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Phase 2a > Neuro > Flashcards

Neuro Flashcards

1
Q

What is an ischaemic stroke?

A

Ischaemic infarction due to occlusion of a vessel by embolism of a thrombus

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2
Q

What is a haemorrhagic stroke?

A

Bleeding from brain vasculature

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3
Q

Risk factors for ischaemic stroke

A

HTN, smoking, DM, heart disease, peripheral vascular disease, hypercholesterolaemia, raised clotting factors

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4
Q

What is the main risk factor for haemorrhagic stroke?

A

HTN

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5
Q

Signs and symptoms of an ACA territory stroke/TIA

A 
o	Leg weakness and sensory disturbance 
o	Gait apraxia  
o	Incontinence
o	Drowsiness
o	Akinetic mutism - decrease in spontaneous 
        speech and movement
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6
Q

Signs and symptoms of an MCA territory stroke/TIA

A 
o	Contralateral upper limb weakness and sensory 
        loss
o	Hemianopia
o	Aphasia
o	Dysphasia
o	Facial Droop
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7
Q

Signs and symptoms of PCA territory stroke/TIA

A 
o	Contralateral homonymous hemianopia
o	Cortical blindness 
o	Visual agnosia - can’t interpret visual information
o	Prosopagnosia
o	Dyslexia
o	Unilateral headache
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8
Q

Symptoms of a hemorrhagic stroke

A

Severe headache, nausea/vomiting, sudden loss of consciousness

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9
Q

What is the act fast campaign?

A 
Stroke management outside of hospital:
   o	Facial asymmetry 
   o	Arm/leg weakness 
   o	Speech difficulty
   o	Time to call 999
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10
Q

Investigations for suspected stroke

A
  • CT/MRI within 1 hour (+ blood count and glucose)

* Further investigations (within 24 hours) – Carotid doppler USS, bloods (FBC, ESR, glucose, clotting, lipids), ECG

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11
Q

Initial management of ischaemic stroke

A 
•   300mg aspirin (2 weeks)
•   Thrombolysis:
     o   Up to 4.5 hours post onset of symptoms
     o   Alteplase – IV to break up clot
•	Thrombectomy
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12
Q

Contraindications for thrombolysis

A

Surgery in last 3 months, recent arterial puncture, history of active malignancy, brain aneurysms, anticoagulation, clotting disorders, severe liver disease, acute pancreatitis

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13
Q

Risk management after ischaemic stroke

A

o Anti-platelet – aspirin and clopidogrel
o Cholesterol – statins
o AF – warfarin, NOAC’s
o Antihypertensives – ACE-i

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14
Q

Management of haemorrhagic stroke

A

Treat as SAH, stop anticoagulants

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15
Q

What is a transient ischaemic attack (TIA)?

A

An ischaemic neurological event with symptoms lasting <24hrs

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16
Q

Causes of TIA

A

• Carotid atherothromboembolism
• Cardioembolism – post-MI, AF, diseased/prosthetic
valve
• Hyperviscosity – polycythaemia, sickle-cell, myeloma
• Vasculitis

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17
Q

Investigations for suspected TIA

A
  • Bloods – FBC, ESR, U&E, glucose, lipids
  • Carotid Doppler ± angiography
  • CT/MRI
  • Echocardiogram
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18
Q

Management of TIA

A
  • Control CV RF’s
  • Antiplatelets – aspirin 300mg (2 weeks)
  • Anticoagulation if cardiac source
  • Carotid endarterectomy – if severe stenosis
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19
Q

What are the DVLA regulations on driving after a stroke/TIA?

A

Prohibited for 1 month

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20
Q

What is a subarachnoid haemorrhage (SAH)?

