Neurological emergencies!! CLEAR! AIMS : To recognize, investigate, and manage the most common vascular neurological emergencies. OBJECTIVES: To describe typical patient presentation with neurological emergencies (SBA format!) To differentiate clinically between. 1. 2. Stroke vs TIA Subarachnoid vs subdural vs extradural haemorrhages Breakdown pathology into WHERE + WHAT CAUSE To identify the most appropriate investigations for each To be familiar with the management principles (Esp. Guidelines for SBAs) of vascular neurological emergencies and name drugs / interventions. There will be SBAs to answer by you!! Don’t be shy ☺ While on night take on the final Friday before start of Easter holidays you are asked to take a history from Wilfred here. He is a 85 yo male who says 2 hours ago his wife noticed his speech began to slur and that his vocabulary became disordered. As he lived nearby he decided to walk to the hospital A+E. Once he got to the hospital he says he is now fine and passes all aspects of the speech exam you perform. He also mentions he had a similar incident 1 week ago where he lost his sight in his Right eye, he described like a curtain coming down over the eye. Both these events seemed to have lasted less than 45 minutes, recovering fully from both. What is the most likely diagnosis? A. Absence seizure B. Ischemic Stroke C. Migraine attack D. Transient Ischemic Attack E. Focal epileptic seizure TIA = “mini stroke” Symptoms resolve <24hours (usually within few minutes) Focal symptoms (transient weakness in arm / Amaurosis fugax ect) Unlikely if generalised symptoms (LOC) Pathology = Micro-emboli ?AF throw off clot (ECG) ?recent MI cause mural clot on dead myocardium (:. ECHO) ?carotid stenosis :. Doppler USS You decided to take a full history from Wilfred. In his PMHx he is Diabetic, with a BP of 155/95 on admission and had surgery last year on his hip after a fall fractured it. He is on no regular medication, has no known allergies and lives at home with his wife Marge in a ground floor flat. He reminds you only his speech was affected for less than 45 minutes and he is 85 yo, as he feels these are important. Based on this information, risk assess Wilfred using ABCD2 scoring system. What is the outcome of you assessment? A. STAT Aspirin 300mg + specialist review within 2 weeks B. Specialist review within 2 weeks C. STAT aspirin 300mg + specialist review within 24 hours D. STAT aspirin 75mg + specialist review within 24 hours E. Specialist review within 24 hours ABCD2 score = predictor those progress to full ischemic stroke High risk Left untreated, 30% of TIA’s progress to ischemic stroke (20% within the first month and 50% within the first year) :. Prevention Key! Age >/= to 60 (1) BP >/= to 140/90 (1) Suspect TIA = Aspirin 300mg STAT Clinical Unilateral weakness (2) Speech disturbance with no weakness (1) Duration of symptoms >60mins (2) 10-59 mins (1) Diabetes Yes (1) 3 or less specialist referral within 7 days 4 or more specialist assessment within 24h Stroke Sudden onset (mins) >24 hours symptoms persist Vascular origin focal territorial signs (usually) CT + MRI (within 48 hours) You are desperate for you final CBD of the module and find 64 yo woman to clerk in A+E. She says she suddenly felt funny about 2 days ago, when her right arm became weak whilst writing a letter. You also notice the right side of her mouth droops and her speech is a bit slurred. You suspect a stroke. What is you top differential on the location of the affected vessel? A. Left ACA infarct B. Right MCA infarct C. Pontine infarct D. Left MCA infarct E. Right ACA infarct Where is the pathology? (1) Where is the pathology? (2) Where is the pathology? – vessel? ANTERIOR CIRCULATION ACA = 2% Leg >> face/ arm MCA = 66% Motor + sensory •Contralateral Hemiparesis (face + arm >> leg) • Contralateral Hemi-sensory symptoms Cortical signs 1. Dominant hemisphere (L) = Broca’s + Wernicke’s Dysphasia 2. Non-dominant hemisphere (R) neglect left side • RARE = Homonymous Hemianopia with extensive lesions (catches temporal and parietal fraction of optic radiation!!) POSTERIOR CIRCULATION 1. PCA OCCIPITAL LOBES Binocular visual symptoms = cortical blindness (hemianopia) + central sparing? 