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NEUROLOGY > EXTRAPYRAMIDAL DISORDERS > Flashcards

EXTRAPYRAMIDAL DISORDERS Flashcards

1
Q

Function of the basal ganglia?

A

It’s like a collection of brakes or accelerators

To fine-tune voluntary movements
It recieves impulses fron the cerebral cortex, processes them and adjusts them and then covey this infromation to the thalamus and then back to the cortex
Ultimately the fine-tuned movement instruction is sent to skeletal muscles via the spinal cord

Also involves in planning, modulation of movements, memory, eye movements, reward processing and motivation

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2
Q

Components of the basal ganglia?

A

Caudate nucleus
Putamen
Nucleus accumbens and olfactory tubercle
Globus pallidus
Subthalamic nucleus
Substantia nigra

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3
Q

Which part of the striatum is part of the basal ganglia?

A

The dorsal striatum

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4
Q

What are the 2 components of the striatum?

A

The caudate nucleus and the putamen

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5
Q

What forms the corpus striatum?

A

The striatum and the globus pallidus

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6
Q

Input nuclei of the basal ganglia?

A

The striatum and the caudate nucleus

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7
Q

What is the nucleus accumbens?

A

The most cranial aspect of the striatum where the caudate nucleus and the putamen join together

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8
Q

Function of striatum?

A

It recieve excitatory glutamatergic inputs from the cerebral cortex.
The synapsing pattern reflects topography of the cortex e.g. caudal parts of the cortex project to the caudal part of the brain the striatum

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9
Q

Structure of the caudate nucleus?

A

Consists of a head, tail and the body
Terminates by connecting with the amygdala at the tail of the caudate nucleus

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10
Q

Function of the caudate nucleus?

A

Integrates sensory information about the spatial position of the body and according to that sends infromation about necessary fine tunes of motor response to that stimuli to the thalamus
Also contributes to body & limb posture and speed &accurary of directed movements

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11
Q

Intrinsic nuclei of the basal ganglia?

A

External globus pallidus
Subthalamic nuclei
Pars compacta of the substantia nigra

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12
Q

Output nuclei of the basal ganglia?

A

Internal globus pallidus
Pars reticulata of the substantia nigra

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13
Q

Function of putamen?

A

To regulate motor functions and influence various types of learning
It uses dopamine

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14
Q

What are the 2 divisions of the globus pallidus?

A

The internal globus pallidus and the external globus pallidus

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15
Q

What are the 2 components of the substantia nigra?

A

The pars compacta and the pars reticulata

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16
Q

Function of the substantia nigra pars compacta?

A

Output to the basal ganglia circuit, supplying the striatum with dopamine through specific D1 and D2 neurones within the nigrostriatal pathways

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17
Q

Function of the substantia nigra pars reticulata?

A

Serves as input - conveys signals from the basal ganglia to the thalamus

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18
Q

Why does the substantia nigra have a dark appearance?

A

Due to the neuromelanin present in the cells in the pars compacta

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19
Q

Arterial supply to the basal ganglia?

A

Middle cerebral artery - main aretry is the lenticulostriate artery

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20
Q

Direct pathway of basal ganglia structure

A

Glutamate neurones project from the thalamus to motor regions of cerebral cortex = excitatory = stimulates movement

Neurones from the globus pallidus internal and substantia nigra pars reticulata project to the thalamus and release GABA = inhibition = suppression of movement to prevent unwanted movements from occurring

Infromation from movement is sent from cortex to striatum via the corticostriatal pathway. Glutamate nuyerones excite neurons on the striatum. Activated stiatam neurones release GABA in the globus pallidus internal and substantia nigra pars reticulata = inhibition of these regions = stops inhibition of neurones in the thalamus which are involved in movement = movement can occur!

