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(SG) condensed phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

Define Transient ischaemic attack

A

Rapid onset of neurological deficit, less than 24hrs.

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2
Q

Define Stroke

A

Rapid onset of neurological deficit, more than 24hrs.

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3
Q

Types of Stroke

A

Ischaemic.

Haemorrhagic.

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4
Q

How does a Transient ischaemic attack clinically present?

A

Depends on the locations of the ischaemia.

Carotid:
Amaurosis fugax, aphasia, hemiparesis, hemisensory loss, hemianopic visual loss

Vertebrobasilar:
Diplopia, vertigo, vomiting, choking and dysarthria, ataxia, hemisensory loss, hemianopic, tetraparesis

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5
Q

How does an ischaemic stroke clinically present?

A

Depends on the location of the infarct.

Cerebal hemisphere (most common): 
Signs contralateral to the affected side. Hemiplegia, hemisensory loss, upper motor neurone facial weakness and hemianopia

Brainstem:
complex, depending on location

Multi-infarct:
Multiple steps progressing to dementia

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6
Q

How does a haemorrhagic stroke clinically present?

A

Severe headache, nausea/vomiting.

Sudden loss of consciousness

-> Stroke (see ischaemic stroke clinical presentation).

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7
Q

Why is a transient ischaemic attack good?

A

It’s completely reversible

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8
Q

Pathophysiology of a Transient ischaemic attack

A

Ischaemia

  • > oxygen deprevation of tissue
  • > transient loss of function
  • > resolve
  • > possible remittance
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9
Q

Pathophysiology of an ischaemic stroke

A

Ischaemic

  • > infarct
  • > Death of neural tissue
  • > Loss of functionality
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10
Q

Pathophysiology of a haemorrhagic stroke

A

Primarily intracerebral haemorrhage.

Risk factors -> small vessel disease and aneurysms

-> rupture and haemorrhage.

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11
Q

Cause of a Transient ischaemic attack

A

Usually passage of microemboli, which subsequently lyse, from atheromatous plaques.

Can be from the carotid, or a cardiac embolus (IE)

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12
Q

Cause of an ischaemic stroke

A

Ischaemic infarction due to occlusion of a vessel, usually by an embolism of a thrombus.

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13
Q

Cause of a haemorrhagic stroke

A

RF: Hypertension,

excess alcohol,

smoking

and age.

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14
Q

Diagnostic test for a Transient ischaemic attack

A

Clinical. ABCD2 score (risk of a stroke).

CT: Infarction check.

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15
Q

Diagnostic test for an ischaemic stroke

A

CT/MRI: rule out bleed.

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16
Q

Diagnostic test for a haemorrhagic stroke

A

CT or MRI: in <24hrs.

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17
Q

Treatments for a Transient ischaemic attack

A

Aspirin, clopidogrel if intolerant.

Control of hypertension.

Adjust risk factors.

Start a statin.

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18
Q

Treatment for an ischaemic stroke

A

Aspirin, IV alteplase in at least 4.5 hours (thrombolytic; IV tissue plasminogen activator),

antiplatelet (aspirin -> lifelong clopidogrel),

maintain glucose,

NBM.

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19
Q

Treatment for a haemorrhagic stroke

A

Stop anticoagulants.

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20
Q

Define Subarachnoid haemorrhage

A

Spontaneous arterial bleeding into the subarachnoid space.

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21
Q

Define Dural haemorrhage

A

Bleed into a space adjacent to the dura.

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22
Q

Types of Dural haemorrhage

A

Subdural.

Extradural.

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23
Q

How does a Subarachnoid haemorrhage clinically present?

A

Mostly asymptomatic until rupture

-> very immediate onset of ‘thunderclap headache’,

usually on the back of the head, with nausea, and loss of consciousness.

Possible ‘warning headaches’ days before.

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24
Q

How does a subdural haemorrhage clinically present?

A

Headache,

drowsiness

and confusion (may fluctuate).

Signs of ICP.

