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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

Define Parkinson’s disease

A

Degenerative movement disorder caused by a reduction of dopamine in the substantia nigra in the basal ganglia.

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2
Q

What is the epidemiology of Parkinson’s?

A
  • Increasing prevalence with age
  • Peak onset is 55-65 years
  • More common in males
  • Higher prevalence in West
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3
Q

Name some potential causes of Parkinson’s disease

A
  • Idiopathic
  • Drug induced - reversible cause of parkinsonism; Dopamine antagonists, CCB, atypical neuroleptics
  • Environmental factors - pesticides, herbicides, heavy metals
  • Parkinson genes - Parkin gene, alpha-synuclein gene mutation
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4
Q

What are the risk factors of Parkinson’s disease?

A

Male
Increasing age (median age is 60)
Family history
Higher risk in non-smokers

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5
Q

What is the pathophysiology of Parkinson’s?

A

Progressive degeneration of dopaminergic neurones in the substantia nigra in the midbrain that project to the striatum of the basal ganglia. This leads to reduced dopamine levels which means the thalamus will be inhibited, causing decrease in movement.

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6
Q

Describe the direct and indirect pathway of the basal ganglia?

A
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7
Q

How are the direct and indirect pathways of the basal ganglia affected in Parkinson’s

A

Direct Pathway: Reduced dopamine leads to less activation of the direct pathway (via D1 receptors). This decreases movement-promoting signals.

Indirect Pathway: Reduced dopamine leads to overactivity of the indirect pathway (via D2 receptors), increasing inhibitory signals that reduce movement.

Overall Effect: Increased inhibition of the thalamus results in less cortical stimulation, leading to the bradykinesia and rigidity characteristic of Parkinson’s disease.

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8
Q

How is gait affected in Parkinson’s?

A

Reduced asymmetrical arm swing
Narrow gait
Small steps and stooped posture
Shuffling steps, drags feet

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9
Q

What are the motor symptoms of Parkinson’s?

A

Unilateral tremor
Rigidity
Bradykinesia

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10
Q

What are the non-motor symptoms of Parkinson’s?

A

Falls, dizziness, orthostatic hypotension
Sleep/fatigue
Mood/cognition - high and lows, depression, anxiety
Vision disturbance/hallucinations
Constipation/swallowing difficulty
Urinary urgency
Sexual function - ED/high sex drive
Anosmia/excessive sweating

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11
Q

How is Parkinson’s diagnosed?

A
  • Clinically based on history and exam
  • May be confirmed in response to Levodopa
  • MRI head: Initially normal but will show atrophy
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12
Q

What is the gold standard treatment for Parkinson’s? What are the side effects?

A

Oral Levodopa - usually combined with a peripheral decarboxylase inhibitor (prevents breakdown of dopamine in the body before it reaches the brain)
e.g co-careldopa or co-beneldopa.

Side effects - Dyskinesias when dose is too high; dystonia (excessive muscle contraction), chorea (involuntary movements), athetosis (writhing hand movements)

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13
Q

Name other potential drug treatments for Parkinson’s?

A

COMT inhibitor - Inhibits Catechol-O-methyltransferase which breaks down dopamine e.g oral Entacapone or Tolcapone.

Monoamine Oxidase B inhibitor - Inhibit MAO-B enzymes which breaks down dopamine. e.g Oral Selegiline or Rasagiline

Dopamine agonists - Used to delay starting L-dopa in early stages
Side effects - Long term use may cause pulmonary fibrosis

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14
Q

What are the non-drug treatments for Parkinson’s?

A

Deep Brain Stimulation - works best in patients who have on/off fluctuations of drug treatment effectiveness

Surgical ablation - of overactive basal ganglia structures

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15
Q

What are the Parkinson plus syndromes?

A

Multiple system atrophy
Progressive supranuclear palsy
Corticobasal degeneration
Lewy-body dementia

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16
Q

Define Parkinson plus syndrome

A

Group of neurodegenerative movement disorders that have a similar presentation to Parkinson’s. However they have a limited response to levodopa and a poor prognosis.

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17
Q

How does an essential tremor differ from a parkinsonian tremor?

A

Bilateral fine tremor
5-8 cycles per second
Improves at rest, worse on intentional movement
Improves with alcohol
No other features of Parkinson’s

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18
Q

What are the differentials for an essential tremor?

