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Nervous System > Lecture 8.2: Parkinson’s Disease (and some other motor disorders) > Flashcards

Lecture 8.2: Parkinson’s Disease (and some other motor disorders) Flashcards

1
Q

What is Parkinson‘s Disease?

A

Chronic Progressive Neurodegenerative disorder that affects the dopaminergic neurons within the substantia nigra as a result, body movements are affected

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2
Q

Parkinson’s: TRAP

A

Tremor (usually starts on 1 side)
Rigidity (stiffness of limbs, neck or trunk)
Akinesia (loss/impairment in power of voluntary mvt)
Posture & Balance

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3
Q

Aetiology of Parkinson‘s Disease (7)

A
  • Mostly Idiopathic (95%)
  • Rarely Genetic (autosomal dominant & recessive)
  • Medicine Related
  • Toxins
  • Vascular (multiple white matter infarcts)
  • Traumatic
  • Post-Infectious (post encephalitic parkinsonism)
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4
Q

What Medicines can contribute to Parkinsonism? (2)

A
  • Antiemetics
  • Antipsychotics
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5
Q

What Toxins can contribute to Parkinsonism? (3)

A
  • Manganese
  • Carbon Disulphide
  • MPTP
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6
Q

What percentage of nigrostriatal dopaminergic neurones need to be lost before classical symptoms are noted?

A

> 50%

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7
Q

During a preclinical phase extending back for several years before the development of the motor deficit, what symptoms may be present? (5)

A
  • Hyposmia
  • Constipation
  • Anxiety
  • Depression
  • Rapid Eye-Movement (REM) sleep behaviour
    disorder (dream enactment)
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8
Q

Features of a Parkinson’s Tremor (4)

A
  • 4-6Hz noticeable at rest
  • ‘Pill-rolling’ – rhythmic flexion/extension of fingers,
    supination-pronation of forearm
  • Increases during stress
  • Reduces on movement
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9
Q

Clinical Features of Parkinson’s: Rigidity

A
  • Increased tone = resistance to passive movement
  • ‘cog-wheel’ = rachet like interruptions
  • Due to tremor in muscles
  • Creates a more flexed posture
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10
Q

Clinical Features of Parkinson’s: Akinesia (Bradykinesia)

A
  • Slowness of voluntary movement
  • Reduction in automatic movement (e.g arm swing
    when walking)
  • Mask-like face, reduced blinking
  • Power retained
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11
Q

Management of Parkinson’s (3)

A
  • Precursors of Dopamine
  • Inhibitors of Dopamine metabolism
  • Dopamine receptor agonists
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12
Q

Levodopa (L-dopa)

A
  • Precursor of dopamine converted both peripherally
    and centrally by decarboxylation
  • Majority converted peripherally so need to block
    peripheral decarboxylase
  • Dopamine stored in brain and one dose can last
    several hours
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13
Q

Side-Effects of Levodopa (L-dopa) (4)

A
  • Nausea
  • Hypotension
  • Hallucinations
  • Nightmares
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14
Q

What are Selegiline & Rasagiline? What do they do?

A
  • Selective MAO inhibitors
  • Reduce metabolism of central dopamine
  • Complement L-dopa
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15
Q

What are Entacapone & Tolcapone? What do they do?

A
  • COMT inhibitors
  • Increase dopamine availability
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16
Q

What are Pramipexole & Ropinirole? What do they do?

A
  • Dopamine receptor agonists
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17
Q

What is Huntington’s Disease?

A
  • Huntington‘s disease is a inherited Autosomal
    Dominant neurodegenerative disease
  • It causes the progressive breakdown of nerve cells
    in the brain and progressive movement disorder
    with dementia
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18
Q

What chromosome is Huntington’s associated with?

A
  • Chromosome 4
  • CAG trinucleotide repeats
19
Q

What parts of cerebrum atrophy in Huntington’s? (3)

A
  • Cortex
  • Caudate
  • Putamen
20
Q

Clinical Presentation of Huntington’s Disease (8)

A
  • Changes in Mood
  • Anxiety
  • Irritability
  • Memory Loss
  • Quickly putting food in mouth (like chipmunks)
  • Chorea
  • Dystonia
  • Slow or unusual eye movements
21
Q

Treatment of Huntington’s Disease (5)

A
  • No treatment only management of symptoms
  • Psychological support
  • Speech therapist
  • Antipsychotics
  • Tetrabenazine – FDA approved for managing Chorea
    but can cause Parkinsonism as it depletes dopamine
    and also may increase risk of depression
22
Q

What is Wilson Disease?