A

Bleeding into the space between the arachnoid and the pia mater

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21
Q

Epidemiology of SAH

A

Usually 35-65yrs

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22
Q

Symptoms of SAH

A

o Sudden-onset excruciating headache, ‘thunder clap’
o Vomiting, collapse, seizures, coma
o Preceding ‘sentinel’ headache

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23
Q

Signs of SAH

A

o Neck stiffness
o Kernig’s sign (6hrs after) – inability to straighten leg
when hip flexed 90 degrees
o Retinal subhyaloid and vitreous bleeds
o Pupil changes

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24
Q

Causes of SAH

A

o Berry aneurysm – 90%
o Arteria-venous malformation – 15%
o Encephalitis, vasculitis, tumour

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25
Q

Risk factors for SAH

A

Previous aneurysm, smoking, alcohol misuse, HTN, FH, bleeding disorders

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26
Q

Investigations for suspected SAH

A

o Urgent CT – star pattern within 24hrs
o Lumbar Puncture (12 hours after symptoms) –
bloody or increase in pigments (bilirubin) -> straw
coloured
o CT angiography

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27
Q

Management of SAH/haemorrhagic stroke

A

o Re-examine CNS often – BP, pupils, GCS
o Fluids
o CCB (nimodipine) – reduces vasospasm
o Dexamethasone – cerebral oedema
o Surgery – endovascular coiling vs surgical clipping
(craniotomy)

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28
Q

Differential diagnosis for suspected SAH

A

Meningitis, migraine

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29
Q

Differential diagnosis for suspected TIA

A

Migraine with aura, hypoglycaemia, focal epilepsy

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30
Q

What is the main complications of SAH?

A

Cerebral ischaemia

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31
Q

Cause of subdural haematoma

A

Trauma – can be minor or forgotten (up to 9 months ago) -> rupture of bridging veins

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32
Q

Risk factors for subdural haematoma

A

Age, falls, anticoagulation

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33
Q

Symptoms of subdural haematoma

A 
o   Fluctuating level of consciousness 
o   Gradual physical or intellectual slowing 
o   Headache 
o   Personality change 
o   Unsteadiness
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34
Q

Signs of subdural haematoma

A

Raised intracranial pressure, seizures

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35
Q

Investigations for subdural haematoma

A

CT/MRI – crescent-shaped collection of blood over one hemisphere

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36
Q

Management of subdural haematoma

A

o Reverse clotting abnormalities

o Surgery if >10mm - craniotomy

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37
Q

Cause of extradural haematoma

A

Skull fracture -> rupture of middle meningeal artery and vein

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38
Q

Signs and symptoms of extradural haematoma

A

o Lucid interval – hours-days
o Increasingly severe headache, vomiting, confusion,
seizures, hemiparesis
o -> pupil dilation, coma, bilateral limb weakness,
breathing irregular -> death

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39
Q

Differentials for subdural haematoma

A

Stroke, dementia, CNS masses

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40
Q

Differentials for extradural haematoma

A

Epilepsy, carotid dissection, CO poisoning

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41
Q

Investigations for suspected extradural haematoma

A

o CT – biconvex/lens-shaped, +/- midline shift
o Skull x-ray
o DO NOT LP

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42
Q

Management of extradural haematoma

A

o Surgery – craniotomy, clot evacuation ± ligation of
bleeding vessels
o Mannitol IVI

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43
Q

What is an epileptic seizure?

A

Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excessive, hypersynchronous neuronal discharges in the brain

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44
Q

Causes of epilepsy

A
  • 2/3 idiopathic
  • Structural – cortical scarring, development, stroke
  • Other – autoimmune
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45
Q

Defining features of an epileptic seizure

A

• 30-120 seconds
• ‘Positive’ ictal symptoms
• Postictal symptoms
• Stereotypical seizures/syndromal seizure types
• May occur from sleep
• May be associated with other brain dysfunction
• Typical seizure phenomena – lateral tongue bite,
déjà vu ect.

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46
Q

Common postictal symptoms

A

Headache, confusion, myalgia, temporary weakness or dysphagia

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47
Q

What are the two main types of epileptic seizures?

A

Focal (partial) seizures, generalised seizures

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48
Q

What are the 2 main types of focal epileptic seizures?

A

o Partial seizures without impairment of consciousness

o Partial seizures with impairment of consciousness

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49
Q

What are secondary generalised epileptic seizures?

A

Occur following a primary partial seizure, typically convulsive

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50
Q

What are the 3 main types of primary generalised epileptic seizures?

