Motor systems

Question 1

Describe the functional segregation of motor control

Answer 1

Functional segregation

Motor system organised in a number of different areas that control different aspects of movement

Question 2

Describe the hierarchical organisation of motor control

Answer 2

Hierarchical organisation
high order areas of hierarchy are involved in more complex tasks (programme and decide on movements, coordinate muscle activity)
lower level areas of hierarchy perform lower level tasks (execution of movement)

Question 3

Summarise motor system hierarchy

Answer 3

The motor cortex (both primary and association) receives information from other cortical areas and sends commands to the thalamus (via basal ganglia) and brainstem
Information from the thalamus then feeds back to the motor cortices
The motor cortex passes commands to the spinal cord ( to control muscles of the body) and brainstem to control muscles of the face, head and neck
The cerebellum and basal ganglia adjusts the commands received from other parts of the motor control system to fine-tune the movement
Cerebellum feeds to thalamus and brainstem
Basal ganglia feeds to the thalamus

Question 4

Outline the hierarchy in motor control

Answer 4

o Level 4 (highest) – association cortex.
o Level 3 – motor cortex.
o Level 2 – brain stem and cerebellum (side loop structure (SLS)).
o Level 1 (lowest) – basal ganglia (SLS (e.g. caudate nucleus)) and spinal cord

Question 5

What are the 3 main areas of the motor cortex

Answer 5

Has got 3 main areas:

1. Primary motor cortex or M1 – Broadmann’s area 4.
2. Premotor cortex – Broadmann’s area 6.
3. Supplementary motor area – Broadmann’s area 6

Question 6

Describe the primary motor cortex (M1)

Answer 6

Location: precentral gyrus, anterior to the central sulcus
Function: control fine, discrete, precise voluntary movement
Provide descending signals to execute movement
 Betz cells exist in layer V of the cerebral cortex. They are the biggest cells in the cerebral cortex- pyramidal cells
They are found in the 5th layer of grey matter
The corticospinal tracts originate from here
M1 is in the frontal lobe

Question 7

Describe the somatotopic organisation of the primary motor cortex

Answer 7

 The somatotopic organisation of the primary motor cortex is known as Penfield’s motor homunculus.
Organisation: somatotopic - whereby face and lips are most lateral, moving medially to control hands > arms > legs > feet (anterior cerebral artery); more sensory receptors = larger area
 The face and hands have a large area of the brain to control them because they have more fine control.

Question 8

Summarise the motor homunculus

Answer 8

Each area of the body which is under motor control is represented in the primary motor cortex and these representations are arranged somatotopically: the foot is next to the leg which is next to the trunk which is next to the arm and the hand.

The amount of brain matter devoted to any particular body part represents the amount of control that the primary motor cortex has over that body part. A lot of cortical area is required to
control the complex movements of the hand and fingers, and these body parts have larger representations in M-I than the trunk or legs, whose muscle patterns are relatively simple

Question 9

State the descending motor pathways

Answer 9

Corticospinal (pyramidal) and subcorticospinal tracts:

Cortico-spinal tracts (CST)
Rubrospinal tracts
Reticulospinal tracts
Vestibulospinal tracts
Organization of CST

Question 10

Summarise the descending pathways

Answer 10

Integration of inputs from somatosensory cortex into layer IV of M1
Layer V (grey matter) contains pyramidal cells – the large Betz cells are visible
Projects to white matter below layer VI and then to internal capsule
Travels via cerebral peduncles to medulla where fibres come together as pyramids
Fibres decussate – 80% cross to form lateral corticospinal tract and 20% remain uncrossed forming anterior corticospinal tract
Tracts project to ventral horns and motoneurons

Question 11

Describe the lateral and medial descending pathways

Answer 11

Lateral
•	Lateral corticospinal tract
•	Rubrospinal tract
Medial 
•	Anterior corticospinal tract
•	Reticulospinal tract
•	Vestibulospinal tract
•	Tectospinal tract

Question 12

Broadly, what is the function of the lateral and medial descending pathways

Answer 12

Lateral 
•	Control of proximal and distal musculature
•	Voluntary movements or arms and legs
Medial
•	Control of axial muscles 
•	Balance and posture

