neurological Flashcards
stroke:
- two different types?
- difference between a stroke and a TIA?
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)
stroke:
- risk factors for stroke? 11
- rarer causes of stroke? 6
- 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
stroke: focal signs in:
- cerebral infarcts?
- brainstem infarcts?
- lacunar infarcts?
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
aphasia:
- two different types?
- name of areas of brain?
- signs/symptoms?
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”
stroke:
- bloods? 4
- imaging? 1
- 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
immediate + secondary treatment for stroke:
- ischaemic? 5
- haemorrhagic? 4
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
differential diagnoses for stroke or TIA? 12
- 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
sub-arachnoid haemorrhage:
- most common cause?
- 2 other causes?
- unmodifiable risk factors? 5
- modifiable risk factors? 3
- 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
symptoms associated with a large berry aneurysm (nb not ruptured)?
common anatomical locations? 2
mass effect
- painful third nerve palsy (down + out)
- junction of posterior communicating with internal carotid
- junction of anterior communicating with anterior cerebral
sub-arachnoid haemorrhage:
- main symptom?
- other symptoms? 4
- signs? 3
- 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)
sub-arachnoid haemorrhage:
- investigations? 2
CT (if first 48 hours)
LP
- looking for xanthochromia
- use if CT negative (but only after 12 hours!!)
sub-arachnoid haemorrhage:
- immediate treatment? 2
- later treatment? 1
- stabilise & keep BP >160
- give NIMODIPINE (Ca channel blocker, reduces artery spasm)
- neurosurgery (endovascular clipping - or surgical clipping if weird shape)
differential diagnosis for a ‘thunder clap’ headache? 6
- SAH (25%)
- idiopathic (50%)
- meningitis
- migraine
- hemorrhagic stroke
- cortical vein thrombosis
peripheral neuropathy:
- what are polyneuropathies?
- types of causes of polyneuropathies?10 (incl examples)
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)
symptoms (+ signs) of:
- sensory neuropathy? 6
- motor neuropathy? 4
- autonomic neuropathy? 7
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
commonest mononeuropathy?
- nerve roots?
- symptoms? 3
- clinical tests? 2
- treatment? 3
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
seizures:
- pathogenesis of epilepsy?
- definition of epilepsy?
- what % have idiopathic causes of epilepsy?
- risk factors for epilepsy? 5
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
non-epileptic causes of seizures:
- metabolic? 5
- other? 8
- 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
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?
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
symptoms of post-ictal state:
- common to all types?
- seen in frontal lobe?
- seen in frontal lobe?
- 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)
seizures/epilepsy:
- bloods? 5
- other investigations? 2
- 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)
FIRST line drug treatments for:
- generalised tonic-clonic, tonic, atonic + myoclonic? 2
- absence seizures? 3
- partial seizures +/- secondary generalisation? 1
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
drug treatment for prolonged or repeated seizures, incl status epilepticus
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
meningitis:
- 2 commonest causative organisms?
- risk factors? 3
- young or old age
- absent or non-functioning spleen
- immunocompromised (get odd organisms)
meningitis:
- signs/symptoms? 11
- 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)
3 signs of meningism?
- neck stiffness
- photophobia
- positive Kernig’s sign
= pain + resistance on passive knee extension with hip fully flexed
meningitis:
- bloods? 5
- other investigations? 2
- treatment?
- 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!!
bacterial meningitis differential diagnoses:
- other causes of meningitis? 3
- other neurological? 4
- other? 2
- 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
migraine:
- risk factors? 3
- triggers for attacks? (incl acronym) 9
- 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%
migraine:
- three types?
- typical presentation of attacks?
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
migraines:
- investigations?
- treatment of attacks? 3
- meds for prevention? 2
- what drugs are contraindicated for migraines WITH aura?
- 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)
migraines
- differential diagnoses? 4
- 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
tension headache:
- classical presentation?
- risk factors?
- investigations?
- management?
- what can mimic it? 3
- 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
parkinsons disease:
- three groups of motor signs?
- non-motor features? 7
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
parkinsons disease:
- investigations?
- initial drug treatments? 2
- later drug treatment? 1 (incl side effects)
- other management needed?
- 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
non-idiopathic causes of Parkinsonism:
- drugs? 3
- other? 3
- antipsychotics
- metoclopramide (an anti-emetic)
- prochlorperazine (another anti-emetic)
- repeated head trauma (e.g. boxing)
- encephalopathy post flu
- HIV
