neurological Flashcards

1
Q

stroke:

  • two different types?
  • difference between a stroke and a TIA?
A

Ischaemic (80%)
- further subdivided into thrombotic (atherosclerosis) + embolic (norm AF)

Haemorrhagic (20%)
- nb these are intracerebral and don’t include sub arachnoid, subdural or epidural haemorrhages

TIA is effectively a minor ischaemic stroke
- symptoms/signs last LESS THAN 24 HOURS (with no residual damage)

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2
Q

stroke:

  • risk factors for stroke? 11
  • rarer causes of stroke? 6
A
  • age
  • HTN (main one for haemorrhagic)
  • diabetes
  • smoking
  • hyperlipidaemia
  • high alcohol consumption
  • polycythaemia
  • COCP
  • AF
  • valvular heart disease
  • ischaemic heart disease
  • carotid artery dissection
  • venous sinus thrombosis (similar risk factors to VTE, but rarer)
  • vasculitis
  • cocaine (causes vasoconstriction)
  • antiphospholipid syndrome (autoimmune, hypercoaguable state)
  • haemophilis
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3
Q

stroke: focal signs in:
- cerebral infarcts?
- brainstem infarcts?
- lacunar infarcts?

A

cerebral infarcts (50%)

  • contralateral sensory loss
  • contralateral hemiplegia (initially placid then rigid)
  • dysphasia
  • homonymous hemianopia
  • frontal sparing!!

brainstem infarcts (25%)

  • quadriplegia
  • disturbances of gaze or vision
  • locked-in syndrome

lacunar infarcts (35%)
= basal ganglia, internal capsule, thalamus + pons
- ataxic hemiparesis
- pure motor
- pure sensory
- cognition/conciousness intact (except thalamic stroke)

nb signs can be localising but often more generalised and imaging is only way to identify specific area
- symptoms are hugely variable!!

nb haemorrhagic strokes can give meningial signs (photophobia, neck stiffness etc) but may not

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4
Q

aphasia:

  • two different types?
  • name of areas of brain?
  • signs/symptoms?
A

Expressive aphasia
= Broca’s area
- dominant (norm left) frontolateral cortex
- patient knows what they want to say but can’t say it (may be frustrated)
- can understand speech and aware that they are struggling to speak
- “infront of central sulcus, where motor area is - so damage to this area reduces ability to do motor part of speech”

Receptive aphasia
= Wernicke’s area
- dominant (norm left) posterior part of superior temporal gyrus
- speech if fluent but makes no sense
- difficulty in comprehending what is being told to them
- often think they are making sense and don’t realise there is a problem
- “wernickes area is behind central sulcus so affects sensory, also W has corners like the corner between parietal + temporal lobes where this area is found”

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5
Q

stroke:

  • bloods? 4
  • imaging? 1
A
  • glucose
  • FBC (to identify polycythaemia)
  • ESR (can be high in vasculitis)
  • INR (if on warfarin)
  • CT (to differentiate between bleed or clot!)

nb can also US or doppler carotid to look for atherosclerosis

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6
Q

immediate + secondary treatment for stroke:

  • ischaemic? 5
  • haemorrhagic? 4
A

ischaemic
+ stabilise vital signs
+ 300mg aspirin
+ consider thrombolysis with rTPA (if onset of symptoms <4.5hrs)
- lifestyle + med changes for secondary prevention
- carotid endarterectomy if carotid artery stenosis of >70%

haemorrhagic
\+ stop AND reverse any anticoagulation
\+ stabilise vital signs
\+ craniotomy (if large haematoma)
- antihypertensive medication

REHABILITIATION for both types with SALT, physiology + other input

nb do not lower blood pressure in the acute setting as this will further reduce cerebral perfusion

