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Neurology Flashcards

1
Q

What are the types of seizure?

A

*Generalised tonic-clonic: muscle tensing and jerking
*focal: hearing/speech/memory/emotions affected
*Absence: blank, stare into space
*Atonic: lapses in tone
*Myoclonic seizure: sudden brief muscle contraction

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2
Q

What is status epilepticus?

A

Seizure lasting > 5 minutes or >3 seizures in one hour, medical emergency

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3
Q

What is the management of status epilepticus?

A

*ABCDE
*high conc oxygen
*Test blood glucose
*IV lorazepam 4mg, repeat after 10 minutes
*After 2 doses of lorazepam if seizure continues, give IV phenytoin or phenobarbital

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4
Q

What are the acute causes of status epilepticus?

A

*Hypoxia
*Stroke
*Metabolic abnormalities
*Alcohol intoxication/withdrawal
*Poor anticonvulsant therapy adherence

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5
Q

What is the definition of epilepsy?

A

The tendency to have recurrent unprovoked seizures

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6
Q

What investigations should you carry out in suspected epilepsy?

A

*EEG
*MRI brain
*ECG

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7
Q

What is the management of generalised tonic clonic seizures?

A

Sodium valporate first line

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8
Q

What is the management of focal seizures?

A

Carbamazepine or lamotrigine

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9
Q

What is the management of absence seizures?

A

Sodium valporate

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10
Q

What is the management of atonic seizures?

A

Sodium valporate

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11
Q

What is the presentation of a stroke?

A

*Sudden weakness of limbs
*Sudden facial weakness
*Sudden onset dysphasia
*Sudden onset visual or sensory loss

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12
Q

What are the risk factors for ischaemic stroke?

A

*Cardiovascular disease
*Previous stroke/TIA
*Hypertension
*Smoking
*Vasculitis
*Thrombophilia
*Combined contraceptive pill

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13
Q

What investigations should you carry out in suspected stroke?

A

*Not contrast CT (diffusion weighted MRI is gold standard)
*Serum glucose
*Serum electrolytes, UEs, FBC
*Cardiac enzymes
*ECG
*Prothrombin time and PTT

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14
Q

What is the management of ischaemic stroke?

A

*Admit to hyperacute stroke unit within 4 hours
*Swallow function assessment
*If <4.5 hours of onset, IV alteplase
*If >4.5 hours, consider mechanical thombectomy
*Start aspirin within 24 hours 300mg OD
*Atorvastatin after 48 hours

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15
Q

Wernicke’s aphasia

A

Receptive, impaired comprehension, can speak fluently but sentences may not make any sense

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16
Q

Broca’s aphasia

A

Expressive aphasia, can understand but cannot speak properly

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17
Q

TACS

A

Total anterior circulation
*All 3 of:
- Unilateral weakness
- Homonymous hemianopia
- Higher cerebral dysfunction

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18
Q

PACS

A

Partial anterior circulation
Two of:
- Unilateral weakness
- Homonymous hemianopia
- Higher cerebral dysfunction

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19
Q

POCS

A

Posterior circulation
One of:
- CN palsy and contralateral motor deficit
- bilateral motor/sensory deficit
- isolated homonymous hemianopia
- cerebellar dysfunciton
- conjugate eye movement disorder

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20
Q

LACS

A

Lacunar
One of:
- pure motor
- pure sensory
- sensori-motor
- ataxic hemiparesis

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21
Q

What is a TIA?

A

Transient neurological dysfunction secondary to ischaemia without infarction. Symptoms resolve within 24 hours

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22
Q

What is the management of TIA?

A

*300mg PO OD aspirin, once confirmed, switch to 75mg PO OD clopidogrel
*Atorvastatin
*If AF: anticoagulate

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23
Q

Tension headache

A

*Associated with stress/depression/alcohol/skipping meals/dehydration
*Mild ache, band like pattern around the head

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24
Q

What is the management of tension headaches?

