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290 Cards in this Set
- Front
- Back
what is stereognosis
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ability to perceive the form of an object using touch
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what is graphestheisa
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ability to recognize writing on skin purely by the sensation of touch
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what is the clinical term for a type of sensation
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modality
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a patient is experiencing extreme pain who smiles and enjoys it, has an inappropriate expression of what
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affect
|
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if a person has complete loss of sensation in a part of the skin, where will the lesion be
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Peripheral (PNS)
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when a person experiences loss of one sensory modality, where will the lesion be
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central (CNS)
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what differentiates a tract from a pathway
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a tract is a bundle of axons with a common origin, course, and destinations, whereas a pathway is a series of synaptically linked neurons that share a common function; tracts are often included as parts of pathways
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what distinguishes sensory info from afferent info
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sensory info is consciously experience, wherease afferent info contains both conscious and subconscious input
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what do the medial division fibers consist of and what do they initially run into when entering the spinal cord
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large, myelinated fibrer
enter into the fasciculus gracilis or cuneatus |
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what do the lateral division fibers consist of and what do they initially run into when entering the spinal cord
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small, unmyelinated fibers
enter into the dorsolateral sulcus |
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After a sensory axon enters the spinal cord, what normally occurs and how does this differ b/w medial and lateral division fibers
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it bifurcates into an ascending and descending branch
medial divions: long ascending and short descending with collateral innervation of 6-8 segments lateral division: short ascending and short descending with collateral innervation to 2-3 segments |
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what fibres distribute mainly to the posteromarginal nucleus, substantia gelatinosa, and the neck of the dorsal horn
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lateral division fibrs
vs. the medial division fibers which have a much more widespread distribution |
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what functions are the medial division fibers associated with
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movement reflexes, stretch reflexes, and fine localization of touch
vs. lateral division fibers carrying pain and temperature |
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what are the possible effects of a single spinal afferent
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reflexes (via spinal cord)
perception (via thalamus/cortex) "subconscious" data (via brainstem/cerebellum) |
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what is the cutaneous innervation associated with C1
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nothing
starts at C2-back of head |
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what spinal cord segments provide cutaneous innervation to the neck
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C3, 4 (shoulders are C5)
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where do 1st, 2nd, and 3rd order afferents originate and terminate
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1st: PNS --> DRG --> Spinal cord/brainstem
2nd: SC/BS --> crosses midline --> VP nucleus of the thalamus 3rd: VP nucleus --> PLIC --> cortex (area 3, 1, 2) |
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what are examples of rapidly adapting receptors
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meissner's corpuscles
pacinian corpuscles merkel's discs ruffini corpuscles |
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what modalities are carried in the DCML parthway and which is unique to it
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fine touch
conscious proprioception vibration** |
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which division fibers are associated with DCML and in what nuclei will the 1st order synapse
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medial division afferents
travel in fasciculus gracilis and cuneatus and synapse in their respective nuclei |
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Where do the second order neurons of the DCML pathway cross over and where do they project to?
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at the medial leminiscus (immediately after leaving the nucleus gracilis and cuneatus) and project to the VPL nucleus
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Where do the 3rd order neurons of the DCML pathway project to, specifically
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primary sensory cortex (S1)
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Below midthoracic level, into what fasciculations do axons of the DCML enter
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fasciculus gracilis
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after crossing over, what do the 2nd order neurons of the DCML travel in
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medial lemnicus
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where in the VPL do axons from the nucleus gracilis and cuneatus synapse, respectively
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gracilis - lateral
cuneatus - medial |
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after leaving the lateral part of the VPL, where in the cortex do signals from the lower extremitiy synapse
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medially (in the somatopic map - S1)
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if a patient has a lesion in the medial part of the medial lemniscus, where would the deficit be
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in the contralateral side of the upper extremity
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on the somatopic map, what two sections separate the angle at the midline which separate the supply of MCA from ACA
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angle - hip and knee
MCA/ACA - trunk and hips |
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what kind of touch is esp important in the DCS
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time coded touch (graphesthesia/stereognosis)
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what does a loss of vibration indicate
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a lesion in the DCML (almost exclusively)
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Which modalities are located in the ALS
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pain
temperature crude touch/pressure |
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Which fibers are found in the ALS
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Adelta dibers (small, myelinated)
C fibers (small, unmyelinated) |
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What type of axonal endings (receptors) are associated with the ALS
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undifferentiated (naked nerve endings)
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where do Adelta and C fibers of the ALS enter the spinal cord and where do they initially travel to
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enter in the lateral division of the dorsal root
ascend and descend for 1-3 segments in the dorsolateral tract (Lissauer's tract) to synapse in the dorsal horn |
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Where in the dorsal horn do the Adelta and C fibers synapse
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Adelta: laminae I (posteromarginal nucleus) and V (nucleus proprius)
C: lamina I and II (substantia gelatinosa) |
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Where do the 2nd order neurons of the ALS decussate and where do they ascend
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in the ventral white commissure at approx their level of origin and ascend in the ALS tract
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What distinguishes the ALS from the DCML system when looking at 2nd order neurons
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the 2nd order neurons of the ALS do not all go to the VPL thalamus, but split off earlier in the brainstem to synapse in mult. areas of the brain and they decussate at different level
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to what areas do the 2nd order neurons of the ALS send their axons to
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reticular formation
PAG intralaminar nucleus of the thalamus (CM - centromedian) VPL (main pathway) |
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what is found b/w the 1st and 2nd order neurons of the ALS and what is its purpose
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an interneurons - modulates input (reduces pain)
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how do the axons of the ALS distribute somatotopically
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same as those of the DCML but less defined (only counts for the spinothalamic division - those going through the VPL)
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How do fibers of the ALS running into the PAG function
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they synapse on neurons that descend and cause release of serotonin from the raphe nuclei, which subsequently causes inhibition of 2nd order neurons of the ALS (i.e. it has an analgesic role)
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complete unilateral loss of pinprick sensation can be caused by what
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a lesion of the ALS in the upper spinal cord/ brainstem in the contralateral side
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what type of deficits are caused by damage to the ALS
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deficits in pinprick sensation, temperature, itch/tickle, and sexual sensations
