Neurological Emergencies Lecture Notes PDF

Neurological Emergencies Robert Gourlay, BSc. BSc (Med) MD CCFP (EM)  Objectives Discuss clinical features, diagnosis, and management of patients presenting to the ER with headache. Discuss clinical features, diagnosis, and management of pat...

Neurological Emergencies Robert Gourlay, BSc. BSc (Med) MD CCFP (EM)  Objectives Discuss clinical features, diagnosis, and management of patients presenting to the ER with headache. Discuss clinical features, diagnosis, and management of patients presenting to the ER with seizures. Discuss clinical features, diagnosis, and management of patients presenting to the ER with suspected stroke. Headache  Headache Headaches can be categorized into two broad groups: Primary Headaches The headache IS THE DISEASE Secondary Headaches The headaches is a SYMPTOM of ANOTHER DISEASE process.  Primary Headache Tension Headache Migraine Headache Cluster Headache  Tension Headache The most prevalent headache type. Poorly understood mechanism. Previously believed to be a result of sustained contraction of pericranial muscles - this is now debunked. Believed to be a result of “heightened sensitivity of the peripheral nervous system and increased excitability with misrepresentation of signals by the central nervous system”.  Tension Headache Bilateral. Non-throbbing. Mild/moderate intensity. NO associated features. May have cranial muscle, cervical paraspinal muscle tenderness. NORMAL neurological exam. NORMAL diagnostic evaluation (if performed).  Tension Headache Diagnostic Criteria At least two of the following: Bilateral location Pressing or tightening (non-pulsating) quality Mild or moderate intensity Not aggravated by routine physical activity such as walking or climbing stairs Both of the following: No nausea or vomiting No more than one of photophobia or phonophobia  Tension Headache Treatment: First line: simple analgesia (NSAIDS, Acetaminophen, Aspirin). Second line: above, plus addition of caffeine In the ER: IV/IM NSAID, Metoclopermide /Diphenhydramine. Avoid medication overuse headache: limit analgesia to twice/day, less than 9 days/month. Avoid opioids.  Migraine Headache An episodic disorder with the hallmark feature being a severe headache, with photosensitivty and nausea. Again... incompletely understood. Primary neuronal dysfunction leads to a sequence of changes both intracranially and extracranially. Neuronal sensitization? Serotonin? Calcitonin? Cardiac shunt? Hereditary?  Migraine Headache Common. ~12% of the population. Women > Men Without aura = 75% of cases. Most common in 3rd decade of life.  Migraine Headache Recurrent attacks that unfold as a "cascade of events": Prodrome Aura (25% of patients) Migraine headache Postdrome  Migraine Headache 1. Prodrome Occur 24-48 hours prior to onset. Frequent yawning, irritability, depression, food cravings, neck stiffness. 2. Aura One or more "focal neurologic" symptoms, preceding or during the headache. Can be visual > sensory > language > motor. Can occur in absence of headache (acephalegic migraine).  Migraine Headache 3. Migraine Headache P - pulsatile O - onset (insideous) U - unilateral N - nauseating D - debilitating (intensity) S - sensitivity (photo/phonophobia) 4. Postdrome Feeling drained / exhausted. Head movement may cause headache return.  Migraine Headache Precipitating Factors Menstruation Visual stimuli Weather changes Dietary nitrates Fasting Wine Sleep disturbance? Aspartame?  Migraine Headache Diagnostic Criteria 5 attacks fulfilling ALL below criteria: ***Not better accounted for by another diagnosis Headache lasting 4 to 72 hours At least two of the following characteristics: Unilateral location Pulsating quality Moderate or severe pain intensity Aggravation by or causing avoidance of routine physical activity During headache at least one of the following: Nausea, vomiting, or both Photophobia and phonophobia  Migraine Headache Treatment NSAIDS Triptans Combination of NSAIDS & Triptans Triptans most effective during prodrome / aura (known as abortive therapies) In the ER: antiemetics / dopamine receptor antagonists (Metoclopermide / Prochlorperizine) Consider Dexamethasone to reduce recurrence.  Cluster Headache Recurrent SEVERE headache attacks with associated autonomic symptoms. Complex and incompletely understood mechanism: Hypothalamic activation which subsequently activates the trigeminal autonomic reflex.  Cluster Headache Rarest of the primary headache syndromes. ~0.1% lifetime prevalence. Male > Female (4:1) Genetic predisposition? Associated with smoking?  