A

o Absence seizures
o Myoclonic seizures
o Primary generalised tonic clonic seizures

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51
Q

Signs and symptoms of an absence seizure

A

Brief <10 second pauses, stops talking mid-sentence then carries on where left off

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52
Q

Signs and symptoms of a myoclonic seizure

A

Sudden jerk of limb, face or trunk, violently disobedient limb

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53
Q

Signs and symptoms of generalised tonic clonic seizures

A

Loss of consciousness, limbs stiffen (tonic) then jerk (clonic), post-ictal confusion and drowsiness

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54
Q

Investigations for epilepsy

A
  • Look for provoking causes
  • EEG if differentials ruled out
  • MRI – structural lesions
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55
Q

Differentials for epileptic seizures

A

Syncope, non-epileptic seizures

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56
Q

What is syncope?

A

Paroxysmal event in which changes in behaviour, sensation and cognitive processes are caused by insufficient blood or oxygen supply to the brain

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57
Q

Features of syncope

A 
o   Situational 
o   Typically from sitting or standing 
o   Rarely from sleep 
o   Presyncopal symptoms 
o   5-30 seconds 
o   Recovery within 30 seconds 
o   Cardiogenic syncope – less warning, heart disease
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58
Q

What is a non-epileptic seizure?

A

Paroxysmal event in which changes in behaviour, sensation and cognitive function caused by mental processes associated with psychosocial distress

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59
Q

Features of a non-epileptic seizure

A

o Situational
o 1-20 minutes
o Dramatic motor phenomena or prolonged atonia
o Eyes closed ictal crying and speaking
o Surprisingly rapid or slow postictal recovery
o History of psychiatric illness/somatoform illness

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60
Q

Pharmocological management of epilepsy

A
  • Focal – 1st line Carbamazepine/Lamotrigine
  • Primary generalised– 1st line Valproate/Lamotrigine
  • Surgery – if drugs fail
  • Vagus nerve stimulation – palliative
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61
Q

What advice should be given to someone with suspected epilepsy?

A

Advice about dangers – swimming, driving, heights
– until diagnosis
o Contact DVLA and avoid driving until seizure-free
for > 1year

62
Q

What are the DVLA guidelines for someone with epilepsy?

A

Avoid driving until seizure-free for >1 year

63
Q

What is Parkinson’s disease?

A

Progressive nervous system disorder with loss of dopamine producing neurones in the substantia nigra, affects movement

64
Q

Epidemiology of Parkinson’s

A

Adult onset

65
Q

Cause of Parkinson’s

A

Unknown, genetic predisposition

66
Q

Pathology of Parkinson’s

A

Dopamine producing neurones in the substantia nigra (pars compacta) undergo degeneration (darker areas disappear, Lewy bodies in damaged neurones) -> movement affected

67
Q

Investigations for suspected Parkinson’s

A
  • Mainly clinical assesment
  • MRI and CT - atrophy of the Substantia Nigra
  • PET - reduced dopamine supply
68
Q

Signs and symptoms of Parkinson’s

A

Tremour at rest
Ridgidity
Akinesia
Posture stooped

69
Q

Pharmacological management of Parkinson’s

A

• Levodopa - dopamine precursor, with co-beneldopa
• Dopamine agonist (Ropinirole, pramipexole) -
reduced risk of dyskinesias in short-medium term, 1st
line in younger patients (< 60 yr)
• MAO-B inhibitor (Selegiline) – not very powerful,
most likely to be neuroprotective
• Anti-cholingerics (Benztropine) - younger patients only

70
Q

SE’s of levodopa

A

Dyskinesia, painful dystonia, N&V, psychosis, hallucinations

71
Q

SE’s of dopamine agonists

A

Drowsiness, compulsive behaviour (gambling), hallucinations

72
Q

SE’s of anti-cholinergics

A

Dry mouth, dry eyes, constipation

73
Q

Complications of late stage PD

A
  • Wearing off – medication doesn’t work as long as before
  • On-Dyskinesias – hyperkinetic, choreiform movements whenever drugs work
  • Off-Dyskinesias – fixed, painful dystonic posturing, typically of feet, when drugs don’t work
  • Freezing – unpredictable loss of mobility
74
Q