A

Analgesia, reassurance, relaxation techniques

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25
Q

Migraine

A

*At least 5 attacks, lasting 4-72 hours
*Unilateral, pulsating, moderate to severe pain, worsened by routine physical activity
*Causes nausea/vomiting and/or photo/phonophobia
*Preceded by prodrome and aura, followed by postdrome

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26
Q

What is the prevention of migraine?

A

*Avoidance of triggers
*If 4-5 attacks a month, prophlaxis:
- propranolol
- topiramate
- amitryptiline
- candesartan
- flunarazine
*≥15 headaches a month with 8+ being migraines and failed on 3 prophylactics, consider onabotulism toxin A

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27
Q

Acute treatment of migraine

A

Sumatriptan or aspirin 900mg or ibuprofen

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28
Q

Cluster headaches

A

*Severe/very severe unilateral orbital, supraorbital and/or temporal pain
*Last 15-180 minutes
*One every other day up to 8 a day
*Also associated with one of:
- lacrimal injection
- nasal congestion or rhinorrhea
- forehead/ facial sweating/flushing
- eyelid oedema
- sensation of fullness in the ears
- miosis/ptosis

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29
Q

What is the management of cluster headaches?

A

100% oxygen, subcutaneous triptan

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30
Q

Trigeminal neuralgia

A

*unilateral, electric shock like pains
*Abrupt onset and termination
*Limited to the distribution of the trigeminal divisions
*Pain evoked by light touch

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31
Q

Thunderclap headache

A

*Sudden onset severe, occipital headache
*Associated nausea, meningism, seizure

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32
Q

Investigations thunderclap headache

A

Non contrast head CT within 12 hours, if negative after 12 hours from headache onset, lumbar puncture

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33
Q

Why do you have to wait 12 hours from onset to do a lumbar puncture in thunderclap headache?

A

To allow for xanthochromia to develop

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34
Q

What are the causes of thunderclap headache?

A

*Subarachnoid haemorrhage
*Intracerebral haemorrhage
*Arterial dissection
*Cerebral venous sinus thrombosis
*Ischaemic stroke
*Bacterial meningitis

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35
Q

Presentation of raised pressure headache

A

*Worse on lying down, improved on standing
*Worse in the morning
*Worse on valsalva (coughing, laughing)
*Worse on exertion
*Transient visual obscurations with changes in posture
*Persistent nausea and vomiting
*Papilloedema/optic disc swelling
*Impaired visual acuity, reduced fields, poor colour vision
*III or VI nerve palsy
*Focal neurological signs

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36
Q

What are the causes of raised intracranial pressure?

A

*Idiopathic intracranial hypertension
*Trauma
*Infection: meningitis
*Hydrocephalus
*Tumour

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37
Q

What is MS?

A

Demyelinating central nervous system condition clincially defined by 2 episodes of neurological dysfunction (brain, spinal cord, optic nerve) that are separated in space and time

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38
Q

What is the presentation of MS?

A

*Visual disturbance in one eye, painful movement of eye, loss of colour discrimination (particularly red)
*Peculiar sensory phenomena: wetness/burning sensation
*Ataxia: sensory or cerebellar

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39
Q

What is Lhermitte’s sign?

A

Electric shock sensation down the spine into the limbs when flexing the neck due to disease in the dorsal column of the spinal cord

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40
Q

What investigations should you carry out in suspected MS?

A

*MRI brain and spinal cord
*FBC and metabolic panel, VIt B12 and TSH to exclude other pathologies
*Lumbar puncture - oligoclonal bands
*visual evoked potentials

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41
Q

What are the patterns of disease in MS?

A

*Relapsing-remitting
*Primary progressive (has never been relapsing remitting)
*Secondary progressive (was once relapsing-remitting)

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42
Q

What is the management of an MS relaspe?

A

*Methylprednisolone:
- 500mg orally for 5 days
- 1g IV for 3 days
*Give PPI for gastro protection

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43
Q

What is the presentation of Parkinsons?

A

*Bradykinesia
*Rigidity
*Resting tremor
*Postural instability
*Fatigue
*Depression, anxiety
*Constipation
*Dementia
*Speech difficulties (hypophonia and dysarthria)

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44
Q

What are the exclusion criteria for parkinson’s?