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7
Q

differential diagnoses for stroke or TIA? 12

A
  • seizure (+ post-ictal states)
  • migraine
  • syncope
  • sub-arachnoid, sub-dural or epidural bleed
  • other mass lesion
  • hypoglycaemia
  • hyponatraemia
  • MS
  • focal neuropathy (e.g. bells palsy)
  • hyperglycaemia
  • other encephalopathies
  • trauma
  • functional hemiparesis
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8
Q

sub-arachnoid haemorrhage:

  • most common cause?
  • 2 other causes?
  • unmodifiable risk factors? 5
  • modifiable risk factors? 3
A
  • berry aneurysm (70%)
  • congenital arteriovenous malformations (15%)
  • idiopathic, no lesion found (15%)
  • age 35-60
  • female
  • bleeding disorder
  • mycotic anerysm
  • FH of SAH
  • smoking
  • alcohol misuse
  • HTN
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9
Q

symptoms associated with a large berry aneurysm (nb not ruptured)?

common anatomical locations? 2

A

mass effect

  • painful third nerve palsy (down + out)
  • junction of posterior communicating with internal carotid
  • junction of anterior communicating with anterior cerebral
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10
Q

sub-arachnoid haemorrhage:

  • main symptom?
  • other symptoms? 4
  • signs? 3
A
  • sudden ‘thunderclap’ headache (norm in occipital region)
  • seizures
  • nausea/vomiting
  • collapse/LOC
  • coma

nb coma/drowsiness may last for days

  • meningeal irritation (neck stiffness + positive kernige sign)
  • focal euro signs (e.g. 3rd nerve palsy)
  • subhyaloid haemorrhages (between retina + vitreous membrane)

nb can get a less severe ‘warning headache’ a few days prior (indicative of a little leak)

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11
Q

sub-arachnoid haemorrhage:

- investigations? 2

A

CT (if first 48 hours)

LP

  • looking for xanthochromia
  • use if CT negative (but only after 12 hours!!)
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12
Q

sub-arachnoid haemorrhage:

  • immediate treatment? 2
  • later treatment? 1
A
  • stabilise & keep BP >160
  • give NIMODIPINE (Ca channel blocker, reduces artery spasm)
  • neurosurgery (endovascular clipping - or surgical clipping if weird shape)
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13
Q

differential diagnosis for a ‘thunder clap’ headache? 6

A
  • SAH (25%)
  • idiopathic (50%)
  • meningitis
  • migraine
  • hemorrhagic stroke
  • cortical vein thrombosis
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14
Q

peripheral neuropathy:

  • what are polyneuropathies?
  • types of causes of polyneuropathies?10 (incl examples)
A

disorders of peripheral or cranial nerves
- distribution is usually symmetrical + widespread (often glove + stocking distribution)

Metabolic

  • DM
  • renal failure
  • hypothyroidism
  • hypoglycaemia
  • mitochondrial disorders

vasculitides

  • polyarteritis nodosa*
  • rheumatoid arthritis
  • wegner’s granulomatosis

malignancy

  • paraneoplastic syndromes
  • polycythaemia rubre vera

inflammatory

  • guillian-barre
  • CIDP
  • sarcoidosis

infections

  • leprosy
  • HIV
  • syphilis
  • lyme disease

nutritional

  • low thiamine (B1) or B12 (incl dt alcohol misuse)
  • low vit E or folate
  • high vit B6

inherited syndromes

  • charcot-marie-tooth
  • refum’s syndrome
  • porphyria
  • leucodystrophy

toxins

  • lead
  • arsenic

drugs

  • alcohol
  • vincristine (chemo)
  • isoniazid
  • phenytoin
  • cisplatin
  • nitrofurantoin
  • metronidazole

(finish from page 508)

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15
Q

symptoms (+ signs) of:

  • sensory neuropathy? 6
  • motor neuropathy? 4
  • autonomic neuropathy? 7
A

sensory:

  • numbness
  • pins & needles (burning, feels funny)
  • affects extremities first (glove + stocking)
  • difficulty handling small objects (eg buttons)
  • signs of trauma on hands/feet
  • diabetic + alcoholic neuropathies are typically painful

motor:
(nb often progressive, may be rapid)
- weak or clumsy hands
- difficulty in walking (falls, stumbling)
- wasting + weakness most marked in distal muscles (eg foot drop)
- reflexes reduced or absent

autonomic:

  • postural hypotension
  • erectile dysfuntion/ejaculation failure
  • decreased sweating
  • constipation
  • nocturnal diarrhoea
  • urine retention
  • horners syndrome
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16
Q

commonest mononeuropathy?

