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Neurology > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

What is the extrapyramidal system?

A

Part of the motor system network causing involuntary actions i.e. autonomic control of the muscles

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2
Q

What makes up the extrapyramidal system?

A

Basal ganglia: modulate fine motor planning and sequencing

Thalamus: processes information between basal ganglia and cerebral hemispheres

Brainstem nuclei: form the descending spinal pathways responsible for posture, muscle tone and reflexes

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3
Q

Which neurtransmitter is implicated in most movement disorders?

A

DA

Excess: Huntington’s

Deficiency: Parkinson’s

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4
Q

Examples of movement disorders

A

Parkinson’s

Huntington’s

MS

MND

SMA

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5
Q

Classic presentation of Parkinson’s

A

68 year old male with tremor in left hand

Slowing of movements and increasing stiffness in arms and legs

Unilateral tremor, worse at rest

Difficulty starting movements

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6
Q

Key differentials when presented with a patient who may have Parkinson’s

A

Drug-induced symptoms

Vascular parkinson’s

Parkinson’s plus syndrome

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7
Q

Epidemiology of Parkinson’s

A

20 in 100,000

Peak age 75yrs

Higher in non smokers

15% have FHx (park2 gene mutation associated with early onset)

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8
Q

Aetiology of Parksinon’s

A

Decrease in DA neurones in sub. nigra pars compacta (we also have a pars reticulata which contains GABAergic neurones)

  • 15% have 1st degree FHx
  • Loss of DA neurones is combined with accumulation of alpha synuclein in Lewy bodies which collect in neurones that remain - causing them to become defective

Decreased DA signalling leads to an increase of inhibitory output from the basal ganglia leading to hypokinesis

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9
Q

What are the clinical features of Parkinson’s?

A

Hyperkinetic motor features

Resting tremor (asymmetrical at start), restless legs syndrome (can precede diagnosis by many yrs), acting out dreams in sleep

Hypokinetic motor features

Bradykinesia/ akinesia, micrographia, rigidity, postural instability, difficulty with fine motor skills, loss of spontaneous blinking + serpentine stare 🐍

Bradykinesia

Shuffling gait, difficulty initiating movement, no arm swinging when walking, pausing at door frames

Non-motor features

Anosmia (90%), sleep disorders, dementia, depression, psychosis

Autoimmune features

Bladder and bowel dysfunction, dystonia, postural hypotension

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10
Q

Which symptoms of Parkinson’s often precede the others?

A

Restless legs and anosmia

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11
Q

Which system is associated with rigidity?

A

Rigidity = increased tone in all muscles, associated with the extrapyramidal system

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12
Q

What is spasticity?

A

Increased tone in the upper limb flexors and lower limb extensors associated with the pyramidal system/ UMN dysfunction

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13
Q

Investigations for Parkinson’s

A

Bedside: congitive test to exclude dementia, ask about sense of smell

Bloods: LFTs/ copper studies: exclude Wilson’s

Imaging: SPECT - shows dopamine levels in basal ganglia: people with PD and Parkinson’s + show symmetrical reduced uptake whereas drug-induced uptake is symmetrical and normal

MRI: can be used to identify specific patterns of gegeneration in Parkinsons + syndromes

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14
Q

Parkinson’s differentials

A

Resting tremor: different from cerebellar and essential tremor as these are both worse on movement - do cerebellar tests

Rigidity and not spasticity (rigidity = increased tone in both directions, not velocity dependent etc)

Drug induced: antipsychotics

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15
Q

What is the Glabellar tap?

A

Repetitively tap patients nose - after a while they should stop blinking but patients with Parkinson’s continue to blink

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16
Q

What has to be present for the diagnosis of Parkinson’s?

A

Bradykinesia

+ one of:

  • Tremor
  • Rigidity
  • Postural instability
17
Q

MRI findings in Parkinson’s plus

A

Midbrain atrophy: prpgressive supranuclear palsy

Parietal cortex atrophy: corticobasal degeneration

Pontocerebellar tract atrophy: multiple systems atrophy

18
Q

Principles of management of Parkinson’s

A

Requires management of both hyperkinetic and hypokinetic symptoms, mood and sleep disturbance

Treatment started early because it has long term benefits

19
Q

Medical management of Parkinson’s

A

Levodopa - dopamine precursor 1st line for those who have a reduced QoL due to motor symptoms

  • Then add dopamine agonists or monoamine oxidase B inhibitors if needed
  • Modafanil for daytime sleepiness
  • Orthostatic HTN: review medication
  • Psychosis: quetiapine (only treat if patient unable to cope)
20
Q

Levodopa

A

Precursor of DA, given with carbidopa (dopa decarboxylase inhibitor) which prevents peripheral metabolism allowing it to cross BBB

Benefits: improves hypokineses

Downside: no effect on hyperkinesis and non-motor symptoms

Duration: works for 5-10yrs

Adverse effects: most remains peripheral so GI upset e.g. N&V, stiffness, dyskinesia, ‘on-off effect’ symptoms return before next dose given, psotural hypotension, hallucinations, excessive sleepiness, impaired impulse control, hypersexuality

