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Junior Medicine & Surgery > Neurological History > Flashcards

Neurological History Flashcards

0
Q

Headaches

How would you firstly investigate the headache?

A

SOCRATES

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1
Q

Headaches

A patient presents with a headache, what are the sinister causes that must be ruled out?

A

VIVID

VASCULAR - subarachnoid haemorrhage, subdural or extradural haematoma, cerebral venous sinus thrombosis, cerebellar infarct

INFECTION - meningitis, encephalitis

VISION THREATENING - temporal arteritis, acute glaucoma, pituitary apoplexy, posterior leucoencephalopathy, cavernous sinus thrombosis

INTRACRANIAL PRESSURE (RAISED) - SOL, cerebral oedema (trauma, altitude), hydrocephalus, malignant HTN

DISSECTION - carotid dissection

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2
Q

Headaches

What questions would you ask to rule out reg flags? And what would a ‘yes’ to these questions suggest?

A
  1. Decreased consciousness - + headache = SAH; + head trauma = subdural (if fluctuating) or extradural (if preceded by a lucid period); meningitis; encephalitis
  2. Sudden onset, worst headache ever - SAH (especially if the onset of the severe headache was instantaneous)
  3. Seizures or focal neurological deficit - intracranial pathology
  4. No previous episodes - suggests new pathology. If >50 = temporal arteritis until proven otherwise
  5. Reduced visual acuity - temporal arteritis or carotid art dissection (= decreased blood flow to retina); acute glaucoma (NB TIA also present with transient blindness (amaurosis fugax) but not with headache)
  6. Headache worse when lying down + morning nausea - raised intracranial pressure
  7. Progressive, persistent headache - expanding SOL
  8. Constitutional symptoms - weight loss, night sweats, fever = malignancy, chronic infection (TB), chronic inflam (temporal arteritis)
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3
Q

Headaches

What basic observations would you make on examination to exclude sinister causes?

A
  1. GCS - SAH, subdural and extradural
  2. BP and pulse - malignant HTN
  3. Temperature - fever + headache = meningitis, encephalitis
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4
Q

Headaches

List some focal neurological signs that may coexist with a headache, and what pathology they may indicate

A
  1. Focal limb deficit - intracranial pathology
  2. 3rd nerve palsy - ptosis, mydriasis (dilated pupils), eye down & out = SAH when rupture of aneurysm of the posterior communicating art
  3. 6th nerve palsy - convergent squint (one eye deviates in because can’t be abducted out) = nerve compressed directly by a mass or indirectly by raised IC
  4. 12th nerve palsy - tongue deviation to side of lesion = carotid dissection
  5. Horner’s syndrome - ptosis, miosis (constricted pupil), anhydrosis (dry skin around orbit) - result of interruption of the ipsilateral sympathetic pathway = carotid artery dissection (neck pain?) or cavernous sinus lesion
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5
Q

Headaches

Inspection of the eye may reveal what? And what may this indicate?

A
  1. Exophthalmos - retro-orbital process = cavernous sinus thrombosis
  2. Cloudy cornea, fixed dilated pupil = acute glaucoma
  3. Papilloedema on fundoscopy = raised ICP
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6
Q

Headaches

What other findings O/E would you look for? And what do positive findings suggest?

A
  1. Reduced visual acuity - temporal arteritis or carotid dissection. (Reduced retinal blood flow) or acute glaucoma
  2. Scalp tenderness - temporal arteritis
  3. Meningism - stiff neck, photophobia and headache = infection (meningitis or encephalitis) or SAH
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7
Q

Headaches

What positive bedside tests indicate meningitis?

A

KERNIG’S SIGN
Person lies supine. Flex hip and knee to 90. Positive sign: pain when passively extending the knee.

BRUDZIŃSKI’S SIGN
Positive sign: flexion of neck = involuntary flexion of knee and hip

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8
Q

Headaches

What is temporal arteritis?

A

Unknown aetiology.
Appears in people >50.
Characterised by formation of immune, inflammatory granulomas in the tunica media of medium/large arteries –> block the arteries.
Presentation: jaw claudication (block mandibular branch of external carotid); headache & scalp tenderness (block superficial temporal branch of external carotid); visual disturbances (block posterior ciliary arteries) –> ophthalmological emergency
Manage with high-dose corticosteroids

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9
Q

Headache

Causes of non-sinister headaches?

A 
Tension-type headache
Migraine 
Sinusitis 
Medication overuse headache 
Temporomandibular joint dysfunction syndrome 
Trigeminal neuralgia 
Cluster headache
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10
Q

Headaches

What are primary and secondary headaches?

