Neurology Flashcards

1
Q

Define syncope

A

Transient global cerebral hypoperfusion

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2
Q

Name 3 causes of syncope

A

Reflex/neurally mediated (happens when nervous system controlling HR and BP malfunctions in response to emotional stress), cardiogenic, orthostatic/postural hypotension

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3
Q

Name 3 types of reflex/neurally mediated syncope

A

vasovagal, situational eg. coughing/swallowing/micturition, carotid sinus hypersensitivity- on head turning/shaving

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4
Q

Name 4 risk factors for cardiogenic syncope

A

conditions that predispose to tachyarythmias = long QT, SVT (Wolff-Parkinson White), bradyarrhythmias (heart block), cardiac ischaemia, structural heart disease (AS, hypertrophic cardiomyopathy), age >60, fainting during exertion/lying down

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5
Q

What are the symptoms of vasovagal syncope

A

nausea, pallor, sweating, visual fields closing in and then fainting

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6
Q

How long does vasovagal syncope last

A

Briefly- 1 min approx

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7
Q

Is there post-ictal symptoms in vasovagal syncope

A

No

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8
Q

What investigations would you do in a patient with suspected syncope?

A

ECG, bloods- glucose, FBC, UEs, tilt table test

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9
Q

What is the treatment for reflex/neurally mediated syncope

A

Education, avoiding triggers and tilt table training- but this is not very effective

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10
Q

What is the treatment for cardiogenic syncope

A

treat the cause eg. pacemaker for bradycardia and anti-arrhythmic drugs

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11
Q

What is the treatment for orthostatic syncope

A

check any medications that might be causing eg. ACEi CCB, beta blockers , water intake and can take fludrocortisone

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12
Q

Define a seizure

A

Clinical manifestation of abnormal and excessive discharge of cerebral neurones

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13
Q

Define epilepsy

A

a recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures

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14
Q

Name 5 causes of epilepsy

A

idiopathic, cerebral haemorrhage, stroke, head injury, CNS infections eg. encephalitis, neurodegenerative disease eg. Alzheimers, metabolic disorders eg. hypoxia, hypoglycaemia, hypernatraemia, hypercalcaemia, drugs, developmental disorders

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15
Q

What is the difference between focal and generalised epileptic seizures?

A

Focal- features localised to part of one hemisphere of the brain. often caused by structural disease. Generalised- features cannot be localised to one part. causes= idiopathic, genetics/FMH, lack of sleep, alcohol, photosensitivity

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16
Q

Name and describe the two types of focal seizures?

A

Simple partial seizures - with awareness and one abnormal motor or sensory sx (depending on the lobe affected)|, complex partial seizures- loss of awareness and complex movements (commonly from temporal lobe)

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17
Q

What symptoms would occur with a simple partial seizure of the temporal lobe?

A

automatisms (e.g lip smacking, grabbing ,singing), abdominal rising sensation/pain, deja vu, dysphasia, hippocampal sx- fear, panic

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18
Q

What symptoms would occur with a simple partial seizure of the frontal lobe?

A

Motor features- posturing, leg/head movements) motor arrest, behavioural changes, dysphasia, post-ictal Todd’s palsy

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19
Q

What symptoms would occur with a simple partial seizure of the parietal lobe?

A

sensory disturbances (tingling, numbness, pain) and motor symptoms

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20
Q

What symptoms would occur with a simple partial seizure of the occipital lobe?

A

Visual symptoms- flashes, spots and lines

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21
Q

Name and describe the four types of generalised seizures?

A

generalised tonic clonic seizures (stiffening and jerking of limbs, LOC, post-ictal sx of confusion and drowsiness), myoclonic (sudden jerk of one limb), absence (spacing out) and akinetic (sudden loss of tone in limb- no LOC)

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22
Q

What are some of the post-ictal symptoms in a GTCS?

A

confusion, drowsiness, urinary incontinence, LATERAL tongue bite (tongue moves back in seizures so more to bite), injury- dislocation of the shoulder

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23
Q

What is the likely cause of a FIRST seizure in older age? (2)

A

Tumour! primary= glioblastoma, secondary= brain mets (from lung, breast, thyroid, kidney, colon, skin) or vascular- stroke, MI

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24
Q

What investigations would you do in a patient with suspected epilepsy?

A

Bloods- glucose, FBC, UE, ECG, and 24h ECG, CT, MRI, EEG (normal doesn’t exclude)

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25
Q

What is the drug treatment for epilepsy? name the side effects of each drug

A

Focal seizures= carbamazepine (SE leukopenia, blurred vision) or lamotrigine (rash, fever)
Generalised seizures= sodium valproate (SE teratogenic, liver failure) or lamotrigine

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26
Q

What is the surgical treatment for epilepsy?

A

Resection or vagal nerve stimulation (palliative)

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27
Q

Define non-epileptic seizures

A

Episodes of movement/sensation/experience that resemble epileptic seizures but without cerebral discharges

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28
Q

What is the cause of non-epileptic seizures?

A

psychological distress - trauma for example childhood sexual abuse

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29
Q

What are the symptoms of non-epileptic seizures?

