Medicine - Neurology Flashcards
Define ‘seizure’ and ‘epilepsy’
seizure = transient occurrence of S/Sx due to abnormal neuronal activity in the brain Epilepsy = at least 2 unprovoked episodes of a seizure caused by spontaneous, intermittent, abnormal electrical activity in the brain
What is the pathophysiology of epilepsy?
Imbalance between excitatory (glutamate/aspartate) and inhibitor (GABA) signalling
Commonest at the extremes of life, and 2/3rds are idiopathic
What are the two main types of epilepsy?
Focal and generalised
Describe focal epileptic seizures and the subtypes
area of local cortical abnormality in an otherwise normal brain
originates in 1 hemisphere
EEG shows localised discharge and they are easy to diagnose as features correlate to one area e.g. visual/jerking…
3 subtypes:
- without impaired consciousness
- with impaired consciousness
- evolving to bilateral convulsive seizures
Describe generalised epileptic seizures and the subtypes
Originate in one brain area but rapidly spread to involve bilateral networks, show widespread electrical discharge throughout with no features attributable to a single hemisphere. Usually as patients are born with an issue in neurotransmitter metabolism/ion channels which leads to CNS hyper-responsiveness
4 subtypes:
- absence seizures (<10s, always start in childhood, often mistaken for poor concentration at school)
- myoclonic seizures (sudden involuntary muscle group contractions, may cause patients to fall over, usually provoked e.g. alcohol, tired)
- tonic clonic seizures (pt becomes rigid (tonic) and then begins jerking (clonic), may have tongue biting, unconsciousness, headache afterwards)
- atonic (akinetic) seizures (brief loss in muscle tone, usually resulting in heavy falls +/- LOC)
What are possible triggers for seizures?
missed drugs sleep deprivation alcohol exhaustion infection flickering lights
What are the differentials for seizure/epilepsy with LOC?
migraine
panic attack
syncope
NEAD (non-epileptic attack disorders)
What are the key questions to think about when investigating epilepsy?
1) where is the epilepsy arising from? = EEG
2) what is the cause of the epilepsy? = structural (CT/MRI), metabolic (bloods), infection/inflammation (bloods, CXR, CSF)
3) are the attacks truly epileptic? = ambulatory EEG, videotelemetry
What are the three types of epilepsy treatment?
1) Lifestyle
- psychosocial therapies
- avoid triggers
2) Pharmacological
- carbamazepine
lamotrigine
levetiracetam
pregablin
gabapentin
phenytoin
sodium valproate
benzos
3) Surgery
- considered if a single epiletogenic focus can be identified e.g. low grade tumour
Which AED are Na channel antagonists?
Carbamazipine
Lamotrigene
Phenytoin
Which AED are Ca channel antagonists?
Pregablin/gabapentin
Which AED are SVA2 vesicle antagonists which stops neurotransmitter release?
Levetiracetam
Which AED are GABA metabolism inhibitors?
Sodium valproate
How do benzodiazepines work?
GABA agonists, reduce post-synaptic excitability, used in epilepsy
What is status epilepticus and how is it treated?
life threatening, continuous seizures without regaining consciousness after 5+ minutes
Cruicial to recognise as rapid termination helps prevent serious brain injury
Treatment:
A-E
Bloods (FBC, coag, BM, U&E, LFT, anti-epileptic drug levels)
If seizure >5 mins: diazepam/lorazepam
If seizure >30 mins: phenytoin loading, thiamine, glucose, benzodiazepines, general anaesthetic
One the status is controlled, commence long term anti-convulsant therapy
Define a stroke, its two types:
Sudden death of brain cells (caused by hypoxia from ischaemia/haemorrhage) leading to focal neurological deficit in a defined vascular distribution
90% ischaemic = small vessel occlusion due to thrombus/embolus
10% haemorrhagic
What are the risk factors for a stroke?
HTN!!!!!! smoking PVD DM OCP hyperlipidaemia increased clotting tendancies
Describe the 4 classifications of stroke and their features:
1) TACS = total anterior circulation syndrome (ICA/prox MCA occlusion) which presents with:
- hemianopia
- hemiparesis
- higher cortical dysfunction
2) PACS = partial anterior circulation syndrome (MCA occlusion) which present with:
- 2H’s
- higher cortical dysfunction
3) POCS = posterior circulation syndrome (PCA/cerebellar communicating artery) presents with:
- isolated hemianopia
- brainstem syndrome
4) LACS = lacunar syndrome (perforating artery/small vessel damage) present as:
- pure motor/sensory stroke
What are the differentials for a stroke?
head injury hypo/perglycaemia subdural haemorrhage tumour migraine drugs encephalopathy
What is the immediate management strategy of a stroke?
