Neuro 1 - Stroke, Headache, Seizures Flashcards

1
Q

Define TIA

A

Sudden onset neurological dysfunction caused by ischaemia, without acute infarction (previous definition of <24h, but even short periods of ischaemic can cause tissue damage)

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2
Q

What is the commonest cause of TIA?

A

Arterial embolism or thrombosis in the carotid, vertebral or cerebral arteries

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3
Q

What is the most common location for TIA?

A

Anterior circulation (carotid territory) 90%

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4
Q

What are the symptoms of anterior circulation TIA?

A

Hemiparesis
Hemi-sensory disturbance
Dysphasia
Amaurosis fugax

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5
Q

What are the symptoms of a posterior circulation TIA?

A

Loss of consciousness (brainstem)
Bilateral motor or sensory dysfunction
Binocular blindness
Vertigo/diplopia/dysarthria

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6
Q

What is the pathophysiology of amaurosis fugax?

A

Temporary reduction in the retinal, ophthalmic, or ciliary artery blood flow, leading to retinal hypoxia

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7
Q

What are the causes of amaurosis fugax?

A

Giant cell arteritis

TIA - internal carotid or ophthalmic atherosclerosis

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8
Q

What is transient global amnesia?

A

Episodes of confusion/amnesia lasting several hours, followed by complete recovery

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9
Q

What is Todd’s paralysis?

A

Focal weakness of the body following a seizure

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10
Q

What are the differentials for TIA?

A
Migraine with aura
Hypoglycaemia
Focal epilepsy
Todd's paralysis
Subdural haematoma
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11
Q

Give three investigations in the diagnosis of TIA

A

ECG - AF
Echo - cardiac cause
Carotid Doppler - stenosis

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12
Q

What are the features of the ABCD2 score?

A

Age >60 = 1 point
BP>140/90 = 1 point
C = clinical features (unilateral weakness 2 points, dysarthria w/o weakness 1 point)
D = duration >60m 2 points, 10-59m 1 point
Diabetes 1 point

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13
Q

An ABCD2 score of what indicates a high risk of stroke after TIA?

A

4 or more

OR AF, multiple TIA in one week, or TIA on anticoags

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14
Q

What is the management of TIA?

A

Lifestyle
Control HTN, DM, AF
2 weeks aspirin/300mg aspirin/300mg clopidogrel loading dose
Long term antiplatelets - clopidogrel 75mg OD
Statin

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15
Q

What is the management of high-risk TIA patients?

A

Refer within 24h (low risk refer within 7d)

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16
Q

How long can you not drive for following a TIA?

A

4 weeks

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17
Q

Give three causes of stroke

A

Cardiac emboli
Atherosclerosis
Vasculitis

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18
Q

Give three risk factors for stroke

A
Smoking
Hypertension
Diabetes mellitus
Age
Heart disease/AF
Previous TIA
Alcohol
Polycythaemia
Thrombophilia
COCP
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19
Q

What are the three symptoms required for total anterior circulation stroke?

A
Unilateral weakness (and/or sensory deficit) or face, arm, and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia etc)
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20
Q

What is the criteria for a partial anterior circulation stroke?

A

2 of the 3 symptoms for Total

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21
Q

What does the anterior circulation comprise?

A

ACA, MCA

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22
Q

What is the criteria for posterior circulation syndrome?

A

One of: cerebellar or brainstem syndrome, loss of consciousness, and isolated homonymous hemianopia

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23
Q

Where is the location of a subcortical/lacunar stroke?

A

Midbrain

Internal capsule

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24
Q

What is the criteria for lacunar syndrome

A

One of: unilateral weakness (and/or sensory deficit) of face and arm, arm and leg, or all 3; pure sensory loss, ataxic hemiparesis

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25
Q

What is required before thrombolysis is initiated and why?

A

Urgent CT head

Rule out haemorrhagic stroke

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26
Q

What is the treatment of ischaemic stroke?

A
IV alteplase (tissue plasminogen activator) within 4.5 hours of symptom onset
Clopidogrel 24 hours after thrombolysis
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27
Q

What is the treatment of ischaemic stroke after 4.5 hours has passed after onset?

A

300mg aspirin OD for two weeks, then lifelong clopidogrel

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28
Q

What is a subarachnoid haemorrhage?

A

Bleeding into the subarachnoid space

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29
Q

What are the risk factors for SAH?

A

Hypertension
Aneurysm (and predisposing conditions e.g. PKD)
Family history

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30
Q

What is the most common cause of SAH?