Cluster Headache Several short lived attacks per day: Unilateral Severe Orbital / temporal / supraorbital Autonomic Symptoms: Parasympathetic activity, sympathetic impairment Ptosis / myosis Lacrimation / rhinorrhea / conjunctival injection Circadian Pattern: Bouts may last a few days to a few months - asymptomatic in between.  Cluster Headache At least one of the following symptoms or signs ipsilateral to the headache: Conjunctival injection and/or lacrimation Nasal congestion and/or rhinorrhea Eyelid edema Forehead and facial sweating Miosis and/or ptosis A sense of restlessness or agitation Attacks have a frequency between one every other day and eight per day; during part (but less than half) of the active time-course of cluster headache, attacks may be less frequent. *Not better accounted for by another diagnosis  Cluster Headache Treatment High flow Oxygen! Triptans Intranasal lidocaine Consider preventative therapy with either a CCB (Verapamil) or glucocorticoid (Prednisone).  Secondary Headaches Must entertain a broad differential, as the headache is a symptom of another disease process. A helpful tool to develop a differential diagnosis: VITAMIN C Scope of this lecture is not to discuss ALL possibilities, but let’s focus on a few life threatening conditions.  Subarachnoid Hemorrhage Rupture of a cerebral artery aneurysm. Blood enters the subarachnoid space (under arterial pressure). CSF outflow obstruction - resulting in hydrocephalus. May progress to increased intracranial pressure followed by brain herniation and death.  Subarachnoid Hemorrhage SAH occurs in ~10-15 per 100,000 people. Slight female predominance. Typically 4th - 6th decade of life. Risk factors include: Hypertension Smoking Family History of SAH / Aneurysm  Clinical Features: SAH Presents as a sudden severe headache. "Worst headache of my life" Brief LOC, or altered LOC Nausea, vomiting Meningismus * Up to 10% patients die prior to reaching hospital.  Diagnosis: SAH CT Brain Fresh blood appears white (hyper-dense) on non-contrast CT. In SAH you see it fill the basilar cisterns. ~98% sensitive < 6 hours, 92% at 24 hours, ~50% at day 5. Lumbar Puncture Unfortunately the gold standard. Mandatory if there is a strong suspicion of SAH despite a normal CT. Elevated opening pressure, RBC's, xanthochromia.  Treatment: SAH Identify the etiology CT or MR angiography Catheter angiography (Gold Standard) Admit to Hospital Neurosurgical consultation Endovascular or microsurgical clipping withing 24-48 hours. Discontinue anticoagulants. Frequent neurological assessment (neuro vitals Q1H - Q4H). Maintain normothermia. Maintain euvolemia, and monitor for hyponatremia. Prevent vasospasm - Nimopidine? Control blood pressure ( heparin bridge to oral anticoagulation.  SNNOOP 10 S - SYSTEMIC Symptoms (including fever) N - NEOPLASM history N - NEUROLOGICAL Deficit O - ONSET "Abrupt" O - OLDER Age (Over 50) P - PATTERN CHANGE P - POSITIONAL P - PRECIPITATED (by coughing, sneezing or exercise) P - PAPILLEDEMA P - PROGRESSIVE P - PREGNANCY or PEURPERIUM P - PAINFUL EYE P - POST TRAUMATIC P - PATHOLOGY OF IMMUNITY (HIV) P - PAINKILLER OVERUSE (or NEW drug onset)  Giant Cell Arteritis Giant cell arteritis (GCA / Temporal arteritis) is an autoimmune vasculitis. If missed can result in permanent morbidity and mortality. The vasculitis involves the medium and large vessels arising off the aortic arch. Typically affected branches are the cranial arteries, but can affect any systemic artery.  Giant Cell Arteritis Women > Men Lifetime risk: 1% Women and 0.5% Men Risk Factors: Age > 50 (typically > 70) Caucasian ethnicity  Giant Cell Arteritis Clinical Features Constitutional symptoms Fever, fatigue, weight loss Headache Scalp / (temporal artery) tenderness Jaw claudication or trismus Vision loss Transient monocular (amaurosis fugax) Permanent  Giant Cell Arteritis Diagnosis High index of suspicion Elevated inflammatory markers: ESR / CRP Temporal artery biopsy Treatment Initiate glucocorticoids (Prednisone) immediately if your suspicious (even before you confirm the diagnosis). Consult Rheumatology and Opthalmology. Stroke  Stroke Permanent or transient brain ischemia as a result of: Vessel occlusion (Ischemic Stroke) Vessel rupture / hemorrhage (Hemorrhagic Stroke)  Ischemic Stroke 80% of cerebrovascular accidents. Results from: Thrombus (formed in an artery reduces blood flow distally) Embolus (debris originating elsewhere in the circulatory system travels to and blocks arterial access to a particular brain region) Systemic Hypoperfusion (secondary to a cardiac arrest, arrhythmia, pulmonary embolism, hemorrhage etc)  Hemorrhagic Stroke 20% of cerebrovascular accidents. Intracerebral Hemorrhage Most fatal form of stroke. Bleeding results from rupture of arterioles or small arteries. The bleeding is directly into the brain, forming a localized hematoma. Subarachnoid Hemorrhage Rupture of arterial aneurysms. Aneurysm rupture releases blood directly into the CSF under arterial pressure.  