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what is the DRG a homolog to in the trigeminal system
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sensory ganglia of CN V and the mesencephalic nucleus
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what is the spinal homolog to the cheif sensory nucleus of V
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dorsal column nuclei (nucleus gracilis and cuneatus)
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What are the homologs in the spinal system to the spinal trigeminal nucleus and tract
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spinal trigeminal nucleus: laminae I/II in the dorsal horn (posteromarginal nucleus and substantia gelatinosa)
spinal trigeminal tract: dorsolateral funiculus |
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how do pain and temperature sensation from the face reach the spinal trigeminal nucleus
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from the receptor they travel through a ganglion and descend in the spinal trigeminal tract to the spinal trigeminal nucleus
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after crossing the midline fairly quickly, in what tract do the 2nd order neurons of the trigeminal pain pathway travel and where do they synapse
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VTTT and synapse in the VPM nucleus
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how do the locations where the 2nd order neurons conveying pain and temp input synapse differ, regarding body and facec
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VPL: body
VPM: face (think of general somatotopic arragments) |
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What do the 3rd order neurons of the trigeminal sensory pathway travel through and where do they synapse
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travel through the PLIC to synapse in S1 (lateral portion) goes for pain, temperature, touch, and pressure
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where do most of the pain pathways of the trigeminal nerve travel to before synapsing
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the caudal 1/3 of the medulla
|
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where do the 1st order neurons of touch and pressure pathways of the face have their cell bodies and where do they synapse
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cell bodies in the trigeminal ganglia
synapse in the cheif sensory nucleus of CN V |
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in what tract do decussation axons from 2nd order neurons of touch and pressure pathway of CN V travel and where do they synapse
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travel in VTTT
synapse in VPM |
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how do the pathwats of 2nd order neurons of touch and pressure modality of CN V different from the rest of the body
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besides decussating and traveling in VTTT, some neurons remain ipsilateral and travel in DTTT to synapse on VPM
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why is pinprick sensation a more reliable modality than touch and pressure in the face
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b/c ALL pain fibers cross over whereas some touch and pressure fibers do not
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what type of neurons are involved in proprioception of the face and where are their cell bodies located
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pseudounipolar neurons - cell bodies in mesencephalic nucleus
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what differentiates visceral sensation from somatic sensation
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afferents, perception, and innervation (density) is different; CNS pathway is bilateral; pain is often referred
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Does the NS have the capacity to create new information
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no, it can only process it
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how does the concept of entropy relate to the NS
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in the process of transmitting information, some is always lose
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where is the neuron does most of the information processing occur
|
axon hillock
|
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what is the purpose of having interneurons
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they aid in the processing of information
|
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even though the individual neuron is slow, what aspect of the NS causes info processing to be fast
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its parallel nature (many cells working at the same time)
|
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what differentiates b/w transduction and representation
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transduction: link b/w physical stimulus and input tp nervous system
representation: link b/w nervous system and preception |
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What type of potential is the receptor and how it is referred to
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graded potential
referred to as a generator potential (since graded potential is genereated at sensory endings of axon) |
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Besides the receptor potential, what is another example of a graded potent
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synaptic potential
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What is the concept called which states that the receptor potetial amplitude is proportional to the number of open channels (caused by stimulus)
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Amplitude modulation (AM)
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how does stretching a muscle induce an action potential in the muscle spindle
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when stretched, tethers b/w the ions channels induce a conformational change allowing the passage of ions
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Where are action potentials usually generated at sensory terminals
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at the trigger zone (first node of Ranvier)
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what type of channels are found in the trigger zone of sensory terminals
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voltage-sensitve channels
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What does AM-FM conversion refer to
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the conversion of a sensory stimulus to an action potential
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What happens when the amplitude of a stimulus is increased
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the frequency of action potentials increase
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How does the firing rate differ when a static stimulus is applied to either a slow-adapting or fast-adapting receptor
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slow-adapting: fires continuously
fast-adapting: only fires when the stimulus is applied and when it is removed |
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How can a continuous stream of action potentials be genereated in a fast-adapting receptor
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the intensity of the stimulus must be constantly changing
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What type of conversion happens at the synapse
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FM-AM conversion
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What happens when the action potential frequency (FM) increases at the synapse
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more neurotransmitter is released (which determines the AM via the number of channels opened)
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What does computation refer to regarding action potentials
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the processing of various PSPs coming from different sources to determine action potential frequency
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how are sensory systems segregated
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by modality (vision, hearing, touch, etc)
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What is meant by calling an axon a labeled line
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stimulation of that axon will signal the type, location, and amplituse of the stimulus to the cortex (i.e. make us aware of its modality, location, and strength)
|
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Which type of receptor is good for coding the intensity of a stimulus
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slow-adapting (or tonic) receptors
|
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When does the rapidly-adapting receptor fire
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when the stimulus changes (always when the amplitude increases, and sometimes when it decreases)
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Which type of receptor allows extraction of dynamic information regarding the stimulus (i.e. velocity and acceleration)
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rapidly-adapting receptor
|
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What type of response do the Pacinian corpuscle and the free nerve ending exert, respectively
|
Pacinian: rapidly-adapting
Free nerve ending: slow-adapting |
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Why is the range of the stimulus intensity that we can perceive limited
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b/c each receptor has a physiological range of intensities at which it can response, and once the stimulus goes outside that range we can no longer preceive it
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How does the CNS judge stimulus intensity
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by looking at how many axons are firing due to a particular stimulus
|
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What determines the receptive field of a particular sensory neuron
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the area of skin which will elicit discharge in that central neuron
|
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how are the receptive fields represented in the cortex
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axons with adjacent RFs in the skin will also have adjacent projections and connections in the sensory cortex
|
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What tells the CNS where the RF of a certain sensory neuron is located?
