Neuro Flashcards
Summarise stroke and TIA
Pathophysiology: ischaemia or haemorrhage disrupting blood supply.
TIA = transient neurological dysfunction secondary to ischaemia without infarction
Bamford-Oxford Class- Total ACA: Have all 3: 1. Unilateral weakness/ sensory deficit face/ arm/ leg, 2. homo hemi, 3. dysphasia/ visuospatial issues
Partial ACA: 2/3 above
PCA: 1 of: Cranial nerve palsy + contralateral motor/ sensory deficiy; bilateral motor/ sensory deficit; eye movement disorder; cerebellar dysfunction; homo hemi
Lacunar: Pure sensory/ motor/ sensori-motor, ataxic hemiparesis
RF: CVD/ PVD, previous stroke, AF, carotid artery disease, COCP
Ix: CT brain to exclude haemorrhage
Mx:
Admit, exclude hypoglycaemia, 300mg aspirin post CT, alteplase (thombolysis) in 4.5 hrs, thrombectomy offered potentially depending on time and location
TIA: aspirin, secondary prevention at TIA clinic (statin, clopidogrel, carotid endartectomy, htn, DM control)
Summarise ICH
RF: head injury, aneurysms, tumours, anticoagulants
Presentation: Headache, seizures, weakness, vomiting, LOC, neuro sx
Extradural: Middle meningeal artery in temporo-arietal region, between skull and dura mater at pterion, on CT had a lens shape and doesnt cross cranial sutures. Often initially improve and then worsen.
Subdural: rupture bridging veins, occuring between dura and arachnoid. Has a crescent shape and can cross suture lines. More frequent in elderly or alcoholics.
Ix: CT head (shape, midline shift, ventricular compression), FBC, clotting
Mx: Admit, discuss neurosurgery, intubate if GCS <8, correct clotting abnormalities, correct hypertension
CT guidelines:
Urgent if: GCS <13; open or depressed skull #, basal skull #; seizure; focl neuro deficit; 1+ vomit
Within 8hrs + LOC/ amnesia: >65; bleeding/ clotting disorders; dangerous mechanism of injury
Summarise subarachnoid haemorrhage
Pathophysiology: Bleeding occurs into the subarachnoid space where the CSF is located. Usually due to berry aneurysm in circle of willis.
Presentation: thunderclap headache during strenuous activity, neck stiff, photophobia, visual changes, focal neurology
RF: htn, smoking, alcohol excess, cocaine, fhx, black, female, SCD, connective tissue disorders, ADPKD, neurofibroma
Ix: CT head first line where will see hyperattenuation subarachnoid. Blood will be in interhem spheric fissure, basalcisterns and ventricles.
LP if CT negative - xanthochromia. Angio once confirm diagnosis to find source of bleeding
Mx: neurosurgery - coiling/ clipping, nimodipine to prevent vasospasm
Summarise multiple sclerosis
Pathophysiology: Demyelination of the neurones in CNS via autoummune inflammation. At first re-myelination occurs but later on it stops.
RF: genetics, EBV, low vitamin D, smoking, obesity, young, woman
Presentation: Sx generally last days to weeks, optic neuritis is often first. Central scotoma. This is an enlarged blind spot.
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect. Weakness, incontinence, trigeminal neuralgia, numbness, paraesthesia, lhermittes sign upon neck flexion, ataxia
Types: relapse-remit, secondary progress (relapse-remit becomes progression with no remission), primary progressive
Ix: MRI, shows periventricular lesions. LP shows oligoclonal bands. Macdonalds criteria
Mx: MDT, relapse treated with methylprednisolone, exercise, mx neuropathic pain, depression, urge incontinence, spasticity, Interferon beta preventative
Summarise MND
Pathophysiology: Progressive, fatal condition affecting upper and lower motor neurones. ALS is most common, progressive bulbar palsy affects swallowing and talking.
Presentation: usually middle aged man with possible affected relative., progressive weakness, usually starting in upper limbs, fatigue, clumsy, drop things/ trip over, dysarthria .
Mix UMN and LMN signs.
Ix: clinical diagnosis
Mx: riluzole slows progression, NIV, MDT, end of life care planning
Summarise PD
Pathophysiology: Reduction of dopamine in the substantia nigra basal ganglia (controls co-irdinating habitual/ voluntary/ patterned movements.)
TRIAD of bradykinesia, resting tremor and rigidity
Presentation: Typically older man, unilateral pill rolling tremor which worsens with distraction; cogwheel rigidity (gives ways in little jerks); smaller handwriting; shuffling gait; difficulty initiating movement; difficulty turning; reduced facial movements; depression; insomnia; postural instability; anosmia; dementia
Ix: Made based on sx - Parkinson’s disease society have criteria
Mx:
Levodopa + drug that stop levodopa being broken down before it gets to the brain e.g. co-benyldopa or co-careldopa
SE: dystonia, chorea, athetosis
Dopamine agonists e.g. cabergoline
SE: pulmonary fibrosis
Monoamine Oxidase B inhibitors (inhibit enzymes that break down dopamine) e.g. selegiline
COMT inhibitor eg entacapone prolongs levodopa effect
Summarise Parkinson’s plus syndromes
Multiple system atrophy –> degeration neurones, leads to parkinsonisms, cerebellar dysfunction and autonomic dysfunction e.g. sweating, ED, consipated
Dementia with lewy bodies –> visual hallucinations, delusions, dementia first feature
(Progressive supranuclear palsy and corticobasal degeration)
Summarise benign essential tremors
RF: age and fhx
Presentation: Older, fine tremor, symmetrical, worse on voluntary movement, with stress/ tiredness/ coffee, better with alcohol, not there during sleep.