Neurones from the substantia nigra pars compacta travel to the striatum via the nigrostriatal pathway and release dopamine in the striatum = facilitates activity in direct pathway

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21
Q

Indirect pathway of the basal ganglia structure

A

GABA neurones project from globus pallidus external to the Subthalamic nucleus = inhibition on glutamate neurones in Subthalamic nucleus

Signals from cerebral cortex causes activation of GABA neurones in the striatum which projects to the globus pallidus external and inhibits thr activity of neurones there. This prevents globus pallidus external neurones from inhibiting the neurones in the Subthalamic nucleus

Projections from the cortex activate the Subthalamic nucleus neurones and stimulate GABA neurones in the globus pallidus internal and substantia nigra pars reticulata = project to the thalamus = inhibits thalamic neurones that travel the motor regions of the cerebral cortex to stimulate movement = therefore inhibits movement

This antagonises the activity of the direct pathway and acts to keep unwanted movements from occurring

Neurones from the substantia nigra pars compacta travel to the striatum via the nigrostriatal pathway. These can modulate the activity of the indirect pathway through dopamine release in the striatum = inhibition of activity in indirect pathway = facilitation of movement

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22
Q

What broadly causes movement disrders?

A

Disturbance of the cerebellum and extrapyramidal system e.g. basal ganglia, thalamus, Subthalamic nuclei and red nucleus

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23
Q

Positive symptoms of movement disorders?

A

Chorea
Athetosis
Ballismus
Dystonia
Tremor
Rigidity

(Due to disinhibition of undamaged parts of the motor system)

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24
Q

Negative symptoms of movement disorders?

A

Hypokinesia and bradykinesia

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25
Q

What is a tremor?

A

An involuntary, regular, rhythmic, oscillatory movement produced by alternating or irregularly synchronous contractions of antagonistic muscles

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26
Q

Types of tremor?

A

Physiological
Exaggerated physiological e.g. thyrotoxicosis or anxiety
Essential tremor
Dystonic tremor
Cerebellar tremor
Parkinsonian tremor
Functional tremor

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27
Q

What is an essential tremor?

A

An autosomal dominant condition that affects both upper limbs usually

There is often a strong FHx

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28
Q

Features of an essential tremor?

A

It’s a postural tremor i.e. worse if arms are outstretched
Improved by alcohol and rest
It’s the most common cause of titubation (a head tremor)

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29
Q

Why does alcohol improve an essential tremor?

A

Alcohol enhances GABA which is inhibitors and dampens the excessive firing of neurones

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30
Q

Management of essential tremor?

A

Propranolol first line

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31
Q

What is titubation?

A

Head tremor

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32
Q

Type of tremor seen in parkinsonism?

A

Resting, pill-rolling tremor

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33
Q

Causes of tremor?

A

Parkinsonism
Essential tremor
Anxiety
Thyrotoxicosis
Hepatic encephalopathy
CO retention
Cerebellar disease
Drug withdrawal e.g. alcohol or opiates

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34
Q

What type of tremor does cerebellar disease cause/

A

An intention tremor

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35
Q

What is an intention tremor?

A

Involuntary, thyroid muscle contractions that occur during purposeful, voluntary movement e.g. reaching for something
Most commonly affects the upper limbs

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36
Q

What is myoclonus?

A

A brief, involuntary, shock-like contraction of a group of muscles; Irregular in rhythm and amplitude, asynchronous and asyemmetrical

Can cause whole body to jerk or just an area

Caused by abnormal discharges in the CNS of motor neurones or interneurones

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37
Q

What is chorea?

A

“To dance”
Brief, semi-directed, irregular movements that are not repetitive or rhythmic, but appear to flow from one muscle to the next

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38
Q

What is hemiballismus?

A

Unilateral - affects ipsilateral arm & leg
Intermittent, sudden involuntary large movements

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39
Q

What is athetosis?

A

Slow, involuntary, convoluted, writhing movements of hands and feet
Slow, sinuous movements that flow into 1 another

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40
Q

What is dystonia?

A

Sustained muscle contractions causing abnormal, often repetitive movements or postures
Movements are typically twisting, patterned or tremulous
It can be focal, segmental or generalised
Tremor is often a feature
Often worsened by voluntary movements

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41
Q

Where is the lesion likely in a patient with athetosis?