A

PRIMARY - if headache removed, no harmful pathology

SECONDARY - the headache is one of many ossicle symptoms that result from the pathology - e.g. Head trauma, intracranial lesion, SAH etc

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11
Q

Headaches

Give non-sinister causes of SECONDARY headaches?

A

Sinusitis
Medication overuse headaches
Temporomandibular joint dysfunction syndrome

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12
Q

Headaches

In addition to pain history (SOCRATES), what other Qs should you ask to characterise non-sinister headaches?

A
  1. Does the patient suffer any other type of headache? - must take the Hx of the separate types. E.g. Patients with migraines are more likely to get medication overuse headaches too
  2. Any triggers? - migraines: chocolate, cheese, caffeine, wine
  3. How disabling are the headaches - migraines (incapable of performing daily tasks), cluster headaches (disabling at night, normal in day), tension (Normal activities)
  4. Aura?
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13
Q

Headaches

What do you know about Tension-Type Headaches?

A 
Very common.
Bifrontal pain.
Pain = pressure/tightness around head like a band.
No Associated symptoms. 
Last <few hours. 
Not particularly disabling.
Triggers = stress and fatigue.
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14
Q

Headaches

What do you know about migraines?

A

Common - not as common as tension headaches.
2:1 f:m
Migraines attack in the same pattern each time in an individual.
Unilateral.
Aura (migraines with aura aka classical migraine; migraine without aura aka common migraine).
Pain = throbbing or pulsatile.
Sensitivity to light, sound + nausea.
Last 4-72 hours.
Some people can suffer from migraine without aura - differentials for this include TIA or epilepsy.

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15
Q

Headaches

What do you know about sinusitis?

A

Presentation: facial pain coming on over hrs - days + coryzal symptoms (symptoms of inflammation).
Pain = tight (like tension) + exacerbated by movement.
Last several days over the time course of the infection.

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16
Q

Headaches

What dyiu know about medication overuse headaches?

A

Common.
5:1 f:m
Seen particularly in patients with migraine meds and analgesics - usually taking 35 doses of 6 different meds per week.
Presentation: like migraines (throbbing/pulsatile) or tension-type (tight band around head).

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17
Q

Headaches

What do you know about temporomandibular joint syndrome?

A

Common in 20-40y/os
4:1 f:m
Presentation = headache + dull ache in muscles of mastication that may radiate to jaw &/or ear + clicking jaw.

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18
Q

Headaches

What do you know about cluster headaches?

A

Mainly affects men.
Presentation= headaches occur in clusters for 6-12 weeks every 1-2 years. Attacks happen at same time every day (like an alarm). Pain focussed in one eye. Wakes people up and can cause suicidal thoughts. Pain lasts 20-30 mins.

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19
Q

Blackouts

Are the terms ‘syncope’ and ‘loss of consciousness’ interchangeable?

A

No. LOC can be either syncopal or non-syncopal. Syncope is a form of LOC which is the result of hypoperfusion of the brain

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20
Q

Blackouts

How can you classify LOC?

A

Into syncopal or non-syncopal

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21
Q

Blackouts

What can the ‘syncopal’ causes be subdivided into?

A

Reflex
Cardiac
Orthostatic
Cerebrovascular

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22
Q

Blackouts

What are the non-syncopal causes of blackouts? (Order from most common to least)

A 
Intoxication (alcohol & sedatives) 
Head trauma
Metabolic - hypoglycaemic
Epileptic seizure 
Non-epileptic seizure 
Narcolepsy
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23
Q

Blackouts

Examples of ‘reflex’ causes of syncopal blackouts?

A

Vasovagal syncope

Carotid sinus hypersensitivity

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24
Q

Blackouts

What are the ‘cardiac’ causes of syncope?

A

Arrhythmia
Anything causing outflow obstruction - aortic stenosis, hypertrophic obstructive cardiomyopathy
Massive PE

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25
Q

Blackouts

Orthostatic causes of syncope?

A

Dehydration
Drugs - anti hypertensives
Autonomic instability

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26
Q

Blackouts

What are the cerebrovascular causes of syncope?

A

Vertebrobasilar insufficiency

Aortic dissection

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27
Q

Blackouts

Main cause of LOC in patients aged 25?

A

Vasovagal syncope

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28
Q

Blackouts

How does vasovagal syncope present?

A

Triggered by fear, straining, fear, pain.
Pre-syncopal sensation - nausea, clammy, pale
Lasts seconds
May twitch or be incontinent
Rapid recovery on sitting or lying

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29
Q

Blackouts

Main cause of LOC in middle aged people?

A

Vasovagal syncope + cardiac arrhythmias

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30
Q

Blackouts

Why do middle aged people mainly present with cardiac arrhythmias?

