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Phase 2a > Neuro > Flashcards

Neuro Flashcards

1
Q

What is a stroke (cerebrovascular accident)?

A

When the blood supply to part of the brain is cut off

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2
Q

What can cause a stroke?

A

Small vessel occlusion/ thrombosis in situ
Cardiac emboli, CNS bleeds e.g. aneurysm rupture
Subarachnoid haemorrhage

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3
Q

What are the modifiable risk factors for strokes?

A

High BP, smoking, diabetes, heart disease, peripheral vascular disease

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4
Q

What medical conditions act as risk factors for strokes?

A

Hypertension, carotid artery stenosis, vasculitis, hyper viscosity

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5
Q

What is the ischaemic pathology of a stroke?

A

Sustained occlusion of a cerebral artery leads to ischaemic necrosis of the territory of the brain supplied by the affected artery

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6
Q

What is the haemorrhagic pathology of a stroke?

A

Hypertension due to ruptured Charcot-Bouchard aneurysms

Haematoma forms which destroys the brain structure and causes a sudden rise in intracranial pressure

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7
Q

Which manifestations of a stroke point to a haemorrhagic cause?

A

Meningism, severe headache, coma

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8
Q

Which manifestations of a stroke point to an ischaemic cause?

A

Carotid bruit, AF, past TIA, IHD

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9
Q

How do cerebral infarcts present?

A

Visuo-spatial deficit, dysphasia, spasticity (UMN)

Contralateral sensory loss or hemiplegia

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10
Q

How do brainstem infarcts present?

A

Quadriplegia, disturbances of gaze and vision, locked-in syndrome (aware but can’t respond)

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11
Q

How do lacunar infarcts present?

A

5 syndromes: Ataxic hemiparesis, pure motor, pure sensory, sensorimotor, dysarthria

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12
Q

How are strokes diagnosed?

A

FAST, CT/ MRI for haematoma, ECG: AF, CXR: LV hypertrophy

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13
Q

How are strokes managed?

A

Ischaemia - thrombolysis with IV Altepase
Aspirin for 2 weeks, then clopidogerol
Haemorrhagic - control BP (beta blocker)
Surgery - Clot evacuation

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14
Q

How can strokes be primarily prevented?

A

Control risk factors - hypertension, diabetes mellitus, cardiac disease, quit smoking. Use lifelong anticoagulant in AF and prosthetic heart valves

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15
Q

How can strokes be secondarily prevented?

A

Lower BP and cholesterol
Anti-platelet agents after stroke
Anticoagulation after stroke from AF

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16
Q

What is a transient ischaemic attack?

A

An ischaemic (usually embolic) neurological event with symptoms lasting <24h (often much shorter)

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17
Q

What are the causes of TIAs?

A

Atherothromboembolism from the carotid, cardioembolism, hyper viscosity, vasculitis

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18
Q

Explain the ABCD2 score for strokes

A 
Age: 60+
BP: 140/90mmHg +
Clinical features: unilateral weakness (2 points), speech disturbance without weakness
Duration: 60+ = 2 points, 10-50 = 1
Diabetes
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19
Q

What indicates a high risk of stroke?

A

ABCD2 score 4+

AF, more than one TIA in one week

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20
Q

What is amaurosis fugax?

A

Occurs when the retinal artery is occluded, causing unilateral progressive vision loss ‘like a curtain descending’

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21
Q

What is a differential diagnosis for a TIA?

A

Focal epilepsy

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22
Q

How are TIAs investigated?

A

FBC, CXR, ECG, Carotid Doppler with angiography r CT

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23
Q

How are TIAs managed?

A

Control CV risk factors; high BP (beta blocker), diabetes, smoking
Antiplatelet drugs - aspirin (immediate)/clopidogrel
Statins - simvastatin

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24
Q

What is a carotid endarterectomy?

A

Surgery to remove a build-up of plaque in the carotid artery

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25
Q

What is a subarachnoid haemorrhage?

