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357 Cards in this Set
- Front
- Back
- 3rd side (hint)
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normal height of the palpebral fissure?
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9-12mm
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orientation of the pupillary muscle constrictors and dilators?
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Constrictors--> oriented in a circular fashion around the pupil (sphincter)
Dilators--> oriented longitudinally in a radial fashion from the pupil |
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anisochoria
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when pupils are >0.4mm different in size
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normal pupil size in ambient light
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2mm-6mm
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Muscles of the pupil are under what kind of control?
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both under autonomic nervous control.
Dilators--> sympathetic innervation. Nerve from the ventral horn enters paravertebral ganglia (T1,T2) , ascend up and synapse in the superior cervical ganglion, "hop on" to the internal carotid artery there, then hops to the opthalmic division of the trigeminal nerve. Then travels as a brach of the nasal ciliary nerve as the long cilliary nerve and goes to the pupil in a longitundinal fashion. another branch will go to mullers muscles Constrictors--> parasympathetic innervation. by way of the 3rd nerve from the Edinger Westphal nucleus to the short cillary ganglia, and to the pupil |
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Mullers muscles
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smooth muscles that pull the upper and lower eye lids slightly up and down, increasing the height of the palpebral fissure. innervated by sympathetic fibers (superior tarsal muscle, and also one to the lower lid as well) . this makes sense because sympathetic innervation also dilates the pupil so this along with it allows that new diameter of pupil be able to receive light
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adie's syndrome
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chronically dilated pupil, caused by damage to the parasympathetic postganglioic fibers of the cercvical ganglia
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Edinger Westphal nucleus (accessory parasympathetic cranial nerve nucleus of the oculomotor nerve (cranial nerve III), supplying the constricting muscles of the iris.)
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myosis
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small pupil
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mydriasis
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large puil
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compresssion of the 3rd nerve (as in an aneurysm) VS. vascular damage to the 3rd nerve (as in diabetes)?
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for compression, one of first signs is change in pupillary diameter (larger) because they are on the surface and will be affected first with compression. In vascular things like DM see pupillary sparing because nerve affected from inside out so last ones to be affect are those of the pupil.
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direct light reflex
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illumination of one eye causes pupillary constriction in that same eye
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indirect light reflex
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illumination of one eye causes pupillary constriction in the other eye
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mechanism of the direct and indirect light reflexes
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illuniate the eye and you activate receptors in all 4 retinal quadrants . Fibers go to optic nerve some cross some stay. collateral branches from the tract break off and terminate in the PTN (pretectal nucleus). Some cells cross the posterior commissure and some stay on same side and go to edinger westphal nucleus. that then gives rise to axons of the 3rd nerve, synapse on cillary ganglia, then to pupillary consrtictors. because of crossing over at posterior commissure as well as the fact that edinger westphal nuclei are connected, that is why a unilateral stimulus gives rise to a bilateral response
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Accomodation reflex
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focus on distant object and then have pt look at your thumb right in front of the nose. Eyes should ADduct, pupils get smaller, and lens become rounder in order to get the object in focus. The muscle important here is the ciliary muscle, which is a circularly oriented muscle. see next side of slide as well
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When the muscle contracts, the AP diameter gets larger. you cannot visualize this but tension is taken off the zomules and the lens becomes rounder
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"wiring" of the accomodation reflex
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pupillary constriction by way of the pupillary constrictor muscles and lens accomodation by way of cilliary body constriction (both of these CN III, parasympathetic division). medial rectus muscle also contracts but by way of CNIII, CNIV, and CNVI alpha motor neurons.
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Swinging flashlight test
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looking at the responses in each pupil as you swing light between the eyes. Should see sustained pupillary constriction throughout. an abnormal response would show paradoxical response (dilation)
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Congruous deficit
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similarly shaped deficits (may be different in sides). congruity is a signature of location, occuring commonly in lesions affecting the optic radiation (postgeniculate lesion)
TOP in pic |
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incongruous deficit
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deficits of different shapes. Most commonly due to lesions that are PREgeniculate
BOTTOM in pic |
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Name the visual deficit and where is the lesion?
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Right Central Scotoma. Also see
increase in the blind spot in the right eye. Lesion is right in the middle of the R fovea and R macula |
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Name this visual deficit
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Bilateral Cecocentral Scotomas,
There is continuity with the central part, maculovision, and the blindpot. |
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Name this visual deficit and lesion
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Right Homonymous Hemianopsia with Macular involvement
The lesion is on the left side, behind the chiasm. It is congruent, so likely in the optic radiations. Because it is affecting the R temporal field, which project on the L nasal part of the retina, which cross at the chiasn. On the L side, the L nasal visual field projects to the L temporal retinal field. These fibers laterally remain uncrossed Note that the visual field on the right is larger because if you are taking out the optic tract and 53% of the fibers cross, we can presume if complete deficit, a larger deficit seen in the fibers that have crossed |
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Name this visual deficit and lesion
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Left Homonymous Hemianopsia with Macular Sparing
This pt may not even know they have visual field defect because macular area is spared. likely not a handicapping lesion |
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Name this visual deficit and lesion
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Left Superior Homonymous Quadrantanopsia
Lesion is post -chiasmatic, and post geniculate (because if pre, more likely to get the optic tract and would have hemianopsia). This is a lesion in the temporal lobe, acting on fiber of Meyer's Loop. "Pie in the sky deficit" |
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Name this visual deficit and lesion
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Right Inferior Homonymous Quadrantanopsia
Lesion is in the parietal lobe, affecting fibers in the medial part of the geniculate nucleus, projecting to cuneate gyrus |
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Name this visual deficit and lesion
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Right Anopisa with a Left Superior Temporal Quadrantanopsia
R sided lesion, prechiasmatic. Affecting Wilbrand's knee area ie in a pt with a pituitary adenoma, esp if a postfixed optic chiasm |
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Right temporal crescent defect
Lesion on the L side, in the |
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any retrochiasmatic lesion will affect...
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both eyes, and deficit occurs contralaterally
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1. Which side demonstrates the abnormal response?
2. Do the observations suggest a sympathetic or parasympathetic lesion? |
1. RIght
2. Sympathetic Anisochoria worse in the dark than in the light--> implies sympathetic injury. |
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1. Which side demonstrates the abnormal response?
2. Do the observations suggest a sympathetic or parasympathetic lesion? |
1. Left
2. Parasympathetic anisochoria worse in the light than in the dark--> implies parasympathetic injury |
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1. Which side demonstrates the abnormal response?
2. Do the observations suggest an afferent or an efferent pupillary deficit? |
1. Left
2. 2nd nerve injury and not 3rd because pupils are the same size. if 3rd nerve was injury, pt would have anisochoria at rest. This is actually called RAPD. Afferent pupillary deficit |
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See anisochoria, down and out of the R eye, suggestive of a 3rd nerve injury. Tool on the r is so that lid doesnt fall down (pt would normally have ptosis)
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3rd nerve injury and eye findings
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Anisochoria, with myopsia on the contralateral side, normal sized pupil on ptosis side. Down and outward orientation of the affected eye. Ptosis on the affected side which does not resolve with upward gaze
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What do you see? Where is the lesion?
