Motor system

Question 1

Primary motor area

Answer 1

Precentral gyrus
Pyramidal tracts
Simple fine movement e.g. hand

Question 2

Premotor PMC (more ventral/caudal/to the side) and supplementary motor areas SMA (dorsal)

Answer 2

Programming of complex movement
Lies in the frontal lobe, immediately rostral to the primary motor area

Question 3

Frontal eye field

Answer 3

Immediately rostral to the PMC
Saccadic eye movement to the opposite side
Right FEF - saccade to left

Question 4

Anterior cingulate gyrus

Answer 4

Goal or emotion directed movement

Question 5

Motor decussation of pyramidal tracts?

Answer 5

FORAMEN MAGNUM, MEDULLA OBLONGATA
Ventral - crosses later, TRUNK
Lateral corticospinal tracts LIMB

Question 6

Pyramidal tract: corticospinal course

Answer 6

1. Motor cortex
2. Corona radiata
3. Post. limb of internal capsule
4. Cerebral peduncle
5. Longitudinal pontine bundle
6. Pyramid (medulla)
7. lateral column in spinal cord

Question 7

Pyramidal corticobulbar tract course

Answer 7

1. Motor cortex
2. Corona radiata
3. GENU of internal capsule
4. Cerebral peduncle
5. Longitudinal pontine bundle
6. Pyramid (medulla)
7. lateral column in spinal cord

Question 8

Extrapyramidal system

Answer 8

Basal ganglia
- Caudate
- Lenticular
- Subthalamic nucleus
- Substantia nigra

Question 9

Which region of the substantia nigra atrophies in PD?

Answer 9

Pars compacta

(not pars reticularis)

Question 10

Non-pyramidal motor pathways

Answer 10

NON-VOLUNTARY = parallel control of LMN
1. Red nucleus
2. Reticular formation
3. Vestibular nuclei

Question 11

Rubrospinal tract

Answer 11

From red nucleus.
FLEXOR MUSCLES OF UPPER EXTREMITY

Question 12

Medial reticulospinal tract

Answer 12

From pontine RF. IPSILATERAL CONTROL
EXTENSOR MUSCLES OF UPPER & LOWER EXTREMITIES.

Question 13

Lateral reticulospinal tract

Answer 13

From medullary RF. CONTRALATERAL
Inhibits gamma motor neurons and
LOSS OF MUSCLE TONE

Question 14

Vestibulospinal tracts

Answer 14

1. Lateral tract = EXTENSOR MUSCLES OF UPPER & LOWER
2. Medial tract = CONTRACTION OF NECK MUSCLES in response to postural changes
   Remark: balance is always ipsilateral

Question 15

What is the main neuron in the cerebellum?

Answer 15

Purkinje = only output tract

Question 16

Deep cerebellar nuclei from medial to lateral

Answer 16

1. Fastigial nucleus
   2&3. Globose n., Emboliform n.
2. Dentate nucleus

Question 17

Fxn of Flocculonodular lobe (vestibulocerebellum)

Answer 17

Vestibulo-ocular (VOR through MLF) and vestibulospinal reflexes (head & neck, muscle tone)

Question 18

Fxn of vermis (spinocerebellum)

Answer 18

Control muscle tone & postural control (upgrade from flocculonodular)
AFFERENT
1. Spinocerebellar
2. Cuneocerebellar
3. Vestibular nuclei

EFFERENT
1. Vestibulospinal tract
2. Fastigial nuclei sends signals to RF and then down the reticulospinal tract

Question 19

Cerebellar hemisphere / cerebro or pontocerebellum

Answer 19

Cortical motor areas sends signals to the cerebellar hemisphere through the pontine nucleus. These PONTOCEREBELLAR fibers decussate before reaching the cerebellum.

The DENTATE nucleus sends decussating fibers to the cortical motor area again through the thalamus.

The cerebellar hemispheres also work with the inferior olivary nucleus (RUBROSPINAL, RED NUCLEUS)

Remark: the multiple decussations are from attempts to keep the cerebellum controlling ipsilateral and cortex controlling contralateral.

Question 20

Inferior cerebellar peduncle

Answer 20

Mostly inputs
1. Spinocerebellar tract: mossy fibers
2. Inferior olive

Question 21

Middle cerebellar peduncle

Answer 21

Pontocerebellar fibers

Question 22

Superior cerebellar fibers

Answer 22

1. Dentate To Thalamus
2. INTERPOSED N. to red nucleus
3. FASTIGIAL n. to vestibular n.

Question 23

Lesions above motor motor decussation (medulla, foramen magnum)

Answer 23

Contralateral hemiplegia

Question 24

Lesions below motor motor decussation (medulla, foramen magnum)

Answer 24

Ipsilateral hemiplegia

Question 25

LMN lesion, anterior horn cell disease

Answer 25

Flaccid (gamma) paralysis (alpha motor neuron) Hyporeflexia Severe muscular atrophy Muscle fasciculation Clonus negative Babinski's sign: flexor

Question 26

UMN lesion (specifically, Pyramidal tract lesion)

Answer 26

Weakness/paralysis Atrophy of disuse Clonus: positive or sustained Babinski's: extensor

Question 27

Decorticate rigidity vs decerebrate rigidity

Answer 27

Decorticate rigidity is due to a lesion above the brainstem whereas decerebrate rigidity is caused by a lesion between the midbrain and the pons. Specifically, upon decerebrate rigidity, caused when a lesion in the midbrain, pons, or diencephalon. Decorticate rigidity occurs when lesions occur in the cortical white matter, internal capsule, thalamus, cerebral peduncle, and basal ganglia.

Question 28

Lewy body

Answer 28

Intraneuronal inclusion body composed of alpha-synuclein in Parkinson's disease

Question 29

Extrapyramidal lesions

Answer 29

- No paralysis or weakness - Abnormal muscle tone: RIGIDITY (dystonia) - Decreased movement - Increased involuntary movement

Question 30

Cogwheel rigidity

Answer 30

Parkinson

Question 31

Festinating gait, decreased arm swing, stooped posture, difficulty initiating gait

Answer 31

Parkinson

Question 32

Hemiballismus: ischemia of

Answer 32

Contralateral subthalamic n.

Question 33

Huntington's disease

Answer 33

In Huntington disease, the caudate nucleus atrophies, the inhibitory medium spiny neurons in the corpus striatum degenerate, and levels of the neurotransmitters gamma-aminobutyric acid (GABA) and substance P decrease. Huntington disease results from a mutation in the huntingtin (HTT) gene (on chromosome 4), causing abnormal repetition of the DNA sequence CAG, which codes for the amino acid glutamine. The resulting gene product, a large protein called huntingtin, has an expanded stretch of polyglutamine residues, which accumulate within neurons and lead to disease via unknown mechanisms. The more CAG repeats, the earlier the onset of disease and the more severe its expression (phenotype). The number of CAG repeats can increase with successive generations when the father transmits the mutation and, over time, can lead to increasingly severe phenotypes within a family (called anticipation).

Question 34

chorea

Answer 34

Involuntary jerking or writhing movements

Question 35

Deep brain stimulation of GPi or subthalamic n. may help with

Answer 35

Hyperkinetic disorders or Parkinson's disease

Question 36

Vermis lesion in cerebellum

Answer 36

Trunkal ataxia Wide-based gait Nystagmus

Question 37

Cerebellar hemisphere lesion

Answer 37

Dysdiadochokinesia Dysmetria Intention tremor Rebound phenomenon Dysarthria

Question 38

Lateral reticulospinal tract lesion or injury

Answer 38

SPASTICITY HYPERREFLEXIA