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
what is the 2 most common neurodegenerative diseases
1-alzheimer's 2-parkinson's
26
what are the treatment options of parkinson's disease
-Dopamine-based medication : L-Dopa (dopamine precursor). -Deep Brain Stimulation
27
what entails deep brain stimulation for parkinson's treatment
-Insertion of an electrode deep into the brain -Repetitive and regular electrical stimulation. -targeted structures: subthalamic nucleus, globus pallidus internal.
28
degeneration of caudate and putamen neurons is associated with what disease
huntington's
29
what movement disorder does huntington's cause
hyperkinesia (rapid and jerky motions with no clear purpose)
30
in ataxia what does dysfunction of the Cerebrocerebellum cause
Lack of voluntary coordination of muscle movements (e.g.,failure to predict motor movement, patients will overshoot intended target)
31
in ataxia what does dysfunction of the vestibulocerebellum cause
Loss of balance and gait difficulty
32
cause of ataxia
genetic disease