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Pass Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What is morton’s neuroma?

A

A benign neuroma affecting the intermetatarsal plantar nerve, most commonly the third inter-metatarsophalangeal space

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2
Q

Features of morton’s neuroma?

A

Forefoot pain, worse on walking (like a pebble in their shoe) or a burning paiin
Mulder’s click - hold the neuroma between finger and thumb. Other hand squeezes the metatarsals together. Click may be heard
Distal loss of sensation

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3
Q

How to treat morton’s neuroma?

A

Avoid high-heels
Metatarsal pad
Corticosteroid injection

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4
Q

Proportion of ischaemic to haemorrhagic stroke

A

85% ischaemic

15% haemorrhagic

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5
Q

Risk factors of ischaemic stroke

A 
Age
HTN
Smoking
Hyperlipidaemia
DM
AF
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6
Q

Risk factors for haemorrhagic stroke

A

Age
HTN
AVM
Anticoagulation therapy

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7
Q

What classification system do we use for strokes?

A

Oxford Stroke Classification

Bamford classification

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8
Q

Total anterior circulation stroke

A

A large stroke affecting areas supplied by middle and anterior arteries

Needs all 3 of:
Unilateral weakness (and/or sensory deficit) of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)

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9
Q

Partial anterior circulation stroke

A

Just the anterior circulation is compromised

2/3 of:
Unilateral weakness (sensory deficit) of face, arm, leg
Homonymous hemianopia
Higher cerebral dysfunction (visuospatial disorder, dysphagia)

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10
Q

Posterior circulation syndrome

A

Damage to the area of the brain supplied by the posterior circulation

One of the following required:
Cranial nerve palsy + contralateral deficit
Bilateral motor/sensory deficit
Horizontal gaze palsy
Cerebellar dysfunction (vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

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11
Q

Lacunar syndrome

A

Subcorticol stroke secondary to small vessel disease

No loss of higher cerebral functions

One of the following:
Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis
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12
Q

What is the ROSIER score?

A

A scoring system for stroke. If score is >0, stroke is the likely diagnosis

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13
Q

Aspirin and stroke

A

Aspirin 300mg orally/rectally as soon as haemorrhagic stroke has been excluded

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14
Q

Thrombolysis

A

Thrombolysis with alteplase should be given if:
Within 4.5 hours of onset of stroke symptoms
Haemorrhage definitely excluded

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15
Q

Thrombolysis contraindications

A 
Previous intracranial haemorrhage
Seizure with stroke
Stroke/traumatic brain injury past 3 months
Active bleeding
GI bleeding type problems
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16
Q

Thrombectomy

A

Within 6 hours of symptom onset

If ischaemic stroke in the proximal anterior circulation confirmed by CTA/MRA

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17
Q

Statins and anticoagulants

A

Statins shouldn’t be started till 48 hours after stroke

Anticoagulants shouldn’t be started for 2 weeks after stroke

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18
Q

Secondary prevention of stroke

A

Clopidogrel 75mg daily

Aspirin plus dipyramidole if clopidogrel is contraindicated

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19
Q

Transient ischaemic attack

A

A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemic, without acute infarction

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20
Q

Treatment of TIA

A

Give aspirin, 300mg immediately

If patient has had multiple TIAs, discuss the need for admission or observation with stroke specialist

Clopidogrel long term

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21
Q

When should carotid artery endarterectomy be considered

A

Stroke/TIA in carotid territory

Carotid stenosis >70%

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22
Q

What is the first-line investigation in stroke

A

Non-contrast CT head scan

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23
Q

Extradural haematoma

A

Collection of blood between the skull and the dura

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24
Q

Extradural haematoma CT scan

A

Biconvex collection around the edge of the brain (oval coming from the edge)

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25
Q

Features of extradural haematoma

A

Low impact trauma
LOC
Lucid interval
Rapid decline of consciousness

Dilated pupil due to 3rd cranial nerve compression as a result of mass effects (it also causes uncal herniation)

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26
Q

Treatment of extradural haematoma

A

Craniotomy

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27
Q

Subdural haematoma

A

Collection of blood under the dura mater most often caused by trauma (high impact)

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28
Q

CT imaging of subdural haematoma

A

Crescenteric collection (i.e. following line of the skull)

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29
Q

Treatment for subdural haematoma

A

Decompressive craniectomy

Burr hole drainage if chronic

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30
Q

Chronic subdural haematoma

A

Typically presents weeks after mild injury. Patients are often on anticoagulants, or are alcoholics

Patients will have progressive confusion, LOC, weakness etc.