A

In the lentiform nucleus in the basal ganglia

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42
Q

Where is the lesion likely in a patient with chorea?

A

Caudate nucleus

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43
Q

Causes of chorea?

A

Inherited e.g. huntingtons, Wilson’s
Sydenhams (as a consequence of rheumatic fever)
Hormonal and endocrine - typically oestrogen-related e.g. in pregnancy or SE of contraceptive pill
Degenerative
Drugs e.g. phenytoin, neuroleptics
Structural - stroke, tumours, trauma
SLE
Polycythemia vera

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44
Q

Causes of athetosis?

A

Birth hypoxia or kernicterus
Hepatic encephalopathy

All other causes same as chorea:
Inherited e.g. huntingtons, Wilson’s
Sydenhams (as a consequence of rheumatic fever)
Hormonal and endocrine - typically oestrogen-related e.g. in pregnancy or SE of contraceptive pill
Degenerative
Drugs e.g. phenytoin, neuroleptics
Structural - stroke, tumours, trauma
SLE
Polycythemia vera

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45
Q

Where is the lesion likely to be in a patient who has hemiballismus?

A

Subthalamic nuclei

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46
Q

What is considered the commonest form of tremor?

A

Dystonic tremor

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47
Q

Causes of dystonia?

A

Genetics
Drug-induced e.g. parkinsonian medications and neuroleptics
Related to trauma
Idiopathic

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48
Q

What is parkinsonism?

A

An umbrella term for the clinical syndrome involving bradykinesia plus at least one of tremor, rigidity or postural instability

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49
Q

Causes of parkinsonisms?

A

Parkinson’s disease
Drug induced e.g. antipsychotics and metoclopramide
Degenerative: Progressive supranuclear palsy, Multiple system atrophy
Metabolic: Wilsons disease
Infection: Post-encephalitis, prion disease e.g. cruz-felt Jakob disease
Dementia pugilistica
Toxins e.g. CO, MPTP, mercury

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50
Q

What is dementia pugilistica?

A

A form of chronic traumatic encephalopathy
Caused by chronic head trauma
Commonly seen in boxing

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51
Q

Red flags to diagnosing parkinsonsism and a cause that is not parkinsons disease?

A

Recent use of dopamine blocking drugs
Lack of the typical tremor (resting pill-rolling)
Symmetrical signs (parkinsons is usually asymmetrical i.e. affects 1 side more than the other)
Early cognitive dysfunction
Early balance disturbances eg. In PSNP where people tend to fall backwards
Significant and early autonomic dysfunction e.g. MSA
Poor response to usual parkinsons medications

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52
Q

Dementia with Parkinson’s vs dementia with Lewy body?

A

The only real difference is that in Lewy body dementia, the dementia occurs first before the motor symptoms (may also have recurrent visual hallucinations & act out dreams)
In parkinsons, the motor symptoms occur first and then dementia follows

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53
Q

What is parkinsons disease?

A

A chronic, progressive neurodegenerative condition resulting from the loss of the dopamine-containing cells of the substantia nigra
The dopamine deficiency within the basal ganglia leads to a movement disorder with classical parkinsonian motor symptoms

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54
Q

How much dopaminergic cell activity must be lost for parkinsons disease to be clinically apparent?

A

At least 50%

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55
Q

Cause of parkinsons?

A

Dopamine denervation due to Lewy body deposition and cell death in the substantia nigra
A large number of extra-nigral and non-dopaminergic brain regions are also affected
Minority of people have a FHx - associated with early-onset i..e <40

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56
Q

Most common cause of parkinsonisms?

A

Parkinson’s disease

57
Q

Epidemiology of parkinsons disease?

A

Common
Mean age of diagnosis is 65
Increases with age - nearly 2% of over 80s
Prevalence higher in men
Lifetime risk is 2.7%

58
Q

Complications of parkinsons disease?

A

Motor complications e.g. deteriorating function, dyskinesia, falls, NMS
Mental health problems
Autonomic dysfunction e.g. orthostatic hypotension, syncope, excessive salivation, sweating, bladder and bowel problems, sexual problems
Sleep disturbances

59
Q

Symptomatic progression of parkinsons disease?

