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4th Year Long term conditions > Neurology > Flashcards

Neurology Flashcards

1
Q

Pathology of Parkinson’s disease

A

Dopaminergic neurones in the substantia migrans degenerate.

Progressive, adult onset movement disorder.

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2
Q

What are the two parts of the substantia nigra and which is affected in Parkinson’s disease?

A

Pars reticulata

Pars compacta - affected area

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3
Q

Which neuro pathway is affected in Parkinson’s disease and what is its function?

A

Nigrostriatal pathway - helps to stimulate the cerebral cortex and initiate movement

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4
Q

What are the cardinal motor signs of Parkinson’s disease?

A
  • Bradykinesia
  • Resting tremor
  • Rigidity
  • Postural instability
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5
Q

What does bradykinesia look like in a patient?

A
  • Slow to initiate movement
  • Actions slow and decrease in amplitude with repetition
  • Gait is shuffling, pitched forward
  • Decreased arm swing and freezing at obstacles or doors (due to poor simultaneous motor and cognitive function)
  • Expressionless face
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6
Q

Is Parkinson’s disease unilateral or bilateral?

A

Symptoms often begin on one side of the body or even in one limb on one side of the body. As the disease progresses, it eventually affects both sides. However, the symptoms may still be more severe on one side than on the other.

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7
Q

Non motor symptoms of Parkinson’s disease

A
  • Reduced sense of smell (can lose sense of smell years before motor symptoms)
  • Sleep disturbances
  • Autonomic dysfunction
    • postural hypotension
    • constipation
    • urinary symptoms
    • dribbling of saliva
  • Neuropsychiatric complications
    • depression
    • dementia
    • psychosis
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8
Q

Does Parkinson’s disease have a treatment that will stop the progressive neurodegeneration?

A

No - treatments only aim to control symptoms and will not affect the underlying disease

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9
Q

What are the pharmacological treatments for Parkinson’s disease?

A
  • Levodopa
  • Dopamine agonists
  • MAO-B inhibitors
  • COMT inhibitors
  • Anticholinergics
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10
Q

Why is levodopa (precursor to dopamine) given instead of dopamine?

A

Levodopa can cross the blood brain barrier while dopamine cannot.

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11
Q

What is levodopa combined with and why?

A

Levodopa is administered with carbidopa - a dopa decarboxylase inhibitor that isn’t able to cross the blood brain barrier

  • Levodopa is converted to dopamine by dopa decarboxylase (within nigrostriatal neurones and by peripheral dopa decarboxylase)
  • Periperal dopa decarboxylase can metabolise levodopa into dopamine before it gets to the blood brain barrier. Dopamine can be further metabolised into other catecholamines such as epinephrine which can have side effects such as arrhythmias
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12
Q

When should levodopa be started?

A

Efficacy of this therapy reduces over time, requiring larger and more frequent dosing, with worsening side effects and response fluctuations.

It may be wise to start levodopa late eg >70 years or when symptoms seriously interfere with life.

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13
Q

Side effects of levodopa

A
  • Compulsive gambling, hypersexuality, binge eating, or obsessive shopping (can develop in patient on any dopaminergic therapy)
  • Dyskinesia - involuntary movements
  • Wearing off - the effects of the drug wear off before the next dose
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14
Q

Why should levodopa not be withdrawn suddenly?

A

It risks acute akinesia and neuroleptic malignant syndrome

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15
Q

How do anticholinergics work? Who should they be used for?

A

They balance acetylcholine with dopamine

They cause confusion in the elderly and have multiple side effects - limit use to younger patients

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16
Q

How do COMT inhibitors and MAO-B inhibitors work?

A

They inhibit enzymes which metabolise dopamine which increases the dopamine concentration in the brain

17
Q

MAO-B inhibitor examples, use and side effects

A

Rasagiline, selegiline

An alternative to dopamine agonists in early Parkinson’s disease

Side effects include postural hypotension and atrial fibrillation

18
Q

Other causes of Parkinsonism

A
  • Lewy body dementia
  • Wilson disease
  • Pick disease
  • Encephalitis
  • Neurosyphilis
  • Side effects of:
    • antipsychotics (haloperidol) - blocks dopamine receptors
    • metclopramide - dopamine antagonist used to treat vomiting
19
Q

What is myasthenia gravis?

