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Clinical neurology Flashcards

1
Q

Bilateral sensory involvement LMN diseases

A

Polyradiculopathy
Polyneuropathies- Guillain Barre
Mononeuritis multiplex

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2
Q

What is Guillain-Barre?

A

Acute inflammatory demyelinating polyradiculoneuropathy
Often follows gastroenteritis- commonly campylobacter jejuni
Progresses over days to weeks and may lead to respiratory muscle failure

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3
Q

Possible causes of polyneuropathies

HINT: A DANG THERAPIST

A 
Acquired or inherited 
Diabetes
Amyloid
Nutritional- B12 deficiency 
Guillain Barre
Toxic 
Hereditary- Charcot Marie Tooth, Friedrick's ataxia 
Endocrine 
Recurring/ Renal
Alcohol 
Pb toxicity/ porphyria 
Infection
Systemic- SLE, sarcoid, hypothyroid, syphilis 
Tumours- paraneoplastic

Around 50% are idiopathic

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4
Q

How is Duchenne muscular dystrophy inherited?

A

X-linked recessive

Dystrophin absence

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5
Q

Signs of Duchenne muscular dystrophy

A

Proximal lower limb weakness from the age of 4, gradually spreads to rest of muscles over time
Calf pseudohypertrophy (from infiltration)
Eventual spread to cardiac and respiratory muscles
Gower’s manoeuvre (when asked to stand from sitting)

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6
Q

Acquired myopathies usual clinical features

A

Proximal muscle weakness, usually symmetrical and more weakness than pain
Polymyositis/dermatomyositis
Often affect the pelvic girdle more than the shoulder

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7
Q

Investigations into acquired myopathies

A 
CK- in the 1000s
ESR
EMG to confirm spontaneous activity 
Biopsy
Genetic analysis 
Antibody testing
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8
Q

LMN, bilateral, purely motor potential issues

A

Myopathy- acquired- inflammatory, endocrine, metabolic- hereditary
Anterior horn cell
NMJ- MG, MG crisis, Lambert-Eaton, botulism

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9
Q

Presentation of myasthenia gravis

A

Fluctuating weakness
Proximal, ocular and bulbar- ptosis, diplopia, dysphonia, dysarthria, dysphagia
MG facies- snarl
Fatiguability
No atrophy/ fasciculations, normal tone and reflexes as not a nerve pathology `

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10
Q

What is the Tensilon Test?

A

Short acting anticholinesterase is given IV to see if there is any improvement

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11
Q

What imaging is done in MG?

A

CT of thymus looking for thymoma

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12
Q

Treatment for MG

A

Anticholinesterase inhibitors- pyridostigmine, propantheline
Immunosuppression- especially in acute- pred, IVIg, plasmapheresis
Thymectomy

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13
Q

Unilateral LMN signs

A

Radiculopathy
Plexopathy
Mononeuropathy

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14
Q

Causes of plexopathy

A 
Features reflect motor and sensory findings extending over multiple nerve roots
Trauma- Erb's palsy and Klumpkeys 
Neuralgic amyotrophy
Thoracic outlet syndrome 
Malignant infiltration 
Radiotherapy (may be years later)
Compression
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15
Q

Radiculopathy clinical features

A

Shooting, electric, sharp pain radiating down the limb

Can be across multiple levels if polyradiculopathy

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16
Q

ALS MND stands for

A

Amytrophic lateral sclerosis- Motor neuron disease

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17
Q

ALS differentials

A 
UMN and LMN signs
cervical spondylotic radiculomyelopathy 
Spinal tumour 
Spinal conus medularis lesions
Vit B12 deficiency- sub acute degeneration of the cord and peripheral neuropathy
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18
Q

Treatment for ALS

A 
No cure
Riluzole used to prolong life (1-2 months)
Supportive-
CPAP/NIPPV
PEG
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19
Q

What is MS?

A

Demyelinating disorder of the CNS

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20
Q

Who gets MS?