2. Rest of vertebro-basilar circulation: A. CEREBELLUM - Ataxia of limbs and gait B. BRAINSTEM (ipsilateral CN defects) • III, IV,VI - diplopia • V - facial paraesthesia • VII - facial weakness • VIII - vertigo • IX, X, XII - dysarthria, dysphagia • Long tracts – bilateral limb symptoms • RAS – coma 68yo lady presents to A+E with sudden onset Right side weakness in arms + legs. PMH = HTN + hypercholesterima Exam = R facial weakness also no hemianopia + speech normal + no sensory loss BP 210/100 Diagnosis? A. Left MCA infarct B. Left ACA infarct C. Lacunar infarct D. PCA infarct E. Spinal infarct Where is the pathology? –subcortical? Lacunar Syndromes (main 3 shown) • Occlusion of deep penetrating arteries to subcortical structures (i.e internal capsule). • Usually ischaemic (microatheroma) in a single perforating artery :. very localised symptoms • MRI needed possibly very small infarct! NO CORTICAL SIGNS!!! :. NO dysphasia, inattention, apraxia, consciousness problems and visual problems (i.e. hemianopia) Syndrome Symptoms Location of lesion Hemiparesis Face + arm + leg of one side (+/- dysarthria /dysphagia) Internal capsule (posterior limb) Pure Sensory Contralateral paraesthesia/ anaesthesia Thalamus (VPLN) Mixed sensorimotor Thalamus + posterior internal Contralateral hemiparesis + sensory change Not respect vascular boundaries capsule (close proximity) again (leg + arm) Pure motor {NB. most common = 1/3 to ½ of lacunar strokes } Subcortical infarcts MCA HAEMORRHAGE vs ISCHEMIA INFARCTION (70%) In situ thrombus (Vessel already in head) EMBOLI! (Different sources from outside brain) A) PFO B) Mural C) AF D+E ) aortic + carotid Systemic hypo-perfusion (bilateral watershed infarct) INFARCTION (70%) In situ thrombus: 1. Large vessel :Arteriosclerosis in-situ atheroma (rupture thrombus) = ?CVS risk factors 2. Small vessel disease Lacunar stroke (microathermoa) EMBOLI! 1. Vertebral / Carotid A. atheroma rupture (?CVS risk facotrs) B. dissection trigger (?collagen disorder) 2. Cardiac emboli = AF/ previous MI (mural thrombus ) 3. Patent Foramen Ovale –young + DVT paradoxical embolism skips across (R.Atrium L.Atrium BRAIN!) Systemic hypo-perfusion global bilateral watershed deficits at border zones between major cerebral arterial territories (post - cardiac arrest) Younger (RARE) • Vasculitis (PAN + WG or post systemic disease i.e. SLE/ Bechet’s) • Venous infarction (Venous thrombosis – Sagittal > lateral > straight) • PFO • Clotting abnormality (prothrombotic) – Factor 5 Leiden + APS • Collagen disorder :. Dissection! HAEMORRAGE (30%) problems mainly from mass effect + pressure around area Reasons to think more about haemorrhage: – Poorly controlled hypertension – Severe headache at onset + Vomiting – Drowsiness early on + progressive Small vessel disease (again but different nature) A) HTN = major risk factor!! 1.HTN arteriopathy 2. Charcot-Buchard microanyerysms B) Alzheimer’s = major risk factor Cerebral Amyloid Angiopathy (CAA) Arterio-venous malformations Iatrogenic = anticoagulation/ antiplatelet HAEMORRAGE (30%) problems mainly from mass effect + pressure around area Reasons to think more about haemorrhage: – Poorly controlled hypertension –– Severe headache at onset + Vomiting – Drowsiness early on + progressive Small vessel disease (again but different nature) HTN = major risk factor!! HTN arteriopathy Weaken Blood vessel wall • hyaline build up (chronic HTN) • Fibronid necrosis (malignant HTN) Alzheimer’s = major risk factor Charcot-buchard microanyerysms (<250microns) commonly lenticulostraie arteries of MCA supplying BG + IC = chronic HTN cause turbulent blood flow at Right angle bend Cerebral amyloid deposition in vessel wall- (beta 40 amyloid) peripheral and