Airway (if GCS < 8 = airway management) Breathing - CXR, ABG CIrculation (HR, BP, ECG?AF) IV access and bloods (FBC, U&E, coag screen, lipids) Disability (glucose) Everything else (full neuro exams)
CT head -> rule out haemorrhage! Then if ischaemic…
- if <4.5hrs since onset: tPa (alteplase), use NIHSS score, then CT 24hrs later to check there has not been any haemorrhage
- if >4.5hrs since onset, give dual antiplatelet therapoy (aspirin/clopidogrel)
Thrombectomy may be used for pts who have/have not received thrombolysis (with alteplase)
What are 5 contra-indications to thrombolysis?
pt on warfarin/doacs intracranial haemorrhage coagulopathy recent head trauma patient has severe HTN (>200mmHg systolic) history of ischamic heart disease
What is involved in the later management of a stroke?
- swallow screen within 24hrs
- try to work out the cause: 24hr ECG tape (?paroxysmal AF), carotid doppler (?stenosis), DM?, ECHO (?patent foramen ovale)
2o prevention:
- Antiplatelet/anticoagulation
- BP lowering medications
- Cholesterol lowering (statins - atorvastatin 80mg), smoking cessation, carotid revascularisation
- diet
- exercise
What is the definition of a TIA?
transient ischaemia attack
usually due to an ischaemic (embolic) event where symptoms last <24hrs (in a stroke symptoms last >24hrs)
*Prompt management is KEY as without intervention a proportion of patients will go on to develop a stroke within 1/52
What are the 4 causes of a TIA?
Atheroembolism (e.g. from carotid artery)
Cardioembolism (post MI, AF, prosthetic valve)
Hyperviscosity (myeloma, sickle cell disease)
Vasculitis (rare, non-embolic cause of TIA symptoms)
How is a TIA managed and what risk scores are used?
(same investigations as a stroke)
Usually managed in the same way as a stroke, but patient will be asymptomatic/their symptoms will have passed by the time they are in hospital
1) control RFx: BP, lipids, smoking cessation, diet
2) antiplatelet medications: aspirin, clopidogrel
3) carotid endarterectomy
ABCD2 score: calculates the risk of a stroke/CV event following a TIA
Age >60
BP >140/90
Clinical features: unilateral weakness (2)/speech disturbance (1)
Duration of symptoms: >1hr (2), 10-59mins (1)
Diabetes?
Define MS and the 4 subtypes of MS
Inflammatory plaques of demyelination in the CNS
Defined as 2 episodes of neurological dysfunction separated in time and space (>30 days apart, in multiple body sites)
May be clinical isolated (episodes of neurological dysfunction due to CNS inflammation but no radiological signs) or radiologically isolated (classical MS presentation on scans but no clinical/physical signs)
- primary progressive
- secondary progressive
- relapsing remitting
- progressive relapsing
What is the pathophysiology of MS?
cause unclear, genetics + environment (EBV, smoking, low sunlight/vit D)
leads to autoimmune mediated CNS demyelination, demyelinated areas undergo inflammation and heal poorly leading to axonal damage and loss of neurological function
What are the signs/symptoms of MS?
CNS that is affected therefore UMN signs!
Cognitive -> amnesia, poor mood, poor executive functioning
Motor -> transverse myelitis (weakness and sensory loss below level of lesion)
Sensory -> paraesthesia, reduced vibration, dyaesthesia
GI -> swallowing disorders, constipation
Eye -> optic neuritis (painful central field visual loss)
Cerebellum -> tremor, falls, limb ataxia
Bladder -> incontinence
What investigations should be carried out if MS is suspected and how is it diagnosed clinically?
Diagnosed clinically by 2 episodes of demyelination, disseminated in time and space:
Imaging
- MRI of brain/SC
Bloods
- FBC (exclude differentials like vitamin deficiencies, infections)
- TFTs
- VitB12 levels
- CSF (looks for oligoclonal Ig bands/cell count)
What are the treatments for MS?