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NOT the location in the sensory cortex, but the labeled line
|
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What are derivative sensations and what are some examples of them
|
sensations derived from multiple primary sensations (modalities)
includes wetness, tickle, itch |
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Which two sensory fibers types have the fastest conduction and why
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Aalpha and Abeta, because they have the largest diameter and are myelinated
|
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Which two sensory fibers types have the slowest conduction and why
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Adelta and C, because they have the smallest diamter
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What differentiates C type fibers from A type fibers
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C type fibers are unmyelinated and smaller
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Which motor fiber type is unmyelinated
|
Type IV (all other myelinated with Type I being the fastests, then II, then III)
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What fibers are associated w/ touch and which with pain/temperature
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Touch: Aalpha and Abeta
Pain/temp.: Adelta and C |
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How are different sub-modalities represented in the somatosensory map
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they are intermingled by segregated to some extent as the level of the individual neurons
|
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What is acuity and how is it measured clinically
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a measure of sharpness of resolution
determined by measured the two-point discrimination threshold (and taking the reciprocal) |
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What two factors determine the acuity at a point on the skin
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receptive field size
number of RFs contacted by the stimulus |
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Which will have a higher innervation density, the finger or the arm, why
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the finger since it has many more sensory axon RFs contacted by the stimulus
|
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What types of stimuli are transmitted by nociceptive axons
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potentially tissue-damaging stimuli (not by exacerbated touch, vibration, or temp)
|
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How do the conduction velocity and duration of the stimulus differ b/w Adelta and C fibers
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Adelta: fast, pain lasts only the duration of the stimulus
C: slow, pain outlasts the duration of the stimulus |
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What type of nociceptive stimuli are carried by Adelta and C fibers, respectively, and how does their onset differ
|
Adelta: sharp, buring, but tolerable pain, with a rapid onset
C fibers: dull, aching, intoleravle pain with a slow onset |
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Which type of pain has central representation similar to that of touch and which does not
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Fast pain: well localized just like touch
Slow pain: not well localized, since it is relayed polysynaptically and through nonspecific nuclei of the thalamus leading to widespread coritcal representation |
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How does morphine exemplify the difference b/w pain and nociception
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patients can still identify that the stimulus is noxious (still havs nociception) but the affect of pain is missing
|
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What sets phantom pain, carpal tunnel syndrome, and trigeminal neuralgia apart from most forms of pain
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they are not caused by tissue damage
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lesions in what part of teh NS cause extreme, excruciating pain
|
thalamus
|
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what is the cause of referred pain
|
convergence of cutaneous and visceral info onto the same neuron
|
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how does central pain come about
|
chronic nociceptive input can cause pain cells in lamina V to become spontaneously active, producing central pain
|
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what is the best way to prevent both chronic pain and addiction in cancer or burn patients, requiring morphine
|
use a carefully controlled systemic drip as opposed to a patient controlled drip
|
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which types of surgical innervation for pain relief give the patient profound, by transient relief
|
dorsal rhizotomy
anterolateral tractotomy |
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what is the mechanism by which morphine analgesia works
|
binds to the same receptors as endogenous opoids such as endorpins, enkephalins, and dynorphins
|
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how does activation of endogenous opoid receptors decrease pain
|
afferents activate neurons in the PAG, these project to the medullary nucleus raphe magnus and nucleus reticularis gigantocellularis whose descending axons cause inhibition of pain
|
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by what mechanism do the descending axons from the medullary nucleus raphe magnus cause inhibition of pain
|
axons synapse to excite interneuons on the spinal cord (through 5-HT) which in turn causes the inhibition of C fibers by secreting enkephalin
|
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by what mechanisms do the descending axons of the nucleus reticularis gigantocellularis cause inhibition of pain
|
axons synapse to excite interneurons in the SC (through NE) which in turn cause inhibiton of thalamic projectio neurons of the ALS through a non-opoid polysynaptic pathway
|
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what mediates stress-induced analgesis
|
thalamic and cortical projections to PAG
|
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what is the mechanism by which gate control inhibits pain
|
stim of large diameter fibers (by rubbing skin) excites interneuons which in turn have an inhibitory effect on C fiber synaptic transmission (thus inhibiting pain)
|
|
what types of clinical applications use the gate control concept to manage pain
|
acupuncture/acupressure
dorsal column stimulation transcutaneous electric nerve sitmulation |
|
What is it called when a single afferent neuron splits to synapse on multiple interneurons
|
divergence
(vs. convergence) |
|
what is the mechanism called by which a reflex pathway be inhibited through higher centers
|
gating
|
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what are the two types of gating control mechanisms and how does each work
|