occipital location!! (CONGO RED GREEN!!) AVM (younger <45yo) abnormal shunt between arteries + veins :. easy pop Coagulation disorder Iatrogenic = Already on aspirin, clopidogrel or warfarin Haemorrhagic transformation Embolic stroke embolus re-canalised starved endothelium beyond it that have been damaged by ROS from ischemia reperfusion with thrombolysis Oxidative burst break blood vessels haemorrhagic transformation Other Brain tumour related Cocaine use = surge BP What you going to do?.... ABCDE exclude Hypoglycaemia + maintain homeostasis (O2 + normoglycemia + fluids + temperature) Clinical assessment F.A.S.T (community) / ROSIER ?Haemorrhagic Ischemia confirmed :. Restore Blood flow YES  (Indication for thrombolysis?) NO NBM!!! PR if cant swallow IMMEDIATE BRAIN IMAGING!!! = high suspicion of haemorrhage! Block vs bleed CT INFARCT Hypodense = dead tissue = infarct WEDGE SHAPE!!! HAEMORRAGE Hyperdense = acute blood on show Fe in it makes it show up!! The CT evolution of ischemic infarct Hard to see very early • ?hypodensity • ?oedema (neutrophils enter after 15-24 hours) Macrophages begin eating up brain liquefactive necrosis cystic resorption of necrotic tissue (neutrophils disappear after 5 days) Astrocytosis proliferation + gliosis scar edge of cyst (Gliotic cavity last for years!) Thrombolysis The CT shows ischemic infarct and you want to start tPA (atelplase). Current guidelines recommend this be started within what time frame of onset of initial symptoms? A. Within 3 hours B. Within 3.5 hours C. Within 4 hours D. Within 4.5 hours E. Within 5 hours TIME = BRAIN!!! Core = Infarcted tissue :. unsalvageable Penumbra – Surrounding ischaemic area = Some blood supply from collateral vessels – Tissue not yet irreversibly injured but does expand out overtime!! – Target of acute therapies – Aim to preserve function and reduce disability After 24 hours have pasted you set up the 300mg Aspirin. Just as you come towards him with the aspirin he shocks you with a story of how he once nearly died last time he took aspirin due to his Asthma. Now what are you going to do?? A. Administer the 300mg aspirin anyway + monitor patient regularly B. Administer only 75 mg/day + monitor patient regularly C. Don’t administer the aspirin + substitute with Warfarin D. Don’t administer the aspirin + substitute it for Clopidogrel E. Don’t administer the aspirin + substitute it for Heparin Clopidogrel =ADP receptor antagonist blocks platelet aggregation Heparin (accelerate ATIII) UF = IV LMWH= Sub.Cut Warfarin = inhibits synthesis of clotting factors II, VII, IX and X (vit K dependant) Ischemic Stroke management 1. Primary prevention = if there is no previous history of stroke or transient ischaemic attack (TIA) 2. secondary prevention = if there has been such an event Acute Reopen the artery Thrombolysis Prevent early recurrence • Aspirin 300mg OR 2nd line - Clopidogrel 75mg • Anticoagulation if indicated Protect from secondary brain damage • Maintain physiology and homeostasis may need monitor + treat cerebral oedema = common cause of death inside 1 week via herniation (esp. large MCA infarct) • Treat complications (aspiration= NBM / DVT = mobilise early) Longterm: Lifestyle: MANAGE YOUR MODIFIABLE RISK FACTORS!! Drugs: Antiplatelet Drugs (Aspirin75 mg) Anti-hypertensive (>130/80 aim) Statin (even if cholesterol ok in 1st place!) begin 48 hours after stroke ANY QUESTIONS SO FAR? A 40-year-old female presents with vomiting preceded by “The WORST EVER headache” that was localised in the occipital region, and came on suddenly while playing tennis. On examination she was conscious and alert with photophobia and neck stiffness (Kernigs’s postive), but she is afebrile. What is your top Ddx? A) Subdural haemorrhage B) Ischaemic Stroke C) Subarachnoid haemorrhage D) Meningitis E) Migraine Common Vignettes BUZZ words - SAH Clinical presenting signs: Sudden-Onset “Thunderclap Headache” “Worst Headache of my life” (?occipital) Unilateral big pupil (post. Communicating artery aneurysm CN III palsy) CN VI palsy (raised ICP – False Localising Sign) Retinal (subhyaloid) Haemorrhages Altered Mental Status (low GCS) Meningism signs without fever What next? Management: ABC ITU support CT head 5% will be normal :. DOES NOT EXCLUDE!! WHAT DO WE DO NOW TO PROVE SAH? LP (after 12 hours = allow RBC lysis :. xanthachomia to develop) Cell counts Xanthochromia (protect CSF from light) May see red of blood but unreliable as “tap truama” will clear up on serial LP (true SAH will remain bloody) High yield BUZZ words of pathology - SAH 1. Cerebral berry (saccular) aneurysms rupture (70-85%) conditions associated: adult polycystic kidney disease (i.e. ballotable kidneys) Ehlers-Danlos syndrome weak collagen in vessels Coarctation of the aorta diversion upwards = increase flow to brain 2. Arterio-venous malformations (10-15%) 3. Traumatic (usually less serious) 4. Tumours rapid angiogenesis = poor vessel quality Treatment - SAH Bed rest + analgesia + monitor CNS signs Maintain cerebral perfusion levels IV fluids (prevent hypotension) Nimodipine (CCB) believed to reduce cerebral artery spasm :. STOPS secondary ischemia. Neurosurgical transfer + cerebral angiogram (GOLD STANDARD) = clipping off/ endovascular coiling the aneurysm to prevent re-bleeding may be employed. Evacuation may be considered High yield BUZZ words SAH Complications: 1. Re-bleeding = 30% of patient in first few days 2. Obstructive hydrocephalus (due to blood in ventricles) 3. Communicating hydrocephalus (blood block arachnoid granulations :. Fail drain into systemic circulation) 4. Vasospasm = leading to secondry cerebral ischaemia 78 year old man is brought in by his carer with fluctuating episodes of confusion over the past 5 days. Between these episodes he is apparently his normal self. He also complains of a mild constant headache and seemed mildly confused when you speaking to him. You are told he had a fall a week ago but appeared uninjured and he cant remember if he hit his head or not. He is on warfarin for atrial fibrillation. Examination: Mildly disorientated but alert, afebrile with no neck stiffness At this point what is your top differential? A. Recurrent TIA’s B. Stroke C. Subdural D. Extradural E. SAH High yield BUZZ words – Subdural Trauma can be mild + many weeks ago :. Patient may forget! Common vignettes Elderly + alcoholics + On antiplt / anticog. Insidious onset (can be over weeks) Fluctuating consciousness levels + focal neurology Treatment - Subdural Stop the warfarin. Some can be managed conservatively if small bleed Neurosurgical advice +/-transfer = May need evacuation Burr hole Address cause of fall + monitor INR A 14yo boy is brought into A+E by a worried mum. One hour ago he was hit on the side the head by a cricket ball during a match and collapsed to the ground, complaining of a sore head. After a couple minutes however he got back up and felt Ok, continuing to play. After 30 minutes however he suddenly collapsed to the ground and lost consciousness near the end of the game. What type of injury is he most likely to have sustained? A. Cerebral contusion B. Subarachnoid haemorrhage C. Intraventricular haemorrhage D. Extradural haemorrhage E. Subdural haemorrhage High yield BUZZ words– Extradurals Severe head Trauma (temporal region) Lucid interval = compensation M-K doctrine until herniation (coning) DEATH (hours) Torn middle meningeal art. Young patient Treatment - Extradural Repeated physical examinations assess your level of consciousness ?symptoms that may appear such as headache, arm or leg weakness Burr holes / craniotomy = relieve pressure + remove hematoma Quick comparison imaging EXTRADURAL SUBDURAL Egg shaped hyperdense area = cranial sutures limit spread Cresentic inner skull table, Remember CT can miss over the cerebral convexity small bleed in 2% :. May in the parietal region (most need LP to confirm common location) ? Any hydrocephalus Acute Chronic (secondary) Hyperdense SAH