Question 13

Describe the lateral corticospinal tract

Answer 13

Lateral corticospinal tract: supplies skeletal muscles in distal parts of limbs
Upper motor neurone emerges from primary motor cortex and travels through internal capsule
UMN passes through cerebral peduncle of midbrain, travelling through pons
UMN undergoes pyramidal decussation in the medulla
UMN descends down contralateral lateral corticospinal tract to the correct spinal level
UMN synapses to Lower motor neurone in ventral horn
LMN exits cord via the ventral root

Question 14

Describe the anterior corticospinal tract

Answer 14

Anterior corticospinal tract: supplies muscles of the trunk and proximal limbs
Upper motor neurone emerges from primary motor cortex and travels through internal capsule
UMN passes through cerebral peduncle of midbrain, travelling through pons
UMN DOES NOT undergo pyramidal decussation in the medulla, remaining ipsilateral
UMN descends down ipsilateral half of anterior corticospinal tract to the correct spinal level
UMN synapses to LMN in contralateral ventral horn to Lower motor neurone
LMN exits cord via the ventral root

Question 15

Describe the corticobulbar pathways

Answer 15

Corticobulbar pathway: supplies the muscles of the head, neck and face - carrying the motor cranial nerves (V, VII, IX and XII)
Upper motor neurone emerges from head region of motor cortex
UMN passes through corticobulbar tract to brainstem
UMN synapses to CN in contralateral brainstem motor nuclei
CN passes out of brainstem to innervate muscles

Question 16

Describe the differences in synaptic transmission of the upper and Lower motor neurones

Answer 16

 Upper to lower motor neurones NT = glutamate.

 Lower neurone to muscle fibres NT = ACh.

Question 17

What is the function of the rubrospinal tract

Answer 17

It is an alternative pathway that allows voluntary motor commands to be sent down the spinal cord meaning that the body can compensate for a lesion in the primary motor cortex.
It also has a role in movement velocity.

Question 18

Describe the structure and function of the vestibulospinal tract

Answer 18

The lateral vestibulospinal tract originates at the lateral vestibular nucleus.
The medial vestibulospinal tract originates at the medial vestibular nucleus.
They mediate postural adjustments and head and eye movements

Question 19

Describe the structure and function of the reticulospinal tract

Answer 19

It originates in the reticular formation in the brainstem then goes down the spinal cord to innervate muscle. 
It is involved in complex actions:
•	Orienting 
•	Stretching 
•	Maintaining a complex posture

Question 20

Describe the structure and function of the tectospinal tract

Answer 20

It originates in the superior colliculus (brainstem)

Its function is not known but is most likely involved in reflexive turning of the head to orient to visual stimuli.

Question 21

Describe the premotor cortex

Answer 21

Location: frontal lobe anterior to M1
Function: planning of movements and their coordination
Regulates externally cued movements
e.g. seeing an apple and reaching out for it requires moving a body part relative to another body part (intra-personal space) and movement of the body in the environment (extra-personal space)

Question 22

Describe the supplementary motor cortex

Answer 22

Location: frontal lobe anterior to M1, medially
Function: planning complex movements; programming sequencing of movements
Regulates internally driven movements (e.g. speech)
SMA becomes active when thinking about a movement before executing that movement (rehearsing a dance)

Question 23

Describe the role of the association cortices

Answer 23

Brain areas not strictly motor areas as their activity does not correlate with motor output/act
Posterior parietal cortex: ensures movements are targeted accurately to objects in external space
Prefrontal cortex: involved in selection of appropriate movements for a particular course of action- personality impact and influence of previous experiences

Question 24

Give some important definitions relating to the motor system

Answer 24

Lower motor neuron
		Spinal cord, brainstem
Upper motor neuron
		Corticospinal, corticobulbar
Pyramidal
		Lateral corticospinal tract
Extrapyramidal
		Basal ganglia, cerebellum

Question 25

What are the negative signs of an upper motor neurone lesion

Answer 25

Loss of function (negative signs):
Paresis: graded weakness of movements
Paralysis (plegia): complete loss of muscle activity

Question 26

What are the positive signs of an upper motor neurone lesion

Answer 26

Increased abnormal motor function (positive signs) due to loss of inhibitory descending inputs:
Spasticity: increased muscle tone
Hyper-reflexia: exaggerated reflexes
Clonus: abnormal oscillatory muscle contraction
Babinski’s sign
no muscle atrophy

Question 27

What is Babinski’s sign

Answer 27

You stroke the plantar surface of the foot and in a normal subject you will see flexion of the toes (they curl downwards)
In the case of upper motor neurone lesions, the patient will show an EXTENSOR PLANTAR RESPONSE where their toes fan out and their big toe lifts up.