A

Eyes closed, partially responsive, may be emotional, paralysed but conscious, may be shaking with fighting movements (remembering the trauma)

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30
Q

What are the post-ictal symptoms of non-epileptic seizures?

A

Very tired and worn out. Talk dramatically about the event

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31
Q

Apart from syncope, epilepsy and non-epileptic seizures , name 4 other causes of loss of consciousness

A

migraine, hypoglycaemia, acute hydrocephalus (tumour), orthostatic hypotension

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32
Q

How is coma measured?

A

on the GCS scale

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33
Q

What are the 3 components measured by the GCS?

A

Eye opening, motor response and visual response

34
Q

Name 5 causes of coma?

A

drugs/toxins, anoxia, bleeding, infections, infarcts, hypoglycaemia, DKA, SAH, epilepsy, tumour

35
Q

what investigations would you do in an unconscious patient?

A

bloods- glucose, U&E, Ca, phosphate, LFT, clotting, toxicology (alcohol level- , ECG, CT brain, MRI brain, LP (only if safe- can’t do it if abscess/tumour due to high ICP), EEG

36
Q

What are the main symptoms of CO poisoning?

A

Headache, altered awareness and altered behaviour

37
Q

Patient presents with fever, cough, marked confusion. is in a coma with serial seizures. The CT shows low density and volume loss in the temporal lobe. What is the diagnosis?

A

Herpes simplex encephalitis. (acute deterioriation in conscious level= think of encephalitis)

38
Q

Define status epilepticus

A

Non self- limiting manifestation of an epileptic seizure

39
Q

Name the 4 types of status epilepticus and describe

A

GTCS (seizure lasts 90s, then unresponsive and then another seizure), myoclonic, absence (confused, slow, lasting >5s and doesnt stop), focal- unusual

40
Q

Name 5 causes of status epilepticus

A

ALCOHOL (no.1 cause of status epilepticus in those without epilepsy), NON-COMPLIANCE (no.1 cause in epileptics), stroke (haemorrhage/ischaemic), malignancy, infections- meningitis, encephalitis, , drugs, trauma, metabolic- hypogylcaemia, hypocalcemia, hyponatraemia, hypokalaemia, thiamine deficiency (leading to Wernicke’s encephopathy and Korsakoff’s syndrome)

41
Q

What investigations would you do in suspected status epilepticus?

A

Bloods- FBC, WBC (infection?), U&Es, glucose, Ca, toxins- drug and alcohol levels, EEG, CT/MRI if suspecting stroke/haemorrhage

42
Q

How do you treat status epilepticus? (1st and 2nd line drugs)

A

Initially- check airway is clear and give O2 if necessary. 1st line: BENZOs (lorazepam IV in hospital, midazolam buccal if at home). 2nd line: phenytoin infusion (anti-seizure, Na channel blocker stopping the repeated action potentials)

43
Q

How do benzodiazepines work to treat status epilepticus?

A

They bind to GABA receptors, enhancing the effect of GABA in producing sedative, anti-convulsive, muscle relaxant and anti-anxiety effects

44
Q

What is the definition of a stroke?

A

Sudden onset of focal neurological signs lasting longer than 24h , of presumed vascular origin

45
Q

Name 5 causes of stroke

A

small vessel thrombosis, cardiac emboli (MI, AF, endocarditis), atherothrombolism (from carotids eg), haemorrhage (trauma, increased BP, aneurysm rupture, anticoagulation), subarachnoid haemorrhage, carotid artery dissection

46
Q

What are the risk factors for stroke? modifiable and non-modifiable

A

non-modifiable: age, sex, FMH of vascular disease, ethnicity (afro-carribean and asian). modifiable: HTN, smoking, AF, excess alcohol intake, hyperlipidaemia, diabetes, obesity, carotid artery disease, recreational drugs . in younger people= ASD/VSD in heart, AF, sickle cell disease, aortic dissection, OCP

47
Q

What arteries does an anterior circulation stroke affect and what symptoms would this produce?

A

involves the carotid system (ACA, MCA). symptoms= unilateral contralateral weakness of arm and face, sensory loss, dysphasia, homonymous hemianopia, amarausis fugax

48
Q

what arteries does a posterior circulation stroke affect and what symptoms would this produce?

A

basilar and vertebral arteries. symptoms: bilateral symptoms- dysarthria, dysphagia, diplopia, dizziness, ataxia, diplegia (paralysis)

49
Q

What symptoms would a brainstem infarct produce?

A

quadriplegia, locked in syndrome, eye movement abnormalities

50
Q

What are the 5 stroke syndromes produced by a lacunar infarct?

A

ataxic hemiparesis, pure motor, pure sensory, sensorimotor and dysarthria

51
Q

where does a lacunar infarct occur most commonly?

A

in basal ganglia, thalamus, pons and internal capsule

52
Q

What investigations would you do in a patient with stroke?

A

CT! bloods- FBC, ESR, clotting (looking for thrombophilia/thrombocytopaenia), U&Es, LFTs, glucose (hyper/hypo), cholesterol (dyslipidaemia-> ischaemia), carotid duplex (US), Echo (if pt <55 and previous cardiac disease to see thrombus)

53
Q

What are the indications for an immediate CT scan in a patient with stroke?