Hypodense Summary – All easily testable material TIA + Stroke WHERE + WHAT (anatomy + pathology). SCORING SYSTEMS + GUIDELINES for management Extra Dural + Subdural + SAH Compare and contrast common presenting vignettes Investigations results can be OSCE picture station Other bits worth looking over not covered…Soz CHA2DSVA2S = scoring system in AF (see appendix) Venous sinus thrombosis Other causes of raised ICP Headaches Extra vascular essentials (1) CHA(2)DS(2)VAS = stroke risk scoring system in AF C Congestive HF 1 H Hypertension (constantly >140/90 or on meds) 1 A Age >/= 75 2 D Diabetes 1 S Prior stroke/ TIA 2 V Vascular disease (Peripheral artery disease/MI) 1 A Age 65-74 1 S Sex (female) 1 Score Risk Management 0 LOW Nothing 1 MEDIUM Aspirin (OR oral anticog. Warfarin) 2 HIGH Warfarin Neurological Emergencies (Non-vascular) Veronica Melchionda 25 March 2013 What and Why Topics covered Importance Status epilepticus Extremely interesting! Meningitis Potentially fatal Encephalitis Will encounter as FY1/2 GCA, MG, GBS Tx varies greatly with Dx Cauda equina Wernicke’s encephalopathy Other Impact on QoL, NHS cost Exams: SBAs & OSCEs Aims & objectives AIMS: To recognize, investigate, and manage the most common non-vascular neurological emergencies. OBJECTIVES: 1. To describe typical patient presentation with neurological emergencies and their common pathologies. 2. To identify the most appropriate investigations for each. 3. To differentiate between epilepsy & status, meningitis & encephalitis, cord compression & cauda equina, and between the auto-immune inflammatory emergencies. 4. To be familiar with the management principles of neurological emergencies and name drugs/interventions/care needed. STATUS EPILEPTICUS What do you know? Reminder of Epilepsy Classification Provoked Simple Partial/Focal Complex Definitions: Generalized = entire brain Partial = one area 2º generalized Seizure Absence Myoclonic Generalized Absence = petit mal Tonic/clonic = grand mal Simple = without LOC Complex = with LOC Tonic-clonic Tonic Atonic THEN WHAT IS STATUS E? = prolonged seizure acitivity + failure to regain LOC (≥30min but in practise >5min). Convulsive or non. Ddx? Status epilepticus Epidemiology: incidence (1/3) vs recurrence (1/3) vs 2º (1/3), ± previous hx, especially under 5’s and over 40’s. Mortality 10-20% S.E. Aetiology Invx Electrochemical stages EEG progression of seizures Systemic physiological stages • Compensation • Decompensation Normal Neuronal damage Excessive activation of glutamate receptors. Status E Management 1. DR ABC ITU (resus) 2. Consider aetiology TREAT EARLY! +BM Intubation Ventilation Diazepam IV/PR 10mg ± repeat after 15min Earl y Lorazepam IV 4mg ± after 10min Thiopentone GA (IV then infusion) Established Phenobarbitone IV 10mg/kg +ECG ± Phenytoin IV 15mg/kg + ECG DIAZEPAM (short action <30min) LORAZEPAM (long action 3-10hr) 50% recurrence in 2hr < chance seizure occurrence Complications of Status E Factor CNS metab consumptn Metabolic derangement Oxygen BP Temperature Other organ effects Effect INFECTION What do you know? **USE ACCURATE DESCRIPTIONS!! (onset, anatomy, pathology, aetiology) Meningitis vs Encephalitis What’s do they each mean? MENINGITIS ENCEPHALITIS Organism Confusion/LOC Seizures Meningism Headache Fever Typical PC/ *Meningism signs = Kernig’s (on leg ext) & Brudzinski’s (on neck flex) signs, high pitched cry in infants *meningiococcal septicaemia ± meningitis = life-threatening, assoc w arterial thrombosis Culprit Organisms *IS = immunosuppressed Encephalitis Meningitis Non-bacterial Gram +ve Organism Type Examples Mycobactium tuberculosis diplococcus (all ages) Streptococcus pneumoniae!!! Viral Syphilis, lyme coccus (neonates) Group B streptococci HSV1&2 VZV & CMV Enteroviruses Mumps & Measles Influenza Tropical (Japanese, West Nile, rabies) Viral: HSV2, Enteroviruses, mumps, VZV, EBV, HIV, etc Fungal: cryptococcus neoformans*, histoplasma capsulatum (HSV1 is most common) bacillus