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25
Q

How does an extradural haemorrhage clinically present?

A

Head injury

  • > Unconscious
  • > Lucid recovery
  • > Rapid deterioration (with focal neurological signs),

with loss of consciousness.

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26
Q

Where does a subdural haemorrhage occur?

A

Beneath the dura

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27
Q

Where does an extradural haemorrhage occur?

A

Above the dura

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28
Q

Pathophysiology of a Subarachnoid haemorrhage

A

Berry aneurysms are an acquired lesion that occur most commonly at bifurcations.

Can cause a mass effect if they are large.

Rupture causes a rapid release of arterial blood into the SA space

-> increased ICP and possible CVA.

Sentinel headaches due to leaking aneurysms

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29
Q

Pathophysiology of a subdural haemorrhage

A

Rupture of a vein running from the hemisphere to the saggital sinus (bridging veins).

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30
Q

Pathophysiology of an extradural haemorrhage

A

Fractured temporal bone

  • > rupture of the middle meningeal artery
  • > bleed.
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31
Q

Cause of a Subarachnoid haemorrhage

A

Spontaneous.

70% due to rupture of berry aneurysms (usually at branch points in the circle of willis).

10% due to congenital arteriovenous malformation.

20% other vascular cause.

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32
Q

Cause of a subdural haemorrhage

A

Almost always head injury (often minor).

But can be delayed for up to 9 months after the incident.

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33
Q

Cause of an extradural haemorrhage

A

Injuries that fracture the temporal bone.

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34
Q

Epidemiology of a Subarachnoid haemorrhage

A

5% of strokes.

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35
Q

Epidemiology of a subdural haemorrhage

A

Elderly and alcoholics.

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36
Q

Diagnostic tests for a Subarachnoid haemorrhage

A

CT scan: Star pattern

Lumbar puncture (12hrs after symptoms):

Bloody, or Increase in pigments (xanthochromia) making it straw coloured.

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37
Q

Diagnostic test for a subdural haemorrhage

A

CT: Appears crescent shaped.

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38
Q

Diagnostic test for an extradural haemorrhage

A

CT: Appears like a convex lens.

DONT DO LP.

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39
Q

Treatments for a Subarachnoid haemorrhage

A

Bed rest, supportive measures for hypertension,

CCB,

IV saline to replace salts,

dexamethasone for cerebral oedema.

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40
Q

Treatments for a subdural haemorrhage

A

Surgical removal of the haematoma.

Mannitol: Reduced ICP in small dose.

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41
Q

Treatments for an extradural haemorrhage

A

Surgical drainage

Mannitol: Reduced ICP in small dose

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42
Q

Complications of a Subarachnoid haemorrhage

A

50% die in hospital.

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43
Q

Define epilepsy

A

Transient abnormal electrical activity in the brain

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44
Q

Define Parkinson’s disease

A

Neurodegenerative loss of dopamine-secreting cells from the substantia nigra.

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45
Q

Types of epilepsy

A

Generalised tonic clonic (Grand mals).

Absence (Petite mals).

Myoclonic, tonic and akinetic.

Partial.

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46
Q

How does generalised tonic clonic (Grand mals) epilepsy clinically present?

A

Sudden onset of rigid tonic phase followed by convulsion (clonic) phase.

Back and forth rhythmically.

Tongue biting,

incontinence of urine,

followed by drowsiness/coma.

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47
Q

How does absence (Petite mals) epilepsy clinically present?

A

Usually childhood.

Cease activity, stares and pales.

Tends to develop into grand mals.

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48
Q

How does Myoclonic, tonic and akinetic epilepsy clinically present?

A

Muscle jerking (myoclonic),

intense stiffening (tonic) or cessation of movement,

falling and loss of consciousness (akinetic).

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49
Q

How does partial epilepsy clinically present?

A

Simple (not affecting consciousness or memory)

or complex (affecting).

Symptoms depending on focus of seizure.

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50
Q

How does Parkinson’s disease clinically present?

