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Phase 3A > Neurology Peer Teaching > Flashcards

Neurology Peer Teaching Flashcards

1
Q

Name 3 primary headaches

A

Migraine
Cluster headache
Tension headache

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2
Q

Name some secondary headaches

A 
Meningitis
SAH
GCA
Medication over use
IIH
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3
Q

Name headaches which arent primary or secondary headaches

A

Trigeminal neuralgia

Painful neuropathies

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4
Q

What is classic migraine

A

Migraine with aura

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5
Q

What is common migraine

A

Migraine without aura

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6
Q

Name triggers for migraine

A 
Cheese
OCP
Caffeine
Alcohol
Anxiety
Travel
Ecercise
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7
Q

Give some examples of migraine auras

A

Reversible visual symptoms (unilateral blindness, flashes, fortification)
Reversible dysphagic sppech disturbances, numbness, tingling

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8
Q

Features of migraine

A 
4-72hrs
Unilateral, pulsing
Moderate to severe
Acitivity = worse
N and V
Photo/phonophobia
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9
Q

First line management of an acute migraine attack

A

Aspirin +- metoclopramide

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10
Q

Second line management of an acute attack

A

Sumatriptan

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11
Q

Prophylaxis of migraine

A

Propanolol

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12
Q

Features of cluster headaches

A 
Severe, short lived
15mins- 180mins
Unilateral eye pain
Ipsilateral autonomic features
Headaches in clusters
Restless during attack
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13
Q

Do migraine patients move around

A

No

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14
Q

Do cluster headache patients move around

A

Yes

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15
Q

Treatment of an acute cluster headache attack

A

SC sumatriptan

100% Oxygen

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16
Q

Cluster headache prophylaxis

A

Verapamil

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17
Q

Features of tension headache

A

30 minutes- a week
Bilateral pressing
Not associated with activity or nauseau

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18
Q

Treatment for tension headache

A

Reassurance that self limiting. Stress is cause. <15 a month, then paracetamol but be wary of MOH

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19
Q

Who more commonly gets cluster headaches

A

Men

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20
Q

Who gets giant cell arteritis

A

Over 50s

Associated with polymyalgia rheumatica

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21
Q

Symptoms of GCA

A 
Headaches
Scalp tenderness
Jaw claudication
Unilateral vision loss
Temporal artery tenderness
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22
Q

Investigations for GCA

A

ESR (often v high) Temporal artery biopsy

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23
Q

Treatment of GCA

A

PO Prednisolone

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24
Q

What can cause a headache of raised intracranial pressure

A

Space occupying lesion, intracranial tumour or idiopathic intracranial hypertension

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25
Q

Features of a headache of raised intracranial pressue

A

Generalised ache
Aggravated by bending, coughing or straining.
Worse in morning or after prolonged recumbency

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26
Q

Accompanying symptoms fo headache of raised intracranial pressure

A

Vomiting
Visual obscurations
Progressive focal neurological signs
Papilloedema, enlarged blind spots, reduced visual acuity

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27
Q

What investigation do you do for suspected headache of raised ICP

A

Urgent imaging with CT or MRI

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28
Q

Describe idiopathic intracranial hypertension

A

Fat young women, papilloedema is marked so they might get optic atrophy.

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29
Q

3 cardinal presenting symptoms of brain tumours

A

Symptoms of raised ICP
Progressive neurological defecity
Focal or generalised epilepsy

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30
Q

Which cancers met to brain

A

Lung
Breast
RCC
GI

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31
Q

What cells do most brain tumours come from

A

Glial cells

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32
Q

Which tumour makes up 90% of gliomas

A

Astrocytoma

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33
Q

Name two gliomas

A

Astrocytoma

Oligodendroblioma

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34
Q

What can be used to treat cerebral oedema

A

IV dexamethasone

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35
Q

What can be used to treat raised ICP

A

IV mannitol

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36
Q

What treats glioblastoma multiforme

A

Temozolamide

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37
Q

How do you treat brain tumours

A 
IV dexamethasone (for cerebral oedema)
IV mannitol (for ICP)
Anticonvulsants (epilepsy)
Surgical excision
Adjuvant chemo-radiotherapy
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38
Q