A

In early disease the motor symptoms are usually unilateral
It’s progressive so by later disease its usually bilateral

60
Q

Symptoms of Parkinson’s disease?

A

Resting tremor
Gradual onset progressive bradykinesia
Rigidity

Others:
Postural instability
Gait disorders - shuffling, festination or freezing
Mental health problems - usually depression + insomnia + Cognitive impairment
Anosmia
Hypomima - reduced facial expression
Sleep disturbance
Fatigue
Autonomic dysfunction e.g. postural hypotension, hyperhidrosis
Dysphagia
Drooling
Blurred vision and eye opening ataxia
Constipation & urinary incontinence

61
Q

Describe the bradykinesia seen in parkinsons disease?

A

Slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of sustained repetitive actions e.g. finger tapping

Poverty of movement can also be seen - sometimes referred to as hypokinesia

62
Q

How can hypokinesia present in parkinsons disease?

A

Reduced or flat facial expression
Reduced blinking
Difficulty with fine movements e.g. handwriting, buttoning clothes
Slow, short shuffling gait with reduced arm swinging
Freezing gait

63
Q

Type of rigidity seen in parkinsons disease?

A

Lead-pipe rigidity or cogwheel rigidity

64
Q

What is lead-pipe rigidity?

A

Constant resistance felt when a limb is passively flexed in the presence of increased tone without tremor

65
Q

What is cogwheel rigidity?

A

Cogwheel rigidity refers to resistance that stops and starts as the limb is moved through its range of motion. Like going through the cogs!! This is with a tremor

66
Q

When does the resting tremor in Parkinson’s disease typically improve?

A

On moving, with mental concentration and during sleep

67
Q

What is a pill-rolling tremor?

A

Simultaneous rubbing movements of the thumb and index fingers against each other e.g. appears they are rolling a small object between their fingers

68
Q

Drug causes of parkinsonisms?

A

Antipsychotics - usually first-generation e.g. haloperidol
Anti-emetics e.g. prochlorperazine and metoclopramide

More rarely:
Antidepressants e.g. SSRIs
CCB
Cinnarizine
Amiodarone
Lithium
Cholinesterase inhibitors e.g. donepezil
Sodium valproate
Methyldopa
Pethidine

69
Q

What typically worsens the resting tremor seen in parkinsons?

A

Stress or being tired

70
Q

How can drug-induced Parkinsonism present differently to parkinsons disease?

A

Motor symptoms have a rapid onset and are bilateral
Rigidity and resting tremor are uncommon

71
Q

What can you do if you have difficulty differentiating between an essential tremor and Parkinson’s disease?

A

123I‑FP‑CIT single photon emission computed tomography (SPECT).
A type of functional Neuroimaging that can assess dopamine levels

72
Q

What are the 2 types of multiple system atrophy?

A

MSA-P - predominant parkinsonian features
MSA-C - predominant cerebellar features

73
Q

Features of multiple system atrophy?

A

parkinsonism
autonomic disturbance - erectile dysfunction, postural hypotension and atonic bladder, urinary retention
cerebellar signs - ataxia

74
Q

What is multiple system atrophy?

A

A rare, neurodegenrative disorder characterised by autonomic dysfunction, Parkinsonisms and ataxia
Usually affects ~55
Its caused by progressive degeneration of neurones in the basal ganglia, inferior oligarch nucleus and cerebellum

75
Q

What is progressive supranuclear palsy?

A

Aka Steele-Richardson-olszewski syndrome
It’s a ‘Parkinson Plus’ syndrome

A late-onset (~63) neurodegenerative disease involving gradual deterioration and death of specific volumes of the brain
Involves accumulation of tau protein in the brain

76
Q

Features of progressive supranuclear palsy?

A

Postural instability and falls - tend to have a stiff, broad-based gait. Particularly falls backwards
Impairment of vertical gaze e..g difficulty reading or ascending stairs
Parkinsonism with bradykinesia being prominent - symmetrical
Cognitive impairment - mostly frontal love dysfunction

77
Q

pathophysiology of drug-induced parkinsonism

A

Medications which reduce dopamine levels from the basal ganglia = brain cannot transmit signals to correctly coordinate movement

78
Q

Advice about driving for patients with parkinsons?