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drooping of the R eye (decreased pupedral height). Also loss of sympathetic innervation of the pupils on the R so constriction on the ptosis side. also see ptosis on the R because loss of innervation in Muller's muscles. This ptosis RESOLVES when looking up because not a 3rd nerve injury. This is Horner's Syndrome
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label the 6 muscles of the eye
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Levator palpebrae superioris
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O: Lesser wing of spheroid bone, superior and anterior to optic canal
I: Superior tarsus and skin of superior eyelid N: Oculomotor nerve (CN III); deep layer (superior tarsal muscle) is supplied by sympathetic fibers A: Elevates superior eyelid |
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Listing's plane and movements of the eye
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divides the eye into anterior and posterior planes
movement about the x axis permits elevation (supraduction) and depression (subduction) of the eye movement about the y axis permits intorsion (incylcoduction) and extorsion (excyloduction) movement about the z axis permits eye adduction or eye abduction |
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Eye intorsion (incylcoduction) vs extorsion (excycloduction)
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eye rotated nasally vs eye rotated laterally, along the y axis
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medial rectus muscle of the eye
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O: common tendinous ring
I: sclera, just posterior to the corneoscleral junction, anterior to listings plane N: CNIII A: Adducts eyeball |
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Superior rectus muscle of the eye
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O: common tendinous ring
I: Sclera just posterior to corneoscleral junction N: CNIII A: elevates*, adducts, and intorsion of the eyeball (3 actions because its pull is not parallel to just one axis) |
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Inteferior rectus muscle of the eye
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O: common tendinous ring
I: Sclera just posterior to corneoscleral junction N: CNIII A: depresses*, adducts, and extorsion of the eyeball (3 actions because its pull is not parallel to just one axis) |
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superior oblique muscle of the eye
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O: Body of the sphenoid bone
I: into the sclera, deep to the superior rectus muscle, behind listings plane N: Trochlear A: abducts, depresses, and intorsion* of the eye |
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inferior oblique muscle of the eye
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O: anterior part of the floor of the orbit
I: sclera, deep to the lateral rectus muscle N: CNIII Action: elevates, adducts, and extorsion* of the eye |
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nerves of the eye
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Occulomotor nerve: arises from BOTH sides of the occulomotor complex and goes on to innervate the SR, MR, IR, and IO
trochlear nerve: arises from the contralateral side and innervates the SO Abducens: arises from the ipsiateral side and innervates the LR All enter the orbit through the superior orbital fissure |
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aneurysms of the cavernous part of the internal carotid will affect which nerve? What is the clinical presentation
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Abducens nerve. Eye will be in abduction (strabismus)
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The third nerve always passes through what area? How is this clinically relevant?
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always passes over gruber's ligament (petroclinoid ligament). branches of the posterior communicating artery can compress the third nerve. Only the LR and SO will be working in this case so eye will be extorted and depressed. pupil will be big because you knock out parasympathetic fibers
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Sherrington’s Law
(law of reciprocal innervation) |
antagonist muscles operating on the same eye are reciprocally
excited or inhibited. Ie If you tell lateral rectus to contract (EPSP in abducens nucleus) you need to inhibit medial rectus (IPSP in a subnucleus of the occulomotor nucleus that innervates the MR) |
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Hering’s Law (law of yoked muscles)
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muscles that produce conjugate eye movements are similarly excited or inhibited. Ie to look leftward across the horizon, you have to excite lateral rectus of the L and medial rectus of the R.
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strabismus
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misalignment of the eye typically involving a lack of coordination between extraocular muscles. The clinical symptom or presentation that results is diplopia
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Binoncular eye movements and version movements
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to maintain foveation when distance between eyes and the viewed object does not change. Both eyes will move in the same direction to follow the object.
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Binocular eye movements and vergence movements
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to main foveation when distance between eyes and viewed object increases or decreases. Eyes will each converge or diverge to follow the object.
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MLF
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Located from the rostal midbrain to the caudal medulla.
Highly myelinated and functional before birth. It can be thought of as a bidirectional highway that allows for interconnection of different cell groups. Axons "get off" of the MLF are the occulomotor, abducens, and trochlear nuclei. Axons "get on" (contribute) to the MLF from the gaze centers in the midbain: 1) parabducens nucleus 2) 3 subnuclei: interstital nucleus of Cajal, nucleus of dar, riMLF |
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3 nuclei that induce vertical gaze shift
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iMLF, nD, and iC (mesencephalic nuclei)
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horizontal gaze shift
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nuclei within the PPRF. stimulation of the PPRF induces ipsilateral gaze shift
Excitation of A with stimulate CNVI on the L (adduct the L eye) and CN III (abduct the R eye) |
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unilateral lesion of the PPRF induces?
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contralateral gaze shift. Opposite side works unopposed
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vertical gaze shift
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axons from nuclei in the vertical gaze shift centers go on to EPSP or IPSP CN III or CN IV nuclei.
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Two types of strabismus
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1) observed when patient is using both eye and when there is free vision of both eyes (tropia)
2) observed only when one eye is covered (phoria). |
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what type of strabismus is this (assuming pt is looking straight?
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This is strabismus, specifically esotropia involving the R eye. Suggestive of a right 6th nerve damage
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The R trochlear nerve innervates which superior oblique? axons arise from which trochlear nuclear?
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Ipsilateral superior oblique (Right)
Axons arise from the contralateral trochlear nucleus though (Left) |
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Damage of the the occulormotor nucleus will affect muscles on which side?
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will causes BILATERAL symptoms. The muscle affected on the contralateral side is the superior rectus
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Damage to the occularmotor nerve will affect muscles on which side?
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ipsiateral
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Damage to the trochlear nerve will affect muscle on which side?
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ipsilateral
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Damage to the abducens nerve will affect muscle on which side?
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ipsilateral
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Damage to the abducens nucleus will affect muscle on which side?
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ipsilateral
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Describe the eye issue on the L
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The eye is in supraduction and extorsion. Superior oblique damage would show this presentation. The inferior oblique is working relatively unopposed and the superior rectus is working unopposed.
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patient is holding with head tilt to the Right side with tilting in of the chin. Which nerve damage does this suggest and why?
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Damage to the trochlear nerve on the contralateral side. This maneuver will correct for the supraduction and extorsion present in the L eye
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We see strabismus, specifically exotropia with subduction. We also see ptosis that would not resolve with looking up. This is highly indicative of 3rd nerve injury
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Pt has head turned to the L side in order to see properly straight ahead. Which nerve is affected and on which side?
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abducens nerve on the L side. the L eye will be intorted (abducens innervates the lateral rectus). So to correct, pt will move head to the L
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which muscle/nerve is affected if pt sees like this?
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superior oblique muscle, right trochlear nerve injury so R eye is extorted
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for the red glass test, how would the pt with esotropia see the red and white lights?
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lateral displacement of the red dot. image is also likely blurry because image is not falling exactly on the fovea . This is an example of uncrossed diplopia
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Corneal light reflection test
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reflecting light off the cornea. Can visualize the degree of tropia based on how displaced the reflection is from normal
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A. 6th nerve injury on the R. At rest R eye has slight esotropia. This is primary deviation
B. Unaffected eye overadducts when you ask pt to fixate on an object straight ahead with the right eye. Because you are using “a lot of 6th nerve power” on the R and according to Hering’s law, this will happen to the other side as well. This is a secondary deviation tropia, and it is always greater than primary deviation. |
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Single cover test
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Test for evaluating tropia. Cover the fixating eye and observe the response in the non fixating eye.
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cover uncover test
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test for evaluating tropia. cover an eye and observe the response in that eye after you uncover it. When you uncover the good eye you should see a greater response because it would have had to move over way more which the bad eye tried to fixate
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comitant tropia
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the malaligned angle does not change with gaze shift. Suggests UMN injury...lesion above the gaze centers (info to the gaze centers is affected and gaze centers are not changing their command to the muscles irrespective of gaze shift.
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noncomitant tropia
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the malaligned angle does change with gaze shift. Suggests LMN injury...PNS injury
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What kind of issue is this?