A

A spontaneous, non-traumatic bleed into the subarachnoid space (from circle of Willis)

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26
Q

What is the most common cause of a subarachnoid haemorrhage?

A

Rupture of a berry aneurysm - result in extensive bleeding through the subarachnoid space

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27
Q

What are the risk factors for a subarachnoid haemorrhage?

A

Smoking/alcohol excess, raised BP, bleeding disorders, PKD, aortic coarctation

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28
Q

How do subarachnoid haemorrhages present?

A

Sudden severe headache, vomiting, neck stiffness, collapse, seizures, coma

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29
Q

What is a differential diagnosis of a subarachnoid haemorrhage?

A

Benign thunderclap headache

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30
Q

How are subarachnoid haemorrhages diagnosed?

A

Macroscopy - blood present within SA space, with abundant clots around circle of Willis
CT - urgent

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31
Q

How are subarachnoid haemorrhages managed?

A

Well hydrated - maintain cerebral perfusion
CCB - nimodipine, reduces vasospasm and consequent morbidity
SURGERY URGENT

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32
Q

What are cerebral contusions?

A

Bruises on the surface of the brain

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33
Q

When do cerebral contusions occur?

A

When the brain suddenly moves within the cranial cavity and is crushed against the skull

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34
Q

What is a subdural haemorrhage?

A

Bleeding from bridging veins between cortex and venous sinuses, resulting in accumulating haematoma

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35
Q

When are subdural haemorrhages common?

A

When patients have a small brain e.g. alcoholics, dementia

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36
Q

Between what layers do subdural haemorrhages occur?

A

The dura and the arachnoid

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37
Q

What causes a subdural haemorrhage?

A 
Lowered intracranial pressure
Minor trauma (up to 9 months previous) - 	Results from tearing of delicate bridging veins that traverse the subdural space to drain into the cerebral venous sinuses
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38
Q

How do subdural haemorrhages present?

A

Fluctuating levels of consciousness, insidious physical/ intellectual slowing, sleepiness, headache, personality change

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39
Q

Why is there raised intracranial pressure in subdural haemorrhages?

A

The massive increase in oncotic and osmotic pressure sucks water into the haematoma, gradual rise in ICP

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40
Q

How are subdural haemorrhages diagnosed?

A

CT/MRI shows clot - look for crescent-shaped collection of blood over 1 hemisphere (sickle-shape differentiates subdural from extradural)

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41
Q

How are subdural haemorrhages managed?

A

Address the cause, surgical evacuation of the clot

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42
Q

What is an extradural haemorrhage?

A

Bleeding from the middle meningeal artery with a characteristic lucid period

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43
Q

Between what layers do extradural haemorrhages occur?

A

Dura and the skull

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44
Q

Why is there a lucid period for extradural haemorrhages?

A

Accumulation of extradural blood is slow, as the firmly adherent dura is slowly peeled away from the inner surface of the skull

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45
Q

What causes an extradural haemorrhage?

A

Traumatic skull fracture - temporal or parietal bone causing laceration of the middle meningeal artery and vein
Tear in a dural venous sinus

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46
Q

How do extradural haemorrhages present?

A

Severe headache, vomiting, confusion, seizures
Continued bleeding Ipsilateral pupil dilates, coma deepens, bilateral limb weakness
Death - respiratory arrest

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47
Q

How long may the lucid interval for extradural haemorrhages last?

A

A few hours to a few days before a bleed declares itself by low GCS (Glasgow coma scale) from rising ICP
Patients may appear well for several hours following a head injury but then quickly deteriorate as the haematoma enlarges and compresses the brain

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48
Q

How are extradural haemorrhages diagnosed?

A

CT - haematoma

Skull X-ray may be normal or show fracture lines crossing meningeal vessels

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49
Q

How are extradural haemorrhages managed?

A

Urgent clot evacuation

Care of the airway and lowering ICP often require intubation and ventilation

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50
Q

What is epilepsy?