A

Parkinson’s - most important to rule out
Hyperthyroidism
MS
Huntington’s
Iatrogenic - e.g salbutamol

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19
Q

How is essential tremor treated?

A

Propanolol - non selective BB

Primidone - Barbituate used in epilepsy, dose increased slowly to reduced SE (drowsiness, ataxia, nausea - all common SEs)

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20
Q

Describe Multiple System Atrophy and its pathophysiology

A

Rare condition where neurones in multiple areas of the brain degenerate, including the basal ganglia (leading to parkisonian features). Also leads to autonomic and cerebellar dysfunction. Caused by the spread of alpha synuclein and inclusions of tau and ubiquitin proteins.

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21
Q

How does Multiple System Atrophy present? How does it differ from Parkinsons?

A

Two types, MSA-P which has predominantly parkinsonian features or MSA-C which has predominantly features of cerebellar ataxia. May change through disease course.

Dysautonomia - ED (usually presents 6-8 months before motor symptoms, unlike parkinsons), constipation, urinary frequency, incontinence, abnormal sweating and late onset orthostatic hypotension.

Cognitive function is well maintained

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22
Q

How does corticobasal degeneration affect the brain?

A

Tau astrocytic plaque and inclusions in the glia (non-nerve cells), leading to severe gliosis (proliferation of glial cells in response to injury causing scarring) and nerve loss. Involving parts of cerebrum and basal ganglia.

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23
Q

How does corticobasal degeneration present?

A

Asymmetric movement disorder:
Extreme rigidity, muscle jerking, dystonia, alien limb.

Cognitive impairment:
Aphasia
Executive dysfunction
Visuospatial deficits
Behavioural change

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24
Q

How does PSP affect the brain?

A

Neurofibrillary tangle of tau proteins form (different to Alzheimers) in various structures including basal ganglia, oculomotor nucleus, cerebral cortex.

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25
Q

What are the various, predominant features of PSP?

A

Gait dysfunction
Oculomotor dysfunction - unable to move eyes vertically, focus or control lids
Speech/language disorder
Frontal presentation - Behaviour change (apathy, loss of inhibition etc), loss of executive function
Corticobasal syndrome - similar symptoms as CBD

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26
Q

What is a stroke?

A

Stroke is any sudden onset in neurological deficit. Can be due to Ischaemic or Haemorrhagic (Intracerebral + SAH). Lack of blood supply leads to irreversible cell death.

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27
Q

In an ischaemic what is the area surrounding the infarcted area called? Why is it significant?

A

The penumbra - area of oedema around infarct. Deficits of this area can be reversed with rehabilitation and quick treatment

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28
Q

What are the causes of an ischaemic stroke?

A

Atherothromboembolism - e.g from carotid artery

Cardioembolsim - AF, post MI, valve disease, IE

Hyperviscosity syndrome - e.g waldenstrom’s macroglobulinemia (WBC cancer)

Hypoperfusion - systemic blood loss

Vasculitis

Fat emboli - long bone fracture

Venous sinus thrombosis - infection, injury, pregnancy, inflammatory conditions

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29
Q

What are the risk factors for an ischaemic stroke?

A

Increasing age
Male
Hypertension
Smoking
Diabetes
Recent/past TIA
Hyperlipidaemia
Heart disease - IHD, AF, valve disease
Combined oral contraceptive pill
Black, Asian
Peripheral vascular disease
Clotting disorder
Vasculitis
Alcohol
Infective endocarditis
Carotid bruit

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30
Q

What investigations should be done if an ischaemic stroke is suspected?

A

Immediate CT scan -
Distinguish ischaemic from haemorrhagic, shows site of infarct, may be negative in first few hours

Diffusion-weighted MRI -
More sensitive, for confirmed diagnosis

Blood tests -
Glucose (rule out hypoglycaemia), FBC (polycythaemia), ESR (vasculitis), U&Es, cholesterol, INR (if on warfarin)

ECG -
In AF or MI

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31
Q

What is the immediate management for an ischaemic stroke?

A

Urgent CT to exclude haemorrhagic
Immediate 300 mg loading dose of Aspirin continue for 2 weeks

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32
Q

When should thrombolysis be used? What are the risks and contraindications?

A

IV Alteplase infusion - Has to be within 4.5 hours of symptom onset
Risk of massive bleeding. Contraindications (Hx of stroke in diabetes patient, severe stroke, stroke in last 3 months, intracranial neoplasm)

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33
Q

What is the time frame for thrombectomy in an ischaemic stroke affecting the proximal anterior circulation?

