pathophysiology of the motor system Flashcards

1
Q

what are the symptoms of a frontal lobe lesion

A

-Difficulty with executive functions: hard to manage his daily plans, decision-making problem, not organized…etc.
-Change in personality and behavior: more aggressive, less compassion, social isolation…etc.

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2
Q

upper motor neuron lesion (site of lesion, m. weakness, m. tone, m. atrophy, fasciculation, tendon reflex, plantar reflex)

A

-site of lesion: cortex, brainstem, spinal cord
-m. weakness: yes (plegia)
-m. tone: increased (spasticity)
-m. atrophy: disuse atrophy
-fasciculation: no fasciculations
-tendon reflex: hyperreflexia
-plantar reflex: positive babinski sign

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3
Q

lower motor neuron lesion (site of lesion, m. weakness, m. tone, m. atrophy, fasciculation, tendon reflex, plantar reflex)

A

-site of lesion: ant horn, roots, nerves, neuromuscular junction
-m. weakness: yes (myopathy)
-m. tone: decreased (hypotonia)
-m. atrophy: denervation atrophy
-fasciculation: fasciculations
-tendon reflex: hyporeflexia
-plantar reflex: negative babinski sign

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4
Q

what kind of lesion causes hyporeflexia: absence or weak extension of the leg

A

lower motor neuron lesion

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5
Q

what kind of lesion causes hyperreflexia: strong extension of the leg

A

upper motor neuron lesion

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6
Q

upper motor neuron lesion causes _____ on the reflex circuit

A

lack of control

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7
Q

what does the distribution of facial weakness provide

A

important localizing clues indicating whether the underlying injury involves the lower motor neuron (LMN) or the upper motor neuron (UMN)

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8
Q

injury to the primary motor cortex causes a weakness of what facial m.
what input is lost and intact

A

contralateral inferior facial muscles:
Ø Input to inferior facial muscles from the UMN in primary motor cortex is lost.
Ø Input to superior facial muscles from the UNM in the premotor areas (cingulate gyrus) remains intact.

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9
Q

injury to the corticobulbar tract causes a weakness of what facial m.
what input is lost and intact

A

contralateral inferior facial muscles:
Ø Input to inferior facial muscles from the UMN in primary motor cortex is lost.
Ø Input to superior facial muscles from the UNM in the premotor areas (cingulate gyrus) remains intact bc this input projects bilaterally

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10
Q

injury to the facial motor nucleus or its n. causes a weakness of what facial m.
what input is lost and intact

A

all m. of facial expression on the same side of the lesion:
Ø Input to inferior and superior facial muscles from the LMN is lost.

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11
Q

what is aphasia

A

Aphasia is a disorder in the comprehension and/or expression of language

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12
Q

what are the 2 diff types of aphasia

A

-Broca’s (motor) aphasia: loss of the ability to produce language.
-Wernicke’s aphasia: difficulty understanding speech.

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13
Q

why is broca’s aphasia also called non-fluent aphasia

A

Characterized by the loss of the ability to produce language,

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14
Q

why is broca’s aphasia also called motor aphasia

A

Lesion in the Broca’s area: the posterior inferior frontal gyrus (inferior part of the motor cortex)

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15
Q

what is broca’s aphasia mostly caused by

A

stroke

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16
Q

what does the severity of broca’s aphasia varies from and what does it depend on

A

The severity of the problem varies from the complete loss of the ability to speak to struggle to speak depends on the size of the affected area.

17
Q

is there a possibility of recovery w broca’s aphasia

A

yes, Possibility of recovery by speech therapy.

18
Q

what is multiple sclerosis

A

an immune-mediated inflammatory disease that causes the demyelination of the nerves of central nervous system

19
Q

what happens w multiple sclerosis when it affects motor neurons, sensory neurons or optic fibers

A

motor neurons: m. weakness
sensory neurons: loss of sensation
optic fibers: visual disturbances

20
Q

what is myasthenia gravis

A

a neuromuscular disease that causes weakness in the muscles (e.g. drooping of eyelids, difficulty swallowing, shortness of breath)

21
Q

what happens with myasthenia gravis

A

-Acetylcholine (Ach) receptors blocked (or destroyed) by antibodies (autoimmune disease).
-Reduced transmission of Ach in the muscle.
-Impaired muscle contraction.

22
Q

what is the treatment for myasthenia gravis

A

Cholinesterase inhibitors: inhibit the metabolism of Ach by the cholinesterase enzyme (i.e., keep more Ach in the synaptic cleft), Thus, boost signals between nerves and muscles to improve muscle strength

23
Q

parkinson’s disease is the degeneration of what neurons

A

substantia nigra’s neurons (loss of dopaminergic neurons)

24
Q

what does parkinson’s cause

A

igidity, tremor and akinesia (i.e. inability to initiate and stop movement)

25
Q

what is the 2 most common neurodegenerative diseases

A

1-alzheimer’s
2-parkinson’s

26
Q

what are the treatment options of parkinson’s disease

A

-Dopamine-based medication : L-Dopa (dopamine precursor).
-Deep Brain Stimulation

27
Q

what entails deep brain stimulation for parkinson’s treatment

A

-Insertion of an electrode deep into the brain
-Repetitive and regular electrical stimulation.
-targeted structures: subthalamic nucleus, globus pallidus internal.

28
Q

degeneration of caudate and putamen neurons is associated with what disease

A

huntington’s

29
Q

what movement disorder does huntington’s cause

A

hyperkinesia (rapid and jerky motions with no clear purpose)

30
Q

in ataxia what does dysfunction of the Cerebrocerebellum cause

A

Lack of voluntary coordination of muscle movements (e.g.,failure to predict motor movement, patients will overshoot intended target)

31
Q

in ataxia what does dysfunction of the vestibulocerebellum cause

A

Loss of balance and gait difficulty

32
Q

cause of ataxia

A

genetic disease