Cortical motor function, basal ganglia and cerebellum

Question 1

Where is the primary motor cortex located?

Answer 1

precentral gyrus, anterior to central sculls (separates frontal and parietal lobes)

Question 2

What is the function of the primary motor cortex?

Answer 2

control fine, discrete and precise voluntary movement by providing descending signals to execute movement

Question 3

How is the primary motor cortex organised?

Answer 3

somatotropic - face and lips are most lateral, moving medially to control hands > arms > legs > feet. More sensory receptors = larger area.

Question 4

Where is the premotor cortex located?

Answer 4

frontal lobe, anterior to primary motor cortex (inferiolateral to supplementary motor cortex)

Question 5

What is the function of the premotor complex?

Answer 5

Planning of movements.

Question 6

Where is the supplementary motor area located?

Answer 6

frontal lobe, anterior to primary motor cortex (superiomedial to premotor cortex)

Question 7

What is the function of the supplementary motor area?

Answer 7

planning complex movements and programming sequencing of movements e.g. speech.

Question 8

What is the function of the posterior parietal cortex.

Answer 8

ensures movements are accurately targeted to objects in external space.

Question 9

What is the role of the prefrontal cortex?

Answer 9

selection of appropriate movements for a particular course of action.

Question 10

What does the lateral corticospinal tract innervate?

Answer 10

skeletal muscles in distal parts of limbs.

Question 11

Outline the course of the lateral corticospinal tract. 6 steps.

Answer 11

1. Upper motor neurone emerges from primary motor cortex and travels through internal capsule 2. UMN passes through cerebral peduncle of midbrain, travelling through pons 3. UMN undergoes pyramidal decussation in the medulla 4. UMN descends down contralateral lateral corticospinal tract to the correct spinal level 5. UMN synapses to Lower motor neurone in ventral horn 6. LMN exits cord via the ventral root

Question 12

What does the anterior corticospinal tract innervate?

Answer 12

muscles of trunk and proximal limbs.

Question 13

Outline the course of the anterior corticospinal tract. 6 steps.

Answer 13

1. Upper motor neurone emerges from primary motor cortex and travels through internal capsule 2. UMN passes through cerebral peduncle of midbrain, travelling through pons 3. UMN DOES NOT undergo pyramidal decussation in the medulla, remaining ipsilateral 4. UMN descends down ipsilateral half of anterior corticospinal tract to the correct spinal level 5. UMN synapses to LMN in contralateral ventral horn to Lower motor neurone 6. LMN exits cord via the ventral root

Question 14

What does the corticobulbar pathway innervate? Which motor cranial nerves does it carry?

Answer 14

Supplies muscles of head, neck and face. Carries V, VII, XI, XII.

Question 15

Outline the course of the corticobulbar pathway? (4 steps).

Answer 15

1. Upper motor neurone emerges from head region of motor cortex 2. UMN passes through corticobulbar tract to brainstem 3. UMN synapses to CN in contralateral brainstem motor nuclei 4. CN passes out of brainstem to innervate muscles

Question 16

Compare paresis and paralysis.

Answer 16

Paresis - graded weakness of movements. Paralysis - complete loss of muscle activity.

Question 17

How are UMN lesions associated with increased function? Give some examples of this.

Answer 17

Loss of inhibitory descending inputs. Spasticity - increased muscle tone. Hyper-reflexia - exaggerates reflexes. Clonus - abnormal oscillatory muscle contraction.

Question 18

What are the effects of a LMN lesion?

Answer 18

Weakness Hypotonia Hyporeflexia Muscular atrophy Fasciculations: damaged motor units producing spontaneous action potentials - visible twitch Fibrillations: spontaneous twitching of individual muscle fibres

Question 19

What is apraxia?

Answer 19

Disorder of skilled movement due to damage to inferior parietal or frontal lobe - most commonly caused by stroke and dementia.

Question 20

Compare the signs of upper and lower motor neuron disease.

Answer 20

Upper: Increased muscle tone (spasticity of limbs and tongue) Brisk limbs and jaw reflexes Babinski’s sign Loss of dexterity Dysarthria Dysphagia Lower: Weakness Muscle wasting Tongue fasciculations and wasting Nasal speech Dysphagia

Question 21

Name and elaborate one some important components of the basal ganglia.