A

A recurrent tendency to spontaneous episodes of abnormal electrical activity within the brain which manifest as seizures

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51
Q

What are partial/focal epileptic seizures?

A

Originating within networks linked to one hemisphere and often seen with underlying structural disease

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52
Q

What are generalised epileptic seizures?

A

Features not referable to one hemisphere, consciousness always impaired

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53
Q

What are the causes of epilepsy?

A

Idiopathic
May be associated with underlying structural lesions e.g. neoplasms, metabolic conditions e.g. electrolyte disorders, infections, rare genetic diseases

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54
Q

What is an aura of an epileptic seizure?

A

Aura: implies a focal seizure, often from the temporal lobe. May be a strange feeling in the gut or flashing light

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55
Q

What general symptoms might occur after an epileptic seizure (post-ictally)?

A

Headache, confusion, myalgia

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56
Q

What symptoms may occur after an epileptic seizure affecting the temporal lobe?

A

Emotional disturbance, dysphasia, hallucinations

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57
Q

What symptoms may occur after an epileptic seizure affecting the frontal lobe?

A

Motor features such as peddling movements of the legs. Motor arrest, dysphasia or speech arrest

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58
Q

What symptoms may occur after an epileptic seizure affecting the parietal lobe?

A

Sensory disturbances - tingling, numbness, pain. Motor symptoms

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59
Q

What symptoms may occur after an epileptic seizure affecting the occipital lobe?

A

Visual phenomena such as spots, lines, flashes

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60
Q

How is epilepsy diagnosed?

A

Thorough history - often from a witness of a seizure
Ask about triggers e.g. flickering lights
Rule out provoking causes e.g. trauma, stroke, alcohol withdrawal
MRI: structural lesions

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61
Q

How is epilepsy managed pharmacologically?

A

Anti-Epileptic drugs
Status-Epilepticus - IV Lorazepam
Focal: carbamazepine
Generalised: Sodium valproate

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62
Q

How is epilepsy managed non-pharmacologically?

A

Psychological therapies - relaxation, CBT

Surgical intervention - neurosurgical resection

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63
Q

What are the different subtypes of generalised seizures?

A

Absence - brief pauses
Tonic-clonic - loss of consciousness. Limbs stiffen then jerk
Myoclonic - sudden jerk of a limb, face or trunk
Tonic - sudden sustained stiffening of the body not followed by jerks
Atonic - sudden loss of muscle tone causing a fall

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64
Q

What is dementia?

A

A neurodegenerative syndrome with progressive decline in several cognitive domains

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65
Q

What are the different types of dementia?

A

Alzheimer’s, Lewy body, Parkinson’s, vascular

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66
Q

What causes vascular dementia?

A

Cumulative effect of many small strokes - Multiple infarcts caused by vascular occlusion due to thrombosis commonly due to atherosclerosis

67
Q

What is characteristic about Lewy body dementia?

A

Lewy bodies in brainstem and neocortex. These accumulate within neurones and lead to damage and cellular loss

68
Q

What are some ‘other’ causes of dementia?

A 
Alcohol/ drug abuse
Repeated head trauma
Pellagra - lack of nicotinic acid
Huntington's and Parkinson's
Familial autosomal dominant Alzheimer's
69
Q

How is dementia diagnosed?

A

Look for reversible/ organic causes: raised TSH/ low B12
MRI can identify other reversible pathologies e.g. subdural haematoma
History - timeline of decline and domains affected
Cognitive testing - mental state exam to identify anxiety, depression or hallucinations

70
Q

What is the 6CIT Dementia test?

A 
Six item cognitive impairment test
What year is it?
What month is it?
Give an address with 5 parts
Count 20-1
Say months of the year in reverse
Repeat address
71
Q

How is dementia managed?

A

Healthier lifestyle, social support, Acetylcholinesterase inhibitor e.g. Rivastigmine

72
Q

What is vascular dementia?