A

An autosomal recessive genetic disorder of impaired copper transport and excretion caused due to the loss of function of the ATP7B copper-binding protein

23
Q

Normal Cu Metabolism

A
  • Loading of Cu onto protein ceruloplasmin for safe
    transport in blood
  • Excretion of excess Cu via bile in faeces
24
Q

Cu Metabolism in Wilson’s Disease

A
  • No loading of Cu onto protein ceruloplasmin
  • No excretion of excess Cu via bile in faeces
  • Increased levels of toxic Cu in blood, liver, brain,
    other organs
25
Q

Clinical Features in Wilson’s Disease (10)

A
  • Tremor
  • Involuntary Movements
  • Dysphagia
  • Dysarthria
  • Lack of Coordination
  • Spasticity
  • Dystonic Postures
  • Muscle Rigidity
  • Kayser-Fleischer Rings
  • Liver Failure
26
Q

What are Kayser-Fleischer Rings?

A

Dark rings that appear to encircle the iris of the eye

27
Q

Investigations for Wilson’s Disease (3)

A
  • Raised Urinary Copper (100 μg/24 hours)
  • Reduced Caeruloplasmin (<20mg/dL)
  • Serum Copper (25 μg/dL)
28
Q

Treatment of Wilson’s Disease (4)

A
  • Penicillamine (chelates copper and increases
    excretion)
  • Trientine (Syprine)
  • Zinc Acetate
  • Liver Transplant
29
Q

What is Wernicke Encephalopathy?

A

A degenerative brain disorder caused by the lack of vitamin B1

30
Q

Triad of Wernicke Encephalopathy Symptoms

A
  • Ataxia
  • Ophthalmoplegia
  • Confusion
31
Q

What can cause Wernicke Encephalopathy?

A
  • Alcohol Abuse
  • Dietary Deficiencies
  • Prolonged Vomiting
32
Q

What is Vertebrobasilar Insufficiency?

A
  • Inadequate blood flow through the posterior
    circulation of the brain, supplied by the 2 vertebral
    arteries that merge to form the basilar artery
  • The vertebrobasilar arteries supply the cerebellum,
    medulla, midbrain, and occipital cortex.
33
Q

Clinical Presentations of Cerebellar Infarct (3)

A

Ipsilateral Limb:
* Ataxia
* Lateropulsion
* Hypotonia

34
Q

What is Multiple Sclerosis (MS)?

A
  • MS is an autoimmune disease
  • Caused by myelin-reactive T cells in the peripheral
    circulation that become activated by a trigger
  • Invade the central nervous system and cause
    destruction of myelin and axons directly and by
    initiating the release of various inflammatory
    mediators
35
Q

Risk Factors for MS (6)

A
  • Geography
  • Vitamin D deficiency
  • Obesity
  • EBV exposure
  • Smoking
  • Gut Microbiome
36
Q

When is typical disease onset of MS?

A

Between 20 to 40 year olds

37
Q

Signs and Symptoms of MS (10)

A
  • Fatigue
  • Vision Problems (Optic Neuritis)
  • Incontinence
  • Muscle stiffness and spasms
  • Relative Afferent Pupillary Defect (Marcus Gunn
    Pupil)
  • Bilateral Internuclear Opthalmoplegia
  • Pseudobalbar Palsy
  • Memory loss, depression
  • Ataxia
  • Intention Tremor
38
Q

What is Pseudobulbar Palsy is characterised by? (4)

A
  • Dysarthria
  • Dysphagia
  • Facial and Tongue Weakness
  • Emotional Lability
39
Q

What are Clinical Signs of MS? (2)

A
  • Lhermitte’s Sign
  • Uhthoff’s Phenomenon
40
Q

What is Lhermitte’s Sign?

A

An intense burst of pain like an electric shock that runs down your back into your arms and legs when you move your neck

41
Q

What is Uhthoff’s Phenomenon?

A

Transient worsening of neurological symptoms when the body becomes overheated in hot weather, exercise, shower, saunas, or hot tubs

42
Q

What is Charcot’s Neurological Triad for MS?

A
  • Nystagmus
  • Dysarthria
  • Intention Tremor
43
Q

Treatments of MS (6)

A
  • High Dose Corticosteroids
  • Plasmapheresis
  • Interferon Beta
  • Glatiramer Acetate
  • Ocrelizumab
  • Natalizumab

Nervous System (18 decks)

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