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This is right esotropia. it is an example of a noncomitant tropia. 6th nerve injury on the R, likely in the PNS eye does respond to gaze shift
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alternate cover test
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test for evaluating phorias
alternately cover each eye and observe the response in the uncovered eye |
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eye movements initiated in brodman area eye are which kind of movements-- volitional or pursuit?
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volitional (this is in the frontal cortex)
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excitation of brodman area 8 on the R does what?
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Contralateral gaze shift, mediated by the MLF
for horizontal movement, PPRF of the contralateral side is stimulated, PPRF on the ipsilateral inhibited |
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immediately after stroke that kills area 8 on the R..eyes will be shifted to which side?
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eye will be shifted to the R. After some time, pt's gaze will return to straight ahead but will lose ability to move eyes to the L
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stroke that involves areas 8, 4, and 6 on the R
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inability to shift eyes to the L. L-sided hemiparesis as well
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Pursuit movements
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fibers project from the eye to the lateral geniculate, then areas 17 and the 18/19. then from these ares to the superior colliculi and then to the occulomotor nucleus which goes back to the eye
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parietooccipatal lesion will affect what kind of gaze movments?
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pt will pretty much alway be able to pursue movements from the periphery to primary gaze. But movement from primary gaze to the ipsilateral side is what is impaired. You would also have a homonymous hemianopsia on the contralateral side
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"Strong muscle contraction with one to three beats of clonus. Reflex spread to the contralateral side may be noted"
Which reflex grade is this? |
4+ (abnormal)
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"Strong muscle contraction with sustained clonus. Reflex spread to the contralateral side may be noted"
Which reflex grade is this? |
5+ (abnormal)
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Titubation
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Nodding movement of head or body seen with midline cerebellar lesions,
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Check and rebound
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Patient, with eyes closed, is unable to return a limb that has been tapped and displaced to its original position, overshoot occurs
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Astasia
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A lack of motor coordination marked by an inability to stand, walk or even sit without assistance due to disruption of muscle coordination
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Marcus-Gunn pupil (Relative afferent pupillary defect (RAPD))
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Defect in optic nerve leads to problem with direct light reflex in involved eye, when light source is rapidly moved from intact eye to involved eye, the pupil in the involved eye dilates
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How would right abducens nerve (CNVI) palsy affect horizontal gaze?
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Leftward gaze would appear normal. On attempting rightward gaze, the right eye would only shift to the middlle-ish, not all the way over to the right
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Pretectal nuclei on each side of the midbrain are connected to each other through?
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posterior commisure
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Describe the parasympathetic innervation to the sphinter pupillary muscle in response to direct + indirect light reflex?
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Light shines on eye signal is carried to both pretectal nuclei of the brainstem (because crossing fibers). The pretectal nuclei are connected by the posterior commisure. Each pretectal nuclei stimulates their respective Edinger Westhpal nucleus, which is where the presynaptic parasympathetic outflow originates. Travels with the third nerve into the orbital area and synapses in the ciliary ganglion. From here the postganglionic nerve project and go to the sphincter muscle as well as the ciliary body
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depolarization in hair cells of the cochlea is due to what?
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vibration of the basilar membrane causes "rubbing" of cochlear hair cells against the membrane tectoria, causing the hair cells to bend. Bending of the hair cells forward, closing off K+ channels. This causes reduced K+ efflux and depolarization of the membrane
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contraction of the tensor tympani has what result?
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"stiffens" the tympanic membrane, less movement of the TM, and lessens the movement of the ossicles, dampens sound; protective mechanism
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contraction of the stapedius has what result?
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restricts movement of the stapes foot plate, lessens compression on the oval window and dampens sound; protective mechanism
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embryological origin of the tensor tympani muscle?
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1st branchial arch, supplied with the trigeminal nerve
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detection of low and high frequency by hair cells--which parts of the basilar membrane?
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hair cells located at the base respond to high frequency sounds, hair cells located at the apex respond to low frequency cells
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movement of the hair cells towards the longest cilia on the hair cell-- does this depolarize or hyperpolarize?
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depolarize
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dorsal cochlear nucleus preferentially responds to which frequency tones?
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high frequency
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what structure does the central process coming from the spiral ganglia to reach the cochlear nuclei pass through to get there?
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interior auditory meatus
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all thalamocortical projections pass through which limb of the internal capsule?
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posterior limb
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auditory and visual projections of meyers loop from the medial and lateral thalamus respectively pass through which part of the internal capsule (specifically)?
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posterior limb, sublenticular part
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superior transverse temporal gyrus
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aka Heschl's gyrus. receives primary auditory input from the medial geniculate. This is Brodmann's area 41.
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innervation to the stapedius
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branches come from the superior olivary nucleus; facial nerve
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4 types of "dizziness" a patient may describe
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1) vertigo (illusion of movement)
2) pres-yncope (feeling faint, no LOC) 3) disequilibrium (sense of imbalance, no vertigo) 4) lightheadedness (ill-defined, often r/t meds) |
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functions of the vestibular system
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1) maintain visual acuity in response to changes to head and body postion]
2) facilitate muscle activity required to maintain upright position |
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firing of hair cells in the macula
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they are always being acted on by gravity and thus have a basal firing rate that helps to detect orietnation in space. these cells also respond to linear acceleration and head tilt which causes stones to shift and bending of the cilia. Bend increased firing rate
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dizziness at rest suggests issue which which receptor system- the macula or cristae?
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macula
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of the 4 vestibular nuclei, which is most significant in regards to the vestibular system?
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lateral vestibular nucleus (deiter's nucleus). contains the largest cell bodies of the 4). Important role in vestibulospinal tracts. Implicated in opisthotonis, sign of decerebrate rigidity
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Oscillopsia
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inability to maintain visual fixation with movement. caused by issue regarding the vestibular system communication with the extraocular nuclei
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ocular counter roll
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eye movement in the opposite direction than the direction the head rotated, mediated by the vestibular system. when the head movements, you induce act movement of fluid in 2 corresponding canals in each side in opposing directions. Activate vestibular nuclei on the side you are turning to and inhibit the other side. Activate the ipsilateral MR (III) and inhibit the ipsilateral LR (VI) and vice versa on the other side in order to activate contralateral gaze shift.
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Describe the ocular counter roll when you tilt to L shoulder in the sagittal plane? Which muscles are involved? Which otolitic organs will you excite?
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Right eye extorts and L eye intorts. Oblique muscles are involved. Note that this movement of intorsion has not cortical input (NOT VOLUNTARY!) only through reflexes.
Activate the otolithic organs on the downgoing side (ipsilateral side) |
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Left jerk nystagmus
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on spinning to the L, fluid in the semicircular canal moves to the right. the eyes move slowly to the right (driven by the vestibular system), then fast to the left (reset driven by the cerebral cortex)
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post-rotational nystagmus
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after rotating and stop, fluid moves in the opposite direction very briefiy. If you have been rotating to the L, and you stop, now the fluid which was moving to the R goes to the L. So it gives you a brief right jerk nystagmus
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damage to R vestibular apparatus will have which type of nystagmus?
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Left jerk nystagumus, fast to the left, slow to the right. (nystagmus named by opposite ear)
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fast reset component of nytagmus requires intact what input?
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cortical input. if you have a pt without this, you will just see the slow contralateral gaze shift component mediated by the vestibular system
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cold irrigation stimulation
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inhibition of ipsilateral vestibular system . eyes gaze to the side that has been irrigated and induce jerk nystagmus to the contralateral side
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irrigate L ear with cold water?
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Right jerk nystagmus
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If you do cold irrgation on an unconscious patient on the L ear and pt's eyes tonically deviate to the cold irrigated side. Where is the problem/ reason for unconsciousness?
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brainstem is intact (because vestibular response is there), but cerebrum is not (area 8)
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CN 9, 10, 11 pass through which opening of the cranium?
