Neurology Flashcards
Epilepsy and features of seizures
= recurrent tendency to spontaneous intermittent abnormal electrical activity in the brain, manifesting as seizures
- 2/3rds idiopathic
- otherwise - SOL, stroke, cortical scarring
- in first seizure, need 2week referral to specialist
- only withdraw drugs once seizure free for 2years
- must contact DVLA and avoid driving until 1yr seizure free
- prodrome (hours/days preceding, of change in mood or behaviour)
- aura (implies focal seizure from temporal lobe, deja vu / strange smells / flashing lights)
- seizure (various, be aware for tongue biting and incontinence)
- post-ictal (headache, confusion, myalgia, temporary weakness (Todd’s palsy) for hours after)
Types of seizures
Generalised seizures (no localising features to a single hemisphere)
- absence - <10s pauses, presents in childhood
- tonic-clonic - LOC, stiffening and jerking, with post-ictal phase. EEG shows bisynchronous epileptiform activity in both hemispheres.
- myoclonic - sudden jerk of limb
- atonic - sudden fall, no LOC
- –> give sodium valproate first line, then lamotrigine
Focal/partial seizures (originating in networks linked to one hemisphere)
- without impaired consciousness (simple) - just focal motor/sensory/autonomic/psychic symptoms
- with impaired consciousness (complex) - commonly from temporal lobe with post-ictal confusion
- in 2/3rds, evolves to GTCS when electrical disturbance spreads
- –> give carbamazepine or lamotrigine first line, then other
Febrile seizures (not epilepsy!) - age 3mo-5yrs, where high fever but no evidence of intracranial infection or defined cause - self-limiting
Status epilepticus
- life threatening!
- where >30mins of continuous seizure, or repetitive seizures without regaining consciousness
- need multiple drugs (IV lorazepam / buccal midazolam, phenytoin infusions, ICU intervention)
Localising features of focal seizures
Temporal lobe
- automatisms (lip smacking, chewing, swallowing) or manual movements (grabbing, fiddling), or complex actions
- dysphasia
- deja vu or jamais vu
- emotional disturbance
- sensory hallucinations
- delusional behaviour
Frontal lobe
- motor (posturing/peddling legs)
- Jacksonian march
- behavioural disturbance (psychogenic)
Parietal lobe
- sensory (tingling, numbness, pain)
- motor
Occipital lobe
- visual spots, lines, flashes
Parkinson’s disease
= loss of dopaminergic neurons in substantia nigra, Lewy bodies in basal ganglia, brain stem and cortex
- 90% idiopathic, 10% mutations in PARK genes so dysregulated alpha synuclein (familial)
Extrapyramidal triad:
- bradykinesia (slow to initiate, decrease amplitude in repetition, shuffling gait with reduced arm swing, expressionless face)
- rigidity (cogwheel, in rapid pronation/supination)
- tremor (worse at rest, pill-rolling)
+ non-motor symptoms: autonomic dysfunction (postural hypotension, constipation, dribbling, urinary frequency); sleep disturbance; change in sense of smell; depression / dementia / psychosis
= overall, reduced voluntary movements and increased involuntary movements
- signs ALWAYS worse on one side, if not then another cause (MRI)
Parkinson’s disease management
- for symptom control only, no slowing disease progression
1st line
- physical activity encouraged
- levodopa - dopamine precursor which can cross BBB (dopamine can’t)
- carbidopa - dopa decarboxylase inhibitor given alongside levodopa to prevent conversion to dopamine in periphery
- – beware therapy reduces effectiveness with time, so don’t start too early (when >70yrs or serious interference with life)
- – never withdraw suddenly
2nd line
- anticholinergics eg procylidine
Surgery
- to ablate problematic areas of brain tissue
- or to deep brain stimulation into subthalamic nucleus
Multiple sclerosis
= inflammatory plaques of demyelination in CNS, disseminated in space and time (multiple sites, with >30d between attacks)
- classic in 20-40yo white women, 1st presentation with temporary unilateral optic neuritis (pain and loss of vision)
- autoimmune, so fhx and HLA-DRB1 allele are risk factors
Episodic symptoms, on background of progressive deterioration
- motor - spastic weakness, myelitis
- cerebellar - DANISH P
- sensory - dyaesthesia, pins and needles, reduced vibration sense, trigeminal neuralgia
- sexual/GU - erectile dysfunction, anorgasmia, urinary retention
- GI - swallowing disorder, constipation
- eye - diplopia, hemianopia, optic neuritis, visual phenomena, pupil defects
Ix
- clinical diagnosis (McDonald criteria)
- MRI for white matter tract lesions
- CSF - oligoclonal bands (IgG, so CNS autoimmunity), lymphocytosis, raised protein
- neurophysiology
Mx
- lifestyle - exercise, stop smoking, lower stress
- steroids for flare ups (no more than 3 per year)
- disease modifying drugs - dimethyl fumarate, alemtuzumab for relapsing-remitting
- gabapentin for spasticity, botulinum toxin for tremor, self-catheterisation etc in symptom control
Space occupying lesion
- present with signs of raised ICP usually (+ focal neurology, seizures and personality change)
- primary or metastatic tumour
- aneurysm
- abscess (following local infection eg otitis media/dental abscess)
- chronic subdural haematoma
- granuloma
- cyst
Ix
- CT ± MRI
- biopsy?