A

Classically white, young women who live at the poles

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21
Q

Types of MS

A

Clinically isolated syndrome
Relapsing-remitting
Primary progressive
Secondary progressive

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22
Q

How can MS be diagnosed

A

Two events demonstrating dissemination over space and time

Can be done faster now by radiological imaging

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23
Q

Management of MS

A

Acute- corticosteroids to rapidly induce recovery
Disease modifying therapy- interferons and monoclonal antibodies
Symptomatic management- spasticity, bladder, bowel, pain, depression/low mood
MDT

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24
Q

Types of trigeminal autonomic cephalalgias

A

Cluster headaches
Paroxysmal hemicrania
Short-lasting unilateral neuralgiform headache (with conjunctival injection and tearing)

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25
Q

Cluster headache important other differentials

A

Migraine
Other types of TACs
Secondary causes of chronic headache
Hypnic headache

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26
Q

Primary headache causes

A

Migraine
Tension type
Trigeminal autonomic cephalalgias
Other- exercise/ sex-induced

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27
Q

Secondary headache causes

A

Injury
Medication overuse
Cranial or cervical vascular disorder (carotid or vertebral artery dissection)
Venous sinus thrombosis
Non-vascular- idiopathic intracranial hypertension
Painful cranial neuropathies

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28
Q

Presentation of venous sinus thrombosis

A

Recurrent presentations
Procoagulant state
Headache with signs of raised ICP
Normal CT head (possibly anti-delta sign)

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29
Q

Signs of idiopathic intracranial hypertension

A

Papilloedema- compression of the optic nerves and subsequent visual loss
Other cranial neuropathies
Raised LP opening pressure

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30
Q

Management of IIH

A

Conservative- analgesia, weight loss (ultimate treatment), life-style
Medical- Acetazolamide, topiramate, furosemide
CSF drainage/ shunting

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31
Q

Acetazolamide

A

MOA: Carbonic acid anhydrase inhibitor
S/E: haemorrhage, metabolic acidosis, nephrolithiasis, abnormal sensation
AVOID in pregnancy (especially 1st trimester) and sulphonamide reactions

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32
Q

Causes of cerebellar dysfunction

HINT: MAVIS

A 
MS
Alcohol
Vascular
Inherited 
Space occupying lesion
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33
Q

Pyramidal tracts

A

Originate in the cerebral cortex

Voluntary control of musculature of the face and body

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34
Q

Extrapyramidal tracts

A

Originate in the brainstem

Involuntary and autonomic control of musculature- tone, balance, posture and locomotion

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35
Q

What is Uhthoff’s phenomenon?

A

Transient worsening of neurological symptoms when the body becomes overheated

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36
Q

Lhermitte’s phenomenon

A

Electric shock like complaint down the spine from flexion of the neck due to a cervical plaque

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37
Q

Clinical findings of MS due to optic nerve involvement

A

RAPD
Central scotoma
Red desaturation
Optic disc atrophy

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38
Q

Causes of carotid artery dissection

A

Traumatic- hyperextension
Iatrogenic- previous surgery, endartectomy
Spontaneous- HTN, smoking
Connective tissue disorder- Marfan’s, Ehlers-Danlos

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39
Q

Signs and symptoms of a carotid artery dissection

A 
MCA thrombotic events 
Headache
Amaurosis fugax
Limb/facial weakness
Neck swelling
Horner's (partial if post-ganglionic)
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40
Q

What is Eagle syndrome?

A

Rare mimic of carotid artery dissection- calcified or elongated stylohyoid ligament compresses the carotid artery

41
Q

Treatment of carotid artery dissection

A

Conservative- modification of risk factors
Medical- aspirin
Surgical- reconstruction

42
Q

Miller-Fisher syndrome

A

Less severe version of Guillain-Barre which causes ophthalmoplegia, areflexia, ataxia
Always self-limiting, does not require treatment
Anti-GQ1b antibodies

43
Q

Tests to diagnose MND and why

A 
TFTs- thyrotoxicosis 
HbA1c and BM- diabetic amyotrophy 
CK- polymyositis/ dermatomyositis 
EMG- confirms MND pattern of fibrillation and fasciculations and loss of lower motor neurons 
Normal nerve conduction
Genetic analysis
44
Q