A

Because cardiac arrhythmias are usually secondary to ischaemic heart disease (which occurs as atherosclerosis develops with age)

31
Q

Blackouts

Why are cardiac arrhythmias not that main cause of blackouts in the elderly population?

A

Because they are likely to have died from other atherosclerosis-related diseases (cardiac or stroke) before reaching old age.

32
Q

Blackouts

How do cardiac arrhythmias typically present?

A

LOC without warning with no obvious trigger (eg when watching the TV) - sitting or lying down
Lasts seconds
May twitch or be incontinent
Rapid, spontaneous recovery

33
Q

Blackouts

Main cause of LOC in elderly patients?

A

Orthostatic/postural hypotension caused by medications (eg anti hypertensives)

34
Q

Blackouts

How would an epileptic patient’s LOC present?

A

BEFORE - aura (partial seizure) or no warning (generalised seizure)

DURING- lasts minutes. The same thing happens to them every time - tongue biting. May also have twitching or incontinence (but these may also happen in vasovagal and arrhythmia syncopes)

AFTER - slow recovery. Confused for 5-30 mins

35
Q

Blackouts

LOC caused by turning head suggests?

A

Carotid sinus hypersensitivity

36
Q

Blackouts

LOC following standing indicates?

A

Postural/Orthostatic hypotension

37
Q

Blackouts

LOC following straining, fear, pain etc suggests?

A

Vasovagal syncope

38
Q

Blackouts

LOC whilst sitting or lying down suggests?

A

Cardiac arrhythmia

39
Q

Blackouts

LOC when exercising indicates what?

A

Cardiac pathology, eg aortic stenosis or a cardiomyopathy

40
Q

Blackouts

If a patient is out for seconds to minutes what does this indicate?

A

Vasovagal syncope or arrhythmias.

41
Q

Blackouts

What is virtually pathognomonic of epileptic seizures?

A

Tongue biting

42
Q

Blackouts

What medications would you look for in a drug history?

A
  1. Insulin/oral hypoglycaemics
  2. Anti hypertensives - ABCD: ACE-inhibitors, B-blockers, Ca channel blockers, diuretics
  3. Vasodilators - GTN, isosorbide mononitrate
  4. Anti-arrythmics - these can paradoxically predispose people to anti arrhythmias
  5. Antidepressants - hypotension is an SE
43
Q

Blackouts

What defines Orthostatic hypotension ?

A

> 20mmHg drop in systolic BP on standing.

Or

> 10mmHg drop in diastolic

44
Q

Blackouts

What investigations would you carry out?

A 
Pulse oximetry - hypoxia 2ndary to PE?
Bloods: FBC (anaemia), U&Es (electrolyte abnormality), cap B glucose 
ECG: may need to also do a 24 hour tape
EEG (epilepsy) 
CT head/MRI (epilepsy)
45
Q

Collapse

What groups can the causes of collapse be split into ?

A
  1. Neurogenic
  2. Cariogenic
  3. Metabolic
  4. Psychogenic
46
Q

Collapse

Give examples of neurogenic causes of collapse

A

Epilepsy
Posterior strokes
Tumour –> epilepsy

47
Q

Collapse

Give examples of cardiogenic causes of collapse?

A 
Vasovagal 
Arrhythmias - bradycardia (if slow enough = hypoperfusion), VT & VF (if fast enough) 
Orthostatic/postural hypotension
Anaemia 
Shock 
Carotid sinus sensitivity
48
Q

Collapse

What can cause bradycardia?

A

B-blockers
Mobitz Type 2 heart block (because it can progress to 3rd degree HB)
3rd degree HB

49
Q

Collapse

Give examples of metabolic causes of collapse?

A

Hypoglycaemia

Hyperkalaemia

50
Q

Collapse

What can cause hyperkalaemia?

A

Drugs - spironolactone, ACEi
Renal failure (AKI or CRF)
Cell lysis - haemolytic anaemia, tumours, post-op
Dehydration

51
Q

Collapse

What investigations would you do to investigate CVS cause?

A

Pulse oximetry
BP and pulse - shock: hypotensive and tachycardic
Bloods: FBC (anaemia), U&Es (electrolyte balance and renal function)
ECG: telemetry, 24hour tape, 2wk event monitor
Lying-standing BP (orthostatic hypotension)
Tilt table test (vasovagal and carotid sinus sensitivity)

52
Q

Collapse

A lying-standing drop in BP of what would be indicative of postural hypotension?

A

Systolic >20 mmHg

Diastolic >10mmHg

53
Q

Collapse

How would you investigate the metabolic causes of collapse?

A

Finger prick glucose (<7mmol random)

U&ES

54
Q

Collapse

How would you investigate neuro cause of collapse ?

A

EEG

CT head/MRI head

55
Q

Stroke

How can a stroke be classified and what are common causes of these?

