Motor Disorders Flashcards

1
Q

Where is the cerebellum located

A

In posterior cranial fossa
Inferior to occipital lobe, separated by tentorium cerebelli
Posterior to Pons, separated by 4th ventricle

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2
Q

What are the structural divisions of cerebellum

A
Anatomical lobes:
Anterior lobe
Posterior lobe
Flocculonodular lobe 
Separated by primary fissure and posterolateral fissure 

Anatomical zones:
Vermis
Intermediate zone
Lateral hemispheres

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3
Q

What are the functional divisions of cerebellum

What are their functions

A

Vestibulocerebellum:
Balance and ocular reflex (fix gaze)
Input from vestibular system, output to vestibular nuclei

Spinocerebellum:
regulate movements by error correction (enable reliable delivery of signals over unreliable channels)

Cerebrocerebellum:
planning movements, motor learning, coordination of muscle activation
Input from cortex and pontine nuclei, output to Thalamus and red nucleus

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4
Q

What is the overall function of cerebellum

A

Coordination
Precision of movements
Motor learning

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5
Q

What is the blood supply of cerebellum

A

Superior cerebellar artery
Anterior inferior cerebellar artery
Posterior inferior cerebellar artery

SCA + AICA from basilar artery
PICA from vertebral artery

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6
Q

What are possible causes of cerebellar dysfunction

A
Stroke/TIA
Tumours (can cause hydrocephalus)
Thiamine deficiency 
Toxins: alcohol, barbiturates,phenytoin 
Multiple sclerosis
Infection: meningo-encephalitis, HIV
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7
Q

What are the clinical features of cerebrocerebellum and spinocerebellum lesion

A
IPSILATERAL signs: 
Dysdiadochokinesia / dysmetria 
Ataxic gait  
Nystagmus 
Intention tremor 
Slurred speech 
Hypotonia
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8
Q

What is dysdiadochokinesia

A

Difficulty in carrying out rapid alternating movements

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9
Q

What is dysmetria

A

Lack of coordination characterised by overshooting of hand past intended position

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10
Q

What is ataxic gait

A

Wide and slow gait with tendency to fall on side of lesion

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11
Q

What is nystagmus

A

Involuntary eye movement, maximal on gaze towards lesion

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12
Q

What is intention tremor

A

Tremor when attempting voluntary and precise movements

Amplitude increases as you reach the target

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13
Q

How might lesion in vestibulocerebellum manifest

A

Loss of balance

Abnormal gait with a Wide stance

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14
Q

How might midline lesions present

A

Truncal ataxia on ipsilateral side

Hydrocephalus: compression of 4th ventricle, leading to signs of raised ICP

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15
Q

How might a cerebral hemisphere lesion present

A

Limb ataxia on Ipsilateral side

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16
Q

What is ataxia

A

Lack of coordination of voluntary movement, involving balance, coordination, speech

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17
Q

What is the basal ganglia

A

Group of subcortical nucleiin forebrain:
Lentiform nucleus (Globus Pallidus interna and externa, Putamen)
Subthalamic nucleus
Caudate nucleus
Substantia nigra pars compacta

18
Q

What is the role of basal ganglia

A

Acts as a feedback circuit, to modulate and refine cortical activation
Main function as editing motor plan: reduce excitatory input to cortex to inhibit excessive movements

19
Q

What does editing motor plan involve

A

Stimulation of direct pathway to facilitate appropriate movements
Stimulation of indirect pathway to inhibit inappropriate/excessive movements

20
Q

How does basal ganglia facilitate appropriate movement

A

Putamen receives cortical input for appropriate movement
Activation of direct pathway
Putamen inhibits Globus Pallidus Interna
Loss of inhibition of thalamus by GPi
Increased thalamic activity
Increased motor cortical activity
Increased descending motor signal / movement

21
Q

How does basal ganglia inhibit inappropriate movement

A
Putamen receives input from cortex (for inappropriate movement) 
Putamen stimulates indirect pathway 
Putamen inhibits GPe 
Loss of inhibition of STN by GPe
Stimulation of GPi
Thalamic inhibition by GPi
Decreased motor cortex stimulation 
Decreased descending motor signal / movement
22
Q

What is the role of substantia nigra pars compacta

A

Regulate Putamen activity by release of dopamine
Dopamine excites direct pathway + inhibits indirect pathway
Overall increased thalamic activity
Increased motor cortical activity and movement

23
Q

What is Parkinsons Disease

A

Progressive neurodegenerative disorder involving degeneration of dopaminergic neurones of Substantia nigra pars compacta

24
Q

Clinical triad of PD

A

Bradykinesia
Tremor
Rigidity

25
Q

Clinical features of PD

A
Bradykinesia 
Tremor
Rigidity
Postural instability 
Shuffling gait 
Reduced facial expression 
Hypophonia
Micrographia 
Lewy body dementia
26
Q

What is bradykinesia

A

Slowness of movement

27
Q

What type of tremor do you get with PD

A
Resting tremor:
Lips and tongue
Pronation-supination of forearm
Flexion-extension of fingers
Pill-rolling - index/middle fingers against thumb pad
28
Q

What is rigidity

What are features of rigidity

A

Stiffness

Cog wheeling - tremor superimposed on rigidity

29
Q

What is Huntington’s disease

A

Autosomal dominant progressive neurodegenerative disorder involving degeneration of GABA neurones of indirect pathway

30
Q

What is the age of onset for HD

A

30-50

31
Q

What are clinical features of HD

A

Chorea
Athetosis
Abnormal eye movements

Personality changes
Dementia

32
Q

What is chorea

A

Increased involuntary movements, Type of hyperkinetic movement disorder
Presents with dance-like movements: not repetitive but flow from one muscle to next

33
Q

What is athetosis

A

Slow, involuntary snake like movements of hands, feet

34
Q

What would occur to the basal ganglia feedback mechanism if STN was damaged

A

Reduced stimulation/activity of GPi
Loss of inhibition of thalamus by GPi
Increased thalamic thus cortical activity
Increased descending motor signals + movement
Hyperkinesia (loss of inhibition)

35
Q

What is a possible cause of STN damage

A

Small vessel stroke

36
Q

How may STN lesion present

A

Ballismus:
Repetitive, large amplitude involuntary movements of proximal limbs.
Movements appear violent, continuous and random

Hemiballismus in stroke
Type of chorea

37
Q

How do you perform a Romberg’s test

A

Ask patient to stand with eyes closed

Look for INCREASED loss of balance

38
Q

What sensory inputs does Balance require

A

Vision
Vestibular function
Proprioception
Balance requires at least 2/3 of inputs

39
Q

What is a Romberg’s test testing

A

Proprioception and vestibular function

Loss of vision on standing means balance is dependent on both proprioception and vestibular function
Loss of balance with no vision means either of the inputs are not working

40
Q

What might Romberg’s test be used to investigate

A

Ataxia

41
Q

What does a +ve Rombergs test mean

A

Ataxia is sensory in nature

42
Q

What does a -ve Romberg’s test mean

A

Ataxia is cerebellar in nature:

Patient is ataxic but no increase in ataxia with eyes closed