21
Q

Dopamine agonists

A

Example: ropinirole

DA agonists are 1st line in young patients

Not as efficacious as levodopa

Cause the same adverse effects as levodopa

22
Q

Monoamine oxidase inhibitors

A

E.g. selegiline

Work by preventing breakdown and reuptake of DA, promoting its action for longer

Used to decrease the on-off effect and bridge between doses of levodopa/ DA agonists

Adverse effects: dyskinesia, insomnia

23
Q

Management of non-motor symptoms of Parkinson’s

A

Fludrocortisone: orthostatic hypotension

Laxatives: bowel dysfunction

Anti-cholinergics: bladder dysfunction

Anti-depressants: mirtazapine

Dietician

24
Q

Surgery in management of Parkinson’s

A

Deep brain stimulation: offer to those whose symptoms continue despite use of drugs

Levodopa carbidopa intestinal gel: given via percutaneous pump into jejunum

25
Q

Complications of Parkinson’s

A

Infections: UTIs, URTIs (due to dysphagia)

MI and stroke

Trauma injuries due to falls

26
Q

What can be given to make sure levodopa reaches CNS?

A

Carbidopa - dopa decarboxylase inhibitor, prevents peripheral breakdown of levodopa

Essential because dopamine cannot cross BBB

27
Q

Which genetic condition is often misdiagnosed as Parkinson’s?

A

Wilson disease

Abnormal copper accumulation

Wilson’s tested for in young patients presenting with Parkinson-like features

In Wilson disease: if ceruloplasmin level is low, measurement of 24-hour urinary copper excretion and slit-lamp examination for Kayser-Fleischer rings must be performed.

28
Q

Discuss drug-induced Parkinsonism

A

Depletion of DA activity in basal ganglia, symptoms are symmetrical and tremor is more postural than resting

Causes:

Reserpine, tetrabenzine: deplete pre-synaptic DA, used to treat hyperkinetic movement disorders e.g. Huntington’s

Antipsychotics

Antiemetics: metoclopramide

29
Q

What are the Parkinson + diseases?

A

Group of 4 neurodegenerative disorder that cause Parkinsonism

  1. Multiple system atrophy
  2. Progressive supranuclear palsy
  3. Lewy body dementia
  4. Corticobasal degeneration

*Patients tend to present in their 50-60s

30
Q

How do Parkinson’s + diseases differ from Parkinson’s?

A

Less prominent remor, poor response to levodopa, disease specific symptoms (later mentioned), distincitve MRI changes in Parkinson’s +

31
Q

Multiple systems atrophy

A

One of the parkinson + diseases

  • Stiffness and slowness early on, gradual damage to neurones and proliferation of astrocytes in CNS, loss of neurones in several areas inc. cerebellum

Symptoms

  • Palsy of vocal cords (croaky quivering voice), orthostatic hypotension, impotence, xerostomia, urinary dysfunction

MRI: decreased size of cerebellum and pons hot cross bun sign in pons - think cross, think multiple systems crossing think multiple system atrophy

32
Q

Progressive supranuclear palsy

A
  • Includes difficulty moving eyes: trouble reading as can’t look down
  • Fast walking
  • Bumping into people
  • Falls
  • Disinhibition
  • Anxiety
  • Surprised look

MRI: midbrain and frontotemporal atrophy - hummingbird sign

33
Q

Corticobasal degeneration

A

Sudden onset, higher order dysfunctione.g. sensory loss, acaculia, dementia

Alien hand syndrome in 60% - diagnostic

34
Q

You have a patient with features of Parkinson’s although tremor is not very pronounced - you give them levodopa but they don’t respond. Thoughts?

A

Parkinson+ syndromes don’t respond to levodopa and are less associated with a resting tremor

35
Q

What questions could you ask to differentiate between the types of Parkinson’s?

A

Have you ever had a stroke? Vascular PD

Any risk factors for vascular disease? Smoking, DM, known atherosclerosis

Taking any anti-psychotic medication? Or other causative medication

36
Q

Examination in Parkinson’s

A

Cogwheeling

Tremor worse at rest

Slow at rising from chair

Low, monotonous voice

Face expressionless

When asked to tap hand on table, speed of tap declines progressively

Shuffling gait

Glabbellar tap

37
Q

Prognosis of Parkinson’s

A

Most patients respond well with a period of stability but higher doses of medication required

Increased fluctuations between mobile & immbolie states and dyskinesia

Mid 70s: unresponsive to medications, dysphagia, loss of postural stability, falls

Rate of progression over 10-20yrs

38
Q

Consequence of suddenly stopping Parkinson’s medication?

A

Neuroleptic malignant syndrome

Lack of dopamine triggers massive glutamate release causing neurotoxicity and muscle damage

Pyrexia, muscle stiffness, HTN, tachycardiam agitated, raised CK, AKI due to rhabdomyolysis

39
Q

Name some causes of tremor

A
  • Parkinsonism: worse at rest
  • Essential tremor: worse if arms outstretched, often strong family history, improved by rest
  • Anxiety
  • Thyrotoxicosis: usually combined with weight loss, tachycardia, feeling hot
  • Hepatic encephalopathy
  • Carbon dioxide retention
  • Cerebella disease: intention tremor, past appointing, nystagmus
  • Drug withdrawal

Neurology (23 decks)

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