A

*Cerebellar signs
*Limited to the lower limbs for >3 years
*Vertical gaze palsy
*No response to L-Dopa
*Normal FP-CIT scan

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45
Q

What are the drug options for parkinsons?

A

*L-Dopa: sinemet (Levodopa and carbidopa)
*Dopamine agonist: ropinerole, rotigotine, pramipexole
*MAO-B inhibitor
*COMT inhibitor

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46
Q

MAO-B inhibitor

A

Selegiline, rasagiline

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47
Q

COMT inhibitor

A

Entracapone, opicapone

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48
Q

What are the side effects of L-Dopa

A

*nausea
*Vomiting
*Postural instability
*Confusion
*hallucination

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49
Q

What are the side effects of dopamine agonists?

A

*Daytime somnolence
*Impulse control disorders
*nausea, vomiting, postural hypotension

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50
Q

What are the complications of advanced parkinsons?

A

*Motor complications
*Change in posture
*Increased falls
*L-Dopa induced dyskinesia
*Poor balance
*Swallowing and speech difficulties
*Dementia, hallucinations, psychosis

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51
Q

What are the treatment options for advanced parkinson’s?

A

*Apomorphine pen injection
*Intrajejunal duodopa infusion
*Deep brain stimulation

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52
Q

What are the other causes of parkinsonism?

A

*Drug induced
*PSP: progressive supranuclear palsy
*MSA- multi systems atrophy
*Vascular Parkinsonism
*Lewy body dementia
*Corticobasal degeneration

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53
Q

What drugs can causes parkinsonism?

A

*Lithium
*Antipsychotics
*CCB
*Metoclopramide

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54
Q

What are the signs of MSA?

A

*Poor response to l-dopa
*Autonomic dysfunction
*Speech difficulties

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55
Q

What are the signs of PSP?

A

*Vertical gaze palsy
*Postural instability

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56
Q

What are the signs of vascular parkinsonism?

A

*Lower extremities
*Symmetrical

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57
Q

What is cervical spondylosis?

A

Osteoarthritis of the spine including the spontaneous degeneration of the disc or facet joints

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58
Q

What is the presentation of cervical spondylosis?

A

*Spontaneous onset of neck pain
*Cervical muscle pain and spasm
*Headaches/occipital pain
*Weakness or numbness
*Radiating arm pain
*Reflex changed (reduced in radiculopathy, increased in myelopathy)

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59
Q

What investigation should be carried out in suspected cervical spondylosis?

A

Cervical MRI (order if pain remains after 4-6 weeks)

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60
Q

What is the management of cervical spondylosis?

A

*Axial neck pain: physio, NSAIDs, muscle relaxant if spasm
*Cervical spondylitiic radiculopathy: NSAIDs, physio, consider prednisolone
*Degenerative cervical myelopathy: consider surgical decompression

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61
Q

What is myasthenia gravis?

A

Autoimmune condition of the post synaptic membrane at the neuromuscular junction in skeletal muscle. Circulation of antibodies against the nicotinic acetylcholine membrane

62
Q

What is the presentation of myasthenia gravis?

A
  • muscle strength fatiguability
  • ptosis due to eyelid weakness
  • diplopia due to extraocular muscle weakness
  • slurred speech
  • problems with swallowing and chewing
63
Q

Investigation for myasthenia gravis

A
  • serum acetylcholine receptor antibody analysis
  • muscle specific tyrosine kinase
  • edrophonium test
64
Q

Management of myasthenia gravis

A

Pyridostigmine or neostigmine

65
Q

What are the types of MND?

A
  • amytrophic lateral sclerosis
  • progressive bulbar palsy
  • progressive muscular atrophy
  • primary lateral sclerosis
66
Q

What is the presentation of MND?