A

DVLA days that group 1 and 2 may drive as long as safe vehicle control is maintained at all times

79
Q

First line medical treatment for parkinsons disease if motor symptoms are affecting the patient’s quality of life?

A

Levodopa

80
Q

First line medical treatment for parkinsons if motor symptoms are not affecting the patient’s quality of life?

A

Oral MAO-B inhibitors OR levodopa OR oral/transdermal dopamine agonists

81
Q

Examples of oral MAO-B inhibitors?

A

Selegiline, rasagiline or safinamide

82
Q

Examples of oral dopamine agonists that can be used for parkinsons disease?

A

Pramipexole or ropinirole

83
Q

Example of transdermal dopamine agonist that can be used for parkinsons?

A

Rotigotine

84
Q

Levodopa vs MAO-B inhibitors vs dopamine agonists for Tx of parkinsons?

A

Levodopa typically provides more improvement in motor symptoms and daily functioning, fewer adverse effects but may cause more motor complications
Oral MAO-B usually provide less improvement in motor symptoms and daily functioning, fewer motor complications and fewer adverse effects
Dopamine agonists provide less improvement in motor symptoms and daily functioning, fewer motor complications but more adverse effects e.g. excessive sleepiness, hallucinations and impulse control disorders

85
Q

Specific adverse efefcts of dopamine agonists for parkinsons disease?

A

Excessive sleepiness
Hallucinations
Impulse control disorders

86
Q

What are impulse control disorders?

A

A group of behaviour disorders characterised by impulsivity
E.g. failure to resist an urge or temptation or having an inability to not speak on a thought
E.,g. Gambling or hypersexuality

87
Q

What can be used to manage parkinsons when pt have developed dyskinesia or motor fluctuations despite optimal levodopa therapy?

A

Additional of a dopamine agonist, MAO-B inhibitor or a COMT inhibitor as an adjunct

88
Q

What are COMT inhibitors and give 2 examples?

A

Oral Catechol-O-methyl transferase inhibitors
Entacapone or opicapone

89
Q

Who are impulse control disorders most common in?

A

Can occur with any dopaminergic therapy
More common with:
Dopamine agonist therapy - this doubles the risk!
History of previous impulse behaviours
History of alcohol consumption or smoking

90
Q

How can we medically manage drooling of saliva in Parkinson’s disease?

A

Glycopyrronium bromide

91
Q

Non motor sympotms of parkinsons?

A

Constipation
N&V
Pain
Sleep disturbance and daytime sleepiness
Depression and anxiety
Dementia and cognitive impairment
Impulse control disorders and psychotic symptoms
Orthostatic hypotension
Speech and swallowing problems & weight loss
Excessive salivation and sweating
Bladder and sexual problems

92
Q

How is levodopa given for management of parkinsons motor symptoms?

A

Nearly always given combined with a decarboxylase inhibitor e.g. carbidopa
This prevents the peripheral metabolism of levodopa to dopamine outside of the brain as decarboxylase is the enzyme for this = reduces the SE

93
Q

Common adverse efefcts of levodopa

A

Major: with years of use there is motor fluctuation and dyskinesias

Dry mouth
Anorexia
Palpitations
Postural hypotension
Psychosis
End of dose wearing off : symptoms worsen towards end of dosage interval
On-off phenomenon: large variations in motor performance
Dyskinesias at peak dose

94
Q

What are dyskinesias?

A

Involuntary, erratic movement disorders e.g. dystonia, chorea, athetosis

95
Q

What is important information to give patients about stopping levodopa?

A

It’s important not to acutely stop levodopa as this can cause acute dystonia

96
Q

How do MAO-B inhibitors work to manage Parkinson’s?

A

They inhibit the breakdown of dopamine secreted by dopaminergic neurons in the substantia nigra

97
Q

Moa of COMT inhibitors for parkinsons?

