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Neurology > Neuro - Parkinson's, Trigeminal Neuralgia, MS > Flashcards

Neuro - Parkinson's, Trigeminal Neuralgia, MS Flashcards

1
Q

Parkinson’s Disease (PD) - what is it?

A

Progressive reduction in amount of dopamine in the basal ganglia

Degeneration of dopaminergic neurons in the substantia nigra

Lead to disorders of movement

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2
Q

PD - what are the characteristic featurs?

A

Triad:

  1. Bradykinesia
  2. Cog-wheel rigidity
  3. Resting tremor (unilateral)

Characteristically asymmetrical, one side affected more than the other

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3
Q

PD - pathophysiology

A

The basal ganglia are a group of structures situated in the middle of the brain

Responsible for coordinating habitual movements such as walking or looking around, controlling voluntary movements and learning specific movement patterns

Part of the basal ganglia called the substantia nigra produces a neurotransmitter called dopamine

Dopamine is essential for the correct functioning of the basal ganglia

In Parkinson’s disease, there is a gradual but progressive fall in the production of dopamine

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4
Q

PD - what are the features of the characteristic resting tremor?

A

The tremor in Parkinsons has a frequency of 4-6 Hz, meaning it occurs 4-6 times a second

“pill rolling tremor”

More pronounced when resting and improves on voluntary movement

The tremor is worsened if the patient is distracted

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5
Q

PD - what are the features of the characteristic bradykinesia?

A

Bradykinesia describes how their movements get slower and smaller

This presents in a number of ways:

  • Their handwriting gets smaller and smaller
  • They can only take small steps when walking (“shuffling gait”)
  • They have difficulty initiating movement
  • They have difficulty in turning around when standing, having to take lots of little steps
  • They have reduced facial movements and facial expressions (hypomimia)
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6
Q

PD - what are some other features?

A
  • Depression
    • Sleep disturbance and insomnia
  • Loss of the sense of smell (anosmia)
  • Postural instability
  • Cognitive impairment and memory problems
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7
Q

PD - how to distinguish between PD and drug-induced parkinsonism?

A

In drug-induced parkinsonism:

  • Motor symptoms are generally rapid onset and bilateral
  • Rigidity and rest tremor are uncommon
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8
Q

PD - what are two drug examples which can cause drug-induced parkinsonism?

A

Metaclopramide - can cross BBB

Antipsychotics

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9
Q

PD - how do you distinguish between Parkinson’s tremor and Benign essential tremor?

A

Parkinson’s tremor - asymmetrical, worse at rest, improves with intentional movement, no change with alcohol

Benign essential tremor - symmetrical, improves at rest, worse with intentional movement, improves with alcohol

Opposite to one another

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10
Q

PD - what is Multiple System Atrophy?

A

This is a rare condition where the neurones of multiple systems in the brain degenerate

Affects basal ganglia as well as multiple other areas

Degeneration of the basal ganglia lead to a Parkinson’s presentation

Degeneration in other areas lead to autonomic dysfunction (causing postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (causing ataxia).

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11
Q

PD - what is Progressive Supranuclear Palsy and what are the clinical features?

A

It is a ‘Parkinson Plus’ syndrome

Features

  • postural instability and falls
    • patients tend to have a stiff, broad-based gait
  • impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)
  • parkinsonism
    • bradykinesia is prominent
  • cognitive impairment
    • primarily frontal lobe dysfunction
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12
Q

PD - how do you diagnose?

A

Clinical diagnosis based on symptoms and examination

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13
Q

PD - 1st line management?

A

For first-line treatment:

if the motor symptoms are affecting the patient’s quality of life: levodopa

if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor

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14
Q

PD - what is levodopa?

A

synthetic dopamine given orally to boost their own dopamine levels

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15
Q

PD - what is levodopa combined and taken with?

A

It is usually combined with a drug that stops levodopa being broken down in the body before it gets the chance to enter the brain

These are peripheral decarboxylase inhibitors - examples are carbidopa and benserazide.

Combination drugs are:

  • Co-benyldopa (levodopa and benserazide)
  • Co-careldopa (levodopa and carbidopa)
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16
Q

PD - what is the main side effect when the dose is too high, and there is too much dopamine?

