Exam 2 First Half Flashcards

(51 cards)

1
Q

Name the cortical areas involved in motor activity and describe their general role in the production/control of movement.

A
  1. ) Frontal lobe
    a. ) Primary motor cortex (M1) – 4
    - Execution

b. ) Premotor cortical areas (pka secondary motor cortex) – planning area
i. SMA (supplementary motor area) and PMC (premotor cortex) – 6
- Program: design and sequence of complex movements involving groups of muscles (including orienting them correctly)
- Transmit: send above program to M1 for execution

ii. FEF (frontal eye field) – 8
- Coordinate eye movements by projecting to brain stem centers

  1. ) Parietal lobe
    a. ) Posterior parietal cortex – 4
    - Visual guidance of movement via sensory integration

b. ) Primary somatosensory cortex (S1) – 3, 1, 2
- Does not produce movement.
- Influences movement by modulating sensory input from visceral/somatic structures reaching spinal cord through descending “filters”

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2
Q

Describe layer V of the cerebral cortex.

A
  • Cortex of brain is composed of 6 layers. 5th layer is prominent in motor cortex and contains pyramidal cell bodies, which are the output (UMNs) of the motor cortex forming descending motor tracts (of which there are 5 tracts).
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3
Q

Describe and draw the origin of, course, decussation, location in spinal cord and pattern of termination of the corticospinal tract. Distinguish between anterior and lateral corticospinal tracts.

A
  1. ) Origin: 5th layer of cerebral cortex
  2. ) Course: corona radiata – internal capsule (posterior limb) – midbrain (basis pedunculi) – pons (basal) – medulla (pyramid)
  3. ) Decussation: vast majority decussate at caudal medulla, others continue descent
  4. ) Lateral corticospinal tract: crossed fibers in the lateral funiculus at all spinal cord levels. Most fibers terminate in cervical cord, remainder in T and LS cord where they synapse with LMNs (mostly via interneurons, some directly) in the ventral horn of the grey matter to UL and LL muscles.
  5. ) Anterior corticospinal tract: uncrossed fibers in the anterior funiculus in only the cervical and upper thoracic cord levels. Fibers decussate (via AWC) at their level of termination with LMNs (mostly via interneurons, some directly) in the ventral horn of the grey matter to axial muscles (neck, shoulder, trunk)
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4
Q

Describe the function(s)/role of the corticospinal tract.

A
  • Lateral corticospinal tract (LCST): UL and LL function, especially distal muscles of the UL (skilled, well-defined manipulation of fingers)
  • Anterior corticospinal tract (ACST): movement of the axial muscles (neck, shoulder and trunk)
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5
Q

Describe and UMN and LMN

A
  • UMN refers to the pyramidal neuron in 5th cortical layer of the brain that carries output from the motor cortex via descending motor tracts and synapses with LMN residing in ventral horn of spinal cord which run in peripheral nerves to terminate in skeletal muscle.
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6
Q

List and describe the deficits resulting following an UMN lesion involving corticospinal tract anywhere from motor cortex to decussation in brainstem or spinal cord. Which side of the body is affected?

A
  • Side of body affected = contralateral to lesion
  1. ) Spastic paralysis (to passive motion) with the following initial/temporary series of changes
    - Initially paresis (weakness) or flaccid paralysis / hypotonia and hyporeflexia
    - Regain of proximal limb musculature
    - Hypertonia: inhibitory signals are eliminated or diminished resulting in gamma motor neurons becoming overactive
    - Spasticity: exaggeration of stretch reflex d/t passive motion
  2. ) Hyperreflexia: d/t excess stimulation of gamma motor neurons
  3. ) Muscle atrophy (mild)
  4. ) Babinski sign: dorsiflexion of big toe, fanning of remaining four
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7
Q

List and describe deficits resulting following a lesion involving the corticospinal tracts at the spinal level or LMNs in peripheral nerves. Which side of the of the body is affected?