gating by interneurons: descending control signal directly inhibits interneuron
gating by presynaptic inhibition: descending control signal causes presynaptic inhibition of excitatory input into the interneuron/motor neuron |
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by what mechanism can a single stimulus cause a reflex, that far outlasts the stimulus itself
|
reverberating circuits: interneurons synapse on each other, creating a circle that continuously activates itself and the motor reflex
|
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How does the spinal cord maintain the rhythmic alternating activity (half-center model) as seen in walking
|
both flexors and extensors are stimulated simulataneously, but inhibitory interneurons allow only one of the antagonisitic muscle groups to contract at once; when the inhibition of one group dies out the antagonisistic muscle group will contract, until the cycle repeats itself
|
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how is stiffness of the joint generated, as in holding a heavier object
|
normally, contraction of flexors causes the extensors to relax; but by causing inhibition of the Ia inhibitory interneuron innervating the extensors, dual contraction is possible and stiffness in the joint is generated
|
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what is the interneuron called that creates a negative feedback loop b/w a motor neuron and itself
|
renshaw cell (inhibitory interneuron) - prevents muscular damage from tetanus
|
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what does stimulation of the renshaw cell cause
|
inhibition of the agonisitc muscle group and disinhibition of the antagonist muscle group
|
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what are the three negative feedback systems that control muscle stretch, muscle forece, and firing rate of motor neurons
|
stretch: muscle spindle
force: golgi tendon organ firing: renshaw cell |
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which internuron has a larger number of convergence inputs, making it a very important integrating system for motor imput
|
Ib inhibitory interneurons (receives input from Ib afferents, joint afferents, cutaneous afferents, and descending pathways)
|
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when pinching skin on the ventral aspect of the leg, which muscle group contracts and which is inhibited
|
anterior group (underlying pinched skin) contracts while the posterior group is inhibited
|
|
when stepping on a nail with the right foot, interneurons innervating what muscles are excited
|
excitationn if right flexors and left exntensors; inhibition of right extensors and left flexors
|
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what happens to the scratch reflex when the stimulus generating the reflex is increased in intensity
|
both amplitude and duration of the scratch reflex is increased (but rhythm remains constant)
|
|
what occurs when the intensity of stimulation of the mesencephalic locomotor region is increased in a walking animal
|
speed of movement increases with increased stimulus (from slow walk to gallop)
|
|
where is goal-directed locomotion generated
|
in supraspinal systems
|
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what differentiates the comatose patient with a lesion to the upper brain stem from one with a lesion to the cortex in comparing their response to a noxious stimulus
|
upper brain stem: decebrate posture (arms extended)
cortex: decorticate posture (arms flexed) |
|
what types of movement are generated by the cortex and spinal corrd
|
cortex: voluntary movement
spinal cord: reflex response and rhythmic motor patterns |
|
what charachterizes rhythmic motor patterens and what are some examples
|
initiation and termination are voluntary, but the on-going sequence is stereotyped
e.g. walking, running, chewing |
|
What two systems are used to regulate slow and rapid movements
|
slow movements: negative feedback systems (does NOT use advance inforamtion)
Rapid movments: feedforward control system (use advance information) |
|
What are the two main types of intrafusal muscle fibers found in the muscle spindle and what are their subtypes
|
Dynamic: dynamic nuclear bag fibers
Static: static nuclear bag fibers and static nuclear chain fibers |
|
What type of afferent axons are associated with the static intrafusal muscle fibers
|
Type II (whereas type Ia axons are associated with both static and dynamic intrafusal fibers)
|
|
What are the efferent axons associated with the intrafusal muscle fibers
|
dynamic gamma motor axon
static gamma motor axon |
|
Where is the golgi tendon organ located and in what fashion
|
b/w the tendon and the muscle, connected in series to the muscle
(vs. the muscle spindle being connected in parallel) |
|
by what mechanism does the golgi tendon organ generate an AP
|
stretching of the muscle causes the encapsulated organ to lengthen, and in effect causes the Ib afferent axons to become compressed by the collagen fibers that comprise the golgi tendon organ
|
|
What aspect of the muscle contraction does the golgi tendon organ register
|
muscle force
(vs. the muscle spindle registering muscle length) |
|
What happens to the frequency of APs generated by the muscle spinsle and golgi tendon organ when a muscle contracts
|
muscle spindle: decreases (since muscle length decreases)
GTO: increases (since the force on the muscle increases) |
|
What happens to the frequency of APs generated by the muscle spinsle and golgi tendon organ when a muscle stretches
|
both increase, but that of the muscle spindle does so to a greater extent (b/c length increases more than force)
|
|
When a muscle undergoes stretch, what happens to the frequency of APs registered at the Type Ia and tpye II axons of the muscle spindle
|
Type Ia: increase drastically (since it reads both static and dynamic changes)
Type II: simple decrease in AP frequency |
|
When a muscle contracts (via stim of alpha motor neurons), what prevents the muscle spindle from becoming limp
|
simultaneous firing from gamma motor neurons causing the muscle spindle to contract, thus allowing it to continue registering muscle length
|
|
how does the firing frequency of type Ia axons differ when either the static or dynamic gamma fibers are stimulated
|
static gamma fibers: baseline firing frequency increases, everything else remains the same
dynamic gamma fibers: baseline does not change much, but firing frequency during dynamic phase is greatly enhanced |
|
how does stimulation of dynamic gamma motor neurons cause an increase in sensitivity of the dynamic nuclear bag fibers
|
the dynamic gamma motor neurons innervate the polar regoin of a fiber, causing teh ends of the fiber to become more viscous and thus less stretchy; the central regions, where Ia axons are located, wii therefore experience more stretch
|
|
What is the difference in firing frequency of the static and dynamic gamma motor neurons when comparing fast walking and imposed movments
|
Fast walking: high static/low dynamic
imposed movement: low static/high dynamic beam walking: high static/high dynamic |
|
When a type Ia axon from a muscle spindle enters the spinal cord, what does it synapse on?
