Neurology Flashcards

1
Q

Where is the most common location for TIA embolus? (1)

What symptoms do patients with this present with? (3)

A

Anterior circulation - originating from atherosclerotic plaque in the carotid artery.

Hemiparesis, dysphasia, amaurosis fugax

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2
Q

How do patients with posterior circulation TIAs present? (4)

A
Bilateral motor and sensory dysfunction
Loss of consciousness
Binocular blindness
Vertigo
Diplopia
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3
Q

What vessel is typically involved in a posterior circulation stroke? (1)

A

Vertebrobasilar

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4
Q

What is the pharmacological management following TIA? (3)

A

300 mg aspirin for 2 weeks
Longterm - Clopidogrel
Statin

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5
Q

What are the features of an anterior circulation stroke, what is the difference between a total and partial anterior circulation stroke? (4)

A

Unilateral weakness/hemiparaesis
Homonymous hemianopia
Higher cerebral dysfunction - dysphasia, visuospatial disorder

Partial will only have 2 of the 3 features. Partial typically affected the anterior cerebral artery, with middle being total.

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6
Q

How does the paralysis vary in middle cerebral artery strokes compared to anterior?

A

In anterior - lower limbs are affected more than the upper limbs and there is less sensory loss

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7
Q

Which artery is most commonly affected in ischaemic stroke? (1)

A

Middle cerebral artery

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8
Q

What is the function of Broca’s and Wernicke’s areas? (2)

A

Broca’s - Production of speech

Wernicke’s - comprehending speech

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9
Q

What is Weber’s syndrome? (3)

A

Midbrain stroke
Affects CNIII (Occulomotor)
With contralateral hemiplegia/paresis

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10
Q

What is a lacunar stroke? What is the most common type? (3)

A

A stroke of a penetrating artery
There is an absence of cortical signs
Pure motor

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11
Q

What is required before treatment in a stroke? (1)

A

Head CT - differentiate between ishcaemic and haemorrhagic

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12
Q

What is the treatment for ischaemic stroke? (4)

A

ABCDE
IV alteplase thrombolysis within 4.5 hours of symptom onset
Aspirin 24 hours following thrombolysis
VTE prophylaxis and early mobilisation

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13
Q

What are causes of intracerebral haemorrhage? (5)

A
Hypertension
Cerebral amyloid angiopathy
Ruptured AV malformation
Coagulation disorders or use of anticoagulants
Vasculitis
Neoplasms
Traumatic brain injury
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14
Q

What is the main cause of subarachnoid haemorrhagic strokes? (1)

A

Berry aneurysms in the circle of Willis

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15
Q

What are risk factors for subdural haematoma? (5)

A

Head injury
Cerebral atrophy/increased age
Alcohol misuse
Anticoagulation medication

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16
Q

What is the typical delay between injury to symptoms in subdural versus extradural haematoma? (2)

A

Subdural - Days to weeks

Extradural - Minutes to hours followed by a lucid period then relapse in hours to days

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17
Q

What is seen on CT in a subdural haematoma? (1)

A

Crescent-shaped mass

Density decreases the older the bleed is

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18
Q

What is seen on CT in an extradural haematoma? (1)

A

Hyperdense biconvex shape

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19
Q

What is the management of subdural and extradural haematoma? (3)

A

ABCDE
Mannitol for raised ICP
Stabilise and refer to neurosurgery

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20
Q

Name some red flags in a patient presenting with migraine (4)

What should be done if a patient presents with red flags? (2)

A

Onset > 50 years old
Change in pattern
Abnormal neurological exam
Posteriorly located headache

Neuroimaging (MRI) and lumbar puncture

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21
Q

What is used to manage migraines acutely? (2)

A

Triptans (Sumatriptan)

Simple analgesia

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22
Q

What is used for migraine prophylaxis? (3)

A

1) Propranolol or Topiramate

2) Amitryptaline

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23
Q

What is the management for acute cluster headache? (2)

A

Oxygen and triptans

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24
Q

What is used for cluster headache prophylaxis? (1st and 2nd line) (2)

A

1) Verapamil

2) Lithium

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25
Q

What is used in the acute management of trigeminal neuralgia? (1)

A

Carbamazepine (anticonvulsant)

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26
Q

What condition must be excluded in trigeminal neuralgia? (1)