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31
Q

Subarachnoid haemorrhage

A

A bleed deep to the subarachnoid layer of the meninges

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32
Q

Causes of subarachnoid haemorrhage

A

Most commonly caused by trauma

If non-traumatic: ruptured aneurysm or AVMs

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33
Q

Features of subarachnoid haemorrhage

A

Sudden onset severe headache
Neck stiffness
Photophobia

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34
Q

Hydrocephalus

A

Excessive volume of CSF fluid within the ventricular system of the brain, caused by an inbalance between CSF production and absorption

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35
Q

Symptoms of hydrocephalus

A

Due to raised ICP:

Headache - worse in the morning (due to lying down)
Nausea/vomiting
Papilloedema
Coma

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36
Q

Obstructive (non-communicating) hydrocephalus

A

A structural pathology blocks the flow of CSF, causes include:
Tumours
Acute haemorrhage
Developmental abnormalities

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37
Q

Non-obstructive (communicating) hydrocephalus

A

Due to an imbalance of CSF production and absorption

Increased production:
Choroid plexus tumour (very rare)

Failure of reabsorption at the arachnoid granulations:
Meningitis, post-haemorrhagic

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38
Q

What is normal pressure hydrocephalus

A

Non-obstructive hydrocephalus with large ventricles but normal ICP

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39
Q

Triad of features in normal pressure hydrocephalus

A

Dementia
Incontinence
Disturbed gait

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40
Q

Investigating hydrocephalus

A

CT head first line
MRI head
LP - both diagnostic and therapeutic

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41
Q

When should you not perform LP in hydrocephalus

A

Obstructive hydrocephalus - difference in pressures between brain and spinal cord will cause brain herniation

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42
Q

Treatment of hydrocephalus

A 
External ventricular drain
Ventriculoperitoneal shunt (this treats it long term)

If obstructive, may need surgery

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43
Q

Multiple sclerosis

A

A chronic cell mediated autoimmune disorder characterised by demyelination in the CNS

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44
Q

MS epidemiology

A

M:F 1:3
Age 20-40
30% likelihood of twin concordance in monozygotic twins

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45
Q

Relapsing-remitting MS

A

Most common form
Acute attacks last for 1-2 months, followed by periods of remission
Don’t quite get back to previous function after relapses

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46
Q

Secondary progressive MS

A

This is where you are relapsing remitting but develop more signs in between relapses
65% of people with relapsing remitting go on to develop secondary progressive

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47
Q

Primary progressive MS

A

10% of patients

Progressive deterioration from onset

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48
Q

Features of multiple sclerosis

A

Non-specific features
75% have significant lethargy

Visual:
Optic neuritis
Optic atrophy
Uhthoff’s phenomenon

Sensory
Pins/needles
Numbness
Trigeminal neuralgia

Motor
Spastic weakness

Cerebellar
Ataxia

Other
Urinary incontinence
Sexual dysfunction
Intellectual deterioration

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49
Q

How do we diagnose MS

A

Lesions disseminated in time and space

Usually an MRI head

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50
Q

Management of MS

A

Acute relapse:
High dose steroids given for 5 days (methylprednisolone)

Chronic:
DMARDs - beta interferon

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51
Q

Trigeminal neuralgia

A

Severe unilateral pain
Can be evoked by light touch though also occurs spontaneously
Usually limited to 1 or more sections of the trigeminal nerve

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52
Q

Management of trigeminal neuralgia

A

Carbamazepine

Referral to neurology if failure to respond

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53
Q

Myasthenia gravis

A

Autoimmune disorder resulting in insufficienct functioning acetylcholine receptors

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54
Q

Features of myasthenia gravis

A

Muscle fatigue (that gets worse as the day goes on, is better after rest)

Extraocular muscle weakness - diplopia
Proximal muscle weakness
Ptosis
Dysphagia

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55
Q

Associations with myasthenia gravis

A 
Thymomas
Pernicious anaemia
RA
SLE
Thymic hyperplasia in 50-70%
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56
Q

How do we investigate myasthenia gravis

A

Single fibre electromyography
CT thorax (to exclude thymoma)
Creatine Kinase is NORMAL
Autoantibodies are present in 85-90%

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57
Q

Management of myasthenia gravis

A

Long-acting anticholinesterase inhibitors - pyridostigmine
Immunosuppression: prednisolone
Thymectomy