A

Has to be within 6 hours of symptom onset, if CTA/MRA confirms PAC stroke.
Consider 6-24 hours of symptom onset, if proximal anterior circulation and diffusion weighted MRI or CT perfusion scan indicates potential to salvage brain tissue

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34
Q

What is the time frame for thrombectomy in an ischaemic stroke affecting the proximal posterior circulation?

A

Consider thrombectomy w/ IV thrombolysis (if not contraindicated) if imaging shows proximal posterior circulation stroke, 6-24 hours of symptom onset

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35
Q

How should BP be controlled in an ischaemic stroke?

A

Not usually lowered in ischaemic strokes, consider below 185/110 if treating with IV thrombolysis.

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36
Q

What is the treatment for an ischaemic stroke caused by venous thromboembolism?

A

Full anticoagulation therapy (full dose heparin and warfarin (if not contraindicated))

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37
Q

What is the long term management for an ischaemic stroke?

A

SALT support, rehabilitation, after 2 weeks of aspirin switch to 75mg Clopidogrel

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38
Q

Define intracerebral haemorrhage?

A

Sudden bleeding into brain tissue due to rupture of blood vessels, leading to infarction due to O2 deprivation. Pooling of blood increases ICP. 10% of strokes, 50% mortality

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39
Q

What is the aetiology of an intracerebral haemorrhage?

A

Hypertension - causes stiff, brittle vessels prone to rupture, microaneurysms
2° to ischaemic stroke - bleeding after reperfusion
Head trauma
AV malformations
Vasculitis
Vascular/Brain tumours
Cerebral amyloid angiopathy - amyloid beta deposits in small/medium vessels
Carotid artery dissection

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40
Q

What are the risk factors for an intracerebral haemorrhage?

A

Hypertension
Age
Alcohol
Smoking
Diabetes
Anticoagulation/Thrombolysis

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41
Q

What is the pathophysiology of increased ICP due to intracerebral haemorrhage?

A

Pooling of blood puts pressure on brain,
May cause CSF obstruction - hydrocephalus,
Leading to midline shift/tentorial herniation ,
Eventually coning - brain stem compression - Death

42
Q

What is the immediate treatment for intracerebral haemorrhage?

A

Stop anticoagulants immediately
Reverse with clotting factor replacement if needed (Beriplex + vitamin k if on warfarin)

43
Q

How should BP be controlled in an intracerebral haemorrhage?

A

Consider rapid BP lowering if <6 hours before onset and systolic BP is between 150-220 mmHg
Aim to lower below 140 mmHg systolic

Contraindicated - underlying structural cause, GCS below 6, early neurosurgery, poor prognosis

44
Q

How is increased ICP treated?

A

IV mannitol, consider mechanical ventilation if risk of coning.

45
Q

What is the surgical treatment in strokes?

A

Decompressive hemicraniectomy
Shunting - in hydrocephalus

46
Q

What is the Bamford classification?

A

Sub-categories of cerebral infarction on the basis of presenting symptoms and signs: lacunar infarcts (LACI); total anterior circulation infarcts (TACI); partial anterior circulation infarcts (PACI); and posterior circulation infarcts (POCI).

47
Q

Using the Bamford classification define a TACS, what are the symptoms?

A

Total anterior circulation syndrome (large cortical stroke in ACA/MCA territories). All 3 of:

Contralateral weakness (and/or sensory deficit) of face, arm + leg

Homonymous hemianopia

Higher dysfunction – dysphasia, visuospatial disorder

48
Q

Define PACS using the Bamford classification, what are the symptoms?

A

Partial anterior circulation infarct (cortical stroke in ACA/MCA territories). 2 of:

Contralateral weakness (and/or sensory deficit) of face, arm + leg

Homonymous hemianopia

Higher dysfunction – dysphasia, visuospatial disorder

49
Q

Define POCS using the Bamford classification, what are the symptoms?

A

Posterior circulation syndrome (supplied by posterior circulation e.g brainstem, cerebellum). 1 of:

Cerebellar / brainstem syndrome – e.g. quadriplegia, locked in syndrome

LoC

Isolated homonymous hemianopia

Cranial nerve palsy AND contralateral motor/sensory deficit

50
Q

What are the symptoms in a Lacunar syndrome (Bamford classification)?