Listeria (v. young/old, IS) monocytogenes Gram –ve Organisms cocco-bacilli (children) Haemophilus influenzae diplococcus (young-adults) Neisseria meningitidis!!! Bacterial Meningo (often) Listeria TB, Syphilis Lyme, Brucella Leptospirosis Other Toxoplasma, Trypano, inflamm., haem, metabolic, drug bacillus E. coli, Klebsiella (v. young/old, IS) Meningococcal Pneumococcal *ABC + ITU if necessary Mx Meningitis (±CT) LP w paired BM + empirical abx • IV Benpen/cef OR chloramph if pen allergy • CSF stain (gram, ZN, India) & culture & PCR • IV dexamethasone (high dose) • Contacts’ prophylaxis w PO rifamp Meningo/p IV ceftriaxone/cefotaxime neumo (vanco or rifamp if DR) H. influenz IV chloramphenicol Listeria High dose ampicillin TBM 9mo of TB drugs Viral N/A (self-limiting, benign) Encephalitis CT or MRI (better) EEG (non-specific slow wave/periodic complexes) CSF/blood PCR (98% sens) + viral serology IV aciclovir 10mg/kg TDS if HSV (or ganciclovir if CMV) Supportive & symptomatic tx N= neutrophil/PMN L= lymphocyte Interpreting CSF Results Normal Bacterial meningitis Viral meningitis TB/fungal meningitis Cryptococcal meningitis Appearance Clear & colourless Turbid/pus Clear Fibrin web/ viscous / Pressure (cmH2O) 5-20 >30 Normal or mildly up / / WBC /µl (differential) <5 (90% L, 10% N) >200 (mostly N) 50-200 (mostly L) 50-200 (mixed/L) 5-100 (mostly L) PROTEIN (g/L) 0.45 High (>1.5) Moderate (<1.0) Moderatehigh (>1.0) Lowmoderate GLUCOSE mM (ratio*) 2.5-3.5 (>60%) <2.2 (<40%) Normal (>60%) 1.6-2.5 (<40%) Low/normal *ratio is CSF:plasma glucose (% of blood glucose) Complications Meningitis Hydrocephalus (CSF obstruction, esp TBM) Encephalitis Neuro sequelae ex dysphasia Cerebral oedema, SIADH Venous sinus thrombosis Subdural empyema, Cerebral abscess Memory impairment in HSV ( short-term amnesia) Cerebral oedema Arteritis & endarteritis (±occlusion) Delirium (from high fever) Septic shock, DIC, adrenal haemorrhages (=WF syndrome) *thus, watch out for focal neuro! Seizures Coma INFLAMMATORY Important bc of neuromuscular respiratory failure – arbitrary 1L vital capacity cut off before assisted ventilation Mr GB 1. Hx of infx 2. Sensory (minor) 3. Motor (predom) progressive symmetrical ascending Guillain-Barre’ Syndrome = acute autoimmune (post-infx) demyelinating polyradiculoneuropathy Invx (mb normal initially): LP, EMG & nerve conduction ± ab screen, MRI Most common culprits Mx: Monitoring (ECG, VC), IV Ig/plasmapheresis, ventilation. + LMWH, physio, aspiration care Px: most good recovery w rehab. Death in 5-10% • aspiration, PE, sepsis COMPLICATIONS • CN, resp muscle weakness • autonomic instability (arrhthymias) Mrs MG Fatigability of muscle • Prox muscle neck, trunk, girdles • Ocular ptosis, diplopia Myasthenic crisis • bulbar dysphagia w nasal regurg, dysarthria, aspiration • Respiratory Myasthenia gravis = NMJ transmission disorder due to post-synaptic AchR ab • Bimodal age/sex distribution ± thymus pathology • Invx: Tensilon test, AchR ab, EMG changes, CT/MRI chest (thymoma), MRI brain. • Mx: • ABC- respiration (VC) & swallow (NBM) • Pyridostigmine (s.e.), prednisolone, azathiorpine • Thymectomy, plasmapheresis/IV Ig Miss GC Pain over thickened, tender, often non-pulsatile temporal arteries with: Transient visual loss (25%) Jaw claudication Scalp tenderness Systemic fts Giant Cell Arteritis = Granulomatous temporal arteritis αPMR Invx: V. raised ESR (60-100), CRP temporal artery biopsy Mx: IV hydrocortisone then pred ASAP (high dose) Rarer complications Resect ≥1cm bc of skip lesions CORD COMPRESSION Miss CA Limb weakness gait Lumbar/sciatic pain Poor bladder/bowel control Sexual dysfunction Spinal cord compression >L1 Cauda equina syndrome <L1 UMN (leg ± arms) L1 LMN (±UMN if conus) PMHx -surgical sieve Saddle area paraesth, bladder/bowel probls Sensory level, reflex level Absent ankle reflex ± foot drop Complications: permanent paraplegia *both extensor plantar Mx: MRI asap + assessment surgery same day recovery. Dexamethasone while waiting urgent decompressive laminectomy/radio. *Check vit B12. On MRI: ? SIGNS? ? SIGNS? METABOLIC Wernicke’s emcephalopathy Wernicke-Korsakoff syndrome EtOH Hx W’s encephal. K’s psychosis • Long term use, binge, gastritis, vomiting, malnutrition etc • TRIAD (ocular, ataxia, confusion) • TRIAD (amnesia confabulation, lack of insight, personality ∆ apathy) Mx: high dose IV thiamine (± BM) diet, PO thiamine *Pathology Glasgow Coma Scale (/15) EYE opening (max 4) 1. 