A

An autoimmune condition that causes muscle weakness that gets worse with activity and improves with rest.

20
Q

Myasthenia gravis preferentially affects:

A
  • Young women 20s and 30s
  • Older men 60s and 70s
21
Q

Describe the link between myasthenia gravis and a thymoma

A

10-20% of patients with myasthenia gravis have a thymoma

20-40% of patients with a thymoma develop myasthenia gravis

22
Q

Which auto-antibodies cause myasthenia gravis?

A
  • Acetylcholine receptor antibodies (85%)
  • Muscle-specific kinase (MuSK) antibodies (10%)
  • Low-density lipoprotein receptor-related protein 4 (LRP4) antibodies (<5%)
23
Q

How do acetylcholine receptor antibodies cause myasthenia gravis?

A

These bind to the postsynaptic neuromuscular junction receptors. This blocks the receptor and prevents the acetylcholine from being able to stimulate the receptor and trigger muscle contraction. As the receptors are used more during muscle activity, more of them become blocked up. This leads to less effective stimulation of the muscle with increased activity.

These antibodies also activate the complement system within the neuromuscular junction, leading to damage to cells at the postsynaptic membrane. This further worsens the symptoms.

24
Q

How do MuSK and LRP4 antibodies cause myasthenia gravis?

A

MuSK and LRP4 and important proteins for the creation and organisation of the acetylcholine receptor. Destruction of these proteins by autoantibodies leads to inadequate acetylcholine receptors. This causes the symptoms of myasthenia gravis.

25
Q

Symptoms of myasthenia gravis

A

The characteristic feature is weakness that gets worse with muscle use and improves with rest. Symptoms are typically minimal in the morning and worst at the end of the day.

  • Diplopia
  • Ptosis
  • Weakness in facial movements
  • Difficulty with swallowing
  • Fatigue in the jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
26
Q

The symptoms of myasthenia gravis most affect:

A

The proximal muscles and muscles of the head and neck

27
Q

How do the symptoms of myasthenia gravis fluctuate throughout the day?

A

Symptoms are typically minimal in the morning and worst at the end of the day.

28
Q

How severe are the symptoms of myasthenia gravis?

A

The severity of symptoms can vary dramatically between patients. They can be mild and subtle or life threateningly severe.

29
Q

How would you examine someone with myasthenia gravis?

A
  • There are a few ways to elicit fatiguability in the muscles:
    • Repeated blinking will exacerbate ptosis
    • Prolonged upward gazing will exacerbate diplopia on further eye movement testing
    • Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
  • Check for a thymectomy scar.
  • Test the forced vital capacity (FVC)
30
Q

What tests are used to diagnose myasthenia gravis?

A
  • Testing directly for the relevant antibodies:
    • Acetylcholine receptor (ACh-R) antibodies (85% of patients)
    • Muscle-specific kinase (MuSK) antibodies (10% of patients)
    • LRP4 (low-density lipoprotein receptor-related protein 4) antibodies (less than 5%)
  • A CT or MRI of the thymus gland is used to look for a thymoma
  • The edrophonium test can be helpful where there is doubt about the diagnosis
31
Q

Treatment options for myasthenia gravis

A
  • Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine) increases the amount of acetylcholine in the neuromuscular junction and improves symptoms
  • Immunosuppression (e.g. prednisolone or azathioprine) suppresses the production of antibodies
  • Thymectomy can improve symptoms even in patients without a thymoma
  • Monoclonal antibodies - Rituximabis a monoclonal antibody that targets B cells and reduces the production of antibodies
32
Q

What is a myasthenic crisis?

A

A severe complication of myasthenia gravis. It can be life threatening. It causes an acute worsening of symptoms, often triggered by another illness such as a respiratory tract infection. This can lead to respiratory failure as a result of weakness in the muscles of respiration.

33
Q

Treatment for myasthenic crisis

A

Patients may require non-invasive ventilation with CPAP or full intubation and ventilation.

Medical treatment of myasthenic crisis is with immunomodulatory therapies such as IV immunoglobulins and plasma exchange.

4th Year Long term conditions (5 decks)

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