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ABCD score in TIA| stroke guidelines | MMSE | GCA | Coma evaluation

ABCD score in TIA

Src:Rothwell'05/30, Lancet (PMID=15993230)

A=age[yr]>=60: 1

B=BP[mmHg]>140 and/or DBP>=90: 1

C=Clin feat: unilat weakn: 2; speech disturb w/o weakn: 1, other: 0

D=Duration[min]: >=60: 2, 10-59: 1, <10: 0

Score predicts 7-day risk of stroke (95% of all strokes occur with scores 5-6):

6: 31%; 5: 12%; 0-4: <1%

Stroke guidelines

http://www.rcplondon.ac.uk/pubs/books/stroke/stroke_conciseguide_2ed.pdf

TIA: clinic <=7/7, if likely TIA: Aspirin 300 od (or other antiplatelet), hospital if >1 TIA / 7d

Urgent CT if: bleeding diathesis, dcrd GCS, unexplained progressive/fluctuating symptoms, papilloedema/meningism/fever, severe HA at onset, indications for thrombolysis or early anticoagulation

PROGRESS trial

http://www.ncbi.nlm.nih.gov/pubmed/12958329

Fransen(2003)Stroke(12958329): Effects of a perindopril-based blood pressure-lowering regimen on disability and dependency in 6105 patients with cerebrovascular disease: a randomized controlled trial.

BACKGROUND AND PURPOSE: We sought to quantify the effects of blood pressure lowering on long-term disability and dependency among patients with cerebrovascular disease. METHODS: We performed a randomized, double-blind, placebo-controlled trial. A total of 6105 participants with a history of stroke or transient ischemic attack in the past 5 years were recruited from 172 hospital outpatient clinics in 10 countries. Subjects were randomly assigned to the following groups: active treatment (angiotensin-converting enzyme inhibitor perindopril [4 mg/d] for all patients, with the diuretic indapamide added at the discretion of treating physicians) or matching placebo(s). Measurements were disability (defined as a Barthel Index score < or =99/100) and dependency (a positive response to the following question: "In the last 2 weeks has the patient required regular help with everyday activities?"). RESULTS: The median duration of follow-up was 4 years. At the last available assessment, 19% of the active treatment group and 22% of the placebo group were disabled (adjusted odds ratio, 0.76; 95% CI, 0.65 to 0.89; P<0.001). Twelve percent of the active treatment group and 14% of the placebo group were dependent (adjusted odds ratio, 0.84; 95% CI, 0.71 to 0.99; P=0.04). The effects of treatment appeared to be mediated primarily through the prevention of disability and dependency associated with recurrent stroke. Four-year treatment with the study drug regimen would be expected to result in the avoidance of 1 case of long-term disability for every 30 (95% CI, 19 to 79) patients. CONCLUSIONS: Among individuals with cerebrovascular disease, a perindopril-based blood pressure-lowering regimen not only reduced the risk of stroke and major vascular events but also substantially reduced the risks of associated long-term disability and dependency. 

Antithrombotic therapy [ JBS-2'05: www ]

CAD/PAD: Aspirin [/Clopidogrel] 75 od for life

Cerebral infarct/TIA (non-haemorrhagic cerebrovasc dis): if SR Asp [/Clopidogrel if Asp contraind; or if further events on Asp] 75-150 od + Dipyridamol MR 200 bd for 2 years; consider Anticoag if moderate risk (aged 60-75 w/o additional RF) or hi risk (age>75, or >60 with additional RF: Htn, DM, LV dysfx)

W/o established CVD: aged>50 with CVD risk>=20%, or if DM and {>=50y | DM duration>10y | antihypertensive treatment} once BP<150/90

Mini Mental State Examination

http://www.medicaleducation.co.uk/resources/Miniment.pdf

Coma: Evaluation [postgradmed]

  • Coma: due to

(1) diffuse insult to both hemispheres
(2) focal ARAS lesion (upper pons, midbrain, diencephalon)

(1) structural/surgical
(2) metabolic/medical

  • Most common causes

(1) Stroke
(2) cran trauma
(3) intoxication

  • Hx & Exam

(1) respir pattern
(2) pupillary responses
(3) eye movements
(4) motor responses

  • 1) Respiratory pattern:

Cheyne-Stokes breathing: usu. bilat. or diencephalic insult; may signify impending herniation from unilateral mass lesion; central neurogenic hyperventilation (RR 40-70): usu lesions central tegumentum of pons; apneustic breathing: dorsolat. lower half of pons; cluster breathing: high medullar damage; ataxic breathing: medullary (usu preterminal)

