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.
Summarise Charcot-Marie-Tooth Disease
Pathophysiology: AD inherited disease affecting myelin of sensory and motor nerves
Presentation: pes cavus, inverted champagne bottle legs, loss ankle dorsiflexion + other weakness in legs and hands; hyporeflexia; hypotonia; reduced sensation
Differentials: Other neuropathies - alcohol, B12, CKD, DM, isoniazid; amiodarone; cisplatin; vasculitis
Mx: MDT: PT, OT, podiatry, ortho input
Summarise Gullian-Barre Syndrome
Pathophysiology: Acute polyneuropathy. Infection triggers (campylobacter jejuni, CMV, EBV) as immune system creates antibodies against these pathogens which also target proteins on the myelin sheaths.
Presentation: 4 weeks post infection starts. Symmetrical ascending weakness, reduced reflexes, loss sensation, can spread to CN
Ix: Brighton criteria for diagnosis - clinical. Supported by reduced signals on NCS. LP shows raised protein.
Mx: IV Ig/ plasma exchange, supportive care, VTE prophylaxis, intubate if severe
80% recover
15% left disabled
5% die (PE leading cause)
Summarise Neurofibromatosis
Pathophysiology: Inherited AD, NF1 neurofibromin protein made by mutation on chromosome 17; NF2 merlin protein, mutation chromsome 22. Make neuromas.
Presentation:
NF1 –> 6+ cafe au lait spots; Fhx; axillary freckles; bony dysplasia; Lisch nodules (yellow-brown spots on iris), glioma optic nerve, neurofibromas
NF2 –> acoustic neuromas (hearing loss, tinnitus, balance issues), schwannomas CNS
Ix: clinical criteria, genetic testing, CT lesions
Mx: symptomatic, monitor complications
Complications –> epilepsy, renal artery stenosis, LD, scoliosis, cancers, CNS tumour
Summarise Tuberous Sclerosis
Pathophysiology: Mutations in TSC genes.
Presentation: Ash leaf spots (depigmented); shagreen patches (pigmented, thickened, dimpled); angiofibroma (papules nose+cheeks); subungal fibromata (fibroma nailbed); cafe au lait spots; poliosis (patch white hair); epilepsy; LD; PKD; hamartomas.
Starts childhood usually.
Mx: supportive
Summarise tension headaches
Presentation: tight band across forehead, associated with stress/ depression/ alcohol/ dehydration
Mx: reassure, analgesia, relax, hot towels
Summarise sinusitis
Presentation: inflammation over ethmoid/ maxillary/ frontal/ sphenois sinuses . Tender over these. Mostly viral. Can irrigate with saline or use steroid nasal spray. Only use abx if suspect bacterial.
Summarise Migraines
Presentation: moderate to severe pain lasting 4-72 hrs; throbbing; unilateral; photo/phonophobia; aura (visual, hemiplegic); N+V
Triggers: stress, chocolate, cheese, caffeine, smells, lights, dehydration, menstruation, poor sleep, trauma
Mx:
Triptans (5HT R agonists) as soon as migraine starts; NSAIDs; antiemetics.
Prophylaxis: Propranolol, topiramate, amitrptyline
Acupuncture
Summarise Cluster headaches
Presentation: Classically 30-50 yr male smoker. Severe unilateral headache occuring in clusters of attacks, lasting 15m to 3hrs. Eyes are red and swollen with miosis, ptosis, nasal discharge and sweating.
Mx:
Acute - triptans SC, high flow oxygen 15-20 mins
Prophylaxis: verapamil, lithium, prednisolone
Summarise syncope
Pathophysiology: vagus nerve recieves strong stimuli e.g. pain/ emotions –> parasympathetic NS –> relaxation SM in blood vessels –> hypoperfusion brain tissue —> LOC and fall to reperfuse brain
Presentation: Prodrome ( hot, sweaty, dizzy, vision blurred, headache), unconscious few seconds and may twitch. Groggy after but not as severe as postictal. May be incontinent.
Causes:
Primary: dehydrated, standing in warmth, pain, blood
secondary: hypo, anaemia, infection, anaphylaxis, arrthymia, valvular, HOCM
Ix:
OE: injuries? illnesses? Neuro sx? Cardiac sx? Postual hypotension?
ECG, Echo, Bloods
Mx: address cause
Summarise febrile convulsions
Definition: Occur between 6m and 5 yrs with high fever
Presenation: Typically 2-5 mins tonic clonic seizure with fever, but may last longer and be a partial seizure
Mx: Paracetamol
After first episode advise parents to put child in recovery position and call ambulance if >5 mins
More likely to go onto develop epilepsy
Summarise hydrocephalus
Pathophysiology: CSF build up due to over-production/ poor drainage. CSF is created in the choriod plexus in the ventricles and is reabsorbed by the arachnoid granulations.
