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module 202 neuroscience & behaviour > T2 L9 Parkinson's disease > Flashcards

T2 L9 Parkinson's disease Flashcards

1
Q

What is ballismus?

A

High amplitude flailing of limbs on one side of the body

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2
Q

What is the pathophysiology of ballismus?

A

Inhibition of STN so no excitatory signals are produced to GPi so GPi does not inhibit thalamus so thalamus excites cortex

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3
Q

What is the commonest cause of ballismus?

A

Stroke

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4
Q

What is a tic?

A

Brief, repetitive stereotypic movements with premonitory urge

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5
Q

What are the types of tics?

A

Simplex: blinding, coughing
Complex: jumping or twirling
Plus: motor disorder
Coprolalia: swearing

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6
Q

What can help reduce tics?

A

Distraction & concentration

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7
Q

What can make tics worse?

A

Anxiety

Fatigue

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8
Q

What is Tourette syndrome?

A

More severe expression on a spectrum of tic disorders

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9
Q

What other conditions are associated with tics?

A

50% have ADHD
33.3% have OCD
≥50% have anxiety

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10
Q

What are come causes of tic disorders?

A

Complex genetic inheritance

Post infectious immune

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11
Q

What is chorea?

A

Jerky, brief, irregular contractions that aren’t repetitive or rhythmic
Appear to flow from one muscle to the next
Patient appears fidgety / restless

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12
Q

What is the pathophysiology of chorea?

A

Inhibition of STN –> no excitation signal produced to GPi so no signal to thalamus which causes it to excite cortex

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13
Q

What are some causes of chorea?

A

Huntington’s disease

Drugs- neuroleptics

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14
Q

What is the genetics of Huntington’s disease?

A

Trinucleotide repeat on chromosome 4
Autosomal dominant with complete penetrance
Longer the repeat sequence the earlier the disease presents
Normal is 10-28 repeats
Disease is 36-121 repeats.

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15
Q

What is the clinical presentation of Huntington’s disease?

A

Cognitive - inability to make decisions, multitasking, slowness of thought
Behavioural -irritability, depression, apathy, anxiety, delusions
Physical - chorea, motor persistence, dystonia, eye movements

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16
Q

What is myoclonus?

A

Brief movement
Rapid onset & offset
Positive or negative

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17
Q

What is the pathophysiology of myoclonus?

A

Unknown
Possible imbalance between excitatory & inhibitory neurotransmitters as it is treatable with anti epileptic drugs
Perturbations of motor control system leading to brief disequilibrium which explains why it is present at multiple levels

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18
Q

What are the causes of myoclonus?

A

Juvenile myoclonic epilepsy
Brain hypoxia
Prion disease

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19
Q

What is dystonia?

A

Abnormal twisting posture associated with jerky tremor

Often axial, facial, trunk

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20
Q

What is the pathophysiology of dystonia?

A

Unknown
Functional PET studies suggested abnormal activity in motor cortex, supplementary areas, cerebellum & basal ganglia
Abnormal activity in basal ganglia suggested by dystonia being caused by blocking dopamine receptors & some dystonia being levodopa responsive

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21
Q

What are the causes of dystonia?

A 
Stroke
Brain injury
Encephalitis
Parkinson's disease
Huntington's disease
22
Q

What is a tremor?

A

Involuntary, rhythmic, sinusoidal alternating movements of part of the body
Affect different parts of the body
Different occurrence e.g. rest, postural, kinetic

23
Q

What is the pathophysiology of a tremor?

A

Postulated theory is increased activity in cerebothalamocortical circuit
PD: dopamine dysfunction in pallidum
ET: GABAergic dysfunction in cerebellum

24
Q

What are the types of drug treatment for hyperkinetic movement disorders?

A

Dopamine (D2) receptor blocking agents
Dopamine depleting agents
Atypical anti-psychotics

25
Q

What are some examples of dopamine receptor blocking agents?

A

Haloperidol
Chlorpromazine
Pimozide
Risperidone

26
Q

What are some examples of dopamine depleting agents?

A

Tetrabenazine

Reserpine

27
Q

What are some examples of atypical antipsychotics?