- no LP until after imaging, as in raised ICP risk coning
Signs of symptoms of raised ICP
Early
- headache
- vomiting
- papilloedema
Late - pupillary constriction then dilation - abducens palsy - occipital infarction - hemiparesis - raised BP, low HR (causes false localising signs)
Dementia types
Alzheimer’s most common
- neurofibrillary tangles of hyperphosphorylated Tau and amyloid plaques resulting in gradual decline in cognition
Vascular dementia
- arteriosclerosis and atherosclerosis cause white matter hypoperfusion and demyelination. Sudden onset, stepwise deterioration.
Dementia with lewy bodies
- alpha synuclein destroys neurones in cortex, causing gradual decline in cognition and often visual hallucinations (like Parkinson’s, but first in cortex then in basal ganglia. In late stages of both diseases look the same.)
Frontotemporal dementia
- frontal and temporal atrophy, causing executive impairment, behaviour/personality change, disinhibition, hyperorality
Alzheimer’s disease
- neurone death after deposition of beta amyloid and hyperphosphorylated Tau tangles
- common - 5% of over 65s
- disease process starts 20yrs pre diagnosis
1st - cognitive - memory (short term), understanding, language, anosmia ± aphasia / apraxia / agnosia
2nd - ADLs - loss of functional independence (1yr after diagnosis)
3rd - behavioural - depression, paranoia, aggression, wandering, auditory hallucinations (2yrs after)
Death - 3-10yrs after diagnosis
RFs
- ApoE4
- age
- Fhx
- Downs syndrome
- cerebrovascular disease
- hyperlipidaemia
- smoking, obesity, high sat fats diet
Ix
- AMTS, MOCA
- CT (exclude SOL)
- MRI (atrophy in late stage)
Mx
- home safety and evaluation with OT, ID bracelets, carer, cognitive exercises
- acetylcholinesterase inhibitors eg donepezil, rivastigmine
- BP control
- antidepressants / antipsychotics
Diabetic neuropathy
- complication of T1 or T2DM (more likely if onset early in life, tall stature, HTN), in 50% of diabetics
- as neurones are damaged by excess uptake of glucose
50% asymptomatic
- or peripheral pain, loss of sensation (glove and stocking often, can be in other patterns), dyaesthesia, reduced ankle reflexes, painless injuries/ulcers
+ urinary symptoms and ED (autonomic damage)
Ix
- clinical diagnosis (sensation, reflexes)
- fasting blood glucose
- HbA1c
- nerve conduction studies
- nerve biopsies
Mx
- glycaemic control
- advice re checking feet for injury
- in pain - pregabalin, gabapentin, opioid, topical capsaicin, TENS machine
- bethanechol for bladder dysfunction
- sildenafil for ED
Cervical spondylosis
= degeneration of spinal column, from any cause (usually OA)
- in 80% of over 60s
- mechanical neck and shoulder pain, exacerbated by movement, headaches, radiculopathy in specific roots
- red flags if paraesthesia, heaviness in arms or legs, lack of coordination
Ix
- Xray, CT, MRI (if suspicious symptoms)
- electromyogram, nerve conduction study
Mx
- physio, exercise
- analgesia, NSAIDs
- muscle relaxants
- steroid injections
- surgery if prolapsed disc or spinal cord symptoms
Haemorrhagic stroke
15-20% of strokes
- rupture of vessel (intraparenchymal / subarachnoid / intracerebral)
- if secondary, then underlying anomali
RFs
- HTN
- male, age, fhx
- haemophilia, cerebral amyloid angiopathy, vascular malformation
- anticoagulation
Ix
- CT head (hyper dense where bleed)
- PT, aPTT (exclude coagulopathy)
- BM, TFTs (stroke mimics)
- urgent review by neurosurgeons
- control BP to 120mmHg
- stop all anticoagulation
Ischaemic stroke
80-85% strokes
- embolic cause (AF) - more sudden onset
- thrombolic cause - crescendo symptoms
- pathology is primary vascular, cardiac, or haematological
- if young, think vasculitis, carotid dissection, thrombophilia syndromes
RFs
- age, fhx
- HTN, smoking, DM
- AF, IHD, PVD, carotid artery stenosis, sickle cell disease
Ix
- CT head (late, see hypo-attenuation)
- PT, aPTT (exclude coagulopathy)
- ECG (AF)
- BM, TFTs (stroke mimics
- carotid USS (embolic plaques)
Mx
- rule out haemorrhage by CT!