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jugular foramen
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somatic afferents of bulbar CNS--> superior or inferior ganglia?
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superior (jugular) ganglia
these transmit info from receptors derived from ectoderm and somatic mesoderm. |
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visceral afferent of bulbar CNs--> superior or inferior ganglia?
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inferior (petrosal) ganglia
these transmit info endoderm and splanchnic mesoderm. synapse in the nucleus solatarius |
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Ninth (glossopharyneal) nerve functions
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fibers go to
1) carotid sinus 2) pharyngeal mucosa (afferent limb of gag reflex) 3) taste buds (posterior 1/3 of the tongue) 4) partoid gland (motor) |
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nucleus solitarius receive which fibers?
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receive visceral afferent fibers from the glossopharyngeal nerve
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only muscle derived from the third branchial arch?
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stylopharyngeus (receives efferent fibers from the nucleus ambiguous)
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vagus nerve functions
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Mostly autonomic. go to the carotid body, mucosa of the abdomen, glands, etc
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gag reflex
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input from physical stimulation of receptors on the pharyngeal mucosa comes through the 9th nerve to nucleus solitarius. Acts on nucleus ambiguous to cause construction of pharyngeal muscles through the 10th nerve
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Have pt open mouth and say "ahhh". Uvula deviates to the R. What is the issue??
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Damage to the 10th nerve on the L side.
There is weakness of the L levator veli palatini. uvula deviates to the normal side when say ahhh. note that you are not physically stimulating anything but rather stimulation is coming from the pt's cerebral cortex. afferent lesion |
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Pt with R sided stroke will have weakness tuning the head to which side?
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They will actually have ipsilateral SCM weakness so weakness will be in turning to the hemiparetic side.
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contraction of the genioglossus muscles causes?
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causes protrusion of the tongue
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You ask patient to stick out tongue and notice deviation to the L. What is the issue?
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issue with the L genioglossus muscle which is innervated by L hypoglossal nerve
(ipsilateral muscle issue, ipsilateral nerve involvement) |
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What is the issue?
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atrophy on the L side of the tongue. motor units on the L are dennervated. The lesion is of the L 12th nerve. Tongue will deviate to the L on protrusion
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In patient with suspected hearing loss in the right ear, the Rinne's test reveals that AC>BC. Is this finding suggestive of conductive deafness or sensorineural deafness of the right ear?
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Sensorineural
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In patient with suspected hearing loss in the right ear, the Rinne's test reveals that BC>AC. Is this finding suggestive of conductive deafness or sensorineural deafness of the right ear?
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conductive
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If there is a conduction deficit in the R ear, which way will the sound lateralize during the Weber test?
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the affected R ear
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If there is a sensorineural deficit in the L ear, which way will the sound lateralize during the Weber test?
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The unaffected R ear
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On Rinne test, AC>BC in the suspected bad ear indicates a problem where and in which way?
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Sensorineural deficit on the affected side
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Person with MLF lesion with show what kind of movement of the eyes when turning head to right?
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Normally, the MLF allows the abducens nerve to comminicate with CNIII contralaterally and activate it. if you lose this, only abducen (LR) will function. So movement to the right will allow abduction of the left eye as normal but the right eye will stay in the middle (internal opthalmoplageia)
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Person who is comatose shows the ability upon right rotation of the head to abduct L eye and adduct right eye. Is the brainstem intact?
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yes. Vestibulo-ocular reflexes are intact in this patient
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Comatose pt is tested for "doll eyes" and upon head rotation to the right, eyes stay fixed. What is this indicative of?
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low brain stem damage (vestibulo-ocular reflexes are not intact)
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Caloric test given to a brainstem dead patient, what response would you expect?
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No movement of the eye balls
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Trigeminal reflexes (4)
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1) corneal reflex
2) Lacrimal reflex 3) Jaw jerk 4) Occulocardiac reflex |
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cell bodies for the proprioception component coming from the divisions of the trigeminal nerve is located where?
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mesencephalic nucleus (pain, temp, and fine touch cell bodies are located within the trigeminal ganglion, proprioception is the exception there)
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If you can still feel fine touch on the face but cannot feel pain or temperature, where is the lesion?
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The lower part of the spinal nucleus (which receives fibers for pain and temperature from the trigeminal divisions). Recall that the fibers for fine touch go to the primary pontine nucleus, the the fibers for proprioception goes to the mesencephalic nucleus directly (doesnt pass through the trigeminal ganglion)
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"pathway" of the corneal reflex of the trigeminal nerve
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stimulus to cornea --> long ciliary nerve (branch of nasal ciliary nerve, which is a branch of V1) --> upper part of the spinal nucleus ---> facial nerve nucleus --> temporal and zygomatic branches --> orbicularis oculi --> blink
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trigeminal leminiscus
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made up of the fused ascending ventral (pain and temp) and dorsal (fine touch, proprioception) trigeminothalamic tracts.
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Sensory to the VPM vs VPL?
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Pretty much all the sensations (touch, pain, temp, proprioceptio) from the BODY go to VPL
Pretty much all sensations from the head and neck go to VPM |
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all things innervated by the afferent division of CNV have what embryological origin?
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ectoderm and somatic mesoderm. The sensory division of CNV is GSA (general somatic afferent)
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The motor division of CNV innervates skeletal muscle that are embryologically derived from where?
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Branchial arch derived skeletal muscle. The motor branch of CNV is SVE (special visceral efferent)
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nerves passing through the superior orbital fissure?
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occulomotor, trochlear, abducens, and opthalmic division of CNV
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innervation of the cornea?
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long ciliary branch of V1
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"dermatome" for frontal nerve branch of trigeminal?
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forehead and anterior 2/3 of the scalp
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what types of fibers do the long vs short ciliary nerves carry:
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long ciliary nerve carries sympathetic fibers which dilate the pupil. The short ciliary nerves come from the ciliary ganglion and carry postsynaptic parasympathetic fibers that go to constrict the pupil
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infraorbital nerve
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branch of V2 of the trigeminal. comes through infraorbital canal and supplies the skin of the cheek. also gives rise to the sensory fibers that innervate the upper teeth and gums
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when you bite your tongue, what nerve is being stimulates?
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CNV (V3), specifically the lingual branch. in contrast, taste buds are innervated by branch of CNVII which travels along with the lingual branch
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if patient has numbness on one side of the tongue and loss of taste, where is the lesion?
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the lingual branch of V3. Notes that the numbness issue is actually due to CNV whereas the taste bud piece is due to CNVII, which rides along lingual branch of CNV
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the angle of the mandible is innervated by?
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C2 C3. (NOT 5!)
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nociceptive information from the head and neck travelling through the trigeminal system synapse where?
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That info will go down as spinal tract of V and synapse in the spinal nuclei of 5 They will then go on to form the ventral trigeminothalamic tract
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nonnociceptive information from the head and neck travelling through the trigeminal system synapse where?
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primary and mesencephalic nucleus of V. They will then go on to form the dorsal trigeminothalamic tract
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masseter reflex
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abnormal segmental muscle stretch reflex. normally it is suppressed but in patients with frontal lobe issue, will be able to elicit
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corneal reflex afferent and efferent limbs?
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approach pt eye from the side and touch the cornea with a cotton tip. Response elicited should be bilaterl blinking. This work by: stimulation of cornea --> afferent limb is CNV --> efferent limb is CNVII
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Lacrimation reflex
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irritation of cornea --> long ciliary branch of V1 --> spinal nucleus of V --> synapse on superior salivatory nucleus (pregnaglionic parasympathetic cell bodies here) and outflow through the facial nerve--> pterygopalantine ganglion - -> lacrimal gland
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Derivatives of the 2nd branchial arch is innervated by what?
