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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the cause of cluster headaches?

A

Unknown cause

Superficial temporal artery SM hyperactivity of 5HT

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2
Q

What are the risk factors of cluster headaches?

A

Being male >5:1

Smoking

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3
Q

What are the symptoms of cluster headaches?

A

Severe UNILATERAL pain, around one eye
‘Suicide headaches’
Ipsilateral autonomic features: lacrimation, facial flushing, rhinorrhoea, miosis, ptosis

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4
Q

How long do cluster headaches last (acute phase and cycles) and how often are they?

A

15-160 minutes
Once/twice a day
Often nocturnal
Clusters last 4-12wks, then pain-free periods for months/years

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5
Q

Treatment of cluster headaches?

A

100% OXYGEN for 15 minutes via non-rebreathable mask

SUMATRIPTAN SC 6mg at onset

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6
Q

What are the triggers of cluster headaches?

A

Alcohol
Histamine/nitroglyceride
Disrupted sleep
Sometimes heat, exercise, solvents

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7
Q

What are the red flag signs for headaches (requiring further investigation)?

A

Change in pattern of headache
Onset >50yrs
Onset of seizures
Headache with systemic illness
Personality change
Symptoms suggestive of raised ICP (headache in the morning, on coughing/sneezing/straining)
Acute onset of worst headache ever (?Intracranial aneurysm)

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8
Q

Prophylaxis of cluster headaches?

A

Verapamil
Prednisolone
Lithium
Melatonin

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9
Q

What are the symptoms of trigeminal neuralgia?

A

SUDDEN, UNILATERAL, STABBING pain in trigeminal nerve distribution - ‘electric shock’
Lasting seconds-minutes
A few-100’s of attacks a day
Pain can go into remission for weeks/months, but remission gets shorter as time progresses

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10
Q

What is the cause of trigeminal neuralgia?

A

Compression of the 5th CN - most commonly mandibular/maxillary division
Most commonly by a loop of artery/vein, in 10% of cases by tumour, MS, skull base abnormalities etc

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11
Q

Epidemiology/RF of trigeminal neuralgia?

A

Peak incidence 50-60yrs
More common in females
May be genetic predisposition

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12
Q

Triggers for trigeminal neuralgia:

A

Light touch to face - person, wind
Eating
Bathroom - shaving, brushing teeth
Dental procedures

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13
Q

Ix for trigeminal neuralgia:

A

CLINICAL Dx

MRI sometimes needed - to exclude secondary causes

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14
Q

Mx for trigeminal neuralgia:

A

CARBAMAZEPINE
Or lamotrigine/phenytoin/gabapentin
If drugs fail: SURGERY - Microvascular decompression

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15
Q

What is the likely cause of migraines?

A

Primary brain disorder resulting from altered modulation of normal sensory stimuli and trigeminal nerve dysfunction

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16
Q

What are the symptoms of migraines?

A

Aura - lasting 15-30 minutes
Within 1hr - unilateral, pulsating headache (lasting 4-72hrs)
Prodrome: Precedes headache by hrs/days - yawning, cravings, mood/sleep changes
Aura: Visual, somatosensory (abnormal sensation spreading from fingers-face), motor (stammering/ataxia), speech
Nausea/vomiting
Photo/phonophobia

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17
Q

What are the main types of migraine?

A

Aura + headache
Aura, no headache
Episodic severe headache without aura e.g. premenstrual

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18
Q

What are the triggers for migraines?

A 
CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult (noisy/violent commotion)
Exercise
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19
Q

Management of migraines:

A 
Lifestyle changes
Step 1: NSAIDs +/- anti-emetic
Step 2: Rectal analgesia +/- anti-emetic
Step 3: Anti-migraine drugs
- Triptans
- Botulinum toxin type A injections - last resort
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20
Q

Information about Triptans

A

Have largely replaced Ergotamine
Triptans selectively stimulate seretonin receptors in brain
CI in:
- People with uncontrolled HTN
- People with/at risk of coronary heart disease/cerebrovascular disease
- People with coronary vasospasm (Prinzmetal’s angina)
Rare SEs:
- Arrythmias
- Angina +/- MI

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21
Q

Prevention of migraines:

A

Remove triggers
If 2+/month or not responding to drugs:
1st line: Propanolol, amitriptyline, topiramate or Ca+ channel blockers
2nd line: Valproate, pizotifen, gabapentin

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22
Q

What is a tension headache and how is it treated?