A

Rest tremor, rigity and bradykinesia developing over several months.

Characteristic stoop.

Pill rolling tremor.

TRAP (tremor akinesia akinesia postural instability).

Usually one side over the other at the start.

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51
Q

Pathophysiology of epilepsy

A

Uncontrolled electrical activity in the brain.

Innervation of muscle fibres can cause physical movements (as per tonic clonic)

and sensory disturbance possible (particularly in partial).

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52
Q

Pathophysiology of Parkinson’s disease

A

Progressive loss of dopamine secreting cells from the substantia nigra

-> alteration in neural circuits within basal ganglia that regulates movement.

Also loss from non striatal pathways accounts for neuropsychiatric pathology.

Thought to be due to abnormal accumulation of alpha-synuclein bound to ubiquitin which forms lewy bodies in cytoplasm.

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53
Q

Causes of epilepsy

A

Can be triggered by flashing lights.

Broadly unknown cause, but some genetic association.

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54
Q

Causes of Parkinson’s disease

A

Unknown.

Some genetic link (alpha-synuclein gene and parkin gene),

some environmental link.

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55
Q

Epidemiology of Parkinson’s disease

A

Less common in smokers.

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56
Q

Diagnostic tests for epilepsy

A

Short term video EEG.

CT,

MRI.

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57
Q

Diagnostic tests for Parkinson’s disease

A

Clinical,

MRI

and CT (Atrophy of the Substantia nigra).

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58
Q

Treatment for generalised tonic clonic (Grand mals) epilepsy

A

AED: Sodium valproate (not in child bearing age women).

Lamotrigine.

Seizure control: Diazepam (or lorazepam).

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59
Q

Treatment for absence (Petite mals) epilepsy

A

AED: Sodium valproate.

Ethosuximide.

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60
Q

Treatment for partial epilepsy

A

AED: Lamotrigine carbamazepine, Phenytoin

Seizure control: Diazepam (or lorazepam).

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61
Q

Treatment for Parkinson’s disease

A

L-DOPA with peripheral DOPA decarboxylase inhibitor (carbidopa).

Dopamine agonists (ropinirole)

MAO-B inhibitors: Selegiline.

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62
Q

Define Huntington’s disease

A

AD neurodegenerative,

loss of GABA + Ach,

but dopamine spared.

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63
Q

Define a migraine

A

Recurrent headache for 4-72hrs with visual

and/or GI disturbance.

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64
Q

Define giant cell arteritis

A

Granulomatous arteritis.

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65
Q

Define Trigeminal neuralgia

A

Knife like pain in trigeminal sensory divisions.

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66
Q

Types of migraine

A

Aura

Without aura

Variant

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67
Q

How does Huntington’s disease clinically present?

A

Rrelentlessly progressive.

Chorea.

Personality change.

Later, dementia.

Occasionally prodromal phase of psychotic and behavioural symptoms.

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68
Q

How does a migraine aura clinically present?

A

Characteristically unilateral.

Visual disturbance (zig zaggy lines).

Photosensitivity.

Nausea.

Sometimes premonitory symptoms.

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69
Q

How does a migraine without aura clinically present?

A

Characteristically unilateral.

Photosensitivity.

Nausea.

Sometimes premonitory symptoms.

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70
Q

How does a variant migraine clinically present?

A

Unilateral motor or sensory symptoms resembling a stroke.

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71
Q

How does giant cell arteritis clinically present?

A

Headache, scalp tenderness, jaw claudication.

Superficial temporal artery may be firm, tender and pulseless.

Weight loss, malaise and fever.

Blindness in 25% of untreated (amaurosis fugax).

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72
Q

How does Trigeminal neuralgia clinically present?

A

Severe, short lasting, paroxysmal knife/electric shock like pain in one or more sensory divisions of the trigeminal nerve.

Almost always unilateral.

Usually specific trigger (washing, shaving, eating).

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73
Q

What is giant cell arteritis associated with?

A

Polymyalgia rheumatica.