  • nerve roots?
  • symptoms? 3
  • clinical tests? 2
  • treatment? 3
A

carpal tunnel syndrome
= median nerve (C6-T1)

  • aching pain in hand + arm (esp at night)
  • parasthesiae in thumb, index + middle fingers)
  • may be sensory loss + weakness/wasting over/of thenar eminence

Tinel’s test: tap over wrist to induce symptoms

Phalen’s test: maximal wrist flexion for 1 min mauy elicit symptoms

nb neither of these are very reliable

  • splinting
  • local steroid injection
  • decompression surgery
17
Q

seizures:

  • pathogenesis of epilepsy?
  • definition of epilepsy?
  • what % have idiopathic causes of epilepsy?
  • risk factors for epilepsy? 5
A

seizure = occurrence of signs +/or symptoms due to abnormal, excessive or synchronous neuronal activity in the brain

epilepsy = enduring predisposition to generate epileptic seizures

epilepsy = two or more unprovoked (or reflex) seizures occurring more than 24 hours apart

nb unprovoked means there wasn’t a secondary provocation like a low blood sugar or hypoxia, triggers like flashing lights, stress, alcohol count as unprovoked

2/3rds are idiopathic

  • FH
  • cortical scarring (eg following old head injury)
  • developmental
  • following a stroke
  • space occupying lesion
18
Q

non-epileptic causes of seizures:

  • metabolic? 5
  • other? 8
A
  • hypoxia (incl post-syncope)
  • high OR low sodium
  • high OR low glucose
  • low calcium
  • uraemia
  • trauma
  • stroke
  • haemorrhage
  • raised ICP
  • alcohol (or benzodiazepine) withdrawal
  • infection (meningitis, encephalitis, syphilis, HIV)
  • high temp
  • drugs (tricyclics, cocaine, tramadol, theophylline)

nb things like stroke can cause a seizure as there are happening, this is not epilepsy! - however if, due to the secondary hypoxia + brain damage, a person then goes on to have further seizures then this is then epilepsy

19
Q

definitions of seizures:

partial seizures?

subtypes of partial:

  • simple partial?
  • complex partial?
  • partial w secondary generalisation?

primary generalised seizures?

subtypes of generalised:

  • absence?
  • tonic-clonic?
  • myoclonic?
  • atonic?
A

partial seizures:
= focal onset with features referable to a part of one hemisphere (often seen w underlying structural disease)

simple partial:

  • awareness is NOT impaired
  • focal motor, sensory, autonomic or psychic symptoms
  • no post-ictal symptoms

complex partial:

  • awareness IS impaired
  • may have simple partial onset (=aura)
  • post-ictal confusion can occur (more common is from temporal lobe, less so if from occipital lobe)

partial w secondary generalisation:

  • 2/3rds of partial seizures spread
  • causing a typically convulsive generalised seizure

primary generalized seizures:
= simultaneous onset with no localising features

absence:

  • brief (<10 sec) pauses
  • eg suddenly stop in convo then carry on again
  • presents in childhood

tonic-clonic

  • loss of consciousness
  • limbs stiffen (tonic) then jerk (clonic) (nb may have one without the other)
  • post-ictal convusion + drowsiness

myoclonic

  • sudden jerk of a limb, face or trunk
  • patient may be thrown to the ground or have a violently disobedient limb

atonic

  • sudden loss of muscle tone -> fall
  • no LOC
20
Q

symptoms of post-ictal state:

  • common to all types?
  • seen in frontal lobe?
  • seen in frontal lobe?
A
  • headache
  • confusion
  • myalgia
  • sore tongue

frontal (ie motor cortex)
- todd’s paresis (temporary weakness)

temporal
- dysphasia

nb there are a lot of different localising signs for focal seizures but probably beyond 3rd year (see page 495 in mini oxford clinical handbook for more info)

21
Q

seizures/epilepsy:

  • bloods? 5
  • other investigations? 2
A
  • FBCs
  • U+Es
  • LFTs
  • glucose
  • calcium
    (all looking for secondary causes of seizure)
  • 12-lead ECG (cardiac syncope is key DD)
  • EEG

nb may require CT/MRI of head if suspect a physical cause (eg space occupying lesion)

22
Q

FIRST line drug treatments for:

  • generalised tonic-clonic, tonic, atonic + myoclonic? 2
  • absence seizures? 3
  • partial seizures +/- secondary generalisation? 1
A

generalised tonic-clonic, tonic, atonic + myoclonic
= lamotrigine (better tolerated + less teratogenic)
= sodium valproate

absence
= sodium valproate
= lamotrigine
= ethosuximide

partial +/- generalisation
= carbamazepine

nb these are for preventionof seizures not during seizures

also nb there are many other drugs and usage depends on co-morbidities, interactions and plans for pregnancy

23
Q

drug treatment for prolonged or repeated seizures, incl status epilepticus

A

rectal or IV benzodiazepines
- eg diazepam, lorazepam

nb this makes sense as these are GABA agonists and so act as CNS depressors, reducing the neuronal excitability quickly

24
Q

meningitis:

  • 2 commonest causative organisms?
  • risk factors? 3
A
  • young or old age
  • absent or non-functioning spleen
  • immunocompromised (get odd organisms)
25
Q

meningitis:

- signs/symptoms? 11

A
  • neck stiffness
  • headache
  • photophobia
  • non-blanching rash
  • fever
  • muscle ache/joint pain
  • cold hands + feet
  • pallor
  • nausea/vomiting
  • irritability/not-settling
  • seizures

nb also signs of sepsis (reduce cap refill, fast pulse etc)

26
Q

3 signs of meningism?

A
  • neck stiffness
  • photophobia
  • positive Kernig’s sign
    = pain + resistance on passive knee extension with hip fully flexed
27
Q

meningitis:

  • bloods? 5
  • other investigations? 2
  • treatment?
A
  • U&Es
  • LFTs
  • FBC
  • glucose
  • BLOOD CULTURE
  • CT head (if focal signs, paipiloedema, seizures etc)
  • lumbar puncture + culture/PCR

resus + empirical Abx (once culture back, change Abx)

nb if signs of sepsis do BUFALO!!

28
Q

bacterial meningitis differential diagnoses:

  • other causes of meningitis? 3
  • other neurological? 4
  • other? 2
A
  • viral meningitis
  • fungal meningitis (esp if immunocompromised)
  • autoimmune meningitis (eg SLE)
  • encephalitis
  • subarachnoid haemorrhage
  • brain/CNS malignancy
  • brain/CNS abscess
  • septicaemia
  • malaria or dengue fever
  • look up other causes of non-blanching rash
29
Q

migraine:

  • risk factors? 3
  • triggers for attacks? (incl acronym) 9
A
  • FH (v important)
  • female (2:1)
  • obesity

CHOCOLATE

C - Chocolate
H - Hangovers
O - Orgasms
C - Cheese
O - Oral contraceptives
L - Lie-ins
A - Alcohol
T - Tumult (stress/distressed)
E - Exercise

nb triggers are only seen in 50%

30
Q

migraine:

  • three types?
  • typical presentation of attacks?
A

migraine withOUT aura

  • unilateral throbbing/pulsating headache
  • lasting 4-72 hours
  • nausea/vomitting + fatigue
  • photophobia +/or photophobia
  • worsened by moving around/daily activities

migraine WITH aura

  • see above, PLUS….
  • aura precedes headache by minutes + may occur during
  • auras can be visual (distorting visions of lines, dots, zig zags, scotoma +/or hemianopia), sensory (e.g. parasthesia in arms) +/or motor (dysarthria, ataxia, ophthalmoplegia etc)

migraine variants

  • get unilatreral aura-like symptoms but without the headache
  • poorly understood
31
Q

migraines:

  • investigations?
  • treatment of attacks? 3
  • meds for prevention? 2
  • what drugs are contraindicated for migraines WITH aura?
A
  • none needed, all on history

unless suspect a different cause

treatment for attacks

  • NSAIDs (least likely to induce a post-analgesia headache)
  • a triptan (e.g. sumitriptan)
  • antiemetic (e.g. metoclopramide)

only use drugs for prevention if attacks are very frequent and disabling and medication-overuse headaches are occurring dt repeated treatment of acute attacks

prevention

  • topiramate (an anti-epileptic - nb a teratogen)
  • propranolol

^nb these are first line, consult neurologists if failure of these

COMBINED oral contraceptive pill (though fine if no aura)

32
Q

migraines

- differential diagnoses? 4

A
  • tension type headache
  • meningitis
  • subarachnoid haemorrhage
  • TIA

nb in TIAs, the maximum deficit is present immediately + headache is unusual

if take good history then normally easy to rule out other causes

33
Q

tension headache:

  • classical presentation?
  • risk factors?
  • investigations?
  • management?
  • what can mimic it? 3
A
  • BI-lateral tightening pain around head
  • non-pulsating
  • no nausea/vomiting (though anorexia may occur)
  • often radiates to neck
  • may be tenderness of scalp muscles
  • stress/sleep disturbance
  • squinting
  • poor posture
  • dehydration
  • noise

nb similar headaches may be caused by depression, caffeine withdrawal etc but these don’t technically count as tension headaches

  • BP + papilloedema
  • relaxation techniques (yoga, massage, light exercise)
  • mild painkillers (paracetamol or ibuprofen)
  • analgesia-overuse headaches
  • migraine without aura
  • pain referred from neck

always make sure to ask about social history and OTC drug Hx in these presentations

34
Q

parkinsons disease:

  • three groups of motor signs?
  • non-motor features? 7
A

slow tremor

  • worse at rest
  • ‘pill rolling’
  • one side worse

rigidity/increased tone

  • cogwheel rigidity
  • postural instability

brady/hypokinesia

  • slow to initiate movement
  • freezing at obstacles and doors
  • low blinking rate + reduced facial expressions
  • micrographia
  • festinating gait
  • reduced arm swing

non-motor

  • reduced sense of smell
  • constipation
  • frequency/urgency
  • dribbling of saliva
  • visual hallucinations
  • dementia
  • depression
35
Q

parkinsons disease:

  • investigations?
  • initial drug treatments? 2
  • later drug treatment? 1 (incl side effects)
  • other management needed?
A
  • none, all clinical exam/history findings
  • dopamine agonists (e.g. ropinirole, pramipexole etc)
  • monoamine oxidase B inhibitor (inhibits catabolism of dopamine)

levodopa (with a peripheral decarboxylase inhibitor)

  • therapeutic range gradually gets narrower the longer the usage
  • if too much = dyskinesias + chorea
  • get ‘on/off’ effect
  • physio (to prevent falls)
  • psych support (esp if hallucinating)
  • increasing level of care needed
36
Q

non-idiopathic causes of Parkinsonism:

  • drugs? 3
  • other? 3
A
  • antipsychotics
  • metoclopramide (an anti-emetic)
  • prochlorperazine (another anti-emetic)
  • repeated head trauma (e.g. boxing)
  • encephalopathy post flu
  • HIV