Causes: congenital cerebral aqueduct stenosis, arnold-chiari malformations, arachnoid cysts
Presentation: as cranial bones don’t fuse at the sutures until 2yrs will have large forehead from pressure on cranial bones; bulging fontanelle; poor tone; FTT
Mx: Shunt (drain CSF from ventricles into peritoneal cavity)
Summarise Plagiocephaly and Brachycephaly
Pathophysiology: Abnormal head shapes. Plagio = flattening one bit of head
Brachy = flat back of head
Cause: Baby spending lots of time in one position –> skull bones and sutures mould with gravity
Mx: Exclude craniosynotosis, look for congenital muscular torticollis, advise change in positioning
Summarise Spinal Muscular Atrophy
Pathophysiology: AR condition causing progressive loss of LMN.
Presentation: age onset and prognosis depends on type. Weakness. LMN signs (fasiculations, wasting, hypotonia and reflexia)
Mx: MDT, PT, NIV, PEG feding
Summarise Craniosynostosis
Pathophysiology: skull sutures close prematurely –> abnormal shaped head and raised ICP
Presentation:
Depends on site of the affected suture to the abnormal shape. Small head in proportion to body, fontanelle closure <1 yr
Ix: XR, CT
Mx: Monitoring with potential surgical reconstruction
Summarise muscular dystrophy
Presentation: Proximal muscle weakness, Gower’s sign
Duchennes: X-linked recessive, defective gene for dystrophin. Progressive.
Beckers: less severe version Duchenne’s
Myotonic dystrophy: prolonged muscle contraction e.g. can’t let go after shaking a hand
Mx: MDT, steroids, creatinine supplements
Summarise cerebral palsy
Definition: Permanenet neurological damage due to issues at birth.
Causes: Infections (ante and postnatal); trauma; birth asphyxia; prematurity
Types: Spastic/ pyramidal: hypertonia (UMN) Dyskinetic/ athetoid/ extrapyramidal: hyper + hypotonia; athetoid movements; oro-motor issues (basal ganglia) Ataxia (cerebellar) Mixed
Patters:
Monoplegia/ hemiplegia (unilat)/ diplegia (all, legs>arms)/ quadriplegia (all, severe)
Presentation:
Failure to meet milestones; abnormal tone; hand preference <18m; coordination/ speech issues; feeding issues; LD
Mx: MDT, baclofen for spasticity
Summarise strabismus
Strabismus: eyes are misaligned Ambylopia: affected eye becomes passive compared to other eye esotropia: inwards eye Exotropia: outwards eye Hypertropia: upwards eye Hypotropia: downwards eye
Causes: Idiopathic, hydrocephalus, CP. SOL, trauma, paralytic
O/E: Fundoscopy for retinoblastoma, acuity, eye movements. Hirschberg’s test shows if is a pseusostrabismus by looking at corneal reflection to see if central and symmetrical.
Mx: Treat early so doesn’t become permanent. Eye patch/ atropine to cover good eye, refractive errors correct with glasses
Summarise Meningitis
Pathophysiology: inflammed meninges, most commonly n.meningidis (gram negative diplococci). Meningococcal septicaemia = infection in blood stream –> non-blanching rash via DIC. Most common cause in neonates = GBS
Presentation: Usually young, stiff neck, headache, N+V, fever, malaise, non-blanching rash, bulging fontanelle, poor feeding, hypotonia, Brudzinski’s sign (flex neck to chest –> flex hips and knees), kernigs sign (straighten knee with hip at 90 degrees –> spinal pain)
Ix:
LP-
Bacterial: cloudy, high protein, low glucose, high neutrophils, culture +ve
Viral: normal protein and glucose, high lymphocytes
Blood with PCR
HIV test in encephalitis
Mx: Cefotaxime + amoxicillin for listeria if <3m Ceftriaxone older Aciclovir is viral Notifiable disease Dexamethasone to stop hearing loss Ciprofloxacin for prophylaxis
Complications:
Hearing loss, seizures, LD, memory loss, neuro deficits
Summarise Brown Sequard Syndrome
Causes: Trauma, tumour, infection, inflammation or vascular event in spinal arteries leading to hemisection spinal cord
Pathophysiology: Pain and temperature = spinothalamic tract which decussate in the spinal tract.
Proprioception and light touch = dorsal columns which decussate in the medulla.
Corticospinal = motor neurones and decussates in the medulla.
Presentation: Ipsilateral loss proprioception and light touch + weakness, contralateral loss pain and temperature.
