PATHOPHYSIOLOGY OF MOTOR SYSTEM

Question 1

What happen with a lesion on frontal lobe

Answer 1

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.

Question 2

symptom of upper motor lesion

Answer 2

Site of the lesion :
Cortex, brainstem, spinal cord:
Muscle weakness : Yes (plegia)
Muscle tone : increased (spasticity)
Muscle Atrophy: Disuse Atrophy
Fasciculation (muscle twitching): No Fasciculations
Tendon (stretch) reflex: Hyperreflexia
Plantar reflex(Babinski Sign) : Positive Babinski Sign

Question 3

lower motor neuron lesion symptom

Answer 3

site of lesion: Anterior horn, roots, nerves, neuromuscular junction

muscle weakness: Yes (myopathy)
muscle tone: decreased (hypotonia)
muscle atrhophy: Denervation Atrophy
fasciculation: Fasciculations
tendon reflex: Hyporeflexia
babinski sign: Negative Babinski Sign

Question 4

what is hyporflexia during LMN lesion

Answer 4

absence or weak leg extension

Question 5

what is hyperreflexia of UMN lesion

Answer 5

strong extension of the leg

Question 6

Injury to the primary motor cortex (lesion A) causes a weakness of the

Answer 6

contralateral inferior facial muscles:
Input to inferior facial muscles from the UMN in primary motor cortex is lost.

Question 7

Injury to corticobulbar tract (lesion B) causes a weakness of the

Answer 7

contralateral inferior facial muscles:
Input to inferior facial muscles from the UMN in primary motor cortex is lost

Question 8

Injury to the facial motor nucleus or its nerve (lesion C) causes a weakness of

Answer 8

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

Question 9

what is aphasia

Answer 9

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

Question 10

what is broca aphasia

Answer 10

loss of the ability to produce language.
also called non-fluent aphasia.

Question 11

what is wenickes aphasia

Answer 11

difficulty understanding speech

Question 12

where is the broca area

Answer 12

the posterior inferior frontal gyrus (inferior part of the motor cortex). For that is also called motor aphasia.

Question 13

broca aphasia is mostly caused by

Answer 13

stroke

Question 14

what is multiple sclerosis

Answer 14

an immune-mediated inflammatory disease that causes the demyelination of the nerves of central nervous system so the propagation of AP is stop

Question 15

what is myasthenia gravis

Answer 15

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

Question 16

what happen whit myasthenia gravis

Answer 16

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

Question 17

treatment of myasthenia gravis

Answer 17

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.

Question 18

treatment of myasthenia gravis

Answer 18

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.

Question 19

what is parkinson disease

Answer 19

Degeneration of the substantia nigra’s neurons: i.e. loss of dopaminergic neurons.
Causes: rigidity, tremor and akinesia (i.e. inability to initiate and stop movement).
2nd most common neurodegenerative disease after Alzheimer’s disease.

Question 20

what is the 2nd most common neurodegenerative disease after Alzheimer’s disease.

Answer 20

parkinson

Question 21

direct pathway of parkinson disease

Answer 21

the transient inhibition from the caudate/putamen to the globus pallidus internal is diminished (no activation of D1). Thus, the tonic inhibition of the globus pallidus internal on the thalamus is increased, which results in decreased excitation of the motor cortex (i.e. akinesia, difficulty to initia

Question 22

indirect pathway of parkinson disease

Answer 22

the transient inhibition from the caudate/putamen to the globus pallidus external is increased (no activation of D2). Thus, the tonic inhibition of the globus pallidus external on the sabthalamic nucleus is decreased, which results in increased excitation of the globus pallidus internal. The latter exerts more tonic inhibition of the thalamus, which results in decreased excitation of the motor cortex (i.e. akinesia, difficulty to stop movement).

Question 23

parkinson treatment option

Answer 23

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

Deep Brain Stimulation:
Insertion of an electrode deep into the brain
Repetitive and regular electrical stimulation.
Targeted structures: subthalamic nucleus, globus pallidus internal.

Question 24

what is hungtington disease

Answer 24

Degeneration of caudate and putamen neurons. The size of the caudate and putamen is dramatically reduced.
Causes a movement disorder: hyperkinesia