A

Temporal arteritis

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27
Q

Name causes of peripheral neuropathy (4)

A
Diabetes
Alcohol misuse
Vitamin deficiency - B12
Infective/Inherited - Lyme disease, EBV, Shingles
Drugs - Isoniazid, cisplatin, phenytoin
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28
Q

What are the mechanisms that can lead to peripheral neuropathy? Give an example of a condition in each. (6)

A

Demyelination (damage to Schwann cells) - Guillan Barre Syndrome
Axonal degeneration - Multiple sclerosis
Wallerian degeneration - Infarction
Compression - Carpal tunnel syndrome
Infiltration - Leprosy, inflammation, malignancy

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29
Q

What organisms typically lead to Guillain Barre syndrome? (3)

A

Campylobacter
EBV
CMV

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30
Q

How does Guillain Barre present? (5)

A
1-3 weeks post infection. 
Symmetrical, ascending muscle weakness +/- numbness
Loss of reflexes
Autonomic dysfunction
Neuropathic pain
Can be respiratory involvement
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31
Q

What tests should be done in suspected Guillain Barre syndrome?

A
Nerve conduction study
Lumbar puncture
Spirometry - to monitor resp function
LFTs - elevated indicates higher severity
Serology - antiganglioside antibodies
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32
Q

What is seen on lumbar puncture in Guillain Barre? (1)

A

Elevated proteins

Normal cell count

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33
Q

What is the management for Guillain-Barre syndrome? (2)

A

Plasma exchange and IV immunoglobulins

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34
Q

What is the most common inheritance pattern in Charcot-Marie-Tooth? (1)

A

Autosomal dominant

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35
Q

How does Charcot-Marie-Tooth present? (4)

A

Foot drop
Loss of sensation
Loss of reflexes
Peroneal muscle atrophy and ‘inverted champagne bottle’ appearance

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36
Q

What is the triad of Parkinsonism? (3)

A

Rigidity, bradykinesia, resting tremor

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37
Q

What is the pathology behind Parkinson’s disease? (4)

A

Progressive degeneration of dopaminergic receptors in the substatia nigra of the basal ganglia.
Lewy bodies develop.
There is loss of dopamine and melanin in the striatum.

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38
Q

What do Lewy bodies consist of? (2)

A

Ubiquitin and alpha-synuclein

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39
Q

What are the features of a Parkinsonian tremor? (6)

A
Pill rolling
Micrographia
Improves with activities
Postural instability
Cog-wheeling
Brisk reflexes
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40
Q

Name some non-motor symptoms of Parkinson’s (4)

A
Depression
Anosmia
Visual hallucinations
Constipation
Urinary frequency/urgency
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41
Q

Describe a Parkinsonian Gait (4)

A

Stooped
Small, shuffling gait
Narrow base
Reduced arm swing

42
Q

What is the gold standard management for Parkinson’s? (2)

How do the drugs work? (2)

A

Levodopa + Carbidopa
Levodopa is a precursor to dopamine that crosses the blood brain barrier
Carbidopa is decarboxylase inhibitor that prevents Levodopa being converted to Dopamine in the peripheral circulation.

43
Q

What is used to delay starting levodopa in Parkinson’s? (2)

A

Monoamine Oxidase Inhibitors - Rasagiline

Dopamine agonists - Pramiprexole, Ropinirole

44
Q

What are limitations/disadvantages of Levodopa? (3)

A

Decreased efficacy and duration of action over time
On/Off effect
Levodopa induced dyskinesia

45
Q

What are the symptoms of progressive supranuclear palsy? (4)

A

Early postural instability
Vertical gaze palsy
Cognitive impairment
NO tremor

46
Q

What are the symptoms of multiple system atrophy? (4)

A

Early autonomic dysfunction - Postural hypotension, bladder dysfunction
Cerebellar signs

47
Q

What are the Parkinson-plus syndromes? (3)

A

Progressive Supranuclear Palsy
Multiple system atrophy
Lewy-body dementia

48
Q

How are Lewy body dementia and Parkinson’s differentiated clinically? (1)

A

In Parkinson’s motor symptoms occur a year or more before dementia
In Lewy body the two occur closer together or at the same time

49
Q

What is the cause of Huntington’s Disease? (2)

A

A mutation of chromosome 4 with an extended glutamine sequence consisting of multiple CAG repeats