A

Subcortical stroke due to small vessel disease. 1 of:

Pure motor stroke – contralateral weakness of face, arm, leg, or all 3

Ataxic hemiparesis – ipsilateral weakness + clumsiness (mostly affects legs)

Pure sensory stroke – contralateral numbness, tingling, pain, or burning

Mixed sensorimotor stroke

Clumsy hand dysarthria

51
Q

Define Subarachnoid haemorrhage

A

Spontaneous bleeding between arachnoid and pia mater usually due to rupture of a cerebral aneurysm. Mainly communicating branches of the circle of willis.

52
Q

What is the epidemiology and prognosis of SAH?

A

Age 35-65

High mortality (50% die straight away), 10-20% more from rebleeding, 50% left with significant disability.

53
Q

What are the risk factors for SAH?

A

Hypertension
Known aneurysm
Previous SAH
Smoking
Alcohol
FHx
Bleeding disorders
PKD
Coarctation of aorta
Connective tissue disorders - ED, Marfan’s
associated with berry aneurysm

54
Q

What is the aetiology for SAH?

A

Traumatic injury
Aneurysmal rupture - berry (70-80%) at communicating branches
AV malformations - abnormal artery and venous connections (15% of cases)
Idiopathic

55
Q

Describe the pathophysiology of the complications of SAH?

A

Tissue ischaemia - due to bleeding loss, causing cell death
Raised ICP - Blood into cranial space, space occupying lesion
Blood causing meningism - could obstruct CSF outflow (hydrocephalus)
Vasospasm - bleeding irritates other vessels causing ischaemic injury

56
Q

What are the symptoms of SAH?

A

Thunderclap headache - typically occipital, excruciating
Sentinel headache - Before main rupture, early sign - 6% cases
Nausea, vomiting, seizures, visual disturbance, LoC, photophobia

57
Q

What are the potential clinical signs seen on examination of a patient with SAH?

A

Meningeal irritation - Neck stiffness, Kernig’s (leg raise - pain), Brudzinski (neck raise - hip\knee flexion)
Retinal, vitreous and subhyaloid bleeds w/ or without papilloedema
Focal neurological signs - e.g 3rd nerve palsy (fixed dilated pupil)
Increased BP

58
Q

Give 4 potential differentials for SAH

A

Headache - mainly migraine, cluster also
Meningitis
Intracerebral haemorrhage
Carotid/vertebral artery dissection

59
Q

What investigations can be used to confirm SAH?

A

Immediate CT head - detects >95%, star shaped sign
Lumbar puncture - if normal ICP, after 12 hours (xanthochromia - confirms SAH, raised red cells)
MR/CT angiography - establish source, in all patients fit for surgery

60
Q

How is SAH treated?

A

IV fluids - maintain cerebral perfusion, keep BP below 160 mmHg
Nimodipine - Ca2+ antagonist, reduce risk of vasospasm
Neurosurgery - Endovascular coiling or surgical clipping, ventricular drainage/shunting (hydrocephalus)
Antiepileptics - used to treat seizures

61
Q

Define Multiple Sclerosis

A

Chronic T cell mediated response of the CNS leading to demyelination within the brain and spinal cord, occurring sporadically over years. Affects the white matter of the brain, targeting oligodendrocytes.

62
Q

Which groups of people are most likely to be affected by MS?

A

Presents typically between 20-40 years
More common in women
More common in white populations

63
Q

What are some of the potential causes of MS?

A

Unknown
Genetic/environmental factors
EBV in childhood may increase risk
Low levels of sunlight and vitamin D

64
Q

Describe the pathophysiology of MS

A

T-cell mediated, activating B cells to produce autoantibodies against myelin, targets oligodendrocytes resulting in sites of demyelination. Myelin does regenerate, however it is less efficient and is temperature dependent (resulting in Uhtoff’s phenomenon).

Repeated demyelination eventually leads to incomplete recovery and permanent neurological deficits.

65
Q

What are distinct areas in the brain affected by MS?

A

Optic nerves, brainstem/cerebellum connections, corpus callosum (connects both hemispheres), cervical cord (corticospinal and dorsal tracts). MS lesions must be disseminated in time and space.

66
Q

What are the patterns of presentations of MS?

A

Primary progressive MS

Secondary progressive MS

Relapsing-remitting MS

67
Q

Define Clinically Isolated Syndrome?

A

Not MS as not Disseminated in time and space. However, it is more likely to develop MS if lesions seen on MRI.