Features of trigeminal neuralgia

A

Stabbing sharp pain in CN V distribution
Unilateral
Second to 2mins

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39
Q

Triggers of trigeminal neuralgia

A

Washing face
Shaving
Eating
Talking

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40
Q

What is the neurological examination like in trigeminal neuralgia

A

Normal

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41
Q

First line treatment of trigeminal neuralgia

A

Carbamazepine

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42
Q

What is a subarachnoid haemorrhage

A

Spontaneous bleeding into the subarachnoid space

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43
Q

What are causes of SAH

A

Rupture of berry aneurysms

Congenital AVMs

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44
Q

Describe features of SAH

A

Sudden onset occipital headache
N and V
reduced consciousness
Meningeal irritation signs

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45
Q

Name 3 signs of meningeal irritation

A

Neck stiffness
Kernigs sign positive
Photophobia

46
Q

What is kernigs sign positive

A

Hip flexed to 90 degrees, then patient cant straighten leg

47
Q

Investigations for SAF

A

CT head
LP if CT normal
MR angiography

48
Q

What does LP show in SAH

A

Xanthochromia (only after 12 hours)

49
Q

Management of SAH

A

Bed rest, analgesia, supportive measures.

Nimodipine

50
Q

What is nimodipine

A

CCB

51
Q

Why is a CCB given to SAH patients

A

Prevents cerebral artery spasm

52
Q

What is a subdural haematoma

A

Accumulation of blood in the subdural space following rupture of veins running from hemisphere to sagittal sinus

53
Q

Who gets subdurals

A

Head injury
Elderly
Alcoholic

54
Q

Symptoms of subdural haematoma

A 
Headahc 
Confusion
Fluctuating LOC
Personality change
Latent period
55
Q

Gold standard investigation of subdural haematoma and the finding

A

CT Head

Crescent shaped lesion

56
Q

Management of subdural

A

Surgical removal of the haematoma

57
Q

What is an extradural haematoma

A

Collection of blood between the dura mater and the skull

58
Q

What causes an extradural

A

Rupture of the miffle meningeal artery following head injury, usually ssociated with temproal bone skull dracture

59
Q

Extradural presentation

A

Brief LOC, lucid interval of recovery. If severe headache, decreased consciousness and signs of raised ICP

60
Q

What is the gold standard investigation for extradural and the finding

A

CT scan

Biconvex haematoma

61
Q

Treatment of extradural haematoma

A

Evacuation of the clot through burr holes or open craniotomy

62
Q

What is multiple sclerosis

A

Inflammatory demyelinating autoimmune disease of the CNS. Characterised by multiple plaques of demyelination in the brain and spine

63
Q

What must plaques be for them to be MS

A

Disseminated both in time and place

64
Q

Who gets MS

A

Young adult, women more than men

65
Q

Which sites are most commonly affected by MS

A

Periventricular region of the hemispheres
Brainstem, cerebellum
Cervical cord
Optic nerves

66
Q

Name the 4 types of MS

A

Benign
Relapsing remitting
Secondary progressive
Primary progressive

67
Q

Which is the most common type of MS

A

Relapsing remitting

68
Q

Define relapsing remitting MS

A

Clearly defined relapses with full recovery or with some residual deficit upon recovery. There is no disease progression between relapses.

69
Q

Define secondary progressive MS

A

When the disease starts with a relapsing-remitting picture, but eventually recovery from each successive relapse becomes less complete

70
Q

Eye signs in MS

A

Optic neuritis => optic atrophy

  • unilateral visual loss
  • painful eye movement
  • reduced colour vision
71
Q

Spinal cord lesion sensory symptoms (MS)

A 
Numbness
Tingling
Burning
Band like sensation
Lhermittes
Altered temperature sensation
72
Q

What is Lhermittes symptom

A

Electric shock like sensation down the limbs on flexion of the neck

73
Q

When is Lhermittes present

A

MS

Vit B12 deficiency

74
Q

Spinal cord lesion motor symptoms (MS)

A

Weakness
Clumsiness
Tonic spasms

75
Q

Spinal cord lesion sphincter symptoms (MS)

A

Urinary
Constipation
Faecal incontinence
Erectile dysfunction

76
Q

Cerebellum lesion symptoms (MS)