50
Q

What are the first symptoms of Huntington’s? (1)

A

Prodromal phase - mild psychotic and behavioural changes

51
Q

In which areas is neuronal loss seen in Huntington’s? (2)

A

Caudate nucleus and putamen of the basal ganglia

52
Q

How are neurotransmitters affected in Huntington’s? (3)

A

GABA and ACh are reduced

Normal Dopamine

53
Q

What can be used for symptom management in Huntington’s? (3)

A

Benzodiazepines
Sodium valproate
Tetrabenazine
Antidepressants, antipsychotics

54
Q

What are the variants of motor neurone disease? What nerves are affected in each one? (4)

A

Amyotrophic lateral sclerosis - UMN and LMN
Primary lateral sclerosis - UMN
Progressive muscular atrophy - LMN
Progressive bulbar palsy - UMN and LMN of lower cranial nerves

55
Q

What dementia is amyotrophic lateral sclerosis associated with? (1)

A

Frontotemporal dementia

56
Q

What is the management of motor neurone disease? (4)

A

Riluzole - extends life by approximately 3 months
Baclofen for muscle spasms
Non-invasive ventilation
PEG tube feeding

57
Q

What imaging is used to visualise the plaques in multiple sclerosis? (1)

A

MRI

58
Q

What are the clinical features of Multiple Sclerosis? (4)

A

Unilateral optic neuritis
UMN signs - Spasticity, weakness, hyperreflexia
Symptoms are worse in the heat or after exercise (Uthoff’s phenomenon)
Cerebellar signs

59
Q

What is Lehrmitte’s sign in multiple sclerosis? (2)

A

Neck flexion leads to an electric shock sensation down the trunk and limbs

60
Q

What investigations should be order in suspected multiple sclerosis and what would be seen in each? (6)

A

MRI brain and spinal cord - Periventricular lesions, cervical spinal cord lesions

Lumbar puncture - Raised protein, oligoclonal bands

FBC, TSH, metabolic panel, B12 - exclusionary

61
Q

How are relapses treated in multiple sclerosis? (1)

A

IV methyprednisolone

62
Q

What is the most common cause of death in multiple sclerosis? (1)

A

Aspiration pneumonia

63
Q

What antibodies are associated with Myasthenia Gravis? (2)

A

AChR antibodies

anti-muscle-specific tyrosine kinase (MuSK) antibodies

64
Q

What muscles are affected first in Myasthenia Gravis? (1)

A

Extraoccular muscles

65
Q

What is Lambert-Eaton Myasthenic syndrome? (1)

A

Presents similarly to Myasthenia Gravis but is associated with small cell lung cancer

66
Q

What investigations are done in suspected Myasthenia Gravis? (4)

A

Serum antibodies (MuSK, antiACh)
CT chest - Thymic hyperplasia
Tensilon test - IV endrophonium increases power
Neurophysiology

67
Q

What class of drug is used for symptom control in Myasthenia Gravis? (1) Name two examples (2)

A

Acetylcholinesterase inhibitors - Pyridostigmine, neostigmine

68
Q

What surgery can improve symptoms in Myasthenia Gravis? (1)

A

Thymectomy

69
Q

What is the management for a Myasthenic crisis? (3)

A

Intubation and mechanical ventilation
Plasmapheresis and IV immunoglobulins
Corticosteroids

70
Q

What is seen on blood tests in Duchenne muscular dystrophy? (1)

A

Elevated creatinine kinase

71
Q

Which cancers metastasise to the brain? (5)

A

Lung, breast, prostate, colorectal, melanoma and kidney

72
Q

What is the most common high grade brain tumour? (1)

A

Astrocytoma

73
Q

What is the diagnostic criteria for brainstem death? (4)

A

1) Patient must suffer from a condition that has lead to irreversible brain damage
2) Potentially reversible causes have been excluded
3) There is coma, apnoea and absence of brainstem reflexes that have been formally demonstrated

The diagnosis must be made by two doctors

74
Q

What are the brainstem reflexes examined in suspected brainstem death? (6)

A
Pupils unresponsive to light
Absent corneal reflex
Absent oculovestibular reflex
No cranial nerve motor response
No gag or cough reflex
75
Q

What lobe is affected in this seizure presentation -

A sense of deja vu and strange smells followed by repetitive, non-purposeful movements (1)

A

Temporal lobe

76
Q

What lobe is affected in a seizure with Jacksonian march? (1)

A

Frontal lobe

77
Q

What is first line for generalised tonic-clonic seizure prophylaxis? (2)

A

Sodium Valproate or Lamotrigine

78
Q

What is first line prophylaxis for absence seizures? (2)

A

Sodium Valproate or Ethosuximide

79
Q

What is the management for status epilepticus?