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facial nerve
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autonomic and afferent component of the facial nerve is carried by which of the branches?
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nervus intermedius
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what muscles are innervated by the facial nerve?
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innervation of the lacrimal gland
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fibers from the superior salvitory nucleus, travels to pteryopalatine ganglion and synapses there. postsynaptic fibers run up to the lacrimal gland
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what is the visceral association nucleus called? (target of visceral affernts)
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nucleus solatarius
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geniculate ganglion contains which type of fibers?
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contains afferent fibers, both visceral and somatc
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what is the somatic associated nucleus called? (target of somatic afferents)
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contains both visceral and somatic spinal nucleus of 5
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Lesion here would cause what kind of symptoms?
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IT would affect both the facial and the abducens (because facial fibers come up and wrap around the abducens). Patient would present with ipsilateral facial weakness and esotropia of the affected side, with difficultly gazing to the ipsilateral side (LR is not working)
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somatotropy of the facial nucleus?
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dorsal --> upper face
ventral --> lower face note that fibers from the cerebral cortex are weird. innervation to the upper face receives bilateral inneration whereas the lower face receives fibers only from the contralateral cerebral cortex. so upper 7 issue = spare the upper face but rest of contralateral face is weak vs lower 7 issue= whole contralateral face weakness |
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testing frontalis
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raises the eyebrows (is telling you about integrity upper facial nucleus(
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testing orbicularis orbis
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purse lips (is telling you about integrity of lower facial nuclus)
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testing risorius
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show your teeth (is telling you about integrity of lower facial nuclus)
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what are the two possible nerve lesions you may suspect in this patient?
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this is definitely an issue with the facial nerve. It could be a left lower 7th nerve palsy or right upper 7th nerve palsy. upper face decifits are unclear
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say that the left side showed ptosis and that you suspect an issue with muller's muscle. what else would you except to see in the affect eye?
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pupil would be constricted (muller's muscle--> sympathetic fibers)
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increased palpebral height on the L (paralysis of orbicularis oculi), risorius issues, frontalis issues. see complete L paralysis so know it is a peripheral issue not central. LMN
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What issue does this guy have
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right 7th LMN
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bells phenomenom. Upward and outward movement of the eye, when an attempt is made to close the eyes; (relfexive contraction of the superior rectus when the orbicularis oculi contracts) It becomes noticeable only when the orbicularis oculi muscle becomes weak. note that this guy also has bell's palsy
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What issue is this? what other signs would the patient have?
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THis is a right UMN 7th nerve issue. Pt will also have L sided hemiparesis. Babinski sign will be present on the L. (typical stroke presentation)
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ROSTRAL MIDBRAIN
arrow-Occulomotor complex 1- medial leminiscus 2- brachium of the inferior colliculis 3- superior cerebellar peduncle 4- cerebral peduncle lesion in 2 would cause bilateral hearing loss, worse in the contralateral ear |
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ROSTRAL MIDBRAIN
Rostral- red nucleus is present as well as the superior colliculis Occulomotor is present at this level (2 components of= GSE and GVE) Arrow shows the occulomotor complex, the lighter part = edinger westphal nucleus |
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At the intercollicular level
1- brachium of the inferior colliculis 2- trochlear nucleus (occupying the ventral midbrain) 3- MLF 4- medial leminiscus 5- decussation of the superior cerebellar peduncle |
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Level of the inferior colliculi
1- Lateral leminiscus 2- commisure of the inferior colliculis |
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Arrow- axons of the facial nerve
2- abducens nucleus 1- facial nucleus |
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Identify. What symptoms would you expect with lesion of 2
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Level of the ponto-medullary junction
1- facial nucleus 2-Spinal tract of the trigeminal nerve ("lisseur's tract of V"). Notes that if there is a lesion here, ipsilateral issues with nociceptive stimulation 3- spinal nucleus of the trigeminal nerve |
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level of the medulla,
1 – hypoglossal nuclei 2- MLF medial medullary syndome-- loss of medial leminiscus, tectospinal, and MLF. |
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1- vestibular nuclei
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1- nucleus solitarius
2- tract of solitarius |
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1- nucleus gracilias
2- nucleus cuneatus 3- lateral cuneatus 4- spinal nucleusof 5 5- spinal tract of 5 |
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transitioning from the medulla to the spinal cord, what does the spinal nucleus of V become?
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dorsal horn, substancia gelatinosa
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Patient has difficulty with the heel to shin test, spefically moving the right heel down the left shin. Where is the lesion most likely?
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Right cerebellar hemisphere. This is called dysmetria
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touch, pain, temperature of the face go where in the brainstem??
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the trigeminal system. this is like that anterolateral system but for head/face area
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How many sympathetic ganglion do the head and neck have and what are they?
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1) ciliary ganglion
2) pterygopalantine ganglion 3) submandibular ganglion 4) otic ganglion |
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Facial nerve has what 4 type of fibers? What the the corresponding nuclei in the brainstem for each of these ?
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1) branchiomtor--> go to the primary facial nucleus
2) parasympathertic fibers --> superior salivatory nucleus 3) taste sensation to the anterior 2/3 of the tongue --> nucleus solitarius 4) pain, touch, temp fibers for external ear --> spinal nucleus of V |
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Taste to the anterior 2/3 of the tongue is provided by what nerve? Pain and temp to the anterior 2/3 of the tongue is provided by what nerve?
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TASTE --> Facial
PAIN/TEMP --> Trigeminal, lingual branch of V3 |
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geniculate ganglion contains which cell bodies?
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afferents that are part of the facial nerve--> taste sensation from the anterior 2/3 of the tongue (special visceral afferents) and pain/touch/temp fibers coming from the external ear (general somatic afferent)
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Complete 3rd nerve palsy
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Eye with dilated pupil looks down and out with ptosis. Patient will also have diplopia
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What kind of findings would you see during the swinging flashlight test when testing a patient with RAPD?
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RAPD= relative afferent pupillary defect. It is often due to small or previous damage to the optic nerve on one side, lets say the left. What happens then with the swinging flashlight test is that when the light eye is illuminated, the L eye strongly constricts but when the L eye is illuminated, it only weakly constricts. So during the swinging flashlight test, the affected eye appears to dilate when light is shone directly on it--> this is called a marcus gunn pupil
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one and a half syndrome
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This is when the PPRF complex as well as both MLF are damaged. Lets say that it is the right PPRF. So what would happen is that you would lose the ability to gaze rightward and then on leftward gaze, only the left eye would move outward.
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3 layered cerebral cortex and what kind of things are located there?
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Accounts for 10% of the whole thing. (90% of it is 6 layered)
Cortical regions involved in encoding experiences into synaptic changes so you can recall them later--> those cortices are the 3 layered ("oldest" evolutionarily) |
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What type of cortical areas are the oldest evolutionarily?
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the 3-layered areas. These areas are involved in memory storage
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areas at the top? area at the bottom?
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top is where the pia mater is, bottom is transition of white to gray matter
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less densely packed area contain what in this stain?
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dendrites and axons (things that occupy space that are not Nissl)
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names of the 6 layers of the cerebral cortex?
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external= closer to the pia surface
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what can you say about the axons in the granular layer?
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likely to be interneurons, commincate with nearby cells within the same hemisphere (as opposed to pyramidal cells which likely communicate more at a distance)
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max amount cortical neurons is presents when?
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before birth (end of the 2nd trimester)
note that the size of the brain growth through life is due to increase in the size and branching of dendrites as well as glial cells |
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primary somatosensory cortex -- what brodman area?
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3, 1, 2
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agnosias involve an abnormality in which area(s) of the brain?