Differential diagnosis for Parkinson’s

A
  • Normal pressure hydrocephalus
  • Essential tremor - no structural pathology
  • Cerebellar ataxia – intention tremor
  • Huntington’s disease
  • Generalised dystonia
75
Q

Cause of cluster headache

A

Unknown

76
Q

Epidemiology of cluster headache

A

M>F, smokers

77
Q

Signs and symptoms of cluster headache

A

o Rapid onset
o Excruciating pain around one eye, watery,
bloodshot, swelling, facial flushing, rhinorrhoea,
miosis ± ptosis
o Pain unilateral, usually same side
o 15-180mins, once or twice per day
o Chronic or episodic with pain-free periods of months
or years

78
Q

Management of cluster headache

A

o Acute – 100% oxygen for 15 mins, sumatriptan SC
o Avoid triggers – e.g. alcohol
o Corticosteroids, verapamil, lithium

79
Q

Epidemiology of migraines

A

F>M, associated with FH and obesity

80
Q

Symptoms of migraine

A

o Aura lasting 15-30min followed by 1hr unilateral
throbbing headache
o Or – isolated aura with no headache
o ‘Common migraine’ – episodic severe headaches without aura, often premenstrual, unilateral, N&V, ± photophobia/phonophobia

81
Q

What are the common triggers of migraines?

A 
Chocolate
Hangovers
Orgasms
Cheese/caffeine
Oral contraceptives
Lie-ins
Alcohol
Travel
Exercise
82
Q

Prophylactic treatment of migraines

A

Prophylactic treatment – propranolol, topiramate, botulinum toxin type A injections (botox)

83
Q

What medications can be taken during a migraine attack?

A

Oral triptan +NSAID/paracetamol

84
Q

What is a common SE of triptan and in which patient group is it contraindicated?

A

Arrythmias, do not give if IHD

85
Q

Non-pharmological therapies for migraines

A

Warm or cold packs, rebreathing into paper bag (↑PaCO2), acupuncture

86
Q

Classification of headaches

A

o Infrequent episodic – 1day/month
o Frequent episodic – 1-14days/month for 3 months
o Chronic – 15days/month for 3 months

87
Q

Signs and symptoms of a tension headache

A

o Lasts 30mins to 7days
o Bilateral
o Pressing/tightening quality
o Mild-moderate intensity
o Not aggravated by routine physical activity
o No nausea or vomiting
o No more than one of photophobia or phonophobia

88
Q

Management of tension headaches

A

Analgesics (aspirin, NSAIDs), tricyclic antidepressants (amitriptyline)

89
Q

What is multiple sclerosis (MS)?

A

Inflammatory plaques of demyelination in the CNS disseminated in space and time

90
Q

Epidemiology of MS

A

F>M average age 30yrs

91
Q

Cause of MS

A

Combination of environment, genetics and chance

92
Q

Pathophysiology of MS

A

Genetic susceptibility + environmental trigger -> activated autoreactive T-lymphocytes -> inflammatory attack with demyelination -> demyelination heals poorly -> progressive disability

93
Q

Signs and symptoms of MS

A

• Vision problems - optic neuritis, double vision,
blurred vision, nystagmus
• Spasticity
• Numbness and tingling
• Lhermitte’s sign - electric shock-like sensation on
flexion of neck
• Dizziness and vertigo
• Bladder and sexual dysfunction
• Fatigue
• Pain - worse with heat (hot bath, exercise)

94
Q

Diagnostic criteria for MS

A

o Two or more CNS lesions disseminated in time and
space
o Exclusion of conditions giving a similar clinical
picture – SLE, AIDs etc.

95
Q

What are the 3 main patterns of MS progression?