A

Rupture of berry aneurysm

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31
Q

What are the symptoms of SAH?

A
Thunder clap headache
Vomiting
Nuchial rigidity
Decreases consciousness
Papilloedema
Seizures
CNS deficits e.g. cranial nerve signs
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32
Q

What is the name of the prodrome in SAH caused by a small leak of the aneurysm?

A

Sentinel headache

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33
Q

What is seen on CT in SAH?

A

Star shaped lesion (blood filling gyral patterns)

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34
Q

When should a lumbar puncture be performed in SAH?

A

CT head negative but high clinical suspicion AND

No raised ICP

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35
Q

What is seen on lumbar puncture in SAH if performed?

A

Xanthochromic CSF

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36
Q

What is the treatment of SAH?

A

Dexamethasone
Neurosurgery
Nimodipine reduces risk of vasospasm

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37
Q

What is the cause of a subdural haematoma?

A

Tearing of bridging veins between venous sinuses and cortex

Usually deceleration injury during violent head movement

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38
Q

What type of blood is seen on SDH?

A

Clotting

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39
Q

What are the signs and symptoms of acute SDH?

A

Interval between injury and symptoms can be days-weeks-months
Signs and symptoms of raised ICP
Confusion and seizures

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40
Q

What is seen on CT in acute SDH?

A

Hyper dense crescent shaped mass

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41
Q

What is the most common condition affecting elderly patients with a change in personality and decreased GCS?

A

Chronic subdural haematoma

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42
Q

What is an extradural haematoma?

A

Collection of blood between the dura mater and the bone

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43
Q

What causes an EDH?

A

Fracture of the temporal or parietal bone causing laceration of the middle meningeal artery

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44
Q

What age group usually gets EDH?

A

Young adults

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45
Q

What are the symptoms of EDH?

A

Brief post-traumatic LOC
Lucid interval for hours or days
Followed by altered consciousness
Then headache, n+v, confusion, seizures

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46
Q

Rapid increase in ICP equals

A

Ipsilateral pupillary dilatation, signs of brain stem compression, death

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47
Q

What is seen on CT in EDH?

A

Hyperdense biconvex (lemon) shape adjacent to the skull

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48
Q

What is the treatment of EDH?

A

Craniotomy and clot evacuation

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49
Q

What is the commonest primary headache?

A

Tension

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50
Q

What are the characteristics of tension headaches?

A

Bilateral, non-pulsatile, chronic daily headache
Tight band
Pressure behind the eyes
Mild-moderate pain

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51
Q

What is the treatment of tension headaches?

A

Lifestyle advice

Symptomatic treatment - paracetamol, NSAIDs, NOT OPIOIDS

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52
Q

What is the only prophylactic treatment for tension headaches recommended by NICE?

A

Acupuncture

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53
Q

What is a medication overuse headache?

A

Headache worsens whilst on regular analgesia, especially opioids

54
Q

What is a theory behind the pathophysiology of migraine?

A

Neuronal hyperexcitability

Cortical spreading depolarisation

55
Q

What are the risk factors for migraine?

A

Female

Genetics

56
Q

What are the characteristics of a migraine headache?

A

Moderate to severe, lasts 4-72h
Unilateral, pulsatile, throbbing, aggravated by movement
N+v, photo/phonophobia

57
Q

What is an aura?

A

Evolving and reversible focal deficit

58
Q

What is the treatment of migraine?

A

Avoid triggers

Sumatriptan + NSAID/para + anti-emetic if needed

59
Q

What is the treatment of migraine in children aged 12-17?

A

Nasal triptan

60
Q

When is migraine prophylaxis indicated?

A

2+ attacks a month

Acute treatment needed more than twice a week

61
Q

What medication is used for migraine prophylaxis?

A

Propanolol

Topiramate

62
Q

What are the characteristics of cluster headaches?

A

Rapid onset
Excruciating crescendo unilateral pain around one eye
Wakes patient from sleep
Occurs in clusters of 1-2x/day, 5-12 weeks

63
Q

What are the risk factors for cluster headaches?

A

Male

Smoking

64
Q

What are the facial symptoms of cluster headaches?

A
Watery and bloodshot eye
Lid swelling
Lacrimation
Facial flushing
Rhinorrhoea
Miosis and ptosis
65
Q

What is the treatment of cluster headaches?

A

100% 15L oxygen 10-20 minutes
Sumatriptan
Avoid alcohol

66
Q

What is first line prophylaxis for cluster headaches?