A
  • Side of body affected = ipsilateral to lesion
  1. ) Decrease in muscle strength
  2. ) Hypotonia: alpha and gamma motor neurons affected
  3. ) Hyporeflexia / areflexia: lesion affects sensory and/or motor neurons (alpha and gamma)
  4. ) Muscle atrophy (severe)
  5. ) Fibrillations (1 muscle fiber) using electrical recordings
  6. ) Fasciculations (groups of muscle fibers) seen grossly
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8
Q

List the arterial blood supply to the corticospinal tracts. Describe where motor deficits would occur following occlusion to these vessels.

A
  1. ) Primary motor cortex (M1)
    - Medial surface by ant cerebral artery = contralateral leg/foot deficit
    - Lateral surface by middle cerebral artery = contralateral trunk, UL and face deficit
  2. ) Internal capsule
    - Lenticulostriate arteries of middle cerebral artery (to anterior and posterior limbs) = contralateral deficit
  3. ) Midbrain
    - Post cerebral artery = contralateral deficit
  4. ) Pons
    - Pontine arteries of basal artery = contralateral deficit
  5. ) Caudal medulla
    - Ant spinal artery = bilateral deficits (supplies both LCST and ACST)
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9
Q

Name the origin and termination of the following tracts: corticotectal, corticorubral and corticoreticular tracts.

A
  1. ) Corticotectal: visual association cortex (18/19) of occipital lobe to oculomotor accessory nuclei (to EOM via MLF: medial longitudinal lemniscus) and superior colliculus (to C and T-spine via tectospinal tract)
  2. ) Corticorubral: sensorimotor cortex to the red nucleus of midbrain (to upper spinal cord via rubrospinal tract)
  3. ) Corticoreticular: sensorimotor cortex descend with corticonuclear and corticospinal fibers to reticular formation (pons and medulla). Here pontine nuclei give rise to medial (pontine) reticulospinal tract to all spinal cord levels. Medullary nucleus gives rise to lateral (medullary) reticulospinal tract to all spinal cord levels.
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10
Q

Describe the input, origin, course, termination and function(s)/role of the tectospinal, rubrospinal, reticulospinal and vestibulospinal tracts.

A
  1. ) Tectospinal
    - Input = corticotectal tract
    - Origin: superior colliculus
    - Course: crosses in spinal cord
    - Termination: C&T spinal cord levels
    - Function: reflex movements of eyes, neck/head, upper thorax in response to auditory, vestibular or cutaneous stimuli
  2. ) Rubrospinal
    - Origin: red nucleus of midbrain
    - Course: crosses midbrain and descends to
    - Termination: upper spinal cord
    - Function: excitatory to the distal flexor muscles of the UL (hand/digits) and inhibitory to the distal extensor muscles of the UL (hand/digits). This is insignificant given we have corticospinal tract.
  3. ) Reticulospinal* both play role in modulation of muscle tone and posture maintenance
    a. ) Medial (pontine) reticulospinal tract
    - Origin: pontine nuclei
    - Course: ipsilateral in anterior funiculus
    - Termination: all spinal cord levels
    - Function: standing – excitatory influence on motor neurons that innervate paravertebral and limb extensors, inhibition to the flexors

b. ) Lateral (medullary) reticulospinal tract
- Origin: medullary nucleus
- Course: ipsilateral in anterior funiculus
- Termination: all spinal cord levels
- Function: lying down – inhibitory influence on motor neurons that innervate the paravertebral and limb extensors, excitation to the flexors

  1. ) Vestibulospinal
    a. ) Medial vestibulospinal tract
    - Origin: medial vestibular nuclei
    - Course: medial longitudinal fasciculus
    - Termination: bilaterally at C and upper T spinal cord levels onto alpha and gamma motor neurons that innervate neck muscles
    - Function: maintain balance in response to vestibular input, control neck musculature to control head movement to keep image on the retina

b. ) Lateral vestibular nuclei
- Origin: lateral vestibular nucleus
- Course: lateral vestibular spinal tract
- Termination: all spinal cord levels onto interneurons (mostly) and alpha motor neurons
- Function: maintenance of posture and balance – how? Excitatory to antigravity muscles, inhibit LMNs that innervation limb flexor muscles. Same function as medial reticulospinal tract.