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74
Q

Pathophysiology of Huntington’s disease

A

Presence of mutant Huntingtin protein

  • > unknown process
  • > Loss of neurones in the caudate nucleus and putamen of the basal ganglia
  • > Depletion of GABA and Ach.

Dopamine spared.

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75
Q

Pathophysiology of a migraine

A

Changes in brainstem blood flow

  • > unstable trigeminal nerve nucleus and nuclei in the basal thalamus
  • > release of vasoactive neuropeptides (CGRP and substance P)
  • > neurogenic inflammation; vasodilatation and plasma protein extravasation.

Aura: Cortical spreading depression is a self propogating wave of neuronal and glial depolarization that spreads across the cortex.

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76
Q

Pathophysiology of giant cell arteritis

A

Chronic inflammation of the medium-large arteries, particularly the aorta and its extracranial branches.

Blindness: inflammation and occlusion of the ciliary and/or central retinal artery

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77
Q

Pathophysiology of Trigeminal neuralgia

A

Possibly as a result of compression of the trigeminal nerve by a loop of artery or vein.

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78
Q

Cause of Huntington’s disease

A

Autosomal dominant.

CAG repeats in Huntingtin protein gene on chromosome 4.

No. of repeats -> indicative of age of onset.

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79
Q

Cause of a migraine

A

Genetic and environmental factors.

Precipitants: chocolate, cheese and too much/little sleep.

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80
Q

Cause of giant cell arteritis

A

Unknown

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81
Q

Cause of Trigeminal neuralgia

A

Unknown

82
Q

Epidemiology of Huntington’s disease

A

Usually onset in middle age.

83
Q

Epidemiology of a migraine

A

More in women.

Usually presents before 40.

84
Q

Epidemiology of giant cell arteritis

A

Principally over 50s.

85
Q

Epidemiology of Trigeminal neuralgia

A

Mostly in old age.

86
Q

Diagnostic test for Huntington’s disease

A

Genetic diagnosis

87
Q

Diagnostic test for a migraine

A

Clinical.

Neuroimaging: Rule out mass lesions

88
Q

Diagnostic test for giant cell arteritis

A

ESR: elevated, (50/50 rule; over 50yrs with over 50 ESR).

Histology: Temporal artery biopsy.

89
Q

Diagnostic test for Trigeminal neuralgia

A

Clinical.

MRI.

90
Q

Treatments for Huntington’s disease

A

Treat chorea symptoms (benzodiazepines, sodium valproate)

Genetic counselling.

91
Q

Treatments for a migraine

A

Passes in sleep.

Painkillers: Paracetamol / NSAIDs.

In severe: Triptans (serotonin agonists).

92
Q

Treatment for giant cell arteritis

A

High dose of steroids: Oral prednisolone immediately.

93
Q

Treatment for Trigeminal neuralgia

A

Anticonvulsant: Carbamazepine.

94
Q

Complications of Huntington’s disease

A

Death, usually from infection.

95
Q

Define Spinal cord compression

A

Compression of the spinal cord.

96
Q

Define Cauda equina syndrome

A

Compression of the spinal cord at the level of the cauda equina.

97
Q

Define Multiple sclerosis

A

Autoimmune demyelination of the CNS.

98
Q

Types of Cauda equina syndrome

A

Cord ends around L2

99
Q

Types of Multiple sclerosis

A

Benign,

Relapsing-remitting,

secondary chronic progressive

and primary progressive.

100
Q

How does Spinal cord compression clinically present?

A

Progressive weakness of the legs with upper motor neurone pattern and eventual paralysis.

Hours to days onset.

Arms affected if lesion is above thoracic spine.

Sensory loss below lesion.

101
Q

How does Cauda equina syndrome clinically present?

A

Low back pain.

Bilateral sciatica.

Lower limb motor weakness and sensory deficit (saddle anaesthesia).

Bowel and/or bladder dysfunction.

Sexual dysfunction.

102
Q

How does Multiple sclerosis clinically present?

A

Typically young adult.