A

Clozapine
Olanzapine
Aripiprazole

28
Q

What is an ocylogyric crisis?

A

Very characteristic acute response to certain drugs
Fixed stare, upward deviation of eyes
Neck extension
Trunk extension
Jaw spasms & possible tongue protrusion
Acute dystonic reaction

29
Q

What is neuroleptic malignant syndrome?

A 
Acute medical emergency due to D2 blocking drugs
Rigidity / muscle breakdown - raised CPK
Fever
Autonomic instability
Confusion
30
Q

What is Parkinsonism?

A

Akinetic rigid syndrome

Symptoms: slowness of movement, stiffness, shaking

31
Q

What are the physical signs of Parkinsonism?

A

Slowness & poverty of movement
Voluntary movements are harder to initiate
Rigidity
Rest tremor

32
Q

What are the non-motor signs of Parkinsonism?

A

Mood - depression, anxiety
Dementia - slowed thought, mental inflexibility
Autonomic involvement - postural hypotension, hyper salivation
Sleep disturbance - restless legs, REM, parasomnia

33
Q

What are the neurodegenerative causes of Parkinsonism?

A

Idiopathic - Parkinson’s disease
Diffuse lewy body disease
Atypical parkinsonism
Multiple system atrophy, progressive supra nuclear palsy, corticobasal degeneration

34
Q

What are the secondary causes of Parkinsonism?

A

Drugs - haloperidol, MPTP
Cerebrovascular disease
Hydrocephalus
Toxicity / metal deposition disorders

35
Q

What are the genetic causes of Parkinsonism?

A

Metabolic - Wilson’s disease

Rare familial causes

36
Q

What is the pathophysiology of Parkinsonism?

A

Decreased dopamine input –> reduced activation of direct pathway & reduced inhibition (higher activity) of indirect pathway. This leads to reduced movements.

37
Q

What is Parkinson’s disease?

A

Neurodegenerative condition primarily affecting dopaminergic cells of substantial nigra

38
Q

What is the histological hallmark of Parkinson’s disease?

A

Lewy bodies

39
Q

What were some early drug therapies for Parkinson’s disease?

A

Amatadine - initially anti flu agent. Glutamate agonist
Anticholinergics - procyclidine, benzhexol. Limited by side effects
Mono-amine oxidase inhibitors

40
Q

What are monoamine oxidase inhibitors?

A

Prevent breakdown of monoamine chemical transmitters

2 isoforms: MAO-type A (serotonin, adrenaline, noradrenaline, dopamine). MAO-type B (dopamine)

41
Q

What is non selective MAO-I used for?

A

Depression (moclobemide)
Rarely used due to problems metabolising dietary amines / tryptophan leading to risk of hypertensive crisis from cheese, red wine & marmite

42
Q

What is more selective MAO-IB used for?

A

Parkinson’s disease
Selegiline, rasagiline
No dietary restrictions

43
Q

What is entacapone / tolcapone used for?

A

Reduced peripheral metabolism of L-DOPA. Also reduces central but to a lower extent

44
Q

What are the pros & cons of entacapone / tolcapone?

A

Pros: increases duration & efficacy of action of L-Dopa
Good for wearing off with L-Dopa inbetween doses

Cons: makes dyskinesia worse, diarrhoea
Liver disease with tolcapone

45
Q

Where is L-DOPA absorbed?

A

Duodenum

46
Q

What affects L-DOPA absorption?

A

Poor gastric motility / constipation & diet / protein load

47
Q

What do dopamine agonists do?

A

Bypass degenerating nigrostriatal neurons
Directly activate dopamine receptors
No need for enzymatic conversion
More stable & longer acting

48
Q

What are the pros of amorphine?

A

Very instant effect as given by s/c infusion

Reduces dyskinesia by allowing continuous dopaminergic stimulation

49
Q

What are the cons of amorphine?

A

Only for right patients

Skin nodules

50
Q

What is the favoured target for deep brain stimulation?

A

Subthalamic nucleus for Parkinson’s disease
Pallidum for dystonia
Thalamus for tremor

51
Q

What is the future for non-drug therapies?

A

Neurorestorative (stem cells)

Neuroprotective (growth factors)

module 202 neuroscience & behaviour (39 decks)

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