Lecture 11: Motor Systems Flashcards

(46 cards)

1
Q

If a pt moves his hand down and back indicating he cannot perform the motor sequence although he knows the position of the limb, this is called ____________. If he raises his left hand and assures you that its his right, this right-eft disorientation is called ____________

A

Apraxia; agnosia

**With agnosia they can do the movement but doesnt know the difference, however they will pick up a pencil with their dominant hand -> this is an automatic-voluntary dissociation

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2
Q

The ___________ lobe incorporates motivation and memory. A pt who has a disturbance of the ___________ lobe is often apathetic and difficult or impossible to test for any cognitive activity

A

Prefontal lobe; frontal lobe

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3
Q
**A pt has the inability to demonstrate how to produce a voluntary cough. This iscalled:
A. Agnosia
B. Agraphia
C. Apraxia
D. A phobia
E. Automatic-voluntary dissociation
A

C. Apraxia

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4
Q

About 40-60% of the corticospinal fibers originate from the _______________ cortex. This area controls precise and individual movements of the digits and distal extremities. The _____________ cortex is located anterior to the precentral gyrus and includes Broca’s speech area and the frontal eye field

A

Primary motor cortex; premotor cortex

**Premotor and supplementary cortices are involved in ideation and programming of movements

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5
Q

How does the premotor cortex receive input from the cerebellum?

A

Ventral anterior nucleus of the thalamus

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6
Q

Where do corticospinal and corticobulbar tracts arise?

A

From large pyramidally shaped neurons -> cells of Betz located in primary motor and premotor cortices

These fibers descend from these areas as part of the corticorubrospinal and corticoreticulospinal pathways, respectively

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7
Q

Explain the corticospinal tract up to the point of decussation

A

Descends through the corona radiata, internal capsule, cerebral peduncles, pons and upper medulla -> in the lower medulla, the majority of the fibers decussate at the pyramidal decussation and form the lateral corticospinal tract -> remaining uncrossed fibers continue as the anterior corticospinal tract

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8
Q

Where do upper extremety motor fibers of the CST versus lower extremity motor fibers decussate?

A

UE decussate more superior and medial compared to the more inferior and lateral decussation of the LE at the lower boundary of the cervicomedullary jnx

UE CST fibers assume a medial position in LCST

LE assume a more lateral position

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9
Q

What does a espionage of the upper portion of the pyramidal decussation result in?

A

Paralysis of UE without LE involvement -> referred to as bell’s cruciate paralysis

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10
Q

Where do direct versus indirect corticobulbar fibersterminate?

A

Direct terminate directly upon LMNs of the trigeminal, facial and hypoglossal motor nuclei

Indirect terminate in the reticular formation surrounding the brainstem motor nuclei

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11
Q

Where do direct corticobulbar fibers decussate?

A

Lower pons between the levels of entrance of the trigeminal and abducens nerves

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12
Q

What is the function of indirect corticobulbar fibers?

A

Play a role in recovery from lesions involving the direct corticobulbar fibers and have a role in physical therapy

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13
Q

What is the cause of supranuclear facial palsy?

A

Unilateral lesions of the corticobulbar fibers above the level of the facial nucleus

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14
Q

What are the symptoms of supranuclear facial palsy?

A

The contralateral mimetic muscles on the lower quadrant of the face are paralyzed

Upper quadrant facial muscles are unaffected by unilateral lesions of the corticobulbar fibers due to bilateral innervation of the facial nucleus

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15
Q

How do the lesions causing supranuclear facial palsy versus bell’s palsy differ?

A

Most common sites for lesions causing supranuclear facial palsy = facial region of motor cortex and genu of internal capsule

Bell’s palsy = central lesion of facial nerve

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16
Q

What are the symptoms of Bell’s palsy?

A

Ipsilateral paralysis of the mimetic muscles

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17
Q

What does the basal ganglia include?

A
Globus pallidus 
Caudate nucleus
Putamen
SUbstantia Nigra
Red nucleus 
Subthalamus
Nucleus accumbens
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18
Q

What is the paleostriatum?

A

Same thing as the globus pallidus

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19
Q

What structures comprise the striatum (neostriatum)?

A

Caudate
Putamen
Nucleus accumbens

20
Q

What structures comprise the corpus striatum?

A

Globus pallidus
Caudate nucleus
Putamen

21
Q

What structures comprise the enticular nucleus?

A

Globus pallidus

Putamen

22
Q

What structures comprise the dorsal striatum?

A

Caudate nucleus

Putamen

23
Q

In what part of the brain is the globus pallidus in and what is it one of the principal sources of?

A

Its part of the diencephalon

One of the principle sources of efferents from the basal ganglia

24
Q

Where is the caudate nucleus located and what is it functionally similar to in its connections?