Answer 21

Lentiform nucleus (putamen and external globus pallidus) Caudate nucleus - large anterior head, and thins out to tail Subthalamic nucleus Substantia nigra - part of the midbrain, projects to ganglia Ventral pallidum - DAergic neurones projecting to brain Claustrum - layer of grey matter Nucleus accumbens - reward centre Nucleus basalis of Meynert - ACh-ergic projections to cortex for memory

Question 22

How does the direct pathway of the basal ganglia initiate movement?

Answer 22

striatum communicates with internal globules pallid us and thalamus. Thalamus sends signals to motor cortex –> movement.

Question 23

How does the basal ganglia receive information?

Answer 23

from the cerebral cortex via the striatum - two pathways arise.

Question 24

What is the role of the indirect pathway of the basal ganglia?

Answer 24

inhibit undesired movement through inhibition of the thalamus.

Question 25

Outline the pathology of Parkinson’s disease.

Answer 25

neurodegeneration of the dopaminergic neurones originating in the substantia nigra and projecting to the striatum .

Question 26

Give the clinical signs of Parkinson’s.

Answer 26

Bradykinesia: slowness of small movements e.g. Handling a knife Hypomimic face: expressionless and mask-like face Akinesia: difficulty in the initiation of movements Rigidity: increased muscle tone causing resistance to externally imposed joint movements Tremor: 4-7Hz tremor, beginning on one hand, spreading to rest of body over time

Question 27

Outline the pathology of Huntingdon’s disease.

Answer 27

genetic neurodegenerative disorder; excess CAG repeats (35+) in Huntingtin gene on Chr4 - leading to degeneration of GABAergic neurones in the striatum, caudate and then putamen

Question 28

Give the clinical signs of Huntingdon’s.

Answer 28

Choreic movements: rapid and jerky involuntary movement in the body (hands and face affected first, then legs and rest of body) Speech impediment Difficulty swallowing Unsteady gait Cognitive decline and dementia

Question 29

Where is the cerebellum located?

Answer 29

posterior to 4th ventricle.

Question 30

How does information flow into and out of the cerebellum?

Answer 30

via transverse fibres running to the pons.

Question 31

How does the inferior olive nucleus input into the cerebellum?

Answer 31

project to Purkinje cells using climbing fibres and then synapse with dendritic trees of Purkinje cells.

Question 32

How do other inputs synapse?

Answer 32

to granule cells via mossy fibres then onwards via parallel fibres.

Question 33

How does the cerebellum output information?

Answer 33

One output from Purkinje cells via white matter to thalamus

Question 34

Where is the vestibulocerebellum?

Answer 34

Question 35

Where is the spinocerebellum?

Answer 35

Question 36

Where is the cerebrocerebellum?

Answer 36

Question 37

What is the role of the vestibulocerebellum?

Answer 37

Regulation of gait, posture and equilibrium

Coordination of head movements with eye movement

Question 38

What is the role of the spinocerebellum?

Answer 38

Coordination of speech

Adjustment of muscle tone

Coordination of limb movements

Question 39

What is the role of the cerebrocerebellum?

Answer 39

Coordination of skilled movements

Cognitive function, attention and language processing

Emotional control

Question 40

outline the cortical structure.

Answer 40

3 layers.

Outermost - molecular layer; few neurones

Middle - piriform layer; Purkinje cells - project to nuclei in white matter, huge dendritic trees

Innermost - granular layer; small neurones involved in processing

Question 41

How does damage to different areas of the cerebellum have different effects?
Compare vestibulocerebellar, spinocerebellar and cerebrocerebellar syndromes.

Answer 41

Vestibulocerebellar syndrome: damage (tumour) leads to gait ataxia and tendency to fall even when sitting, eyes opened

Spinocerebellar syndrome: degeneration/alcohol related atrophy leads to abnormal gait and wide-based stance

Cerebrocellar syndrome: mainly affects arms and skilled movement, leading to tremor and speech problems

Question 42

Give the main signs of cerebellar dysfunction.

Answer 42

Ataxia: general impairments in movement coordination and accuracy - disturbances of posture or gait: wide-based, staggering (“drunken”) gait

Dysmetria: inappropriate force and distance for target-directed movements

Intention tremor: increasingly oscillatory trajectory of a limb in target directed movement

Dysdiadochokinesia: inability to perform rapidly alternating movement

Scanning speech: staccato due to impaired speech muscles