A

80mg verapamil TDS

67
Q

What is trigeminal neuralgia?

A

Paroxysms of intense, debilitating pain in the distribution of the trigeminal nerve

68
Q

What is the peak age of onset of trigeminal neuralgia?

A

50 years

69
Q

What causes the pain in trigeminal neuralgia?

A

Compression of the trigeminal nerve causing demyelination and excitation of the nerve

70
Q

What is a risk factor for trigeminal neuralgia?

A

Hypertension

71
Q

What are the characteristics of trigeminal neuralgia?

A

Sudden, unilateral paroxysms of knife-like/electric shock pain
Mandibular –> maxillary and ophthalmic
Lasts seconds to minutes
Triggers- eating, shaving, talking

72
Q

How is trigeminal neuralgia diagnosed?

A

MRI to exclude secondary causes or other pathologies

73
Q

What is the treatment of trigeminal neuralgia?

A

Carbamazepine

Neurovascular decompression

74
Q

What is temporal arteritis?

A

Inflammatory granulomatous vasculitis of large cerebral arteries

75
Q

What are the symptoms of GCA?

A
Temporal pulsating headache
Scalp tenderness
Jaw claudication
Amaurosis fugax
Systemic: fatigue, fever, myalgia
76
Q

How is GCA investigated?

A

Pulseless temporal artery
Raised ESR and CRP
Biopsy within 1 week (skip lesions)

77
Q

What is the treatment of GCA?

A

Prednisolone 12 months
Visual symptoms - IV methylprednisolone 3 days
PPIs and bisphosphonates from long term steroid use

78
Q

What condition presents in 50% GCA patients?

A

Polymyalgia rheumatica

79
Q

What is the most common cause of encephalitis?

A

Herpes simplex virus 1 and 2

80
Q

Which lobes of the brain are most affected in encephalitis?

A

Frontal and temporal

81
Q

What are the main symptoms of encephalitis?

A
Features of a viral infection
Decreased consciousness
Behavioural change
Focal neuro deficit
Seizures and coma
82
Q

How is encephalitis diagnosed?

A

LP: culture CSF: increased protein and lymphocytes, decreased glucose
FBC and blood film, cultures
CT/MRI, EEG

83
Q

What is seen on EEG in encephalitis?

A

Diffuse abnormal slow wave changes

84
Q

What is the treatment of viral encephalitis?

A

Urgent acyclovir

85
Q

What are the symptoms of meningitis?

A
Fever
Headache
Meningism
Altered GCS
Seizures
Non-blanching petechial rash
86
Q

What are the CSF findings in bacterial meningitis?

A

Neutrophils
Raised protein
Low glucose

87
Q

What are the CSF findings in viral meningitis?

A

Lymphocytes
Normal protein
Normal glucose

88
Q

What is the treatment of bacterial meningitis in adults?

A

IV ceftriaxone

GP - IM benzylpenicillin

89
Q

What antibiotic is used to treat listeria in pregnant/older patients?

A

Ampicillin

90
Q

What is the prophylaxis of meningitis?

A

Rifampicin

91
Q

What is the organism usually responsible for triggering GBS?

A

Campylobacter jejuni

92
Q

What is seen on nerve conduction studies in GBS?

A

Slow nerve conduction
Prolonged distal motor latency
Conduction block

93
Q

What is the pathophysiology of GBS?

A

Molecular mimicry –> demyelination

94
Q

What other investigations are used in the diagnosis of GBS?

A

LP: increased proteins
Spirometry: decreased FVC = ITU

95
Q

What is the treatment of GBS?

A

IVIG 5 days

96
Q

What is epilepsy?

A

A recurrent tendency to spontaneous, intermittent, abnormal electrical activity in the brain

97
Q

What is a seizure?

A

The clinical manifestation of dyssynchronous neuronal discharge

98
Q

What is a primary generalized seizure?

A

Bilaterally symmetrical discharge involving both hemispheres

Consciousness lost from the start

99
Q

What is a partial seizure?

A

One hemisphere is involved at onset

100
Q

Give four types of primary generalised seizures

A
Generalised tonic-clonic
Clonic or tonic
Absence
Atonic
Myoclonic
101
Q

What are the tonic and clonic phases of a grand mal seizure?

A

Tonic - rigid stiff limbs

Clonic - generalised, bilateral, rhythmic jerking

102
Q

What are three types of partial seizure?

A

Simple partial
Complex partial
Partial seizure with secondary generalization

103
Q

What are the characteristics of a simple partial seizure?