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58
Q

Treatment of myasthenic crisis

A

Plasmapheresis

IV Immunoglobulins

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59
Q

What is Guillain-Barre

A

An immune mediated demyelination of the peripheral nervous system

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60
Q

Which antibody is associated with Guillain-Barre

A

Anti-GM1

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61
Q

Features of Guillain-Barre

A

Progressive weakness of all four limbs
Usually affects lower limbs first

Often triggered by an infection (classically campylobacter jejuni) - so a history of gastroenteritis

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62
Q

Investigations in Gullain-Barre

A

LP - raised protein with normal WCC
Nerve conduction studies

Can see papilloedema on fundoscopy

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63
Q

What is Miller Fisher syndrome

A

A variant of Guillain-Barre associated with areflexia, ataxia and ophthalmoplegia

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64
Q

Treatment of Guillain-Barre

A

IV immunoglobulins
Plasmapheresis
Painkillers

Most people make a full recovery in less than a month

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65
Q

Features of discitis

A 
Back pain
Pyrexia
Rigors
Sepsis
Changing lower limb neurology
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66
Q

Causes of discitis

A

Staphylococcus aureus is most common
Viral
TB

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67
Q

How to diagnose discitis

A

MRI

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68
Q

Treatment of discitis

A

IV abx for 6-8 weeks

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69
Q

Complications of discitis

A

Sepsis

Epidural abscess

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70
Q

What else should we look for in discitis?

A

Look for bacterial endocarditis

Discitis is usually the result of a bacteraemia

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71
Q

Huntington’s chorea

A

An autosomal dominant inherited neurodegenerative condition

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72
Q

What is the genetic defect in Huntington’s chorea

A

Trinucleotide repeat disorder - repeat expansion of CAG

Disease often is seen earlier with each generation due to more repeats

Defect is in Huntingtin gene on chromosome 4

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73
Q

Pathophysiology of Huntington’s chorea

A

Degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia

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74
Q

Features of Huntington’s

A 
Chorea
Personality changes
Intellectual impairment
Dystonia
Saccadic eye movements (rapid)
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75
Q

What is chorea

A

Quick abnormal involuntary movements of hands and feet, comparable to dancing

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76
Q

What is dystonia

A

Sustained/repetitive muscle contractions resulting in twisting movements and abnormal postures

77
Q

What can we give for dystonia

A

Procyclidine, benzos, dopaminergic drugs

78
Q

What is motor neuron disease

A

A neurological condition of unknown cause which can present with both upper and lower motor neuron signs

79
Q

Features of motor neuron disease

A

No sensory signs
Mixture of upper and lower motor neuron signs
Fasciculations
Unusual to develop <40 years of age

80
Q

Diagnosis of motor neuron disease

A

Clinical

Can perform nerve conduction studies to exclude a neuropathy

81
Q

Amylotrophic lateral sclerosis

A

50% of motor neuron disease patients
Typically LMN signs in arms
Typically UMN signs in legs

Familial cases - gene responsible is on chromosome 21

82
Q

Primary lateral sclerosis

A

Type of motor neuron disease

UMN signs only

83
Q

Progressive muscular atrophy

A

Type of motor neuron disease
LMN signs only
Distal before proximal
Best prognosis

84
Q

Progressive bulbar palsy

A

Type of motor neuron disease
Palsy of the tongue
Muscles of chewing/swallowing/facial muscle lose function
Carries worst prognosis

85
Q

Management of motor neuron disease

A 
Riluzole (mainly for ALS)
Respiratory care (BIPAP)

Prognosis: poor - 50% of patients die within 3 years

86
Q

Focal seizures

A

Start in a specific area on one side of the brain

87
Q

Focal seizures types

A 
Focal aware (previously called simple partial)
Focal impaired awareness (previously called complex partial)

Can be motor (Jacksonian march)
Non-motor (deja vu, jamais vu)

88
Q

Generalised seizures

A

Engage or involve both sides of the brain at onset

89
Q

Generalised seizures types

A

Motor - generalised tonic-clonic

Non-motor - absence seizures

90
Q

General rule for prescribing anti-epileptics in epilepsy

A

Don’t prescribe till 2 seizures

Sodium valproate for generalised
Carbamazepine for partial

91
Q

Management considerations in epilepsy

A

Driving - can’t drive for 6 months following seizure (or 12 months if established epileptic)
Pregnancy - anti-epileptics tend to be teratogenic (esp. sodium valproate)
Contraceptives - some anti-epileptics can affect the efficacy of these