68
Q

What is the most common presenting pattern of MS? Describe it

A

Relapsing-remitting MS - is the most common pattern at initial diagnosis. It is characterised by episodes of disease and neurological symptoms followed by recovery. In MS the symptoms occur in different areas with different episodes and are unpredictable. May or may not leave permanent deficit

69
Q

Describe the pattern of Primary progressive MS

A

There is a worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions.

70
Q

What is the pattern of Secondary progressive MS?

A

Is where there was relapsing-remitting disease at first, but now there is a progressive worsening of symptoms with incomplete remissions. Symptoms become more and more permanent.

71
Q

How can these patterns be further defined?

A

Relapsing-remitting - Active (new symptoms or MRI lesions)/Non Active and Worsening (overall worsening of disability)/Non

Primary and Secondary MS - Active/Non Active and Progressing (overall worsening of disability over time regardless of relapses)/Non progressing

72
Q

How does an attack of MS initially present?

A

Initially monosymptomatic with symptoms progressing over 24 hours, usually resolves within days to weeks

73
Q

What are the various presenting symptoms of MS?

A

Optic neuritis

Eye movement abnormalities - Internuclear ophthalmoplegia + Conjugate lateral gaze disorder

Focal weakness

Focal sensory symptoms

Ataxia

74
Q

Define Optic Neuritis

A

Most common presenting symptom, due to demyelination of optic nerve.
Unilateral central scotoma/reduced vision, with pain on eye movement, RAPD

75
Q

Explain eye movement abnormalities in MS

A

Double vision due to lesions in abducens nerve. 2 key signs:
Internuclear ophthalmoplegia - Nerve fibres connecting cranial nerves 3,4 and 6 (eye movement), thus the muscles controlling eye movement are affected.

Conjugate lateral gaze disorder - Disordered in 6th nerve palsy, meaning affected eye will not move laterally (adduct - towards nose)

76
Q

What are examples of focal weakness in MS?

A

Bell’s palsy, limb paralysis, horner syndrome, incontinence, sexual dysfunction

77
Q

What are the types of focal sensory symptoms that may present in MS?

A

Trigeminal neuralgia, numbness, paresthesia, Lhermitte’s sign (indicates disease in dorsal column, sharp pain down spine on neck flexion

78
Q

What are the causes of ataxia in MS?

A

Can be sensory or cerebellar, sensory due to a loss in proprioception (positive Romberg’s + pseudoathetosis). Cerebellar lesions can cause cerebellar signs (disturbance of balance, coordination and speech)

79
Q

What are potential differentials for MS?

A

Autoimmune (cerebral SLE, sarcoidosis, sjogrens),
CNS infection,
Metabolic (B12 deficiency, copper deficiency, mitochondrial disease),
Vascular
Neoplasm

80
Q

How is MS diagnosed?

A

Requires 2 or more attacks affecting different parts of CNS, usually over the course of a year.
Other causes of symptoms must be ruled out.

MRI brain/spinal cord: Diagnostic if multiple lesions seen in CNS and history fits
LP - reveals oligoclonal bands in 90% of patients, not specific to MS
Nerve conduction - reduced in demyelination

81
Q

What lifestyle factors may improve symptoms of MS?

A

Reduced stress, healthy diet, vitamin D supplements, stop smoking

82
Q

What is the acute and chronic management for MS?

A

Acute relapse: 500 mg methylprednisolone for 5 days, 1g IV methylpred for 3-5 days if not responding or if attack is severe

Frequent relapse/chronic management:
Interferon beta (anti-inflammatory cytokines, SE - depression, flu-like symptoms, teratogenicity unclear)
DMARDs - IV Alemtuzumab or IV Natalizumab, Dimethyl fumarate

83
Q

Describe treatment for symptom management in MS

A

Spasticity - Physio, Baclofen (GABA analogue reduces Ca influx), botox, Tizanidine
Urinary urgency/frequency - intermittent self catheterisation
Incontinence - Doxazosin (anti Ch alpha blocker drugs)

84
Q

What is Huntington’s Chorea?

A

Huntington’s is an autosomal dominant condition that causes a progressive deterioration in the nervous system, leading to chorea. It is characterised by a lack of inhibitory neurotransmitter GABA.

85
Q

Define Chorea

A

Continuous flow jerky, semi-purposeful movements, may interfere with voluntary movements but cease with sleep.

86
Q

What is the epidemiology of Huntington’s?

