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487 Cards in this Set
- Front
- Back
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What is snell’s law of refraction?
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shows the distoration of the angle of light ray when it enters a different medium than the one it is currently in, when a light ray enters water it is refracted (bent), summarized by the equation: n1*sin(theta1) = n2*sin(theta2)
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What are the normal index of refractions for water and the eye?
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water has an index of refraction of 1.33, the normal eye has 1.38
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What are the refractive characteristics of the eye?
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when light travels through a curved surface, the light rays converge on a single point, since an image is made up of a large number of points of light, an image will form where the light rays converge
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What is the focal point of a convex lens?
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found behind the lens, when light hits the convex lens light converges at a spot behind the lengs, called a positive converging lens
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What is the focal point of a concave lens?
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found in front of the lens, when light hits the concave lens light diverges, have to superimpose the light backwards to front of lens to find focal point, has a negative (diverging) lens
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What is focal distance or length (f)?
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it is the distance of the focal point (point of image formation) from the lens, basic unit of focal power is the diopter (D), D = 1/f, 1 D = 1/1 meter (ex: +10 D lens has a f = 10 cm)
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What is focal power?
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focal power = refractive index / focal length
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What is the radius of the cornea, index of refraction and length of the eye?
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radius = 0.66 cm, n = 1.38 and length of eye = 2.4 cm
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What happens in patients with glaucoma?
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have aqueous humor drainage problems, leads to high levels of intraocular pressure that can reduce the blood supply to the eye and eventually damage retinal neurons
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What happens in patients with cataracts?
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have opaque lens, caused by alterations in the composition of the cornea which can significantly reduce their transparency and have serious consequences for visual perception, account for half the cases of blindness in the world
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What controls accommodation of lens?
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the level of curvature of the lens, accommodation leads to an INC in the diameter of the lens, accommodation allows for focusing on near objects and involves the contraction of the ciliary muscle which reduces the tension in the zonule fibers and allows the elasticity of the lens to INC its curvature (parasympathetic innervation)
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What happens to the lens when viewing far objects?
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lens is made relatively thin and lfat and has the least refractive power, the force from the zonule fibers is greater than the eleasticity of the lens and the lens assumes the flatter shape
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How does the ciliary muscle relax the lens?
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occurs when looking at closer obejects, causes relaxation of tension in the zonule fibers, allowing the inherent elasticity of the lens to INC its curvature, accompolished by the sphincter-like contraction of the ciliary muscle, when it contracts the attachment points of the zonule fibers move toward the central axis of the eye reducing the tension on the lens
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What happens during accommodation?
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the edinger-westphal nucleus (responsible for accommodation and papillary light reflex) sends a signal to the ciliary ganglion, via parasympathetics on CN III the ciliary muscles contracts, the zonule fibers relax and the lens round up
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What are some of the optical properties of the eye?
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1. anterior surface of cornea- +48.5 refractive power
2. posterior surface of cornea- -5.9 refractive power 3. anterior surface of lens- +5.0 4. posterior surface of lens- +8.3 5. total (at rest)- ~56 6. maximal accommodation- ~69 because the total lens power can be INC to about 25-26 |
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What structure is primarily responsible for refractive power?
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anterior curvature of the cornea but the lens curvature can be modified as well
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What happens to accommodation with age?
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it deteriorates with age, at some point, usually during middle age, the accommodative ability of the eye is so reduced that near vision tasks like reading become difficult, this is called presbyopia, caused by a loss of lenses elasticity therefore max curvature the lens can achieve when the ciliary muscle contracts is gradually reduced
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How is presbyopia corrected?
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conbex lenses for near-vision tasks
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What is myopia?
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is nearsightedness, cannot bring distant objects into clear focus, can be caused by the corneal surface being too curved or by the eye being too long, with the lens as flat as it can be, the image of distant objects focuses in front of the retina, corrected with concave lens
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What is hyperopia?
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is farsightedness, can be caused by the eyeball being too short or the refracting system too weak, even with lens completely rounded up the image is out of focus on the retinal surface (focusing at some point behind it), corrected with convex lens
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What is emmetropia?
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have normal vision
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What is astigmatism?
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it is a refractive error, vision is blurred due to irregular curvature of the cornea or lens, the cornea may not be perfectly round but may have a football shape
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What is the optic disk?
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the region where the ganglion cell axons leave the retina to form the optic nerve, it is also characterized by the entrance and exit of the ophthalmic arteries and veins that supply the retina, contains the blind spot (has no photoreceptors)
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What is the macula lutea?
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it can be seen as a distinct area at the center of the optical axis, is the region of the retina that has the highest visual acuity, yellow spot that contains yellow pigment (xanthophyll), high concentration of cones
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What is the fovea?
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is a depression or pit about 1.5 mm in diameter that lies at the center of the macula, area of greatest visual acuity
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From proximal to distal what are the different layers of the retina?
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nerve fiber layer -> ganglion cell layer (have ganglion cells) -> inner plexiform layer -> inner nuclear layer (has amacrine, horizontal and bipolar cells) -> outer plexiform layer -> outer nuclear layer -> photoreceptor outer segments (has rods and cones) -> pigment epithelium
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What are the fibe basic classes of neurons in the retina?
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photoreceptors, bipolar cells, ganglion cells, horizontal cells and amacrine cells, cell bodies are located in the inner and outer nuclear and ganglion cells layers and the processes are in the inner and outer plexiform layer
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What is the retinal pigment epithelium?
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the outer (distal) wall of the retina, is a thin, melanin-containing structure that reduces backscattering of the light that enters the eye and plays a critical role in maintaining the phototransduction machinery of retinal photoreceptors
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What are the different types of photoreceptors?
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rods and cones, have an outer segment adjacent to epithelial layer and has membraouns light sensitive disks and an inner segment that contains the cell nucleus and gives rise to synaptic terminals that contact bipolar or horizontal cells
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What is the three neuron chain?
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photoreceptor cell -> bipolar cell -> ganglion cell, most direct pathway of info flow from photoreceptors to the optic nerve, light is absorbed in the outer segment of the photoreceptor initiaiting a cascade of events (phototransduction)
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Describe the synpases at the different layers.
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photoreceptors cell bodies are found in the outer nuclear layer, synapse with bipolar cells at the outer plexiform layer, bipolar cell cell bodies are in the inner nuclear layer, axons synapse with ganglion cells at the inner plexiform layer, axons of ganglion cells form the optic nerve
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Describe where the horizontal and amacrine cells cell bodies and processes are.
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have cell bodies in the inner nuclear layer, horizontal processes are in outer plexiform layer while the amacrine processes are in the inner plexiform layer
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What does the horizontal cell do?
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enable lateral interactions between photoreceptors and bipolar cells that are thought to maintain the visual system’s sensitivity to contrast over a wide range of light intensities (luminance)
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What do the amacrine cells do?
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are postsynaptic to bipolar cell terminals and presynaptic to the dendrites of ganglion cells, many classes available, one class has a role in the pathway that transmits info from rod photoreceptors to retinal ganglion cells, another class is critical for generating the direction-selective responses exhibited by a specialized subset of ganglion cells
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Describe the distribution of rods and cones in the retina.
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cones are present at a low density throughout the retina with a sharp peak in the center of the fovea (foveola, also has a one-to-one relationship with bipolar and ganglion cells), rods are present at high density throughout most of the retina with a sharp decline in the fovea, rods are absent in the foveola, the INC density of cones in the fobea is accompanied by a striking reducing in the diameter of their outer segments, there is also a lack of receptors at the optic disk where retinal ganglion cell axons gather to exit the retina
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What is the approx. number of rods and cones in the retina?
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90 million rods and 4.5 million cones
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What is the capillary supply to the foveola?
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there is a lack of capillaries here, the overlying cellular layers and blood vessels are displaced so that light is subjected to a minmum of scattering before photons strike the outer segments of the cones in the foveola, this avascular region of the fovea is thus dependent on the underlying choroid and pigment epithelium for oxygenation and metabolic substances
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Describe the range of luminance values over which the visual system operates.
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has an exceptional range, at the lowest levels of illumination only rods are activated, cones begin to contribute to perception at about the level of starlight and are the only receptors that function under relatively bright conditions
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At what luminance is their best acuity? other levels of acuity?
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best acuity from 2-4 (found in indoor lighting), no color vision and poor acuity occurs at ~< -3.5, good color vision occurs when rod saturation begins at ~> 0.5, damage beings at ~ 8
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What is scotopic vision?
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occurs at the lowest levels of illumination, where only ythe rods are activated
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What is photopic vision?
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as illumination level INC, cones become more and more dominant in determining what is seen, in this type of vision the contribution of rods to vision drops out nearly entirely because their response to light saturates and all their membrane channels are closed, this is the vision associated with normal indoor lighting vision
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What is mesopic vision?
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occurs in levels of light at which both rods and cones contribute, assocated with starlight and moonlight
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Describe the structure of the rods and cones.
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are generally similar in structure, have disks and cytoplasmic space in the outer segment with a plasma membrane covering the cell, mito and nucleus in the inner segment, cones are smaller and have a triangular shape in the arrangement of their disks
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Describe the shedding and recycling of photoreceptor disks in the retinal pigment epithelium.
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the life span of photoreceptor disks is about 12 days, they migrate from the proximal portion of the outer segment distally towards the retinal epithelium, expended disks are shed from the outer segment and phagocytosed into the retinal epithelium where it will be biochemically cycled back to newborn photoreceptor disks
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Describe the differential responses of rods and cones to light flashes.
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for moderate to long flashes, the rod response continues for more than 600 ms (for the rods the greater the intensity of light, the longer the response), whereas even for the brightest flashes tested the cone response returns to baseline in roughly 200 ms (duration of response is independent of intensity of light flash)
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Why is there a difference in the response between rods and cones to different intensities of light flashes?
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because of the level of signal conversion between the two, each rod bipolar cell synpases from 15-30 rods, additional convergence occurs at downstream sites in the rod pathway, in the center of the fovea, a single cone contacts a single bipolar cell and this bipolar cell contacts a single ganglion cell, convergence makes the rod system a better detector of light because small signals from many rods are pooled to generate a large response, one-to one relationship good for acuity
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What happens to membrane potential of rods and cones when hit with a light flash of varying intensities?
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it hyperpolarizes with the level of hyperpolarization dependent on the intensity of the light flash, the most intense flash response produces a response of -65 mV which is at a saturated level
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What role of cyclic GMP-gated channels in the outer segment membrane play in phototransduction?
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are responsible for the light-induced changes in the electrical activity of photoreceptors
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Describe the process of phototransduction in the dark.
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in the dark, cGMP binds to the Na+ permeable channels in the plasma membrane of the outer segment, keeping them open and allowing Na+ and other cations to enter the outer segment depolarizing the cell, Na+ influx and K+ efflux occurs leading to depolarization
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Describe the process of phototransduction in the light.
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absorption of photons leads to a DEC in cGMP levels closing the cation channels and resulting in receptor hyperpolarization, there is a reduce Na+ influx but still K+ efflux leading to hyperpolarization
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How does hyperpolarization cause a change in transmitter release?
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in the dark, photoreceptors are relatively depolarized and the number of Ca channels (and thus transmitter release) in the membrane is high, in light Ca channels close and less transmitter is released
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How is the [cGMP] reduced when a photon hits a rod or cone?
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the photon hits retinal which is coupled to one of several opsins (which tune the molecules absorption of light to a particular region of the spectrum), when a photon hits retinal it changes it from a cis to trans form, this activates transducin which activates PDE which hydrolyzes cGMP, leads to a huge signal amplification
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What role does intracellular Ca2+ play in light adaptation?
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Ca2+ in the outer segment inhibits the activity of guanylate cyclase (which makes cGMP) and activates rhodopsin kinase (which phosphorylates rhodopsin and blocks its ability to activate transducin), also reduces the affinity of cGMP-gated channels for cGMP, light induced closure of channels in the outer segment membrane leads to a reduction in Ca2+ concentration and a reduction in Ca2+0mediated inhibition of these elements of the cascade, the potoreceptor’s sensitivity to photon capture is reduced
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What is the time course differences between cones and rods in dark adaptation?
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cone adaptation (from 0 – 10 mins in dark) occurs before rod adaptation does (from 10 – 45 mins)
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Describe the absorption spectra of rods and cones.
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cones have 3 different pigments for cones (short, medium and long frequencies), 1 for rods
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Describe the genetics of cone pigments and color vision.
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there are substantial differences in the aa sequences of rhodopsin and the S-cone pigment (blue), and between the S and M-cone (green) pigments, but there aer only a few aa differences that separate the M and L cone (red) pigment sequences
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What is protanopia?
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color vision that has a loss of long wavelength sensitive cones, a severe type of color vision deficiency caused by the complete absence of red retinal photoreceptors, it is a form of dichromatism in which red appears dark. It is hereditary, sex-linked, and present in 1% of all males
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What is deuteranopia?
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color vision that has a loss of medium wavelength sensitive cones, deficiency in which the green retinal photoreceptors are absent, moderately affecting red-green hue discrimination. It is a form of dichromatism in which there are only two cone pigments present. It is likewise hereditary, sex-linked, and present in 1% of all males
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What is the perception of light intensity dependent on?
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on the context and background
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What are the two types of ganglion cells?
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1. on-center-turning on a spot of light in the receptive field of this center produces a burst of APs, INC their discharge rate to luminance increments in the receptive field center, if exposed to darkness, then there are no APs in the time period of dark exposure but there is a sudden INC in AP firing after stimulus is removed
2. off-center-tunring on a spot of light in the receptive field reduces the rate of discharge and when the spot of light is turned off, the cell responds with a burst of APs, INC their discharge rate to luminance decrements in the receptive field center, if exposed to light, then there are no APs in the time period of light exposure but there is a sudden INC in AP firing after stimulus is removed |
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What happens if an on center that has an activated center has its surrounding also hit with ligt?
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reduces the AP discharge rate
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What happens to the rate of discharge of an on-center cell to a spot of light as a function of distance from the center?
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maximally stimulated with light hits only the center, starts to DEC as only part of the light hits the center and the other part of the light hits the surrounding, is at a minimal level when the light hits only the surrounding, reaches the 0 level when the light hits neither the center or surrounding
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What happens to the rate of discharge when on-center ganglion cell approaches a light-dark edge?