A

Main side effect of dopamine is when the dose is too high patients develop dyskinesias

Abnormal movements associated with excessive motor activity

Examples are:

  • Dystonia: This is where excessive muscle contraction leads to abnormal postures or exaggerated movements.
  • Chorea: These are abnormal involuntary movements that can be jerking and random.
    • Athetosis: These are involuntary twisting or writhing movements usually in the fingers, hands or feet
17
Q

PD - what are COMT inhibitors, how do they work, and what is the main example?

A

Entacapone

Inhibitors of catechol-o-methyltransferase (COMT)

The COMT enzyme metabolises levodopa in both the body and brain

Entacapone is taken with levodopa (and a decarboxylase inhibitor) to slow breakdown of the levodopa in the brain - it extends effective duration of the levodopa

18
Q

PD - what are examples of dopamine agonists, how do they work and what is their main side effect?

A

These mimic dopamine in the basal ganglia and stimulate the dopamine receptors

Used to delay the use of levodopa and are then used in combination with levodopa to reduce the dose of levodopa that is required to control symptoms

SE - with prolonged use, pulmonary fibrosis

  • Bromocryptine
  • Pergolide
  • Carbergoline
19
Q

PD - what are MOA-B inhibitors, how do they work, and what are some examples?

A

Monoamine oxidase enzymes break down neurotransmitters such as dopamine, serotonin and adrenaline

The monoamine oxidase-B enzyme is more specific to dopamine and does not act on serotonin or adrenalin

These medications block this enzyme and therefore help increase the circulating dopamine

Similarly to dopamine agonists, they are usually used to delay the use of levodopa and then in combination with levodopa to reduce the required dose

  • Selegiline
  • Rasagiline
20
Q

Trigeminal Neuralgia (TN) - what is it?

A

Trigeminal neuralgia is a pain syndrome characterised by severe unilateral pain

The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur

21
Q

TN - what is the presentation of the pain?

A

Unilateral disorder characterised by brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve

22
Q

TN - how is the pain evoked?

A

The pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously

23
Q

TN - what are red flag symptoms?

A
  • Age of onset before 40 years
  • Sensory changes
  • Deafness or other ear problems
  • History of skin or oral lesions that could spread perineurally
  • Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
  • Optic neuritis
    • A family history of multiple sclerosis
24
Q

TN - management?

A

1st line - Carbamazepine

Failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology

25
Q

Multiple Sclerosis (MS) - what is it?

A

Chronic and progressive autoimmune condition that involves demyelination of the myelinated neurones in the central nervous system

This is caused by an inflammatory process involving the activation of immune cells against the myelin

26
Q

MS - what are the three types of disease patterns?

A

Relapsing-remitting disease (RRD) - commonest, acute attacks, then periods of remission

Secondary Progressive Disease - RRD patients who have deteriorated, and have developed neuro signs between relapses

Primary Progressive Disease - 10% cases, progressive deterioration from onset, more common in older people

27
Q

MS - who does it more commonly affect and at what age?

A

Females

20-40

28
Q

MS - what are the salient symptoms and signs, visual, sensory, cerebellar, others?

A

Visual:

  • Optic neuritis - most common presentation
  • Uhthoff’s phenomenon - worsening of vision following body temperature rise, such as after exercise
  • Internuclear opthalmoplegia

Sensory:

  • Pins/needles
  • Numbness
  • Trigeminal Neuralgia
  • Lhermitte’s syndrome - paraesthesia in limbs on neck flexion

Cerebellar:

  • Ataxia
  • Tremor

Others:

  • Urinary incontinence
  • Sexual dysfunction
  • Intellectual deterioration
29
Q

MS - how do you diagnose?

A

Diagnosis requires evidence of dissemination (spreading) of lesions throughout time and space

MRI - high signal T2 lesions, periventricular plaques, Dawson fingers

CSF - find oligoclonal bodies

Visual evoked potentials - test for demyelination, delayed, but well preserved waveform

30
Q

MS - management of acute relapses?

A

Acute relapses - high dose steroids, oral/IV methylprednisolone

Shortens acute relapses

31
Q

MS - disease modifying drugs?

A

Beta-interferon - reduce relapse rate up to 30%, decreases lesion accumulation, prevents immune activation

Natalizumab - prevents lymphocytes crossing BBB

32
Q

MS - management for spasticity?

A

1st line - Baclofen and gabapentin

Physio

33
Q

MS - drug that can be given for fatigue?

A

Amantadine

34
Q

MS - drugs that can be given for urinary incontinence?

A

anticholinergic medications such as tolterodine or oxybutynin

Neurology (4 decks)

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