Question 28

Why is atrophy not seen in upper motor neurone lesions

Answer 28

The lower motor neurones are still in tact and they have a role in providing nutrients to the muscle.
There will still be partial atrophy due to muscle disuse.

Question 29

Describe apraxia

Answer 29

A disorder of skilled movement. Patients are not paretic but have lost information about how to perform skilled movements

Lesion of inferior parietal lobe, the frontal lobe (premotor cortex, supplementary motor area)

Any disease of these areas can cause apraxia, although stroke and dementia are the most common causes

Question 30

What is apraxia caused by

Answer 30

A disorder of skilled movement not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea).
It is caused by the loss of information on how to perform skilled tasks rather than loss of motor command to the muscles.

Question 31

Describe the features of lower motor neurone lesions

Answer 31

Weakness
Hypotonia (reduced muscle tone)
Hyporeflexia (reduced reflexes)
Muscle atrophy
Fasciculations: damaged motor units produce spontaneous action potentials, resulting in a visible twitch
Fibrillations: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination

Question 32

Describe motor neurone disease

Answer 32

Motor Neurone Disease – A disease that affects both UPPER and LOWER motor neurones;
 Motor neurone disease = Amyotrophic Lateral Sclerosis (ALS).
 These are progressive neurodegenerative disorders (can affect upper and then lower or the other way around).

Question 33

Describe ALS

Answer 33

Most common cause of MND

Lesions of both upper and lower

Question 34

What are the key features of MND

Answer 34

Progressive neurodegenerative disorder of the motor system
Spectrum of disorders
Amyotrophic Lateral Sclerosis (ALS)

Question 35

What are the upper motor neurone signs of MND

Answer 35

Increased muscle tone (spasticity of limbs and tongue)
Brisk limbs and jaw reflexes 
Babinski’s sign
Loss of dexterity
Dysarthria
Dysphagia

Question 36

What are the lower motor neurone signs of MND

Answer 36

Weakness
Muscle wasting
Tongue fasciculations and wasting
Nasal speech
Dysphagia

Question 37

Summarise the premotor area

Answer 37

Located laterally in front of M-I. Six-times larger than M-I PMA activity seems to facilitate multiple columns in M-I preparing them for action.

Involved in planning – particularly using external (e.g. visual) cues

Question 38

Summarise the SMA

Answer 38

Supplementary motor area (SMA) (medial region of Brodmann area 6)

Located medially in front of leg area of M-I

Stimulation of neurons in SMA elicits complex movements involving many muscle groups rather than the highly specific movements generated by M-I stimulation. For example movements following SMA stimulation often involve the entire hand or arm or in same cases even postural movements of the whole body.

The SMA is Involved in motor planning of internally driven voluntary movements

SMA lesions result in lack of spontaneous movements and speech

Imaging studies (PET) show activity even when thinking about movement.

Question 39

Summarise the structure and roles of the SMA and PMA

Answer 39

The principal areas of the cerebral cortex concerned with motor control beside the primary motor cortex (M-I) are the supplementary motor area (SMA) and premotor area (PMA).

SMA and PMA are also somatototpically organized.

Intracortical motor pathways. Somatotopically related areas of each of the 3 motor areas are precisely interconnected. The SMA and PMA are reciprocally interconnected and both independently provide reciprocal connection to M-I which receive afferents not only from these motor areas but also from sensory areas.

M-I Stimulation of M-I produces muscles movement at stimulus intensities far lower than those for any other part of the cerebral cortex.

Small group or populations of motor neurons are controlled by small population of cortical neurons. The control is directed at the most distal muscles of an extremity and related to the most
delicate and precise movements, as such is quite specific.