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rate of firing is dependent on how many surrounding and center portions are hit with light
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Describe the circuitry for receptive field center responses.
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when light hits the cone photoreceptive disks causes hyperpolarization and it releases glutamate (a transmitter) that binds to mGluR6 recetpors of on0-center bipolar cells (inhibiting it causing depolarization) and AMPA kainite receptors on off-center bipolar cells (stimulating it causing hyperpolarization), these changes then release glutamate which stimulate the on-center and off center ganglion cells respectively
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What is depth of focus?
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pupillary constriction INC depth of focus, pupillary dilation DEC depth of focus
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What are the three methods used by the visual system in depth perception?
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1. relative object size
2. moving parallax-when you move your head from side to side, objects that are close to you move quickly across your retina, far object move very little, your brain takes this info and can tell roughly how far away something is from you 3. stereopsis |
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What is stereopsis?
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each eye receives a slightly different image of an object on its retina because each eye is 2 inches apart, the difference is greater when an object is close to your eyes, images on the retina become more similar the farther they are from your eyes
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What is the importance of the lateral genicular nucleus (LGN)?
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target of the optic tract axons in the diencephalon, is the gateway to the cortex, optic tract axons synapse here and neurons here send their axons to the cerebral cortex via the internal capsule (via the optic radiation)
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What is the pretectum?
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is coordinating center in the pupillary light reflex, a collection of neurons that lies between the thalamus and midbrain, the initial component of the papillary light reflex pathway is a bilateral projection from the retina to the pretectum, these neurons then project to the Edinger-Westphal nucleus
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What is the purpose of the Edinger-Westphal nucleus?
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contains preganglionic parasympathetic neurons that send their axons via CN III to terminate on neurons in the ciliary ganglion, neurons here innervate the constrictor muscles of the iris which DEC the diameter of the pupil when active
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What is the important of the hypothalamus in retinal ganglion cells?
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important for circadian rhythm, retinohypothalamic pathway is the route by which variation in light levels influences the broad spectrum of visceral functions that are entrained to the day/night cycle
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What is the importance of the superior colliculus?
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important in visual reflexes, coordinates head and eye movements to visual targets
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Describe the pathways connecting the eye and brain.
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retinal ganglion cells -> optic nerve -> optic chiasm -> lateral geniculate nucleus (-> optic radiation -> striate cortex), superior colliculus, pretectum or hypothalamus
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Describe how parasympathetic innervation controls the size of the pupils.
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there are bilateral projections from the retina that go to the pretectum, these give off projections that enter both Edinger-Westphal nucleus (preganglionic parasympathetic), even if only one eye is shined with light, neurons here terminate in the ciliary ganglion and neurons in the ciliary ganglion innervate the papillary constrictor muscles
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Describe how sympathetic innervation causes dilation of the pupils.
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the hypothalamus innervates spinal nerves T1-T3 which supply the sympathetic fibers to the internal carotid plexus via the superior cervical sympathetic ganglion, sympathetics on the internal carotid artery enter the brain and give sympathetics to the ophthalmic division of CN V, V1 gives off a long ciliary nerve branch (which has sympathetics on it) or enters the ciliary ganglion and gives off short ciliary nerve branches (which also have sympathetics) and innervates the pupillodilator muscles of the iris which can cause dilation of the pupils
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What causes blindsight?
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occurs following damage of the visual cortex or lesions of the pathways to the visual cortex (geniculo-striate pathway), the subcortical pathways (to the midbrain, superior colliculus) remain and mediate blindsight, when a patient is presented with visual stimuli, such patients deny seeing anything but asked to gues where in the visual field the stimulus might be they are often able to locate it accurately
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Describe the visual field projection onto the right and left retina.
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there are two retinas, temporal and nasal, points in the binocular visual field on the left and right side fall on the nasal retina of the left and right eye respectively and the temporal retina of the right and left eye respectively, points in the left and right visual field outside of the binocular visual field project to the nasal retina of the left and right eye only, therefore the only time that projections enter the temporal retinal is when the left and right eye observe something in the right and left binocular visual field respectively
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Which type of retina crosses at the optic chiasm?
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only the retinal ganglion cells in the nasal retina cross at the optic chiasm, as a result info from the left visual field is carried in the right optic tract and info from the right visual field is carried in the left optic tract
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When does information from the right and left eye mix?
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does not happen until the level of the visual cortex (in the striate cortex), info from the right and left eye remains segregated in the LGN, individual geniculate neurons are strictly monocular, driven either by the left or right eye but not by both
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What is the basis of steropsis?
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binocular disparities are thought to be the basis for it, when the eyes are fixed on a point, points that lie beyond the plane of fixation or in front of the point of fixation project to non-corresponding points on the two retinas, when these disparities are small the images are fused and the disparity is interpreted as small differences in depth, when disparities are large double vision occurs
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What is the course of the optic radiation from the LGN to the striate cortex?
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from the LGN axons carrying info about the superior portion of the visual field (inferior retinal quadrants) sweep around the lateral horn of the ventricle in the temporal loop (Meyer’s loop) before reaching the occipital lobe (to the lingual gyrus), those carrying info about the inferior portion of the visual field travel in the parietal lobe (to the cuneus)
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Describe the representation of the fovea in the retinotopic projection to visual cortex.
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the fovea is greatly over-represented in the retinotopic projection to visual cortex, found on the posterior portion of the brains at the left and right calcarine fissure, the area of central vision (fovea) is represented over a disproportionately large part of the caudal portion of the lobe, whereas peripheral vision is represented more anteriorly
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Describe the location of some additional secondary visual cortex areas.
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V1 (primary visual cortex) is found posterior-medial aspect of the occipital lobe, there are also additional visual areas surrounding it (V2, V3, V4 (surrounding V1 on the medial aspect) VP (ventral posterior), MT (middle temporal) and MST (medial superior temporal area)
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What are the different layers in the visual cortex?
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there are 6 principal cellular layers that differ in cell packing density, cellular morphology and connections, layer 4 has A, B and C subdivisions
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Where are pyramidal cells located?
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pyramidal cells (which have prominent apical and basilar dendrites) are the most numerous cell type in the neocortex, found in all cell layers except 4C
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What is located in 4C?
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is dominated by spiny stellate neurons whose dendrites are confined to this layer
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Where do lateral (laminar) geniculate axons terminate most heavily?
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in 4C and 4A layers with less dense projections to layers 1, 2/3 and 6, terminations in 2/3 are patchy
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Describe the interlaminar connections between the different layers in the visual cortex.
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neurons in layer 4C give rise to axons that terminate in more superficial layers (4B and 2/3), axons of layer 2/3 neurons terminate heavily in layer 5, axons of layer 6 neurons terminate in layer 4C
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Where do connections with extrastriate cortex arise from?
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layers 2/3 and 4B, are ascending pathways
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Where do descending projections to the lateral geniculate nucleus and superior colliculus arise from?
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lateral geniculate from layer 6 neurons while those projecting to the superior colliculus reside in layer 5
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What do the circular retinal ganglion cells receptive fields form?
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several circular RGC receptive fields combine to form elongated fields on individual neurons in cortex, the simplest possible hypothetical connections by which synaptic excitation from several on-center cells converging on a single cell in visual cortex could result in a simple receptive field
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What role do slit detectors, line detectors and edge detectors in visual cortex have?
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receptor fields are organized to provide information about lines and borders, the left cell is most effectively activated by a slit of light in the center (slit detector), the middle cell by a dar bar in the center (line detector) and the right cell by an edge with dark on the left (edge detector)
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How does stimulus orientation affect neuron activation in visual cortex?
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neurons in the primary visual cortex respond selectively to oriented edges, neurons in the primary visual cortex typically respond vigorously to a bar of light oriented at a particular angel and less strongly to other orientations
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How are the orientation preferences in the visual cortex mapped?
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by using color coding to specify a specific orientation and color coding specific parts of the visual cortex to the orientation preferred there, colors indicate the average preferred orientation of columns at a given location
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Explain how circuitry is used in explaining red-green sensitivity of distinct ganglion cells.
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the green-sensitive ganglion cells receives excitatory input form the green sensitive cone and inhibitory input form the red sensitive cone, the red sensitive ganglion cell input is the opposite, the antagonistic interaction means that the perception of one color is associated with depression of sensitivity to the other color in the pair
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What are the different types of ganglion cells?
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1. P-have smaller cell bodies and dendritic fields, important in spatial color, terminate in 4C-beta
2. M-have large diameter cell bodies and large dendritic fields, important in motion, terminate in layer 4C-alpha 3. K-have small cell bodies and intermediate size dendritic fields, terminate in 2/3 |
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Describe the columnar organization of the striate cortex.
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shows that right eye and left eye inputs are still segregated in layer 4, the striate cortex is organized into intersecting sheets of cells, one set of sheets representing progressively changing optimum stimulus orientation and the other an alternation of dominance of input of left and right eyes, right half of the retina of both eyes projects to the right hemisphere and inputs from correspoinding points of the two retinae converge on single cells within the striate cortex
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What are some different types of visual field defects?
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1. lesion on the right optic nerve-loss of vision in the right eye
2. lesion at optic chiasm-bitemporal hemianopsia 3. lesion of right optic tract-left homonymous hemianopsia (loss of left temporal of left eye and left nasal or right eye) 4. lesion of right optic radiation-left superior quadrantanopsia (loss of superior temporal of left eye and superior nasal of right eye) 5. lesion of right striate cortex-left homonymous hemianopsia with macular sparring |
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What are anopsias? scotomas
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anopsias are large visual defects, scotomas are smaller visual defects
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What is the somatic sensory system?
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takes sensory information from the body into the CNS, there are two pathways to the thalamus and cortex (TVP and pain and temperature)
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Describe the pathway of touch, vibration and proprioception (TVP).
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TVP is via the dorsal columns of the spinal cord or trigeminal ganglia, via the medial lemniscus through the medulla, pons and midbrain to the thalamus, through the internal capsule to the primary somatic sensory system, axons from the spinal cord synapse at the gracilis (midline, lower limb) and cuneatus nucleus (lateral to gracilis, upper limb) then synapse at the medulla to enter the middle lemniscus
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Describe the pathway of pain and temperature (P&T).
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via anterolateral system (AKA spinothalamic tract) through the medulla, pons and midbrain to the thalamus through the internal capsule to the primary somatic sensory system, cross at the spinal cord at the level it enters
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What are the primary afferent neurons?
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encode a mechanical, chemical or thermal stimulus into APs that are conducted into the spinal cord, they are similar for TVP and P&T
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Where is the receptor of the primary afferent neurons?
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in periphery (skin, muscle, blood vessels), often inserted into a specialized capsule important in encoding the stimulus, receptor specializations in the skin include mechanoreceptors (Meissner’s, Ruffini’s, and Pacinian corpuscles, Merkels disks)
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Where is the cell body of the primary afferent neurons?
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found in the dorsal root ganglia (AKA spinal ganglia) or brainstem ganglia, no dendrites, normally there is no synaptic input to the cell body in the ganglia, DRG has no synapses, APs pass right through usually, very different from autonomic ganglia
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Where are the terminals of the primary afferent neurons?
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found in the spinal cord, some connections in the cord at the level of entry, some branches go up and down the cord and synapse at different levels
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Describe the size of the components of the primary afferent neurons.
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the cell body is 50 microM across, the axon is 5 microM across, 30 cm into the cord and 120 cm into the body
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What are some properties of A fibers?
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they are large diameter fibers and conduct fast, A-alpha conduct faster than A-delta, A-beta are the fastest and for TVP and are found in mechanoreceptors, A-delta are the slow and found in P&T as free nerve endings
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What are some properties of C fibers?
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are small diameter and conduct slowly, are free nerve endings for pain, temperature and itch, C are slowest
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Describe the transduction in a mechanosensory afferent.
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little is known about how these neurons transducer stimuli into APs, channels that open in response to stretch, temperature and chemicals is known, deformation of the capsule leads to a stretching of the membrane of the afferent fiber INCing the probability of opening stretch-sensitive cation channels in the membrane
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What is a generator potential?
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a stimulus that results in a change in membrane permeability and a depolarization, if sufficiently depolarized an AP is generated and propagates to central targets
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What are the different receptor responses?
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receptors have individual responses to a stimuli, slowly adapting mechanoreceptors continue responding to a stimulus whereas rapidly adapting receptors respond only at the onset of stimulation, these functional differences allow the mechanoreceptors to provide information about the static (via slowly adapting) and dynamic (via rapidly adapting) qualities of a stimulus
***note...meissner's and pacinian are inhibited (don't fire spikes) when stimulated, rufini and merkels disk are stimulated when a stimulus hits |
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What are rapidly adapting afferents good for?
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are thought to be particularly effective in conveying info about changes in ongoing stimulation such as those produced by stimulus movement
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What are slowly adapting afferents good for?
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suited to provide info abouth the spatial attributes of the stimulus such as size and shape
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What is the receptive field of a stimulus?
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the receptive field of a somatic sensory neurons is the area of skin within which a tactile stimulus evokes a sensory response, the area of the skin surface over which stimulation results in a significant change in the rate of APs
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What determines the size of the receptive field?
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largely a function of the branching characteristics of the afferent within the skin, smaller arboizations (formed by more branching) result in smaller receptive fields
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What is two-point discrimination?
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is the minimum interstimulus distance required to perceive two simulateneously applied stimuli as distinct, the ability to distinguish one or two tactile stimuli varies over the body, at the finger tips and lower face is ~ 2mm, at the thigh and leg ~ 40 mm, all the thalamus knows is that a neuron is firing APs
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what is a dermatome?
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territory innervated by each spinal nerve, each spinal nerve innervates a dermatome (which can be revealed during herpes zoster flares), map shows sharp clear boundaries but in reality they are not distinct, overlap is more extensive for TVP than for P&T
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What is haptics?
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active tactile exploration, complete characterization of a stimulus requires varying the stimulus, this is accomplished by manipulation to activate multiple primary afferent neurons and requires dynamic interactions between motor and sensory systems
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what are the two different TVP pathways?
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1. via dorsal column (medial lemniscus)-info from the body and back of head is collected by neurons with cell bodies in the spinal ganglia and enter cord via the dorsal roots
2. trigeminal (trigeminothalamic system)-info from the face (including teeth) is collected by neurons with cell bodies in trigeminal ganglion, enter brainstem via trigeminal (CN V) |
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What happens to axons that enter the cord and branch?