A

Bilateral, non-pulsatile headache +/- scalp muscle tenderness - no vomiting/sensitivity to head movements
Tx - Massage or anti-depressants may be helpful

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23
Q

What are the 4 causes of stroke?

A

Small vessel occlusion or thrombosis in situ
Cardiac emboli (e.g. increased risk in AF, endocarditis, MI - emboli comes from the heart)
Atherothromboembolism (e.g. from carotids - emboli comes from a vessel)
CNS bleeds (e.g. due to increased BP, trauma, aneurysm rupture)
Other causes: Sudden BP drop of >40mmHg, carotid artery dissection, vasculitis, anti-phospholipid syndrome etc)

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24
Q

Risk factors for stroke

A 
Increased BP
Smoking
DM
Heart Disease (vascular, ischaemic, AF)
Past TIA
the Pill
Alcohol etc
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25
Q

What are the different sites of infarcts that cause a stroke?

A 
Cerebral infarct (50%) - contralateral sensory loss/hemiplegia, initially flaccid becoming spastic, dysphagia, homonymous hemianopia
Brainstem infarct (25%) - wide range of effects, including quadriplegia, disturbed gaze/vision, locked-in syndrome
Lacunar infarct (25%) - occlusion of small penetrating arteries in the basal ganglia, internal capsule, thalamus, and pons
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26
Q

Immediate management (1st hour) for suspected stroke?

A

1) Protect the airway
2) Pulse, BP & ECG
3) Blood glucose
4) Urgent CT/MRI - if thrombolysis considered, cerebellar stroke, unusual presentation, high risk of haemorrhagic stroke
- – otherwise can wait (aim <24hrs)
- – Diffusion-weighted MRI is most sensitive, but CT helps to rule out a primary haemorrhage
5) Thrombolysis (consider if <4.5 hours)
6) ‘Nil by mouth’ - consider only if swallowing may be dangerous, do NOT over hydrate (risk of cerebral oedema)
7) Antiplatelet agents - once hemorrhagic stroke excluded, give aspirin

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27
Q

Thrombolysis in acute non-hemorrhagic stroke:

A

If neuroimaging performed, expert clinicians available and pt seen within 4.5 hours -> consider reperfusion with IV RECOMBINANT TISSUE PLASMINOGEN ACTIVATOR (ALTEPLASE)

  • May cause small increase in (usually minor) intracranial haemorrhage
  • Always do CT 24hrs post-lysis to check for bleeds
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28
Q

In which groups is thrombolysis contraindicated?

A 
Major infarct/haemorrhage on CT
Mild/non-disability defect
Arteriovenous malformation (AVM) or aneurysm
Severe liver disease, portal hypertension or varices etc
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29
Q

Primary prevention of stroke

A

Control RFs

Lifelong anticoagulation for - rheumatic/prosthetic heart valves on L side, consider in chronic AF

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30
Q

Secondary prevention of stroke

A

Control RFs
Antiplatelet agents - Clopidogrel
Anticoagulation after stroke from AF - start warfarin if indicated 2 weeks after stroke

31
Q

Investigations for stroke (in the longer term) to determine management + identify risks for further strokes

A

Look for:

1) Hypertension
2) Cardiac source of emboli - 24hr ECG (AF), CXR (enlarged L atrium), Echo
3) Hypo/hyperglycaemia, dyslipidaemia
4) Vasculitis (raised ESR, ANA +ve)
5) Prothrombiotic states (thrombophilia, antiphospholipid syndrome)
6) Hyperviscosity (polycythaemia, SCD)
7) Thrombocytopaenia
8) Genetic tests

32
Q

Complications of stroke:

A 
Aspiration pneumonia
Pressure sores
Contractures (shortening of muscle tissue)
Constipation
Depression
33
Q

Cardiac causes of stroke (source of >30%):

A 
Non-vascular AF - do CHADS2 score
External cardioversion
Prosthetic valves
Acute MI
Paradoxical systemic emboli - via venous circulation with patent foramen ovale, ASD, VSD
Cardiac surgery
Valve vegetation from SBE/IE
34
Q

What is a transient ischaemic attack?