|
an excitatory neuron of the homonymous muscle, an excititatory neuon of a synergistic muscle, and an inhibitory neuron of an antagonistic muscle
|
|
by what mechanism does the inverse myotatic reflex work
|
- muscle contraction increases the force generated by the muscle; this leads to increased firing frequency of type Ib afferents via the goligi tendon organ; type Ib afferents synpase on inhibitory interneuons in the spinal cord causing inhibition of muscle contraction; the type Ib afferents also synapses on excitatory interneuon innervating the antagonisitic muscle
|
|
Tracts in which part of the brainstem act on flexor-biased muscles
|
lateral parts
(vs. medial for extensor) |
|
which corticies add to the descendin corticobulbospinal tracts
|
primary motor cortex
primary sensory cortex premotor cortex (supplementary motor area) posterior parietal cortex |
|
what parts of the body does the corticobulbar tract innervate
|
head and face
|
|
which corticospinal tract innervates the axial musculature
|
ventral
(vs. lateral innervating the appendicular muscle) |
|
What is the key distinction b/w the sensory and motor homunculi
|
the motor homunculus has a larger representation of for the hand
|
|
where in the internal capsule do the motor tracts innervating the head and neck travel
|
corticobulbar tracts run through the genu of the internal capsule
|
|
where in the internal capsule do the corticospinal tracts travel
|
PLIC
|
|
which arteries supply most of the internal capsule and which supplies only the ventral part of the posterior limb
|
most if the IC: medial and lateral striate arteries
ventral PL: anterior choroidal |
|
Where do corticospinal fibers decussate
|
at the pyramidal decussation
|
|
After decussating, in what part of the spinal cord do the lateral corticospinal fibers travel?
|
lateral funiculus
|
|
How does the path of the ventral corticospinal fibers differ from those of the lateral corticospinal fibers?
|
ventral fibers do not decussate, travel in the anterior funiculus (vs. lateral), and terminate on the medial motor cell groups (vs. lateral)
|
|
What differentiates upper motor neurons from lower motor neurons
|
lower motor neurons connect directly to the muscle
upper motor neurons then, lie proximal to the LMN |
|
What is the major tract associated with upper motor neuron disease
|
corticospinal tract
|
|
What changes in reflexes are seen in upper motor neuron disease?
|
increased muscle stretch reflex
Babinski/Bing sign present Abdominal/cremasteric reflexes not present |
|
Which motor neuron disease is associated with spastic weakness and clonus
|
UMN disease
|
|
What word defines a series of involuntary muscular contractions due to sudden stretching of the muscle?
|
clonus
|
|
What is characteristic of a Hoffmann's sign?
|
flicking the terminal phalanx of the third or fourth finger causes flexion of the terminal phalanx of the thumb and/or index finger
|
|
What type of gait is seen frequently following stroke (and is also associated with upper motor neuron disease)?
|
hemiparetic gait (weakness on one side while walking)
|
|
Where does the corticorubral tract terminate?
|
red nucleus
vs. corticoreticular tract terminating in the reticular formatoin |
|
What type of lesion is associated with one-sided drooping of the lower face?
|
corticobulbar lesions (contralateral side)
|
|
Which motor tract travels close to the lateral corticospinal tract and is thus flexor-biased?
|
rubrospinal tract
|
|
What type of movement is associated with the rubrospinal tract?
|
voluntary, fine activity of distal extremities; coarser activity of proximal flexors
|
|
Damage to which spinal tract causes hand movements to become clumsy?
|
rubrospinal tract
|
|
After taking away all of the nuclei and tracts in the brain stem, what is left?
|
reticular formation
|
|
Which tract carries out reflexive control of posture?
|
reticulospinal tract
|
|
Which reticulospinal tract is flexor-biased and which is extensor-biased?
|
flexor-biased: medullary reticulospinal tract
extensor-biased: pontine reticulospinal tract |
|
Which spinal cord tracts maintain posture and reflexes by controlling the midline extensor muscles, and how does each accomplish this specifically?
|
lateral vestibulospinal tract: keeps center of gravity b/w feet
medial vestibulospinal tract: provides a stable platform for the eyes (cervical levels only) |
|
Where does the tectospinal tract originate and what is its function?
|
superior colliculus: helps coordinate eye and head movement
|
|
Which tract is located all around the spinal cord gray matter and what is its function?
|
propriospinal tract: coordinate activity of axial and distal musculature
|
|
Which motor nuclei are interconnected with long propriospinal neurons and which with short propriospinal neurons?
|
long: medial motor nuclei
short: lateral motor nuclei |
|
What types of muscle paralysis are associated with upper motor neuron disease and lower motor neuron disease, respectively?
|
UMN: spastic paralysis
LMN: flaccid paralysis |
|
What clinical signs are associated with lower motor neuron disease?
|
flaccid muscle weakness / paralysis
muscle wasting decreased or absent MSR muscle fasciculations/fibrillations sensory deficits (stocking/glove; following dermatomes or parts of dermatomes) |
|
What are poliomyelitis and amyotrophic lateral sclerosis (ALS) examples of?
|
LMN
|
|
What does damage to CN VII (nucleus of nerve) lead to?
|
Bell's Palsy
|
|
What causes Brown-Sequard syndrome and how does it present clinically?
|
lateral hemisection of the spinal cord: leads to ipsilateral loss of vibration and proprioception, and contralateral loss of pain and temperature (also ipsilateral spastic paralysis)
|
|
What types of muscle paralysis are associated with upper motor neuron disease and lower motor neuron disease, respectively?
|
UMN: spastic paralysis
LMN: flaccid paralysis |
|
What clinical signs are associated with lower motor neuron disease?