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abnormal association cortices (this is where the interpretation occurs)
Agnosia= ability to perceive but not recognize |
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inability to perform a previously learned motor act?
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Apraxia. issue with the "program writing cortices" in the parietal and frontal lobe, integrative association cortices are not working
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which of the subcortical white matter types are the inner pyramidal fibers?
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descending projection fibers
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VPL and VPM of the thalamus gives rise to fibers that ascend where?
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ipsilateral projection, goes to post-central gyrus, brodman areas 3,1,2 --> associated with senstations experiences from the body (VPL) and the head/face (VPM)
go through the posterior limb of the internal capsule |
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DM gives rise to thalamocortical projections that ascend where in the cerebral cortex?
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ipsilateral projection, goes to frontal lobe, anterior cingulate part and orbital cortex--> associated with nociceptive judgement of a stimulus; also important in psych health
go through the anterior limb of the internal capsule |
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Lateral geniculate of the thalamus gives rise to fibers that go where?
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ipsilateral projection, goes to brodman area 17, important in visual projections
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CM of the thalamus gives rise to projections that project where?
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project (right back) to the striatum
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Medial geniculate of the thalmus have fibers that project where?
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travel through the posterior limb, sublenticular part, and project to the auditory cortex (superior transverse temporal gyrus)
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thalamocortical projections vs reticulocortical projections
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thalamocortical projections are more focused--there is a specific gyri for most of them, the reticular projections are more widespread, more collateral branches. this is important in the function of the reticular formation because is is involved in consciousness/awareness and maintaining brain consciousness at all times
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metathalamic nuclei
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MG and LG
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3 major transmitter systems associated with the reticular formation?
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serotonin, NE, and DA
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where are the axons of the monoaminergic fibers coming out of the reticular formation found?
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MFB- medial forebrain bundle. . largely unmyelinated fibers, important in the reward and pleasure
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nucleus of meynert
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home of cholinergic cells, just medial to the nuclelus accumbens (located in the ventral pallidum below the anterior commisure) extensive cholinergic projections from here. among the first nuclei that die in pts that develop alzheimer's dementia
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corticobulbar (aka corticonuclear) fibers are located in which limb of the internal capsule?
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TRICK! its the genu
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commissural fibers- what do they do
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interhemispheric fibers, involved in interhemispheric communication
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label the 4 parts of the corpus callosum
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fibers of the corpus callosum connect what in the brain?
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between lobes in each hemisphere (so like occipital to occipital or frontal to frontal). Note that it connects AREAS not specific gyri or specific targets
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what part of the corpus callosum is this?
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body- this is the frontal lobe (can see lateral ventricle an the nucleus accumbens)
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which areas of the brain are LEAST connected areas by the corpus callosum?
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PRIMARY sensory and motor cortices (ie 3,1,2,4,17,etc) because you want to be able to separate tactile stimuli hitting R vs L hand, for example. these cells do not really give rise to commisural fibers. commisural fibers arise from association cortices, modality specific and integrative.
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splenum connects which lobes?
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occipital lobes and the posterior parts of the parietal and temporal lobes
this is a pretty big connecting part of the brain (forceps major) |
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unique function fo the anterior commisure:
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1) in addition to interconnnecting 6layer cortices, also interconnects 3 layers cortices (limbic system)
2) contains crossing fibers from the olfactory system 3) interconnect nuclei of the telencephalon ("nucleonuclear projections"), internuclear projections from the amygdloid on each respective side the anterior commisure is phylogentically "older" than the corpus callosum |
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what do you see and what types of things you would see on this patient on physical?
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agensis of the corpus callosum
would see nothing! these people are symptom free. they were born this way so compensation. |
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association fibers
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intrahemispheric fibers
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uncinate fasiculus
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runs from the temporal lobe to the frontal lobe. implicated in uncinate epilepsy
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arcuate fasiculus
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connects wiernicke's area and broca's area, two integrative cortices. phylogenetically "new" intrahemispheric bundle
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cingulum
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connects the limbic system, important in formation of new memories
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reticular formation-- cell body size of the cells of the lateral 1/3 vs medial 2/3
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small in the lateral 1/3 and large in the medial 2/3
note that its the larger medial cells that will give rise to efferent axons the function of the lateral 1/3 area is the RECEPTIVE (afferent) area |
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cells in the reticular formation that synthesize 5HT are located where?
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close to the midline, clusters in the midbrain, pons, and medulla, but all near midline. these are called the raphe nuclei
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locus coeruleus of the reticular formation?
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NE projections both rostrally and caudally from
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monoaminergic pathways
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phylogenetically very old. have huge collateral branches as well. these cells do not play a role in any sensory modality, they keep cells at a level so that when specific projections come from elsewhere, those cells are ready to fire. keep cortical and subcortical cells close to threshold. if you drop these levels, system dial down their receptivity (become sleep, lethargic, or even coma)
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reticular nucleus of the thalamus separate what structures?
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thin layer of cells that separates the external medullary lamina of the thalamus and the internal capsule
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reticular nucleus function
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inhibit effect on thalamic neurons that excite cells in the cortex. way to modulate thalamocortical activity
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Deactivate the ascending reticular activating system?
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system goes down--this would put a patient in coma or stupor (unresponsiveness)
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coma (as defined by plum and posner)
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state of unarousable, unconsciousness in which the individual lies with eyes closed
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key components or hallmark of delirium?
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transient and organic (ie due to metabolic condition, so reversible), characterized mainly by problem with attention
patient is typically oriented to time and place but not person or situation |
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arousal
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LEVEL OF CONSCIOUSNESS
primitive set of automatic responses, involve phylogenetically old network of nuclei and pathways located in the BRAINSTEM- thalamus and reticular formation. Damage to the brainstem= problems with arousal |
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Awareness
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CONTENT OF CONSCIOUSNESS
ability to integrate multiple sensory experience that result in a meaningful and authentic understanding of their environment and themselves. The "neural substrate of awareness" is NOT the brainstem, rather above the tentorium, specially the cerebral cortex |
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A patient with brainstem (infratentorial) damage will have impaired arousal or awareness?
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both, but by the book, more decrease in arousal
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A patient with cortical damage will have impaired arousal or awareness?
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both, but by the book, more decreased awareness
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evaluating the functional integrity of midbrain, pons, medulla?
|
different reflexes allow for you to test the integrity of different areas of the brainstem.
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pupillary reflexes--> evaluating integrity of which part of the brainstem?
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the rostral midbrain
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corneal reflex --> evaluating integrity of which part fo the brainstem?
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pons/ pontomedullary junction
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oculocephalic reflex (dolls eye reflex) or oculovestibular reflex (cold caloric)--> evaluating integrity of which part of the brainstem?
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pontomedullary area/vestibular system
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gag reflex --> evaluting integrity of which part of the brainstem?
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rostral medulla
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testing response to non-noxious and noxious stimuli is testing what part of the brainstem?
|
long tracts passing through RT
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Decreased arousal suggests damage where? What are the common mechanisms of this type of injury?
|
BRAINSTEM
most commonly due to primary causes = trauma or ischemia or secondary causes = compression |
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decreased awareness suggests injury where? What is it usually due to?
|
cerebral cortex
Most often due to toxic or metabolic disease. This is a temporary state usually-- brain cells are "poisoned but not dead" |
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a patient who is "lethargic" responses how to non-noxious and noxious stimuli?
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they appear drowsy at resting state but will become alert to non-noxious/verbal stimulus. They respond normally to noxious stimuli
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an obtunded patient will respond to non-noxious and noxious stimuli how?