A

Autosomal dominant condition with full penetrance - all gene carriers will develop disease, it is incurable

Asymptomatic until 30-50, presents with mild symptoms

Rare, prevalence is 5 per 100000

87
Q

Define the aetiology and risk factors of Huntington’s

A

Aetiology:
Mutation affecting HTT gene on chromosome 4
Trinucleotide repeat disorder, repeat expression of CAG sequence

Risk factors:
FHx
Parent with Huntington’s - child has 50% risk

88
Q

What is the pathophysiology of Huntington’s?

A

CAG sequence repeats 36 or more times (usually 10-35), leading to the translation of an expanded polyglutamine sequence in the huntingtin gene.

Progressive cerebral atrophy with marked loss of neurons in the caudate and putamen - specifically a loss of GABA-nergic and cholinergic neurons

Decrease ACh and GABA synthesis
Loss of GABA results in reduced inhibition of dopamine therefore these is excessive thalamic stimulation = chorea

89
Q

What is anticipation?

A

Anticipation - worse in successive generations more CAG repeats leading to increased severity and earlier onset

90
Q

Describe the clinical presentation of Huntington’s

A

Typically insidious onset with mild psychotic, behavioural and cognitive problems.

Chorea develops: Progressive, jerky, explosive, rigid involuntary movements.

Dysarthria, dysphagia and abnormal eye movements
Associated with seizures, depression, dementia

91
Q

What are other causes of chorea?

A

Sydenham’s chorea (rheumatic fever)
Wilson’s disease
SLE
Stroke of the basal ganglia
Creutzfeldt-Jakob disease - prion protein forms and causes irreversible damage to nerve cells

Huntington’s is the most common cause

92
Q

How is Huntington’s diagnosed?

A

Mainly clinical
Genetic testing
CT/MRI - shows caudate nucleus atrophy and increased size of lateral ventricles, not useful in early disease

93
Q

Explain the treatment for Huntington’s?

A

No treatment to prevent progression
Family, genetic counselling

Symptom management - Benzodiazepines, Sulpiride (neuroleptic, depresses nerve function), Tetrabenazine (dopamine depleting agent)
Antidepressants - SSRI
Antipsychotic medication - neuroleptics, Haloperidol
Treat aggression - Risperidone

94
Q

Define Guillain Barre Syndrome

A

Acute inflammatory paralytic polyneuropathy that affects the peripheral nervous system (targeting schwann cells), causing an acute symmetrical, ascending weakness and sensory symptoms. Usually triggered by an upper resp tract or GI infection.

95
Q

What factors increase the risk of GBS?

A

More common in males
Peak ages 15-35 and 50-75 years
History of respiratory or GI infections 1-3 weeks prior to onset
Vaccinations
Post pregnancy - incidence increases in months after delivery

96
Q

What is the pathophysiology of GBS?

A

GBS is usually triggered by infection, thought to occur due to molecular mimicry. The B cells of the immune system produce antibodies against the pathogen and create antibodies against the antigens on the pathogen. These antibodies also match proteins on the schwann cells in the PNS this leads to autoantibody mediated nerve cell damage.
This leads to demyelination resulting in an acute polyneuropathy

97
Q

How does GBS present?

A

Symmetrical ascending muscle weakness starting usually 4 weeks post infection, may advance quickly and lead to paralysis
The proximal muscles are more affected e.g. trunk, respiratory and cranial nerves (especially facial)
Neuropathic pain + peripheral loss of sensation
Reduced reflexes
Symptoms peak 2-4 weeks after onset

98
Q

Name other causes of acute paralysis that should be considered as differentials of GBS

A

Hypokalaemia
Stroke
Brainstem compression
Encephalitis
Spinal cord compression
Myasthenia gravis

99
Q

How is GBS diagnosed?

A

Nerve conduction studies - Diagnostic if clinical history matches, showing conduction block/reduction
Lumbar puncture - raised protein, normal white cell count + glucose
Spirometry - to monitor FVC if respiratory involvement

100
Q

Outline the treatment for GBS and include the management for respiratory involvement

A

If FEV1:FVC <1.5L/80% ventilate and admit to ICU, monitor FVC 4 hourly

IV immunoglobulin: decreases the duration and severity of paralysis
Contraindicated: In patients with IgA deficiency, screen before therapy

Plasma exchange (alternative to IVIg)

VTE prophylaxis (low molecular weight heparin + compression stockings) - PE is the most common cause of death

Phase 3a (9 decks)

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