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863 Cards in this Set
- Front
- Back
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What are 5 testable components of sensations
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- touch (light, discriminative)
- temperature (hot, cold) - position sense - vibration - pinprick |
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What is steriognosis
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the use of touch to identify an object
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What is graphesthesia
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the ability to identify a number written on the skin with your finger, tests the ability to sense touch that is changing rapidly
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What 2 systems are responsible for gathering general sensation from the neck down and transmitting it to the brain
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- dorsal column-medial lemniscus pathway
- anterolateral system |
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What 3 tracts/systems make up the ALS
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- spinothalamic
- spinoreticular - spinomesencephalic |
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What system is responisble for gathering sensation information from the chin up
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trigeminal pathways
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What are 4 subjects you should address when recording sensory deficits of a patient
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- modality
- topography - level of sensation - affect |
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What does modality refer to
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type of sensation
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Why is the modality of a sensory deficit important
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different modalities have different pathways
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What does topography of a sensory deficit refer to
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where
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what does level of sensation usually refer to
give an example |
- quality; usually talking about touch
example: can feel touch, but are unable to do steriognosis or graphesthesia |
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How is affect associated w/ sensation
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- emotional concomitants; how they interpret different sensations
example: patient interprets painful sensation as bad |
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What might improper affect suggest?
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- some brain lesions may can have correct modality, topography, and a good level of sensation but their affect is different
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describe sensation deficits associated with damage to a peripheral nerve
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- lose all modalities, in a nerve field distribution
-- a complete loss of sensation to an area almost always suggests lesion of a peripheral nerve since there is sensory overlap in spinal nerve and CNS regions |
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describe sensation deficits associated with damage of dorsal root of a spinal nerve
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- lose all modalities, but with a dermatomal distribution
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What type of lesion would be required in order to see complete anesthesia along a dermatome
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in order to see complete anesthesia along a dermatome, the dorsal roots of 3 adjacent spinal segments would have to be involved in the lesion because sensation overlaps by 1 segment in either direction
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What does the loss of one modality of sensation indicate? why
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CNS = modality dissociation
- modalities run together in the PNS, so if one modality is affected, but not others, you have a CNS lesion |
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What is a tract
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- a tract is a bundle of axons in the CNS, with a common origin, course, destination (or termination) and (usually) function
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What are tracts usually named according to
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- often named according to origin and ending
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what are neural pathways
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- a pathway is a series of synaptically linked (related) neurons that share a common function
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compare/contrast tracts and pathways
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- tracts are often included as parts of pathways, such that pathways are often tracts linked end to end
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What are some possible functions of pathways
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- pathways mediate reflexes, may serve sensory, motor, or other functions
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contrast afferent and sensory
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- not all afferent information contributes to your conscious experience. Some information brought into the CNS on afferent fibers is interpreted by the CNS and function is modulated w/ out you knowing (e.g. blood pressure)
- sensory however, specifically refers to afferent info coming into the CNS that you are aware of (e.g. pain) |
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describe the physical appearance of the medial division fibers
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- very thick, and heavily myelinated fibers
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What are the 2 main roles of medial division fibers
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- contribute mostly to reflexes and fine localization of touch
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Where do medial division fibers enter the spinal cord
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- enter the spinal cord, not right at the dorsal horn, but at the dorsal funiculus
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describe the branching pattern of medial division fibers
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- generally give off a long ascending branch and a short descending branch
- the ascending and descending branches give off many collateral branches - ascending branch may go all the way to the brain - collaterals = branches from an axon |
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What are 3 basic types of collaterals given off by ascending and descending branches of medial division fibers
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- to the dorsal horn = touch sensation
- to the intermediate gray = propriospinal reflexes - through the ventral horn, synapse on the motor neuron = muscle stretch receptors |
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What do collaterals synapsing on the dorsal horn facilitate
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touch sensation
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What do collaterals synapsing on the intermediate gray facilitate
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propriospinal reflexes
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What do collaterals synapsing on motor neurons facilitate
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muscle stretch reflexes
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describe the physical appearance of the lateral division fibers
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small, unmyelinated to lightly myelinated
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what do lateral division fibers carry
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- carry pain, temperature, and some touch
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where do lateral division fibers enter the spinal cord
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go straight into the dorsolateral sulcus
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describe the branching pattern of lateral division fibers
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- after entering at the dorsolateral sulcus, they bifurcate and give off short ascending and descending branches
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What is the extent of the reach of ascending and descending branches of the lateral division fibers
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- ascending and descending branches go to 2-4 adjacent branches
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Where do collaterals of the lateral division fibers synapse? (generally? 3 specifically?)
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synapse in the dorsal part of the dorsal horn
- posterior marginal nucleus - substantia gelatinosa - neck of the dorsal horn |
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What are 3 general functions of afferent neurons
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- reflexes
- subconscious "data" - cortex for perception |
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Where are the multiple actions of a single motor neuron seperate
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individual action become separated at the synaptic level
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What type of subconscious "data" is required for skeletal muscle
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propriceptive "data"
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Where is subconscious proprioceptive "data" sent
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proprioceptive fibers will also synapse on a neuron that will project to the cerebellum
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Why is it important that the cerebellum receive data about muscle position
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cerebellum is important for coordination of movement, but it is important that it always has incoming information about muscle position
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In general sensory systems, where is the NCB of primary afferent (I-aff) neurons found
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dorsal root ganglion
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Where do the central processes of primary afferents project to? which side?
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- they reach the ipsilateral spinal cord or brainstem and synapse
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describe the course of the second order neurons in the SC or BS
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second order neurons (projection cells) project across the midline to the ventral posterior nucleus of the lateral thalamus and end
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Where do projection sensory neurons (II) synapse
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VPL nucleus
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What type of neurons make up third order sensory neurons
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thalamic neurons
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through what do thalamic neurons (III) pass
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their axons pass through the posterior limb of the internal capsule (PLIC)
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where do thalamic neurons (III) synapse
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the primary sensory cortex (S-1 or area 312)
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What is the DC-ML system responsible for
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- touch
- pressure - proprioception - vibration |
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Which 2 sensations of the DC-ML system are used for testing the integrity of this system
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vibration and position sense?
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Which sensation of the DC-ML system is unique to this system
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vibration
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What class of sensation receptors are found on the end of peripheral processes of the first-order neurons of the DC-ML system
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rapidly adapting neurons
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What are 2 rapidly adapting receptors associated w/ DC-ML system
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- Meissner's corpuscle
- Paccinian corpuscle |
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what does it mean to be a rapidly adapting receptor
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can fire an action potential then quickly recover and fire another one
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what part of the dorsal root are primary afferents of the DC-ML system found in
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become part of the medial division of the dorsal root
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what do the central processes of first order neurons of the DC-ML system do once they enter the spinal cord
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they branch and enter the dorsal columns (fasciculus gracilis or cuneatus) and ascend to the medulla
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where do first order neurons synapse on projection neurons of the DC-ML system
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synapse on projection neurons in the gracile and cuneate nucleus
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what is the medial lemniscus made up of
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projection neurons of the gracile and cuneate nucleus that generate axons that cross at the midline and form the ML
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Where do projection DC-ML neurons project to
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VPL nucleus of the thalamus
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What do the thalamic projections (thalamic neurons) of the DC--ML system pass through
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PLIC
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Where do thalamic projections of the DC-ML system project to
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ipsilateral S1 (primary sensory) cortex
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Describe the route of central processes of first order neurons innervating innervating an area of skin below T6 as part of the DC-ML system
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central processes of dorsal (posterior) root ganglia (DRG or PRG) neurons from below T6 enter the spinal cord just medial to the dorsal horn
- they then bifurcate and one of the branches joins the fasciulus gracilis (adjacent available DC), turns cranially and travels up to the gracile nucleus in the medulla. An excitatory nt will be released here to stimulate the projection neurons |
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Where do first order neurons from below T6 synapse in the DC-ML system
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gracile nucleus
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describe the course of projection neurons from pathways below T6 in the DC-ML, where do they synapse?
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immediately axons coming from the projection neurons in the nucelus gracilis will cross the midline and ascend as part of the lateral portion of the ML
- they end by synapsing on thalamic neurons in the lateral portion of the VPL nucleus in the thalamus |
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Where do axons of thalamic sensory neurons of pathways from below T6 in the DC-ML system project to
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Axons of the thalamic neurons in the thalamus extend projection through the posterior limb of the internal capsule, through the corona radiata, to the medial surface of the posterior paracentral lobule in the primary sensory cortex
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What is the role of the posterior paracentral lobule in S1
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the medial surface of the posterior paracentral lobule in S1 is solely responsible for sensation in the leg, thigh, and foot
- specifically within this region, the divisions are broken down even further such that there are regions solely responsible for each area of skin (e.g. big toe) |
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describe the course of 1st order axons of pathways from above T6 in the DC-ML system. Where do they synapse
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- central processes of DRG neurons above T6 will enter the spinal cord medial to the dorsal horn, bifurcate and one axonal branch will ascend as part of the fasciulus cuneatus
- these axons will synapse on projection neurons in the cuneate nucleus |
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describe the route of projection neurons in the pathways above T6 in the DC-ML system, where do they synapse
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projection neurons from the cuneate nucleus will immediately cross the midline and ascend as the medial portion of the ML
- synapse on thalamic neurons in a more medial portion of the VPL nucleus of the thalamus |
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Where do axons from the 3rd order sensory neurons of pathways from above T6 in the thalamus project to in the DC-ML system
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thalamic neurons in the thalamus send projections through the PLIC, through the corona radiata, to the lateral surface of the primary sensory cortex on the postcentral gyrus
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compare and contrast the location of: 1st order sensory neurons from pathways above and below T6
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above T6: in the fasciculus cuneatus
below T6: in the fasciculus gracilis (medial to the axons above T6) |
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compare and contrast the location of: NCBs of projection sensory neurons from pathways above and below T6
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above T6: cuneate nucleus
below T6: gracile nucleus |
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compare and contrast the location of: axons of projection sensory neurons from pathways above and below T6
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when projection neurons cross the midline and form the medial lemniscus, axons from above T6 are more medial than axons below T6
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compare and contrast the location of: NCBs of thalamic sensory neurons from pathways above and below T6
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above T6: in the more medial portion of the VPL nucleus in the thalamus
below T6: in the more lateral portion of the VPL nucleus in the thalamus |
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compare and contrast the location of: cortical projection of pathways above and below T6
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above T6: to the lateral surface of the primary sensory cortex in the postcentral gyrus
below T6: to the medial surface of the posterior paracentral lobule in the primary sensory |
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What part of the primary sensory cortex receives input from the spinal nerves via the DC-ML system
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- thumb
- index finger - middle finger - ring finger - little finger - hand - wrist - forearm - elbow - arm - shoulder - head - neck - trunk - hip - leg - foot - toes - genitals |
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What part of the primary sensory cortex receives input from the trigeminal nerve/system
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- intra-abdominal
- pharynx - tongue - teeth, gums, and lower lip - lips - upper lip - face - nose - eyes |
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Where on the primary sensory cortex is the lower limb represented
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most medial and superior part, receives input from DC-ML
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Where on the primary sensory cortex is the face represented
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lower half, towards the top, receives input from the tigeminal system
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Where in relation to the representation of the face is the hand represented on the primary sensory cortex
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the hand is on the upper half (DC-ML) at about 11 and the face is on the lower half (trigeminal) a little after 9
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Where on the primary sensory cortex is the mouth (teeth, gums, jaw, tongue, pharynx, etc.) represented
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lower half (trigeminal) from about 8-9
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What part of the face has the largest representation on the primary sensory cortex
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lips/mouth
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contrast the area of the primary sensory cortex devoted to representing the face to the area devoted to representing the trunk
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- the face has a much larger area than the trunk
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Which would you expect to lead to more sensory loss, a CVA in the ACA or MCA
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- ACA supplies the part of the primary sensory cortex that receives sensory innervation for the lower limb,
- while the rest of the primary cortex is supplied by the MCA |
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Where would expect to see sensory deficits from someone who had a stroke in their ACA
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lower limb
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What 4 types of sensation would you expect a patient with a complete loss of the DC-ML to be deficient in
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- discriminative touch, esp. time coded (movement related, ex. graphesthesia)
- vibratory sense (best way to test this system is vibration) - essential for sterognosis - position sense |
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What is the anterolateral system (ALS) responsible for
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- detection of noxious stimuli (pain and temp.)
- some touch |
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What type of receptors are found in the ALS
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- naked nerve endings = undifferentiated nerves, detect noxious stimuli, chemoreceptors, mechanoreceptors
- specific receptors for hot and cold |
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How do you test ALS
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test the ability to sense pinprick sensation
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explain how primary afferents of the ALS "synapse" on projection afferents in the spinal cord, where does this occur?
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- primary afferents enter the spinal cord in the lateral funiculus and brach off to give short branches that ascend and descend in the dorsolateral funiculus.
- These branches synapse on a short interneuron near the entry level in spinal gray matter - these short interneurons projects to a projection neuron deeper in the gray matter - these neurons send their axons immediately across midline to ascend (via ALS) to the thalamus (VPL) to the primary sensory cortex |
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Breify describe the route of projection sensory neurons in the ALS
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- these short interneurons projects to a projection neuron deeper in the gray matter
- these neurons send their axons immediately across midline to ascend (via ALS) to the thalamus (VPL) to the primary sensory cortex |
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Where are the thalamic sensory neurons of the ALS found
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VPL nucleus
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where do the axons of thalamic ALS sensory neurons project to
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primary sensory cortex
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do all processes of the projection sensory axons of the ALS go the VPL thalamus? Where else do axonal branches from the projection sensory neurons synase? (3)
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- in the brainstem, many branches come off the projection neuron and go to places other than the VPL of the thalamus, including:
-- reticular formation (RF) -- Periaqueductal grey (PAG; mesencephalic) -- Intralaminar nuclei of the thalamus (intralaminar nuclei send projections to many parts of the cortex) |
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What is the sontramedian nucleus
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the largest of the intralaminar nuclei of the thalamus
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Do all axons of thalamic neurons of the ALS pathway project to the primary sensory cortex
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no, because intralaminar nuclei of the thalamus can send projections to the many parts of the cortex
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describe the physical characteristic of neurons of the ALS pathway
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small, slightly myelinated to unmyelinated fibers make up this pathway (C fibers and Agamma fibers)
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What is the role of the interneuron b/w the 1st and projection neurons of the ALS pathway
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to modulate pain
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Where are descending and ascending branches of 1st order ALS neurons found
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- central processes of DRG 1st order neurons of ALS enter the dorsolateral fasciculus and branches into ascending and descending branches
- branches synapse in the dorsal horn of the spinal cord |
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Where do 1st order neurons of the ALS synapse
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in the dorsal horn of the spinal cord
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Where do ALS neurons cross the midline? Which ones cross the midline
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- axons of projection ALS neurons cross the midline immediately (at the same level which the 1st order neurons synapse) and ascend in the ALS (located in the anterior and lateral white matter of the spinal cord)
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What is the anterior white commissure made up of?