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11
Q

Which tracts neutralize the effects of gravity?

A
  • Medial (pontine) reticulospinal tract
  • Vestibulospinal tract
  • These receive messages from cerebellum
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12
Q

Functional classification of tracts. Include what tract consists of

A
  1. ) Ventromedial (anteromedial) group
    - Consists of: anterior corticospinal tract, medial/lateral vestibulospinal tracts, medial/lateral reticulospinal tracts, tectospinal tract
    - Function: gross movement of trunk and proximal limb musculature to maintain balance
  2. ) Lateral group
    - Consists of: lateral corticospinal tract, rubrospinal tract
    - Function: influence mostly the distal muscles of the limbs (muscles that control digits)
  3. ) Cortical group
    - Consists of: only lateral corticospinal tract
    - Function: distinct, fractionated movements of digits
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13
Q

Function of tectospinal tract – think about deficit with lesion

A
  • Reflex turning of head and upper trunk in direction of startling stimulus
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14
Q

Function of rubrospinal tract – think about deficit with lesion

A
  • Stimulates motor neurons that innervate distal flexor muscles of the UL; supplements lateral corticospinal tract
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15
Q

Function of reticulospinal tracts – think about deficit with lesion

A
  • Influence antigravity muscles; role in muscle tone and posture maintenance
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16
Q

Function of vestibulospinal tracts – think about deficit with lesion

A
  • Balance

- Lateral vestibulospinal tract is involved in muscle tone

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17
Q

Describe Brown-Sequard syndrome.

A
  • Hemisection of spinal cord
    1. ) Loss of discriminative sense ipsilateral at or below level of lesion d/t FG and FC involvement carrying DC-ML fibers
    2. ) Loss of pain/temp sense contralateral ~ 2 segments below level of lesion d/t ALS fiber involvement.
    3. ) Loss of reflex activity ipsilaterally
    4. ) UMN signs below level ipsilaterally
    5. ) LMN signs at level of lesion ipsilaterally
  • note all ipsilateral except pain/temp
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18
Q

What in the spinal cord is affected with a poliomyelitis infection

A
  • LMNs. LMN signs
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19
Q

Describe combined systems disease (aka subacute combined degeneration).

A
  • Deficiency in vit B12 intake or metabolism
  • Degeneration of dorsal and lateral funiculus (heavily myelinated tracts)
  • Dorsal funiculus (FG/FC) = loss of discriminative touch, two-point discrimination, vibratory sense, proprioception ipsilaterally
  • Lateral funiculus (lateral corticospinal) = UMN signs ipsilateral
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20
Q

Describe neurological deficits seen with occlusion of the anterior spinal artery.

A
  • Anterior spinal artery supplies anterior 2/3rd of spinal cord, ie. the anterior and lateral funiculi and most of the grey matter resulting in following;
    1. ) ALS damage = loss of pain/temp sensation several levels below level of lesion
    2. ) Anterior horn damage = LMN weakness
    3. ) Lateral corticospinal tract damage = UMN signs
    4. ) Loss of sphincter function = incontinence
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21
Q

Describe neurological deficits seen with occlusion of the posterior spinal arteries.

A
  • These arteries supply the posterior 1/3rd of the spinal cord, ie. the dorsal funiculi and posterior part of dorsal horns resulting in following:
    1. ) Posterior white column damage = loss of proprioception, vibratory sense and fine touch discrimination
22
Q

Which part of the spinal cord is most susceptible to interruption of blood flow? Why?