A

TEMPORARY occlusion of part of the cerebral circulation

Symptoms last <24hrs

35
Q

What are the signs of a TIA?

A

Features mimic a stroke in the same arterial territory

36
Q

What do multiple stereotypical TIA suggest?

A

Critical intracranial stenosis (commonly the superior division of the MCA)

37
Q

In TIA, if emboli pass to the retinal artery, what can this cause?

A

Amaurosis fugax (one eye’s vision is progressively lost - like curtains descending)

38
Q

Investigations of TIA?

A 
Bloods - FBC, ESR, U&amp;Es, glucose, lipids
CXR
ECG
Carotid doppler +/i angiography
CT/diffusion-weighted MRI
Echo
39
Q

Management of TIA?

A

TIMING is crucial - assess ABCD2 score
Risk of stroke in 90 days dramatically decreases if treated in 72hrs
Control CVS RF: BP, smoking, lipids, DM
Antiplatelet drugs: Clopidogrel/aspirin
Warfarin if cardiac emboli
Carotid endarterectomy - if >70% stenosis at the origin of the internal carotids artery, surgery should be performed within 2 weeks of TIA
Avoid driving for 1 month

40
Q

Causes of unilateral vision loss?

A

Vascular:
- central retinal artery/vein occlusion
- Anterior ischaemic optic neuropathy (can be arteritic: due to ischaemia of the arteries supplying the nerve, or non-arteritic)
Optic neuritis
Retinal detachment (flashes/floaters)
Vitreous haemorrhage (flashes/floaters - associated with diabetic retinopathy/macular degeneration)
Acute angle closure glaucoma (pressure in eye rises suddenly - painful red eye, nausea + vomiting)

41
Q

What is papilloedema?

A

Optic disc swelling caused by increase in ICP

42
Q

What changes will you see on fundoscopy for Anterior Ischaemic Optic Neuropathy?

A

Swollen optic disc

This is a cause of vision loss that occurs in GCA, also has non-arteritic causes

43
Q

Fundoscopy findings for central retinal artery occlusion?

A

This artery supplies the whole retina

Findings: Pale optic disc, cherry red spot at macula

44
Q

Fundoscopy of central retinal vein occlusion?

A

Dilatation of branch veins
Multiple retinal haemorrhages
Cotton wool patches

45
Q

Investigations for unilateral vision loss?

A

History + exam
Visual evoked potential (VEP)/MRI (optic neuritis)
Fluorescein angiography (CRVO)
Tonometry - intraocular pressure measure (glaucoma)
USS - vitreous haemorrhage/retinal detachment

46
Q

What are the symptoms of optic neuritis?

A

Reduced visual acuity over a few days
PAIN on eye movements
Exacerbated by heat/exercise
Afferent pupillary defect (light swing test)
Dyschromatopsia (can’t see colours normally)

47
Q

What is the cause of optic neuritis?

A

Inflammation of the optic nerve, often associated with MS, can occur as clinically isolated syndrome, other causes - infection (lyme, syphilis, HIV), B12 deficiency, arteritis

48
Q

What is the ‘course’ of optic neuritis?

A

Vision usually recovers in about 6 weeks

49
Q

Treatment of optic neuritis?

A

Steroids

50
Q

What are the requirements for a diagnosis of MS?

A

Multiple CNS lesions, causing symptoms that:
Last >24 hours
Are disseminated in time (>1m apart) and space (clinically/on MRI)

51
Q

Typical features of MS:

A 
Usually MONOSYMPTOMATIC
Visual loss (optic neuritis)
Numbness/tingling in the limbs
Sensory disturbances
Cerebellar symptoms
Bladder involvement/sexual dysfunction
Lhermitte’s (electric shock sensation that runs down the back -> limbs) &amp; Uhthoff’s phenomenon (worsening of symptoms due to heat/exercise)
Fatigue
Cognitive impairment
52
Q

What are the signs of cerebellar disease?