  • 2) Pupillary responses:

bilat. reactivesymmetrical: almost always metabolic/medical coma [exception: cerebell haemorrh]; unreactive, unequal, dilated pupil: possible uncus herniation (part of temp lobe)=neurosurg emergency [DD: expanding PCA aneurysm]; pinpoint pupils: pontine lesions [pontine haemorrhage, large brainstem/pontine infarction]

  • 3) Eye movements:

1) resting position: if dysconjugate in horizontal plane ["skew" deviation]: usu brainstem lesion; 2) spontaneous eye movements: roving, slow, conjugate lat. to-and-fro movements: usu. metabolic cause, or bilat lesions above brainstem; paralysis of spontaneous and reflex lat. eye movements: usu pontine lesion; ocular dipping: often diffuse cerebral damage; 3) reflex eye movements (oculocephalic reflex, "doll's eyes"): absent in brainstem dysfx; use 50mL ice water if unstable neck: eyes deviate to cold ear

  • 4) Motor responses:

absent spontaneous movements on one side only: contralat. hemispheric or brainstem lesion; decorticate posturing (flexed elbows and wrists, adducted shoulder, extended legs): lesion above brainstem; decerebrate posturing (internal rotation and adduction of shoulder, extension of wrists, elbows and legs): usu. bilat. midbrain/pontine lesion (red nucleus), occas. metabolic (e.g. hypoglycaemia); cortical reflex myoclonus: with anoxic injuries or metabolic encephalopathies (eg HE); rhythmic myoclonus: brainstem injury

  • Immediate Ix and Treatment:

(1) if lo BG: iv Dextrose + thiamine

(2) if narcotic OD: iv naloxone; benzodiazepine OD: flumazenil [if not epileptic]

  • Investigations:

(1) U&Es, LFTs, FBC, PT, aPTT, +- ABG, +- alcohol level & urine drug screen

(2) arterial ammonia, TFT, cortisol

(3) CT head; LP

(4) EEG (non-convulsive status epilepticus: 8%?!)

(5) if icrd ICP: hyperventilate (pCO2<25mmHg), mannitol 1g/kg IVI

Epilepsy Syndromes (GIM teaching, Preston, June 2008, Dr Majeed)

Episodic neurological events: epilepsy / migraine / ischaemia (rarer: metabolic, alcohol related, ...)

Pos. vs neg. symptoms: epilepsy=pos. symptoms (flashing lights, ...); ischaemia=neg. symptoms (vision loss, ...); migraine with aura=pos. (P&N) & neg. symptoms (hemiplegia)

Onset: migraine aura: ~5mins (max 60) vs. epil/TIA: sudden (seconds)

Specific features: diplopia: vertebrobasilar TIA (NOT migraine/epil); deja vu=epilepsy

Basilar migraine (5%): can be with confusion, impaired consciousness

Epilepsy: evolution of symptoms: clonic activity: early phase: lo amplitute + hi frequency; late phase: hi amplitude + lo frequency (NB: not observed in psychogenic seizures!)

True epileptic seizure: postictal confusion, cyanosis if prolonged

Psychogenic seizures: more in females with lo IQ under stress in presence of other; often pelvic thrusting, back arching, erratic movements, often eyes closed, no lateral tongue bite, no postical confusion

Prodrome in syncope (usu. minutes): lightheadedness, visual (as opposed to taste/smell=epil) symptoms: darkening/blurring, buzzing

Hyperventilation: often P&N

Provoking factors: epil: sleep deprivation, alcohol withdrawal, flashing lights, often in the morning; syncope: postural change, micturition, heat, prolonged standing, neck movement [NB: not infrequent: jerks, eye-rolling, vocalisation]

NB: syncope may turn into reflex-anoxic seizure (e.g. if prevented from lying down)

Progression of idiopathic epilepsy syndromes: Childhood Absence Epilepsy -> Juvenile Absence Epilepsy -> Juvenile Myoclonic Epilepsy -> Adult Onset Idiopathic Generalized Epilepsy

Generalized Absences (very short, usu. unaware afterwards) vs Complex Partial Seizure (often minutes, often aware of event afterwards)

New generalized seizure after age>30y: 70% Focal Onset Secondary Generalized Epilepsy vs 30% Idiopathic Generalized Epilepsy

When to start AED? after 1st seizure in US, but not in UK

AED: dcr risk of further seizure in 2yrs from 40% to 20%

NB: Any unexplained LOC (e.g. seizure): don't drive (or bath: shower instead) for 12/12 and tell DVLA

When to stop AED? usu don't if Hx of myoclonic jerks 

Choice of AED: dep on type epil, childbearing age, SE, ...