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projection axons crossing the midline
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What are 2 major target areas in the midbrain for branches from projections of ALS neurons
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- deep layers of the tectum (superior colliculus)
- periaqueductal grey matter (PAG) |
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Where are place the branches from projections of ALS neurons can go
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- projection axons go thru the ALS, anteriolateral part of the medulla, pons, and midbrain, giving off branches all the while
- branches of projection axons may drop off in the tegmentum of the pons, reticular formation, or other brainstem regions |
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Where do major (terminal) branches of projection ALS neurons go to synapse on thalamic neurons (2)?
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- major branches go to the VPL nucleus of the thalamus, synapse on thalamic neurons,
- projections also go to the intralaminar (medial thalamic) nuclei of the thalamus and synapse on other thalamic neurons |
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Where do thalamic ALS neurons in the VPL nucleus of the thalamus project to? How?
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- they project to the cortex in a very specific pattern, with pathways innervating medial structures projecting to the lateral cortex and pathways innervating lateral structures projecting to the medial cortex
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Where do thalamic ALS neurons in the intralaminar nuclei project to? How?
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they synapse on other thalamic nuclei and project to a very wide spread area of the primary sensory cortex
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Contrast the evolution of the ALS system to that of the DCS system, why did it occur this way
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- ALS pathway evolved long before the DCS system
- b/c advantageous for noxious stimuli: caused escape reflexes to develop and would allow cognitive system to make judgments to avoid harmful stimuli |
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How is the ALS associated w/ the raphe nuclei
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- at the midbrain level (esp. PAG) activates neurons in the raphe nuclei which project downward and inhibits/minimizes synaptic activity in the ALS pathways, uses serotonin and helps to reduce the amount of pain sensation being carried up
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What would a lesion of the ALS at the level of T6 cause?
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loss of pinprick sensation and temperature to opposite side below T6
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Where would a lesion to the ALS have to be if you were to lose pinprick sensation to one entire side of the body from neck down
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a lesion would have to be at the very top of the spinal cord
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Relatively, what proportion of the primary sensory cortex is devoted to pain?
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- relatively small part is devoted to pain
- the pain system is very complex and involves many parts of the brain |
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What deficits are seen in patients w/ ALS lesions
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- loss of pinprick
- temperature deficit - itch and tickle - sexual sensation deficit |
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What is itch and tickle
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complex compounds of both touch and pain
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What is one drastic way that extreme chronic pain (often in cancer patients) is treated
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- cut or interupt the ALS system
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How is surgical interuption of the ALS system acheived
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by sticking an electrode into the spinal cord through an IV foramen
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What are the trigeminal homologs of the DRG? (2)
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- sensory ganglion of V
- mesencephalic nucleus (contains NCBs of proprioceptive neurons) |
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what is the trigeminal homolog of the dorsal column nuclei (gracile and cuneate nucleiu)
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cheif sensory nuclei (part of the touch pathway)
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What is the trigeminal homolog of the dorsal part of the dorsal horn (nucleus proprius and substantia gelatinosa)
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spinal nuclei
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What is the trigeminal homolog of the dorsolateral fasciculus (DLF)
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trigeminal spinal tract
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What does the mesencephalic nucleus contain
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NCBs of proprioceptive neurons
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What type of sensation is the cheif sensory nucleus of V responsible for
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part of the touch pathway
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Where do afferents carrying pain, temp, and touch on CN V enter the CNS
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enter at the pons
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what do trigeminal afferents do once they enter the brain? and where do they synapse?
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- fibers descend as spinal tract of V and synapse in the caudal spinal nucleus
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describe the course of projection trigeminal sensory neurons, where do they synapse
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- projection cells send axons across midline to form the ascending ventral trigeminal thalamic tract (VTTT) which reaches the VPM tract
- here projection cells synapse on thalamic cells, which send their axons thru PLIC to the primary sensory cortex |
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Where do thalamic sensory neurons of the trigeminal pathway project to? how do they get there
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to the primary sensory cortex via the PLIC
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What is probably found b/w the 1st and projection neurons of the trigeminal sensory pathway
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an interneuron
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What types of receptors are associated w/ noxious stimuli of V
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naked
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describe the physical properties of the neurons of the trigeminal sensory (noxious) pathway
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lightly myelinated to unmyelinated neurons
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what is similar about projection neurons of the trigeminal pain pathway and those of ALS
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also have shootoffs to the intralaminar nuclei, RF, and midbrain
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Where do the most important pain pathway neurons of V synapse in the spinal trigeminal nucleus
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- most important in pain pathway neurons are in the caudal 1/3 of the nucleus
- so that most of the pain pathway from the face descends all the way to the medulla |
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where do projection neurons of the pain pathway of V cross the midline
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at the level of the medulla
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where could a 1 cm lesion be located such that it would cause loss of pinprick sensation on one side of the face, and opposite side of the body
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represents a completely crossed pathway for pinprick (noxious) sensation from the face (in addition to completely crossed system from the vbody)
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pain path via the Vth nerve: course
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- afferent of V enter at the pons and descend to the level of the pons as the spinal trigeminal tract . As they go they give off colaterals that synapse in the spinal trigeminal nucleus
- projection neurons cross the midline and begin to ascend at the level of the medulla - VTTT goes up to the thalamus and axons synapse on the VPM nucleus |
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What is the major difference in the cortical projection of the trigeminal sensory pathway vs. the trigeminal pain pathway, ALS, DCS
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the face is represented bilaterally b/c it sends its axons both contralaterally and ipsilateral
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Where do the 1st order sensory neurons of the trigeminal sensory pathways synapse
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afferents enter the pons and synapse on the cheif sensory nucleus of V
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Where do 2nd order sensory neurons of the trigeminal sensory pathways synapse (2)
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- some projection cells send their axons across midline to join the VTTT which reaches the contralateral thalamic VPM to synapse on
- others send their axons through the DTTT to the VPM on the same side to the synapse |
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Why is the projection of sensation from the lips so expansive
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- they are amazingly sensitive
- beneficial for food seeking behavior |
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Why is touch on the face not a good way for testing for lesions of CN V
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- b/c it is carried to both sides from the cheek up
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how should trigeminal pathways be tested
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pin prick
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describe the physical properties of the trigmeinal sensory neurons
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large caliber myelinated fibers
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What 2 systems use the VTTT
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sensory and pain pathways of the trigeminal pathways
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What is found in the mesencephalic nucleus of V
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primary axons from most CN reach sensory root of V and enter the brain with it, fibers run to mesencephalic nucleus where unipolar cell bodies are found
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Where do "central" projections from the neurons found in the mesencephalic nucleus of V go
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go to motor nuclei for reflexes and other sites as well
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What are central projections from the mesencephalic nucleus of V which synapse in the motor neuron responsible for
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reflexes
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What are 5 differences in visceral sensation and somatic sensation
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- afferents are different (types)
- perception is different - innervation (density) is different - CNS pathways appear to bilateral - pain is often referred (contrast referred pain vs. projected) |
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What are 2 possible explanations for why CNS pathways for visceral sensation are bilateral
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- if cells in the dorsal horn are activated, they may project to the contralateral and ipsilateral sides
- or simply most of the structures that are innervated are located very close to the midline, so when you have part of a structure stimulated, you stimulate neurons that project from both sides of the spinal cord |
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compare/contrast how it would feel if someone touched your stomach (your actual stomach) vs. if the touched your abdominal wall skin
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if someone touched ur viscera you would get some more noxious and uncomfortable sensation
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explain why visceral pain is referred to part of the body wall and not felt in the organ where it is produced. Use the heart attach/arm pit model
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- pain afferent fibers that innervate the heart project to the spinal cord around T1, 2, 3, these fibers synapse in the dorsolateral horn and the substantia gelatinosa. These neurons synapse on some of the same neurons that usually convey pain from the arm pit
- since these neurons have only ever been stimulated by pain in the armpit before, you learn that stimulation in this part of the cortex is associated with the arm pit |
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What are 3 functions of the nervous system
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- homeostasis
- mental events - coordinated movement |
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What are 5 mental events or categories of mental events that the nervous system does
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- sensation
- perception - recollection - cognition - unconscious events |
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What 3 components do all brain functions involve to a varying degree
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1. representation of afferent and efferent information
2. storage of information 3. information processing |
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How does new infomation arrive in the CNS
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- arrives via afferent channels, which limits what we can register
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Can the nervous system make new information? What does it do?
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- it can not make new info, just process it
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what is entropy
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- in the process of transmitting information, some of it is lost as entropy
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how many "computations" can a neuron handle at one time
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- like computers, each computing element (a neuron) does one computation at a time
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How is information acheived in the nervous system
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- most information transmission down axons is via action potentials (all-or-none)
- most information processing occurs at the axon hillock (summation) |
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are action potentials graded
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no, they are all-or-nothing
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where does information processing (summation) occur in the nervous system
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at the axon hillock
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What does parallel processing of the nervous system refer to
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- massively parallel processing (MANY cells can work at the same time in different areas on different subjects with different goals)
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What does serial processing of the nervous system refer to
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- multiple synapses may occur b/w the beginning and end of a pathway
- synapses are not simply for relay of information, but also function in information processing - we know this b/c if they were simply involved in relay, evolution probably simply would have made individual axons longer |
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do individual neurons transmit information slowly or quickly
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- they are slow
- aggregate rate of information processing is fast because of parallel and serial processing |
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How is fast information processing acheived in the nervous system
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aggregate rate of information processing is fast because of parallel and serial processing
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What are 2 sensory neural links
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- transduction
- representation |
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What is transduction, what does it link
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- process by which the first neural signals are generated due to stimuli
- link b/w physical stimuli and input to the nervous system |
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What is representation, what does it link (3)
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- link b/w nervous system and perception
- link b/w nervous system and action - link b/w CNS activities |
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What is a receptor potential
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- graded potential generated at sensory endings of axons
- first potential to occur in a sensory pathway |
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Where are receptor potentials seen
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sensory pathways
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Classify the strength of receptor potentials
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- graded potentials
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What type of sensory neural links are generator potentials associated with
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- generator potentials arise due to non-electrical signals, which causes electrogenic changes in the cell
- representation |
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what type of potential is a receptor potential
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- this is a type of generator potential, like synaptic potentials
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How are receptor potentials achieved
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- stimulus changes channel permeability
- which causes potential changes (changes in relative conductances of ions) - receptor potentials amplitude is proportional to the number of open channels (graded) and controlled by the strength of the stimulus = AM by stimulus |
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What is amplitude modulation (AM)? What determines amplitude?
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- strength of the stimulus
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What is an example of stimulus sensitive channels
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stretch sensitive channels
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describe muscle spindle receptors
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- consist of extensions of neurons wrapped around muscle fibers
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What causes membrane ion channels in muscle spindles to open? how?
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- membrane channels in these extensions are physically tethered to one another
- when a muscle fiber contracts, the muscle spindle must stretch in order to accomadate this change - when the membrane stretches, the connection does not, so the channels are pushed open |
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What determines the amplitude of the receptor potential of a muscle spindle? how?
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- the greater the stretch of the spindle (proportional to the contraction of the muscle fiber), the greater the frequency of an ion channel opening and thus the greater the amplitude of the receptor potential
-- greater chance of action potential in the neuron |
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Where are action potentials generated at sensory terminals
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- usually generated at the 1st node of ranvier (trigger zone)
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What is the trigger zone
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where action potential generation and conduction occur at sensory terminals
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Where, other than the 1st node of ranvier in sensory terminals, are trigger zones located
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postsynaptic neurons at the axon hillock
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What types of channels are located at the trigger zone
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- voltage-sensitive channels (no stimulus-sensitive channels)
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What determines if a action potential will fire at a sensory terminal
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action potentials are generated if passive current from generator potentials is sufficient to exceed threshold
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What causes a receptor potential
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- sufficient stimulus --> change of ion channel permeability at the receptor site --> receptor potential
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What leads to an action potential starting at the trigger zone
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- receptor potential (if sufficient) --> passive current reaches the trigger zone --> opening of voltage gated channels (if depolarization is sufficient to threshold) --> action potential
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increasing the strength of what will increase the likelyhood of an action potential being generated at the trigger zone?