Typical pattern of presentation of MND

initial, progression and sparing

A

Isolated limb weakness (reduced grip or foot drop) which progresses to truncal and bulbar involvement
Progressive bulbar palsy- dysarthria and dysphagia
Usually spares extraocular muscles and sensory and autonomic systems

45
Q

What enhances active MS plaques on MRI T2

A

Gadolinium

46
Q

Differentials for myasthenia gravis

A 
Myasthenic crisis
Lambert-Eaton Myasthenic syndrome
Polymyositis 
Dermatomyositis
Botulism
47
Q

Clinical features of GB

A

Back/leg pain in the initial stages
Progressive, symmetrical weakness of the limbs, classically ascending from the legs first, proximal muscles affected first
Reduced or absent reflexes
Mild sensory symptoms

48
Q

Autonomic dysreflexia occurs in patients that have…

A

A spinal cord injury (often traumatic) above the level of T6

Most commonly triggered by constipation or urinary retention

49
Q

Features of multisystem atrophy

A

Parkinsonian features
Cerebellar signs- ataxia

Autonomic disturbance:
Postural hypotension
Erectile dysfunction
Atonic bladder

50
Q

Features of a bacterial meningitis LP

A 
Turbid appearance
Elevated opening pressure
Very raised WCC
Raised protein
Low glucose
51
Q

Features of a viral meningitis LP

A 
Clear appearance 
Normal opening pressure 
Lymphocyte predominance, raised WCC
Slightly raised protein 
Normal glucose
52
Q

What is Hoover’s sign of leg paresis used to distinguish between?

A

Organic and non-organic paresis of the leg
Synergistic contraction of the contralateral leg if the patient is genuinely trying, no contraction suggests a functional/ non-organic cause

53
Q

Management of possible TIA if the patient is anticoagulated

A

A&E for CT head to exclude haemorrhagic stroke- do not give aspirin 300mg until this is done

54
Q

Conduction dysphasia

A

Classically due to a stroke affecting the arcuate fasciculus- connecting Broca’s and Wernicke’s areas
Speech is fluent and comprehension is intact but poor repetition

55
Q

Clinical features of neuroleptic malignant syndrome

A

Rigidity, hyperthermia, autonomic instability, altered mental state- agitated delirium with confusion
Can cause AKI

56
Q

Management of neuroleptic malignant syndrome

A

Stop causative antipsychotic
IV fluids to prevent renal failure
Dopamine agonist (bromocriptine)
Dantrolene, muscle relaxer

57
Q

Stroke management

A

Exclude haemorrhage (CT head)
Aspirin 300mg (and then for 14 days)
Thrombolysis within 4.5 hours if no contraindications
+ thrombectomy within 6 hours

58
Q

Secondary stroke prevention

A

Follow up in primary care at 6 months and annually
Lifestyle modification
Clopidrogrel 75mg daily
Aspirin if not tolerated and dipyridamole if both not tolerated
Duel aspirin and clopidogrel for 3 months may be initiated
Statin
Treatment for HTN
Weigh up anticoagulation risk vs benefit
Optimise co-morbidities

59
Q

Triad of Wernicke’s encephalopathy

A

Ataxia, ophthalmoplegia (nystagmus most commonly) and confusion
Peripheral polyneuropathy may be seen

60
Q

Treatment of Wernicke’s encephalopathy

A

Urgent replacement of thiamine

IV pabrinex- vit B/C

61
Q

Causes of a third nerve palsy

A 
Vasculitis
DM
Posterior communicating artery aneurysm
MS
Weber's syndrome- ipsilateral third nerve palsy with contralateral hemiplegia- midbrain strokes
Amyloid
62
Q

Features of progressive supranuclear palsy

A

Parkinsonian features- particularly early loss of balance when walking
More rapidly progressive
Ophthalmic and bulbar symptoms more pronounced- problems controlling eye movements and blurring of vision predominant