92
Q

When would you start anti-epileptics after a first seizure

A

If there is a neurological deficit
Brain imaging shows a structural abnormality
EEG shows epileptical activity

93
Q

Status epilepticus

A

IV lorazepam
Buccal Midazolam
Rectal diazepam

Give after 5 minutes, then 15 minutes then at 25 minutes give phenytoin or sodium valproate or levitaretam

If after 30 mins still uncontrolled, general anaesthesia

94
Q

Alcohol withdrawal seizures

A

Peak incidence 36 hours following cessation of drinking
Related to the GABA mediated inhibition in CNS
Give benzos following cessation of drinking to reduce risk

95
Q

Psychogenic (pseudoseizures)

A

Seizure like symptoms but with no electrical discharges

Patients often have a history of mental health problems

96
Q

Dystrinopathies

A 
X-linked recessive conditions
Includes:
Becker's
Myotonic
Duchenne's
97
Q

Myotonic dystrophy

A

An inherited myopathy with features developing at around 20-30 years old

98
Q

Genetics of myotonic dystrophy

A

Autosomal dominant condition with a trinucleotide repeat disorder:
DM1 - CTG repeat chromosome 19
DM2 - ZNF9 gene repeat on chromosome 3

99
Q

Difference between myotonic dystrophy DM1 and DM2

A

Distal weakness more prominent in DM1

Proximal weakness more prominent in DM2

100
Q

Features of myotonic dystrophy

A 
Frontal balding
Myotonic facies (long, haggard)
Bilateral ptosis
Cataracts
Dysarthria
Myotonia
Weakness of arms/legs
Mild mental impairment
DM
Testicular atrophy
Dysphagia
101
Q

What is dysarthria

A

Slow, slurred speech

102
Q

Parkinson’s

A

Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra

103
Q

Triad of Parkinson’s symptoms

A

Bradykinesia
Tremor
Rigidity

(Often asymmetrical)

104
Q

Bradykinesia in Parkinson’s

A

Poverty of movement
Short, shuffling steps with reduced arm swing
Difficulty initiating movement

105
Q

Tremor in Parkinson’s

A

Resting tremor
Worse when tired/stressed, improves with voluntary movemenet
Typically ‘pill-rolling’ (i.e. thumb and index finger)

106
Q

Rigidity in Parkinson’s

A

Lead pipe

Cogwheel - due to superimposed tremor

107
Q

Extra features of Parkinson’s

A 
Mask-like face
Flexed posture
Micrographia
Drooling of soliva
Depression (40%)
Dementia, psychoses, sleep disturbance
108
Q

What drugs typically cause drug induced parkinsonism

A

Typical antipsychotics
Antiepileptics
Calcium channel blockers
GI prokinetics (domperidone, metoclopromaide)

109
Q

Treating Parkinson’s disease

A

Levodopa

Monoamine oxidase B (MAO-B) inhibitor - e.g. selegiline (inhibits breakdown of dopamine)

110
Q

Why do you not stop levodopa suddenly?

A

Acute dystonia

111
Q

Symptoms of lumbar spinal stenosis

A

Back pain
Neuropathic pain
Claudication like symptoms

Positional pain (e.g. walking up hill better than downhill)

112
Q

Lumbar spinal stenosis causes

A

Most commonly degenerative
Tumours
Disk prolapse

113
Q

Imaging in lumbar spinal stenosis

A

MRI scanning

114
Q

Treatment of lumbar spinal stenosis

A

Laminectomy (removing one or more vertebrae)

115
Q

Brown-sequard syndrome

A

Hemisection of spinal cord affecting:
Lateral corticospinal tract
Dorsal columns
Lateral spinothalamic tract

116
Q

What does the corticospinal tract do?

A

This is the tract for the motor pathway (upper motor neurons up until they connect with lower motor neurons)

117
Q

What does the spinothalamic tract do

A

Sensory:
Gross sensation
Pain
Temperature

118
Q

What does the dorsal column do

A

Sensory:
Fine touch
Vibration
Proprioception

119
Q

Where does the dorsal column decussate

A

Brainstem

120
Q

Where does the spinothalamic tract decussate

A

Level at which they enter the spinal cord

121
Q

Where does the corticospinal tract decussate

A

Medulla

122
Q

Brown sequard syndrome features

A

Ipsilateral motor loss (spastic paresis)
Ipsilateral vibration and fine touch loss
Contralateral loss of pain and temperature sensation