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a stronger stimulus will make more stimulus sensitive channels open --> stronger receptor potential --> greater likelyhood of an action potential occuring
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What does AM represent
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- amplitude modulation
- the intensity of a stimulus is represented by the amplitude of receptor potential = AM |
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What component of AM is fixed
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- local current (receptor potential/AM) doesnt travel down an axon (can only travel a short, fixed distance)
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What component of action potentials is fix
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amplitude
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What component of action potentials can be changed
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distance
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What determines the frequency of firing of action potentials
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- it is determined by receptor potential amplitude
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What is frequency modulation (FM)
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action potential frequency is determined by receptor potential amplitude = FM
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where does AM-FM conversion occur
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at the trigger zone (1st node of ranvier)
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contrast the frequency of firing of slowing adapting neurons in which the receptor amplitude is and those in which receptor potential amplitude is high
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- a continuous stimulus only causes an action potential to occur when it changes (usually when the stimulus starts or is taken away)
-- example: you feel your shirt when you put it on, and you feel a difference when you take it off, but you dont feel it all day - if a stimulus gradually becomes stronger, action potentials will fire until the amplitude of the receptor potential plateaus -- example: you are walking toward a pile of dog poop. You first notice the smell when you are 15 feet away. As you get closer, the smell continually gets stronger. If you stand next to the pile for a mintures without moving, you will no longer smell it - rate of discharge is related to the rate of increase in amplitude of the receptor potential |
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how does the firing of slowly adapting receptors change overtime? How long does each change take
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frequency of firing decreases slowly
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why does increased amplitude of receptor potential lead to increased frequency of action potential firings
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- stimulus triggers the opening of receptor channels. Cations diffuse through the channels. These cations will begin to diffuse down the axon, towards the trigger site. If many channels are open, the cation conc within the cell allow enough cations to diffuse to the trigger zone to cause the membrane potential here to reach threshold
- once the membrane potential reaches threshold, all of the voltage-gated ion channels will open and an action potential will fire and propagate down the axon -- cations that enter through receptor channels, diffuse to cause depolarization of the trigger zone - once the AP has fired, repolarization will occur and there will be a period of time when the Na channels here are inactivated - When the Na channels can again open, if there is still a sufficient amount of depolarization at the trigger zone for the membrane potential to reach threshold again, another AP will fire |
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describe FM-AM conversion at the synapse
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- at the CNS end of a sensory axon, some transmitter is released with each presynaptic AP
- AP frequency (FM), therefore determines transmitter concentration in the synaptic cleft (AM) - concentration determines the postsynaptic potential (PSP) amplitude (AM) via number of open channels |
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describe AM-FM conversion at the synapse
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- PSP amplitude (AM) determines postsynaptic action potential frequency (FM)
- this process continues on all the way to the brain, thus the frequency of AP firing at the end of this pathway in the brain is a direct result of the amplitude of the receptor potential and thus the strength of the stimulus |
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What ultimately determines the frequency of firing of a (thalamic) sensory neuron in the brain
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- the amplitude of the receptor potential and thus the strength of the stimulus
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Why is FM-AM conversion necessary
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cant do chemical transmission any other way
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Explain computation at synapses and the axon hillock
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- synapses and axon hillocks are the basis for computation (information processing/ integration):
- computation = AP frequency determined by interactions (summations) among PSPs coming from different sources (excitatory and inhibitory synapses) - in other words, excitatory synapses cause PSP amplitude (AM) to increase, while inhibitory synpases cause it to decrease - these effects sum within the postsynaptic area of the neuron such that PSP amplitude (AM) is determined by the combined effects of all input (it will be greater if there are more excitatory synapses and less if there are more inhibitory synapses) - this amplitude (AM) then determines the firing frequency |
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What type of information is represented by the process of AM-FM, FM-AM conversion transmission
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stimulus intensity
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What type of information, other than stimulus intensity, must be represented in the CNS for consciousness perception
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- type of stimulus: modality
- location of stimulus: localization |
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What are sensory modalities, give examples
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- different forms of perception
-- vision, hearing, touch |
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What determines what type of sensory modality transmitted by a specific receptor, axon, , or input organ
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- specific forms of stimulus energy (e.g. light, sounds, mechanical pressure) determine the sensory modality.
- The type of energy that leads to the greatest change in receptor potential will determine the modality transmitted by that particular pathway |
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Are all sensory receptors the same?
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- no
- specialized receptors have different transduction mechanisms with different adequate stimuli |
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What is a sensory system
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- neurons that are segregated according to modality
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Why might sensory axons be running from peripheral tissue to the CNS be referred to as "labeled lines"
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- electrical stimulation shows each axon is a labeled line, signaling a certain type of stimulus
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What is adaptation
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- constant stimulus produces a response which diminishes with time
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What is another term for slowly adapting neurons
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- tonic
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What are slowly adaptic neurons good for
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- good for intensity coding
-- frequency of discharge represents strength of stimulus |
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What are rapidly adapting neurons also called
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- phasic: on-response, sometimes off-response
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What is responsible for adaptation
|
- adaptation is generally a property of the coupling structures attached to receptor membrane, not the membrane itself
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What is the benefit of rapid adaptation
|
- allows for extraction of dynamic information (related to changes of stimuli)
-- i.e. velocity or acceleration |
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What are 3 types of rapidly adapting receptors
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- Pacinian corpuscles
- meissner's corpuscles - ruffini endings |
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Are bare nerve endings rapidly adapting or slowly adapting
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slowly adapting
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Why is another mechanism, secondary to frequency coding, necessary for representation of stimulus intensity
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- frequency code is inadequate for the physiological range of intensities
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How, basically, is th representation of a large range of intensities acheived?
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- the range can be extended by having sensory receptors with different thresholds
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What kind of stimuli cant sensitive receptors distinguish? why
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- sensitive ones cant distinguish among large stimuli
-- b/c they are already firing as fast as they can |
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What kind of stimuli cant high threshold receptors detect? why?
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- cant detect small stimuli
-- b/c they are below threshold |
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What happens to the number of receptors activated as intensity of a stimulus increases? why?
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- more are recruited into responding pool
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what does recruitment code refer to
|
- number of receptors activated by a specific stimulus at a specific intensity
- CNS interpretation about this code gives information about the intensity of the stomulus |
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Within what range can we detect changes in stimulus intensity
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- we can only detect differences in stimuli intensity b/w the level at which the least sensitive receptors is firing at its lowest frequency and the level at which the most sensitive receptor is firing at its highest frequency
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what does it mean if a sensory neuron discharges
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- discharge of a cell means its receptive field (RF) has been stimulated
- A sensory cell's RF is its "location label" |
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receptive field
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the area of skin that if stimulated will elicit discharge in the central neuron
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localization
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where a stimulus is
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Why can you call the sensory cortex a topographic map
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- due to the same spatial relations at both ends of a axon
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What is the relationship b/w the relative locations of the RFs of 2 axons that innervate the skin and their projections on the sensory cortex
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- if two axons have adjacent RF's (e.g. skin) they have adjacent projections and connections (e.g. sensory cortex)
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What happens on the sensory cortex as the stimulus moves across the skin
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- as the stimulus is moved across the skin, the zone of discharging neurons moves across the sensory cortex
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What would happen if you move the group of cortical neurons that receive afferent input from the big toe, but left all axons and connections in tact
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- a map is not a representation, the location of a neuron in the somatosensory cortex, doesnt tell you where the RF is
- EXAMPLE: if you moved the group of cortical neurons that are responsible for sensation of your big toe from the posterior paracentral lobule to a more lateral portion of the primary sensory (S1) cortex, but left all the axons and connections to the CNS from the big toe, you would still preceive sensation on your big toes as being on your big toe. This information would simply be projected to a different area of the brain, so connections are what is important, not location |
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Can receptors respond to any type of energy other than "adequate" form
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- yes, we can sometimes fool receptors with other forms of energy (e.g. pressing on the eye)
- the brain has no mechanism for distinguishing this |
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What is paradoxical cold
|
- some temperature receptors on the skin will respond to heat and cold, and when you heat them the brain will interpret this as being cold
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What are primary sensations
|
- each modality is perceived as a primary sensation
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What are derivative sensations
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- result from specific combinations of primary sensations integrated by the CNS
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What are 3 examples of derivate sensations
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- sensation of wetness
- itch - tickle |
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What are the 3 major classes of sensory fibers
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A faster than B faster than C (unmyelinated)
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Which of the 3 major classes of sensory fibers is the fastest
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A
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What major class of sensory fibers is the slowest? why?
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C fibers, b/c they are unmyelinated
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What are the 3 subclasses of group A sensory fibers
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alpha faster than beta faster than delta
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What are the 4 major classes of motor fibers
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I faster than II faster than III faster than IV (unmyelinated)
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What are somatosensory submodalities
|
stimulus types within the modality of skin sensation
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What types of fibers are the touch receptors found on (2)
|
most touch receptors have Aalpha or beta axons, and have specialized receptor endings
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What types of axons are most temperature receptors and nociceptors found on
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have Adelta or C axons
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describe segregation of sensory submodalities
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- projections to interneurons are submodality-specific, as interneuron projections
- Hence, submodalities are kept seperate all the way through the cortex - separate private lines for each - however, they are not physically seperate through tracks - stimulation of receptor axons on their labeled line interneurons causes projected sensation of appropriate type (e.g. touch, temp., pain) and location |
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What is the role of receptor fields of sensory axons
|
- receptors have another form of specificity endowed by their receptive fields
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What happens if a sensory axon is stimulated electronically
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- if a receptor axon is stimulated electrically, feeling is projected to the site of its receptive field
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How are RF distributions of the skin perserved throughout the cortex
|
- the specificity is preserved by spatially ordered projections through cortex
- this results in a map of the skin at each level of the somatosensory CNS |
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describe the segregation of submodalities at the level of the individual neurons
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- submodalities are intermingled but segregated to some extent at the level of individual neurons
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What does stimulation of a particular point on the sensory cortex cause
|
- as a consequence, stimulation of cortical points yields projected sensation with specific location on the skin
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What are the 4 major classes of motor fibers
|
I faster than II faster than III faster than IV (unmyelinated)
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What are somatosensory submodalities
|
stimulus types within the modality of skin sensation
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What types of fibers are the touch receptors found on (2)
|
most touch receptors have Aalpha or beta axons, and have specialized receptor endings
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What types of axons are most temperature receptors and nociceptors found on
|
have Adelta or C axons
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describe segregation of sensory submodalities
|
- projections to interneurons are submodality-specific, as interneuron projections
- Hence, submodalities are kept seperate all the way through the cortex - separate private lines for each - however, they are not physically seperate through tracks - stimulation of receptor axons on their labeled line interneurons causes projected sensation of appropriate type (e.g. touch, temp., pain) and location |
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What is the role of receptor fields of sensory axons
|
- receptors have another form of specificity endowed by their receptive fields
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What happens if a sensory axon is stimulated electronically
|
- if a receptor axon is stimulated electrically, feeling is projected to the site of its receptive field
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How are RF distributions of the skin perserved throughout the cortex
|
- the specificity is preserved by spatially ordered projections through cortex
- this results in a map of the skin at each level of the somatosensory CNS |
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describe the segregation of submodalities at the level of the individual neurons
|
- submodalities are intermingled but segregated to some extent at the level of individual neurons
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What does stimulation of a particular point on the sensory cortex cause
|
- as a consequence, stimulation of cortical points yields projected sensation with specific location on the skin
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What are epileptic auras
|
- epileptic seizures are often preceeded by a sensory aura (e.g. tingling on the skin if the seizures are in some specific part of the somatosensory system)
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How are epileptic auras useful in surgically treating severe epilepsy
|
- surgeon will search on the surface of the exposed brain of an awake patient with stimulating electrons until they can replicate the aura
- they will destroy the neurons causing the seizures |
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What is the drawback of surgical treatment of epilepsy
|
- the patient will loose the sense of light touch (assuming we are in the somatosensory cortex), but the seizures will stop
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What is acuity
|
- a measure of sharpness of resolution, how well we resolve details in a percept (e.g. different size letters on an eye chart or different size Braille characters at a drive-up automatic teller)
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What is the two-point discrimination threshold? What is it used to measure?
|
- the minimum separation b/w two objects that can be distinguished by subjects, e.g. measured in meters
- used to measure resolution |
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How are acuity and two-point discrimination threshold related
|
- acuity is the reciprocal (inverse) of two-point discrimination, e.g. m^-1
- therefore high acuity means high resolving power, as reflected by small two-point discrimination threshold |
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What determines acuity at a point on the skin (2)
|
- receptive field (RF) sizes
- numbers of RFs contacted by the stimulus |
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What size of RFs are associated with better acuity
|
- small RFs are better than large ones, b/c in large fields any stimulus in this field, will send the same signal to the brain so it doesnt know where exactly the stimulus is, just that its somewhere within the RF
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What are 2 fcns of the number of RFs contacted by a stimulus
|
- innervation density (number of sensory axon RFs overlapping an area, e.g. RFs/cm^2) on skin, greater density means greater acuity
- map scale (number of CNS neuron RFs overlapping an area, same demensions) on skin |
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What is the highest acuity associated with (what innervation density and what RF size)
|
- small RF size and greater density
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How is innervation density/ map scale measured?
|
RFs/ cm^2 on skin
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How are map scale and RF size related
|
- are reciprocally (inversely) related everywhere in the nervous system
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How is acuity related to RF size
|
- acuity is inversely proportional to RF size
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How is acuity related to map scale
|
- acuity is directly proportional to map scale
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What determines acuity
|
- map scale and RF size work together to determine acuity
- acuity is also proportional to the area of the sensory cortex devoted to a particular area of skin (e.g. lips) |
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|
How is pain normally envoked
|
- by production of AP in nociceptor axons
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Can pain be elicited by high-frequency activity in non-nociceptor skin receptors
|
- pain CANNOT be elicited by high-frequency activity in other skin receptor types (e.g. touch, vibration, temp)
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What type of fibers carry "fast pain"
|
- carried by Adelta fibers
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How long does it take pain travel on Adelta fibers to reach the brain from the finergtip
|
only about 100ms to reach brain from fingertip
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Describe the sensations associated w/ fast pain
|
- sharp, burning, rapid onset
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how long does fast pain last
|
- lasts for the duration of the stimulus
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is fast pain tolerable
|
- yes
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what type of fibers carry slow pain
|
- C fibers
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how long does it take slow pain to reach the brain from the fingertups
|
- as much as 1 second
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describe the sensations associated with slow pain
|
- dull, aching, slow onset
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how long does slow pain last
|
- outlasts the stimulus
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is slow pain tolerable
|
no
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describe the onset of slow pain
|
slow
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Which is more well localized, fast pain or slow pain
|
- fast pain
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where is fast pain relayed through (2)
|
- dorsal horn
- specific thalamic nuclei |
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where is fast pain projected to
|
primary somatosensory cortex
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what type of pain has a polysynaptic pathway
|
- slow pain
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Where is slow pain relayed through
|
- relayed polysynaptically through dorsal horn, reticular formation, and intralaminar nonspecific thalamic nuclei
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describe the cortical projections of slow pain
|
- widespread cortical projections
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Is pain and nociception the same thing
|
- they can be separated
- morphine allows subjects to ID noxious stimuli but affect of pain is still missing - some thalamic lesions cause numbness to touch on opposite side, but subject reports pain - cortical representation of pain has not been IDed, so you cant abalte a portion of the cortex to relieve pain |
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How does morphine work
|
- morphine allows subjects to ID noxious stimuli but affect of pain is still missing
|
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is pain eliminated by thalamic lesions causing numbness to touch
|
some thalamic lesions cause numbness to touch on opposite side, but subject reports pain
|
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|
can a surgical ablation of a portion of the cortex releive pain, why?