A
  • C-spine. Only supplied by anterior and posterior spinal arteries
  • T-L and S spine receives additional blood supplies in radicular arteries from spinal segmental arteries, which anastomose with anterior/posterior spinal arteries.
23
Q

Describe the origin of the corticonuclear (corticobulbar) tract.

A
  • Sensory and motor cortex. Specifically: Premotor cortical areas (SMA, FEF) + primary somatosensory cortex (S1) and primary motor cortex (M1, especially lateral part where face, tongue etc are represented). Think of this tract as the counterpart to the corticospinal tract, except going to nuclei involved in head.
24
Q

Describe the course and pattern of termination (ie. contra/ipsi) of the corticonuclear fibers in the motor nuclei of CNs V, VII, IX, X, XI and XII.

A
  • From sensory and motor cortex, fibers travel through corona radiate through genu of internal capsule, shifting to posterior limb of internal capsule.
  • V: bilateral
  • VII: bilateral in upper half and contralateral in lower half
  • IX – XI (in nucleus ambiguus): bilateral (primarily contralateral) * seems to be some misinformation in slides. Some places say bilateral, others say contralateral. XI says ipsilateral.
  • XII: bilateral except to neurons innervating genioglossus muscle, which only receives contralateral
25
Describe the cortical projections that influence the motor nuclei of CNs III, IV and VI.
- III, IV and VI don’t receive corticonuclear fibers, instead receive messages from a different group of axons originating from frontal and parietal motor eye fields that make stop in reticular formation and produce conjugate eye movements contralateral to side of origin.
26
Describe the deficits following an UMN lesion involving the fibers of the corticonuclear tract that terminate in the facial nucleus.
- Since the corticonuclear fibers terminate bilaterally in the superior half of the facial nucleus and contralateral in the inferior half, UMN lesions to the fibers terminating here spare the upper half of the face. Why? Bilateral projections means that there are backup projections from the other side. Lower half of face shows weakness/paralysis contralateral to lesion.
27
What is the blood supply to the facial nucleus?
- Facial nucleus is in the caudal pons, supplied by the AICA and basilar artery.
28
What occurs to the uvula if there is a lesion to the fibers innervating the nucleus ambiguus?
- Uvula is pulled to the side of the lesion. Lesion produces contralateral deficit. Note: corticonuclear projections to this nucleus are bilateral, but primary contralateral.
29
Deficits to the left trapezius and SCM would indicate a lesion to what side of the corticonuclear motor projections?
- Left side
30
Describe deficits following an UMN lesion involving fibers of the corticonuclear tract that terminate in the hypoglossal nucleus.
- Corticonuclear projections to this nucleus that innervate all muscles of tongue (except those innervating genioglossus) are bilateral. If lesion damages UMN, there are no deficits in most tongue muscles, except for genioglossus, which deviates to side contralateral to the lesion (weak side).
31
Describe the blood supply of the corticonuclear tract along its path.
- Internal capsule: lenticuostriate arteries (branches of middle cerebral)
32
List the nuclei that are the components of the basal ganglia
1. ) Corpus striatum a. ) Caudate nucleus b. ) Lentiform nucleus: putamen and globus pallidus (pallidum) 2. ) Subthalamic nucleus 3. ) Substantia nigra
33
Is corpus striatum the same as striatum?
- No. - Striatum = putamen + caudate nucleus - Corpus striatum = putamen + globus pallidus + caudate nucleus
34
Functions of basal ganglia
1. ) inhibit involuntary movements (tremors, chorea, tics) at rest 2. ) facilitate voluntary movements (getting started, keeping going, stopping an action)
35
Describe major input and output pathways of the striatum (putamen + caudate nucleus)