A

COMT is an enzyme involved in the breakdown of dopamine so it can be used as an adjunct to levodopa to improve dopaminergic activity in the substantia nigra

98
Q

Why do we often delay treatment for parkinsons?

A

Treatment does not alter the natural history of parkinsons
It avoids the complications of drugs
We can introduce the drugs according to the patient’s biological age and functional requirements

99
Q

Why is there an argument for not using Anticholinergics for managing parkinsons?

A

They possibly cause cognitive slowing and confusion
They can cause bladder and bowel dysfunction
They must be used with care, especially in the elderly!

100
Q

Why do you have to be cautious about using MAO-B inhibitors in patients with postural hypotension?

A

As it can increase the risk of cardiac arrhythmias and death

101
Q

2 classes of dopamine agonists?

A

Ergot based and non-ergot based

102
Q

What can ergot-based dopamine agonists cause as complications?

A

Impulse disorders
Organ fibrosis e.g. retroperitoneal and lung fibrosis

103
Q

What is the duodopa gel?

A

A combination of levodopa and carbidopa that is administered as a continous infusion via percutaneous jejunostomy tube
Very expensive!

104
Q

How can we manage the wearing off symtpms, and peak/end of dose dyskinesia and dystonia caused by levodopa therapy?

A

Smaller doses more often
Use in conjunction with other classes of medication to limit total amoutn of levodopa

105
Q

Main side efefcts of COMT inhibitors?

A

Severe diarrhoea especially with entacapone
Can worsen dyskinesia

106
Q

What is hedonistic homeostatic dysregulation?

A

Neuropsychological behaviour disorder associated with substance misuse and addiction

107
Q

How common is cognitive impairment in parkinsons disease?

A

At least 50% of sufferers have some cognitive impairment within5. Years

108
Q

Management of cognitive impairment in parkinsons?

A

Atypical antipsychotics (note you can’t use typical antipsychotics as they are dopamine blocking so worsen motor symptoms)
Cholinesterase inhibitors
Memantine if cardiac arrhythmia or mod-sev dementia

109
Q

Why can parkinsons disease cause hypersalivation and drool?

A

As there can be reduced automatic actions e,g. Swallowing
This creates an inability to manage the flow of saliva

110
Q

Sleep disorders common in parkinsons?

A

Fragmented sleep
Vivid & disturbing dreams
REM sleep behaviour disorder
Restless limbs and akathisia
Daytime hypersomnolence
Obstructive sleep apnoea
Pains nd bladder dysfunction as well as problematic parkinsons Sx can keep pt up

111
Q

Red flags suggesting its not parkinsons?

A

Early balance problems
Symmetrical signs
Opthalmoparesis
Associated pyramidal and cerebellar signs
Absence of resting tremor
Early onset of dementia
Profound autonomic dysfunction
Rapid disease progression
Poor response to levodopa

112
Q

What is a DaTSCAN?

A

A brain scan to diagnose parkinsons disease and differentiate parkinsons syndromes with other diseasese e.g. dementia

113
Q

surgical options for management parkinsons

A

Thalamotomy - surgical destruction of thalamus. Best for drug-resistant tremor
Pallidotomy - surgical destruction of the globus pallidus
Deep brain stimulation
Cell transplants

114
Q

What is deep brain stimulation?

A

A surgical procedure that implants a neurostimulator and electrodes which send electrical impulses to specified targets in the brain responsible for movement control
Can help with parkinsons, essential tremor, dystonia and some neuropsychiatric conditions too

115
Q

What is cell transplant for parkinsons disease?

A

The transplantation product is generated from embryonic stem cells and functions to replace the dopamine nerve cells which are lost in the parkinsonian brain
A new treatment that is still under research process

116
Q

MDT for parkinsons disease?

A

Specialist nurses
PT
OT
Speech therapy
Support groups
Dieticians
Social services
Continence advisors
Psychiatric

117
Q

What is Braak’s hypothesis?