|
flaccid muscle weakness / paralysis
muscle wasting decreased or absent MSR muscle fasciculations/fibrillations sensory deficits (stocking/glove; following dermatomes or parts of dermatomes) |
|
What are poliomyelitis and amyotrophic lateral sclerosis (ALS) examples of?
|
LMN
|
|
What does damage to CN VII (nucleus of nerve) lead to?
|
Bell's Palsy
|
|
What causes Brown-Sequard syndrome and how does it present clinically?
|
lateral hemisection of the spinal cord: leads to ipsilateral loss of vibration and proprioception, and contralateral loss of pain and temperature (also ipsilateral spastic paralysis)
|
|
After the acute phase following transection of the spinal cord, which functions return to normal?
|
Flaccid paralysis, no spinal reflexes, drop in BP, no vascular or visceral reflexes
|
|
After the acute phase following transection of the spinal cord, which functions return to normal?
|
BP, vascular/visceral reflections, reactions of extensor muscles
|
|
What happens to MSRs below the level of the transected spinal cord section in the chronic state?
|
increased response (due to the lack of inhibtion from higher centers)
|
|
How does the latency differ between the muscle proprioceptors and vestibular/visual receptors?
|
proprioceptors: 70-100 msec
vestibular/visual: 140-200 msec stretch reflex latency: 50 msec |
|
Which muscles respond, and in what order, when the platform with a person standing on it moves backwards?
|
Gastrocnemius --> hamstrings --> paraspinals
distal to proximal (vs. anterior tibialis --> quadriceps --> abdominals when moving forward) |
|
By what mechanism are adjustments to posture made when comparing expected and unexpected disturbances?
|
expected: feed-forward system makes postural adjustments prior to disturbance
unexpected: feedback system corrects for postural adjustment after the disturbance |
|
What does the vestibulocollic reflex do?
|
keeps the head stable by counteracting head movements
|
|
Which reflex contracts limb muscles to counteract sway of the body?
|
vestibulospinal reflex
|
|
If vestibular reflexes are destroyed, which reflexes become predominant?
|
Neck reflexes (cervicocollic reflex/ cerviospinal reflex)
|
|
In the cervicospinal reflex, what does bending the neck forward elicit?
|
flexion of the upper extremities
|
|
Which nuclei facilitate motor neurons to axial muscles and extensor muscles?
|
Pontine reticular nuclei
|
|
Which nuclei facilitate flexor motor neurons, inhibit back and neck motor neurons, and inhibit limb extensor motor neurons?
|
medullary reticular nuclei
|
|
Which structure integrates vestibular and other sensory inputs with voluntary motor commands from the cortex?
|
reticular formation
|
|
What type of posture is associated with a lesion above the red nucleus?
|
decorticate posture (flexion)
|
|
In a lesion below the red nucleus, what is found clinically and how is this treated?
|
hyperextension of the extremities
treated by cutting the dorsal roots |
|
Which posture in comatose patients carries a better prognosis?
|
decorticate
|
|
What is the term that describes the use of different motor strategies to achieve the same end-result?
|
motor equivalence
(e.g. writing on paper and blackboard = different muscle groups, but same end-result) |
|
Which processes associated with voluntary movements occur in the posterior parietal cortex, premotor area, and primary motor cortex, respectively?
|
posterior parietal cortex: integrates sensory inpit
premotor area: planning primary motor cortex: performs movement |
|
Which neuron actually send the motor signal from the cortex to the alpha motor neuron in the spinal cord?
|
pyramidal neuron running through the corticospinal tract (= pyramidal tract)
|
|
In the case of an S1 disk herniation, which motor neuron can be affected?
|
LMN (alpha motor neuron)
|
|
What is the purpose of transcranial magnetic induction?
|
test the CST for functionality (causes discharge of pyramidal neurons)
|
|
How does the result of a fMRI differ when comparing a sequential and non-sequential finger sequence?
|
Sequential: visible in motor cortex
Non-sequential: also involves supplemental motor cortex |
|
How does the concept of divergence relate to the pyramidal neuron?
|
one pyramidal neuron can innervate several muscles (regarding a single joint)
convergence states that many pyramidal neurons are needed to forcefully contact a muscle |
|
What concept, regarding cortical representation of muscles, allows for the creation of a wide variety of muscle synergies?
|
the overlap and intermingling of cortical motor cells innervating synergisitc muscles (i.e. those in the hand)
|
|
Which muscle groups, in general, respond to corticospinal neuron firing?
|
flexors
|
|
What aspect of muscle contraction is the red nucleus associated with?
|
dynamic force (speed of movement)
|
|
Which population of motor neurons encode the direction of movement?
|
M-I neurons (each neuron fires when movement is in their preferred direction)
|
|
Which muscles and what types of movement are associated with the primary motor cortex?
|
distal muscles and fine digital movement
|
|
Which area of the cortex controls conditioned and skilled movements?
|
primary motor cortex
|
|
What is the function of the premotor area?
|
receive sensory input from the posterior parietal cortex; then preparse M-1 for the impending motor act (=planning)
|
|
What does the length of the readiness potential preceding a motor act depend on?
|
complexity of the motor act
|
|
When a person is asked to do a mental rehearsal of a finger movement sequence, which cortical area is stimulated?
|
Supplemental motor area (SMA) - vs. both SMA and M-I when actual sequence is performed
|
|
What does a unilateral lesion of the SMA lead to?
|
deficit in coordinating the use of both hands
|
|
Which Brodmann's areas provide sensory input to the posterior parietal cortex?
|
Area 5 (proprioception)
area 7 (visual and auditory) |
|
How does sensory information in the cortex reach M-I?
|
from area 5 to area 7 (integration); then on to the premotor cortex (planning); and into M1 (execution)
|
|
What is the purpose of area 7's projection to the lateral cerebellum?