2. 3. 4. VERBAL response (max 5) 1. 2. 3. 4. 5. MOTOR response (max 6) *minimum of 3 points!! 1. 2. 3. 4. 5. 6. OTHER EMERGENGIES Idiopathic intracranial HTN ADEM Acute encephalopathies Surgical sieve Acute relapse of MS Neuroleptic malignant syndrome Neurosyphilis (tabes dorsalis) Let’s apply your knowledge A Bacterial meningitis B Cerebral tumour C Charcot-Marie-Tooth disease D Diabetic neuropathy E Guillain-Barre syndrome F Motor neurone disease G Multiple sclerosis H Myasthenia gravis I Parkinson's disease J Viral meningitis A 67-year-old male presents with weakness and loss of sensation in his feet and legs. His history includes a flu-like illness two weeks prior to the start of these symptoms. A 45-year-old woman presents with ptosis and diplopia. She also has proximal limb weakness which worsens after exercise. Sensory function is normal. An 18-year-old student presents with headache, neck stiffness and photophobia. The cerebrospinal fluid examination shows 100 lymphocytes, CSF glucose is more than 2/3 blood glucose value and CSF protein is 0.60g/L. Gram stain was negative. EMQ A Bacterial meningitis B Benign intracranial HTN C Brain abscess D Carbon monoxide poisoning E Cluster headache F Giant cell arteritis G Herpes zoster H Intracranial tumour A 70-year-old male presents to his GP with a three week history of headache. He says that they are more frontal, are worse in the evening and he feels that his scalp is tender to touch. A 26-year-old female presents with a two month history of severe headaches that appears to be relieved by standing. On examination, it is noted that she is obese. She has no neurological abnormalities or visual disturbances. A 24-year-old student has a 24 hour history of an ear infection, with photophobia, neck stiffness and a headache. Cerebrospinal fluid shows a white cell count of 500/mm3, almost all of which are polymorphs. SBA a. Blood neutrophil leucocytosis b. FHx of PKD c. Fluctuating LOC d. Hx of DM e. Hx of opiate abuse An 18-year-old man presented with a history of a sudden onset of a frontal headache and photophobia. He had neck stiffness and a temperature of 38°C. Which one of the following findings would suggest a diagnosis of subarachnoid haemorrhage rather than bacterial meningitis? SBA a. CT head followed by lumbar puncture and then IV antibiotics b. IV antibiotics followed by CT head and subsequent LP c. IV antibiotics followed by lumbar puncture d. IV antibiotics only e. Lumbar puncture followed by IV antibiotics A 19-year-old medical student is admitted as an emergency case to a university hospital, as he was found semi-conscious at home. On examination he has a Glasgow coma scale of 12, is febrile at 39.5°C, has a pulse of 120/min, has a blood pressure of 105/60 mmHg, is photophobic and has meningism. The patient has been cannulated and blood cultures have been sent. What is the most appropriate next step? Take home messages Beware of the clinical presentation patterns of neurological emergencies, when to prioritize treatment over investigations. Don’t forget ABC/ITU in management and the surgical sieve when considering aetiology. Differences between epilepsy & status, meningitis & encephalitis, cord compression & cauda equina, and between the auto-immune inflammatory emergencies. Investigations and management principles of neurological emergencies and name drugs/interventions/care needed. Thank you Feel free to contact me with any questions at [email protected] *Feedback Any questions?