A 
DANISH
Dysdiodochokineasia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
77
Q

Best investigation for MS

A

MRI and gadolinium contrast

78
Q

What does CSF electrophoresis show in MS

A

Oligoclonal bands of IgG

79
Q

What do you need for diagnosis of MS

A

Lesions should be disseminated in time (2 attacks) and space (MRI)

80
Q

Acute treatment of MS attack

A

IV methylprednisolone

81
Q

Chronic treatment of MS

A

Beta interferon (immune modulation)
mab (natalizumab)
Immunosuppression (azathioprine)

82
Q

Describe pathophysiology of myasthenia gravis

A

Autoimmune destruction of Ach receptors at NMJ. Depletes working post synaptic receptor sites.

83
Q

What is Myasthenia gravis associated with

A

Thymoma, RA, SLE, T1DM, Addisons, hyperthyroid (AI)

84
Q

Clinical features of MG

A 
Ptosis, eyelid droop after looking up
Diplopia
Myasthenic snarl
Dysarthria
Voice fades
Tendon reflexes normal but faitgue
Sensory exam normal
85
Q

Does Myasthenia affect motor or sensory

A

Only motor

86
Q

Investigations for myasthenia gravis

A

Antibodies
CT thorax
Ice test
Tensilon test

87
Q

What antibodies do you look for in myasthenia

A

Anti-AChR

MuSK

88
Q

What are you looking at on CT thorax for myasthenia

A

Thymus (thymoma common)

89
Q

What is the tensilon test for myasthenia

A

Very short acting anti acetylcholinesterase will show improvement in muscle strength

90
Q

Immediate treatment of myasthenia gravis

A

Pyridostigmine
Prednisolone
Thymectomy

91
Q

What type of drug is pyridostigmine

A

Acetylcholinesterase inhibitor

92
Q

What is a potential long term consequence of myasthenia

A

Myasthenic crisis with weakness of respiratory muscles

93
Q

Name 4 treatable causes of delerium

A

Vitamin B12 deficiency
Folat deficiency
Neurosyphilis
HIV related

94
Q

Describe the onset of alzheimers dementia

A

Gradual, progressive

95
Q

Vascular dementia onset

A

Abrupt or gradual

96
Q

Lewy body dementia onset

A

Insideous, progressive with fluctuations

97
Q

Frontotemporal dementia onset

A

Insidious onset, 50s and 60s, rapid progression

98
Q

Alzhiemers dementia pathology/ imaging

A

Generalised atrophy
Beta amyloid plaques
Neurofibrillary tangles

99
Q

Vascular dementia pathology/ imaging

A

Strokes
Lacunar infarcts
White matter lesions
Vulnerable to cerebrovascular events

100
Q

Pathology/ imaging of lewy body dementia

A

Generalised atrophy

lewy bodies in cortex and midbrain

101
Q

Pathology/ imaging of frontotemporal dementia

A

Frontal and temporal atrophy

Pick cells and pick bodies in cortex

102
Q

Alzhimers disease signs and symptoms

A 
Memory loss
Language defecit
Rapid forgetting
Impaired visuospatial
Normal gate and neuro exam
Late affective disturbances and behaviour
103
Q

Vascular dementia signs and symptoms

A

Focal neurological signs

Signs of vascular disease

104
Q

Lewy body dementia signs and symptoms

A 
Fluctuating cognition
Visual hallucinations
Neuroleptic sensitivity
Shuffling gait
Increased tone
Tremors
Falls
105
Q

Frontotemproal dementia signs and symptoms

A 
Disinhibition
Socially inappropriate behaviour
Poor judgement
Apathy
Decreased motivation
Poor executive function
106
Q

Dementia vs delerium onset

A

Delerium acute, dementia insidiouds

107
Q

Dementia vs delerium consciousness

A

Delirium altered, dementia normal

108
Q

Dementia vs delirium course

A

Dementia progressive deterioration, delirium flucuating

109
Q

Dementia vs delirium sleep wake cycle

A

Dementia normal, delirium altered

110
Q

Dementia vs delirium speech

A

Delirium incoherent rapid or slow speech. Dementia difficulty finding words

111
Q

Dementia vs delirium perceptual disturbance

A

Delirium common, dementia late stage

Phase 3A (25 decks)

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