Motor pathways Flashcards

1
Q

What is the general hierarchy of movement?

A

Movement is hierchical-higher levels are involved in complex parts-program and decide on movement, coordinate them
Lower-just execute (move the limbs)
1ary motor complex is the in the primary gyrus, but helped by Basal ganglia, thalamus, cerebellum, brain stem etc

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2
Q

What is the role of cerebellum for movement? And basal ganglia?

A

Usually movements pass by it, leading to refining-smaller motor movements. Basal ganglia has a similar role “modulatory”W

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3
Q

What is the role of the brain stem and spinal cord for movement?

A

lower tier-just exercuting the orders. Brain stem-Head and face, spinal-rest of the body

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4
Q

Where and what is the primary motor cortex? How is it organised?

A

Precentral gyrus, anterior to central sulcus
Control fin, discrete and VOLUNTARY movement
Neurons can be huge and extend down into the spinal cord
Somatotopic organisation (motor humonculus)-lower limbs are higher up the brain (matters in stroke-anterior cerebral artery)-and not all areas are the same size (hands are massive)

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5
Q

What is the wiring of the 2 descending motor pathway?

A

Most are lateral-cortical tract:
Motor area-pass by basal ganglia internal capsule, via cerebral peduncle of midbrain (mickeymouse ears), then pons (not visible, but where cerebellum links), then pyramidals in the medulla. END OF MEDULLA PASS OVER
(Still no synpase)-then down via lateral corticalspinal tract to the appropriate level, where synapse with lower motor neuron (in ventral horn)-and to the muscle
Other pathway doesnt cross over (ipsilateral)-descend in anterior cortical spinal tract till the right level WHERE IT THEN CROSSES OVER (usually do the intercostal and similar)

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6
Q

What is the cortical bulbar pathway?

A

It refers to the motor neurons that go the brainstem-and act in cranial nerves
Like hypoglossal nucleus, in the medulla (near center because motor), then to tongue. do cross over

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7
Q

What is the pre-motor cortex? What is its role?

A

Anterior and down from primary motor cortex

Role in planning of movement and regulate externally cued movement (how you interact with the environement

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8
Q

What is the Supplementary motor cortex

A

Also anterior to motor, but more medial than pre-motor
Role in planning complex movements, and programming spequencing of movement (Like talking and stuff)
The area thatll actvate when thinking of movement

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9
Q

What is the association cortex?

A

Not stricktly motor but have a role
Posterior parietal cortex: Ensure movements are targeted accuratly in space (like picking an apple-not missing it)
Prefrontal cortex: Selection of appropriate movement-personality involvment in action (like picking up a hot plate

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10
Q

Define upper motor neuron, lower motor neurons, pyramidal and extrapyramidal

A

Lower-those in the ventral horn, and the bulbar ones in the brain stem
Upper-corticospinal and corticobulbar (the ones in the brain)
Pyramidal-exactly the lateral corticospinal tract (so pyramidal problem are there)
Extrapyramidal-basal ganglia, cerebellum (so extrapyramidal problems are there)

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11
Q

What are the main problems with upper motor lesions

A

Loss of function: (negative signs)
Paresis-graded weakness of movement, Paralysis (plegia)-complete loss

abnormal function (positive sign-loss of inhibitory)
Spasticity-increased muscle tone
Hyper-reflexia-
Clonus-Abonrmal repeated muscle contraction
(Babinski’s sign-movement of toes after stimulating bottom of foot)

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12
Q

What is Apraxia?

A

Damage to the inferiot parietal lobe/frontal lobe (premotor/supplementary)
Not weak or aything, but loss of organising of skilled movement
eg: lose ability to put buttons together, etc
Any disease can cause it, but more commonly stroke and dementia

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13
Q

What are consequences of lower motor lesions?

A

Weakness, hypotonia, hyporeflexia, (over time-muscle atrophy), fasciculations (damaged units create spontanous AP-twitch), fibrillations-twitching of individual muscle fibre (seen with EMG)

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14
Q

What is motor neuron disease?

A

Rare, but progessive neurodegenerative disorder of motor system (both upper and lower motor neurons)
Most common one is Amyotrophic lateral sclerosis (ALS)
Varied phenotype and cause (but signs are what are expected-tones increase-rigid tongue, hands, etc)
Usually distal to proximal, until respiratory

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15
Q

What are the different parts of the basal ganglia?

A
Caudate nucleus-the higher part (head and tail) and Lentiform neucleus (putament and external globus pallidus (internal also there))
Caudate, Putamen and external-striatum
Subthalamis nucleus, substantia nigra (in midbrain, but project to ganglia)
Ventral pallidum (dopagenic), claustrum  grey matter), nucleus accumbens (reward system-bottom of lentiform) , nucleus basalis of Meynert (cholinergic to forebrain-memory)
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16
Q

What are the functions of the basal ganglia?

A

Elaborating associated movement-swinging arms when walking, changing facial expression with emotions
Also order of movement
The wiring is still unclear

17
Q

What is the general organisation of basal ganglia wiring?

A

Unsure still but
Striatum to ext globus pallidus (close to subthalamic) and substantia nigra (parkinsons), and more
Importantly, parkinsons seems to be between substancia nigra and striatum

18
Q

What are the 2 main presentations of Parkinsons?

A

Either the slight tremor, or inability to initiate movement (want to move but cant)
Also (trunk forward-Kyphoisis, unsteady when walking, sudden start of running)
affect senses and inttelect later in disease

19
Q

What is the general neuropathology in parkinsons?

A

Thought to be loss of dopanergic neurons in the substancia nigra, that wires to the basal ganglia via nigrostrital fibers-to all of striatum (but in brainstem)
Nearly awlays gone in parkinsons patients (60% loss before symptoms)

20
Q

What are the motor signs of parkinsons?

A
Bradykinesia-slowness of movement
Hypomimin face-expressionless, masklike
Akninesia-diffculty initiating movements
Rigidity-muscle tone increase
Tremor at rest (pill rolling tremor of wrist)-spread
21
Q

What is Huntingtons disease?

A

Genetic disease, based on Huntingtin of Chr4, AD
Based on CAG repeats in DNA (35 repeats is cutoff)
Degeneration of GABAnergic neurons in striatum, caudate and then putamen (very basal ganglia)

22
Q

What are the motor signs of Huntingtons?

A

Choreic movements-rapid jerky movements of hands and face (proximal to distal (rare in neuro))
Speech impariment, difficulty swallowing, unsteady gait, cognitive decline, dementia

23
Q

What is the wiring of the cerebellum

A

Lots of fine sulci, but only 3 layers
Outermost-molecular layer (not too many neurons), Then main processing cells in primiform (Pukinje cells), which have massive dendritic trees
THen granular layer (processing)
Inferior olive (medulla) project to pukinje via climbing fibres. Other input vua mossy fibre and via parallel fibres
ONLY 1 output from pukinje cells via DEEP NUCLEU

24
Q

What are the 3 main areas of the cerebellum?

A

Vestibulocerebellum-regulation of gait, posture and equilibrium
Spinocerebellum-coordination of speech, muscle tons, limb movement (input from spinal cord)
Cerebrocerebellum-coordination of skilled movement (cognitive function, attention, processing of language, emotion)
Each area lesions will cause associated symptoms

25
Q

What are the main signs of cerebellum dysfunction?

A

Deficits only happen upon movement
ATAXIA-staggerring drunken gait
Dysmetria-losing ability to judge how much force/distance needed for a movement
Intention tremor-thinking of an action leads to tremor
Dysdiadochokinesia-inabulity to perform rapidly alternating movements
Scanning speech (staccato delivery of speech)