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Junior Medicine & Surgery > Neurological History > Flashcards

Neurological History Flashcards

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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
Blackouts What are the 'cardiac' causes of syncope?
Arrhythmia Anything causing outflow obstruction - aortic stenosis, hypertrophic obstructive cardiomyopathy Massive PE
25
Blackouts Orthostatic causes of syncope?
Dehydration Drugs - anti hypertensives Autonomic instability
26
Blackouts What are the cerebrovascular causes of syncope?
Vertebrobasilar insufficiency | Aortic dissection
27
Blackouts Main cause of LOC in patients aged 25?
Vasovagal syncope
28
Blackouts How does vasovagal syncope present?
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
29
Blackouts Main cause of LOC in middle aged people?
Vasovagal syncope + cardiac arrhythmias
30
Blackouts Why do middle aged people mainly present with cardiac arrhythmias?
Because cardiac arrhythmias are usually secondary to ischaemic heart disease (which occurs as atherosclerosis develops with age)
31
Blackouts Why are cardiac arrhythmias not that main cause of blackouts in the elderly population?
Because they are likely to have died from other atherosclerosis-related diseases (cardiac or stroke) before reaching old age.
32
Blackouts How do cardiac arrhythmias typically present?
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
Blackouts Main cause of LOC in elderly patients?
Orthostatic/postural hypotension caused by medications (eg anti hypertensives)
34
Blackouts How would an epileptic patient's LOC present?
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
Blackouts LOC caused by turning head suggests?
Carotid sinus hypersensitivity
36
Blackouts LOC following standing indicates?
Postural/Orthostatic hypotension
37
Blackouts LOC following straining, fear, pain etc suggests?
Vasovagal syncope
38
Blackouts LOC whilst sitting or lying down suggests?
Cardiac arrhythmia
39
Blackouts LOC when exercising indicates what?
Cardiac pathology, eg aortic stenosis or a cardiomyopathy
40
Blackouts If a patient is out for seconds to minutes what does this indicate?
Vasovagal syncope or arrhythmias.
41
Blackouts What is virtually pathognomonic of epileptic seizures?
Tongue biting
42
Blackouts What medications would you look for in a drug history?
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
Blackouts What defines Orthostatic hypotension ?
> 20mmHg drop in systolic BP on standing. Or >10mmHg drop in diastolic
44
Blackouts What investigations would you carry out?
``` 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
Collapse What groups can the causes of collapse be split into ?
1. Neurogenic 2. Cariogenic 3. Metabolic 4. Psychogenic
46
Collapse Give examples of neurogenic causes of collapse
Epilepsy Posterior strokes Tumour --> epilepsy
47
Collapse Give examples of cardiogenic causes of collapse?
``` Vasovagal Arrhythmias - bradycardia (if slow enough = hypoperfusion), VT & VF (if fast enough) Orthostatic/postural hypotension Anaemia Shock Carotid sinus sensitivity ```
48
Collapse What can cause bradycardia?
B-blockers Mobitz Type 2 heart block (because it can progress to 3rd degree HB) 3rd degree HB
49
Collapse Give examples of metabolic causes of collapse?
Hypoglycaemia | Hyperkalaemia
50
Collapse What can cause hyperkalaemia?
Drugs - spironolactone, ACEi Renal failure (AKI or CRF) Cell lysis - haemolytic anaemia, tumours, post-op Dehydration
51
Collapse What investigations would you do to investigate CVS cause?
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
Collapse A lying-standing drop in BP of what would be indicative of postural hypotension?
Systolic >20 mmHg | Diastolic >10mmHg
53
Collapse How would you investigate the metabolic causes of collapse?
Finger prick glucose (<7mmol random) | U&ES
54
Collapse How would you investigate neuro cause of collapse ?
EEG | CT head/MRI head
55
Stroke How can a stroke be classified and what are common causes of these?
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
Stroke What are the Risk factors?
``` CVS RF Smoking Diabetes HTN Hypercholesterolaemia FHx (of stroke, heart disease) ``` + age, AF, carotid artery stenosis
57
Stroke Main causes of cerebral infarct?
60% - atherosclerosis or carotid arteries and aortic arch 20% - valvular heart disease 20% - disease in the vessels of the brain itself
58
Stroke In what artery do most cerebral infarcts present?
Middle cerebral
59
Stroke How would a middle cerebral artery infarct present?
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
Stroke On examination what would you find of a cerebral infarct?
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
Stroke Investigations or cerebral infarct?
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
Stroke Are cerebral haemorrhages clinically distinguishable from cerebral infarcts?
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
Stroke Haemorrhages are nearly always the result of what?
Uncontrolled HTN
64
Stroke Other than uncontrolled HTN, what else can cause haemorrhage?
Cocaine Aneurysm Clotting disorders Tumours
65
Stroke How would you investigate a haemorrhage?
CT head/MRI
66
Stroke How would you initially manage any stroke patient?
ABC - maintain airway, prevent hypoxia, hydrate. Treat fever + hyper/hypoglycaemia
67
Stroke How should you treat a patient with ischaemic stroke provided no contraindications?
Thrombolysis
68
Stroke Give some examples of absolute contraindications for thrombolysis
1. Previous intracranial haemorrhage 2. Major surgery/trauma 200/120 Etc
69
Stroke If someone cannot be thrombolysed, how would we treat them?
ASPIRIN - 300mg/day for 2 weeks, then 75mg forever (NB. be aware of asthmatics and GI bleed patients. If aspirin hypersensitive give clopidogrel)
70
Stroke What might warfarin be given to ischaemic infarct patients?
Once cause is known. Eg AF. INF or 2-3
71
Stroke What could you do for a patient who has carotid artery stenosis?
Carotid endartectomy (if obstruction >60%)
72
Stroke How would a haemorrhages stroke patient be managed?
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
Stroke What may an MDT be made up of to rehabilitate the patient?
Physiotherapist - prevent spasticity and contracture Speech therapist - for dysphasia and dysphagia Occupational therapist - see how they are coping at home
74
Stroke What steps may be taken to enable primary prevention?
1. Control risk factors - smoking, DM, HTN, hypercholest, obesity 2. Lifelong anticoagulation - AF, rheumatic heart disease, prosthetic valves
75
Stroke What steps may be taken to enable secondary prevention
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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