1. ) Input a. Cortex (via corticostriate fibers) b. Thalamus (via thalamostriate fibers) c. Substantia nigra (via nigrostriate fibers) 2. ) Output a. Globus pallidus (via striatopallidal fibers) b. Substantia nigra (via striatonigral fibers)
36
Describe major input and output pathways of the pallidum
1. ) Input a. Striatum (via striatopallidal fibers) b. Subthalamus (via subthalamic fasciculus) 2. ) Output a. Thalamus (via pallidothalamic fibers = lenticular fasciculus + ansa lenticularis + thalamic fasciculus joining ventral anterior and ventral lateral and carrying cerebellar fibers) b. Subthalamus (via pallidosubthalamic fibers aka subthalamic fasciculus) c. Substantia nigra (via pallidonigral)
37
What are the major inputs to the basal ganglia? Major outputs?
- Major input = cortex to striatum (corticostriate, thalamostriate, nigrostriatal) - Major output = pallidum to thalamus then cortex (pallidothalamic fibers, pallidosubthalamic, pallidonigral, thalamocortical fibers)
38
Describe the basic pathway interconnecting cortex and basal ganglia as reflected in the four circuits traversing them comparing components of the “open” and “closed” loops.
- Closed loop pathway = cortex – striatum – pallidum – thalamus – cortex - Open loop pathway feeds information into the closed loop. - Distinct circuits that utilize the above structure to convey distinct information to the basal ganglia 1. ) Motor (supplementary motor cortex – striatum – pallidum – VL nucleus of thalamus): provides sequence information. - Open circuit from: somatosensory cortex, primary motor cortex and premotor cortex. 2. ) Association (prefrontal cortex – striatum – pallidum – VA/dorsomedial nucleus of thalamus): planning and direction of movement. - Open circuit from: premotor cortex and posterior parietal cortex. 3. ) Oculomotor (frontal eye field – striatum – pallidum – VA/dorsomedial nucleus of thalamus & superior colliculus): integration of eye movements and visual guidance - Open circuit from: prefrontal cortex, posterior parietal cortex 4. ) Limbic (anterior cingulate gyrus, orbitofrontal cortex – striatum – pallidum – VA/dorstomedial nucleus of thalamus): emotional and motivational influences on movements. - Open circuit from: medial/lateral temporal lobes, hippocampus, amygdala, entorhinal area
39
Compare and contrast the direct and indirect pathways through the basal ganglia
- Direct = excitatory pathway that facilitates flow of information from thalamus resulting in greater excitation of cortex = voluntary movements, hyperkinesia - Indirect = inhibitory pathway that decreases activity in the thalamus lessening excitatory output to the cortex = inhibition of involuntary movements = hypokinesia
40
True/False. Basal ganglia lesions lead to paralysis.
- False. Lesions here lead to extrapyramidal syndromes such as dyskinesia, athetosis, bradykinesia, chorea.
41
Neuroanatomical features of Parkinson’s dz
- Death of dopaminergic cells in pars compacta of substantia nigra. Characterized by rigidity, slowness of movement, slumped posture d/t excessive inhibition with lack of facilitation. Also resting tremor d/t lack of suppression of involuntary movement
42
Define: dyskinesia, athetosis, hemiballismus, bradykinesia, chorea.
- Dyskinesia: unintential, disorderly, purposeless movement. Occur at rest. - Athetosis: slow, vermicular involuntary movements usually of hands and feet. Results from degeneration of the lateral segment of the globus pallidus, so ventrolateral nucleus of thalamus sends spontaneous signals to the motor cortex. - Hemiballismus: involuntary ballistic (violent striking) movements on only one side of the body affecting only proximal muscles of a limb. Results from a cerebral vascular lesion of the ganglial branch of the posterior cerebral artery involving the contralateral subthalamic nucleus. - Bradykinesia: slowness of execution of movement. - Chorea: sequence of rapid, jerky, some-what agile and flowing movements involving mainly the hands and feet, the tongue and facial muscles.
43
What two signs must be present to define Tourette’s syndrome and what one sign, in particular, makes it unique among all extrapyramidal syndromes?