63
Q

Features of corticobasal degeneration

A

Cortical and basal ganglia involvement
Parkinsonism
Often presents unilaterally and then progresses bilaterally
Apraxia, limb dystonia, cognitive features, visual-spatial impairment

64
Q

Cushing’s triad and other features of raised ICP

A

Irregular breathing
Widened pulse pressure
Bradycardia

Papilloedema
Headache
Vomiting
Reduced consciousness

65
Q

LP of bacterial meningitis

A 
Cloudy and turbid appearance 
Elevated opening pressure 
Primarily polymorphonuclear leukocytes- neutrophils elevated
Low glucose 
Raised protein
66
Q

LP of viral meningitis

A 
Appears clear 
Normal or elevated opening pressure 
Raised WBC- primarily lymphocytes 
Normal glucose
Raised protein
67
Q

LP of fungal meningitis

A 
Clear or cloudy appearance 
Elevated opening pressure
Elevated WBC
Low glucose 
Elevated protein
68
Q

LP of TB meningitis

A 
Appears opaque
Elevated opening pressure
Elevated WBC
Low glucose 
Grossly raised protein
69
Q

LP of subarachnoid haemorrhage

A 
Blood stained initially 
Xanthochromia after 12 hours
Elevated opening pressure
Elevated WBC
Elevated RBC
Elevated protein
Normal glucose
70
Q

Guillain Barre LP results

A

Albuminocytologic dissociation- raised protein without a raised WBC

71
Q

Indications for LP

A

Diagnostic- MS, GB, meningitis, subarachnoid haemorrhage, encephalitis, idiopathic intracranial hypertension, normal pressure hydrocephalus
Therapeutic- IIH

72
Q

Normal pressure hydrocephalus triad of signs

A

Instability- ataxic gait
Cognitive dysfunction
Incontinence

73
Q

Contraindications for LP

A

Meningococcal septicaemia
Intracerebral haemorrhage
Raised ICP in a non-communicating hydrocephalus
Congenital malformations- chiari, spina bifida
Coagulopathy or anticoagulated

74
Q

Meniere’s disease

A

Increased pressure of the endolymphatic system leading to recurrent attacks of vertigo lasting >20 minutes but <24 hours
Fluctuating sensorineural hearing loss
Aural fullness
Tinnitus

75
Q

Vestibular schwannoma clinical features

A

Unilateral sensorineural hearing loss
Slow progression leading to CN being effected- 5,6,7,9,10
Absent unilateral corneal reflex
Bilaterally associated with NF2

76
Q

BPPV clinical features

A

Occurs on head movement due to disruption of debris
Brief episodes of mild-intense vertigo
Dix-Hallpike manoeuvre shows fatigable nystagmus
Epley manoeuvre clears debris

77
Q

Vestibular neuronitis clinical features

A

Recent viral infection
No deafness or tinnitus
Abrupt onset, severe, associated with nausea and vomiting

78
Q

Drugs that can cause ototoxicity

A

Loop diuretics

Aminoglycosides ie gentamycin

79
Q

Spinal cord tract changes in sub-acute degeneration of the spinal cord

A

Dorsal column loss causing sensory and LMN signs
Corticospinal cord tract loss causing UMN signs
Spinothalamic tracts remain intact and so there is no pain or temperature change even in extreme cases

80
Q

How many beats of clonus is normal?

A

3 or less

81
Q

Management of cluster headaches

A

Keep calm, 100% high flow oxygen for 15 mins and sumatriptans at onset
Education to avoid triggers- could be alcohol
Consideration of corticosteroids in the short term or verapamil prophylaxis

82
Q

Treatment of trigeminal neuralgia

A

Patient education
Carbamazepine prophylaxis or lamotrigine/ phenytoin/ gabapentin
Surgery can be used if medication fails- microvascular decompression

83
Q

Triggers of migraines

A 
Chocolate
Hangovers
Orgasms
Cheese/ caffeine 
Oral contraceptives
Lie-ins
Alcohol
Travel
Exercise
84
Q

Differentials for migraine headaches

A 
Trigeminal autonomic cephalalgias (including cluster)
Tension headache
Cervical spondylosis 
Raised ICP
TIA
85
Q

Management of migraines

A

Patient education about triggers
Medical prophylaxis- propranolol, topiramate

During an acute attack- oral triptan combined with ibuprofen or paracetamol. Anti-emetics. Warm or cold compress, rebreathing into a paper bag. 10 sessions of acupuncture

86
Q

What is a Stokes-Adams attack?