A

A disease characterised clinically by dementia and histopathologically by injury to the brain parenchyma, associated with a wide range of cerebrovascular lesions

73
Q

How does vascular dementia present?

A

Impairment of executive function and slowing of mental processing may be prominent, particularly with diffuse subcortical involvement
Stepwise progression and focal neurology

74
Q

How does dementia with Lewy bodies present?

A

Progressively worsening dementia very similar to Alzheimer’s disease
Fluctuating levels of cognition, recurrent visual hallucinations, features of parkinsonism

75
Q

What is Alzheimer’s?

A

A neurodegenerative disease characterised clinically by dementia and histopathologically by neuronal loss in the cerebral cortex, in associated with numerous amyloid plaques and neuro-fibrally tangles

76
Q

What causes Alzheimer’s?

A

Environmental and genetic factors play a role
Accumulation of beta-amyloid peptide results in progressive neuronal damage, neurofibrillary tangles, raised number of amyloid plaques and loss of acetylcholine.

77
Q

What is the temporal lobe responsible for?

A

Hearing, Language comprehension, semantic knowledge, memory, emotional behaviour

78
Q

How does Alzheimer’s present?

A

Progressive memory loss - starts with day to day and new learning, increases to managing daily activity such as finances.
Agnosia, delusions, loss of motor skills.
Late - agitation, restlessness, wandering

79
Q

How do the terminal stages of Alzheimer’s present?

A

Reduced speech, immobility, incontinence

80
Q

How is Alzheimer’s diagnosed?

A

Macroscopy: cortical atrophy with narrowing of gyri and widening of sulci.
Microscopy: abundant neuritis plaques and neurofibrillary tangles in the cerebral cortex

81
Q

How is Alzheimer’s managed?

A

Prevention - cognitively active, control vascular risk factors
Support, medications - memantine, acetyl choline esterase inhibitors

82
Q

What is Parkinson’s disease?

A

A neurodegenerative hypokinetic movement disorder characterised clinically by parkinsonism and histologically by neuronal loss and Lewy bodies concentrated in the substantia nigra

83
Q

What is the pathology of Parkinson’s?

A

Lack of dopamine release results in movement disorder (loss of dopaminergic neutrons in substantia nigra)

84
Q

How does Parkinson’s present?

A

Typically unilateral. Classic triad of tremor (pill rolling of thumb over fingers), rigidity (hypertonia), bradykinesia (slow to initiate movement - shuffling, forward gait)

85
Q

What conditions can be seen with Parkinson’s progression?

A

Dysphagia, dementia, depression - debilitating

86
Q

How is Parkinson’s diagnosed?

A

Clinical and based on core features of bradykinesia with resting tremor/ hypertonia
MRI to rule out structural pathology
A clinical response to dopaminergic therapy is supportive

87
Q

How is Parkinson’s managed?

A

Treatment with dopaminergic drugs eases symptoms but doesn’t slow progression
Patients on long term treatment with LEVODOPA develop severe dyskinesias as a side effect

88
Q

What is Huntington’s chorea?

A

An inherited neurodegenerative disorder caused by mutation of the HTT gene

89
Q

What is the pathology of Huntington’s?

A

Gene protein Huntingtin (HTT) which interacts with many other proteins is mutated, which is thought to be cytotoxic to neurones in the caudate nucleus and putamen. Atrophy and neuronal loss of striatum and cortex lead to loss of neurotransmitter GABA

90
Q

How does Huntington’s present?

A

Decrease of GABA and unbalanced dopamine activity result in chorea - Uncontrolled, random, jerky movements
Motor, neuropsychiatric, and cognitive decline, ultimately terminating in dementia

91
Q

How is Huntington’s diagnosed?

A

Diagnosis is clinical

Chorea, slowness of fine finger movements, abnormal eye movements e.g. broken pursuit

92
Q

How is Huntington’s managed?

A

Chorea - sulpiride
Depression - seroxate
Psychosis - haloperidol
Aggression - risperidone

93
Q

What features of a headache point towards secondary causes?