Transient Ischemic Attack Transient episode of focal brain, spinal cord or retinal ischemia, without resultant infarction. Typically last minutes. Must resolve in < 24 hours. Must have NO EVIDENCE of tissue infarction on follow up imaging.  Epidemiology of “stroke” US Data on "stroke": 87% ischemic, 10% intracerebral hemorrhage, 3% subarachnoid hemorrhage. Lifetime risk 25% Men > Women (Age < 75) Women > Men (Age > 75) Indigenous > African American > Caucasian > Hispanic > Asian / Pacific  “Localizing the Lesion” We can clinically predict the culprit vessel in ischemic stroke based on the constellation of presenting symptoms, or “stroke syndrome”.  Anterior Cerebral Artery Contralateral paralysis of leg/foot Arm to a lesser extent Contralateral sensory loss over leg/foot Gait apraxia Akinetic mutism  Middle Cerebral Artery Paralysis of contralateral face / arm / leg Sensory deficits for contralateral face / arm / leg 2-point discrimination Pinprick Vibration Speech deficits Motor aphasia Expressive aphasia Receptive aphasia Paralysis of conjugate gaze to opposite side  Posterior Cerebral Artery Cortical blindness Homonymous hemianopsia Topographic disorientation Memory deficits Hallucinations  Vertebrobasilar Stroke "Posterior circulation" Vertigo Truncal ataxia Auditory phenomena Visual field defects Diplopia Dysphagia, Dysarthria, Hoarseness Drop attacks Hemisensory extremity symptoms  Lacunar Stroke Non-cortical infarcts resulting from occlusion of a penetrating branch off a large vessel. May be purely motor or purely sensory. Typically lack "cortical signs" such as: Aphasia Agnosia Neglect Apraxia Hemianopsia Stupor / Coma / LOC Seizures  Stroke Management History Establish and EXACT time of onset. When was the patient LAST KNOWN TO BE NORMAL Distinguish between stroke mimics: Seizure, syncope, hypoglycemia, migraine, Bell Palsy Rule out ABSOLUTE CONTRAINDICATIONS to treatment: Ischemic stroke or severe head trauma within 3 months Previous ICH Intra-axial intracranial neoplasm GI malignancy or GIB within 3 weeks Intracranial or intraspinal surgery within 3 months  Stroke Management Physical Exam A focused physical exam, paying particular attention to airway, respiratory rate & pattern, temperature and blood pressure. Examine for ABSOLUTE CONTRAINDICATIONS for intervention: Symptoms suggestive of SAH Persistently elevated BP (systolic ≥185 or diastolic ≥110) Active internal bleeding Presentation consistent with infective endocarditis Suspected Aortic Dissection Acute bleeding disorders  Stroke Management Neurological Exam Suspect lesion location based on constellation of symptoms, ”Stroke syndromes”. The three most predictive examination findings: Facial paresis Arm drift/weakness Abnormal speech. National Institutes of Health Stroke Scale (NIHSS) to assess severity, and determine candidacy for intervention.  Stroke Management Treatment Depends on: EXACT TIME of symptom onset Symptom SEVERITY Whether the patient / symptoms are improving or persisting.  Management TIA Determine risk: High risk Symptoms have occurred within 24-48 hours. Fluctuating / persistent symptoms with or without motor involvement. Low Risk Symptoms occurred > 2 weeks ago. Atypical sensory symptoms.  Management TIA: the ABCD2 Score Not a perfect tool, but helpful in providing some idea of patient risk: High score (> 5) ~12% 7-day risk of stroke. Age > 60 +1 SBP > 140 or DBP > 90 +1 ~18% 90-day risk of stroke. Unilateral weakness +2 Speech impairment +1 Low score (< 2) ` Duration > 60 min +2 Duration 10-60 min +1 ~1% 7-day risk of stroke. Diabetes +1 ~3% 90-day risk of stroke.  Management TIA: High Risk TIA Consider admission to hospital and stroke risk stratification as an inpatient. CTA of carotid arteries and circle of Willis or ultrasound of carotid arteries. Initiation of anti-platelet or dual anti-platelet therapy. Blood pressure management. Initiation of a statin. Lifestyle modification.  