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1. Pathway A-forms the dorsal columns of the spinal cord and eventually forms the medial lemniscus pathway, lower limbs are medial gracile tracts while upper limbs, trunk and neck are lateral cuneate tracts, synapse at the gracilis and cuneateus nuclei in the medulla
2. Pathway B-branches enter the dorsal horn at multiple levels (up and down) and synapse (can be all over the place depending on who you believe, includes: Rexed’s laminae III-IV, Rexed’s IV, Rexed’s VI, Rexed’s laminae VII-VIII), important in spinal reflexes |
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What happens to the second-order neurons after synapsing at the dorsal column nuclei for the middle lemniscus pathwya?
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send their axons to the somatic sensory portion of the thalamus as internal arcuate fibers, these cross the midline of the medulla and then form a dorosventrally elongated tract called the medial lemniscus (not a simple pass through, info is mixed, descending inputs added and processing), as they pass through pons and midbrain rotate 90 degrees laterally so that the fibers representing the upper body are eventually located in the medial portion of the tract and those representing the lower body are in the lateral portion
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Where do the medial lemniscus axons synapse?
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synapse with the thalamic neurons located in the ventral posterior lateral nucleus (VPL), form third order neurons that send their axons via the internal capsule to terminate in the postcentral gyrus, lower body axons from the gracilis nucleus synapse at the postcentral gyrus but also at the posterior paracentral lobule
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Describe the VPL nucleus.
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contains a complete representation of the somatic sensory periphery, the thalamus knows everything
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What do lesions of the dorsal columns cause?
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have a modest effect on ability to perform simple tactile tasks, loss of some proprioception and ability to detect direction and speed of a stimulus
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Describe the trigeminothalamic pathway.
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mechanoreceptor info from the face is conveyed by first order neurons in CN V, synapse at principal nucleus and form central processes of trigeminal ganglion cells form the sensory roots of CN V and enter the brainstem at the level of the pons to terminate on neurons in the trigeminal brainstem complex
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What are the components of the trigeminal brainstem complex?
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1. principal nucleus-afferents conveying info from low-threshold cutaneous mechanoreceptors (primary afferent axons) terminate in the principal nucleus, corresponds to the dorsal column nuclei that relay mechanosensory info from the rest of the body
2. spinal nucleus-contains neurons that are sensitive to pain, temperature, and coarse touch |
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Describe the course of the second order neurons of the trigeminothalamic pathway.
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give off axons that cross the midline (after synapsing at principal nucleus) and ascend to the ventral posterior medial (VPM) nucleus of the thalamus by way of the trigeminothalamic tract (trigeminal lemniscus) (axons join the medial lemniscus), neurons in the VPM send their axons to cortical areas SI and SII
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What artery supplies the trunk and leg of the homunculus? arms and face?
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turnk and legs-anterior cerebral artery, arms and face-middle cerebral artery
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Describe the axons in the somatic sensory cortex.
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neurons in primary sensory cortex project to the adjacent secondary somatosensory cortex (SII), axons from SII project to limbic structures, amygdale and hippocampus, these projections mediate functions (tactile, learning, memory)
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What are the descending pathways?
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projections from sensory cortex down to thalamus, brainstem and spinal cord modulate the flow of sensory info, the descending axons outnumber the ascending axons, modulate the ascending flow of info
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What are nociceptors?
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a special class of primary afferent neurons with their cell bodies in the dorsal root ganglia, are unspecialized nerve cell endings that initiate the sensation of pain, composed of C (unmyelinated) or A-delta (lightly myelinated) fibers which conduct relatively slowly (small diameter axons, small diameter cell bodies), several markers, notably capsaicin receptor channels (vanilloid receptors, cloned as VR1), have been proposed
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What are the faster-conducting A-delta nociceptors best at responding to?
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dangerously intense mechanical or to both intense mechanical and thermal stimuli
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What do the majority of unmyelinated C-fiber nociceptors tend to respond to?
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thermal, mechanical and chemical stimuli and are therefore said to be polymodal
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What are the three types of nociceptive afferents supplying the skin?
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A-delta mechanosensitive nociceptors, A-delta mechanothermal nociceptors and polymodal nociceptors (C fibers)
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What happens to nociceptors and non-nociceptive thermoreceptors during a stimulus in the painful range?
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in the painful stimulus range, the axons of thermoreceptors fire APs at the same rate as at lower temperatures, the number and frequency of AP discharge in nociceptive axons continues to INC, nociceptros only fire when the strength of the stimulus reaches high levels
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Do large diameter somatic sensory afferents produce pain when given a large stimulus?
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stimulation at any frequency in humans does not produce sensations that are described as painful, only stimulation of high threshold nociceptors results in pain, stimulation of low threshold mechanoreceptors, thermoreceptors, etc results in a non-painful sensation (intense but not painful)
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What the two categories of pain perception?
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1. sharp first pain-via A-delta fibers, are mechanothermal sensitive, characterized as a sharpt pin
2. delayed second pain-via C fibers, are polymodal (have several kinds of painful stimuli), are delayed, diffuse, and longer lasting sensations, duller longer lasting sensation of pain these two can be anesthiszed separately showing that A-delta is for first and C is for 2nd |
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Describe the transduction of nociceptive signals.
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mechanical, thermal and chemical (pH and neurotransmitter) can excite nociceptors, little is known about the detailed mechanisms but current work is focusing on a family of ion channels called TRP for transient receptor potential
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What are the different types of TRP channels?
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lots of them, there is TRPV1 (AKA VR1, the vanilloid or capsaicin receptor), TRPV2 (AKA VRL-1), these and their fellow TRPs have a variety of functions including temperature and pain sensation
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Describe TRPV1.
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is a capsaicin receptor, are nonselective cation channels opened by heat, low pH, and capsaicin (the hot in hot peppers), mice without VR1 have impaired sensitivity to pain, normal function is unclear, allows for Na+ and Ca2+ to enter
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Describe the central pain pathways of the body and head (but not face).
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P&T afferents enter the cord as do TVP neurons, branch into ascending and descending collaterals forming dorsolateral tract of Lissauer, afferents synapse on dorsal horn neurons (can run up and down for one or two spinal cord segments before synapsing), axons from these secondary neurons (which interact with Rexed’s laminae 1 and 5) cross (at the level it enters the spinal cord) and form the anterolateral tract (spinothalamic tract) to thalamus
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Compare the central pain pathways for TVP and P&T.
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TVP and P&T are on opposite sides below the medulla, are on the same side above medulla
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What happens in a lesion on one side of the spinal cord?
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will result in reduced TVP on the ipsilateral side and reduced pain and temperature sensation on the contralateral side (called dissociated sensory loss)
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Where do the sensory afferents enter the spinal cord and synapse for P&T from upper body (excluding face)? from lower body?
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from upper body synapses at the dorsal horn of the cervical spinal cord, from lower body synpases at the dorsal horn of the lumbar spinal cord
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Describe the central pain pathway for the face.
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P&T from the face come via CN V, have DRG near the pons where the axons initially enter the brainstem, axons then descend (via the spinal trigeminal tract) and synapse at two subdivisions of the spinal trigeminal complex (pars interpolaris and pars caudalis)
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What happens to the axons after they synaps at the pars of the spinal trigeminal complex?
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second order neurons cross the midline, form the trigemino-thalamic tract and terminate in a variety of targets in the brainstem and thalamus, targets gropued into those that mediate the discriminative aspects of pain and those that mediate the affective/motivational aspects
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What is thought to mediate the discriminative aspects of pain?
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thought to be mediated by projections to the contralateral ventral posterior medial nucleus and projections form the VPM to primary and secondary somatosensory cortex, mediates location, intensity and quality of noxious stimulation
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What is thought to mediate the affective/motivational aspects of pain?
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mediated by connections to various targets in the reticular formation and midbrain as well as the midline nuclei of the thalamus, which supply the cingulated and insular regions of the cortex, mediates unpleasantness, anxiety and fear assocated with pain
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What does the anterolateral system supply information to?
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to different parts of the brainstem and forebrain that contribute to different aspects of the experience of pain, those that are responsible for the sensory discrimination of pain (which affects ventral posterior nucleus which affects somatosensory cortex (S1 and S2) and those that are responsible for the affective and motivational responses to pain (amygdala, hypothalamus, periaquiductal grey, superior colliculus, reticular formation and midline thalamic nuclei (which affects anterior cingulated cortex and insular cortex))
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Describe visceral pain.
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some dorsal horn neurons receive input from visceral and cutaneous nociceptors that are referred to another part of the body, some second order nociceptive neurons send their axons via the dorsal column (medial lemniscus pathway) to the ventral posterior nuclear complex of the thalamus, this sends an axons to the insular cortex for processing, ablation of this pathway can reduce pain associated with visceral cancers of abdomen and pelvis
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What is hyperalgesia?
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INC sensitivity to a painful stimulus, following a painful stimulus associated with tissue damage, stimuli in the area of the injury and the surrounding region that would ordinarily be perceived as slightly painful are perceived as significantly more so (ex: INC sensitivity to temp after sunburn)
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What is allodynia?
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previously nonpainful stimuli now cause pain, these can arise (typically following injury or pathology) by peripheral and by central mechanisms, can outlast the pain of the original stimulus by several hours, these once innocuous stimuli activate second-order neurons in the dorsal horn that receive nociceptive inputs giving rise to a sensation of pain
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What is peripheral sensitization?
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results from the interaction of nociceptors with the inflammatory soup of substances released when tissue is damaged, reacts with receptors or ion channels and augments the response of the nociceptive fibers, can have direct or indirect effects on the nerves, nociceptive neurons themselves can release sensitizing compounds
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How does the inflammatory reponse to tissue damage act as peripheral sensitization?
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substances released by damaged tissues augment the reponse of nociceptive fibers, in addition, electrical activation of nociceptors causes the release of peptides and neurotransmitters that further contribute to the inflammatory response
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What are some compounds released during peripheral sensitization?
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proteons, arachidonic acid, bradykinin, histamine, serotonin, prostaglandins, ATP, adenosine, nerve growth factor, CGRP, substance P
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Describe prostaglandins as potent peripheral sensitizers.
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bind to G protein coupled receptors that INC levels of cAMP within nociceptors, also reduce the threshold depolarization of TTX-resistant Na+ channels that are expressed in nociceptors, also release peptides and neurotransmitters which further contribute to the inflammatory response
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Describe cyclooxygenase inhibitors as peripheral sensitizers.
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they reduce pain by inhibiting prostaglandin synthesis, includes aspirin and other cox-inhibitors
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Describe central sensitization.
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refers to an immediate-onset, activity-dependent INC in the excitability of neurons in the dorsal horn of the spinal cord following high levels of activity in the nociceptive afferents, as a result activity levels in nociceptive afferents that were subthreshold prior to the sensitizing event become sufficient to generate APs in dorsal horn neurons, contributing to an INC in pain sensitivity, is a transcription independent mechanism (windup progressive INC in response by a dorsal horn neuron to repetitive stimulation, Ca2+ influx via NMDAR and Ca2+ channels)
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Give an example of central sensitization.
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following injury, light touch will activate dorsal horn neurons that receive nociceptive input (allodynia)
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What are some transcription dependent mechanisms for central sensitization?
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cytokines promote transcription of COX-2 that makes prostaglandins that INC neuronal activity, thus COX-2 inhibitors work peripherally (on the DRG neurons) and centrally (on the spinal cord neurons)
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What is neuropathic pain?
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a chronic, intensely painful experience that is difficult to treat with conventional analgesic medications, damage to the pain pathways can result in the sensation of pain after the injury has healed, can arise spontaneously or it can be produced by mild stimuli that are common to everyday activity
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How does neuopathic pain present?
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a constant burning sensation interrupted by episodes of shooting, stabbing or electric shocklike jolts, can be disabling and cause psychological stress
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Describe the descending control of pain perception.
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the perception and response to a painful stimulus is not determined solely by the magnitude of the stimulus or activity in the primary afferent nociceptor, it depends on its context, is subject to central modulation, there is a disconnect at several locations including the brainstem and spinal cord
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What are primary afferent nociceptive neurons and what role do they play in descending control of pain perception?
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can’t acutely control the sensitivity of the primary afferent nociceptive neurons (PANNs), descending pathways can control the ability of the PANNs to release their neurotransmitter, descending pathways can control the reponse of the dorsal horn neuron and can control the response of the brainstem and cortical neurons
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What is a mechanism of how the descending systems modulate the transmission of ascending pain signals?
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descending pathways activate neurons in the periaqueductal gray (midbrain), the somatic sensory cortex affects the amygdala, hypothalamus and midbrain periaquductal gray, all three of these can affect parabrachial nucleus, medullary reticular formation, locus coeruleus and raphe nuclei, all 4 of these affect the dorsal horn of the spinal cord which affects the anterolateral system
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How is pain modulated in the dorsal horn?
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in the dorsal horn, activity in the descending pathways inhibits nociceptive activity, several neurotransmitters are important (serotonin and enkephalins), activation of low-threshold mechanorecetpros can also inhibit nociceptive activity
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What do opiods do in pain modulation?
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activation of opioid receptors in periaqueductal gray and in spinal cord reduces pain, activation by endogenous or exogenous opiods
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What is the placebo effect?
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can be observed in a variety of clinical situations, for example, anecdotal evidence is strong that placebos work well on warts, the neurochemical basis of the placebo effect is currently being studied, reduction of pain by a placebo can be blocked by naloxone (a compettive antagonist of opiate receptors), the implication is that the placebo causes the release of endorphins
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What are some important points to remember about pain?
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it is important to get a comprehensive history, pain is often under treated, psychological and emotional aspects are always present, realize the plasticity of the nervous system, consider multimodality treatments
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What is the definition of pain?
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an unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of such damage, or both
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What is acute and chronic pain?
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acute pain is pain associated with say surgical pain, while chronic pains is pain that persists beyond the normal time of healing
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What is nociceptive pain?
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pain that affects nociceptors in the skin, muscle, joints and visceral tissues
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What is neuropathic pain?
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primary lesion or dysfunction in the nervous systems, ex-diabetic neuropathy
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What is sypathetical pain?
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matintained pain-reflex sympathetic dystrophy, triad sensory, autonomic and motor
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What is idiopathic pain?