A
  1. INFARCT - 80-90%
    Arterial embolism - eg from carotids, vertebral or basilar arteries or infective endocarditis.
    Thrombus
    Systemic hypoperfusion
  2. HAEMORRHAGE - 10-20%
    In the cerebrum itself (intracranial haemorrhage) or SAH
56
Q

Stroke

What are the Risk factors?

A 
CVS RF
Smoking 
Diabetes 
HTN
Hypercholesterolaemia
FHx (of stroke, heart disease)

+ age, AF, carotid artery stenosis

57
Q

Stroke

Main causes of cerebral infarct?

A

60% - atherosclerosis or carotid arteries and aortic arch
20% - valvular heart disease
20% - disease in the vessels of the brain itself

58
Q

Stroke

In what artery do most cerebral infarcts present?

A

Middle cerebral

59
Q

Stroke

How would a middle cerebral artery infarct present?

A

Symptoms develop over minutes (but very rarely over hours)
FAST - face, arms, speech, timing

Contralateral:
Hemiplegia (paralysis of 1 side of the body)/hemiparesis (weakness)
Homonomous hemianopia (if can’t see L side, stroke in R side)
Aphasia - happens when dominant hemisphere affected - ask whether L or R handed.

60
Q

Stroke

On examination what would you find of a cerebral infarct?

A

UMN LESION SIGNS
Hemiparesis/hemipegia (weakness) - NB seen in upper and lower signs
Hypertonia (spasticity) - physiotherapy can sometimes prevent this.
Hypereflexia
Babinski response (toes go upwards)

61
Q

Stroke

Investigations or cerebral infarct?

A

BP - HTN
Bloods - FBC/platelets/clotting (bleeding disorders), glucose (diabetes), cholesterol (RF for stroke), ESR (raised in temporal arteritis)
CT head/MRI
carotid Doppler - carotid stenosis
ECG - AF
CXR - cardiomegaly (HTN), dilated LV (AF)
Echo

62
Q

Stroke

Are cerebral haemorrhages clinically distinguishable from cerebral infarcts?

A

Not really. Only that cerebral haemorrhages are more likely to:

Lose consciousness
Have sudden onset headache (SAH)
Sudden onset neurological deficit are more likely to progress

63
Q

Stroke

Haemorrhages are nearly always the result of what?

A

Uncontrolled HTN

64
Q

Stroke

Other than uncontrolled HTN, what else can cause haemorrhage?

A

Cocaine
Aneurysm
Clotting disorders
Tumours

65
Q

Stroke

How would you investigate a haemorrhage?

A

CT head/MRI

66
Q

Stroke

How would you initially manage any stroke patient?

A

ABC - maintain airway, prevent hypoxia, hydrate.

Treat fever + hyper/hypoglycaemia

67
Q

Stroke

How should you treat a patient with ischaemic stroke provided no contraindications?

A

Thrombolysis

68
Q

Stroke

Give some examples of absolute contraindications for thrombolysis

A
  1. Previous intracranial haemorrhage
  2. Major surgery/trauma 200/120

Etc

69
Q

Stroke

If someone cannot be thrombolysed, how would we treat them?

A

ASPIRIN - 300mg/day for 2 weeks, then 75mg forever (NB. be aware of asthmatics and GI bleed patients. If aspirin hypersensitive give clopidogrel)

70
Q

Stroke

What might warfarin be given to ischaemic infarct patients?

A

Once cause is known. Eg AF.

INF or 2-3

71
Q

Stroke

What could you do for a patient who has carotid artery stenosis?

A

Carotid endartectomy (if obstruction >60%)

72
Q

Stroke

How would a haemorrhages stroke patient be managed?

A

Treatment is mainly supportive.

If anticoagulants and antiplatelets have been given - give Vit K, Fresh Frozen Plasma (FFP) or platelet transfusions to reverse

Surgery: if haemorrhage mass >3cm

73
Q

Stroke

What may an MDT be made up of to rehabilitate the patient?

A

Physiotherapist - prevent spasticity and contracture

Speech therapist - for dysphasia and dysphagia

Occupational therapist - see how they are coping at home

74
Q

Stroke

What steps may be taken to enable primary prevention?

A
  1. Control risk factors - smoking, DM, HTN, hypercholest, obesity
  2. Lifelong anticoagulation - AF, rheumatic heart disease, prosthetic valves
75
Q

Stroke

What steps may be taken to enable secondary prevention

A
  1. Control risk factors - Smoking, DM, HTN, hypercholest, obesity
  2. Anticoagulation - if embolism stroke: aspirin + warfarin. To decrease risk further add clopidogrel in with the aspirin.

Junior Medicine & Surgery (3 decks)

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