A
  • LMN lesion: muscle wasting, reduced tone, reduced reflexes
  • UMN lesion: increased tone/spasticity, brisk reflexes, upgoing plantar response

There will be an absence of sensory or cerebellar signs

67
Q

Investigation for MND

A
  • Clinical diagnosis
  • Can perform MRI and nerve conduction studies to exclude other diagnoses
68
Q

Amyotrophic lateral sclerosis

A
  • most common
  • UMN in lower limbs
  • LMN in upper limbs
69
Q

Progressive bulbar pasly

A
  • affects muscles responsible for talking and swallowing
  • poor prognosis
70
Q

Progressive muscular atrophy

A

LMN only

71
Q

Primary lateral sclerosis

A

UMN only

72
Q

What are the causes of a predominantly motor peripheral neuropathy?

A
  • Guillain barre
  • Lead poisoning
  • Diptheria
  • Charcot Marie Tooth
73
Q

What are the causes of a predominantly sensory peripheral neuropathy

A
  • diabetes
  • vitamin B12 deficiency
  • alcohol
  • uraemia, chronic kidney disease
  • amyloidosis
74
Q

What is Guillain barre syndrome?

A
  • acute inflammatory demyelinating neuropathy
  • post infectious autoimmune aetiology (e.g. campylobacter, CMV, EBV)
  • progressive weakness over days
  • flaccid, quadraparesis with areflexia
75
Q

Treatment of guillain barre

A

IV immunoglobulin or apheresis

76
Q

What is secondary progressive MS?

A

Relapsing remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses

77
Q

Management of an acute relapse of MS

A

High dose steroids (oral or IV methylprednisolone)

78
Q

Drug options for reducing risk of relapse in MS

A
  • natalizumab IV
  • ocrelizumab
79
Q

Fatigue in MS

A

Amantadine

80
Q

Spasticity in MS

A

baclofen and gabapentin

81
Q

Bladder dysfunction in MS

A
  • get an ultrasound to assess bladder emptying
  • if significant residual volume then intermittent self catheterisation
  • if no significant residual volume then anticholinergics
82
Q

Visual evoked response

A

Delayed but well preserved waveform

83
Q

Where is the lesion in wernickes

A

Superior temporal gyrus

84
Q

What supplies wernickes area?

A

inferior division of the left MCA

85
Q

Where is brocas area

A

Inferior frontal gyrus

86
Q

What supplies brocas area?

A

Superior division of the left MCA

87
Q

What is conduction aphasia

A

Speech is fluent but repetition is poor, they are aware of the errors they are making

88
Q

Area affected in conduction aphasia

A

Arcuate fasiculus

89
Q

Global aphasia

A

All 3 areas: superior temporal gyrus and inferior frontal gyrus and arcuate fasiculus

Severe expressive and receptive aphasia

90
Q

Causes of aphasia resulting in non fluent speech

A
  • Brocas: comprehension intact
  • Global: comprehension impaired
91
Q

Causes of aphasia with fluent speech

A
  • comprehension impaired: wernickes
  • comprehension relatively intact: conduction aphasia
92
Q

Cerebellar vermis lesion

A

Gait ataxia

93
Q

Spinal cord level autonomic dysrefelxia

A

At or above T6

94
Q

Autonomic dysreflexia

A
  • spinal cord injury at or above T6
  • afferent signals triggered by faecal impaction or urinary retention
  • sympathetic spinal reflex
  • parasympathetic prevented by cord lesion
  • extreme hypertension, sweating above the level of the cord, agitation
95
Q

Management of autonomic dysreflexia

A

Removal or control of the stimulus and treatment of life threatening hypertension and/or bradycardia

96
Q

Origin of brachial plexus

A

anterior rami C5 to T1

97
Q

Presentation of brain abscess

A
  • headache
  • fever
  • focal neurology
  • raised ICP: nausea, papilloedema, seizure
98
Q

Management of brain abscess

A
  • surgery: craniotomy and debridement
  • IV metronidazole and 3rd gen cephalosporin
  • intracranial pressure management
99
Q

Which tumours most commonly spread to the brain?

A
  • lung (most common)
  • breast
  • bowel
  • skin (melanoma)
  • kidney
100
Q

What is the most commonly primary brain tumour?