A

• Relapsing/remitting - random attacks over a number
of years, disabilities often accumulate with each
successive attack
• Chronic progressive - slow, unavoidable decline in
neurological functions, primary or secondary to
replasing/remitting
• Benign – few relapses, little disability

96
Q

Lifestyle management of MS

A

Avoid stress, smoking cessation, regular exercise

97
Q

Management of MS relapse

A

Steroids - methylprednisolone

98
Q

Investigations for suspected MS

A 
•   MRI 
•   CSF – electrophoresis 
•   Delayed visual, auditory and somatosensory evoked 
    potentials 
•   Bloods - exclude alternate diagnoses
99
Q

Disease modifying drugs for relapse-remitting MS

A

o Dimethyl fumarate
o Alemtuzumab
o Beta interferons

100
Q

Management of MS symptoms

A

o Spasticity – baclofen/gabapentin
o Tremor – BB
o Urgency/frequency – teach self-catheterisation
o Fatigue – CBT, exercise

101
Q

What is motor neuron disease?

A

A group of neurodegenerative disease’s characterised by selective deterioration of motor neurons

102
Q

What 3 areas are motor neurons lost from in motor neuron disease?

A

Motor cortex, cranial nerve nuclei and anterior horn cells

103
Q

What is the main type of motor neuron disease?

A

ALS/amyotrophic lateral sclerosis – loss of motor neurons in motor cortex and anterior horn, so UMN + LMN symptoms

104
Q

UMN signs

A

Spasticity, brisk reflexes, ↑plantars (Babinski sign)

105
Q

LMN signs

A

Wasting, fasciculation of tongue, back, thigh

106
Q

Symptoms of MND

A
  • No sphincter or sensory loss
  • Stumbling spastic gait
  • Foot-drop ± proximal myopathy
  • Weak grip
  • Weak shoulder abduction
  • Aspiration pneumonia
  • Frontotemporal dementia
107
Q

Investigations and diagnosis of MS

A

• Clinical mainly
• El Escorial diagnostic criteria – more LMN and/or
UMN signs = more likely its MND
• No diagnostic test:
o EMG, NCS – muscle denervation
o LP – exclude inflammatory causes
o MRI of brain/cord – exclude structural causes

108
Q

What drug is used to treat MND?

A

Riluzole – sodium channel blocker

109
Q

What the most common causes of meningitis?

A

Meningococcus, pneumococcus

110
Q

Give 3 routes that infection can enter the CSF

A

o Neurosurgical complications
o Via bloodstream
o Extracranial infection – nasopharynx, ear, sinuses

111
Q

Symptoms of meningitis

A

o Fever
o Headache
o Neck stiffness – ‘meningism’

112
Q

Hospital management of bacterial meningitis

A 
o   Assess GCS 
o   Blood cultures 
o   Broad spectrum antibiotics – ceftriaxone 
o   Steroids IV
o   Lumbar puncture 
o   Inform public health
113
Q

General practice management of suspected bacterial meningitis

A

IM benzylpenicillin and admit

114
Q

Differential diagnosis for meningitis

A

o SAH
o Migraine
o Flu
o Malaria

115
Q

What are the most common causes of encephalitis?

A

Herpes simplex, Varicella Zoster, bacterial meningitis

116
Q

Signs and symptoms of encephalitis

A

o Hours to days – preceding ‘flu-like’ illness
o Altered GCS – confusion, drowsiness, coma
o Fever, seizures, memory loss ± meningism

117
Q

Investigations for suspected encephalitis

A

o MRI head ± EEG
o Contrast CT
o Lumbar puncture – lymphocytic CSF and viral PCR

118
Q

Management of encephalitis

A

o Mostly supportive

o Aciclovir if HSV or VZV

119
Q

Cause of Huntington’s disease

A

Genetic - autosomal dominant, expansion of CAG repeat on Chr. 4

120
Q

Pathophysiology of Huntington’s disease

A

• Loss of neurones in caudate nucleus and putamen
• Atrophy and neuronal loss of striatum and cortex
• Loss of GABA and ACh, dopamine spared ->
dopamine imbalance

121
Q

Signs and symptoms of Huntington’s disease

A

• Initially mild – irritability, depression, incoordination
• Progresses to chorea, dementia ± fits and death
(approx. 15 years)

122
Q

Management of Huntington’s disease

A
  • No treatment prevents progression

* Counselling for patient and family

123
Q

Give a cause of acute peripheral neuropathy

A

Gullian Barré syndrome

124
Q

Give 2 causes of chronic peripheral neuropathy

A

Alcohol, diabetes

125
Q

Pathphysiology of diabetic neuropathy

A

Hyperglycaemia damages retinal endothelium, mesangial cells in glomeruli and Schwann cells in peripheral nerves -> can’t regulate glucose well -> constant hyperglycaemia -> excessive oxidation -> damage

126
Q

What is Guilian-Barre syndrome?