123
Q

Spinal cord compression

A

An oncological emergency that affects up to 5% of patients, usually due to vertebral body metastases

124
Q

Features of spinal cord compression

A 
Back pain (worse on lying down/coughing)
Lower limb weakness
Sensory changes
Lesions above L1 = UMN signs in legs
Lesions below L1 = LMN signs in legs
125
Q

Treatment of neoplastic spinal cord compression

A

Dexamethasone

Urgent oncological assessment for need of radiotherapy or surgery

126
Q

How do we investigate spinal cord compression

A

MRI whole spine

127
Q

What is syringomyelia

A

A collection of CSF within the spinal cord

128
Q

What causes syringomyelia

A

A chiari malformation
Trauma
Tumours
Idiopathic

129
Q

Features of syringomyelia

A

Cape-like (neck and arms) loss of sensation to temperature but preservation of light touch, proprioception and vibration
(AKA spinothalamic tract affected, NOT dorsal column)

130
Q

Investigations in syringomyelia

A 
MRI full spine
Brain MRI (to rule out Chiari malformation)
131
Q

What is a Chiari malformation?

A

A condition in which the brain tissue extends into the spinal canal
It is often associated with syringomyelia (CSF collection in spinal cord)

132
Q

Treatment of syringomyelia

A

Shunt

133
Q

What is acute spinal cord compression characterised by?

A

Upper motor neurone signs

134
Q

What is transverse myelitis

A

Inflammation of both sides of one section of the spinal cord

135
Q

Causes of transverse myelitis

A

Infection
Immune system disorders (SLE, Sjrogen’s)
MS

136
Q

Features of transverse myelitis

A

Pain - sharp in lower back, may go down legs/arms/abdomen depending on where is affected
Abnormal sensation
Weakness in arms/legs
Bladder/bowel problems

137
Q

What is spinal shock

A

Areflexia/hyporeflexia and autonomic dysfunction that accompanies a spinal cord injury

138
Q

Anterior spinal artery syndrome

A

This is a syndrome caused by ischaemia of the anterior spinal artery, it results in loss of function of the anterior 2/3rds of the spinal cord

139
Q

What regions are affected in anterior spinal artery syndrome

A

Anterior 2/3rds of spinal cord:
Corticospinal tracts
Spinothalamic tract
Autonomic fibres

140
Q

Features of anterior spinal artery syndrome

A

Loss of motor function
Loss of pain/touch/temperature sensation
Hypotension

141
Q

Anterior spinal artery syndrome prognosis

A

High mortality rate (>20%)

Unsure on treatment

142
Q

Central cord syndrome

A

Most common form of cervical spinal cord injury

Characterised by loss of motion and sensation in arms/hands

143
Q

Tracts affected in central cord syndrome

A

Corticospinal tract

144
Q

Causes of central cord syndrome

A

Trauma

Common in over 50s due to osteoarthritis causing spondylosis (narrowing of spinal cord)

145
Q

Features of central cord syndrome

A

Dysproportionately greater motor impairment in upper compared to lower extremities
Variable degree of sensory loss
Bladder dysfunction
Urinary retention

146
Q

Treatment of central cord syndrome

A

Immobilisation of the neck
Inpatient physiotherapy

Surgical - cervical spinal decompression

147
Q

Which organisms cause meningitis?

A

Neonates:
Group B strep

3-6 months:
N. meningitidis
Strep pneumoniae

6-60 years:
N. meningitidis
Strep pneumoniae

> 60 years:
Strep pneumoniae
N. meningitidis

Immunosuppressed patients:
Listeria monocytogenes

148
Q

Symptoms of meningitis

A 
Headache
Fever
Nausea/Vomiting
Photophobia
Drowsiness
Seizures
149
Q

Signs in meningitis

A

Neck stiffness

Purpuric rash

150
Q

Bacterial meningitis and CSF

A

Cloudy
Glucose: low
Protein: High
White cells: high

151
Q

Viral meningitis and CSF

A

Clear/cloudy
60-80% of plasma glucose
Normal/raised protein
Raised lymphocytes

152
Q

Vaccines against meningitis

A

Meningitis A, B and C vaccines given 3 times:
2 months
4 months
12-13 months

153
Q

Investigations in meningitis

A 
FBC
CRP
Coagulation screen
Blood cultures
Whole-blood PCR
Blood glucose
Blood gas
LP - if no signs of raised ICP
154
Q