A

Glioblastoma multiforme

101
Q

Location vestibular schwannoma

A
  • benign tumour
  • 8th cranial nerve
  • often seen in cerebellopontine angle
102
Q

Most common primary brain tumour in children

A
  • Pilocytic astrocytoma
103
Q

Brown sequard syndrome

A
  • caused by lateral hemisection of the spinal cord
  • ipsilateral weakness below the lesion
  • ipsilateral loss of proprioception and vibration sensation
  • contralateral loss of pain and temperature sensation
104
Q

Adverse effects of carbamazepine

A
  • P450 inducer
  • dizziness and ataxia
  • drowsiness
  • headache
  • visual disturbance
  • steven johnson syndrome
  • leucopenia and agranulocytosis
  • hyponatraemia secondary to syndrome of inappropriate ADH secretion
105
Q

Why may someone see a return of seizures when starting carbamazepine?

A

Exhibits autoinduction

106
Q

What is in the cavernous sinus?

A

In the lateral wall:
- oculomotor nerve
- trochlear nerve
- ophthalmic nerve
- maxillary nerve

In the sinus
- internal carotid artery
- sympathetic plexus
- abducen nerve

107
Q

Symptoms of cerebellar disease

A
  • Dysdiadochokinesia, dysmetria (past pointing)
  • Ataxia
  • Nystagmus
  • intention tremor
  • slurred staccato speech, scanning dysarthria
  • hypotonia
108
Q

Causes of cerebellar disease

A
  • Freidreichs ataxia
  • cerebellar haemangioma
  • stroke
  • alcohol
  • MS
  • hypothyroidism
  • drugs: phenytoin, lead poisoning
  • paraneoplastic
109
Q

Features of charcot marie tooth disease

A
  • foot drop
  • high arched foot (pes cavus)
  • hammer toes
  • distal muscle weakness
  • distal muscle atrophy
  • hyporeflexia
  • stork leg deformity
110
Q

How long does a cluster headache typically last?

A

15 minutes to 2 hours

111
Q

gold standard imaging cluster headaches

A

MRI with gadolinium contrast

112
Q

Prophylaxis of cluster headaches

A

Verapamil

113
Q

Common peroneal nerve lesion

A
  • foot drop
  • weakness of foot dorsiflexion and eversion
  • weak extensor hallucis longus
  • sensory loss over the dorsum of the foot and lower lateral part of the leg
  • wasting of the anterior tibial and peroneal muscles
114
Q

Which drugs can cause a peripheral myopathy?

A
  • amiodarone
  • isoniazid
  • vincristine
  • nitrofuratoin
  • metronidazole
115
Q

driving after first seizure

A

6 months no seizure if no structural abnormalities of epileptiform waveform otherwise 12 months

116
Q

Stroke/TIA driving

A

one month off if no residual neurological deficit

117
Q

neuropathy EMG

A

Increased action potential duration and amplitude

118
Q

Myopathy EMG

A

Decreased action potential duration and amplitude

119
Q

Management of encephalitis

A

Intravenous aciclovir

120
Q

What virus is responsible for most encephalitis?

A

HSV

121
Q

Features of an essential tremor

A
  • postural : worse if arm is outstretched
  • improved by alcohol and rest
122
Q

Management of essential tremor

A

Propranolol

123
Q

What is the most common cause of foot drop?

A

Common peroneal nerve lesion

124
Q

Foot drop with weak hip abduction

A

L5 radiculopathy

125
Q

What classically triggers guillain barre?

A

Campylobacter jejuni

126
Q

Features of guillain barre

A
  • initially leg/back weakness
  • ascending symmetrical weakness
  • reflexes reduced or absent
  • may have mild sensory symptoms
  • may be a history of gastroenteritis
127
Q

Features of lambert eaton syndrome

A
  • Repeated muscle contractions lead to increased muscle strength
  • limb girdle weakness
  • hyporeflexia
  • autonomic symptoms
128
Q

What muscle heads does the median nerve pass through?