A

An acute inflammatory demyelinating poly-neuropathy

127
Q

Pathophysiology of Guillian-Barre syndrome

A

Infection -> causes antibodies to attack nerves -> paralysis -> recovery

128
Q

Management of Guillian-Barre syndrome

A

IV immunoglobulin 5days

129
Q

What is myasthenia gravis?

A

Autoimmune disease caused by antibodies to ACh receptors -> muscular weakness, fatigability of ocular, bulbar, and proximal limb

130
Q

Pathology of myasthenia gravis

A

Autoantibodies to nicotinic acetylcholine receptors, anti-AChR antibodies or MuSK, at post synaptic membrane of neuromuscular junction, cause receptor blockade/loss

131
Q

Signs of myasthenia gravis

A

• Ptosis
• Diplopia
• Myasthenic snarl on smiling
• Orbicularis fatigability – eyelids separate after
manual opposition to sustained closure
• Voice fades when counting to 50

132
Q

Symptoms of myasthenia gravis

A

Slowly increasing or relapsing muscle fatigue

133
Q

What factors exacerbate myasthenia gravis symptoms?

A

Pregnancy, hypokalaemia, infection, over-treatment, change of climate, emotion, exercise

134
Q

Epidemiology of myasthenia gravis

A

Young females, older males, associated with autoimmune conditions

135
Q

Management of myasthenia gravis

A
  • Symptoms – anticholinesterases (pyridostigmine)
  • Immunosuppression
  • Thymectomy
136
Q

SE’s of anticholinesterases

A

Increased salivation, sweats, vomiting

137
Q

What is a myasthenic crisis?

A

Life-threatening weakness of respiratory muscles during a relapse

138
Q

Causes of spinal cord compression

A

Secondary malignancy, infection, cervical disc prolapse, primary cancer

139
Q

Give a cause of inherited cerebellar ataxia

A

Freidreich’s ataxia (FA)

140
Q

Give 3 causes of acquired cerebellar ataxia

A

o Toxic – alcohol, phenytoin, lithium
o Immune-mediated
o Neurodegenerative – MSA-C

141
Q

Signs and symptoms of cerebellar dysfunction

A

• Dysdiadochokinesis and dysmetria (past-pointing)
• Ataxia – limb/truncal – wide-based, cannot walk heel-
to-toe, worse in dark/eyes closed
• Nystagmus (other abnormalities of eye movements)
• Intention tremor
• Slurred speech
• Hypotonia

142
Q

What tool can be used to assess ataxia?

A

Scale for the Assessment and Rating of Ataxia (SARA)

143
Q

Investigations for suspected cerebellar dysfunction

A

• MRI – rules out structural causes
• Finger-to-nose test
• Romberg’s test – stand with eyes closed – negative
if cerebellar disease

144
Q

What is carpal tunnel syndrome?

A

Entrapment of the median nerve against the carpal tunnel

145
Q

Epidemiology of carpal tunnel syndrome

A

Mainly women

146
Q

Pathophysiology of carpal tunnel syndrome

A

Inflammation of the carpal tunnel -> median nerve gets trapped -> pain and loss of sensation

147
Q

Symptoms of carpal tunnel syndrome

A

o Pain and paraesthesia in the hand, worse at night
o Weakening and wasting of the thenar eminence
o Loss of sensation of median nerve innervation

148
Q

Signs of carpal tunnel syndrome

A

Tinnel’s, Phalen’s test

149
Q

Management of carpal tunnel syndrome

A

o Surgical decompression

o Nocturnal splint and steroid injections for pain relief

150
Q

Management of myasthenic crisis

A

Plasmapheresis

151
Q

What is the first line drug treatment for trigeminal neuralgia?

A

Carbamazepine

Phase 2a (9 decks)

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