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poorly understood pain
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What is the first line of analgesics?
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acetaminophen, aspirin/NSAIDs, +/- adjuvants
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What is the 2nd line of analgesics?
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opioids (sustained release or immediate release), +/- NSAIDs and adjuvants
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What are the analgesics for refractory pain?
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spinal/epidural opioids (+/- clonidine and local anesthetics), selective nerve blocks, neuroabiative procedures, ketamine, total sedation
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What are some examples for the major classes of analgesics?
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1. NSAIDs-ibuprofen, naproxen, ketoprofen, Cox 2 inhibitors
2. P-aminophenol- Tylenol 3. opiates-morphine, oxycodone, fentanyl 4. others-Ca+ channel blockers (ziconotide), anticonvulsants, selective serotonin reuptake inhibitors and alpha-agonists |
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What are the pain targets of certain drug classes?
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1. cortex targetd by anxiolytics, hypnotics, opiods, psychostimulats, anticonvulsants
2. thalamus is targeted by SSRI’s and anticonvulsants 3. spinal cord targeted by opioids, adrenergicagonists, SSRI’s and other drugs 4. receptors are blocked by NSAIDs and local anesthetics |
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What are some reasons for under treatment by analgesics?
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fear of narcotics (addiction, side effects, legal issues), misunderstanding of pain physiology, misunderstanding of pharmacology, fear of children
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What is the goal of surgical pain?
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treat pain with fewest side effects, have to treat pain because of pulmonary function, CV function and mobility
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What are the different types of pain scales?
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verbal pain intensity scale, visual analog scale, 0-10 numeric pain intensity scale, faces pain scale
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What are some pharmacological adjuncts?
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steroids, TCAs (tricyclic antidepressants), muscle relaxants, nerve blocks, epidural injections, spinal injections, clonidine, anti-epileptic drugs
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What are some non-pharmacological adjuncts?
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physical therapy, massage, acupuncture, TENS units, biofeedback, psychological/behavioral therapy, patient participation
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Describe the properties of sound waves.
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1. sound waves are longitudinal vibrations, with the axis of translation of vibrating molecules aligned with the direction of propagation, in contrast, ripples on the surface of water are transverse waves
2. as sound propagates there is no movement of matter, particles just oscillate |
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What does the velocity of sound depend on?
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is independent of its wavelength but is influenced by the medium within which it propagates, the denser the medium, the faster the veolocity of propagation, sound propagates about 4 times faster in water compared to air
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What is the Doppler Effect?
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states that the movement of a sound source alters the frequency perceived by a stationary observer
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Is energy required to initiate sound waves?
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YES, as the wave sound propagates it dies out or dissipates
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How is the velocity of sound found?
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wavelength = velocity/frequency, frequency = 1/period (gives pitch), condensation is top of the sound wave curve (maximum peak of pressure) while a rarefaction is the bottom point (minimal peak of pressure)
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What is resonance?
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it is oscillation caused by a sound wave reaching a solid object, the frequency at which an object tends to oscillate depends upon its composition and is called its resonant frequency
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What causes an echo?
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occurs when sound waves in air reach the surface of a fluid or solid, part of the energy is absorbed and part is reflected (the echo)
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How are different tones composed?
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tones are sounds composed of sine waves of as ingle fundamental frequency, simple arithmetic multiples of this frequency is harmonics
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What is sound intensity and how is it expressed?
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it is the loudness of the sound wave, can be expressed in either absolute or relative units, most common absolute measure is the change in pressure variation caused by sound waves (changeP), for relative changes in sound intensity, the decibel of dB scale (logarithmic ratio) is used (more commonly used)
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How are decibels calculated?
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relative sound energy (dB) = 20 log Pt/Pr, where Pt is test pressure and Pr is reference pressure (2 * 10^-4 dynes/cm^2)
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At what different sound intensities produce permanent damage, discomfort etc?
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1. absolute threshold-40 dB
2. conversation-60 dB 3. heavy traffic-80 dB 4. symphony, auto horn at 2 feet-100 dB 5. thunder-120 dB 6. discomfort and pain-140 dB 7. permanent damage-160 dB |
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What are the three parts of the ear?
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1. external ear-pinna, external audotyr meatus and tympanic membrane (joins to the ossicles transmitting movement to it)
2. middle ear-three ossicles (attaches to the oval window and transmits movement from the ossicles to the fluid-filled cochlea) 3. internal ear-cochlea and vestibular apparatus |
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What are the components of the cochlea?
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1. scala tympani-filled with perilymph (which is like a normal EC solution, high Na+, low K+), inferior part
2. scala vestibule-also filled with perilymph, superior part 3. scala media-cochlear duct that contains the basilar membrane, composed of endolymph (normal IC soluction, high K+, low Na+, but K+ is very high), is where the organ of corti is seen, this is where transduction occurs, sound to nerve impulses |
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What allows for changes in fluid pressure in the cochlea?
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possible because both the oval window of the scala vestibuli into which the stapes fits and the round window of the scala vestibule are flexible membranes, pushing the oval window inward causes the round window to bulge into the middle ear cavity
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Do the oval and round window communicate?
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the compartment of the oval window and that of the round window communicate with each other at the helicotrema so that the perilymph in the two compartments is continuous
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What sepearates the scala tympani from the scala vestibule?
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the basilar membrane, which makes up the floor of the scala media, separates the two compartments over much of their length and is set in motion by the pressure waves
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What does movements of the basilar membrane cause?
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creates a shearing force that bends the stereocilia of the hair cells, the pivot point of the basilar membrane is offset from the pivot point of the tectorial membrane so that when the basilar membrane is displaced the tectorial membrane moves across the tops of the hair cells, bending the stereocilia
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What are some characteristics of the hair cells?
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1. they have hundreds of cilia
2. largest of the cilia is referred to as the kinocilia, others are stereociliar that gives axis of polarity 3. as sound is transmitted from outer ear to middle ear to inner ear there are rolling waves of sound along the basilar membrane, this causes the cilia to move in one direction or antoerh 4. there are inner and outer hair cell types |
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Describe the inner hair cells.
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represent about 25% of the total hair cells, represent 95% of afferent nerve projections to the CNS
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Describe the outer hair cells.
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are vast majority of the hair cells (75%), only 5% of afferent nerve projections, heavily innervated by efferent nerves, have actin filaments, have high sensitivity to low frequency sounds, therefore if individual has a loss of sensitivity to low frequency then there must be a defect in the outer hair cells
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What are the two different mechanisms for encoding different frequencies of sound?
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1. mechanical mechanisms-
2. electrical tuning- |
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Describe the mechanical mechanism for the transduction process.
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mechanical properties of the basilar membrane allow for frequency sensitivity, allows for a tonotopic representation (topogracphical mapping of frequency), points responding to high frequencies are at the base of the basilar membrane where it is stiffer (at the start of the basil membrane, narrower), and the points responding to low frequencies are at the apex (at the end of the basilar membrane, helicotrema ,wide)
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Describe the electrical tuning mechanism for encoding different frequencies of found.
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allows for mechanoelectrical transduction mediated by hair cells, when the hair bundle is deflected toward the tallest stereocillium cation selective channels open near the tips of the stereocilia allowing K+ to flow into the hair cell down their electrochemical gradient, the resulting depolarization of the hair cell opens voltage gated Ca2+ channels in the cell soma, allowing Ca2+ entry and release of neurotransmitter onto the nerve endings of the auditory nerve, Ca2+ also activates K+ channels, K+ exits the cell repolarizing the cell, caused by stretching of the hair cells
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Describe the potential changes that occur within an individual hair cell in the cochlea.
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is +80 mV in the scala media and 0 mV in the scala tympani, the hair cell potential faithfully allows the waveform of the stimulating sinusoids for low frequencies, the stereocilia of the hair cells protrude into the endolymph and has an electrical potential of +80 mV relative to perilymph, body of hair cell is in the perilymph allowing for depolarization between the two
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What happens during hyperpolarization of the hair cell?
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hair cell is compressed, K+ channels are closed and does not allow for K+ to enter, if no K+ is present hyperpolarization occurs, there is no AP propagated down to open voltage gated Ca channels and no neurotransmitter is released, so the afferent nerve to the brain is not fired
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What is the ionic basis for electrical resonance in hair cells?
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oscillations fire due to a depolarizing current injection, the intrinsic frequency of these electrical oscillations is different for different hair cells and seems to depend on the location of the hair cell with respect to the basilar membrane, there seems to be a matching of the electrical frequency of the hair cells and the mechanical properties of the basilar membrane (high freq. at the base)
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What are the major ionic currents implicated in electrical oscillations?
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1. cation (potassium) selective channel
2. calcium current 3. calcium-activated potassium current |
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How does the cochlea break down complex sounds?
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the properties of the cochlea and its hair cells detect complex incoming sounds and break these sounds down into simpler frequency components, which are then relayed to the CNS, this process is analogous to a Fourier Transform
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What is a Fourier Transform?
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is a mathematical theorem which allows any complex wave process to be described in terms of the linear sum of a number simple sine waves of appropriate amplitude, frequency and phase, if there are three pure tones present they can be linearly added in various combinations to form more complex sounds
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Describe the innervation of the hair cell.
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individual hair cells in the cochlea synapse on afferent processes of the bipolar spiral ganglion cells (CN VIII or auditory nerve) whose central (axonal) processes project to the cochlear nuclei in the medulla, there are also efferent axons which innervate the individual hair cells (hair cell is postsynaptic to efferent fibers), the function of which is uncertain, but they may be important in providing CNS modulation of auditory input
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Describe the central pathway of the afferent fibers from the auditory nerve.
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they terminate in the dorsal and ventral cochlear nuclei (found on the rostral medulla in the dorsal, posteroventral and anteroventral sides), fibers from these nuclei either cross the midline (at the medulla (?)) to innervate the superior olivary complex or directly ascend in the lateral lemniscus towards the midbrain
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What happens to the fibers which innervate the olivary nuclei?
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some also project to the trapezoid body where they branch and innervate the olivary complex on the other side, therefore at the level of the lateral and medial superior olivary nuclei, input from cochlea of both ears occurs, from here they ascend in the lateral lemnisucs towards the midbrain
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Where do the fibers from the lateral lemniscus terminate?
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most terminate in the inferior colliculus of the midbrain, from here fibers project to the thalamus and terminate in the medial geniculate nucleus
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After synapsing at the medial geniculate nucleus, where do the fibers go?
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neurons project to two areas of the cortex (primary auditory cortex and the secondary or association auditory cortex) in the temporal gyrus
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What information is taken care of by the primary auditory cortex?
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the frequency spectrum of the cochlea of both ears is represented here, this area is important in the discrimination of tonal and sequential sound patterns
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What information is taken care of by the secondary auditory cortex?
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associated with integrating sound information with information from other areas of the cortex and has to do with interpretation of the meaning of particular sounds
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What is tonotopical mapping?
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it is the spatial organization of the cochlea with respect to frequency response characteristics, occurs throughout the auditory pathways all the way to the auditory cortex, the lateral and medial superior olivary nuclei have bilateral receptive fields and may exhibit excitatory and inhibitory effects from one ear to the other
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What two factors are the auditory neurons sensitive to?
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1. time delay-a time delay measuring neuron is capable of detecting difference in stimulus arrival time between the two ears
2. intensity ratios-some neurons are able to measure the ratio of intensity of input from the two ears, these functions are important in sound localization |
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Describe the different types of deafness.
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nerve deafness is caused by a problem in the inner ear (use cochlear implants for treatement), conduction deafness is caused by conduction deficits of sound through the middle ear (use hearing aids for treatment)
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What is the Weber test?
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a test for hearing, compares air transmitted sounds (x) to bone transmitted sounds (y), hit a tuning fork, put fork to jaw and energy transmitted through the jaw and bypasses the middle ear to the inner ear
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How does nerve deafness present during a Weber test?
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as you test low to high frequency, you note that the air conductance drops off, as you test the bone conductance you note it drops off the same way
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How does conduction deafness present during a Weber test?
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air conductance drops off as you test a patient, bone conductance also drops off while low frequency hearing is bad while high frequency hearing is normal
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What is the purpose of the vestibular apparatus?
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primary organ of equilibrium
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What are the components of the semicircular canals?
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1. SACs-include the utricle and saccule, have dense aggregates of hair cells in macula
2. CANALs-anterior, posterior and horizontal components, have dense aggregates of hair cells in ampulla |
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What is the function of the utricle and saccule?
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sensory cells transmit information about head position relative to force of gravity and linear acceleration or deceleration
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What is the function of the canals?
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sensory cells transmit information about motion or rate of rotation of head
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What is the orientation of the semi-circular canals?
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the planes of the two horizontal canals are parallel, the planes of the right anterior and left posterior canals are parallel, the planes of the left anterior and right posterior are parallel
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Describe the vestibular hair cells.
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vestibular hair cells like those of the cochlea, form synapses onto sensory fibers of CN VIII and in some cases also receive efferent input, each hair cell has about 60-100 non-motile cilia, called stereocilia and one longer motile cilium, called a kinocilium, there are two types (I and II), hair cells are presynaptic to afferent fibers, efferent fibers synapse onto hair cells and/or afferent fibers, extending from the top of each hair cell is a single kinocilium and many stereocilia
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Compare the vestibular hair cells to the auditory hair cells.
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unlike the audtory system, vestibular hair cells are more firmly fixed, while the overlying membranes tend to move and bend the cilia bundles, in all cases, the stimulus which activates the hair cells is a shear force on the hair cell bundle
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Where are the sensory cells in the semicircular canals?
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are embedded in a gelatinous capsule that hangs down from the roof of the ampulla and is called the cupula
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Where are the sensory cells in the utricle and saccule (otolith organs)?
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hair cells in the macula are embedded in the otolithic membrane (so called because in it are otoliths (tiny calcium carbonate particles)), otoliths add mass to the membrane making it more sensitive to gravity
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What is the morphological axis of polarity in the transduction process?
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the kinocilium of each hair cell determines a particular morphological axis of polarity, thus it is the position of the kinocilium which dictates which direction of movement a particular hair cell will respond to
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Describe the different movements of the hair cells.
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forces acting on the head result in displacement of the otolithic membrane of the utricular macula, for each of the positions and accelerations due to translational movements, some set of hair cells will be maximally excited, whereas another set will be maximally inhibited, note that head tilts (backward, forward) produce displacements similar to certain accelerations (forward acceleration, deceleration, respectively)
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How do horizontal canals work?