Two discrete instances or more of CNS dysfunction as a result of demyelination

-> remission to normal in some weeks.

Three characteristic presentations.

Optic: blurred vision, unilateral eye pain.

Brainstem: diplopia, vertigo, dysphagia, nystagmus

Spinal cord: numbness, pins and needles. Possible spastic paresis.

Lhermitte’s sign: tingling down back into limbs on the flex of the neck.

103
Q

What is spinal cord compression?

A

A medical emergency

104
Q

Is cauda equina syndrome a medical emergency?

A

YES

105
Q

What happens in multiple sclerosis?

A

Demyelination plaques disseminated in time and space (Old McDonald Classification).

106
Q

Pathophysiology of Spinal cord compression and Cauda equina syndrome

A

Pressure on the nerves prevent adequate transmission and lead to permanent damage

107
Q

Pathophysiology of Multiple sclerosis

A

Inflammation, demyelination and axonal loss of oligodendrocytes.

Plaques are perivenular, and predilect to particular sites:

Optic nerve, periventricular white matter, brainstem and cerebellar connections, and cervical spinal cord.

Peripheral nerves never affected.

108
Q

Cause of Spinal cord compression

A

Usually vertebral tumour (metastases from lung, breast, kidney, prostate or multiple myeloma).

109
Q

Causes of Cauda equina syndrome

A

Herniation of a lumbar disc (usually L4,L5 / L5,S1).

Tumour.

Trauma.

Infection.

110
Q

Cause of Multiple sclerosis

A

Precise mechanism unknown.

Inflammatory process in brain and spinal cord mediated by CD4 T cells and B cells.

Exposure to EBV in early life predisposes development.

111
Q

Epidemiology of Cauda equina syndrome

A

Can occur at any age.

112
Q

Epidemiology of Multiple sclerosis

A

More common in women.

More common further from the equator.

More common in the young.

Differences: Primary progressive not more common in women.

113
Q

Diagnostic tests for Spinal cord compression

A

MRI.

X-ray

114
Q

Diagnostic tests for Cauda equina syndrome

A

Clinical.

MRI.

PRE: sphincter tone.

115
Q

Diagnostic test for Multiple sclerosis

A

MRI.

CSF: oligoclonal bands of IgG on electrophoresis

VEP: visual evoked potential.

116
Q

Treatments for Spinal cord compression

A

Surgical decompression of the cord.

Correction of pathology.

Dexamethasone reduces oedema around the lesion.

117
Q

Treatment for Cauda equina syndrome

A

Immediate surgical decompression,

removal of causative agent.

118
Q

Treatment for Multiple sclerosis

A

Short courses of steroids (methylprednisolone),

B-interferon.

Immunosuppression (Azathioprine).

119
Q

Define Myasthenia gravis

A

Autoimmune

  • > Ach receptors
  • > Weakness, fatiguability of ocular, bulbar and proximal limbs.
120
Q

Define Motor neurone disease

A

Relentless destruction of upper motor neurones and anterior horn cells in brain and spinal cord.

121
Q

Define Peripheral neuropathies

A

Neuropathy of the peripheral nerves.

122
Q

Types of Motor neurone disease

A

Amyotrophic lateral sclerosis.

Primary lateral sclerosis.

Progressive muscular atrophy.

Progressive bulbar palsy.

123
Q

Types of Peripheral neuropathiesProgressive bulbar palsy.

A

Autonomic

Motor

Sensory

124
Q

How does Myasthenia gravis clinically present?

A

Weakness,

fatiguability of ocular (-> Ptosis),

bulbar (dysphasia, dysarthria) and proximal limbs.

Improves after rest.

125
Q

How does Motor neurone disease clinically present?

A

Varies with type.

Generally: Upper limbs: reduced dexterity, stiffness, wasting of intrinsic muscles of the hand

Lower limbs: tripping, stumbling gait, foot drop

Bulbar: Slurred speech, hoarseness, dysphagia

Overall: Muscle atrophy and spasticity

126
Q

How do Peripheral neuropathies clinically present?