Broad-spectrum AED and order of choice: 1) VPA (Valproate, not for childbearing age!), 2) LTG (Lamotrigine) [=1 if childbearing-age female], 3) LEV (Levitiracetam=Kappra), others: BZD (Clobazane), TPM (=Topiramate),

Narrow-spectrum AED and order of choice (i.e. for Focal onset/lesional epilepsy--i.e. do not use for Idiopathic Generalized Epilepsy, e.g. if Hx of myoclonic jerks): [1) LTG=broad-spec], 2) CBZ, [3) LEV=broad-spec], others: PHT (=Phenytoin), ETX, GBP (=Gabapentin), OXC, TGB, PGB (=Pregabalin)

Important SE and other considerations:
LTG
: SE: severe skin rash: stop!; dose escalation q6w (i.e. bad for quick control, unlike VPA, LEV)!
LEV: SE: behaviour problems, depression
VPA: hand tremor, hair loss, weight gain
Enzyme inducers (CBZ, OXC, PHT, Primidone, TPM): OCP failure rate icr from 0.3->7% (may need dbl dose OCP and other forms of contraception); OCP icrs clearance of LTG: need dose icr of LTG to remain effective

Foetal malformation risk: CBZ 2.2%, VPA 6.2%, LTG 3.2%; preferably stop AED pre-conception until 12/40 (if poss., otherwise LTG/CBZ); give Folate 5mg od (childbearing age) with VPA/LTG (=Folate antagonists)

Paraparesis (GIM teaching, Preston, June 2008, Dr Majeed)

Flaccid paraparesis: Aetiol:
1) Ant horn cells: Polio, SMA=Spinal Muscular Atrophy (NOT classically MND/ALS: also UMN signs!);
2) Root lesions: GBS/CIDP, Lyme;
3) Neuropathies/trauma: axonal--usu. distal (e.g. diabetes); demyelinating--usu. proximal (e.g. CIDP);
4) Neuromusc junction: MG, LEMS;
5) Muscle: herediatry (muscular dystrophia, myotonic dystrophy, ...); acquired: dermato/polymyositis, rhabdomyolysis (e.g. extreme exertion, crush injury, viral, ...), acute myopathies, metabolic: periodic paralysis (lo K, hi K), lo PO4, Cushing's

Spastic paraparesis: Aetiol:
1) parasagittal/paraventricular brain lesion (eg meningioma, sup. sagittal sinus thrombosis, MS/SLE/Sarcoid);
2) spinal cord disease: cervial spondylosis (eg difficulties doing buttons with hands and stereoagnosia + spastic paraparesis!) inflamm (transverse myelitis) SACD (Vit B12), infarction (ant spinal artery thrombosis), intramedullary tu, syringomyelia, cavernoma, extradural disease (mets, abscess--eg TB, Paget's dis of bone, trauma)

Flaccid paraparesis: Ix: check CK; if N also channel AB's, AChR-AB, ganglioside ABs, TFTs; +-EMG/Bx; also MR spine;...

Headaches (GIM teaching, Preston, June 2008, Dr Majeed)

Cluster Headache (CH): 30 (max 120) mins vs Migraine 4-24[-72]h vs Trigem Neuralgia: seconds

CH: always autonomic features in trigem nerve distribution (eg rhinorrhoea, eye redness, facial colour change on one side); precipitated (immediately vs. 4-6h delayed in migraine) by alcohol, cold air, chocolate, GTN; Paroxysmal Hemicrania: like CH, but usu 5-30mins, more frequent, both sexes

CH: pt usu leaves bed b/o severe pain, whereas with migraine pts goes to be (to keep still)

CH Tx: Naproxen/ASA/COX2I, Verapamil, Acetazolamide, CBZ, GABA, steroids, deep brain stimulation

International Headache Society classification:
1) Vascular HA (Migraine, CH),
2) Tension HA (episodic vs chronic),
3) Intracranial pathology (SOL), inflammation of meninges;
4) referred HA

Migraine: common migraine (75%)=w/o aura; classical (20%)=with aura; other (5%)=hemiplegic, basilar, ophthalmoplegic

Migraine characteristics: 4-72h, unilat, pulsating, mod/severe, aggravated by movement, photophobia, phonophobia, N&V, asymptomatic between attacks; diagnostic criteria: at least 5 typical attacks; aura: develops over 5mins, max 60mins; prodrome: depression, irritability, +-hyperactivity, drowsiness; also postdrome

Migraine precipitants: fatigue, overwork, travel, relaxation after stress ('holiday/Sat morning HA')

Migraine Tx: sleep hygiene etc; Aspirin; Triptans (eg nasal, s/c, oral) [not Ergotamines any more!]