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are paired, work together to provide a bilateral indication of head movement, the axis of hair cells are point in a direction like towards the nose (are almost parallel), if turning to the left, the fluid in the left horizontal canal will flow in the axis of the hair cells and INC firing of the afferent fibers of CN VIII, the fluid in the right horizontal canal moves in the opposite direction and DEC firing
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Describe the hair cells in the utricle.
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Hair cells in the macula of the utricle are arranged in a way that their kinocilia do not face in a single direction, therefore they are not uniformly polarized by movement, respond to tilt or linear acceleration
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Describe the response of the hair cell in the utricle.
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The response of a cell is caused by the bending of hair cells by the gravitational force upon the otolithic membrane as shown in Fig 18. The axes of the hair cells all point toward a single imaginary axis of polarization called the striola. A tilt in any direction depolarizes some cells and hyperpolarizes other cells. This dual signal to the CNS is thought to provide information about relative head position. various tilting changes the respone, may be hyperpolarizaiton or depolarization
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Describe the course of the afferent fibers of the transmission pathway for the vestibular system.
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The afferent fibers of the vestibular system have their cell bodies in the vestibular ganglion (Scarpa's ganglion). The ganglion is divided into two portions, a superior division, which innervates the macula of the utricle, part of the macula of the saccule and the crista of the horizontal and anterior semicircular canals, and an inferior division, which innervates the posterior part of the macula of the saccule and the crista of the posterior semicircular canal. Centrally directed axons from cells in Scarpa’s ganglion join with axons from the spiral ganglion in the cochlea to constitute the VIII cranial nerve.
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Where do vestibular fibers of CN VIII project to?
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project primarily to the medulla and pons, where they terminate among the four nuclei of the vestibular nuclear complex: superior, lateral, medial and inferior vestibular nuclei. Each nucleus has a distinctive set of connections to the periphery or CNS. The lateral vestibular nucleus sends axons into the vestibulospinal tract, which have an influence on alpha and gamma motor neurons that innervate antigravity muscles in the limbs. The inferior vestibular nucleus sends axons which terminate in the cerebellum, an important connection for the cerebellar control of posture. Finally, the superior and medial vestibular nuclei send axons to the oculomotor nuclei of the brainstem (via medial longitudinal fasciculus), where they participate in the vestibulo-oculomotor reflex.
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What is the caloric test for the vestibular system?
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irrigate left ear w/ warm H2O, this causes rightward eye movement, if irrigate left ear with cold H2O this causes leftward eye movement, these are true if brainstem is functioning, if not then obviously brainstem is not working
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What are the chemical senses?
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olfaction, taste, trigeminal chemoreception
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Why is smell important?
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crucial in feeding behavior, social interactions and reproduction
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What is the olfactory epithelium?
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an epithelial sheet that lines the interior of the nose, oderants interact with olfactory receptor nueonrs found here
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What is the olfactory bulb?
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is a laminated structure, act as the point where the axons arising form the receptor cells project to, this structure then in turn directs projections to the pyriform cortex in the temporal lobe as well as to other structures in the forebrain via an axon pathway known as the olfactory tract
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What is the cribriform plate?
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is where the olfactory nerve fibers (filae) project through to get to the olfactory bulb, is vulnerable here, separtes the olfacotyr mucosa from the olfacotyr bulb
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What is rhinorrhea and what can cause it?
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is CSF fistula, can be due to injury or congenital malformation (neural tube defect), diagnosis: glucose test
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Describe the olfactory receptor neurons (ORNs).
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have cilia, give rise to unmyelinated axons at their basal surface that transmit olfactory information centrally, at the apical surface gives rise toa single dendritic process that expands into a knowblike protrusion from which several microvilli (olfactory cilia) extend into a thick layer of mucus, exposed to airborne pollutants, allergens, etc. so subjected to continual damage
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Describe the olfactory nerve axons.
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they project to glomeruli with a large convergence of receptor input onto the dendrites of mitral and tufted cells
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What are mitral cells?
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are the main output of the olfacotyr bulb through the lateral olfactory tract, project directly into the primary olfactory cortex (piriform cortex)
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Describe the input to the cortex.
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the direct input to the cortex is a very unusual feature of a sensory system and may account for the strong emotional context of some odors
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Where do the central projections of the olfactory bulb go?
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projects directly to the cortex -> primary olfactory cortex (piriform foctex, olfacotyr tubercle and entorhinal cortex), these regions further project to the thalamus, orbitofrontal cortex and hypothalamus as well as hippocampus, intimate connections with the limbic system may explain the strong emotional connotation and long-lasting memories of smell
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Describe Bowman’s glands in the olfactory epithelium.
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produce mucus, distributed throughout the olfacotyr epithelium, when the mucus layer becomes thicker as during a cold, olfactory acuity DEC significantly, mucus prevents entry of pathogens as well
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Describe the other cell types in the olfactory epithelium
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are basal and sustentacular cells that detoxify potentially dangerous chemicals, also stem cells
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Describe the turnover of ORNs.
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constant turnover of receptor cells, regenerated every 2-3 weeks from stem cells, entire population is replaced within about 6 weeks
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Describe the binding of odorants.
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water soluble ones bind to receptors on cilia, ORNs have direct access to odorant molecules, olfactory cilia do not have the 9+2 arrangement, generation of receptor potentials in response to odors takes place in cilia of receptor neurons, odorants evoke a large inward (depolarizing) current when applied to the cilia but only a small current when applied to the cell body
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Describe the structure of the odorant receptor genes.
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has seven transmembrane domains plus a variable cell curface region and a cytoplasmic tail that interacts with G-proteins, as many as a throusand genes encode proteins of similar structure and each gene is through to encode a receptor protein that detects a particular set of odorant molecules, has variable and conserved aa parts
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What is the molecular biology of the odorant binding to the odorant receptor?
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odorant binds to receptor and activates Golf, Golf has bounded GTP and activates an adenylate cyclase which turns ATP into cAMP, cAMP binds to Na+/Ca+ channel and opens it allowing Ca2+ and Na+ to enter resulting in depolarization, Ca+ binds to a Ca/Cl channel that allows for Cl- to leave (contributes most of the depolarization)
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How is the receptor potential reduced?
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cAMP is broken down by PDE, Ca binds to calmodulin and binds to the Ca/Cl channel, a Na/Ca exchanger is then activated which brings Na+ in and takes out the Ca+ after reaction
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Describe the development of the olfactory system.
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the region of the olfacotyr placode gives rise to cells that migrate into the forebrain and ultimately reside in the hypothalamus, the entire population of gonadotropin-releasing hormone (GnRH) expressing neurons derives from the periphery
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What happens when the migration of the cells from the olfactory placode is compromised (maybe due to a defect in a cell adhesion molecule)?
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development of the olfacotyr bulb as well as the development of the gonads is disturbed, leads to Kallmann’s syndrome (rare)
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Describe the selectivity of odorant receptor proteins.
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is demonstatred by responses to different combinations of molecularly identified odorants, different receptors respond differently to different combinations of odorants
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Compare the interneurons in retina and olfactory bulb.
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although these regions process distinctly different types of sensory information, the overall similarity of their organization and the detailed similarity of some of their local circuits indicates conserved principles in the neural mechanisms for processing both types of information
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Where is the processing of pleasant and unpleasant odors?
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in the cingulated gyrus (?), strong reaction and activity when there is a pleasant smell and very small activity with an unpleasant odor
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What is anosmia?
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loss of smell
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What is hyposmia?
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reduction of smell
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What causes anosmia and hyposmia?
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primarly by viral infections, sinus infections and head trauma, patients won’t complain about unilateral loss, and therefore both sides need to be checked separately, anosmics will typically complain about loss of taste (ageusia) rather than loss of smell
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Describe different scenarios when sense of smell changes.
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sense of smell DEC with age and can be altered in pregnancy, when epileptic seizures originate from olfactory cortex, they can be preceded by olfactory sensations, olfactory hallucinations have also been described, cigarette smoking can induce mucosal hypertrophy and odorants fail to reach the cilia, insurance companies reimburse for anosmia, malingerers need to be distinguaished from true anosmics(complain of aguesia)
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What three cranial nerves mediate taste?
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CN VII, IX and X, all of them via the solitary nucleus in the medulla, from the tongue and epiglottis, CN VII, IX and X project to the nucleus of the solitary tract, which then project to the ventral posterior medial nucleus of thalamus, those project to either the gustatory cortex in either the insula or frontal operculum (in the parietal cortex), another reaches the hypothalamus via the pons (parabrahial nucleus), another to the amygdala
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What is the function of taste?
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to tell whether something should be ingested or not and whether it is pleasurable, the sense of taste also provides information about the identity and concentration of tastants, on the homunculus it projects to the lateral side of the brain, blood supply from middle meningeal artery
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Where are taste buds found and their morphology?
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on the tongue and epiglottis, each taste bud consists of 30-100 receptor cells, the receptor cells have no axon, they release transmitter onto the peripheral processes of ganglion cells, receptor cells die after about 2 weeks and are replaced by division of stem cells (basal cells) in the taste bud, receptor cells have microvilli that extend through the taste pore of the taste bud, at the basal surface is a connection to the gustatory afferent axon
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Describe the different inneravtion of the taste buds?
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1. anterior 2/3-by facial nerve via chorda tympani
2. posterior 1/3-by glossopharyngeal nerve (lingual branch) 3. epiglottis-by vagus via superior laryngeal branch |
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What happens when a tastant binds to a receptor.
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tastants bind to receptors coupled to intracellular signaling pathways or directly open ion channels, INC in Ca2+ results in transmitter release, unclear how many tastants can be distinguished
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What channels and receptors are found in the apical membrane of the taste pore?
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tastant-transducing channels (salt and sour) and G-protein-coupled receptors (sweet, amino acid, and bitter) are limited to the apical domain, intracellular signaling components that are coupled to taste receptor molecules (G-proteins and various second messenger related molecules) are also enriched in the apical domain.
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Describe molecular biology of taste.
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volate-regulated Na+, K+ and Ca channels mediate release of neurotransmitter from presynaptic specialization at the base of the cell onto terminal of peripheral sensory afferents (found in the basal domain), ER releases Ca (via the second messenger pathway) and thse allow for transmitter release
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What is the transmitter found in taste cells?
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serotonin, serotonin receptors are found on the sensory afferents, the TRPM5 channels (which facilitates G-protein coupled receptor-mediated depolarization is expressed in taste cells
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What is the receptor for satly taste transduction?
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cation selectivity of the amiloride-sensitive Na+ versus the H+ sensitive proton channel
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What is the receptor for acids (sour) taste transduction?
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transduced by a proton-permeant, nonselective cation channel that is a member of the transient receptor potential family (TRP)
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What is the receptor for sweet taste transduction?
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heteromeric complexes of the T1R2 and T1R3 receptors transducer stimuli via a PLCbeta-2 mediated, PI2-dependent mechanism that leads to activation of the TRPM5 Ca channel
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What is the receptor for umami (aa) taste transduction?
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heteromeric complexes of T1R1 and T1R3 receptors that transducer stimuli via the same PLCbeta-2/IP2/TRPM5 mechanism
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What is the receptor for bitter taste transduction?
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T2R receptor, associate with the taste cell-specific G-protein gustducin, depolarization depends on PLCbeta-2/IP3/TRPM5 mechanism
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What are the 3 types of taste papillae?
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1. fungiform-anterior tongue
2. foliate-posterior tongue 3. circumvallate-chevron on posterior tongue these papillae correlate somewhat (maximal response) with predominant sensitivities for sweet, salty, sour and bitter (from anterior to posterior) |
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What are the different taste perceptions in the tongue and insular cortex?
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bitter, sour, sweet/umami, salty
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What is ageusia? hypogeusia?
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loss of taste, reduced taste
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What is cacogeusia?
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extremely unpleasant taste
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What causes ageusia or hypogeusia?
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smoking, cystic fibrosis, Bell’s palsy, orophyngeal tumors, chemotherapy (suppresses proliferation of receptor cells
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What is the function of trigeminal chemoreception?
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protect from potentially harmful (noxious) chemical stimuli and initiate their removal, also some solitary receptor cells resembling taste receptors (but innervated by the trigeminal nerve)
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What chemosensitive structures are innervated by the trigeminal nerve?
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nose, cornea, tongue and teeth
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What stimulates the polymodal nociceptive axons of the trigeminal nerve?
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stimulated by irritants, usch as air pollutants, ammonia, ethanol, acetic acids and capsaicin, response is salivation, tearing (to dilute the noxious stimulus) or sneezing
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What is the three neuron to cortex general rule and what is an exception to it?
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receptor cell (optional) -> bipolar/ganglion cell -> sensory nucleus -> thalamus -> cortex, exception is olfaction
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Describe the overall organization of motor control.
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Descending systems (UMN) include the motor cortex (planning, initiating and directing voluntary movements) and brainstem centers (basic movements and postural control) which can be get information from the basal ganglia (gating proper initiation of movement) and cerebellum (sensory motor coordination), UMN sends info to local circuit neurons (which is major, LMN integration) and motor neuron pools (minor, LMN) which can affect skeletal muscles, sensory inputs can effect either the local circuit neurons or motor neuron pools
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Where are UMNs located and what is their input and output?
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are located in the brainstem and cortex, their input is from other UMNs in the brainstem and cortex and from cerebellum and basal ganglia, their output is mostly to local circuit neurons and to some alpha motor neurons, neurons in the cerebellum, basal ganglia and brainstem influence the activity of the UMNs
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What is the purpose of the brainstem and cerebral cortex?
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are UMNs that influence activity of the local circuit neurons and the lower motor neurons
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What is the purpose of the primary motor cortex and premotor cortex?
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they initation movement, select movement and control complex movements
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What is the purpose of the brainstem?
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regulate tone and reflexes (vestibular, somatic, auditory and visual inputs)
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What is the purpose of the cerebellum?
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influence the activity of the UMNs, afferent carry information on how a movements is going for comparision with the intended movement, cerebellum generates output that modifies the activity of the UMN to correct the movement
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What is the purpose of the basal ganglia?
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neurons here influence the activity of the UMNs, activity here suppresses movements and primes the UMN to get a movement going
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What are lower motor neurons?