M-I neurons encode the direction of movement. They also encode (via the firing rate) the force of the muscle contraction and the velocity with which a force is applied.

Question 40

Summarise upper motor lesions

Answer 40

Lesion to the descending motor systems cause an unique set of symptoms

This constellation of symptoms is known as UMN lesions

Clinical features:

Spastic weakness, increases muscle stretch reflexes, no signs of muscle denervation, flexion-reflex-afferent driven reflex reversed (sign of Babinski)

Question 41

Summarise the components of the basal ganglia

Answer 41

Basal ganglia: extrapyramidal structure including:
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 ?function
Nucleus accumbens - reward centre
Nucleus basalis of Meynert - ACh-ergic projections to cortex for memory

Question 42

What is the basal ganglia

Answer 42

The basal ganglia lie deep in white matter of cerebral cortex.
Forebrain nuclei

Question 43

What does the striatum consist of

Answer 43

Globus Pallidus

Caudate and Putamen

Question 44

Describe the cross-section of the basal ganglia in the coronal plane

Answer 44

More anteriorly:
can see head of caudate, nucleus accumbens and putamen
as we move more posteriorly, see tail of caudate on walls of lateral ventricle
putamen and caudate seprated by internal capsule
thalamus pushes the structures out more laterally
golbus pallidus (externus and internus) medial to putamen
see diagrams!!

Question 45

Describe the functions of the basal ganglia

Answer 45

Elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)

Moderating and coordinating movement (suppressing unwanted movements)

Performing movements in order

Question 46

Describe the input into the striatum

Answer 46

From the cerebral cortex (SMA, PMA, primary motor cortex, somatosensory and parietal cortex) projections

two pathways possible after this- direct and indirect pathways

Direct Pathway = excitatory on the motor cortex
Indirect Pathway = inhibitory on the motor cortex

Question 47

Summarise the substantia nigra

Answer 47

The substantia nigra lies in the midbrain and is divided into a ventral pale part, the pars reticulata, which projects to the ventrolateral and ventral anterior thalamic nuclei and the superior colliculus, and a dorsal pigmented part, the pars compacta, which projects to the caudate and putamen. These use dopamine for the transmission of information.
The substantia nigra helps to facilitate the role of the direct pathway by activating cells in the putamen, which in turn releases the ventrolateral nucleus from the inhibitory influence of the globus pallidus.

DA fibres in nigro-striatal pathway

Question 48

Outline the direct pathway

Answer 48

Direct corticostriatal loop
Cortex stimulates the striatum
Striatum inhibits the globus pallidus internus, inhibiting its ability to inhibit the thalamus (ventrolateral)
This effectively encourages the thalamus to fire, and thus stimulates the cortex- supplementary motor area

SNr also involved in direct pathway- diagramaticaly joined with GPi.

Question 49

Outline the indirect pathway

Answer 49

Cortex stimulates the striatum
Striatum inhibits the GPe (GABA and enkephalin) reducing the inhibition of the subthalamic nucleus
The GPi is then excited and in turn inhibits output from the VL thalamus to the cortex- the SMA therefore gets less excitation.

Question 50

Describe how the basal ganglia ensure that the correct motor programmes are carried out

Answer 50

The basal ganglia and cortex form a processing loop.
The basal ganglia enable proper motor programmes (stored in the cortex) via the direct pathway (exicitatory)
The basal ganglia inhibit the competing motor programmes via the indirect pathway
In summary, the basal ganglia and its direct and indirect pathways make sure that appropriate motor commands get transmitted down the hierarchy.

Question 51

Connections with which parts of the brain allow the basal ganglia to have a role in enabling various cognitive, executive and emotional programmes?

Answer 51

Prefrontal association cortex

Limbic system

Question 52

Describe a mathematical representation of the direct and indirect pathways

Answer 52

The easiest way to work through this is mathematically. The direct pathway consists of two inhibitory synapses (let us call them −1). When −1 is multiplied by itself we get +1 (−1 × −1 = +1); therefore the facilitation of movement. The indirect pathway has three inhibitory synapses therefore −1 × −1 × −1 = − 1. Thus the indirect pathway when activated inhibits movement.