A

IV or rectal benzodiazepines (IV Lorazepam, Rectal diazepam)

80
Q

What is first line prophylaxis for partial seizures? (2)

A

Carbamazepine or Lamotrigine

81
Q

What is seen on EEG in West syndrome? (1)

How is this syndrome managed? (2)

A

Hypsarrhythmia

Corticosteroids and vigabatrin

82
Q

What genetic syndrome is West syndrome associated with? (1)

A

Tuberous sclerosis

83
Q

What are the cerebellar signs? (6)

A
Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred, staccato speech
Homonymous hemianopia
84
Q

What is used to manage subarachnoid haemorrhage? (4)

A

Nimodipine - Calcium channel blocker that stops vasospasm
Dexamethasone
NaCl Fluids
Neurosurgery referral

85
Q

What artery is affected most commonly in extradural haemorrhage? (1)

A

Middle meningeal artery

86
Q

What are the triad of symptoms of normal pressure hydrocephalus? (3)

A

Dementia
Gait dyspraxia
Urinary incontinence

87
Q

What is the treatment for normal pressure hydrocephalus? (1)

A

Ventriculo-peritoneal shunting

88
Q

What is the most common genetic mutation in Alzheimers? (1)

A

apoE4

89
Q

What is the pathophysiology of Alzheimers? (3)

A

Amyloid plaques develop in the grey matter of the brain and intracellular neurofibrillary tangles made up of tau proteins develop.
There is atrophy and overall reduction in cholinergic function.

90
Q

Which parts of the brain are affected first in Alzheimers? (2)

A

The hippocampus and medial temporal structures

91
Q

How is vascular dementia managed? (3)

A

Decrease vascular risk - aspirin, warfarin, blood pressure control
Anticholinesterases - Donepezil
Memantine

92
Q

What are Pick bodies? (2)

A

Pathological intracellular inclusion bodies caused by mutations in tau proteins

93
Q

How does frontotemporal dementia present? (2)

A

Early behavioural changes - apathy, disinhibition, impulsivity
Initial preservation of cognitive function

94
Q

What is used to manage frontotemporal dementia? (2)

A

SSRIs

Atypical antipsychotics

95
Q

How are Pick bodies identified? (1)

A

Silver staining

96
Q

What are Lewy bodies? (1)

A

Alpha synucelin and ubiquitin deposits

97
Q

Name some visual signs of multiple sclerosis (4)

A

Blurred vision OR reduced visual acuity
Blurred vision OR reduced visual acuity on exposure to heat e.g. a hot shower (Uthoff’s phenomenon)
Colour desaturation (e.g. seeing the colour red as orange or grey)
Eye pain at rest
Painful ocular movements
Oscilopsia (a visual disturbance in which objects in the visual field appear to
oscillate)

98
Q

Name three tests done in suspected multiple sclerosis and the results expected (6)

A

MRI Head +/- spine - Multiple sclerotic plaques (most commonly seen in periventricular white matter) with finger-like radial extensions (Dawson’s fingers)

Lumbar puncture - Lymphocytic pleocytosis
Oligoclonal bands

Evoked potential testing - usually visual, shows a slowed response

99
Q

Where are sclerotic plaques most commonly seen in multiple sclerosis? (1)

A

Periventricular white matter

100
Q

What histological changes are expected in neurones in multiple sclerosis? (3)

A

Demyelination
Variable oligodendrocyte loss
Hypercellular plaque edge due to infiltration of tissue with inflammatory cells
Perivenous inflammatory infiltrate (mainly macrophages and T-lymphocytes)
Older plaques may have central gliosis

101
Q

What drug can delay progression of disease in multiple sclerosis? (1)

A

Beta interferon

102
Q

What class of drugs is first line for treating Alzheimer’s disease? Give an example (2)

A

Anticholinesterase inhibitors - Rivastigmine, Donepezil