A

Awareness unimpaired
Focal motor/sensory/autonomic symptoms
No post-ictal symptoms

104
Q

What are the characteristics of frontal lobe seizures?

A
Motor features
Jacksonian March (up and down the motor homunculus)
105
Q

What is required for a diagnosis of epilepsy?

A

2 unprovoked seizures >24 hours apart
EEG normal between seizures
MRI to identify structural abnormalities

106
Q

What is the treatment of primary generalised seizures?

A

Valproate or lamotrigine

107
Q

What is the treatment of absence seizures?

A

Valproate or ethosuximide

108
Q

What is the treatment of partial seizures?

A

Carbamazepine or lamotrigine

109
Q

When can a patient drive with epilepsy?

A

Free of daytime seizures for at least one year

110
Q

What is the management of status epilepticus (seizures lasting >30m)?

A

IV lorazepam/rectal diazepam or buccal midazolam (home) (repeat x2)
Phenytoin loading
Rapid sequence induction with sodium thiopental (status epilepticus only)
Ventilation

111
Q

What is SUDEP?

A

Sudden unexpected death in epilepsy

112
Q

What is the pathophysiology of Parkinson’s disease?

A

Loss of dopaminergic neurons
In the substantia nigra pars compacta
Of the basal ganglia

113
Q

What is the common presentation of Parkinson’s disease?

A

Impaired dexterity
Unilateral foot drop
Assymetrical

114
Q

What is the triad of Parkinson’s disease?

A

Rigidity
Bradykinesia
Resting tremor

115
Q

Describe the tremor seen in Parkinson’s

A

Pill-rolling
4-6Hz
Seen at rest, improves with activity
Induced by concentration

116
Q

Describe the Parkinsonian gait

A
Stooped posture
Small shuffling steps
Festinant
Reduced arm swing
Difficulty initiating movement and turning
117
Q

What are three other symptoms of Parkinson’s disease?

A

Micrographia
Serpentine stare, mask
Monotonous speech
Brisk reflexes

118
Q

Give three non-motor symptoms of Parkinson’s disease

A

Depression
Anosmia
Constipation/urinary frequency and urgency

119
Q

What is the gold standard of treatment for Parkinson’s disease?

A

Levodopa combined with a decarboxylase inhibitor, e.g. carbidopa (co-careldopa)

120
Q

What is the function of the decarboxylase inhibitor in Parkinson’s treatment?

A

Prevents peripheral conversaion of L-dopa to dopamine so reduces peripheral side effects of N+V, arrhythmias, alopecia, hypotension

121
Q

What medications are used to delay starting L-dopa (because of its reduced efficacy over time and dyskinetic side effects)?

A

Dopamine agonists - ropinirole

Monoamine oxidase B inhibitors - selegiline

COMT inhibitors - entacapone

122
Q

What are three Parkinson-plus syndromes?

A

Progressive supranuclear palsy
Multiple system atrophy
Corticobasal degeneration
Lewy Body dementia

123
Q

How does PSP differ from Parkinson’s disease?

A

Early postural instability and falls
Vertical gaze palsy (difficulty going downstairs)
No tremor

124
Q

How does multiple system atrophy differ from Parkinson’s disease?

A
Early autonomic features (postural hypotension, bladder dysfunction)
Cerebellar signs (ataxic gait)
125
Q

How does Lewy Body dementia differ from Parkinson’s disease?

A

Dementia occurs prior to or at the same time as motor symptoms in Lewy body

126
Q

What are the symptoms of a cerebral venous sinus thrombosis?

A

Severe but insidious headache

Subtle and non-specific neurology

127
Q

What is the gold standard investigation for cerebral venous sinus thrombosis?

A

MR venogram

128
Q

What is Weber’s syndrome?

A

Midbrain stroke syndrome
Ipsilateral cranial nerve findings, contralateral motor/sensory findings
Posterior inferior cerebellar artery

129
Q

What is the 2nd line prevention of stroke if clopidogrel is contraindicated?

A

Lifelong aspirin and dipyridamole

130
Q

What is the treatment of delirium in normal patients and patients with a history of Parkinson’s disease?

A

Anti-psychotics

Parkinson’s - avoid anti-psychotics and give lorazepam

131
Q

What is a side effect of the dopamine agonist ropinirole?

A

Drowsiness

Pathological gambling

132
Q

Which neurotransmitter is affected in Parkinson’s disease?

A

Dopamine D1 and D2