A

The two heads of pronator teres

129
Q

Median nerve motor supply of hand

A
  • lateral 2 lumbricals
  • opponens pollicis
  • abductor pollicis brevis
  • flexor pollicis brevis
130
Q

Damage to median nerve at wrist

A
  • carpal tunnel syndrome
  • paralysis and wasting of the thenar eminence and opponens pollicis
  • sensory loss to the palmar aspect of the lateral (radial) 2 1/2 fingers
131
Q

Damage to the median nerve at the elbow

A
  • unable to pronate the forearm
  • weak wrist flexion
  • ulnar deviation of the wrist
  • carpal tunnel syndrome
132
Q

Damage to the anterior interosseous nerve

A
  • loss of pronation of the forearm
  • weakness of the long flexors of the thumb and index finger
133
Q

What is the anterior interosseous nerve a branch of?

A

Median nerve

134
Q

Features of neuroleptic malignant syndrome

A
  • pyrexia
  • muscle rigidity
  • autonomic lability: hypertension, tachycardia, tachypnoea
  • agitated delerium with confusion
  • raised creatine kinase
135
Q

Bloods neuroleptic malignant syndrome

A
  • raised creatine kinase
  • AKI
  • leukocytosis
136
Q

Factors suggestive of pseudo seizure

A
  • pelvic thrusting
  • family member with epilepsy
  • female
  • crying agter seizure
  • doesnt occur when alone
  • gradual onset
137
Q

Damage to radial nerve

A
  • wrist drop
  • sesory loss to the dorsal aspect of the 1st and 2nd metacarpals
  • paralysis to triceps (loss of elbow extension)
138
Q

Ankle reflex

A

S1/S2

139
Q

Knee REflex

A

L3/4

140
Q

Biceps reflex

A

C5/6

141
Q

Triceps reflex

A

C7/8

142
Q

Absolute contraindications to thrombolysis

A
  • previous ICH
  • seizure at onset of stroke
  • intracranial neoplasm
  • suspected SAH
  • stroke or traumatic brain injury in last 3 months
  • lumbar puncture in past 7 days
  • GI haemorrhage in past 3 weeks
  • active bleed
  • pregnancy
  • oesophageal varices
  • uncontrolled hypertension >200/120
143
Q

What drug can result in subacute combined degeneration of he spinal cord?

A

Nitrous oxide

144
Q

Features of subacute combined degeneration of the spinal cord

A

Dorsal column:
- distal tingling or burning symmetrically
- impaired proprioception and vibration sense

Lateral corticospinal tract involement
- muscle weakness,hyperreflexia, spasticity
- UMN signs
- brisk knee relex
- absent ankle jerks
- extensor plantars

Spinocerebellar tract
- sensory ataxia leading to gait abnormality
- positive rombergs sign

145
Q

Motor supply of ulnar nerve

A
  • medial two lumbricals
  • adductor pollicis
  • interossei
  • hypothenar muscles: abductor digiti minimi, flexor digiti minimi
  • flexor carpi ulnaris
146
Q

Sensory of ulnar nerve

A
  • medial 1 1/2 fingers
147
Q

Damage to the ulnar nerve at the wrist

A
  • claw hand
  • wasting and paralysis of teh intrinsic hand muscles
  • wasting and paralysis of the hypothenar muscles
  • sensory loss to the medial 1 1/2 fingers
148
Q

Damage to the ulnar nerve at the elbow

A
  • clawing is more severe than wrist lesion
  • radial deviation of the wrist
  • wasting and paralysis of teh intrinsic hand muscles
  • wasting and paralysis of the hypothenar muscles
  • sensory loss to the medial 1 1/2 fingers
149
Q

Features of vestibular schwannoma

A
  • vertigo (CN VIII)
  • hearing loss
  • tinnitus (CN VIII)
  • absent corneal reflex (cranial nerve V)
  • facial palsy if CNVII affected
150
Q

What are bilateral vestibular schwannomas seen in

A

neurofibromatosis type 2

151
Q

investigation vestibular schwannoma

A

MRI cerbellopontine angle

152
Q
A

Finals (37 decks)

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