- Tics (motor and phonetic). Phonetic tics make it unique to other extrapyramidal syndromes.
44
Describe the major functions of the cerebellar cortical areas/lobes.
- Coordinates motor functions in terms of velocity, force, duration, timing, trajectory. - Involved in procedural memory
45
Match deep cerebellar nuclei with associated areas of vestibulocerebellum, spinocerebellum and cerebrocerebellum.
- From midline to lateral are: 1. ) fastigial nucleus 2. ) globose nucleus* 3. ) emoboliform nucleus* 4. ) dentate nucleus * together are referred to as interposed nucleus a. ) vestibulocerebellum: vestibular nuclei (in brainstem) b. ) spinocerebellum: fastigial nucleus and interposed nuclei (globose and emboliform) c. ) cerebrocerebellum: dentate nucleus
46
Discuss the functional role of Purkinje cells and their relationship with deep cerebellar nuclei and the inferior olivary nucleus. Discuss the influence of mossy fibers on the deep cerebellar nuclei.
- Purkinje cells have axons that project into deep cerebellar nuclei and are inhibitory - Fibers from inferior olivary nucleus synapse onto deep cerebellar nuclei are and excitatory. They also synapse onto Purkinje cells and are excitatory. - Mossy fibers (the overwhelming majority of input/tracts to the cerebellum) synapse on the deep cerebellar nuclei and are excitatory. - Therefore depending on the balance, deep cerebellar nuclei has variable output
47
Discuss major input/output pathways to the vestibulocerebellum, spinocerebellum and cerebrocerebellum tracts. Describe location and function of each tract.
1. ) Vestibulocerebellum - Location: flocculonodular lobe - Function: balance, equilibrium, coordination of eye and head movements - Input = vestibular system (vestibulocerebellar) - Output = vestibulospinal tracts, vestibular nuclei, MLF (interconnects CNs III, IV, and VI) 2. ) Spinocerebellum - Location: vermal and paravermal areas - Function: adjust movements based upon proprioceptive feedback, posture and muscle tone - Input = dorsal and ventral spinocerebellar tracts, cuneocerebellar (neck), trigeminocerebellar tracts (face) - Output = vestibulospinal and reticulospinal tracts 3. ) Cerebrocerebellum - Location: lateral hemispheres - Function: preparation (predicting force, velocity and trajectory), precise coordination of motor commands with proprioceptive and vestibular input - Input = corticopontocerebellar tract (receives copy of motor orders), olivocerebellar tract (procedural learning) - Output = dentorubrothalamic tract (feedback to motor cortex), rubrospinal tracts
48
Function of the inferior olivary nucleus and cortico-olivocerebellar pathway?
- Procedural learning? Reinforcing motor skills and the idea that practice makes perfect
49
Why do we care about the homunculus of the cerebellum? Anyone?
Why do we care about the homunculus of the cerebellum? Anyone?
50
Compare and contrast the cerebellum and basal ganglia in terms of alikeness and differences?
1. ) Similar - Both influence motor cortex via thalamus (ventral lateral nucleus) - Modify or adjust motor commands - Lesion to either area does not result in paralysis – no direct link with muscles. 2. ) Different - Basal ganglia has permissive (permission to grant) function in inhibiting involuntary movements and facilitating voluntary movements - Cerebellum has execution function to plan movements ordered by motor cortex, provide corrective feedback to motor cortex and to fine tune ongoing movements.
51
Define the terms: ataxia, dysmetria, dysdiadochokinesia, nystagmus.
- Ataxia: lack of coordination of movements. Seen in lesion of hemispheric zone of cerebellum. - Dysmetria: disorder in which the individual is unable to estminate the distance b/w the moving body part and a target. - Dysdiadochokinesia: inability to carry out rapid alternating movements regularly (eg. rapid pronation/supination of forearm) - Nystagmus: rhythmic spontaneous oscillation of one of both eyes. Seen in lesion of vermal or paravermal areas of cerebellum.