A

Located on surface of inner curvature of lateral ventricle

Functionally similar to putamen

25
What is the largest nucleus of the basal ganglia and where is it located?
Putamen; located lateral to globus pallidus
26
The caudate nucleus and putamen are derived from the _________________ part of the brain and collectively form the ________________
Telencephalon; dorsal striatum
27
The substantia nigra is divided into 2 parts. What are they and what is there function?
Pars reticularis: forms anterior portion and contains serotonin and GABA -> neurons in this zone dont contain melanin and are the source of mos of the efferents from the SN Pars compacta -> contains dopamine and melanin -> cells in pars compacta are principally destroyed in Parkinson’s disease
28
What do pts who have a unilateral lesion of the red nucleus and midbrain tegmentum, such as Benedikt’s syndrome present with?
Ipsilateral oculomotor palsy and contralateral motor dysfunction such as tremor, ataxia or choreiform movements
29
What structure regulates the output of the basal ganglia?
Subthalamus
30
What does a unilateral lesion of the subthalamus result in?
Hemiballismus -> swinging throwing movements of the arms
31
Where is the nucleus accumbens located and what is its function?
Between putamen and caudate nucleus below anterior limb of internal capsule Links the amygdala and hippocampus to dorsomedial nucleus of the thalamus and globus pallidus so it may play a role in motivational and emotional aspects of movement
32
What 2 nuclei are often called the motor nuclei of the thalamus?
Ventral anterior and ventral lateral nuclei -> critical link for the merging, integration and processing of info from the striatum, cerebellum and cortex during all stages of motor pattern develoment
33
What are nigra-thalamic fibers?
Non-dopaminergic fibers that originate from the pars reticularis of the substantia nigra and terminate in the ventral anterior and ventral lateral thalamic nuclei
34
T/F: Fibers from the globus pallidus and substantia nigra do not terminate in the same areas of the VL and VA thalamic nuclei
True -> this distinction was important in stereotaxic surgery for Parkinson’s disease
35
What are Nigra-striatal fibers?
Dopaminergic fibers that originate in the pars compacta of the substantia nigra and terminate in the caudate and putamen (striatum) **The neurons in this area of the substantia nigra are destroyed in Parkinson’s disease
36
The destruction of the inhibitory, GABAnergic fibers in the _____________ fibers are involved in Huntington’s chorea
Stratonigral fibers
37
What are striatonigral fibers?
GABAnergic fibers (inhibitory) that originate in the putamen and terminate in the pars compacta of the substantia nigra and medial/lateral segments **Thought to contribute to Huntingtons disease
38
What is the subthalamic fasciculus?
Reciprocal fiber tracts between globus pallidus (medial and lateral tracts) and the subthalamus -> contain excitatory fibers
39
What is Parkinson’s disease commonly due to?
Loss of neurons in substantia nigra - may also be due to excitotoxicity, oxidative stress, malfunction of mito, toxin exposure
40
What are the symptoms and common treatment method for Parkinson’s?
Sx = tremor at rest, cogwheel rigidity (increased muscle tone), akinesia, bradykinesia, disturbances of eye movements, and loss of postural reflexes Thx = I-dopa or levodopa -> crosses BBB & is converted to dopamine
41
What is huntingtons disease and what are the symptoms?
Untreatable neurodegenerative disorder in which pts lose their ability to fnx due to progressive involuntary movements and dementia Characterized by absent mindedness, irritability, depression, clumsiness and sudden falls; choreiform movements gradually increase until pt is bedridden Cognitive functions and speech progressively deteriorate, severe dementia
42
What is Syndenham’s chorea?
Childhood autoimmune disease that typeically affects children 5-15 and more girls than boys; major manifestation of rheumatic fever (infection with group A beta-hemolytic streptococci) May not appear until 6mo or longer after infection, typically lasts 3-6 weeks, thought to result from Abs against streptococci, which then react with similar epitopes in the basal nuclei
43
What are the symptoms of Syndenham’s chorea?
Rapid, irregular, aimless movements of the limbs, face and trunk Some muscle weakness and hypotonia Irritability, OCD behaviors and anxiety **This is abenign disease and most experience compete recovery
44
What is ballismus and what causes it?
Typically seen as hemiballismus (occurs on one side) -> uncontrolled flinging (ballistic) movements of a limb Common with vascular lesions localized to contralateral subthalamic nucleus or subthalamic fasciculus
45
What is chorea and what causes it?
Rapid, irregular, involuntary, dance-like movements that flow randomly from one body region to another; caused by loss of neurons in the indirect corticobulbar pathway - Characteristic of Huntington disease and tardive dyskinesia, may occur as a side effect in Parkinson’s disease
46
What is Athetiosis?
Continuous writhing of distal portions of one or more extremities -> more obvious in UE and hands/face When more brisk and resemble chorea = choreoathetosis When more intense, sustained and resemble dystonia = athetotic dystonia