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they respond only to noxious stimuli
non-noxious or verbal --> patient shows no response. But to noxious stimuli (like sternal rub), they show a purposeful (ie tries to move away) and lasting (response lasts longer than stimuli) response. |
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a stuporous patient responds to non-noxious and noxious stimuli how?
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no response to non-noxious or verbal stimuli. In response to noxious stimuli, they do respond but in a non-purposeful manner (ie a slight flicker) and the effect is only as long as the stimulus is applied
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a patient in a coma responds to non-noxious and noxious stimuli how?
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will not respond to either period
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pt who has infratentorial lesion will show what kind of signs?
|
will show problems largely with arousal, allow likely to see signs to decreased awareness as well
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Glascow coma scale
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3-15 scale
usually reported as score for each component (E2, V2, M3, total GCS=7) |
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Decerebrate posturing
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both upper and lower limbs extended
MORE CAUDAL LESIONS |
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Decoriticate posturing
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caused by MORE ROSTRAL LESIONS because the rubrospinal pathway is opposing its influenced relatively unopposed. muscle tone= flexion in UPex due to rubro and extension in LOEx due to vestiule
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what is "C"?
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perineurium
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what is "B"?
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epineurium
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what anatomical components are needed for phonation?
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vocal folds
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what anatomical components are needed for resonation?
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pharynx, paranasal sinuses
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What is dysarthria and which structures and nerves are involved?
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problems with articulation (not with language), involving the lips, tongue, jaw. Innervated by CNX (pharynx), CNXII (tongue), CNVII (lips)
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KLM test
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Good bedside test to look for articulation problems.
K--> requires pharynx contraction L--> requires tongue movement M--> requires orbicularis oris / lip movement |
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Arcuate fasiculus is what kind of "bundle" (projection, association, etc?)
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It is an association bundle, because it connects areas within the same hemisphere
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what white matter area does the arcuate fasiculus run through?
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extreme capsule (brodmann areas 39-40).
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What is the thickness of the cerebral cortex in the area that arcuate fasiculus runs through?
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Thickness is about 3mm here, so you would have to go 3mm through the cortex with a lesion until you impinge the underlying arcuate fibers. this is not very deep so with lesion, injury to the arcuate fiber is fairly likely
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Planum temporale on the R vs L?
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The planum temporale is important in language functions. This area is about 10x larger on the L than R (although both hemispheres are involved in language)
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aphasia
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a problem with LANGUAGE (as opposed to articulation, which is dysarthria)
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anomia
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inability to name objects
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2 components of lanugage
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propostitional component --> grammer, syntax, mental dictionary; represented by fluency, comprehension, and repitition. LEFT hemisphere mediated in 95% of R handed people
Prosodic component-- acoustic and intonational functions (rhythm, rate, tempo, melody. RIGHT hemisphere mediated in 95% of R handed people) |
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Lesions in the R hemisphere will affect which component of language?
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prosodic component
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Lexical fluency test
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Evaluate the fluency component of language function
“Say as many words as you can that begin with the letter “S” until I tell you to stop (1 min) (typically use S, A, F) |
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Semantic fluency test
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Evaluate the fluency component of language function
“Name as many items as you can that you can find in a grocery store” (1 min) |
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semantic aphasia
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disorder of language in which the patient uses related word substitions (patient says watch instead of clock, for example). This is a problem with spoken output (frontal lobe lesions, on the L side in 95% of people-broca's area)
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Phonemic aphasia
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disorder of language characterized by sound substitutions“blister” for “sister”, “get” for “met”. THis is a problem with spoken output (frontal lobe lesions, on the L in 95% of people- broca's area
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5 different synonymous names for fluency aphasia?
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motor, expressive, Broca's, anterior, non-fluent aphasia. This means an inferior frontal defect. Patient has trouble with output.
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5 different names for comprehension aphasia?
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sensory, receptive, Weirnicke's, posterior, fluent aphasia. Patient has trouble with input
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semantic dyslexia vs agnostic dyslexia
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patient knows they see written are symbols meant to communicate but can't read it vs do not recognize as symbols meant to communicate
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Patient cannot repeat "No ifs, ands, or buts". Which area is damaged
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arcuate fasiculus. Pt understands the task, and is able to speak, but cannot repeat because communication between weirnicke's and broca's is lost (conductive aphasia)
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Which artery is this perfused by?
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MCA. Has both an anterior and posterior branch. A person which an aphasia in this area would have global aphasia (deficits in broca, arcuate, and weirnicke's)
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lesions here would cause what?
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transcortical motor and sensory aphasias
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praxis
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the ability to perform learned movements
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transitive vs intransitive movements?
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intransitive (do not require a tool)
transitive (require a tool) |
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Dressing apraxia
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R hemisphere dysfunction. message for a program is never sent out
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Lesions assoicated with disconnection apraxias are most often found where?
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subcortical white
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ideational apraxia- what are the characteristics and where is the lesion most commonly?
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-cannot perform an act on command or request
-cannot understand a command or request -cannot select the correct tool for the requested task -cannot perform the act when given the correct tool Lesions are typically in the left parietal lobe |
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Ideomotor apraxias
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-cannot perform an act on command or request
-can understand a command or request -may select the correct tool for the requested task -can perform the act when given the tool UMN, LMN, peripheral nerves all intact. These types of deficits are coritcal and involves the very first steps |
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Pt has agenesis or hypogenesis of the corpus callosum...which side would they have symptoms in?
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no problems with using the right hand but couldnt do things with left hand
The corpus callosum is important in the transfer of info from the left to right hemispheres. lack of these= dont stimulate right motor corticies, and then motor difficulties on the L side |
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Agnosia
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failure to recognize based on sensory characteristics when sensory is intact
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Apperceptive agnosia
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Inability to mentally assemble a visual image.. patient cannot identify a visually perceived object , cannot match objects that are the same presented from a different viewpoint, and cannot draw (copy) objects/images presented visually
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Associative agnosia
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Inability to recognize objects presented visually ..patient cannot identify a visually perceived object . They can match objects presented visually and can draw (copy) objects/images presented visually but cannot name objects drawn.
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Balint syndrome
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Characterized to not see the whole when looking at something. Have "mental tunnel vision" and only recognize a small part of a whole picture.
Lesions are located bilaterally, in the parieto-occpital regions (watershed infarcts) Components are: 1) Simultagnosia (inability to see all parts of the visual field simultaneously ) 2) Ocular Apraxia (inability to move the eyes smoothly to a target difficulty moving the eyes away from central fixation ) 3) Optic Ataxia (difficulty in visually guiding hand movements incoordination of visually guided hand movements) |
pt would only see one part (ie water spilling)
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Prosopagnosia
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Inability to recognize familiar or famous faces
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Second most common site of the circle of willis for an aneurysm? What types of visual issues?
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posterior communicating; 3rd nerve palsy
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blood supply to the internal capsule?
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anterior limb --> from the anterior cerebral artery
genu--> from the middle cerebral artery posterior limb --> from the anterior choroidal artery (branch of the internal carotid) |
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blood supply to the head of the caudate nucleus?
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anterior cerebral artery
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blood supply to most all of the putamen?
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middle cerebral artery
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blood supply to the globus pallidus?
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about half middle cerebral, half anterior choroidal
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Blood supply to the thalamus?
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posterior cerebral artery
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Blood supply to Wernicke's area?
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middle cerebral artery, inferior division
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Blood supply to Broca's area?
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middle cerebral artery, superior division
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Pt has an infarction in the area supplied by the left MCA, superior division. What deficits would you expect?
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This is affecting Broca’s area, so we could expect to see nonfluent aphasia. In terms of motor weakness, we would expect to see contralateral face and arm weakness. Pt may have some sensory loss in these areas as well
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Pt presents with fluent aphasia, right homonymous hemianopsia, sensory loss on the right arm and face. Which cerebral artery is affected?