Question 53

Describe the pathophysiology of PD

Answer 53

In Parkinson’s disease the degeneration of dopaminergic cells in the substantia nigra (SNc) causes loss of dopaminergic terminals in putamen and to lesser extent in caudate. Loss of dopamine to the striatum results in less inhibition of the GPi/SNr and consequently increased inhibitory output from GPi/SNr to the thalamus.
Too much inhibition of thalamus produces decreased facilitation to the motor cortex (particularly SMA): this results in delays in the initiation of movements, slowness of movements (bradykinesia) which are the typical symptoms of Parkinson’s disease.

The lack of excitatory input interferes with the ability of the motor cortex to generate commands for voluntary movement, resulting in poverty of movement.

Question 54

Describe the progressive loss of neurones in PD

Answer 54

It is caused by the progressive depletion of dopaminergic neurones
NOTE: symptoms only appear When 60-80% of the dopamine cells in the substantia nigra have died

Question 55

What may cause the neurodegeneration in PD

Answer 55

Lewy bodies
alpha-synuclein deposits- can effect cognition too

lose neuromelanin- SN becomes pale- ‘locus classicus’

Question 56

What was the original description of PD

Answer 56

“Shaking palsy (paralysis agitans) Involuntary motion, with lessened muscular power, in parts not in action even when supported, with propensity to bend the trunk forward, and to pass from a walking to a running pace: the senses and the intellect being uninjured

Question 57

Describe the main motor signs of PD

Answer 57

Bradykinesia
slowness of (small) movements (doing up buttons, handling a knife)
Hypomimic face
expressionless, mask-like (absence of movements that normally animate the face)
Akinesia
difficulty in the initiation of movements because cannot initiate movements internally
Rigidity
muscle tone increase, causing resistance to externally imposed joint movements
Tremor at rest
4-7 Hz, starts in one hand (“pill-rolling tremor”); with time spreads to other parts of the body

Question 58

Describe the Parkinsonian gait

Answer 58

Walking slowly, small steps, shuffling feet, reduced arm swing
Stooped posture with head and body bent forwards and downwards

Question 59

Summarise the pathophysiology of Huntington’s disease

Answer 59

In Huntington’s disease the degeneration of spiny GABA neurons in the striatum (mainly caudate) results in reduced GABAergic inhibition of GPe and consequently increased
Inhibitory output from GPe to STN, the facilitatory output from STN to GPi/SNr is reduced and there is less inhibitory output from Gpi/SNr to the thalamus. The lack of inhibitory control of
the thalamus on the motor cortex results in unwanted, involuntary movements (dyskinesias and chorea) which are typical of Huntington’s disease.

Question 60

What causes the pathology in Huntington’s

Answer 60

Genetic neurodegenerative disorder
Chromosome 4, autosomal dominant- encodes huntingtin
CAG repeat (>35)
Degeneration of GABAergic neurons in the striatum, caudate and then putamen

Question 61

Describe the motor signs in Huntington’s

Answer 61

Choreic movements (Chorea)
rapid jerky involuntary movements of the body; hands and face affected first; then legs and rest of body (MND s distal to proximal)-
Speech impairment
Difficulty swallowing
Unsteady gait
Later stages, cognitive decline and dementia

Question 62

Where is the cerebellum located and how are the cerebellar hemispheres connected

Answer 62

Cerebellum: posterior to fourth ventricle (posterior aspect of the pons)
Connections: transverse fibres run to pons

Question 63

Summarise the anatomy of the cerebellum

Answer 63

Horizontally divided into 3 lobes: 
§ Anterior. 
§ Posterior. 
§ Flocculonodular. Sagittally divided into 3 zones: 
§ Vermis. 
§ Intermediate hemisphere. 
§ Lateral hemisphere. Connections with the cerebellum are with the SAME side of the body and OPPOSITE cerebral hemispheres. 
§ NT: Glutamate (+), GABA (-

Question 64

Describe the 3 functional units of the cerebellum

Answer 64

The flocculonodular lobe (vestibulocerebellum) involved in the control of posture and eye movements.
•
The vermis with the intermediate part of the hemisphere or paravermis (together known as the spinocerebellum), involved in the control of both postural and distal muscles.
•
The lateral part of the hemisphere (cerebrocerebellum) involved in coordination and planning of limb movements (in conjunction with the basal ganglia)

Question 65

Describe the cortical structure of the cerebellum

Answer 65

Cortical structure: only three layers
Outermost - molecular layer; few neurones
Middle - piriform layer; Purkinje cells - project to nuclei in white matter, huge dendritic trees (receive inputs)
Innermost - granular layer; small neurones involved in processing

Purkinje cells output to the nuclei in the white matter.