A
  • less than 4.5 hours from onset and considering thrombolysis (so if ischaemic stroke)
  • indications for early anticoagulation eg. if have AF
  • on anticoagulation
  • known bleeding tendency
  • decreasing GCS
  • unexplained/progressive sx
  • Papilloedema
  • Severe headache at onset of stroke (SAH)
54
Q

Name 6 differential diagnosis of stroke

A

Seizure (and Todds paresisis- post ictal paralysis), migraines, metabolic eg. hypoglycaemia, subdural haemorrhage, tumours, head injury

55
Q

What is the treatment for ischaemic stroke?

A

Thrombolysis, anticoagulation (if AF), antiplatelets- aspirin for 2 weeks, then clopidogrel, statin (if cholesterol >4) and rehab- OT, physio, speech and language therapists. Secondary treatment: statins, check blood glucose, antihypertensives if necessary, dysphagia screen

56
Q

What drug and method of administration is used in the main treatment of ischaemic stroke (thrombolysis) and what is the importance of the time of administration

A

IV alteplase (tissue plasminogen activator). MUST be administered within 4.5 hours of stroke onset.

57
Q

What is the treatment for haemorrhagic stroke?

A

surgery. supportive treatments

58
Q

What are 5 causes of haemorrhagic stroke?

A

HTN, tumour, vascular malformations (AV malformations), aneurysms, trauma

59
Q

What is the most likely cause of a DEEPER bleed in a haemorrhagic stroke?

A

HTN

60
Q

What is the most likely cause of a CORTICAL/SUPERFICIAL bleed in a haemorrhagic stroke?

A

AV malformations, aneurysms

61
Q

How does hydrocephalus occur in a stroke and what is the treatment?

A

Haemorrhage occurs and a clot blocks the aqueduct obstructing CSF flow through the ventricles causing a build up = hydrocephalus. Tx= clot evacuation

62
Q

Define a TIA

A

The sudden onset of focal CNS symptoms due to temporary occlusion of part of the cerebral circulation- usually by emoli. Sx <24h

63
Q

How does amaurosis fugax occur in a TIA?

A

Emboli in retinal artery

64
Q

Name 4 causes of TIA

A

Atherothrombolism (from carotid- gives carotid bruit), cardiothrombolism (from MI), AF, valve disease

65
Q

What investigations would you do in a patient with a suspected TIA?

A

FBC, U&E, ESR, glucose, lipids, CXR, ECG, carotid doppler, MRI - for previous infarcts

66
Q

What is the acute treatment of a stroke?

A

ABCDE- aspirin, treat BP, order CT and do ABCD2

67
Q

What is ABCD2 in a TIA and what is the clinical significance?

A

Age >60, BP: systolic >140, diastolic >90, clinical features: unilateral weakness, speech disturbance only, duration of TIA >60 mins, 10-60 mins, diabetes. An ABCD2 score >4= assessment within 24h

68
Q

What is the treatment of a TIA (not acute)?

A

Aspirin for 2 weeks then change to clopidogrel, treat risk factors (high BP, alcohol intake, hyperlipidaemia)

69
Q

What is the surgical treatment option for TIA when the cause is atherothrombolism from carotid

A

Carotid endarterectomy and stenting - for symptomatic carotid stenosis

70
Q

Define SAH- subarachnoid haemorrhage

A

spontaneous bleeding into the subarachnoid space

71
Q

What are the causes of SAH?

A

Main- rupture of saccular aneurysms (Berry aneurysms|), AVM, arterial dissection, tumour

72
Q

Name the 3 common sites for a Berry aneurysms

A
  • Junction of posterior communicating artery within internal carotid.
  • junction of anterior communicating with anterior cerebral artery.
  • Bifurcation of MCA
73
Q

What conditions are associated with Berry aneurysms? (3)

A

Polycystic kidneys, coarctation of the aorta, Ehlers- Danlos syndrome (hypermobile joints with increased skin elasticity)

74
Q

Name 5 symptoms of SAH

A

Thunderclap headache- sudden, very painful), depressed GCS, meningisim (neck stiffness, nausea, photophobia), seizures, sentinel headache (previously- from small warning bleed)

75
Q

What are the signs of SAH?

A

neck stiffness, Kernig’s sign, focal neurology

76
Q

What is the big condition associated with SAH?

A

Polycystic kidney disease

77
Q

What would you find on examination of a patient with SAH?

A

Neck stiffness, reduced GCS, 3rd nerve palsy (eye- down and out), extensor plantar reflex/ Babinski, pain on eye movement

78
Q

What investigations would you do in a patient with suspected SAH?

A

CT head, MRI, LP (if CT is negative) = find yellow pigment xanthocromia- due to bilirubin present from breakdown of Hb

79
Q

What is the treatment of a SAH? and what drug is helpful in reducing morbidity?

A

surgical clipping of aneurysms or endovascular coiling. Nimodipine- Ca antagonist- reduces vasospasm and morbidity from bleeding.

80
Q

Name 3 complications of SAH

A

Rebleeding, cerebral ischaemia, hydrocephalus