1) lifestyle: smoking cessation, avoid stress, exercise
2) manage the acute episode: high dose STEROIDS +/- bone protection
3) Disease modifying treatment (to prevent relapses):
- Beta-interferon
- Dimethyl fumerate (reduces WCC)
- ALEmtuzumab (monoclonal AB)
- NATalizumab (monoclonal AB)
- Fingolimod (sequesters lymphocytes in LN’s to prevent them taking part in the immune response)
Define SAH and its causes
spontaneous bleeding into the subarachnoid space
can be traumatic or non-traumatic (e.g. intra-cranial aneurysm)
What is the pathophysiology of SAH?
What are the risk factors for an SAH?
80% due to aneurysm formation
20% due to neoplasia or arterio-venous malformation
aneurysm forms due to haemodynamic stress on the vessel and inflammatory changes, blood then seeps into the subarachnoid space
RFx: smoking, HTN, alcohol, FHx, ADPKD, previous aneurysm, co-arctation of aorta, CTD
What are the signs/symptoms of SAH?
thunderclap headache +/- sentinel preceeding headache N&V photophobia LOC seizures visual/speech/motor disturbances meningism
What investigations should be carried out if SAH is suspected?
Immediate CT
Bloods (FBC, coag, U&E, troponin)
ECG
LP -> only if diagnosis cannot be made from CT, and should be carried out 12hrs after the onset of headache to detect xanthochromia (yellow colour suggesting old blood present from a SAH), also red cell count of CSF
CT angiogram (would reveal any aneurysms)
Describe the WFNS grading system of SAH:
1 - GCS 15 -> no motor deficit 2 - GCS 13-14 -> no motor deficit 3 - GCS 13-14 -> motor deficit 4 - GCS 7-12 -> +/- motor deficit 5 - GCS 3-6 -> +/- motor deficit
How is SAH treated?
Aim = maintain cerebral perfusion and keep hydrated Obs: GCS, CT, pupils, BP Fluids to maintain cerebral perfusion Antiembolic stockings Nimodipine (ca channel blocker) Analgesia
Surgical options: surgical clipping (to exclude aneurysm from circulation) endovascular coil embolisation
What are the complications of SAH?
rehaemorrhage
DVT (as SAH induces a pro-thrombotic state)
Hyponatraemia
Hydrocephalus
Cardiopulmonary complications (MI, sudden arrhythmias, death)
Seizures
Delayed ischaemia
What are the red flags to check for when investigating a patient with a headache?
SNOOP-T Systemic symptoms? Neurological features? Older age of onset? Onset acute? Previous headaches? Trigger e.g. valsalva?
Describe ICP and the Monroe-Kellie hypothesis
Skull contains brain, blood and CSF
Monroe-Kellie hypothesis: an increase in 1 component leads to a decrease in one of the other 2 components
CPP = MAP - ICP
Describe a migraine and its investigation/treatment
Severe unilateral, throbbing headache Usually episodic with triggers (CHOCOLATE) - caffeine - hangovers - orgasms - cheese/chocolate - OCP - lie ins - alcohol - travel - exercise pt likes to curl up in quiet room usually: prodrome with aura (30%) = visual changes Management: - lifestyle: avoid triggers - prophylaxis: B-blockers, TCA, topiramate - during attack: analgesia, triptans, antiemetics
Describe a cluster headache and its investigation/treatment
unilateral severe pain
usually felt around the eyes with: lacrimation, conjuctivitis, rhinorrhoea, Horner’s syndrome
common in middle aged men
?stress related
S/Sx: lasts 10 mins - 1 hr, usually 1-3x a day in clusters which last weeks/months
may be early morning and awake pt from sleep
patient WILL WANT TO PACE AROUND
Management in attack:
- triptans (5-HT serotonin agonists)
- oxygen
- steroids
Preventative:
- verapamil
- steroids
Describe a tension headache and its investigation/treatment
diffuse, dull, band like headache \+/- scalp tenderness usually self-limiting aggravated by noise/light lasts hrs/days varying frequency
No abnormal physical signs
Tx: reassure patient that a sinister cause is unlikely, give analgesia/TCA’s for prophylaxis
NOTE: these headaches can be exacerbated by analgesia over-use so wean off opiates if the patient presents with analgesic/tension headache
Describe a thunderclap headache and its investigation/treatment
abrupt onset of severe headache in <5mins and lasting >1hr
SAH until proven otherwise
Described as being hit over head