A

Can be asymptomatic.

Diabetes: Long history of paresthesia (glove stocking), pain, weakness and wasting, autonomic symptoms; incontinence, sexual dysfunction).

Usually present as foot ulcers (constant damage due to paresthesia).

127
Q

Which neurones does amyotrophic lateral sclerosis affect?

A

UMN + LMN (Most common)

128
Q

Which neurones does primary lateral sclerosis affect?

A

UMN

129
Q

Which neurones does progressive muscular atrophy affect?

A

LMN

130
Q

Which neurones does progressive bulbar palsy affect?

A

UMN + LMN of the lower cranial nerves.

131
Q

Pathophysiology of Myasthenia gravis

A

Autoantibodies to nicotinic acetylcholine receptors (anti-AChR antibodies)

or MuSK (muscle specific tyrosine kinase) at the post synaptic membrane of the neuromuscular junction, causing receptor blockade/loss.

132
Q

Pathophysiology of Motor neurone disease

A

Motor neurones destroyed, namely anterior horn cells of the spinal cord and motor cranial nuclei

  • > LMN and UMN dysfunction
  • > Mixed picture of muscular paralysis
133
Q

Pathophysiology of Peripheral neuropathies

A

Diabetes:

Hyperglycaemia damages 3 cell types; retinal endothelium, mesangial cells in glomeruli and schwann cells in perpheral nerves

(these cell types cannot regulate their glucose well, so constant hyperglycaemia causes excessive oxidation -> damage).

134
Q

Cause of Myasthenia gravis

A

Often associated with thymic hyperplasia,

and in 10% a thymic tumour can be found (50% of those with thymomas have MG).

135
Q

Cause of Motor neurone disease

A

Unknown.

One familial variant involves mutations in free radical scavenging enzyme copper/zinc superoxide dismutase (SOD-1).

136
Q

Cause of Peripheral neuropathies

A

Acute: Guillain barre

Chronic: Diabetes, alcohol.

137
Q

Epidemiology of Myasthenia gravis

A

Women more than men.

138
Q

Epidemiology of Motor neurone disease

A

Middle age, more common in men.

139
Q

Diagnostic tests for Myasthenia gravis

A

Anti-AChR (or anti-MuSK) antibodies in serum.

Nerve stimulation tests: characteristic decrement in evoked potential following motor nerve stimulation.

Ice test: improvement of prosis with ice pack

140
Q

Diagnostic tests for Motor neurone disease

A

Clinical (fasciculation).

EMG: muscle denervation

141
Q

Diagnostic tests for Peripheral neuropathies

A

Nerve conduction studies.

FBC.

Diabetes: As in DM.

142
Q

Treatments for Myasthenia gravis

A

Anticholinesterases: pyridostigmine

Immunosuppressant drugs (if anticholinesterases don’t work): azathioprine.

143
Q

Treatments for Motor neurone disease

A

Sodium channel blocker: Riluzole, slows glutamate release

Symptomatic: Baclofen.

144
Q

Treatments for Peripheral neuropathies

A

Diabetic control.

Amitriptyline for neuropathic pain.

145
Q

Complications of Myasthenia gravis

A

Myasthenia crisis: weakness of the respiratory muscles.

146
Q

Complications of Motor neurone disease

A

Most die in 3 years from respiratory failure due to bulbar palsy and pneumonia.

147
Q

Nerve lesions - Define upper motor nerve lesions

A

Loss of function of upper motor neuron.

148
Q

Nerve lesions - Define lower motor nerve lesions

A

Loss of function of lower motor neuron.

149
Q

Nerve lesions - Define nerve root lesions

A

Compression of the nerve root.

150
Q

Nerve lesions - Define cranial nerve lesions

A

Lesion affecting a cranial nerve.

151
Q

Nerve lesions - Define carpal tunnel syndrome

A

Entrapment of the median nerve against the carpal tunnel.

152
Q

How do upper motor nerve lesions clinically present?