|
cortical representation of pain has not been IDed, so you cant abalte a portion of the cortex to relieve pain
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What is pathological pain
|
pain not caused by a tissue-damaging stimuli
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|
What are 4 examples of pathological pain
|
- phantom pain
- carpal tunnel syndrome - trigeminal neuraligia - thalamic pain |
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What is phantom pain, example
|
- associated with peripheral or central lesions that disconnect the painful part of the body (e.g. amputation, patients will generally have the pain subside accompanied with a perceived shrinking of the missing limb)
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What type of lesion is generally associated with phantom pain
|
- peripheral or central lesion
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|
What causes carpal tunnel syndrome
|
an example of chronic inflammation of nerve which causes AP activity and pain projected to the innervation field of the nerve
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How is carpal tunnel syndrome treated
|
surgical release of pressure
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|
What is trigeminal neuralgia (tic doulourreux)
|
- spasms of intense, intolerable pain so severe that it can lead to suicide
- often triggered by light touch to the face |
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|
How is trigeminal neuralgia treated
|
sometimes treatable with drugs, lesions of trigeminal ganglia
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describe thalamic pain
|
- thalamic lesions may produce thalamic pain
- described as unlike, and more excruicating than any previously experienced pain - totally intolerable |
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What is referred pain
|
- sensations from the viscera are poorly localized, sometimes referred to the skin
|
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Why does referred pain probably occur
|
- probably due to the convergence of cutaneous and visceral information onto same neurons, so that there is a two-part receptive field and the location label is ambiguous
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|
In whom is referred pain from a heart attack not likely
|
women
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|
What is usually women's only symptom of heart attack
|
- very intense nausea
|
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|
What is central pain, what causes it
|
- animal studies show pain cells in lamina V of the dorsal horn can be spontaneously active after periods of excitatory (nociceptive) input and produce central pain (spontaneously). This can occur in the thalamus as well
- usually a result of chronic nociceptive input |
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What 2 locations are associated with central pain
|
- Lamina V in the dorsal horn
- thalamus |
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|
What is central pain generally a result of
|
- chronic nociceptive input
|
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What should be done to prevent central pain
|
- pain should be treated aggresively to prevent chronic pain and central pain
|
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|
How should morphine be used to prevent addiction and chronic and central pain
|
- use of carefully controlled systemic drip morphine
-- example: for cancer or burn patients, NOT patient controlled in order to prevent cyclic over- and under- dosage, may be indicated - when just enough is used to relieve pain, there is a minimal risk of addiction and a decreased risk of chronic pain |
|
|
what can be done to reduce the duration of post surgical pain
|
- some studies suggest pre-emptive use of morphine analgesia reduces duration of postsurgical pain
|
|
|
in whom are dorsal rhizotomys and anterolateral tractotomies used to treat pain, why
|
- can provide immediate and profound, but often transitory relief
- used in terminal patients |
|
|
describe the result of a thalamic lesions of the ventrobasal complex, are they useful in treatment of pain
|
- usually leave affect of pain and pain sensation intact with numbness contralaterally
- this is worthless |
|
|
why are intralaminar lesions suggested for pain relief
|
they are unpredictable
|
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|
why cant cortical lesions be used to treat pain
|
- no direct cortical representation for pain means cortical ablations cant relieve pain
|
|
|
What are 3 endogenous opoids
|
- endorphins
- enkephalins - dynorphins |
|
|
What is the site of action of morphine (molecullary)
|
- binds to the same receptors as the endogenous opoids (endorphins, enkephalins, dynorphins)
|
|
|
What 3 types of activity/substances can activate PAG neurons
|
- opiates
- opioids - activity in the spinoreticular afferents |
|
|
What 2 medullary regions do PAG neurons project to
|
- medullary nucleus raphe magnus (NRM)
- nucleus reticularis gigantocellularis (NRG) - both of these areas have descending neurons which project to the dorsal horn and modulate the relay of pain to higher centers |
|
|
What 2 types of neurons leave the NRG and inhibit the relay of pain in the dorsal horn of the spinal cord
|
- enkophalenergic reticulospinal (NRG) axons
- noradreneric (NE) |
|
|
What 3 regions of the spinal cord are the main nociceptive relay regions
|
- lamina I
- lamina II - lamina V |
|
|
How do enkophalenergic reticulospinal (NRG) axons inhibit the relay of pain
|
- they are traveling in the dorsolateral funiculus and synapse in laminae I, II, and V of the spinal cord, releasing enkaphalen, which inhibits nociceptive neurons found here
|
|
|
How do noradrenergic synapses from NRG spinal neurons inhibit the tranmission of pain
|
synapses from NRG spinal neurons excite interneurons which inhibit thalamic projections (nociceptive) neurons of the ALS system through a non-opioid polysynaptic pathway
|
|
|
what neurotransmitter is released from raphespinal (NRM) axons
|
- serotonin
|
|
|
What do interneurons stimulated by serotonin release
|
secreting enkphalin (endogenous opoid)
|
|
|
How do serotonergic raphespinal neurons block the relay of pain
|
- serotonergic raphespinal (NRM) synapses excite neurons which presynaptically inhibit primary afferent C fibers by secreting enkphalin (endogenous opoid)
|
|
|
Is electrical stimulation of PAG clinically useful, why
|
- has a strong analgesic effect
- could be used to relieve pain in patients, but this structure is buried in the brainstem and the risks outweigh the benefits |
|
|
What are thalamic and cortical projections in the PAG likely responsible for
|
- they may mediate stress-induced analgesia
- example: athletes finishing a FB game with a broken ankle |
|
|
What are the 2 actions of morphine to reduce pain
|
1. block's some excitatory activity
2. increases inhibitory activity |
|
|
What type of sensory input comes through large diameter afferents
|
- light touch
|
|
|
What action do large diameter afferents have on interneuons in the dorsal horn
|
- large diameter afferents excite interneurons in the dorsal horn
|
|
|
What type of sensory input comes through small diameter afferents
|
- pain fibers
|
|
|
What affect do small diamete afferents have on interneurons of the dorsal horn
|
- they are inhibited
|
|
|
What is the effect of interneurons of hte dorsal horn on C fibers, what is the mechanism of action
|
- the interneurons suppress C fiber synaptic transmission by presynaptic inhibition
|
|
|
Why does rubbing your skin, acupuncture, acupressure, dorsal column stimulation, and transcutaneous electrical nerve stimulation work to reduce pain
|
- work by stimulating these large diameter afferents
- drive large diameter axons at the lowest frequency to feel a taping sensation, but not high enough to cause pain - example: bump your shin on a table, rub it to reduce pain |
|
|
What are the 3 levels of motor systems important for generating motor activity
|
- cerebral cortex motor areas
- brain stem - spinal cord |
|
|
How are the 3 levels of the motor system arragned
|
these are arranged hierarchally and in parallel
|
|
|
Explain how motor areas are also connected in parallel. What portions are involved
|
parallel portion of the motor system arrangment is the corticospinal tract
|
|
|
what are 2 motor loops that modify the activity carried out by the motor systems
|
1. basal ganglia and the thalamus
2. cerebellum and the thalamus |
|
|
How is the cerebellum motor loop different from the basal ganglia motor loop
|
- the cerebellum also receives sensory input from the spinal cord and lower sensory systems that it uses to modify movement
|
|
|
What is the corticobulbospinal tract (CBST) made up of
|
- corticobulbar tract to the brain stem
- corticobulbar tract to the spinal cord |
|
|
where does the CBST go
|
- brainstem
- spinal cord - basal ganglia - cerebellum |
|
|
What is the corticospinal (CST) tract made up of
|
- lateral CST
- Ventral CST |
|
|
Where else (other than the brainstem and spinal cord) does the cortex project to directly
|
- cerebellum
- basal ganglia is indirectly |
|
|
What are the lateral motor tracts of the brainstem responsible for
|
flexor biased
|
|
|
What are the medial motor tracts of the brainstem responsible for
|
- extensor biased
|
|
|
What 2 tracts make up the lateral, flexor-biased, tracts of the brainstem
|
- rubrospinal tract
- medullary reticulospinal tract |
|
|
What 3 tracts make up the medial, extensor-biased, tracts of the brainstem
|
- pontine reticulospinal tract
- lateral vestibulospinal tract - medial vestibulospinal tract |
|
|
What are the functions of the tracts originating in the brainstem (3)
|
- integrate vestibular and visual inputs
- modulate the excitability of spinal posture circuits - control eye and head movement |
|
|
What are 2 types of propriospinal fibers
|
- long
- short |
|
|
What are interneurons involved with
|
- reflexive and voluntary motor activity
- link descending fibers with motor neurons |
|
|
do interneurons always need descending input
|
- no
- these can act independently at times, e.g. reflexive withdrawal from noxious stimuli |
|
|
What are motor neurons in the spinal cord
|
- final common pathway to muscles
|
|
|
What is the parallel component of the Basal ganglia
|
CBST
|
|
|
What is the parallel component of the cerebellum
|
CBST
|
|
|
What is the parallel component of the CBST
|
- corticospinal tract, fibers going from the cortex directly to the spinal cord
|
|
|
describe the course of corticospinal fibers
(voluntary activity) |
- CBST originates in the cerebral cortex and fibers pass through the corona radiate, internal capsule, crus cerebri, pyramids, and then decussate in the pyramidal decussation to the opposite side and continue down the spinal cord
|
|
|
What 4 areas contribute fibers to the descending corticospinal tract
|
- posterior parietal cortex (parietal lobe)
-- areas 5, 7, 39, 40, 9% - premotor area (area 6, lateral) and supplementary motor cortex (6 - medial) -- 29% - primary motor cortex -- Broadman's area 4: 31% -- arranged somatotopically (homunluncus) -- cortical motor areas controlling the face and body sensory motor cortex -- areas 3,1, 2, 31% |
|
|
What are 2 ways that axons from these areas can influence the spinal cord
|
- axons of some of these neurons can influence the spinal cord directly
- while some influence the spinal cord indirectly by connecting with brain stem motor nuclei |
|
|
Where is the motor cortex located
|
- precentral gyrus
|
|
|
Where is the supplementary motor cortex located
|
- medial face of the cerebral hemisphere just in front of the primary motor cortex
|
|
|
Where is the premotor cortex located
|
- frontal lobe
|
|
|
Where is the sensory cortex located
|
- postcentral gyrus
|
|
|
Where is the posterior parietal cortex located
|
- portion of the parietal lobe
|
|
|
What areas of the body do fibers passing from the cortex and through the lateral corticospinal tract (LCST) project to
|
- below the hip
- wrist, hands, and fingers |
|
|
What areas of the body do fibers passing from the cortex and through the ventral corticospinal tract (VCST) project to (2)
|
- elbow, shoulder, trunk
- neck |
|
|
What areas of the body do fibers passing from the cortex and through the corticobulbar tract project to
|
- all of the face, mouth, and throat
|
|
|
Where on the primary sensory cortex are neurons that innervate muscles of the leg located?
|
LCST
|
|
|
Where on the cortex are muscles that will innervate muscles of the wrist, hand, and fingers located?
|
LCST
|
|
|
Where on the primary motor cortex are neurons that will innervate the elbow, shoulder, and trunk located?
|
VCST
|
|
|
Where on the primary motor cortex are neurons that will innervate the neck located?
|
VCST
|
|
|
Where on the primary motor cortex are neurons that will innervate the face, mouth, and throat located
|
corticobulbar tract
|
|
|
Note differences in the motor and sensory homunculi.
|
they differ in the amount of cortex representing various parts of the body
|
|
|
What vessels supply blood to the internal capsule (3)
|
- medial striate
- lateral striate - anterior choroidal (posterior limb) |
|
|
give the general route of the corona radiata fibers
|
- corona radiata fibers running to and from cortical regoins to the internal capsule
|
|
|
What afferents (going to the cortex) are found in the internal capsule
|
- thalamocortical fibers
|
|
|
What 8 efferents are found in the internal capsule
|
- corticobulbospinals
- corticopontines - frontopontine - temporopontine - parietopontine - occipitopontine - corticothalamic - corticostriates |
|
|
In the crus cerebri in the midbrain, from the posterior to anterior limb, list the representation of motor fibers
|
face
arm leg trunk |
|
|
In the medullary pyramid, from the posterior to anterior limb, list the representation of motor fibers
|
leg
trunk arm |
|
|
give the 4 structures that fibers of the corticospinal tract pass through before they reach the spinal cord
|
1. corona radiata
2. internal capsule 3. midbrain - crus cerebri 4. pons and pyramidstra |
|
|
What happened to the corticospinal tract in the pons? what does it look like?
|
- track breaks up in the pons, but reunities in the pyramids, maintaining their somatotopy (order), so it looks more spotty here
|
|
|
In the medulla, fibers of what tract makes up the vast majority of fibers in the corticospinal tract
|
- fibers of LCST
- which makes up the vast majority of the fibers of the corticospinal tract cross the midline in the pyramidal decussation, and descend in the lateral funiculus of the spinal cord - fibers in the VCST (anterior CST), which only makes up about 10% of fibers in the CST, do not decussate but continue downward and travel in the anterior funiculus |
|
|
Where do fibers of the LCST cross the midline
|
- pyramidal decussation
|
|
|
Where do fibers of for the corticospinal tract travel in the spinal cord
|
- lateral funiculus
|
|
|
Where do fibers of the corticospinal tract terminate
|
- fibers terminate in the motor cell groups in the ventral horn
|
|
|
Where do fibers of the corticospinal tract synapse
|
- synapse on interneurons and alpha neurons
|
|
|
Where do fibers of the LCST terminate
|
- fibers from the lateral corticospinal tract terminate in lateral motor cell groups
|
|
|
Where do fibers of the VCST terminate
|
- fibers from the anteior (ventral) corticospinal tract terminate in medial cell groups
|
|
|
Where do fibers for the corticobulbar tract terminate
|
- in the brainstem in 8 CN nuclei to innervate the head and face
|
|
|
What 8 CN nuclei do corticobulbar tract fibers terminate in
|
- oculomotor nuclei
- trochlear nuclei - abducens nuclei - facial nuclei - primarily crossed in lower face, bilateral in upper face - ambiguus nuclei - hypoglossal nuclei - primarily crossed for genioglossus muscle - accessory nuclei - trigeminal nuclei |
|
|
are fibers of the corticospinal tract as neat and clean as they appear in the atlas picture, explain
|
- fibers arborize (branch like a tree) along the corticospinal tract while descending and prior to termination, such that one fiber can actually give rise to several terminal axons that can terminate in different cell groups or nuclei
|
|
|
Does one corticospinal fiber always travel strait down to its terminal neuclei and then innervate a single neuclei or cell group?