|
provides it with sensory information used to correct actions during target orientation movements
|
|
In general terms, how do the basal ganglia exert their effect on motor output?
|
indirectly, by modifying the activity of corticobulbospinal tract
|
|
What are the two major functions associated with the basal ganglia?
|
initation of voluntary movement
inhibition of involuntary movement |
|
Which components of the basal ganglia are part of the lenticular nucleus, (neo)striatum, and corpus striatum, respectively?
|
lentiform: putamen + GP
striatum: caudate + putamen Corpus striatum: caudate + putamen + GP |
|
What are the receptive elements of the basal ganglia and from where do they receive input?
|
putamen and caudate: receive input from all areas of the cerebral cortex
|
|
How does the cortical input differ between the putamen, head of the caudate, and body/tail of the caudate?
|
Putamen: motor functions
head of caudate: frontal lobes limbic areas body/tail of the caudate: parietal/occipital/ temporal lobes |
|
Which part of the basal ganglia is responsible for the emotional disturbances associated with basal ganglia disorders?
|
head of the caudate (since ot receives input from the frontal lobe and limbic areas)
|
|
How do the direct and indirect pathways of the basal ganglia differ?
|
direct: putamen --> GPm
indirect: putamen --> GPl --> STn --> GPm |
|
Which substance has a profound modulatory influence on the putamen and caudate, and where is this substance produced?
|
DA - produced in the pars compacta of the substantia nigra
|
|
How do the caudate and putamen downregulate the activity of the substantia nigra?
|
intranuclear connections exist b/w the caudate and putamen with the pars reticulata of the substantia nigra that exert an inhibitory effect through GABA and substance P
|
|
After input into the basal ganglia converge on the medial globus pallidus, where do the major projections travel to?
|
VA/VL and CM of thalamus
|
|
Through which structures do outputs from the medial globus pallidus exert an effect on eye movements and posture?
|
superior colliculus and reticular formation
|
|
By what mechanism does the DIRECT pathway of the basal ganglia generate excitatory effects on the cortical motor areas?
|
through disinhibition (i.e. inhibiting the inhibitory effects on the VA/VL)
|
|
By what mechanism does the INDIRECT pathway of the basal ganglia generate excitatory effects on the cortical motor areas?
|
through inhibition (i.e. by inhibiting the excitatory effects of the STn on the inhibition of the VA/VL)
|
|
Besides modulation of movement, what other areas do the basal ganglia affect?
|
cognition
reward mood regulation |
|
When a disorder is present affecting the prefrontal channel or limbic channel of the basal ganglia, respectively, what function is impaired?
|
prefrontal channel: cognition
limbic channel:emotion/affect |
|
What are the basal ganglia input nuclei and cortical output nuclei associated with the limbic channel?
|
input: nucleus accumbens, ventral caudate, ventral putamen
output: anterior cingulate, oribital frontal cortex |
|
What two structures make up the thalamic fasciculus and how are the pathways of these two structures different?
|
Ansa lenticularis: from GPm it hooks around the IC to the VA/VL
Lenticular fasciculus: from GPm through IC to VA/VL |
|
Which involuntary movements are associated with basal ganglia disease?
|
tremors
athetosis (writhing motions) chorea (abrupt movements) hemiballismus (violent flailing of limbs) dystonia (persistant distorted position) |
|
What causes hemiballismus?
|
subthalamic lesion
|
|
What is the difference between akinesia and bradykinesia?
|
akinesia: difficulty initiating movements
bradykinesia: slowness in executing movements |
|
By what mechanism does a lack of dopamine cause decreased excitation of the premotor cortex in Parkinson's?
|
a lack of DA causes diminished inhibition of the GPm by the caudate/putamen. leading to an increase in the inhibition caused by the GPm on the VA/VL and thus decreased excitation of the premotor area
|
|
What disease are a blank expression and reduced eye-blink frequency associated with?
|
parkinson's
|
|
Does damage to the basal ganglia cause ipsilateral or contralateral motor effects?
|
contralateral (since descending motor tracts decussate)
|
|
What is the cause of Huntington's disease and which structures are affected?
|
gene mutation in huntington gene (autosomal dominant)
involves degeneration of the caudate/putamen and layer III of te cerebral cortex |
|
What personality changes accompany Huntington's?
|
depression
apathy hostility slowed thought processes and forgetfulness |
|
How does Huntington's disease cause increased excitation of the premotor cortex?
|
insult to the caudate/putamen leads to an increased inhibition of the GPm; this is turn means less tonic inhibition of the VA/VL and thus increase excitation of the premotor cortex
|
|
What is the key difference between the mechanisms affecting the basal ganglia in Parkinson's and Huntington's?
|
parkinson's: diminished inhibition of the GPm
Huntingtons: increased inhibition of the GPm remember GPm causes inhibtion of VA/VL |
|
What is the main function of the cerebellum and how does it execute this function?
|
comparator:
compares intention (cortical connections) with performance (proprioceptive info), and compensates for errors |
|
What differentiates internal feedback from external feedback?
of the cerebellum |
internal (what should be happening): from the cortex
external (what is happening): from proprioceptors |
|
After receiving the internal and external feedback, what is the cerebellar response?
|
indirectly adjusts motor activity through connections with the motor and premotor cortices and brainstem to motor nuclei
|
|
What are the nuclei of the cerebellum?
|
Dentate nucleus; Interposed nuclei (= emboliform & globose); Fastigial nucleus
|
|
What is carried in each of the cerebellar peduncles?
|
Inferior: input from the spinocerebellar tracts
middle: input from the cerebral cortex superior: output to red nucleus, thalamus, cerebral cortex |
|
Which three arteries supply the cerebellum?