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Pt has an infarction in the area supplied by the left MCA, inferior division
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Pt presents with UMN type lesion, with purely motor deficits, specfically right hemiparesis. You suspect an infarction in one of the cerebral arteries. Which is the most plausible?
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deep branches of the left MCA
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Pt presents with right hemiparesis, right sided sensory deficits, right homonymous hemianopsia, and both fluent and non-fluent aphasia. Eyes are shifted to the left. Which artery is the cerebral infarction in?
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MCA, stem
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Pt presents with nonfluent aphasia and R face and arm weakness. Which artery is most likely infarcted?
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Left MCA, superior branch
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Pt has left face and arm weakness. as well as some mild sensory loss in these areas. Which cerebral artery is most likely infarcted?
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The right MCA, superior division
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Pt has severe left hemineglect, left visual field deficits. Initially, you also noticed right gaze preference. Which cerebral artery is most likely infarcted?
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right MCA, inferior division
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Pt presents with UMN type lesion, with purely motor deficits, specifically left hemiparesis. You suspect an infarction in one of the cerebral arteries. Which is the most plausible?
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Right MCA, deep branches
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Pt presents with left hemiplegia, left sensory deficits, left homonymous hemianopsia, and profound left hemineglect. They also have a right gaze preference acutely. which cerebral artery is most likely infarcted?
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Right MCA, stem
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Pt presents with right lower leg/foot weakness and sensory deficits, as well as some behavioral abnormalities. Which cerebral artery is mostly likely infarcted?
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left ACA
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Pt has left lower leg/foot weakness of the UMN type and cortical-type sensory deficits . You also notice behavioral abnormalities. Which cerebral artery is mostly likely infarcted?
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right ACA
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Patient presents with right homonymous hemianopsia. Pt also notes alexia (inability to read), but is still able to write. Which cerebral artery is most likely infarcted?
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left PCA
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Pt presents only with left homonymous hemianopsia. You suspect an infarction in a cerebral artery. Which one is most likely
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a small right PCA. Notes that you could also have a right inferior MCA infaraction, except that in those patients you would expect to see other findings, namely left hemineglect.
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A 9-year-old boy presents with progressive severe headaches. Physical examination finds paralysis of upward gaze and increased intracranial pressure, which is the result of a mass producing an obstructive hydrocephalus. A mass located at which site is most likely?
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pineal gland. This is classic is Parinaud's syndrome, also called dorsal midbrain syndrome.
Paralysis of upward and downward gaze along with obstruction of the cerebral aqueduct (producing a noncommunicating hydrocephalus) is consistent with Parinaud syndrome (dorsal midbrain syndrome), a disorder that is frequently the result of a tumor of the pineal gland. |
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A 27-year-old patient with a chief complaint of mild vertigo of 3-months duration is seen by a neurologist. Examination reveals a positional (horizontal and vertical) nystagmus that is bidirectional. The patient reports the absence of tinnitus. What is the most likely etiology of the vertigo?
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this is central vertigo, specifically a lesion in the flocculonodular lobe of the cerebellum. athologic vertigo is generally classified as peripheral (labyrinthine) or central (brainstem or cerebellum). The clinical presentation in this case is most consistent with central vertigo. Positional (especially horizontal) nystagmus (to-and-fro oscillation of the eyes) is common in vertigo of central origin, but absent or uncommon in peripheral vertigo. The chronicity of the vertigo is characteristic of central vertigo, whereas the symptoms of peripheral vertigo generally have a finite duration and may be recurring. Tinnitus and/or deafness is often present in peripheral vertigo, but absent in central vertigo.
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the cerebellum is derived from what embryological brain swelling?
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metencephalon (which came from the rhombencephalon)
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sulcus limitans
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in the floor of the fourth ventricle, the sulcus limitans separates the cranial nerve motor nuclei (derived from the basal lamina from the sensory nuclei derived from the alar lamina
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the thin epidymal pia membrane that marks the tip of the neural tube?
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lamina terminalis
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only unpaired nucleus of the hypothalamus?
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arcuate nucleus
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fornix and the hypothalamus
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fornix comes out of temporal lobe out of hippocampal formation, 'bumps' into anterior commisure, splits and some go posterior and some go anterior. most terminate in the mammilary nuclei. divdies the hypothalamus into two regions
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medial forebrain bundle gets from the brainstem up to the forebrain by passing through what part of the hypothalamus?
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the lateral hypothalamic area
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what are the two magnocellular nuclei of the anterior region of the hypothalamus?
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supraoptic, paraventricular --> cell bodies are a BIG
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1- pituitary stalk
2- hypothalamus 3- optic tract 4- fornix |
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1- mammilary bodies
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projection fiber
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arises in the CORTEX and terminate in a nucleus not in the cortex
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p1 segment of the PCA
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from the origin to where the posterior communicating artery is
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a1 segment of the ACA
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from its origin to anterior communicating artery
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posterior perforated space of the circle of willis
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artifact from the large caliber vessels there from the circle of willis. perforating branches go up to perfuse the red nuclei which have a large metabolic demand
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pituitary hormones get into systemic circulation how?
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dumped into the cavernous sinus then to systemic circulation
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briefly, amygdaloid and hippocampus functions
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amygdala is involved with emotion and hippocampus with the ability to learn and remember
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amygdalofugal projections
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projects to hypothalamus (endocrine response) and thalamus (DM, whihc projects to the prefrontal cortex, where attachment of significant is made)
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human functions associated with the amygdala?
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emotional experiences (feelings) and emotional behaviors (affect)
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amygdaloid body receives input from?
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olfactory bulb, prefrontal cortex on ipsilateral side, thalamus, hypothalamus, and brainstem
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3 layered cortices/archecortex of the limbic system
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hippocampal formatoin = dentate gyrus and hippocampus + (some of the) subiculum (transition zone)
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visual, auditory, and somatosensory areas project to where in the limbic system?
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these pathways give rise to projections that terminate in the enterorhinal cortex (6 layered)
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LTP
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glutaminergic synapses. Important in hippocampal function and learning via synthesis of proteins
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Sommer's sector
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region of the hippocampus that have an extremely low threshold to failure in hypoxic conditions. These cells fail first in the absence of adequate nutrition. clinically important in people who have had MI, can't synthesize proteins using LTP and has trouble with short term memory.
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which cells in the temporal lobe are most suspectible to hypoxia?
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those in Sommer's sector, CA1
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origin of the cells of the fornix?
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cells of the subiculum
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3 targets of the fornix
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mammilary nuclei, hypothalamus, anterior nucleus of the thalamus
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mammilothalamic tract?
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projects from mammilary nucleus to the anterior nucleus of the thalamus
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Papex circuit
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hippocampal formation (subiculum) → fornix → mammillary bodies → mammillothalamic tract → anterior thalamic nucleus → cingulum* → entorhinal cortex → hippocampal formation.
cingulum bundle is key in formation of long term memory |
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working memory v short term v long term
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requires attention v limbic system requires neurochemical changes (protein synthesis, LTP) v associated cortices requires synaptic changes in association cortcies (
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Anterograde amnesia
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for facts and events after an insult
inability to consolidate (store) new information or experience commonly associated with temporal lobe injury |
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Retrograde amnesia
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for facts and events before an insult
inability to retrieve previously learned information commonly associated with association cortex dysfunction |
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foramen of monro (connects the lateral and third ventricles)
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posterior communicating artery
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Your patient presents with an intense pain on his face, arising from stimulation of the corners of his mouth. Which vessel is most likely affected?
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Trigmenial nerve is affected, this is supplied by Superior Cerebellar Artery
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