|
that one fiber can actually give rise to several termianl axons that can terminate in different cell groups or neuclei
|
|
|
What is the function of the corticospinal tract
|
- controls fine (independent, fractionated) movement of distal extremities and coarse regulation of proximal flexors
|
|
|
What is damage to the CST associated with
|
upper motor neuron signs
|
|
|
What are lower motor neurons
|
- neuron that innervate the muscle; includes neurons of the CN nuclei that innervate facial muscles,
-- so neurons dont have to be low in the nervous system to be lower motor neurons |
|
|
What does damage to any part of a lower motor neuron result in
|
will result in a lower motor neuron disease
|
|
|
What determines whether deficits due to an upper motor neuron disease will occur ipsilaterally or contralaterally
|
- depend on whether the lesion is above or below the decussation of the pyramids
|
|
|
What are the acute signs/symptoms of an interuption of CST (2)
|
- flaccid paralysis
- loss of normal resistance to passive movement (muscle tone) |
|
|
What happens to upper motor neuron disease patients after the first few days
|
- after a few days, some voluntary motor control may return, but the sign/symptoms to the left begin
|
|
|
What is spastic weakness
|
increase in muscle tone makes movement difficult
|
|
|
What is clonus
|
rhythmic contraction to ankle/wrist muscles in response to stretch
|
|
|
relatively how many muscles are affected by upper motor neuron disease
|
muscles are affected in large groups
|
|
|
describe babinski sign and normal response
|
- when bottom of foot is stroked with strong metal object the toes exhibit an extensor response, the toes arch upward
- normally the toes would flex downward |
|
|
describe the bing sign and a normal response
|
- normal plantar response with pin stick, foot moves downward
- bing sign, extensor response foot moves up |
|
|
are all sign/symptoms of upper motor neuron disease explained by a CST lesion
|
- all of these signs can not be explained by an upper motor neuron lesion alone
- the timing and course of these changes varies, depending on the cause of the lesion |
|
|
describe how clonus appears after a clinician has struck a patients acheies tendon with a reflex hammer
|
- after the acheiles tendon is hit, the foot will keep jerking repeatedly
|
|
|
describe the babinski sign
|
- as the stick runs up the sole of the foot, the toes fan out
|
|
|
what is the babinski sign characteristic of
|
upper motor neuron damage
|
|
|
describe Hoffman's sign
|
- as the distal phalinx of the middle finger is "flipped" the other fingers and thumb clench together
|
|
|
why does the Hoffman sign occur
|
- sometimes called the upper limb equivalent of the Babinski, but mechanistically they are somewhat different
- for the thumb Rexed's lamina IX is fully inhibited by descending fibers |
|
|
describe hyperflexia
|
reflexes are much more brisk and more jerky
|
|
|
describe hemiparetic gait
|
- one side operates normally and smoothly, but the other side is spastic and may involve some paralysis
|
|
|
what is hemiparetic gait often seen following
|
- a stroke
|
|
|
where do corticobulbar fibers arise
|
- arise from different areas of the cerebral cortex
|
|
|
where do corticobulbar fibers terminate
|
- end in brainstem CN nuclei
|
|
|
what are 2 examples of corticobulbar tracts
|
- corticoreticular tract
- corticorubral tract |
|
|
where do the fibers of the corticoreticular tracts originate
|
- these fibers are from the frontal, parietal, and temporal cortices
|
|
|
where do the fibers of the corticoreticular tracts terminate
|
- terminate in the pontine and medullary reticular nuclei
|
|
|
what does the reticular formation (reticular nuclei) give rise to
|
- the reticulospinal tracts
|
|
|
where do the fibers of the corticorubral tracts originate
|
- includes diffuse fibers from the premotor and motor cortices
|
|
|
where do the fibers of the corticorubral tracts terminate
|
- in the red nucleus
|
|
|
what does the corticorubral tract control
|
- controls fine movement (independent, fractionated) activity of distal extremities, coarser activity of proximal flexors
|
|
|
what does fugal mean
|
- away from, out from
|
|
|
generally, where do corticobulbar fibers terminate
|
throughout the brainstem
|
|
|
constrast the innervation of the upper and lower face
|
- only the upper face in innervated bilaterally
- the lower face is predominately innervated by the contralateral side |
|
|
how is the lower face innervated
|
- predominately innervated by the contralateral side
|
|
|
what are common sites of damage to the corticobulbar projectionsto the upper and lower facial nucleus
|
- in the cortex
- in the internal capsule |
|
|
what does a drooping lower face only on one side indicate
|
- points to a lesion in the contralateral corticobulbar system
|
|
|
why does a lesion in the contralateral corticobulbar system cause a drooping face
|
- because lower face is innervated contralaterally
|
|
|
where does the rubrospinal tract originate
|
- originates in the red nucleus
|
|
|
where does the rubrospinal tract decussate
|
- almost immediately in the ventral tegmental decussation
|
|
|
where does the rubrospinal tract travel in the spinal cord
|
- lateral funiculus
|
|
|
what type of muscles does the rubrospinal tract innervate
|
- distal extremities
- proximal flexors |
|
|
what type of movement of distal extremities the rubrospinal tract involved in
|
- controls voluntary, fractionated, independent activity
- fine movement |
|
|
what type of movement of proximal flexors the rubrospinal tract involved in
|
- coarser activity
|
|
|
what part of the body is the rubrospinal tract particular important for controling
|
- has a large impact on hand movements
- damage leads to very clumsy hand movements |
|
|
how do fibers of the rubrospinal tract control fine movements in the distal extremities
|
- by controling tone in alpha motor neurons innervating contralateral flexors muscles and inhibiting extensor muscles
|
|
|
where is the reticular formation found
|
- in the midbrain, pontine and medullary tegmentum
- nuclei coalesce in reticular formation of the pons and medulla and give rise to reticulospinal tracts -- nucleus pontis oralis and caudalis give rise to the pontine reticulospinal tract -- nucleus gigantocellularis gives rise to the medullary reticulospinal tract |
|
|
what type of movement and reflexes are reticulospinal tracts involved in
|
- involved in sudden reflexive startle responses = quick, reflexive, compensatory movements to maintain posture
|
|
|
what do the medial brain stem motor tracts involved
|
- medial vestibulospinal tracts
- lateral vestibulospinal tracts |
|
|
what is the role of vestibulospinal tracts (VSTs)? how do they accomplish this
|
- they maintain posture and reflexes by controlling the midline extensor muscles
-- the lateral VST keeps the center of gravity b/w the feet -- the medial VST goes to the cervical level only and --- stabilizes the head and provides a stable platform for the eyes --- is joined by the tectospinal tracts in the medulla |
|
|
What joins the medial VST? Where?
|
the tectospinal tracts in the medulla
|
|
|
Where does the lateral VST arise from?
|
arises from the lateral vestibular nuclei
|
|
|
Where does the descending lateral VST travel?
|
descends in the anterior funiculus
|
|
|
Where do fibers in the lateral VST terminate?
|
on the ipsilateral interneurons and motor neurons
|
|
|
What do fibers in the lateral VST act on?
|
- act on medial motor neurons
|
|
|
What do motor neurons influenced by lateral VST fibers control?
|
- control proximal, axial musculature, particulary extensor (antigravity) muscles involved with reflexive control of balance and posture, purpose is to keep center of gravity b/w feet
|
|
|
Where does the medial VST arise?
|
medial vestibular nuclei
|
|
|
Where does the descending medial VST travel?
|
MLF
|
|
|
Where does the medial VST terminate?
|
on the ipsilateral interneurons and motor neurons at cervical and high thoracic level, only innervating muscles of the neck
|
|
|
What do motor neurons on which medial VST fibers synapse control?
|
stabilizes the head to provide a stable platform for the eyes
|
|
|
where do fibers for the tectospinal tract originate
|
superior and inferior colliculi
|
|
|
where do fibers for the tectospinal tract decussate
|
dorsal tegmental decussation
|
|
|
What does the tectospinal tract merge with
|
the medial vestibulospinal tract
|
|
|
where do fibers for the tectospinal tract terminate
|
at cerivical levels
|
|
|
What is the role of the tectospinal tract
|
- coordinates head and eye movement
- orients head and eyes toward sources of auditory or visual stimulation |
|
|
What is the overall role of propriospinal tracts
|
- coordinate the activities of axial and distal musculature
|
|
|
Where (generally) are propriospinal tracts found
|
- run all around the ventral horn, particulary around medial and lateral cell groups
|
|
|
What do the lateral cell groups consist of
|
- corticospinals
- rubrospinals |
|
|
What do the lateral cell groups control
|
- control distal musculaturre of the arms and legs
|
|
|
What propriospinal fibers are associated with the lateral cell groups
|
- short propriospinal fibers run b/w the neurons of the lateral cell groups
|
|
|
Why are the short propriospinal fibers associated with the lateral cell groups
|
- they are short b/c they only have to connect a few spinal cord segments
- b/c only those segments responsible for arm and leg movements have lateral cell groups |
|
|
What do the medial cell groups control
|
- control proximal, axial musculature
|
|
|
What propriospinal fibers associated with the medial cell groups
|
- long propriospinal fibers
|
|
|
Why are the long propriospinal fibers associated with the medial cell groups
|
- these cell groups are long and run through many spinal segments, and thus are connected by long propiospinal fibers
|
|
|
Where are short propirospinal tracts located
|
- on the lateral side of the gray matter
|
|
|
Where are long propirospinal tracts located
|
- on the medial side of the gray matter
|
|
|
What causes lower motor neuron diease
|
- usually caused by a degeneration or trauma to lower motor neurons
|
|
|
what is a lower motor neuron
|
- a neuron that synapses onto muscle
|
|
|
What can caused lower motor neuron disease
|
- selective interuptions of descending motor systems (rarely occur), and are usally accompanied by damage to ascending systems
|
|
|
What are 2 examples of lower motor neuron disease
|
- poliomyelitis
- amytrophic lateral sclerosis (ALS) |
|
|
what are 5 symptoms of lower motor neuron disease
|
- flaccid muscle weakness or paralysis
- muscle wasting - decreased or absent reflexes - signs of muscle atrophy including fasciculations and fibrillations - sensory patterns: stocking and glove: follow dermatomes or fragments of dermatomes |
|
|
What sensory loss patterns follow
|
- stocking and glove: follow dermatomes or fragments of dermatomes
|
|
|
What are fasciculations
|
- small, local, involuntary skeletal muscle contraction arising from spontaneous discharge of a bundle of skeletal muscle fibers
|
|
|
What are fibrillations
|
- muscle twitching involving contraction of individual muscle fibers without coordination
|
|
|
contrast fibrilations with fasciculations
|
- fasciculations involve many fewer fibers that fibrillations
- a common example of fasciculations is an eyelid twitch that many people experience when they are tired |
|
|
give some examples of where lesions causing lower motor neuron disease can occur
|
- facial nucleus (CN VII)
- Hypoglossus nucleus (CN XII) - spinal motor neuron pools |
|
|
Why do fasciculations occur in lower motor neuron disease
|
- muscles need to be innervated to live
- when they become denervated they become hyperactive before they waste away |
|
|
What causes Bell's Palsy
|
- damaged CN VII nucleus or nerve
|
|
|
breifly describe the basal ganglia's communication loop in the cerebral cortex motor area
|
cerebral cortex motor area --> basal ganglia --> thalamus --> cerebral cortex motor area
|
|
|
how were the fucns of basal ganglia originall inferred
|
- from disease and lesions
|
|
|
what are the 2 main functions of basal ganglia
|
1. initiation of voluntary movement
2. inhibition of involuntary movement |
|
|
what are the 6 major nuclei of the basal ganlia
|
- caudate
- putamen - globus pallidus - subthalamic nucleus - substantia nigra - nucleus accumbens |
|
|
what is the name given to the caudate + putamen
|
- (neo) striatum
|
|
|
what makes up the lenticular nucleus
|
- putamen
- globus pallidus |
|
|
what makes up the corpus striatum
|
- caudate
- putamen - globus pallidus |
|
|
What are the 2 parts of the globus pallidus
|
- internal (medial)
- external (lateral) -- medial medullary lamina |
|
|
What are the 2 parts of the substantia nigra
|
- pars compacta: dopaminergic
- pars reticulata |
|
|
What part of the substantia nigra is dopaminergic
|
pars compacta
|
|
|
What is the nucleus accumbens sometimes referred to as
|
ventral palidum
|
|
|
why is the nucleus accumbens considered part of the basal ganglia
|
- relays through areas that follow the basal ganglia loops
|
|
|
What is the function of the expyramidal system
|
- involved with higher aspects of motor control such as initiation of movements, selective facilitation/inhibition of movements
|
|
|
Where is the nucleus accumbens located
|
b/w the head of the caudate and the putamen
|
|
|
What separates the globus pallidus from the putamen
|
external medullary velum (lamina)
|
|
|
where is the internal medullary velum found
|
- separates the external segment of the globus pallidus from the internal segment
|
|
|
input into the basal ganglia comes in via what fibers
|
- corticostriate projections = cortical projections terminate in the caudate and putamen
-- via external and internal capsules |
|
|
where do corticostriate projections originate? where specifically (3)
|
- fibers originate in the motor, sensory, and limbic association areas
|
|
|
where do corticostriate projections terminate
|
- in the caudate and putamen
|
|
|
Where do projections from the motor cortex terminate
|
- putamen
|
|
|
how are the motor cortex projections arranged in the putamen
|
- somatopically
|
|
|
what is the putamen primarily concerned with
|
motor function
|
|
|
what do the corticostriate projections extend downward into
|
external and internal capsules
|
|
|
input from what areas comes into the head of the caudate
|
receives heavy input from the frontal lobes and limbic areas
|
|
|
what is the primary fcn of the head of the caudate
|
emotional aspect of the basal ganglia
-- underlies emotional component of basal ganglia disorders --- eratic behavior, depression, anxiety |
|
|
where does input coming into the body and tail of the caudate come from
|
- parietal, occipital, and temporal lobes
|
|
|
Where is all information incomming to the basal ganglia "funneled" to
|
- everything goes to the GPm
|
|
|
why is all input funneled to the GPm
|
- b/c GPm is responsible for output to the thalamus
|
|
|
where do most afferents (input, corticostriate projections) terminate
|
caudate and putamen
|
|
|
where do corticostriate projections fibers come from
|
- motor, sensory, and limbic association areas
|
|
|
what type of fibers does the putamen primarily receive
|
S1 and M1 fibers
-- sensory/motor aspect |
|
|
describe the direct route of input to the medial portion of the globus pallidus
|
- fibers from the caudate and putamen, drop off colaterals to lateral (GPl) and medial (GPm) segments of globus pallidus (external and internal segments)
- GPm also receives input from pars compacta (PC) of the substantia nigra |
|
|
Describe the indirect route for input into the GPm
|
- colaterals from the putamen and caudate synapse in the lateral segment GPl, synapse on fibers which project to the subthalamic nucleus (STh) and synapse on fibers which then project back to the GPm and the pars reticularis (PR)
|
|
|
fibers from what 4 areas project to the GPm
|
- caudate
- putamen - subthalmic nucleus - Pars Compacta (substantia nigra) |
|
|
how does fibers travels from the GPl to the GPm
|
indirect route through the subthalamic nucleus
|
|
|
what is the clinical significance of the indirect route (genrally)
|
- detour has a large effect on motor fcn when damaged
|
|
|
why is the substantia nigra black
|
- b/c cells of the pars compacta (PC) have melanin
|
|
|
what neurontransmitter does the PC produce
|
dopamine
|
|
|
where does dopaminergic neurons of the PC project to
|
- caudate
- putamen |
|
|
is dopamine an excitatory or inhibitory nt?