A

That sporadic parkinsons disease is caused by a pathogen that enters the body via the nasal cavity and subsequently is swallowed and reaches the gut, initiating lewy pathological in the nose and digestive tract

118
Q

2 enzymes involved in breaking down dopamine?

A

MAO
COMT

119
Q

What is Parkinson’s UK?

A

A charity that funds research to find a cure and help ensure everyone understands the real impact of parkinsons

120
Q

What is Parkinson’s Europe?

A

A charity that works with and campaign with people with parkinsons
They advocate, raise awareness and work with other global parkinsons organisations to provide current info, share good practices and highlight research

121
Q

What is Huntington’s disease?

A

An autosomal dominant genetic condition that causes progressive neurological dysfunction
It’s progressive and incurable.

122
Q

Prognosis of Huntington’s disease?

A

Typically results in death 20 years after initial symptoms develop

123
Q

Genetics of Huntington’s disease?

A

Autosomal dominant
A trinucletodie repeat disorder: repeat exapansion of CAG (this means anticipation may be seen)
Due to a defect in huntingtin gene on chromosome 4 which codes for huntingtin protein

124
Q

What is anticipation?

A

A feature of trinucletodie repeat disorders where successive generations have more repeats in the gene resulting in earlier age of onset and increased disease severity

125
Q

Pathophysiology of Huntington’s disease?

A

Genetic mutation results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia

126
Q

What age does Huntington’s disease occur?

A

After 35 years of age
Usually 30-50

127
Q

Presentation of Huntington’s disease?

A

Chorea
Dystonia
Saccadic eye movements
Personality changes e.g. irritability, apathy, depression
Intellectual impairment
Dysphagia

128
Q

Rigidity vs spasticity cause?

A

Rigidity - extrapyramidal disorders
Spasticity - UMN lesion

129
Q

Diagnosis of Huntington’s disease?

A

Genetic testing

130
Q

Management of Huntington’s disease?

A

Genetic counselling
Physiotherapy to improve mobility, maintain joint function and prevent contractures
SALT
Tetrabenazine for chorea
Manage mental health conditions

Advanced directives and end-of-life care

131
Q

What typically causes death in Huntington’s disease?

A

Aspiration pneumonia
(Note suicide is also a common cause)

132
Q

Pathophysiology of parkinsons disease?

A

Progressive degeneration of dopaminergic neurones within the pars compacta of the substantia nigra in the midbrain for many reasons (not really known)
Lewy bodies (eosinophilic intraneuronal inclusions) are found in the surviving neurones

Nigral cells projecting to the striatum in the nigrostriatal pathway are mostly affected = loss of dopamine in striatum = movement is not smooth, coordinated or controlled

133
Q

What are Parkinson plus syndromes?

A

Other forms of parkinsonism that have clinical features that are not typical of parkinsons disease
Progressive supranuclear palsy, multi system atrophy and corticobasal degeneration

134
Q

What is corticobasal degeneration?

A

A rare disorder characterised by strikingly unilateral involvement with rigidity and dystonia in arms. Can also cause an “alien” arm, tremors, ataxia, slow slurred speech, dementia, difficult swallowing
Areas of the brain die and shrink

135
Q

Which dopamine receptors are excitatory and which are inhibitory?

A

Excitatory - D1-class receptors
Inhibitory - D2-class receptors

136
Q

Risk factors for parkinsons disease?

A

FHx
Genetics
Pesticides

137
Q

Protective factors for parkinsons disease?

A

Smoking
Coffee
Vigorous exercise
Nicotine
Use of NSAIDs
Omega 3 fatty acids

138
Q

why shouldn’t parkinsons medications be stopped abruptly?

A

Can cause dopamine agonist withdrawal syndrome
May also cause acute dystonia

139
Q

Symptoms of dopamine agonist withdrawal syndrome?

A

Anxiety and panic attacks
Dysphoria - sense of unease due to a mismatch between biological sex and gender
Depression
Agitation
Irritability
Suicidal ideation
Fatigue
Orthostatic hypotension
N&V
Diaphoresis
Generalised pain
Drug cravings

NEUROLOGY (16 decks)

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