|
SCA
AICA PICA |
|
How is output generated in the cerebellum?
|
purkinje cells in the cerebellar cortex cause inibition of the deep cerebellar nuclei; these nuclei than project out of the cerebellum
|
|
How do mossy fibers and climbing fibers affect the cerebellar output?
|
they synapse both on the deep cerebellar nuclei directly and indirectly by synapsing in the cerebellar cortex (both fiber types are excitatory)
|
|
Where do mossy fibers arise from and how do the exert their effect on Purkinje cells?
|
spinocerebellar tracts, vestibular nuclei, reticular formation, pontine nuclei
- influence perkinje cells indirectly through synapses with excitatory granule cells |
|
Where do climbing fibers arise from and how do the exert their effect on Purkinje cells?
|
inferior olivary nucleus (contains inputs from all parts of snensory and motor systems:
"climb" around purkinje somata and dendrites |
|
What are the cerebellar functions associated with the lateral hemisphere, intermediate hemisphere, and vermis/flocculonodular lobe, respectively?
|
lateral: motor planning for the extremities
intermediate: distal limb coordination vermis/flocculonodular: proximal lumb/trunk coordination and balance/ vestibulo-ocular reflexes |
|
Which regions of the cerebellum influence the lateral corticospinal tracts?
|
lateral and intermediate hemispheres
|
|
By which tracts does the vermis/flocculonodular lobe influence proximal limb and trunk coordination?
|
anterior corticospinal tract, reticulospinal tract, vestibulospinal tract, tectospinal tract
|
|
Which regions of the cerebellum influence the medial longitudinal fasciculus and what functions are controlled this way?
|
vermis/flocculonodular: controls balance/ vestibulo-ocular reflexes
|
|
What are the three functional divisions of the cerebellum and which anatomical structures make up each of them?
|
cerebrocerebellum: lateral hemisphere/dentate nucleus
spinocerebellum: intermediate hemisphere/vermis/ part of the fastigial nucleus/ interposed nuclei vestibulocerebellum: flocculonodular lobe/ part of the fastigal nucleus |
|
Where do the inputs and outputs to the vestibulocerebellum come from, respectively?
|
inputs: semicircular canals, vestibular nuclei, lateral geniculate nucleus, superior colliculus, visual cortex
outputs: medial and lateral vestibular nuclei |
|
Problems with what functions are associated with damage to the vestibulocerebellum?
|
stance and gait
|
|
Which tracts are associated with the spinocerebellum and how are they divided functionally?
|
cuneocerebellar tract and rostral SCPT: upper limbs
Dorsal SCT and Ventral SCT: lower limb |
|
Which nucleus in the spinal cord gives rise to the dorsal spinocerebellar tract?
|
nucleus dorsalis (Clarke's nucleus) - monitors info from the muscle spindles, GTOs, and joint receptors
|
|
Which spinocerebellar tracts monitor descending information and transmit this back to the cerebellum?
|
ventral SCT (lower limb) and rostral SCT (upper limb): both originate from spinal border cells
|
|
Which is the only tract of the spinocerebellum associated solely with the superior cerebellar peduncle?
|
Ventral SCT: all others run through the ICP (although the rostal SCT also projections through the SCP)
|
|
Which spinocerebellar tract receives information from the muscle spindles, GTOs, and joint receptors of the upper limb and neck?
|
cuneocerebellar tract (from accessory cuneate nucleus - lies lateral to the cuneate nucleus)
|
|
What do cerebellar fibers comingle with when entering the VA/VL?
|
fibers from the thalamic fasciculus
|
|
What functions are associated with the spinocerebellum?
|
controls execution of ongoing movement: regulates muscle tone
|
|
Where do spinocerebellar outputs associated with the vermis and intermediate hemispheres travel to, respectively?
|
vermis: medial cell columns
intermediate hemispheres: lateral cell columns |
|
Where are the cell bodies of the cerebrocerebellum located and where do they synapse?
|
cell bodies in the PMA, SMA, M1, PP: synapse on the deep pontine nuclei
|
|
On which side do symptoms of cerebellar damage manifest themselves and why?
|
ipsilateral: since output from the cerebellum decussates twice before reaching musculature (one up to the cortex, and once coming down it)
|
|
From what structure does output created in the cerebrocerebellum originate and where does it project to?
|
dentate nucleus: projects to the red nucleus and VA/VL
|
|
What clinical sign is associated with damage to the vermis?
|
loss of balance towards the side of the lesion
|
|
What function is associated with the cerebrocerebellum?
|
timing of movements
|
|
What problems are associated with a lesion to the lateral hemisphere or dentate nucleus of the cerebellum?
|
timing of initiation of movements, terminal tremor, temporal coordination of multiple joints, spatial coordination of hand and finger muscles
|
|
How does modification of cerebellar activity occur?
|
through practice and learning
|
|
How does passive limb movement differ between cerebellar damage and damage to the basal ganglia?
|
cerebellum: reduced resistance (hypotonia/pendular reflexes)
basal ganglia: increased resistance |
|
How is ataxia defined?
|
difficultly in executing voluntary movements
|
|
What are the clinical terms used describing errors in range/force of movement, inability to sustain rhythmic alternating movements, and tremor at the end of movement, respectively?
|
dysmetria
dysdiadochokinesiea terminal tremor |
|
What type of gait is associated with midline damage to the cerebellum and why?
|
"drunken sailor's gait"
due to lack of axial musculature control |
|
What problem associated with the eyes is common in cerebellar damage?
|
nystagmus
|
|
What does titubation refer to?
|
a trunk tremor while sitting or walking (due to cerebellar damage)
|