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send their axons out of the brainstem and spinal cord to innervate the skeletal muscles of the head and body, convey control of all commands for movements, whether reflexive or voluntary, to the muscles
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What are the local circuit neurons?
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are the major source of synaptic input to the lower motor neurons
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What is a motor neuron pool?
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each lower motor neuron innervates muscle fibers within a singl muscle, and all the motor neurons innervating a single muscle (the motor neuron pool) are grouped together into a rod-shaped cluster that runs parallel to the long axis of the spinal cord for one or more spinal cord segments
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What are the two types of LMNs in the motor neuronal pools of the ventral horn?
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1. small gamma motor neurons-innervate specialized muscle fibers that in combination with the nerve fibers that innervate them, are actually sensory receptors called muscle spindles, function to regulate sensory input by setting the intrafusal muscle fibers to an appropriate length
2. alpha motor neurons-innervates the striated muscles fibers that actually generate the forces needed for posture and movement, final common pathway |
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What is the input to the alpha motor neurons?
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most are from local circuit neurons nearby in the cord or brainstem (can be excitatory or inhibitory), their input comes from upper motor neurons, some direct input to the alpha motor neurons are from the upper motor neurons and some from the sensory neurons (reflexes)
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Describe the alpha motor neurons.
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each alpha motor neuron innervates from 3-3000 muscle fibers, the alpha motor neurons for a given muscle are clustered in the ventral horns in one or more spinal cord segments
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What is the somatotopic organization of LMNs at the ventral horns of the spinal cord?
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alpha motor neurons for the axial (postural) muscles are located medially wheras those innervating the distal musculature are located more laterally
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What is the somatotopic organization of UMNs?
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UMNs involved in posoture will be projecting medially, UMNs involved in limb movements will be projecting laterally
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What is the location of local circuit neurons associated with posture and limbs?
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located similarly to the UMNs, responsible for receiving the projections from UMNs, local circuit neurons that supply posture are long and have axons that extend over a number of spinal cord segments and terminate bilaterally, neurons associated with limbs (fine control of distal extremities) are short and extend over a few spinal cord segments and terminate only on the same side of the cord
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Describe the motor unit.
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is the alpha motor neuron and the muscle fibers it innervated (gastrocnemius 1:2000, soleus 1:180, eye 1:3), innervation spread throughout the muscle, the muscle fibers in a motor unit are all of the same type and the motor neuron activity is appropriate.
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What are Slow (S) motor units?
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mall red muscle that resists fatigue, fewer fibers per neuron, tend to be continuously active (posture), contract slowly, generate small forces, rich myoglobin, plentiful mito and rich capillary beds, standing
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What are fast fatigable (FF) motor units?
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paler, large forces for short bursts, more fibers per neuron, have larger alpha motor neurons, innervate larger, pale muscle fibers, sparse mito, easily fatigued, for galloping and jumping
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What are fast fatigue-resistant (FR) motor untis?
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more fiber per neuron, are between the S and FF type, intermediate size, not quaite as fast as FF, twice the force of a slow motor unit and are resistant to fatigue, walking and running
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Describe the recruitment of motor neurons.
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as the synaptic activity driving muscle contraction INC the S units are activated first, then FR then FF
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What are the three muscle stretch reflexes?
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1. muscle spindles-help control muscle length (deep tendon reflex, AKA stretch reflex or myotatic reflex), sensory receptors embedded within most mucle
2. golgi tendon organs-help control muscle tension 3. flexion reflex-move you away from an unpleasant even in the periphery all help control muscle length and tension |
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Describe the muscle spindles.
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among the alpha motor nueorns are gamma ones for the same muscle, muscle spindle activate contraction of 8-10 specialized intrafusal muscle fibers (muscle spindles) in proproioception, wrapped by fast 1a primary afferent neurons (proprioception) that sense muscle length, also have group II afferent axons
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Describe the 1a afferents.
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synapse directly on alpha motor neurons driving the homonymous muscle, the 1a afferents also synapse on local circuit neurons that inhibit antagonist muscles
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Describe actions of motor neurons when lifting and filling a cup.
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stretching a muscle spindle leads to INC activity in 1a afferents and an INC in the activity of alpha motor neurons that innervate the sam muscle, 1a afferents also excite the motor neurons that innervate synergistic muscles and inhibit indirectly the motor neurons that innervate antagonists, when lifting against gravity, the antagonist (tricep) is inhibited while synergist (homonymous) is stimulated
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What does activity in the gamma motor neuron and alpha motor neuron do?
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gamma motor neuron will alter the sensitivity of the muscle spindles, activation of alpha motor neuron alone would cause the muscel to shorten and the 1a afferent to shut down, the response of the 1a fiber DEC as the muscle contracts, co-activation of the two causes the spindles to shorten and fills in the information from the 1a, no DEC in 1a firing during muscle shortening
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Therefore what is the purpose of the gamma motor neuron?
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regulate the gain of muscle spindles so they can operate efficiently at any length
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What info does an efficient control center need?
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needs to know the activity in both the gamma efferents and the 1a afferent to know what is going on in the muscle
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What sets the activity of the gamma motor neuron?
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set by the UMN just like the alpha motor neurons, the sensitivyt of the muscle spindles is under constant adjustment, couch potato -> low sensitivity, skiing -> high sensitivity
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What are golgi tendon organs?
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encapsulated afferent nerve endings between the muscle fibers and the tendon, have 1b fibers (which are a bit slower than the 1a muscle spindles), activated by tension not length, arranged in series with extrafusal fibers, located at the junction of the muscle and tendon
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What happens to the GTO with passive stretch and active muscle contraction compared to muscle spindle?
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INC activity in both muscle spindles and GTO but GTO discharge is much less, when the extrafusal muscle fibers contract (via alpha motor neurons) the spindle is unloaded and therefore falls silent whereas the GTO firing INC
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What is an ideal force transducer?
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receptors that do not respond to length or other stimuli, a muscle would undergo the same activity when force is added and/or when stimulating for contraction, golgi thought to be one but doesn’t seem so (Kenyon says that they are not ideal force transducers and that their activity reflects tension and other things related to fiber contraction)
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Describe the negative feedback regulation of muscle tension by GTO.
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1b afferents synaps on local circuit neurons that inhibit alpha motor neurons in the homonymous muscle and neurons that activate the antagonist muscle, if tension gets too big the muscle is relaxed preventing damage, the gains and set points of feedback loops are subject to control via descending pathways, UMNs influence the activity of the alpha and gamma motor neurons
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Describe the spinal cord circuityry responsible for the flexion-crossed extension reflex.
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activation of primary afferent neurons for pain and temperature (by stepping on a tack) leads to excitation of alpha motor neurons to ipsilateral flexors (flexion reflex) and inhibition of alpha motor neurons to ipsilateral extensors, opposite activites in the contralateral limb, crosses extension reflex maintains posture, these reflexes are also subject to adjustment by descending activity
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What is the importance of the spinal cord?
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the spinal cord is capable of organizing and generating sequences of movements without input from cortex, there are pattern generators in the spinal cord
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What happens after transaction of the spinal cord in a cat?
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the hindlimbs will walk on a treadmill, the extensors and flexors cycle correctly, movements continue after sectioning dorsal roots, how does the spinal cord know what to do?
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What is LMN syndrome?
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damage or loss of alpha motor neurons, paralysis (loss of movement), paresis (weakness), areflexia (loss of reflexes), loss of tone, atrophy (in reponse to loss of activation), fibrillations (twitches), fasiculations (twitches of motor units in response to activity in a sick motor neuron
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Give an overview of the organization of the descending motor control.
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lateral white matter is for axons from motor cortex, while medial white matter is for axons from brainstem
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Describe the major pathways for descending motor control in the medial ventral horn.
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the medial ventral horn contains lower motor neurons that govern posture, balance and orienting movements of the head and neck during shifts of visual gaze, these medial motor neurons receive descending input from the pathways that originate mainly in the brainstem, course through the anterior-medial white matter of the spinal cord and then terminate bilaterally
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Describe the major pathways for descending motor control in the lateral ventral horn.
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contains lower motor neurons that mediate the expression of skilled voluntary movements of the distal extremities, these lateral motor neurons receive a major descending projection from the contralateral motor cortex via the main division of the corticospinal tract, which runs in the lateral white matter of the spinal cord
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What is a general overview of what the UMN in the brainstem do?
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UMNs in vestibular nuclei, reticular formation and superior colliculus project primarily to the medial cord controlling posture, movements of many muscles together
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Describe the input, output, projection and function of the vestibular nucleus (brainstem nuclei with UMN).
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1. input-semicircular canals
2. output-vestibulospinal tract 3. projects to-medial and lateral regions of spinal cord 4. function-control axial and proximal limb muscles in posture and balance, vestibuloocular eye movement while the head is moving |
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Describe the input, output, projection and function of the reticular formation (brainstem nuclei with UMN).
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1. input-primary motor cortex via ventral corticospinal tract
2. output-reticulospinal tract 3. projects to-medial region of spinal cord 4. control axial and proximal limb muscles in posture and balance |
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Describe the input, output, projection and function of the superior colliculus (brainstem nuclei with UMN).
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1. input-from upper body proprioceptors, retina, auditory, olfaction, frontal eye field
2. output-colliculospinal tract 3. projects to-brainstem and medial region of cervical spinal cord 4. function-muscles that orient the head, saccads, tomato-somatic reflex |
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Describe the input, output, projection and function of the red nucleus (brainstem nuclei with UMN).
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1. input-motor cortex via lateral corticospinal tract
2. output-reburspinal tract 3. projects to-lateral and intermediate regions of cervical spinal cord 4. function-control muscles of arms and hands (along with direct lateral corticospinal input) |
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Describe the source, decussation and selected destinations of the lateral corticospinal tract from mtor cortex.
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1. source-motor cortex fro limbs and hands
2. cross-pyramids 3. selected destinations-red nucleus, lateral and intermediate regions of spinal cord |
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Describe the source, decussate and selected destnations of the ventral corticospinal tract from the motor cortex.
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1. source-motor cortex for hip, trunk, shoulder, elbow and neck
2. cross-not at pyramids, some crossing in cord (lower end) 3. selected destinations-reticular formation, medial region of spinal cord on both sides |
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Describe the source, decussation and selected destinations of the corticobulbar tract from motor cortex.
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1. source-motor cortex of face
2. cross-yes and no, some do some don’t 3. selected destinations-CN nuclei, trigeminal, facial, ambiguus and spinal accessory nuclei receive input form both sides of cortex (loss of one input can lead to minimal loss of motor function), hypoglossal and part of facial only receive input from contralateral cortex (loss of the input here leads to loss of motor function) |
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Describe the anticipatory maintenance of body posture.
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when pulling against a handle on a wall, the biceps contract, to ensure postural stability contraction fothe gastrocnemius muscle precedes that of the biceps
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Describe the feed forward and feedback mechanisms of postureal control.
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feedforward postural responses are preprogrammed and typically precede the onset of limb movement, feedback responses are initiated by sensory inputs that detect postural instability, UMNs are acting on a prediction of the future
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What is the sequence of events in complex voluntary movements?
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central command (feedforward for anticipated postural instability) affect both limb movement (direction action) and postural adjustment (indirect action), these both affect postural instability which feedback for unanticipated postural instability
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What link motor cortices with the spinal cord?
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both direct and indirect pathways link them, direct go straight through the spinal cord and indirect synapse in the brainstem (superior colliculus and reticular formation
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What is the premotor cortex?
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a complex mosaic of interconnected frontal lobe areas, lateral premotor cortex (activity here sets up an intent to make a movement, selects appropriate movements, responds to external cues), medial premotor cortex (activity here is similar but for internally generated movements)
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What are the early responses in injury to UMNs?
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early responses include spinal shock, flaccidity on contralateral side, loss of reflexes in limbs (postural muscles may retain function because of local circuit neurons that cross over)
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What are the stable responses in UMN syndrome?
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1. babinsky sign (toes curl away) is present in infants and injury
2. spasticity-INC muscle tone 3. hyperactive stretch reflexes 4. hyporeflexia of superficial reflexes-corneal reflex, superficial abdominal reflexes, cremasteric reflex 5. loss of fine movements |
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What do eye movements accomplish?
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move the eye so that an object of interest is focused on the fovea, so a moving object of interest stays on the fovea, keep changing the image focused on the retina (unchanging images disappear)
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What is diplopia and what causes it?
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is double vision, adults with lesions in the extraocular muscles or their nerves have diplopia, this alarming symptom will bring them to the clinic right away
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What strabismus?
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infants with lesions in the extraocular muscles or their nerves have strabismus that can result in loss of function in the affected eye
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What controls the external muscles of the eye?
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controlled by nuclei in the brainstem (III, IV, and VI), injur to the brainstem (trauma, ischemia) can be detected by defects in eye positioning
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What is intorsion? extorsion?
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top towards nose, top away from nose respectively
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What are the effects of the superior oblique muscle?
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varies with the direction of the eye, with abduction, contraction of the superior oblique does more intorsion, with adduction, contraction of the superior oblique does more depression
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What type of muscle are the eye muscles?
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are skeletal muscles, not smooth muscles, they have alpha motor neurons, motor endplates, acetycholine, nicotinic ACh receptors, this is in spite of the fact that the extraocular muscles are rich in muscle spindles, the function of the spindles is unclear, they do have unique properties to meet their unique functions, quick movements of a constant mass
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What nerve innervates the contralateral side?
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CN IV innervates the superior oblique contralaterally, rest is ipsilateral
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Does it matter if there is a lesion in either the nerve or the nucleus or both?
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the answer depends on the nature of the nucleus and the lesion, is the nucleus pure (only lower motor neurons for one eye), is the lesion confined to one nucleus (things are pretty tight in the brainstem)
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Describe CN VI.
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pure, motor neurons to lateral rectus (ipsilateral) only
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Describe CN IV.
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pure, motor neurons to superior oblique (contralateral) only
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Describe CN III.
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mixed, motor neurons to the remaining external muscles of the eye and autonomic to pupil rest (ipsilateral)
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Describe the course of CN IV.
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from trochlear nucleus (caudal midbrain) to superior oblique muscle, the trochlear nerve exits the dorsal surface of the midbrain and crosses over
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What happens with loss of the trochlear nerve?