|
- has either an excitatory or inhibitory effect, depending on what kind of cell it is synaping in
|
|
|
What is the effect of dopamine in the striatum?
|
In the caudate and putamen, it has an excitatory effect on cells.
|
|
|
Is dopamine an excitatory or inhibitory neurotransmitter? Elaborate.
|
Dopamine has either an inhibitory or excitatory effect, depending on what kind of cells it is synapsing in
|
|
|
What part of the substantia nigra do neurons from the caudate and putamen project to?
|
pars reticularis (PR)
|
|
|
What 3 neurotransmitters are released by caudate and putamen neurons projecting to the PR?
|
GABA, Substance P, enkephaline
|
|
|
Are the neurotransmitters released by striatum cells projecting to the PR excitatory or inhibitory?
|
Gaba has a inhibitory effect.
|
|
|
How does the striatum influence the activity of the PC
|
Since there is connection between the PR and PC, the GABA system is one way that the causdate and putamen can regulate activity in the substantia nigra.
|
|
|
where does output from the thalamus go to
|
- outputs go to the thalamus to the contramedian intralaminar nucleus (CM) and the VA/VL nucleus of the thalamus (mingles with fibers from the cerebellum)
|
|
|
Explain why the basal ganglia have an “indirect” effect on motor function.
|
- the basal ganglia has an “indirect” effect on motor function, by means of their connections with supplementary and premotor corticies
- there is no direct projections to the brainstem or spinal cord motor nuclei |
|
|
What other than the GPm gives off fibers that projects to the VA/VL?
|
fibers from the cerebellum
|
|
|
Fibers from where other than the GPm project to the superior colliculus?
|
- outputs from GPm and PR go to the superior colliculus and control eye movement
|
|
|
What is basal ganglia input to the superior colliculus responsible for?
|
controlling eye movements
|
|
|
Fibers from what other than the GPm project to the reticular formation?
|
PR
|
|
|
What is basial ganglia input to the reticular formation responsible for?
|
- impinges on reticulospinal tracts that cause up to reflexively control posture
|
|
|
Are thalamic outputs excitatory or inhibitory?
|
excititory (glutamate)
|
|
|
What neurotransmitter is used by thalamic neurons?
|
glutamate
|
|
|
What is disinhibition?
|
- inhibitory neuons synapsing on anoter inhibitory neuron
- : you can think about disinhibition like multiplying 2 negatives (-2 x -2 = +4) because one inhibitiroy neuron (-) synapsing on another (-) yields an excitatory (+) result. |
|
|
What is disinhibition equivalent to?
|
excitatory
|
|
|
What 2 pathways are responsible for input from the striatum to the thalamus?
|
direct and indirect pathways
|
|
|
Which of the pathways is associated with disinhibition?
|
direct
|
|
|
Which pathway is associated with inhibition?
|
indirect
|
|
|
internal segment of the globus pallidus projects efferent fibers to (3)
|
- VA
- VL - CM |
|
|
Where does the Ansa lenticularis originate
|
in the GPm
|
|
|
What is the course of the Ansa lenticularis
|
- originates in the GPm --> passes ventrally and rostrally around the PLIC --> to Forel's Field H (prerubral field)
|
|
|
Where does the lenticular fasciculus originate
|
GPm
|
|
|
What is the course of the lenticular fasciculus
|
originates in the GPm --> passes through the internal capsule,
|
|
|
What is the lenticular fasciculus also referred to as
|
referred to as Forel's Field H2
|
|
|
What is the thalamic fasciculus also referred to as
|
referred to as Forel's Field H1
|
|
|
How is the thalamic fasciculus formed
|
- formed when fibers from the ansa lenticularis join those of the leniticular fasciculus prior to entering the VA/VL and CM thalamic nuclei
|
|
|
Where do the efferents of the basal gangial that project to cortical areas influence
|
descending motor control
|
|
|
Motor Circuits of the Basal Ganglia: Supplementary motor -> -> -> putamen
|
supplementary motor --> premotor --> motor cortex --> somatosensory cortex --> superior parietal lobule --> putamen
|
|
|
Motor Circuits of the Basal Ganglia: putamen
|
putamen --> internal globus pallidus and substantia nigra
|
|
|
Motor Circuits of the Basal Ganglia: globus pallidus, substantia nigra
|
globus pallidus, substantia nigra --> thalamus (VA, VL, CM)
|
|
|
Motor Circuits of the Basal Ganglia: thalamus
|
thalamus --> supplemtal motor cortex and premotor cortex
|
|
|
Motor Circuits of the Basal Ganglia: supp. motor, premotro
|
- supplementary motor and premotor --> to motor cortex and each other
|
|
|
Motor Circuits of the Basal Ganglia: motor cortical areas
|
- to b.s. and spincal cord
|
|
|
what are signs of basal ganglia disease
|
Involuntary movement
- tremors - athetosis - chorea - hemiballism - dystonia difficulty initiating and executing movements - akinesia - bradykinesia |
|
|
what are the two types of signs for basal ganglia disease
|
- involuntary movements
- disturbances of muscle tone |
|
|
What types of tremors can happen at rest
|
- rhythmic
- involuntary - oscillatory |
|
|
What is athetosis
|
slow writing motions of fingers, hands, and toes
|
|
|
what is chorea
|
abrupt movements of limbs and facial muscles
|
|
|
Motor Circuits of the Basal Ganglia: putamen
|
putamen --> internal globus pallidus and substantia nigra
|
|
|
Motor Circuits of the Basal Ganglia: globus pallidus, substantia nigra
|
globus pallidus, substantia nigra --> thalamus (VA, VL, CM)
|
|
|
Motor Circuits of the Basal Ganglia: thalamus
|
thalamus --> supplemtal motor cortex and premotor cortex
|
|
|
Motor Circuits of the Basal Ganglia: supp. motor, premotro
|
- supplementary motor and premotor --> to motor cortex and each other
|
|
|
Motor Circuits of the Basal Ganglia: motor cortical areas
|
- to b.s. and spincal cord
|
|
|
what are signs of basal ganglia disease
|
Involuntary movement
- tremors - athetosis - chorea - hemiballism - dystonia difficulty initiating and executing movements - akinesia - bradykinesia |
|
|
what are the two types of signs for basal ganglia disease
|
- involuntary movements
- disturbances of muscle tone |
|
|
What types of tremors can happen at rest
|
- rhythmic
- involuntary - oscillatory |
|
|
What is athetosis
|
slow writing motions of fingers, hands, and toes
|
|
|
what is chorea
|
abrupt movements of limbs and facial muscles
|
|
|
What are the signs of basal ganglia disease
|
- involuntary movements
- disturbances of muscles tone (difficulty initiating and executing movement) |
|
|
What are the involuntary movements associated with basal ganglia disease
|
- tremor
- athetosis - chorea - hemiballism - dystonia |
|
|
What are the difficulty initiating and executing movement symptoms associated with basal ganglia disease
|
- akinesia
- bradykinesia |
|
|
What are types of tremors at rest
|
- rhythmic
- involuntary - oscillatory |
|
|
What is athetosis
|
slow writhing motions of fingers, hands, and toes
|
|
|
what is chorea
|
- abrupt movement of limbs and facial muscles
|
|
|
what is hemiballism
|
- violent, flailing; lesion of subthalamic nucleus
|
|
|
What is dystonia
|
- persistent posture causing odd movements, distorted position of trunk and extremities
|
|
|
What is akinesia
|
difficulty initiating movements
|
|
|
what is bradykinesia
|
- slowness is executing movemets
|
|
|
What are symptoms of basal ganglia disease attributable to
|
disturbances in the neurotransmitter systems
|
|
|
When do symptoms of basal ganglia disease worsen
|
with emotional stress
|
|
|
What are the symptoms of Parkinson's disease
|
- tremor at rest
- muscle rigidity (cogwheel type) - akinesia - bradykinesia - reduced eye blink frequency |
|
|
What are the causes of Parkinson's disease
|
- degeneration of substantia nigra pars compacta leads to DA deficit in striatum
-- DA is primarily inhibitory -- 80% of DA neurons lost before symptoms appear |
|
|
What are the treatments for Parkinson's disease
|
- L-DOPA
- MAO inhibitors (L-deprenyl - fetal transplants (midbrain or chromaffin cells) - thalamotomy: lesions of VA/VL or GPm, releives systems - implanted stim electrode |
|
|
What is a thalamotomy, what is it used for
|
- lesions of VA/VL or GPm, releives systems
- relieves symptoms of parkinson's - in cases with unilateral symptoms, lesions found in CL of substantia nigra |
|
|
Where are implated stimulatory electrodes that are used to treat Parkinson's disease
|
- thalamus
- subthalamus - globus pallidus |
|
|
What is the cause of huntington's disease
|
- rare mutation in the huntington gene
- there is a 50% chance of inheriting the gene but the onset is usually not until the 30-40s, now a test for the gene |
|
|
What are symptoms of huntington's disease
|
- motor signs progressively worsen
- dementia - involuntary movements -- athetoid -- chorea - slurred speech |
|
|
what are personality changes associated with huntington's disease
|
- depression
- apathy - hostility - slowed thought process - forgetfulness |
|
|
What is likely responsible for mental deterioration in huntington's disease
|
loss of cells found in the frontal cortex and precentral gyrus
|
|
|
what is the treatment for huntington's disease
|
none, death
|
|
|
what is the biochemical symptoms of huntington's disease
|
- invovles degeneration of caudate and putamen and layer 3 of the cerebral cortex
- loss of striatal gabaergic and cholinergic neurons - induced excitotoxicity from glutamate |
|
|
tardive dyskinesia: iatrogenic
|
due to admisistration of anti-DA drugs (anti-psychotics)
|
|
|
Where does influx of info into the cerebellum come from
|
- come from below in the spinal cord and from the cerebral cortex
|
|
|
Where does outflow from the cerebellum go
|
- back to the spinal cord or brainstem
-- others go back to the cortex and impinge indirectly on other lower systems (BS and SC) |
|
|
what is cerebral input to the cerebellum associated with
|
- communication from cerebral cortical area = plans about ongoing motion
|
|
|
What structure of the cerebellum is at risk from increased intracranial pressure? what is the risk?
|
- tonsil
- subject to herniation through the foramen magnum |
|
|
What is the result of a tonsilar herniation if not relieved immediately by releiving intercranial pressure?
|
it is lethal
|
|
|
What are 3 pairs of deep nuclei of the cerebellum?
|
- fastigal
- interposed - dentate |
|
|
What makes up the interposed nuclei?
|
- emboliform
- globose |
|
|
Generally, what does the superior cerebellar peduncle (SCP) connect?
|
- from the cerebellum to the midbrain (red nucleus and thalamus)
|
|
|
Generally, what does the MCP connect?
|
- fibers from contralateral pons carries info from the cortex to the cerebellum
|
|
|
Generally, what does the ICP connect?
|
- info from the spinal cerebellar tracts (medulla to pons)
|
|
|
Do the peduncles simply carry information into the cerebellum?
|
no, in some of them there is a little bit of info coming out of the cerebellum
|
|
|
What are the 2 divisions of the ICP?
|
- Restiform body
- Juxtarestiform body |
|
|
What 5 fiber classes travel through the restiform body of the ICP?
|
- olivocerebellar fibers (climbin)
- cuneocerebellar fibers - rostral spinocerebellar - dorsal spinocerebellar - arcuocerebellar fibers |
|
|
What 3 classes of fibers travel through the juxtarestiform body of the ICP?
|
- cerebellovestibular
- vestibulocerebellar - cerebellospinal |
|
|
What fibers travel through the MCP?
|
- pontocerebellar
|
|
|
What 4 classes of fibers travel through the SCP?
|
- cerebellorubral
- cerebellothalamic - cerebellooculomotor - ventral spinocerebellar tract |
|
|
What peduncle carries the most output from the cerebellum?
|
ICP
|
|
|
what are the 3 main roles of the cerebellum
|
- compensate for errors in movement
- coordinates limb and eye movements (hand-eye coordination) - maintains balance and muscle tone |
|
|
How does the cerebellum compensate for errors in movement?
|
- by comparing intention (cortical information/ connections) with performance (what's actually going on; proprioceptive info from spinocerebellar tracts)
|
|
|
What info does internal feedback give the cerebellum
|
- what should be happening
|
|
|
What info does the cerebellum receive from external feedback
|
- what is happening
- receives info about movements as they are occuring -- "this is what its doing" |
|
|
What 2 source give external feedback to the cerebellum?
|
- vestibular system
- SCT |
|
|
What 2 areas does the cerebellum influence in order to adjust motor activity?
|
- influences descending motor systems by indirectly adjusting motor activity through connections with the:
-- motor and premotor cortex -- brainstem nuclei |
|
|
Where in the skull is the cerebellum found
|
- posterior cranial fossa
|
|
|
What makes up the cerebellar cortex?
|
- outer gray matter
- inner white matter |
|
|
what are the 3 lobes of the cerebellum
|
- Anterior
- Posterior: seperated from the anterior lobe by the primary fissure - Flocculonodular: seperated from the posterior lobe by the posterolateral fissure |
|
|
What seperates the anterior and posterior lobes
|
- primary fissure
|
|
|
What are lobules
|
- lobes are sep. into 10 lobules
|
|
|
what are folia
|
- shallow fissures that sep. the lobules
|
|
|
What is the functional distinction between the anteior and posterior lobes?
|
there is none
|
|
|
What 3 arteries serve the cerebellum
|
- superior cerebellar artery
- AICA - PICA |
|
|
What artery serves all 3 peduncles
|
AICA?
|
|
|
What artery serves the anterior lobe of the cerebellum
|
SCA
|
|
|
What are the 3 layers fo the cerebellar cortex visible under light microscope?
|
- granule cell layer
- purkinje cell layer - molecular layer (w/ purkinje cell dendrites and other cells) |
|
|
What does the molecular layer of the cerebellar cortex consist of?
|
purkinje cell dendrites and other cells
|
|
|
What is unique about the dendritic arbor of the perkinji cell?