A

Jaw claudication, visual disturbance, severe eye pain, postural, thunderclap

94
Q

What details should be taken in a headache history?

A

Types/number, time-onset/duration, pain - severity/ site, triggers, response, any change in attacks

95
Q

What is a migraine?

A

A recurrent throbbing headache that typically affects one side of the head and is often accompanied by nausea and disturbed vision

96
Q

What are the risk factors for migraines?

A

Smoking, age >35 years, high BP, obesity, oral contraceptive pill

97
Q

What can trigger migraines?

A

Chocolate, hangovers, orgasms, caffeine, alcohol, travel, exercise

98
Q

How do migraines present?

A

Visual or other aura lasting 15-30mins followed within 1h by unilateral, throbbing headache
Episodic headache without aura with nausea, vomiting
Allodynia

99
Q

How are migraines diagnosed?

A

Diagnosis is clinical, based on history.

>5 headaches lasting 4-72 hours + nausea/vomiting + any 2 of; unilateral, pulsating, impairs routine acitvity

100
Q

How are migraines managed?

A

Avoid identified triggers
Prophylactic treatment: propranolol
Severe attack: Oral triptan Mild attack: NSAID

101
Q

What are the characteristics of a tension headache?

A

Most common, tight band pain - feeling of pressure or tightness all around head, scalp muscle tenderness

102
Q

What are the characteristics of a cluster headache?

A

Rapid-Onset of excruciating pain around one eye that may become watery and bloodshot with lid swelling, lacrimation, facial flushing.
Occurs once/twice a day, with clusters lasting 4-12 weeks followed by pain-free periods of months/years

103
Q

How are cluster headaches managed?

A

Acute attack: 100% O2 for 15min via non-rebreathable mask, SC Sumatriptan
Prevention: avoid triggers, corticosteroids

104
Q

What are the characteristics of drug overuse headaches?

A

Headache present on >15days/month. Regular use for >3months of a symptomatic treatment drug e.g. opioids
Headache has developed during drug use.
Withdraw the analgesics

105
Q

What is giant cell arteritis?

A

A vasculitis of medium and large vessels which preferentially affects head and neck arteries

106
Q

How does giant cell arteritis present?

A

Over weeks/months with fever, anorexia, weight loss
Temporal artery - headache, scalp tenderness, jaw claudication
Ocular vessels - blindness

107
Q

How is giant cell arteritis diagnosed?

A

Raised ESR/CRP, raised platelets, low Hb
3 of these criteria present: Age >50, new headache, tenderness, decreased pulsation (temporal artery), ESR >50, abnormal biopsy

108
Q

How is giant cell arteritis managed?

A

Prednisolone immediately

- IV methylprednisolone if visual loss evolving

109
Q

What is trigeminal neuralgia?

A

Neuralgia involving one or more of the branches of the trigeminal nerves, and often causing severe pain

110
Q

How does trigeminal neuralgia present?

A

Paroxysms of intense, stabbing pain, in the trigeminal nerve distribution
Unilateral, face screws up with pain

111
Q

How is trigeminal neuralgia diagnosed?

A

MRI: exclude secondary causes e.g. nerve root compression

112
Q

How is trigeminal neuralgia managed?

A

Carbamazepine, surgery, microvascular decompression

113
Q

What can cause spinal cord compression?

A

Secondary malignant e.g. breast, lung, prostate, thyroid, kidney
Infection, cervical disc prolapse, haematoma

114
Q

How does spinal cord compression present?

A

Bilateral leg weakness, preceding back pain, Urinary: hesitancy, frequency, painless retention

115
Q

How is spinal cord compression diagnosed?

A

MRI, biopsy, CXR to check for primary lung malignancy

116
Q

How is spinal cord compression managed?

A

Urgent dexamethasone in malignancy
Thromboprophylaxis
Epidural abscesses must be decompressed

117
Q

What is Cauda Equina syndrome and what are the signs?