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rare, paralysis of SO muscle, diplopia on looking downward (difficulty descending stairs), head tilt toward the weak muscle compensates, may be the first sign of trochlear lesion, the figure shows a bad left eye
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Describe the course of CN VI.
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abducens nerve from abducens nucleus (pons) to lateral recuts muscle, does not cross over
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What happens with loss of abducens nerve?
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most common palsy due to the long course of the nerve, paralysis of lateral rectus, affected eye fails to abduct on lateral gaze and can intort causing double vision, rotation of head compensates
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Describe the course of CN III.
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from the oculomotor nucleus (under superior colliculus) to superior, inferior and medial rectus and to inferior oblique, no cross over, other neurons in the oculomotor nucleus innervate the levator muscles of the eyelid, the nerve also carries axons from Edinger-Westphal nucleus that drive papillary constriction
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What happens with loss of oculomotor nerve?
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eye is down and out, downward abducted eye due to unopposed action of superior oblique and lateral rectus muscles, ptosis compensated by contraction of frontalis muscle to raise eyebrow and eyelid, dilated pupil, paralysis of accommodation
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What are the 4 types of eye movements?
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saccades, smooth pursuit, vergence and vestibule-ocular eye movements
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What are saccades?
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rapid ballistic movements that put an image on the fovea, a ballistic missle is controlled to the apex of its trajectory then falls freely, a guided missile is controlled for the duration of flight
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What is smooth pursuit movement?
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slower tracking movements to keep a moving image on the fovea (sort of voluntary), keep the image of a moving target on the fovea
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What are vergence movements?
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align the fovea with targets at different distances, move the eyes in opposite directions (conjugate movements) so that the image is positioned on both foveas, tracking something moving towards or away from you
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What near reflex triad?
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tests your oculomotor nerve, vergence adduction of the eyeballs, accommodation of the lens (focus), papillary constriction (INC depth of field)
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Describe the vestibule-ocular movements.
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compensate for movements of the head (driven by the vestibular system), vestibule-ocular movements hold images stable during brief head movements
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What do the semicircular canals in terms of vestibule-ocular movements?
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the semicircular canals detect rotation of the head, this information is used to direct the eyeballs to move in the opposite direction (i.e. to maintain the field of view) works best to correct during acceleration to rapid rotation, during constant or slow rotation, compensatory eye movements cease after 30 sec. (visual cues will then be important)
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What type of signal does the semicircular canal transmit?
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each semicircular canal transmits a tonic signal to the vestibular nerve even when the eyes are still, a pathological imbalance in the signals from the vestibular system will result in nystagmus when the head is still
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What is saccades movement?
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rapid ballistic movements that occur to fix on a target and continue as afterwards (voluntary (reading) or reflexive (e.g. looking at the parts of a picture)), shift the fovea rapidly to a target spotted at the periphery, the system figures out where the eye will point and snaps it to that position, this is not tracking, if the target moves, a whole new saccade will be needed, small or large, the eye movements in REM sleep are saccades
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Describe the neural control of saccades.
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one can record (experimentally) the activity of the motor neurons in the motor nucleus, here one records from a motor neuron in the abducens nucleus, the amplitude of the saccade is encoded in the duration of the burst of APs, this calculation is made upstream, the baseline firing holds the eye in place
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Describe the gaze centers.
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the cell bodies of the LMN that drive the eye muscles are located in the oculmotor, trochlear and abducens nuclei, these neurons receive input from UMN in two gaze centers in the reticular formation
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What generates horizontal movements? vertical movements?
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paramedian pontine reticular formation (PPRF AKA horizontal gaze center) generates all kinds of horizontal movements, rostral interstitial nucleus (AKA vertical gaze center) generates all kinds of vertical movements
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How does the right PPRF signal through the abducens and oculomotor nuclei?
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it allows for one to look at something off to the right, motor neurons to the lateral rectus of the right eye, located in the abducens nucleus are driven directly from the PPRF, in addition neurons in the PPRF also drive inhibitory interneurons that synapse in the contralateral abducens nucleus, thus the opposing rectus muscles are relaxed
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What role do interneurons have in the gaze centers?
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motor neurons to the medial rectus of the left eye are driven through interneurons, these interneurons cross over in the medial longitudinal fasiculus, thus there are two kinds of neurons in the abducens; motor neurons and internuclear neurons
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Describe the higher visual control of eye movement.
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some saccades direct the eye to look at something interesting, UMN in two higher structures important in this type of targeting, superior colliculus (midbrain), frontal eye field (frontal lobe, just rostral to the premotor cortex), these centers generate saccades
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What role does the superior colliculus play in higher visual control?
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the superior colliculus is better documented, the visual field can be mapped onto the superior colliculus such that light on a particular spot on the retina elicits activity in a particular spot in the colliculus, motor neurons in that spot drive saccades to move the eye to shift the image to the fovea
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What else is mapped in the superior colliculus besides the retinal maps?
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audtiroy and somatic stimuli are also mapped here, thus one can look quickly at something that is heard or felt
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What is the output of the frontal eye field?
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goes directly to the gaze centers and also to the superior colliculus and then to the gaze centers, complementary pathways allow for partial compensation for damage in one center
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What is the control of smooth pursuit movements?
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are driven through the PPRF (and verticacl gaze center), the source is not the frontal eye field/superior colliculus, they do saccades, pathways are not known completely, visual areas in the parietal and occipital lobes provide sensory information that is essential for initiation and guidance of smooth pursuit movements, these areas also generate the slow phase of optokinetic nystagmus
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Medial rectus muscle
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adducts eye
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Lateral rectus muscle
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abducts
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Superior rectus muscle
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elevates (primary action), adducts and intorts
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Inferior rectus muscle
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depresses, adducts and excyclotorts
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Superior oblique
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depresses and intorts
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Inferior oblique
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elevates and extorts
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Ductions
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movement of one eye
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Versions
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movement of both eyes, conjugate
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Vergences
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disconjugate movement of eyes
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Strabismus
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misalignment of visual axes
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Phoria
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latent deviation that appears only when fusion disrupted
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Tropia
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manifest deviation, beyond the range of fusional control
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Esotropia
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nasalward deviation of eye, “crossed eye”
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Exotropia
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temporal deviation, “walleye”
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Hypertropia
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vertical deviation, relative to higher eye
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Concomitant
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Angle of deviation remains constant regardless of direction of gaze; range of motion of eyes is, full, without limitation or restriction, Most commonly seen in childhood onset strabismus
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Incomitant
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Angle of strabismus varies with gaze direction; limitation of ocular movements, Patient may exhibit abnormal head posture to maintain binocularity, May be congenital or acquired
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DIAGNOSIS
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Cover test, alternate cover test
Light reflex testing Angle of deviation measured with prisms Motility evaluation – ductions and versions Sensory testing to assess binocularity |
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Comitant strabismus
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PSEUDOESOTROPIA-common in infants: wide flat nasal bridge and epicanthal folds, normal alignment by light reflex and cover tests
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Restrictive strabismus
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1. CONGENITAL FIBROSIS SYNDROME-autosomal dominant, inelastic muscles and ptosis, positive forced ductions
2. GRAVES’ DISEASE-lymphocytic infiltration and secondary fibrosis of extraocular muscles in thyroid disease 3. ORBITAL FRACTURES-carring/entrapment of orbital tissue/extraocular muscles 4. CRANIAL NERVE PALSIES-microvascular, tumor, trauma, aneurysm |
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Neurologic strabismus
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1. THIRD NERVE PALSY – eye down and out, ptosis, +/- pupillary involvement
2. FOURTH NERVE PALSY – oblique diplopia and torsion, bilateral often secondary to trauma 3. SIXTH NERVE PALSY – face turn towards affected side 4. MYASTHENIA GRAVIS – variable strabismus and ptosis, Acetyl Choline receptor antibodies, Tensilon test |
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What is the primary function of the cerebellum?
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to detect difference in motor error (between the intended movement and the actual movement, neuronal activity in the cerebellum changes continually during the course of movement, the neural processing in the cerebellum is dynamic), is a comparator
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What is the clinical presentation of patients with cerebellar damage?
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exhibit problems with range, rate and direction of movement (cerebellar ataxia (fractionation of movements), dysmetria (overshooting and undershooting target when asking pt. to following finger), dysdiadochokinesia (inability to perform rapid, alternating movements), tremor)
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Describe the fibers of the inferior peduncle.
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afferents to cerebellum
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Describe the fibers of the middle peduncle.
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coming form pons, sweeps across to midline from pons to enter the middle peduncle
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Describe the core of white matter in the cerebellum
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core of white matter that lies four pairs of deep cerebellar nuclei, from medial to lateral, (fastigial globose, belliform and dentate), how get info out of the cerebellum, travels out of the superior cerebellar peduncle
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What are the three parts of the cerebellum?
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1. vestibulocerebellum-composed of the floculo-nodular lobe, get info from vestibule complex about whats going on in the outside world, body position
2. spinocerebellum-composed of the midline (associated with big prosimal musculature), vermis and paramedian areas (lateral part is distal muscles), concerned with correction of movement from both distal and proximal musculature, gets input from the spinal cord from muscles 3. cerebrocerebellum-composed of the lateral lobes, responsible for planning and input from the cortex (sensory and motor) |
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Where does the spinocerebellum receive info from?
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receives inpu from the spinal cord related to spindle infor and the cortex related to execution of movements for fine control of proximal and distal muscles
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Where does the cereberocerebellum receive input from?
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receives infput from the premotor cortex and sensory association areas related to the planning of movements
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Where does the vestibulocerebellum receive input from?
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receives input from the vestibular system and the visual system to control eye movements and balance
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Where do the three parts project to?
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spinocerebellum-fastigial and interpositus, cerebrocerebellum to dendtate, vestibulocerebellum to vestibular nuclei, these four deep nuclei associations don’t have nuclei (use vestibulocerebellum as its deep nucleus, fibers run from the deep nuclei back to the vestibulocerebellum)
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What is the cerebellar laterality (how its related to the body)?
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Each cerebellar hemisphere has control over the same side of the body. This is different than what you have learned about other ascending and descending systems so any inputs to the cerebellum from the cortex must cross and inputs from the spinal cord or vestibular nuclei must remain ipsilateral. Similarly, outputs from the cerebellum to the cortex must also cross back on their way up to cortex, always related to the ipsilateral side of the body
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Describe the superior cerebellar peduncle.
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mostly efferent pathway arises from cell bodies in deep cerebellar nuclei and crosses in the midbrain on the way to the thalamus. The correction
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Describe the middle cerebellar peduncle.
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afferent pathway arises from cell bodies in the contralateral pontine gray which got their input primarily from the ipsilateral cerebral cortex, what the muscles are supposed to do
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Describe the middle cerebellar peduncle.
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afferent pathway arises from cell bodies in the contralateral pontine gray which got their input primarily from the ipsilateral cerebral cortex, what the muscles are supposed to do
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Describe the inferior cerebellar peduncle.
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mostly afferent pathway whose fibers come from cells in the spinal cord, inferior olive (has a huge imput to cerebellum, projects to all 3 areas of the cerebellum), vestibular nuclei and ganglion, efferents of this peduncle project to the vestibular nuclei, what the muscles are doing
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What are the neural structures related to the cerebellum?
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Brainstem and spinal cord structures are mostly projecting in, the deep nuclei are projecting out and the VA/VL complex is receiving from the deep nuclei. Cortex is the dominant source of inputs to the pontine nuclei.
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where do the major inputs to the cerebrocerebellum come from?
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cerebral cortex, frontal and parietal lobes, motor and premotor cortex, sensory cortex and cingulated cortex, inputs are concerned with the planning of movements, pontine fibers have the biggest projection into the cerebrocerebellum
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What are the major efferent pathway between the cerebellar cortex and cerebrum?
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cerebellar cortex sends fibers to deep cerebellar nuclei and synapses, gives efferents through the superior cerebellar peduncles, gives collateral to red nucleus and inferior olive, ascends to ventral lateral complex (thalamus) and synapses, then ends at the primary motor and premotor cortex
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Describe the cerebellar afferents.
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1. Cortex to cerebrocerebellum via the pontine nuclei and the MCP. Crossed pathway, pontine nuclei does not go everywhere, goes primarly to cerebrocerebellum for planning
2. Olive to all parts of the cerebellum via the ICP (climbing fibers). talks to all the lobes, Crossed pathway (right where it enters) 3. Vestibular nuclei, accessory cuneate nucleus, and Clarke’s nucleus via the ICP. Uncrossed |
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What is Clarke’s column?
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Clarke’s column is the origin of the dorsal spinocerebellar tract which carries information about muscle length, tension and velocity to the cerebellum from muscles below C7.
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What is the accessory Cuneat nucleus?
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The Accessory Cuneate nucleus is the upper limb equivalent for Clarke’s column carrying muscle information from C7 and above to the cerebellum over the ICP.
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Describe sensory innervation of muscle receptors?
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muscle spinleds enter dorsal horn (type Ia give length and rate of change info while type II give length, type Ib gives tension info), comes in from both sides
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Describe the dorsal spinocerebellar tract.
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Clarke’s column is found between C8 and L3 in the dorsal horn and is the beginning of this pathway to the cerebellum. Muscle information enters the dorsal horn and synapses on cells in Clarke’s column whose axons ascend to the cerebellum in the ICP on the dorsal spinocerebellar tract. (proprio enters and synpase in dorsal horn on cell body then axons ascends to medial where it enters ipsilateral inferior peduncle)
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What about info below L3?
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below L3, info comes in from muscle spindles, but can’t synapse at Clarke’s column, goes up at the dorsal horn and ascends to L3 where it synapses (L3 has largest population of Clarke’s column)
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What about info above C8?
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info comes in, goes up in posterior columns until it gets to the accessory cuneate nucleus where it synapses and etners the cerebellum over the inferior peduncle
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Describe the laterality of the neural circuitry of the cerebellum.
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1. incoming muscle info (from inferior peduncle) to cerebellar cortex
2. cortex processes and projects out of superior peduncle to thalamus to cerebral cortex 3. motor cortex info gives off “collateral” to pontine nucleus and gives off info for middle cerebellar peduncle (is ipsilateral) 4. info from muscles to olive is crossed |
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What are the cell types in the cerebellum, cerebellar circuitry and the layers in the cerebellar cortex?
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1. molecular layer-purkinje cell dendritic tree with numerous parallel fiber endings.