Question 66

Describe the 3 sources of input to the cerebellum

Answer 66

mossy fibres from spinocerebellar pathways
climbing fibres from inferior olive
mossy fibres from pons bringing information from cerebral cortex (these are called corticopontine connections and cross over after synapsing in the pons).
Inferior olive projects to Purkinje cells via climbing fibres
All other input to granule cells via mossy fibres and then onwards via parallel fibres

Question 67

Describe output from the cerebellum

Answer 67

All output from Purkinje cells via deep nuclei
fastigial nucleus (involved in balance and has connections with vestibular and reticular nuclei)
interposed
dentate nuclei are both involved with voluntary movement – they have projections to thalamus and red nucleus

Question 68

Summairse the vestibulocerebellum

Answer 68

The vestibulocerebellum receives information from the vestibular nuclei (changes in head position relative to body position and gravity) and visual information from the lateral geniculate nuclei, superior colliculi and visual cortex. It projects to the vestibular nuclei, and thence to the oculomotor centres, and is involved in the control of axial muscles (balance) and the coordination of head and eye movements.

Question 69

Describe the role of the vestibulocerebellum

Answer 69

Regulation of gait, posture and equilibrium

Coordination of head movements with eye movements

Question 70

Describe the functions of the spinocerebellum

Answer 70

Coordination of speech
Adjustment of muscle tone
Coordination of limb movements

Question 71

Summarise the spinocerebellum

Answer 71

The spinocerebellum receives its main input from the spinocerebellar tract and is concerned with the control of postural muscle tone (by setting GMN drive which affects alpha motor neuron activity through the reflex loop) and movement execution.
The vermis receives information from auditory, visual and vestibular systems, and sensory information from the proximal body. It projects to the ventromedial descending motor pathway and reticular formation.
The intermediate hemisphere receives sensory information from the distal body and projects through the red nucleus (via the superior olive) and thence to the descending rubrospinal tract. It also projects to the contralateral motor cortex (via the thalamus).

Question 72

Describe the function of the cerebrocerebellum

Answer 72

Coordination of skilled movements
Cognitive function, attention,
processing of language
Emotional control

Question 73

Where does the cerebrocerebellum receive inputs from

Answer 73

t receives projections from the cortex 
Main functions are: 
· Coordination of skilled movements 
· Cognitive function 
· Attention 
· Processing of language 
· Emotional control

Question 74

Describe vestibulocerebellar syndrome

Answer 74

Vestibulocerebellar Syndrome
Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)
ataxic gait:- wide based stance (looks drunk)
imbalance when eyes closed (Romberg sign)
nystagmus

Question 75

Describe spinocerebellar syndrome

Answer 75

Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)
Disorder: hypotonia

Question 76

Describe cerebrocerebellar or lateral cerebellar syndrome

Answer 76

Damage affects mainly arms/skilled coordinated movements (tremor) and speech

Tremor and clumsy movements: Movements overshoot or undershoot target (dysmetria)
Coordination problems (dysdiadochokinesia).

Question 77

Describe some deficits that may be apparent upon movement in cerebellar dysfunction

Answer 77

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 (knocking over a cup rather than grabbing it)
Intention tremor
Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
Dysdiadochokinesia
Inability to perform rapidly alternating movements, (rapidly pronating and supinating hands and forearms)
Scanning speech
Staccato, due to impaired coordination of speech muscles

Question 78

State an acquired and inherited form of cerebellar dysfunction

Answer 78

Hereditary – Friedreich’s Ataxia

Acquired – Multiple Sclerosis

Question 79

Summarise neural transmission in the basal ganglia

Answer 79

§ The basal ganglia mediate function of the ipsilateral (same side) cortex.
§ Main NTs; Dopamine (+), Glutamate (+), ACh (+), GABA (-).