A

Spastic weakness.

Decreased control of active movement.

Spasticity.

Clasp-knife response.

Babinski present.

Pronator drift.

153
Q

How do lower motor nerve lesions clinically present?

A

Muscle paresis or paralysis.

Flaccid weakness.

Fasciculations.

Hypotonia.

Hyporeflexia.

Absent Babinski reflex.

154
Q

How do nerve root lesions clinically present?

A

Tingling in the dermatome affected.

Pain, paraesthesia or weakness also possible.

155
Q

How do cranial nerve lesions clinically present?

A

Depends on the nerve affected.

156
Q

How does carpal tunnel syndrome clinically present?

A

Pain and paraesthesia in the hand.

Typically worse at night.

Loss of sensation on median nerve innervation.

Tinnel’s sign.

Phalens test.

157
Q

Pathophysiology of upper motor nerve lesions

A

Lesion of the pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves.

158
Q

Pathophysiology of lower motor nerve lesions

A

Lesion of the nerve fibers travelling from the ventral horn

or anterior grey column of the spinal cord to the muscle.

159
Q

Pathophysiology of carpal tunnel syndrome

A

Inflammation of the carpal tunnel

  • > entrapment of the median nerve
  • > pain and loss of sensation.
160
Q

Causes of upper motor nerve lesions

A

Can be a result of stroke,

MS,

trauma

and cerebral palsy.

161
Q

Cause of lower motor nerve lesions

A

Trauma to peripheral nerves that sever axons.

Potentially sequelae of Guillain-Barre syndrome.

162
Q

Cause of carpal tunnel syndrome

A

Usually idiopathic,

can be associated with hypothyroidism, diabetes, pregnancy, obesity, rheumatoid arthritis and acromegaly.

163
Q

Epidemiology of carpal tunnel syndrome

A

Most common entrapment neuropathy.

164
Q

Diagnostic test for carpal tunnel syndrome

A

Clinical.

Ultrasound apparently.

165
Q

Treatments for nerve root lesions

A

Nerve root injection of steroids,

surgical decompression.

166
Q

Treatments for carpal tunnel syndrome

A

Surgical decompression if unlikely to improve.

Nocturnal splint and steroid injections for relief.

167
Q

Define primary brain tumour

A

Tumour in the brain that arose from associated tissue.

168
Q

Define secondary brain tumour

A

Tumour in the brain that metastasised there from elsewhere.

169
Q

Types of primary brain tumour

A

Glioma,

meningioma,

pituitary adenoma.

170
Q

How do brain tumours clinically present?

A

Progressive focal neurological deficit:

Symptoms depend on location (frontal lobe -> personality change etc).

Speed of deterioration is proportional to growth of tumour.

Raised intracranial perssure: Headaches (worse on cough/leaning forward), vomiting and papilloedema.

Epilepsy: Focal or generalised.

General cancer symptoms: Weight loss, malaise, anaemia etc.

171
Q

Pathophysiology of brain tumours

A

Progressive focal neurological deficit:

Mass effect of the tumour and oedema -> impact functionality of site associated with tumour. Can destroy tissue -> rapid deterioration.

Raised ICP: As tumour grows -> downward displacement of the brain -> pressure on the brainstem (drowsiness) -> respiratory depression -> coma -> death.

False localising signs possible (see left)

Epilepsy: Tumour creates unusual electrical impulses -> seizures.

172
Q

What are some false localising signs of brain tumours?

A

False localising signs:

Raised ICP or the presence of a tumour can cause healthy structures to affect adjacent ones.

E.g., Downward displacement of temporal lobe -> III or VI CN palsy.

173
Q

Cause of primary brain tumours

A

Derived from the skull itself, or adjacent structures.

95% of primary tumours are Gliomas or Meningiomas (others include neurofibromas and lymphomas).

174
Q

Cause of secondary brain tumours

A

Metastases from:

Bronchus,

Breast,

Kidney,

Thyroid,

Stomach,

Prostate.