2. purkinje cell layer-large cell bodies of Purkinje cells, all lined up 3. granule cell layer-granule cells, mossy fibers and climbing fibers entering cortex, contains incoming fibers and granule cells |
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In what layer are the deep cerebellar nuclei?
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are in the white matter layer
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What are mossy fibers?
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originate in: the contralateral pontine nuclei, the ipsilateral Clarke’s column and Accessory Cuneate nucleus, the vestibular nuclei and ganglion, and reach the cerebellar cortex where they excite granule cells. All mossy fibers send an excitatory collateral to the deep nuclei (very important). Any fiber not from the Olive is a mossy fiber.
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What are climbing fibers?
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originate in the contralateral inferior olive and reach all areas of cerebellar cortex where they send an excitatory input to the purkinje cell dendrites after sending an excitatory collateral to the deep nuclei (very important). only come from the inferior olive
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What type of input are the mossy and climbing fibers?
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excitatory inputs, send collateral to deep nuclei, stimulates it first
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Describe the microciruitry of the cerebellar cortex.
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1. Incoming mossy and climbing fibers have an excitatory collateral to the deep nuclei.
2. The Purkinje cells are inhibitory to the deep nuclei and the only way out of the cortex. 3. The only way to get info out of the cerebellum is to turn the purkinje cells off momentarily and allow the deep nuclei to be driven by the mossy and climbing fibers purkinje cells are the only way out of the cortex, is inhibitory, turns off deep nuclei, only way out of the cerebellum is to stop the purkinje fibers from firing, allows deep nucleus to run free |
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What are the most important things to remember about cerebellar circuitry?
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1. All fibers projecting into the cortex are excitatory (mossy fibers, climbing fibers & granule cell parallel fibers) that means the granule cells are excitatory.
2. All cells of the cerebellar cortex except the granule cells are inhibitory (Purkinje cells, stellate cells, basket cells and Golgi cells). 3. The deep cerebellar nuclei (not part of the cerebellar cortex) are excitatory. 4. The only way out of the cortex is an inhibitory Purkinje cell axon which must be turned off to allow the deep nuclei to fire. |
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What are other inhibitory cells on the Purkinje cell?
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Three types of local inhibitory interneurons: Stellate and Basket cells in the molecular layer and Golgi cells in the granule layer. These cells are responsible for inhibitory loops that can turn the Purkinje cells off momentarily. Don’t worry about their exact connections!
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Lesions of the cerebellar hemisphere result in IPSILATERAL
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incoordination/ataxia. For instance, a lesion in the RIGHT cerebellar hemisphere will result in motor incoordination/ataxia of the RIGHT side. A lesion of the inferior or middle peduncle will also cause an ipsilateral deficit. What about the superior peduncle? A lesion of the RIGHT superior cerebellar peduncle before the decussation will also result in motor incoordination/ataxia on the RIGHT side. However, a lesion after the decussation of the superior cerebellar peduncle will result in CONTRALATERAL motor deficits.
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Where does the superior peduncles leave?
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fibers run rostral-ventrally, penduncel gets sucked into the middle, crosses caudal to the red nucleus
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What are some disorders of the cerebellum?
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1. Cerebellar lesions typically result in irregular uncoordinated movement called ataxia.
2. Signs of cerebrocerebellar problems include dysmetria (past pointing), dysdiadochokinesia (inability to perform rapid alternating movements), dysarthria (speech impairment), and intention tremor. 3. Spinocerebellar lesions usually result in unsteady gait (balance) and eye movement abnormalities. 4. Vestibulocerebellar lesions result in problems with balance and eye movements. |
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What is the vestibule-ocular (VOR) reflex?
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When the visual image on the retina shifts its position as a result of head movement, the eyes must move at the same velocity in the opposite direction. when the cerebellum is damaged the VOR fails to operate correctly
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What is Romberg’s sign?
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A test indicating loss of proprioceptive control – increased unsteadiness occurs when standing with the eyes closed compared with standing with the eyes open, does not necessarily test cerebellar function, patients with cerebellar ataxia will generally be unable to balance even with the eyes open, positive in conditions causing sensory ataxia such as general sensory peripheral neuropathies
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What is proprioception?
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proprioception is a sense or perception of movements and position of the body especially limbs
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How is a Romberg’s test performed?
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Romberg's test is performed in two stages. First, the patient stands with feet together, eyes open and hands by the sides. Second, the patient closes the eyes while the examiner observes for a full minute. The examiner is trying to determine whether the patient falls when the eyes are closed.
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How do you determine whether the test is positive or negative?
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Romberg's test is positive if the following two conditions are both met: The patient can stand with the eyes open; and The patient falls when the eyes are closed. Patients with a positive result are said to demonstrate Romberg's sign or Rombergism. They can also be described as Romberg's positive
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How does Romberg’s test work?
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The visual pathway is removed by closing the eyes. If the proprioceptive pathway is intact, balance will be maintained. But if proprioception is defective, both of the sensory inputs will be absent and the patient will sway then fall.
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What is the purpose of the basal ganglia?
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gating proper initiation of movement -> motor cortex for planning, initiating and directing voluntary movements
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Where does the basal ganglia project to?
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does not project directly to either the local sircuit or lower motor neurons, instead they influence movement by regulating the activity of the upper motor neurons
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What does the motor cortex project to?
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along with the brainstem centers (for basic movements and postural control) affects local circuit neurons (for lower motor neurons integration, is also affected by sensory inputs) and motor neuron pools (lower motor neurons) which cause a reaction in a skeletal muscle
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What constitutes the basal ganglia in the motor system?
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a large and functionally diverse set of nuclei (gray matter) that lies deep within the cerebral hemispheres, includes the caudate, putamen and globus pallidus, closely associated with the substantia nigra and subthalamic nucleus
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What types of information affect basal ganglia?
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1. motivation (I will sign my name) from higher-order association cortex
2. context (where? how big? how fast? sitting or standing?) from sensory/motor association cortex after entering the basal ganglia, it sends fibers to the motor cortex for execution of signature |
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Describe the connections of the basal ganglia.
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the cerebral cortex has a transiently stimulatory effect on the caudate and putamen, caudate and putamen can interact with the substantia nigra pars compacta (through input and output) or has a transient inhibitory effect on the internal and external segment of the globus pallidus, the globus pallidus has a tonic negative effect on the subthalamic nucleus, thalamus (VA/VL complex) and superior colliculus, the thalamus is then able to transiently stimulate the cerebral cortex (frontal cortex)
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What is the corpus striatum?
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composed of caudate and putamen, comprise the input zone of the basal ganglia, their neurons being the destinations of most of the pathways that reach this complex from other parts of the brain
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What is the pallidum?
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globus pallidus and substantia nigra pars reticulata
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What is the purpose of the substantia nigra pars compacta and subthalamic nucleus?
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provides input to the corpus stiratum and palladium resepctively
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What is the location of the basal ganglia and connecting centers?
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border the internal capsule in the forebrain and midbrain, substantia nigra found between the cerebral peduncles and red nucleus
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Describe the anatomical organization of the inputs to the basal ganglia.
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1. caudate gets input from frontal cortex and substantia nigra pars compacta
2. putamen gets input from frontal cortex, parietal cortex, temporal cortex and substanctia nigra pars compacta |
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What are the medium spiny neurons?
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cells found in the corpus striatum who have dendrites that act as the destination point of the incoming axons from the cerebral cortex, large dendritic trees of these neurons allow them to integrate inputs from a variety of cortical, thalamic and brainstem structures, axons from here converge on neurons in the pallidum, which includes the globus pallidus and substantia nigra pars reticulata
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What are some different cell types that converge onto a medium spiny neuron?
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from cortical neurons, dopaminergic cells of the substantia nigra and local circuit neurons within the corpus striatum, the arrangement of these synapses indicates that the response of the medium spiny neurons to their principal input (derived from the cerebral cortex) can be modulated by dopamine and the inputs of local circuit neurons, the primary output of the medium spiny cells is to pallidal neurons in the globus pallidus and substantia nigra pars reticulata
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Where does the basal ganglia receive input form?
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from the majority of the cortex, receive cortical projections primarily from the association areas of the frontal, parietal and temporal lobes
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Describe the output (projections) from the basal ganglia.
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the caudate and putamen send inhibitory signals to the sunstantia nigra pars reticulata (which sends an inhibitory signal to the superior colliculus) and globus pallidus internal (which sends an inhbitiory signal to the VA/VL complex of the thalamus which itself sends stimulatory signals to the motor cortex)
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What does inhibition of an inhibitory projection cause?
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excitation, this allows for the concept of gating to initiate movement, a process central to the gating operations of the basal ganglia
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What is the role of the basal ganglia in the generation of saccadic eye movements?
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excitatory signal from cortex stimulates caudate which inhibits substantia nigra pars reticulate which normally inhibit (but now stimulate since the substantia nigra is inhibited from firing its inhibition) now stimulates the superior colliculus which stimulates gaze centers via projections to horizontal and vertical gaze centers
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Describe the direct disinhibition pathway through the basal ganglia.
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transiently inhibitory projections form the caudate and putament project to tonically active inhibitory neurons in the internal segment of the globus pallidus which project in turn to the VA/VL complex of the thalamus, VA/VL complex of thalamus can stimulate frontal cortex
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Describe the indirect disinhibition pathway through the basal ganglia.
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transiently active inhibitory neurons from the caudate and putament project to tonically active inhibitory neurons of the external segment of the globus pallidus, globus pallidus neurons project to the subthalamic nucleus which also receives a strong excitatory input form the cortex, the subthalamic nucleus in turn projects to the globus pallidus where its transiently excitatory drive acts to oppose the dsinhibitory action of the direct pathway, the indirect pathway modulates the effects of the direct pathway
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What happens if there is a reduced input form the substantia nigra?
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Parkinson’s disease, hypokinetic disorder, the dopaminergic inputs provided by the substantia nigra pars compacta are dimished making it more difficult to generate the transient inhibition from the caudate and putamen, the result of this change in the direct pathway is to sustain the tonic inhibition from the caudate and putamen, the result of this change in the direct pathway is to sustain the tonic inhibitrion from the globus pallidus to the thalamus makin gthalmic exciation of the motor cortex less likely
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What happens if there is reduced input from caudate/putamen to globus pallidus externa?
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found in Huntington’s disease, hyperkinetic disorder, this reduction INC the tonic inhibition from the globus pallidus to the subthalamic nucleus making the excitatory subthalamic nucleus less effective in opposing the action of the direct pathway, thus thalamic excitation of the cortex is INC, leading to greater and often inappropriate motor activity
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Describe the body movement loop.
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cortical input from motor, premotor, and somatosensory cortex -> striatum (putamen) -> pallidum (lateral globus pallidus, internal segment -> ventral lateral and ventral anterior nuclei of thalamus -> primary motor, premotor, supuplementary motor cortex
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Describe the oculomotor loop.
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posterior parietal, prefrontal cortex -> caudate (body) -> globus pallidus, internal segment, substantia ngira pars reticulate -> mediodorsal and ventral anterior nuclei -> frontal eye field, supplementary eye field
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Describe the prefrontal loop.
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dorsolateral prefrontal cortex -> anterior caudate -> globus pallidus, internal segment, substantia ngira pars reticulate -> mediodorsal and ventral anterior nuclei -> dorsolateral prefrontal cortex
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Describe the limbic loop.
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amygdale, hippocampus, orbitofrtonal, anterior cingulated, temporal complex -> ventral striatum -> ventral pallidum -> mediodorsal nucleus -> anterior cingulated, orbital frontal cortex
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What are some characteristics of Parkinson’s Disease?
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1. pathogenesis-loss of nigral neurons
2. diagnosis-clinical, not lab or imaging 3. medical Rx-L-Dopa and DA agonists 4. pallidotomy & deep brain stimulation 5. Parkinsonism (neuroleptic induced) 6. Parkinson plus syndromes (Shy Drager, multiple system atrophy) |
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What are some symptoms of Parkinson’s-1?
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tremor, (resting 3-5 Hz), rigidity (cogwheel, paratonia), bradykinesia, slow movement initiation, inability to control inertia (start/stop), loss of balance, retropulsion, shuffling gait, postural change, forward bias
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What are some symptoms of Parkinson’s -2?
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hypominimia (masked facies), hypophonia (soft, low volume, mumbling), kinesis paradoxical, depression, dementia (Alzheimer’s and Lewy body), EMG
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What are some characteristics of Huntington’s Disease?
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1. pathogenesis-loss of striatal neurons
2. symptoms-predominantly chorea, but may see other dyskinesia such as hemiballismus, athetosis and dystonia 3. side effects of antipsychotic medications may limit treatment 4. genetic testing-ethical implications |
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What happens to strength, muscle tone etc during an LMN lesion?
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1. strength-DEC
2. muscle tone-flaccid 3. atrophy-present 4. reflexes-DEC 5. plantars-flexor 6. fasciculations-present |
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What happens to strength, muscle tone etc. during an UMN lesion?
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1. strength-DEC (elective pattern of weakness), extensors in UEs and flexors in LEs
2. muscle tone-spastic 3. atrophy-disuse/less 4. reflexes-INC 5. platars-extensor 6. fasciculations-absent |
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What is spasticity?
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INC resistance to passive movement with sudden collapse (clasped knife collapse, UMN sign), UMN sign = pyramidal sign
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What is rigidity?
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cogwheel and plastic tonus, paratonia (basal ganglion signs), basal ganglion = extrapyramidal sign
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What is limb paresis?
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1. monoparesis-UMN lesion but occasionally LMN lesion
2. hemiparesis, paraparesis and quadriparesis are signs of UMN lesions 3. assocated sensory, autonomic, cerebellar and other signs triangulate the lesion |
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what is ataxia?
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axial vs. appendicular forms, dyssynergia is most general term, testing includes finger to nose, heel to shin, alternating movement balance
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what is hyper- and hypo-reflexia?
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1. hyper-reflexia-3+ with spread, or 4+ (clonus by definition)
2. hypo-reflexia-0 to 2+ may be normal, check for asymmetry (decide which is abnormal, the down or the up reflex) |
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What are some involuntary movements?
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1. myoclonus
2. chorea, dystonia, athetosis 3. tics 4. tremor types-intention (cerebellar origin), resting (basal ganglion origin), sustentation and action tremor (benign essential tremor) |