A

Spinal cord compression at the site of the caudate equina. Back pain and pain down legs, sensory loss in root distribution, bladder/ bowel incontinence

118
Q

What is multiple sclerosis?

A

A relapsing and remitting demyelinating disease of the CNS, in which episodes of neurological disturbance affect different parts of the CNS at different times

119
Q

What is the pathology behind MS?

A

Episodes of demyelination lead to attacks of acute neurological deficit, which develop over a period of a few days and remain for a few weeks before symptom recovery

120
Q

How does MS present?

A

Symptoms highly variable depending on lesion site
Spinal cord: weakness, paraplegia
Optic nerves: impaired vision
Medulla and pons: dysarthria, vertigo

121
Q

How is MS diagnosed?

A

Diagnosis is clinical, based on frequency of attacks and clinical presentation
2+ CNS lesions disseminated in time and space, exclusion of conditions giving a similar clinical picture

122
Q

How is MS managed?

A

Regular exercise, stop smoking
Dimethyl fumarate
Treat relapses - methylprednisolone
Symptom control

123
Q

What is myasthenia gravis?

A

An autoimmune disease caused by production of autoantibodies directed against various antigens of the neuromuscular junction

124
Q

How does myasthenia gravis present?

A

Muscular fatiguability

Muscle groups affected, in order; Extraocular, bulbar face, neck, limb girdle, trunk

125
Q

How is myasthenia gravis diagnosed?

A

Antibodies: increased anti-AChR antibodies, -ve look for MuSK antibodies
EMG: decremental muscle response to repetitive nerve stimulation

126
Q

How is myasthenia gravis managed?

A

Immunosuppression, combination of acetylcholinesterase inhibitors and immunomodulatory therapies

127
Q

What is motor neurone disease?

A

A group of neurodegenerative diseases characterised by selective loss of motor neurones

128
Q

What are the 4 clinical patterns of motor neurone disease?

A

Amyotrophic lateral sclerosis
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

129
Q

What are the clinical features related to lower motor neurone lesions?

A

Muscle tone normal/reduced, muscle wasting, fasciculation, reflexes depressed or absent (everything goes down)

130
Q

What are the clinical features related to upper motor neurone lesions?

A

Muscle tone increases (spasticity), tendon reflexes are brisk, upper limbs extensor muscles weaker than flexors (everything goes up)

131
Q

How is motor neurone disease diagnosed?

A

No diagnostic test. Brain/cord MRI helps exclude structural causes

132
Q

How is motor neurone disease managed?

A

Disease is progressive, fatal within a few years

Riluzole - inhibitor of glutamate release and NMDA receptor antagonist

133
Q

What is Guillain-Barre syndrome?

A

Classical Guillain-Barre syndrome (GBS) is an acute demyelinating polyneuropathy which usually follows 1-2 weeks after an upper respiratory tract or GI infection

134
Q

How does Guillain-Barre syndrome present?

A

Few weeks after infection - symmetrical ascending muscle weakness starts (sudden onset of tingling and numbness of fingers and toes)
Weakness spreads proximally

135
Q

How is Guillain-Barre syndrome diagnosed and managed?

A

Lumbar puncture: increased CSF protein with normal cell count
IV immunoglobulin

136
Q

What are the 3 cardinal presenting symptoms of a brain tumour?

A

Symptoms of raised ICP - headache, reduced conscious level, nausea and vomiting
Progressive neurological deficit
Epilepsy

137
Q

How are secondary brain tumours treated?

A

Surgery, radiotherapy, chemotherapy, best supportive care

138
Q

From what type of cell do most primary brain tumours originate?

A

Glial cells - astrocytoma, oligodendroglioma, gliomas

139
Q

How are glioblastomas treated?

A

Debulking surgery, radiotherapy to maximum tolerated brain dose.

140
Q

What are the features of dexamethasone?

A

Most powerful synthetic steroid, rapidly improves brain performance in all brain tumours. Reduces tumour inflammation/ oedema

141
Q

What are the most common tumours with metastases to the brain?