A

Transient arrhythmia eg bradycardia due to incomplete heart block resulting in decreased cardiac output nad LOC
Falls to the ground with no warning except palpitations, injuries are common as a result of this (screen for these!!)
Pale with a slow or absent pulse
Recovery is within seconds but if prolonged LOC there may be anoxic clonic jerks

87
Q

Blackouts differentialas

A 
Vasovagal syncope- reflex bradycardia and peripheral dilation (situation syncope if triggered specifically)
Carotid sinus syncope 
Epilepsy 
Stokes-Adams attacks
Hypoglycaemia
Postural hypotension 
Anxiety- no LOC 
Factitious
88
Q

Differentials for unilateral foot drop

A 
DM
Early MND
MS
Stroke
Common peroneal palsy
Prolapsed disc
89
Q

Spastic gait description

A

Stiff
Circumduction of the legs +/- scuffing of the toes
UMN lesions

90
Q

Acute management of stroke

A

A-E assessment
CT head to rule out haemorrhage
NBM until swallow screen
300mg aspirin for 14 days
Consider thrombolysis as soon as haemorrhage is ruled out (within 4.5 hours of onset)- best results within 90 minutes- Alteplase
Thrombectomy within 6 hours if large artery occlusion in the proximal anterior circulation

91
Q

Secondary prevention of stroke

A

Control risk factors- treat HTN, hyperlipidaemia, DM, cardiac disease, AF, smoking
14 days of 300mg aspirin
Switch to long-term clopidogrel monotherapy 75mg OD

MDT approach- PT, OT, SALT, specialist nurse, stroke team
Rehabilitation on a stroke ward and into the community

Tests
24 hour ECG
HTN- retinopathy, neuropathy, cardiomegaly
Carotid artery stenosis- carotid doppler US +/- CT angiography

92
Q

Pharmacological treatment of cognitive decline

A

Acetylcholinesterase inhibitors- donepezil, rivastigmine, galantamine- recommended by NICE for dementia
Memantine- NMDA antagonist- late stage AD
Antipsychotics acutely if extreme agitation or psychosis
Vitamin supplementation

93
Q

Todd’s palsy/paresis

A

Weakness following a focal seizure in the motor cortex

94
Q

Extrapyramidal triad of Parkinson’s disease

A

Resting tremor (unilateral presentation, gets better on voluntary movement)- often pill rolling
Hypertonia- cogwheel rigidity
Bradykinesia

95
Q

What is Devic’s syndrome/ NMO

A

Neuromyelitis optica
MS variant with transverse myelitis, optic atrophy
Anti-aquaporin 4 antibodies

96
Q

MND with only LMN signs

A

Progressive muscular atrophy- anterior horn cell lesion so only LMN

97
Q

MND definition

A

Cluster of neurodegenerative diseases characterised by selective loss of neurons in the motor cortex, cranial nerve nuclei and anterior horn cells
UMN and LMN with bulbar inclusion
No sensory or sphincteric disturbance
NEVER affects eye movements

98
Q

Signs of neurofibromatosis type 1

A

Cafe-au-lait spots, adults have more than 5, do NOT predispose to skin cancer
Dermal neurofibromas and nodular neurofibromas, increase in number with age
Lisch nodules on the iris

Mild learning disability common
Malignancy in 5%

Autosomal dominant

99
Q

Signs of neurofibromatosis type 2

A

Bilateral vestibular schwannoma are characteristic
Usually become symptomatic around 20 years old
Meningiomas

Autosomal dominant

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