Migraine prophylaxis: if >1/wk, interfering with QoL, need Triptans >2/wk, if hemiplegic, etc; Rx: Propranolol/Nadolol; Topiramate (SE: wt loss!, CI: renal stones), Epilim, Amitriptyline, Fluoxetine; rarely: Pizotifen/Methysergide (avoid); Tx in pregnancy: Paracet, avoid NSAIDs in 3rd TM; avoid Codeine 2nd TM, Metoclopramide for N&V

Red flags for secondary HA: new/different HA; thunderclap (within secs/mins), focal sy/sx; if age>50 or systemic symptoms (fever, wt loss, jaw claudication): check ESR>50? (GCA)

PD & Parkinsonism (GIM teaching, Preston, 2008, Dr D Gosal)

150 per 100k, 3% if >65y, familial aggregation; Lewy body=misfolded alpha-synuclein aggregates; Clin. features: (5 cardinal) motor (rest. tremor, muscle rigidity, bradykinesia, postural instability,...), and non-motor (esp. later: anxiety, depression, dementia, sleep disturbance,...)

PD Tx: as late as poss (to dcr SE and long-term complications); Early: MAO-B-I (not v. good; Selegeline, Rasageline?); DA=Dopamine Agonists (Ropinirole, Pramipexole, Rotiogotine patch; rarer: Cabergoline/Pergolide: b/o valvular SE; all DA: difficult in elderly b/o behaviour problems: hypersexuality, obsessive gambling,...); L-Dopa + Decarboxylase-I (->honeymoon period ~3yr): Madopar/Sinemet: aim: smallest dose (300-500/d) and least pulsatile to dcr risk of dyskinesia; later Tx: if wearing off: eg more frequent L-Dopa, or Madopar/Sinemet + DA (eg patch); also + Entacapone, Amantadine, Apomorphine, Duodopa via PEJ, PD surgery (pulse generator)

Guillan-Barre syndrome  (GIM teaching, Preston, 2008, Dr Chaouch)

acute fulminant autoimmune polyradiculopathy (CSF: albuminocytologic dissociation=icr Prot w/o pleocytosis, ie WBC<50 (if >50 consider cancer, Lyme, sarcoid)--but may be nml initially; typical NCS after >10days)

progressive, symmetrical limb weakness + areflexia over max 2/52 (mild sensory symptoms), if longer: CIDP; DD: Lyme, HIV, Sarcoid

Care: IVIG/Plasma exchange; supportive care: cardioresp monitoring (BP, FVC: contact ITU if FVC<60% or FVC<20mL/kg or earlier if airway difficulties)

Miller-Fisher variant (5%): triad of ophthalmoplegia +ataxia +areflexia, 90% +ve for GQIB-IgG ABs

Giant Cell Arteritis [emed]

GCA: Diagnostic Criteria

age>50 (peak 70+, rarely <50); new HA; Abnlties of temp arteries; ESR>50, eg 100+ (97%); TA Bx (vasculitis: giant cells) [or: vessel wall oedema on Doppler US] (aim: <7-10d post steroids)

GCA: Symptoms

new onset localized headache

visual symptoms 33% (45% transient: amaurosis fugax/diplopia, 55% permanent: blindness: 50% uni-, 50% bilat: anterior ischaemic optic neuropathy)

systemic: malaise (fatigue, anorexia, fever, malaise, myalgia, night sweats, weight loss)

intermittent claudication 50%, claudication of jaw/tongue

aortic aneurysms/ regurgitation/ dissection, aortic arch syndrome (cf Takayasu arteritis)

DD:

PMR; TIA; Systemic infections; Amyloidosis with vascular involvement; Neoplasms; Atherosclerosis; Other vasculitis

Treatment:

High dose corticosteroids +- steroid sparing Tx

Clin Med (CME)

Acute Neurology

Neurol Problems on ICU, The Heart and brain, Neurol problems in cancer, Neurol and renal disorders, Drug induced neurol disorders

Polymyalgia rheumatica (PMR)

aching prox. extremities, torso and morning stiffness in 2-3 affected areas for 1+mth in aged>50

hi ESR (40-50) with rapid response to small doses steroids e.g. Prednisolone 10mg od

diagnosis of exclusion: consider GCA, RA, Polymyositis, chronic infection, neoplasm