175
Q

Epidemiology of primary brain tumours

A

About 10% of all neoplasms.

176
Q

Diagnostic tests for brain tumours

A

CT and MRI.

Positron Emission Tomography to find occult metastasis.

177
Q

Treatments for brain tumours

A

Surgery: Exploration, removal or biopsy (meningiomas can be fully removed without incident)

Radiotherapy: Gliomas and radiosensitive metastases

Medical: Cerebral oedema can be reduced with corticosteroids. Epilepsy treated with anticonvulsants.

178
Q

Define meningitis

A

Inflammation of the meninges.

179
Q

Define encephalitis

A

Inflammation of the brain parenchyma.

180
Q

Define herpes zoster (shingles)

A

Varicella zoster virus reactivation.

181
Q

Types of meningitis

A

Acute bacterial

Viral

182
Q

How does acute bacterial meningitis clinically present?

A

Headache, neck stiffness, fever.

Photophobia and vomiting.

Kernig’s sign.

Papilloedema.

Progressive drowsiness.

If meningococcal septicaemia: Purpuric, non-blanching petechiae.

183
Q

How does viral meningitis clinically present?

A

As acute bacterial meningitis clinical presentation (bar rash), but usually more benign and self-limiting.

184
Q

How does encephalitis clinically present?

A

Fever,

headache,

altered behaviour

and altered mental status.

Less commonly; hemiparesis, dysphagia, seizure and coma.

185
Q

How does herpes zoster (shingles) clinically present?

A

Pre-eruptive: No skin lesions, but burning itching in one dermatome.

Usually a day or two before eruption.

Eruptive phase: Skin lesions appear (infectious until dried).

Erythmatous, swollen plaques.

Rash does not cross dermatomes.

186
Q

Why is meningitis important?

A

It’s a notifiable disease.

187
Q

Pathophysiology of meningitis

A

Infection of the meninges leads to inflammation of the tissue.

188
Q

Pathophysiology of encephalitis

A

Infection of the brain parenchyma

-> inflammation.

189
Q

Pathophysiology of herpes zoster (shingles)

A

After infection, the virus lies dormant in the sensory nervous system in the geniculate, trigeminal or dorsal root ganglia.

Eventually flares up -> Virus travels down the affected nerve over 3-4 days, causing perineural and intraneural inflammation.

190
Q

Cause of acute bacterial meningitis

A

Infective agents can reach the meninges from ears, nasopharynx, cranial injury or by bloodstream.

Neiserria meningitis and Streptococcus pneumoniae most common cause in adults.

191
Q

Cause of viral meningitis

A

Herpes simplex virus,

Enterovirus.

192
Q

Cause of encephalitis

A

Often presumed viral.

Commonly herpes simplex virus,

coxsackie virus,

ECHO

and mumps.

Can be tick-borne in TBE virus.

193
Q

Cause of herpes zoster (shingles)

A

Varicella-zoster.

Usually occurs in childhood, but lies dormant for years/decades.

194
Q

Diagnostic tests for meningitis

A

Lumbar puncture

-> CSF culture (NOT if signs of raised ICP on CT(because of raised coning).

CT Head scan if suspicion of a mass.

195
Q

Diagnostic tests for encephalitis

A

Viral serology (LP and CSF studies)

CT: Check for space-occupying lesions.

196
Q

Diagnostic tests for herpes zoster (shingles)

A

Clinical,

based on rash within a dermatome.

197
Q

Treatments for acute bacterial meningitis

A

Cefotaxime.

Add ampicillin if risk of listeria.

Follow up based on culture sensitivity results.

Dexamethasone to reduce long term effects.

198
Q

Treatments for viral meningitis

A

Supportive therapy.

Aciclovir for herpetic infection.

199
Q

Treatments for encephalitis

A

If suspected herpes simplex virus, immediately treated with aciclovir.

200
Q

Treatments for herpes zoster (shingles)

A

Oral aciclovir.

(SG) condensed phase 2a (9 decks)

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