- thrombolysis with alteplase (if <4.5 hours, no recent stroke or surgery / on warfarin)
- thombectomy if <12 hours and day time hours at centre (± carotid endarterectomy if at fault)
- aspirin 300mg 7days, aspirin/clopidogrel 75mg for life
- initially don’t worry about HTN and use BP meds yet
- swallow assessment
- RF modification - HTN, statins
Bamford classification of stroke
Total anterior circulation stroke, TACS
- need all three of:
- unilateral weakness ± sensory deficit, of face arm and leg
- homonymous hemianopia
- higher cerebral dysfunction (dysphasia, visuospatial disorder, inattention etc)
Partial anterior circulation stroke, PACS
- need 2/3 of above
Posterior circulation syndrome, POCS
- need one of:
- cranial nerve palse + contralateral motor/sensory deficit
- bilateral sensory/motor deficit
- conjugate eye movement disorder
- cerebellar dysfunction
- homonymous hemianopia
Lacunar syndrome, LACS
- need one of:
- pure sensory stroke
- pure motor stroke
- sensory-motor stroke
- ataxic hemiparesis
Transient ischaemic attack
= symptoms of <24 hrs
- without intervention, ~8% patients will go onto have a stroke within a week
- same RFs and causes of ischaemic stroke
Ix
- CT head (normal)
- bloods (normal)
- carotid doppler ± angiography
Mx
- lifestyle
- optimise BP, DM, lipids
- aspirin 300mg 2 weeks, then clopidogrel 75mg
- no driving for >1mo
Delirium
= acute confusional state, organically caused decline from baseline in mental functioning
Features: - impaired perception, cognition and consciousness - onset hours-days - marked memory deficit - disordered thinking - reversed sleep/wake cycle Hyperactive, hypoactive or mixed
Causes Pain Infection Nutrition Constipation Hydration Medication Environment
Ix
- looking for cause - bloods, urinalysis, CXR, ECG, ABG, LP
Meningitis
Causes
- usually meningococcus (N meningitidis) / pneumococcus
- can be H influenzae, Listeria monocytogenes, viruses, TB (aseptic, clear LP)
Features
- early - headache, fever, myalgia
- late - meningism (neck stiffness, photophobia, Kernig’s sign), low GCS, seizures, petechial non-blanching rash
Ix and Mx
- if raised ICP, ICU input
- blood cultures 1st
- then LP (if not in shock / no rash)
- early abx - ceftriaxone IV (+ amoxicillin if immunocompromised / older)
- dexamethasone if meningism
Subarachnoid haemorrhage
- sudden onset 10/10 thunderclap (occipital) headache
- often followed by vomiting, collapse, seizures, reduced consciousness (sudden rise in ICP)
Causes
- 80% berry aneurysm rupture
- trauma
- arterio-venous malformations
- encephalitis, vasculitis, tumour, idiopathic
- increased risk when HTN, smoking, fhx, polycystic kidneys, aortic coarctation, Ehlers-Danlos syndrome
Ix
- CT head (hyperdense)
- LP if clear CT, done >12hr after headache (xanthochromia)
- bloods - clotting, troponin
- ECG
Mx
- A-E
- surgical clipping or coil embolisation
Encephalitis
- bizarre encephalopathic behaviour
- reduced GCS
- fever
- headache
- focal neurological signs
- seizures
- hx of travel or animal bite
Causes
- viral - HSV1+2, arboviruses, CMV, EBV, VZV, HIV, measles, mumps etc
- non-viral - bacterial meningitis, TB, malaria, listeria
- if no infectious prodrome, think encephalopathy (hypoglycaemia, hepatic, DKA, drugs, hypoxia, Wernicke’s, SLE)
Ix
- bloods - cultures, viral PCR
- contrast CT (see focal bilateral temporal lobe involvement in HSV)
- LP (only after CT, see raised CSF protein and lymphocytes, low glucose, send for viral PCR)
- EEG
Mx
- aciclovir within 30min presentation, for 2 weeks
- supportive
- symptomatic eg phenytoin for seizures
Cerebral abscess
= collection of microbes and dead neutrophils in a capsule of glial cells within brain parenchyma
- suspect when raised ICP, especially with fever and raised WCC
- seizures, fever, localising signs, raised ICP, coma
- following ear / sinus / dental infection; skull #; endocarditis; bronchiectasis
Ix
- CT/MRI (ring-enhancing lesion)
- bloods
- biopsy
Mx
- neurosurgery referral
- abx - vancomycin, metronidazole, ceftriaxone
Raised intracranial pressure
- should be 7-15mmHg for a supine adult
Features
- Cushing’s triad - raised BP, low pulse, low resps (opposite of shock)
- early - early morning headache, papilloedema, vomiting, drowsiness
- late - fixed dilated pupil, occipital infarction, hemiparesis, HTN, pulmonary oedema
Causes
- oedema
- hydrocephalus
- haemorrhage
- SOL
- idiopathic cerebral hypertension
- infection
Ix
- fundoscopy
- CT head
- bloods, any infectious source
- LP if safe, opening pressure
Mx
- sit upright, hyperventilate (so cerebral vasoconstriction)
- osmotic agent eg mannitol to diurise
- treat cause (steroids if tumour)