A

Lung (most common), breast, melanoma, GI tract, kidney

142
Q

What are astrocytomas?

A

CNS tumours formed by glial cells showing astrocytic differentiation. Diffuse, anaplastic, glioblastoma

143
Q

What are oligodendrogliomas?

A

Diffusely infiltrative CNS tumours formed by glial cells showing oligodendrogliomal differentation

144
Q

What are ependymomas?

A

CNS tumours composed of neoplastic ependymal cells arising from the ependymal-lined ventricular system or the spinal canal

145
Q

What are meningiomas?

A

Tumours from meningothelial cells and attached to the inner surface of the dura matter. Majority are benign and correspond to WHO grade I

146
Q

What are medulloblastomas?

A

A primitive embryonal tumour of the cerebellum

147
Q

What are primary CNS lymphomas?

A

Primary extra nodal lymphomas arising in the CNS

148
Q

What is meningitis?

A

Infection of the subarachnoid space. Inflammation of the meninges

149
Q

Which viruses most commonly cause meningitis?

A

Echoviruses, Coxsackie viruses

150
Q

Which bacteria most commonly cause meningitis?

A

Neisseria meningitidis or streptococcus pneumoniae

151
Q

How does infection reach the meninges?

A

Extracranial infection e.g. nasopharynx - nasal carriage
Neurosurgical complications e.g. post op
Via blood stream

152
Q

Describe the pathophysiology of meningitis

A

Blood – CSF – brain barrier
Bacteria enter CSF, and can be isolated from the immune cells due to BBB
Replication – number of bacteria increases
Blood vessels become leaky
WBCs can enter the CSF, meninges and brain
Meningeal inflammation. Brain swelling

153
Q

How does meningitis present?

A

Headache, fever, neck stiffness, photophobia, non-blanching purpuric rash

154
Q

How is meningitis diagnosed?

A

Microbiology: lumbar puncture of CSF fluid shows predominance of lymphocytes in viral, and neutrophils in bacterial
Gram staining: gram negative diplococci

155
Q

How is meningitis managed?

A

Bacterial requires hospital admittance - Glasgow coma score, broad spectrum antibiotics (IV cefotaxime 1st line) and steroids (IV dexamethasone)

156
Q

What is encephalitis?

A

Infection of the brain parenchyma. Inflammation of the brain – confusion due to direct inflammation/infection of brain

157
Q

What causes encephalitis?

A

Viruses - HSV. Herpes simplex, varicella zoster, measles, mumps, rubella, HIV
Rabies, West Nile virus
Malaria, Lyme disease, TB

158
Q

How does encephalitis present?

A

Precedes with ‘flu-like’ illness. Confusion, behavioural changes, altered consciousness seizures in severe cases

159
Q

How is encephalitis diagnosed?

A

Bloods cultures, imaging: MRI highlights abnormalities in temporal lobe
Lumbar puncture: viral PCR on a lymphocytic CSF sample can identify the virus

160
Q

How is encephalitis managed?

A

Urgent antiviral treatment, HSV - acyclovir.

Symptomatic treatment

161
Q

What causes Herpes zoster (shingles)?

A

Varicella-zoster virus (VZV) is highly contagious and most individuals are infected in childhood, leading to chickenpox
Transmitted by respiratory droplets
Infection is lifelong, reactivation of virus in adulthood leads to shingles

162
Q

How does shingles present?

A

Band-like vesicular eruption along the distribution of a sensory nerve. Painful, hyper aesthetic area. Infectious until scabs appear

163
Q

How is shingles diagnosed?

A

Clinical diagnosis (based on a rash within a dermatome) unless immunosuppressed - viral PCR, culture, immunofluorescence

164
Q

How is shingles managed?

A

Oral acyclovir for uncomplicated cases. Aim to give within 48hrs of rash.
Vaccination given at 70 to prevent shingles reactivation

Phase 2a (16 decks)

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