|
- arbor can not be seen in one direction, but if you rotate it 90 degrees it can be seen
|
|
|
Very generally, explain outflow from the cerebellum.
|
efferents
- purkinje cells project first to deep nuclei - neurons in the deep nuclei porject out to the cerebellum |
|
|
inputs to the cerebellum project collateras to what 2 areas?
|
- as afferent fibers come in, they give off collateral to deep cerebellar nuclei and the other terminates in the cerebellar cortex
|
|
|
What does output from the cerebellar cortex effect?
|
- output of the cerebellar cortex is exclusively from purkinje cells and is inhibitory
- inhibition inpinges on deep cerebellar nuclei which then projects out |
|
|
Is output from the cerebellar cortex excitatory or inhibitory?
|
inhibitory
|
|
|
Are cerebellar inputs excitatory or inhibitory?
|
excitatory (2 kinds)
|
|
|
What are the 2 types of afferent fibers which bring info into the cerebellum?
|
- mossy fibers
- climbing fibers |
|
|
What 4 areas do mossy fibers arise in?
|
- spinal cord spinocerebellar tracts
- vestibular nuclei - reticular formation - pontine nuclei |
|
|
How do mossy fibers influence perkinje cells?
|
- influence them indirectly through synapses with excitatory granule cells
|
|
|
Where do climbing fibers arise?
|
- arise in the inferior olivary nucleus
|
|
|
What do climbing fibers synapse on?
|
- inputs from all parts of sensory and motor systems
- "climb" around and synapse on purkinje somata and dendrites - synapse on deep nuclei and cerebellar cortex |
|
|
What is the most excitatory synapse in the NS?
|
climbing fibers
- One climbing fiber can have a major effect on the excitability of a perkinji cell |
|
|
Compare the number of cerebellar afferents to efferents.
|
afferents outnumber efferents 40:1
|
|
|
What are mossy fiber rosets?
|
- area where mossy fibers synapse on granual cells
|
|
|
What do parallel fibers arise from?
|
- granule cells give rise to fibers that climb to the molecular layer and bifurcate to form parallel fibers
|
|
|
What are the 3 functional regions of the cerebellum?
|
- lateral hemispheres
- intermediate hemispheres - vermis and flocculonodular lobe |
|
|
What is the function of the lateral hemisphere of the cerebellum?
|
- motor planning for extremities
|
|
|
What motor pathway is influenced by the lateral hemisphere of the cerebellum?
|
- lateral corticospinal tract
|
|
|
What is the function of the intermediate hemisphere?
|
distal limb coordination
|
|
|
What 2 motor pathways are influenced by the intermeidate hemisphere?
|
- lateral corticospinal tract
- rubrospinal tract |
|
|
What are the 2 functions of the vermis and floccularnodular lobe?
|
- proximal limb and trunk coordination
- balance and vestibuloocular reflexes |
|
|
What 4 motor pathways are involved in vermis and flocculonodular lobe coordination of the proximal limbs and trunk?
|
- anterior corticospinal tract
- reticulospinal tract - vestibulospinal tract - tectospinal tract |
|
|
What motor pathway is involved in control of balance and vestibulo-ocular reflexes by the vermis and the floccularnodular lobe?
|
- medial longitudinal fasciculs
|
|
|
What functional name is associated with the lateral hemisphere?
|
- cerebrocerebellum
|
|
|
What functional name is associated with the intermediate hemisphere (and vermis)?
|
spinocerebellum
|
|
|
What functional name is associated with the folloculonodular lobe (and vermis)?
|
vestibulocerebellum
|
|
|
What makes up the vestibulocerebellum?
|
- flocculonodular lobe and vermis
|
|
|
What nucleus is associated with the vestibulocerebellum?
|
1/2 of the festigal nucleus
|
|
|
What makes up the spinocerebellum?
|
intermediate zone and vermis
|
|
|
What nuclei are associated with the spinocerebellum?
|
- 1/2 of the festigal nucleus and interposed nuclei
|
|
|
What does the spinocerebellum perdominantly communicate with
|
- the spinal cord
|
|
|
What makes up the cerebrocerebellum?
|
lateral hemisphere
|
|
|
What nucleus is associated with the cerebrocerebellum?
|
dentate nucleus
|
|
|
What does the cerebrocerebellum predominately communicate with?
|
cerebral cortex
|
|
|
What 2 functional areas is the festigeal nucleus associated with?
|
- vestibulocerebellum
- spinocerebellum |
|
|
Describe the basics of input into the vestibulocerebellum.
|
receptors in the bony labriynth detect head position --> CN VIII --> flocculonodular lobe and vestibular nuclei
|
|
|
Where does all input to the vestibulocerebellum funnel to?
|
flocculonodular lobe
|
|
|
Describe the basics of output from the vestibulocerebellum?
|
fastigal nucleus --> vestibular nuclei --> vestibulospinal tract
- outflow from the vestibular nucleus then travels to the flocculonodular lobe - Flocculonodular lobe sends output to the festigial nucleus |
|
|
What structures are responsible for vestibular sense
|
- semicircular canals
- vesitbular nuclei - LGB (about body position) - superior colliculus - visual cortex (eyes are important for balance) |
|
|
What are the 2 ways that the simicircular canals detect head postion?
|
- otolith organs (position of head relative to gravity)
- some direct via CN VIII |
|
|
What does the spinocerebellum perdominantly communicate with
|
- the spinal cord
|
|
|
What makes up the cerebrocerebellum?
|
lateral hemisphere
|
|
|
What nucleus is associated with the cerebrocerebellum?
|
dentate nucleus
|
|
|
What does the cerebrocerebellum predominately communicate with?
|
cerebral cortex
|
|
|
What 2 functional areas is the festigeal nucleus associated with?
|
- vestibulocerebellum
- spinocerebellum |
|
|
Describe the basics of input into the vestibulocerebellum.
|
receptors in the bony labriynth detect head position --> CN VIII --> flocculonodular lobe and vestibular nuclei
|
|
|
Where does all input to the vestibulocerebellum funnel to?
|
flocculonodular lobe
|
|
|
Describe the basics of output from the vestibulocerebellum?
|
fastigal nucleus --> vestibular nuclei --> vestibulospinal tract
- outflow from the vestibular nucleus then travels to the flocculonodular lobe - Flocculonodular lobe sends output to the festigial nucleus |
|
|
What structures are responsible for vestibular sense
|
- semicircular canals
- vesitbular nuclei - LGB (about body position) - superior colliculus - visual cortex (eyes are important for balance) |
|
|
What are the 2 ways that the simicircular canals detect head postion?
|
- otolith organs (position of head relative to gravity)
- some direct via CN VIII |
|
|
What are 3 other areas that send input to the vestibulocerebellum?
|
- LGB
- superior colliculus - visual cortex |
|
|
What type of information if sent to the vestibulocerebellum from the lateral geniculate nucleus?
|
about body position
|
|
|
What type of information is sent to the vestibulocerebellum from the visual cortex?
|
- eyes are important for balance
|
|
|
Where does output form the vestibulocerebellum originate?
|
purkinje cells of the flocculonodular lobe
|
|
|
What 2 areas receive projections for the purkinje cells fo the FL lobe? Which area receives more?
|
- fastigal nucleus
- medial and lateral vestibular nuclei - fastigal receives more |
|
|
Where does output from the fastigial nucleus go?
|
goes to the medial and lateral vestibular nuclei --> medial and lateral vestibulospinal tracts
|
|
|
What do the medial and lateral vestibular nuclei give off?
|
medial and lateral vestibulospinal tracts
|
|
|
What are the 2 functions of the vestibulocerebellum?
|
- control of equilibrium and balance
- coordinates head and eye movements |
|
|
How does the vestibulocerebellum control equilibrium and balance?
|
- by controlling axial musculature via the medial and lateral vestibulospinal tracts
|
|
|
What results from damage to the vestibulocerebellum?
|
gait and stance problems
|
|
|
What 5 systems/tracts give input to the spinocerebellum?
|
- from the lower extremities:
-- dorsal and ventral spinocerebellar tracts of the spinal cord - From upper extremities: -- through the cuneocerebellar tracts and rostrospinocerebellar tracts of the spinal cord auditory, visual, and vestibular systems |
|
|
Input from where comes through the dorsal and ventral spinocerebellar tracts?
|
lower extremities
|
|
|
Input from where comes through the cuneocerebellar tract and the rostrospinocerebellar tracts?
|
upper extremities
|
|
|
Where 2 palaces does output from the spinocerebellum originate?
|
vermis and intermediate zone
|
|
|
Where do perkinje cells from the vermis project to?
|
fastigal nucleus
|
|
|
Where do cells from the fastigial nucleus project to (3)?
|
- lateral vestibular nucleus
- reticular formatoin - thalamus |
|
|
Where do cells from the lateral vestibular nucleus project?
|
vestibulospinal tract
|
|
|
Where do cells from the reticular formation project to?
|
reticular tract
|
|
|
What is ultimately effected by output from the perkinji cells of the vermis?
|
medial motor cell column
|
|
|
Where do projections from perkinji cells of the intermediate hemsipher project to?
|
interposed nucleus
|
|
|
Through what do projections from the interposed nucleus pass through?
|
superior cerebellar peduncle
|
|
|
Where do projections from the interposed nucleus go? (2)
|
- red nucleus
- VL thalamus |
|
|
What do projections from the rednucleus travel through?
|
rubrospinal tract
|
|
|
What do projections from the VL thalamus to to?
|
cortex
|
|
|
What do projections from the motor cortex travel through?
|
CBST
|
|
|
What does output from intermediate hemisphere perkinji cells ultimately affect?
|
lateral motor cell columns
|
|
|
What are the 2 functions of the spinocerebellum?
|
- controls execution of ongoing movement via medial and lateral descending motor systems
- regulates muscle tone |
|
|
Where does the dorsal spinocerebellar tract (DSCT) originate?
|
Clarke's nucleus
|
|
|
Where does information traveling in the DSCT originate?
|
muscle spindles, Golgi tendon organs, joint receptors
|
|
|
How does the DSCT reach the cerebellum?
|
inferior cerebellar peduncle
|
|
|
What part of the body does the DSCT carry information about?
|
lower limb and trunk
|
|
|
What makes up the origin of the ventral spinocerebellar tract?
|
spinal border cells
|
|
|
What is the role of spinal border cells?
|
- spinal cord internal feedback
- monitor descending commands; synapse with interneurons and descending neurons; transmit info into the cerebellum |
|
|
Which peduncle does the VSCT pass through
|
superior cerebellar peduncle
|
|
|
The VSCT carries information about what part of the body?
|
lower limb
|
|
|
Where does the cuneocerebellar tract originate?
|
accessory cuneate
|
|
|
Where does the CuneoCBT get the information that it carries?
|
muscle spindles, GTO, joint receptors
|
|
|
What peduncle does the CuneoCBT pass through?
|
ICP
|
|
|
From what body parts does the CuneoCBT carry info?
|
upper trunk, limb, and neck
|
|
|
Where does the Rostral CBT originate?
|
lamina VII, C4-8
|
|
|
What peduncle does the rostral CBT pass through
|
ICP
|
|
|
What body parts does the Rostral CBT carry info from
|
upper trunk and limb
|
|
|
Where do inputs into the cerebrocerebellum originate
|
- pyramidal cells in the sensory, motor, premotor, and visual cortices
|
|
|
Where do inputs into the cerebrocerebellum synapse first?
|
pontine nucleus
|
|
|
Through what do projections from the pontine nucleus pass?
|
middle cerebellar peduncles
|
|
|
What do projections form the pontine nucleus project to?
|
contralateral cerebellum
|
|
|
Where do the outputs of the cerebrocerebellum originate?
|
purkinje cells of the lateral hemisphere
|
|
|
Where do the outgoing fibers from the perkinji cells of the lateral hemisphere synapse first?
|
dentate nucleus
|
|
|
What do projections from the dentate nucleus pass through?
|
superior cerebellar peduncles
|
|
|
What 2 places do projections from the dentate nucleus go?
|
- VL thalamus
- red nucleus |
|
|
Where do fibers form the VL thalamus project to?
|
premotor cortex
|
|
|
Through what do projections from the red nucleus pass?
|
rubrospinal tract
|
|
|
What are the functions of the cerebrocerebellum?
|
- timing of movements
- fine motor commands for movements |
|
|
What are 4 symptoms of lesions of the lateral hemisphere or the dentate nucleus?
|
- problems with timing the initation of movements
- terminal tremor - disorders in temporal coordination of mult joints - disorders in spatial coordination of hand and finger muscles |
|
|
Contrast the difficulty in initiating movement associated with dentate nucleus lesion and basal ganglia lesion.
|
- in the dentate there is problems with timing the initiation of movements
- in the basal ganglia lesions in which the patient is to stiff to start moving |
|
|
What is a terminal tremor?
|
- occurs at the end of movement
-- example: if patient is trying to touch your finger, tremor will get much worse when they get close to ur finger |
|
|
From where does the cerebrocerebellum both receive and send information?
|
receives info from the cortex and returns it to the cortex
|
|
|
How do projections from the cortex reach the pons?
|
Fibers that originate in premotor ares, supplementary motor areas, primary motor, and posterior parietal area, and other parts of cerebral cortex
Project to the pons through the internal capsule and crus cerebri |
|
|
Explain why damage to the cerebrocerebellum causes manifestation of symptoms on the ipsilateral side?
|
double decussation = manifestation of cerebellar damage on the same side as the lesion (lateral system and intermediate zone)
|
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|
The pontocerebellar fibers carry info originating where?
|
cortex
|
|
|
Where do the pontocerebellar fibers originate?
|
pontine nuclei
|
|
|
What do the pontocerebellar fibers pass through to reach the cerebellum?
|
MCP
|
|
|
What are the 4 spinocerebellar pathways?
|
- dorsal spinocerebellar tract
- cuneocerebellar tract - ventral spinocerebellar tract - rostral spinocerebellar tract |
|
|
The dorsal spinocerebellar tract carries informtion originating in where?
|
leg proprioceptors
|
|
|
Where does the dorsal spinocerebellar tract official begin?
|
nucleus dorsalis of clark
|
|
|
Through what does the dorsal spinocerebellar tract pass?
|
ICP
|
|
|
Where does info passing through the cuneocerebellar tract originate?
|
arm proprioceptors
|
|
|
Where does the cuneocerebellar tract originate?
|
external cuneate nucleus
|
|
|
Through what structure does the cuneocerebellar tract pass?
|
ICP
|
|
|
Where does info traveling through the venral spinocerebellar tract originate?