May also affect other areas e.g. head, jaw, vocal cords
Differentials: PD, MS, huntingtons, hyperthyroid, fever, antipsychotics or other drugs
Mx: improve sx with propranolol or primidone
Summarise epilepsy
Pathophysiology: Tendency to have seizures (abnormal electrical activity in the brain)
Types:
Generalised:
Tonic clinic - LOC, musles tense and jerk. Assocaited tongue biting, incontinence, groaning, irregular breathing. Post-ictal period is confusing,
Absence - become blank and unaware lasting ~10-20s
Atonic seizures/ drop attacks - more common in childhood, may indicate lennox-gastaut syndrome
Myoclonic - brief muscle contractions, more common in childhood
Infantile spasm - aka West syndrome, starts around 6m. Treat with prednisolone.
Focal:
Simple Temporal lobe - hallucinationsm flashbacks, deja vu, have consciousness
Complex partial - automatisms, impaired awareness
Ix: electroencephalogram; MRI
Mx:
Generalised: sodium valproate (ethosuximide in absence) –> lamotrigine/ carbamazepine
Focal: carbamazepine/ lamotrigine –> sodium valproate/ levetiracetam
Status epilpeticus: seizure lasting >5 mins or >3 in 1hr
Mx –> ABCDE; secure airway, give oxygen, check glucose, IV lorazepam 4mg x2 -> IV phenytoin (in community buccal midazolam/ rectal diazepam)
Summarise neuropathic pain
Causes: postherpetic neuralgia from shingles; post-surgery, MS, diabetic neuralgia, trigeminal neuralgia, CRPS
Presentation: burning, tingling, paraesthesia, electric shocks, loss sensation
Mx:
1) Amitriptyline, duloxetine, gabaoentin, pregabalin, (carbamazepine in trigeminal neuralgia)
2) Tramadol as rescue in short-term, PT, CBT
Summarise facial nerve palsies
Pathophysiology: Facial nerve exits brainstem at the cerebellopontine angle, passing through the temporal bone and parotic gland. It supplies motor function to various muscles of the face, neck and stapedius. It provides sensory fibres to the anterior 2/3rds of the tongue and parasympathetic supply to the submandibular/ SL salivary glands + lacrimal gland. As the forehead is supplied by UMN on both sides, in a stroke the forehead is spared but not in a LMN lesion.
Causes:
Bell’s Palsy: idiopathic, treated with prednisolone if present with 72 hrs of sx starting. Lubricate eyes.
Ramsay-Hunt syndrome: VZV causes vesicular rash in ear canal, pinna and along CN 7 distribution. Treat with prednislone, aciclovir and lubricate eyes.
Other: infections (e.g. otitis media, HIV); systemic (e.g. sarcoidosis, MS, GBS, DM), tumours (e.g. parotid tumour, acoustic neuroma); trauma
Summarise brain tumours
Presentation: Focal neurological sx which depend on location, raised ICP (papilloedema, headache worse on waking and with straining, vomiting, seizures, visual field defects, 3+6 nerve palsies)
Types:
Most common = mets from lung/ breast/ RCC/ melanoma
Glioma: glioblastoma most malignant
Meningioma: usually benign
Pituitary: bitemporal heminopia, release excess hormones
Acoustic neuroma: hearing loss, tinnitus, balance issues, associated NF2
Mx: Surgery dependent on grade; palliation; chemo; radio
Summarise Huntington’s
Pathophysiology: AD inheritance of a mutation of CAG gene on chromosome 4 with anticipation occuring.
Presentation: 30-50 yrs, insidiuous, progressive, usually starts with cognitive/ psychiatric issues –> chorea, eye movement disorders, dysarthria, dysphagia
Ix: Genetic testing
Mx: MDT, SALT, genetic counselling, end of life planning, symptomatic (Antipsychotics, benzos, dopamine-depleting agents, SSRIs)
Summarise Myasthenia Gravis
Pathophysiology: Autoimmune destruction via antibodies (muscle-specific kinase and low-density receptor related protein) which attack the acetycholine receptors at the neuromuscular junctions. Linked to thymomas.
Presentation: fatigueability, most affecting proximal muscles and small muscle of head–> diplopia, ptosis, difficulty swallowing, jaw fatigue, slurred speech, weakness with repetition of movement O/E. FVC reduced.
Ix: ACh-R Ab, MRI thymus, edrophonium test
Mx: acetylcholinesterase inhibitors (pyridostigmine/ neostigmine); steroids to suppress Ab production; thymectomy; monoclonal Ab
Myasthenic crisis –> ABCDE; BiPAP; intubation; IV Ig; plasma exchange
Summarise Lamert Eaton Syndrome
Pathophysiology: Typically from small cell lung cancer as antibodies are made by the immune system to shut down the voltage-gate Ca channels in the cancer which also damage acetylcholine release in NMJ
Presentation: Proximal/ intraocular/ levator/ oropharyngeal weakness, autonomic dysfunction. Reduced reflexes O/E
Mx: investigate and treat lung cancer, amifampridine allows more Ach release. Steroids, IV Ig, plasma exchange.