Antibiotics in meningitis

A

IV Cefotaxime

+ amoxicillin if aged >50

Can give IV benzylpenicillin instead if meningococcal meningitis

Aciclovir can be given if viral

Can potentially give gentamicin as well (if suspecting listeria)

155
Q

Additional management in meningitis

A

Dexamethasone to reduce neuro sequelae

Prophylaxis should be offered to close contacts if meningoccal

156
Q

What are the potential neurological sequelae of meningitis

A

Sensorineural hearing loss (most common)
Epilepsy, paralysis
Sepsis, intracerebral abscess
Brain herniation, hydrocephalus

157
Q

Meningococcal septicaemia

A

Non-blanching rash

Plus other systemic symptoms (e.g. fever)

158
Q

Treatment of meningococcal septicaemia

A

IV cefotaxime

Treat shock etc.

159
Q

Symptoms of encephalitis

A 
Fever
Headache
Psychiatric symptoms
Seizures
Vomiting

Focal symptoms e.g. aphasia

160
Q

What is aphasia

A

Impairment of language affecting the production or comprehension of speech

161
Q

What is the most common cause of encephalitis in adults

A

Herpes simplex virus 1

162
Q

How do we investigate encephalitis

A

CSF - Lymphocytosis, high protein
PCR for HSV
CT - brain changes
MRI

163
Q

How do we manage encephalitis?

A

IV aciclovir

164
Q

Where does HSV encephalitis most commonly affect

A

Temporal lobes, causing features like aphasia

165
Q

Glioblastoma multiforme

A

Most common primary brain tumour, arising from glial cells (astrocytes, oligodendroctyes) - these are fast growing

166
Q

Imaging of glioblastoma multiforme

A

Solid tumours
Central necrosis
Rim that enhances contrast

167
Q

Treatment of glioblastoma multiforme

A

Dexamethasone treats the oedema

Surgery w/post-op chemo/radiotherapy

168
Q

Meningioma

A

The second most common primary brain tumour in adults, it forms on the tissue of the meninges
They are usually benign

169
Q

Histology of glioblastoma multiforme

A

Pleomorphic tumour cells border necrotic areas

170
Q

Histology of meningioma

A

Spindle cells in concentric whorls with calcified psammoma bodies (calcified collections)

171
Q

Typical locations of a meningioma

A

Falx cerebri
Sup. sagittal sinus
Convexity
Skull base

172
Q

Treatment of meningioma

A

Usually do a CT with contrast first and MRI

Treatment includes observation, radiotherapy and surgical resection

173
Q

What is the function of astrocytes?

A

These are glial cells found in the brain and spinal cord, they help to maintain the blood-brain barrier and aid in the secretion/absorption of neural transmitters

174
Q

Grading of astrocytoma

A

WHO grades I to IV

I is least severe, IV is most

175
Q

Pilocytic astrocytoma

A

Grade I astrocytoma - a slow growing benign tumour

Can be removed with surgery (stereotactic)

176
Q

Anaplastic astrocytoma

A

Grade III astrocytoma

177
Q

Oligodendroglioma

A

Benign, slow-growing tumour common in the frontal lobes

Roughly 10% of primary brain tumours

178
Q

Oligodendroglioma features

A

Seizure - with frontal lobe activity at onset

Headaches with raised ICP

179
Q

Histology of oligodendroglioma

A

Calcifications with ‘fried egg’ appearance

180
Q

Treatment of oligodendroglioma

A

Incurable
Watchful waiting
Anticonvulsants and steroids for brain swelling

181
Q

Ependymoma

A

Tumour of the ependyma (CNS tissue)
In adults it is often spinal
Common location is in the fourth ventricle
Commonly causes hydrocephalus

182
Q

Histology of ependymoma

A

Perivascular psuedorosettes

183
Q

Symptoms of ependymoma

A 
Raised ICP symptoms:
Severe headache
Visual loss (papilloedema)
Vomiting
Drowsiness
Gait change
184
Q

Treatment of ependymoma

A

Maximum surgical resection followed by radiation

185
Q

CNS lymphoma treatment

A

Steroids to reduce swelling/symptoms

Chemotherapy (IV or intrathecally)

186
Q

What does intrathecally

A

Into the CNS by lumbar puncture

187
Q

Cluster headache

A

Pain, once or twice a day
Each episode lasts 15 mins - 2 hours
Clusters typically last 4-12 weeks
Can have watery eyes

188
Q

Treatment of cluster headache

A

100% O2
SC triptan

Verapamil prophylactically

Pass Medicine (24 decks)

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