|
leg interneurons
|
|
|
What cells give rise to projections that pass through the ventral spinocerebellar tract?
|
spinal cord neurons
|
|
|
Through what structure does the ventral spinocerebellar tract pass to reach the cerebellum?
|
SCP
|
|
|
Where does info passing thr the rostral spinocerebellar tract originate?
|
arm interneurons
|
|
|
What cells give off projections that pass through the rostral spinocerebellar tract?
|
spinal cord neurons
|
|
|
Through what structures does the rostral spinocerebellar tract pass to reach the cerebellum?
|
SCP
ICP |
|
|
Where does info passing through the climbing fibers originate?
|
- red nucleus
- cortex - brainstem - spinal cord |
|
|
Where are the cells that give rise to climbing fibers located?
|
inferior olivary nuclei
|
|
|
Through what structure do climbing fibers pass to reach the cerebellum?
|
ICP
|
|
|
Where does informaiton traveling the in vestibular inputs originate?
|
vestibular system
|
|
|
Where are cells that give off projections traveling in the vestibular inputs located?
|
vestibular ganglia
vestibular nuclei |
|
|
Through what structure do vestibular inputs pass to reach the cerebellum?
|
juxtarestiform body
|
|
|
What is the significange of the cerebellum being very plastic?
|
- cerebellar activity is modified by practice and learning = plasticity
|
|
|
What is hypotonia?
|
reduced resistance to passive limb movement
|
|
|
What are pendular reflexes?
|
limb will swing like a pendulum when reflex has been induced b/c no resistance
|
|
|
What is ataxia?
|
difficulties in executing voluntary movement
|
|
|
What are 3 examples of ataxia?
|
- dysmetria
- dysdiadochokinesia - terminal (action) tremor |
|
|
What is dysmetria?
|
errors in the range and force of movement
|
|
|
What is dysdiadochokinesia?
|
cannot sustain rhythmic alternating movements
|
|
|
What is a terminal tremor?
|
esp at the end of a movement
|
|
|
Why do lesions to the cerebrocerebellum cause ipsilateral symptoms?
|
- lesions produce symptoms on the same side b/c the SCP and the corticospinal tract both cross
|
|
|
what is tintubation?
|
- trunk tremors while standing/sitting; interferes with staying erect
-- "drunken's sailor" gait: axial muscles are disturbed |
|
|
What type of gait is associated with cerebrocerebellar lesions?
|
"drunken's sailor" gait: axial muscles are disturbed
|
|
|
What is nystagmus?
|
- eyes move slowly in one direction then rapidly in the other
|
|
|
What will happen if a patient who has a onesided cerebellar hemisphere lesion is told to flex both arms at the same time on a go signal?
|
- a lesion in the right cerebellar hemisphere causes a delay in the initiation of movement
- the left arm will flex later than the right |
|
|
What if the same patient is asked to move his arm from a raised position to touch his nose?
|
- they will exhibit dysmetria (inaccuracy in range and direction) and unsmooth movement with increased tremor upon approaching the nose
|
|
|
Describe the difference between normal alternating movement and dysdiadochokinesia.
|
- dysdiadochokinesia, is an irregular patten of alternating movement
|
|
|
The Romberg test tests the functioning of what system?
|
- vestibulocerebellum
- test done with eyes closed, b/c eyes help u maintain balance; |
|
|
What are 8 Parkison’s syndromes?
|
- parkinson's disease
- drug induced parkingson's disease - progressive supranuclear palsy - multiple system atrophy - lewy body disease - cortico-basal ganglia degeneration - multi-infarct encephalopathy - wilson's disease |
|
|
What is the most common Parkinson’s syndrome?
|
- Parkinson's disease
|
|
|
When does Parkinson’s disease associated dementia occur?
|
- it occurs late and in a minority of patients
|
|
|
Is Parkinson’s disease associated dementia common?
|
no, only occurs in a minority
|
|
|
What are 3 drugs that can cause drug induced Parkinson’s disease?
|
- neuroleptics
- MPTP (a designer narcotic in CA) - reserpine |
|
|
What is the landmark characteristic of Multiple System Atrophy?
|
orthostatic HTN
|
|
|
What is the second most common cause of dementia in the elderly?
|
lewy body disease
|
|
|
What are the cardinal features in Lewy-Body disease?
|
early dementia and hallucinations
|
|
|
Is cortico-basal ganglia degeneration common?
|
no, rare
|
|
|
What are 3 characteristics of cortico-basal ganglia degeneration?
|
- presents with parkinson's syndrome
- progressive dementia - limb apraxia (inability to carry out learned purposeful movement) |
|
|
What causes multi-infarct encephalopathy?
|
a lot of strokes
|
|
|
Which is the most rare Parkinson syndrome?
|
wilson's disease
|
|
|
What causes Wilson’s disease?
|
a genetic disorder
|
|
|
How common is Parkinson’s disease (quantify)?
|
- 1% over the age of 65
|
|
|
What are 3 genetic mutations that may be involved in Parkinson’s disease?
|
- synuclein mutation
- parkinson's mutation - mitochondrial complex I deficiency |
|
|
Which of the 3 mutations is autosomal dominant?
|
synuclein mutation
|
|
|
Which of the 3 mutations is autosomal recessive
|
parkinson's mutation
|
|
|
What are 4 known environmental toxins that can cause Parkinson’s disease or syndrome?
|
- MPTP
- Mn - CO - Cyanide |
|
|
What is MPTP?
|
a designer narcotic that actually causes parkinson's disease
|
|
|
What exactly does Mn toxcicity cause?
|
- causes a unique parkinson's syndrome
- dementia - personality changes -- seen in welders who use Mn rocks |
|
|
Contrast the Parkinson’s syndrome caused by Mn in welders and that seen in other Mn exposures
|
- may cause parkinson's disease in welders
- may cause parkinson's sydrome in non-welders |
|
|
What does CO exposure cause?
|
parkinson's syndrome
|
|
|
What does Cyanide exposure cause?
|
parkinson's syndrome
|
|
|
What are 2 histological or gross slide features of Parkinson’s disease?
|
- substantia nigra appears much lighter in the midbrain of parkinson's patients
- lewy-bodies |
|
|
Contrast the location of Lewy-Bodies in Parkinson’s disease vs. Lewy-Body disease.
|
- can be seen in the cells of the substantia nigra in parkinson's patients, this is a unique feature of parkinson's disease
- lewy bodies are seen in the cortex of patients with lewy body disease |
|
|
What are 7 symptoms of Parkinson’s disease? (originally 6, but I added one that Dr. Gutman said)
|
- asymmetric resting tremor
- cogwheel rigidity - petit pass shuffling gait - bradykinesia - masked face - levadopa (drug) responsive - soft voice with monotone |
|
|
What type of tremor is associated with early Parkinson’s disease?
|
- asymmetric resting tremor
|
|
|
What % of early Parkinson’s patients will have an asymmetric resting tremor?
|
- seen early in 75%
|
|
|
How can you tell a Parkinsonian tremor from a familial action tremor?
|
- an action tremor is seen when the patient is holding their hands out
- asymmetric resting tremor is seen when patient is at rest |
|
|
Describe the Cogwheel rigidity of the limb of a Parkinson’s patient.
|
- arm, when moved passively has a rachet or a cog-like jerk; jerky movement
|
|
|
Describe Petit pas shuffling gait.
|
- walks with short, shuffling steps
- keeping feet touching, or nearly touching the ground |
|
|
What is bradykinesia?
|
slow movement
|
|
|
Describe the masked face of a Parkinson’s patient?
|
- doesnt have a lot of expression
- smile looks painted - staring quality |
|
|
What is the 2nd criteria for Parkinson’s diagnosis (1st being asymmetric resting tremor)?
|
levadopa (drug) responsiveness
|
|
|
What is levodopa?
|
- is a precursor to dopamine
|
|
|
Why does levodopa responsiveness occur?
|
- loss of DA is seen in parkinson's b/c cells in the substantia nigra are dying
- give L-DOPA b/c it can cross the BBB and enhance dopamine production |
|
|
What kind of other drugs (other than levodopa) are used to treat Parkinson’s disease?
|
- requip
- myrapex - dopamine agonist: directly stimulate DA receptors in the striatum |
|
|
What do some patients struggle with after treating Parkinson’s with levodopa for ~6-7 years?
|
- after a while (6-7 yrs) patients get the on/off effect = inadequate response at times (off) and at other times get dyskinesia (on; involuntary movement)
|
|
|
Describe the “on/off” effect associated with levodopa.
|
on/off effect = inadequate response at times (off) and at other times get dyskinesia (on; involuntary movement)
|
|
|
How are patients with “on/off” effect of levodopa now treated?
|
- now treated with 2 stimulators in the subthalamic nucleus if L-DOPA receptors quit working properly
|
|
|
What happens to Parkinson’s patients at night?
|
- all signs of parkinson's go away with sleep
- so patients with a stimulator may turn it off or leave it on |
|
|
When is levodopa normally taken?
|
patients on L-DOPA will take it b/w 6 am and 6 pm, not at night
|
|
|
Why must a patient who is being given a stimulator to treat Parkinson’s be woken up during surgery?
|
- must wake patient up during surgery to insert a stimulator so they can see if it will work; b/c symptoms are suppresed during sleep
|
|
|
What are 12 symptoms that do not usually respond to treatment of Parkinson’s disease with L-Dopa (or stimulator)?
|
- postural instability
- freezing gait - dysphagia - dementia - apathy - depression - constipation - sexual dysfunction - urinary problems - sweating - pain - sleeping disturbances |
|
|
What is freezing-gait
|
- have to really work to start walking
- "stuck to the floor" |
|
|
What is Dysphagia?
|
trouble swallowing
|
|
|
What are 5 treatments/classes of treatments for Parkinson’s disease?
|
- anti-cholinergics
- DA agonists - L-DOPA/ caribidopa - COMT inhibitors - deep brain stim |
|
|
What does Carbidopa do? Why is it given with L-dopa?
|
- caribidopa inhibits DA production in the periphery, but not the CNS b/c it does not cross the BBB, thus it is keeping plasma L-DOPA conc high and saves the L-DOPA for the CNS
|
|
|
How do COMT inhibitors help with Parkinson’s disease
|
break down DA
|
|
|
What are 6 ways that patients that experience the “on-off” effect of levodopa are handled clinically?
|
- more frequent dosing
- alter dietary proteins - DA agonists - COMT inhibitors - apomorphine - STN deep brain stim |
|
|
What is deep brain stimulation in the ventral intermediate nucleus used to treat?
|
- used for tremor
-- bad familial tremor |
|
|
What is subthalmic nucleus (STN) deep brain stimulation used to treat?
|
treat parkinson's patients who experience the on/off effect of L-DOPA
|
|
|
What are 5 side effects of deep brain stimulation?
|
- depression
- dysarthrina - personality and cognitive changes - hemiparesis - suicide |
|
|
What is dysarthrina?
|
problems talking
|
|
|
What is hemiparesis?
|
weakness on one side of the body
|
|
|
What is suicide in patients with STN deep brain stimulation treatment of Parkinson’s disease likely the result of?
|
patients couldnt tolerate the dramatic change b/w being an "invalid" to being high functioning so quickly
|
|
|
What does late Parkinson’s disease treated with a stimulator “look like”?
|
it looks like early in parkinson's
|
|
|
What does cerebral palsy refer to specifically?
|
- motor system abnormality
|
|
|
What is CP due to?
|
due to a static (unchanging) lesion in the brain
|
|
|
When does the lesion associated with CP arise?
|
- it is present from a pre or perinatal period
|
|
|
What is sometimes done instead of diagnosing a patient with CP?
|
- clinicians, often look at the following to define and describe the problem rather than rushing to diagnos with CP, which encompasses a wide range of brain lesions causing motor abnormalities
|
|
|
What are 5 symptoms that may be associated with CP
|
- spasticity
- movement disorder - changing motor patterns - hypotonicity - mixed tone |
|
|
What is spacisticity?
|
- increased muscle tone and brisk reflexes
|
|
|
How is spacisticity tested for in a child?
|
- test by passively moving the limb to grade resistance or by asking the adolescent to walk then run
|
|
|
How is tone tested in a baby?
|
- pick the up from under the sholders and note the stiffness of the baby
|
|
|
Describe the appearance of increased muscle tone.
|
- scissoring of legs = leges extended, stiff, crossed, toes pointed (walking on toes if walking), and elbows and wrists flexed
|
|
|
What are 2 movement disorders associated with CP?
|
- distonic
- choiapitotic |
|
|
What is distonic movement?
|
- slow twisting, stiffening movements
|
|
|
What is choiapitotic movment
|
slow writhing movements
|
|
|
Dispite the fact that the underlying brain lesion doesn’t change, ______ may change through out the patients life and development.
|
motor patterns
- example: start with spasticity then have a motor disorder |
|
|
Relatively how many patient’s with CP experience hypotonicity?
|
a small percentage of patients
|
|
|
What is the most likely course of the symptoms in patients with CP who origionally present with hypotonicity?
|
if they present with hypotonicity at birth they will develop hypotonicity
|
|
|
What is mixed tone?
|
- extremities have increased tone, but trunk has decreased tone
|
|
|
How are relflexes often graded?
|
- often graded based on clonus
|
|
|
What is a +1 reflex?
|
- difficult to obtain
|
|
|
What is a +2 reflex?
|
- normal
|
|
|
What is a +3 reflex?
|
- 2 or 3 beats of clonus
|
|
|
What is a +4 reflex?
|
- 4 or more beats of clonus
|
|
|
In what reflex is clonus seen in mostly
|
- usually clonus is seen more, or only in the ankle jerk
|
|
|
What are 6 developmental or other effects of CP?
|
- increased tone inhibits learning to walk
- speech is more difficult because it is difficult to move their mouth - chewing and swallowing difficulties - constipation - decreased range of motion - life expectancy can be decreased due to complications caused by CP |
|
|
Why is learning to walk particularly challenging for children with CP?
|
- b/c of the increased tone
- 1-2 y/o who are trying to walk, waddle and have a wide gait; since tone increase causes kids to be on their toes, their balance is significant impaired, and since they have scissoring of legs, wide gate is impossible |
|
|
Why is speech often more difficult for CP patients?
|
because it is difficult for them to move their mouth
|
|
|
Why is range of motion decreased in CP patients?
|
- when there is not good movement, you can get contractures (shortening of muscles) such that range of motion is significantly inhibited
|
|
|
How is life expectancy effected by CP?
|
- life expectency is not necessarily decreased by CP, but is usually descreased by complications associated with CP
|