A 
DANISH
Dysdiadochokinesis
Ataxia
Nystagmus
Intention Tremor
Slurred Speech
Hyptonia

(Ataxia is a lack of muscle coordination that impedes speech or movement)

53
Q

Signs of MS:

A 
UMN signs
Spastic paraparesis (of the lower limbs)
Brisk reflexes
Cerebellar signs
Optic atrophy
Relative afferent pupillary defect
Internuclear opthalmoplegia (decreased adduction of ipsilateral eye, nystagmus on abduction of contralateral eye)
54
Q

Investigations of MS:

A 
MRI - lesions of high T2 signal intensity in the white matter of the brain - typically periventricular
LP - oligoclonal bands of IgG in CSF
Evoked potentials (VEP)
55
Q

Pathophysiology of MS

A

Inflammatory, degenerative
Loss of myelin with axon preservation
Axonal loss may contribute to fixed and progressive deficits

56
Q

Differential diagnosis of blackouts?

A

Syncope
Epilepsy
Non-epileptic attacks
Narcolepsy, cataplexy, brain tumour, psychogenic seizures, hypoglycaemia, TIA, Migraine etc

57
Q

Syncope definition

A

Syncope is an abrupt and transient loss of consciousness associated with loss of postural tone that follows a sudden fall in cerebral perfusion

58
Q

Causes of syncope:

A

Neurogenic syncope
Orthostatic syncope
Cardiac syncope

59
Q

What is neurogenic syncope?

A

Caused by enhanced parasympathetic tone and decreased sympathetic tone:
Two elements:
1. cardio-inhibitory response = drop in HR and contractility
2. vasodepressor response = dilatation of blood vessels

60
Q

What are the causes of neurogenic syncope?

A

Vasovagal syncope - prolonged standing, emotional stress, pain, sight of blood
Situational syncope - after/during micturition, coughing, straining
Carotid Sinus syncope - pressing a certain spot in the neck

61
Q

What can cause orthostatic syncope (postural hypotension)? What specific condition should you test for with postural hypotension?

A

Primary (multisystem atrophy)
Secondary (diabetes, drugs)
Condition: Parkinsons

62
Q

Causes of cardiac syncope?

A

Arrhythmias

Valvular heart disease

63
Q

Definition of seizure

A

Clinical manifestations of sudden synchronised discharge of cerebral neurones

64
Q

Definition of epilepsy

A

Recurrent, unprovoked tendency to experience seizures

65
Q

Difference between syncope and seizures; triggers

A

Syncope - Stress/fear, prolonged standing, heat, venepuncture, cough, micturition
Seizures - Sleep deprivation, flashing lights, menstruation,
alcohol and alcohol withdrawal

66
Q

Difference between syncope and seizures; prodrome

A 
Syncope - Hot, visual crowding and loss, feel faint, can
feel dizzy (looks pale)
Seizures - aura (strange feeling in gut, deja vu, strange taste/sound, flashing lights)
67
Q

Investigation of seizures:

A 
Cardiac examination
12-lead ECG - check for prolonged QT
Blood tests (FBC)
EEG
MRI brain
68
Q

Investigations if syncope suggested:

A

24 hr tape
Tilt table
Autonomic function tests

69
Q

Treatment of partial seizures:

A

1st line: Carbamezapine

2nd line: Lamotrigine

70
Q

Treatment of generalised seizures:

A

1st line: Sodium Valproate / Lamotrigine

For G T-C: 2nd line: Carbamezapine / Topiramate

71
Q

Treatment of seizures that are unresponsive to medication:

A

If focal area easily identifiable, consider neurosurgical resection (70% chance seizure-free)

72
Q

What are the early signs of stroke?

A
  • None
  • Hyperdense MCA
  • Loss of grey white matter differentiation and sulcal effacement (disappear)
  • Hypodense basal ganglia
73
Q

Complications of stroke

A

Raised ICP (cerebral oedema, haemorrhage)
Aspiration
Depression
Cognitive impairment

74
Q

What are the roles of the CHA2DS2 VASC or ABCD2 score?

A

CHADS2 - Calculates the stroke risk in patients with AF (within 1 year)
ABCD2 - Calculates the risk of short-term stroke after TIA

Phase 3a (1 decks)

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