Management TIA: Low Risk TIA Can be managed on an out patient basis. As with high risk patients, should have stroke risk stratification. Could consider anti-platelet or statin therapy prior to ER discharge. Lifestyle modification.  Management: Intracerebral Hemorrhage Neurosurgical consultation CTA or MRA Exclude aneurysm or AVM. Reverse anticoagulants. Monitor for signs of increased ICP. Headache, altered LOC, CN VI palsy, Cushings Triad. Hourly neuro-vitals. Aggressive blood pressure management Target SBP < 140  Management “Evolving Ischemic Stroke” IMMEDIATE non-contrast CT Brain to exclude ICH. Are they a reperfusion candidate? Are they in the "window" < 4.5 hours, may be a tPA thrombolysis candidate. 4.5 - 24 hours, may be an endovascular candidate. Initiate Stroke 25 and obtain CT-Angiogram of Carotids & Circle of Willis. Confirm location of lesion.  Management “Evolving Ischemic Stroke” “Outside the Window” Unfortunately patients NOT eligible to immediate intervention. RISK > BENEFIT Patients will require admission to hospital for: Initiation of anti-platelet (or dual) therapy. Initiation of a STATIN Blood pressure monitoring & control Fever prevention SLP assessment Rehabilitative services (OT/PT)  Management “Evolving Ischemic Stroke” Thrombolysis Candidate Recombinant tissue plasminogen activator (rt-PA) Must meet eligibility criteria Must have no contraindications Must be initiated within 3-4.5 hours 5-7% risk of intracerebral hemorrhage as a result of r-tPA.  Management “Evolving Ischemic Stroke” Endovascular Candidate Endovascular Retrievable Stent, Thrombecotmy, Endovascular Catheter Directed tPA. With or without tPA. Different inclusion criteria depending on whether 24 hours apart.  Seizure “Types” Seizures are classified based on whether a the electrical activity is "focal" within the brain or “generalized". Focal seizure with retained awareness Focal seizure with impaired awareness Generalized seizure  Focal Seizure with Retained Awareness Manifest differently from patient to patient depending on the part of the brain involved. May manifest as a focal motor movement, or flashing lights, or loss of speech! No LOC (aware of what is happening) May be preceded by an aura Little to no post-ictal symptoms  Focal Seizure with Impaired Awareness Focal seizure with altered LOC. Most common seizure type in adults with epilepsy. May appear awake, but are unresponsive. Repetitive behaviours (automatisms): Lip smacking Facial grimacing Repetitive words Little to no memory of the event.  Generalized Seizure Abrupt loss of consciousness. Tonic phase (~60 seconds) All muscles (arms, legs, chest and back contract) Patient becomes cyanotic Clonic phase (~60-120 seconds) Full body muscle jerking Tongue biting and incontinence common Post-Ictal phase (15-60 minutes) No recollection. Confusion, myalgias and malaise.  Evaluation Confirm the event was in fact a seizure, and exclude an alternative diagnosis. Careful history Careful examination Appropriate diagnostic tests  History Accurate description of the event (witnesses?) Timing (of event, in relation to sleep) Post-ictal state? Tongue biting or urinary incontinence? Prior similar events? Identifiable trigger? Medications or intoxicants? Family history?  Examination Largely un-revealing following a seizure. MUST exclude CNS infection or intracranial hemorrhage. Meningismus / Kernig / Brudzinski Lateralizing weakness, hyper-reflexia, Babinski Tongue laceration - not sensitive, but highly specific.  Diagnostic Evaluation The minimum: What the neurologist wants: Laboratory Investigations: Lumbar Puncture: Electrolytes / BUN / Glucose / Creatinine If infection suspected EEG: Pregnancy test (B-HCG) If epilepsy suspected CBC with differential MRI Brain: Can be deferred to an outpatient Urinalysis study if initial CT reassuring. Toxicology screen (if indicated) EKG: exclude "cardiac syncope" CT Brain: for all first time seizures in an adult Exclude space occupying lesion  Treatment Depends on whether you’re confident the seizure has resolved, and whether the seizure was provoked or unprovoked. Provoked: quickly identify and treat the underlying infectious, traumatic, or metabolic derangement. Unprovoked: Consider seizure prophylaxis (in consultation with neurology on a case by case basis): ~20-45% seizure recurrence within 2 years. Much higher recurrence risk if: Abnormal EEG Abnormal neuro exam Remote symptomatic insult Occurs during sleep Counsel on dangerous activities: swimming, heights, driving, open fires etc.  Treatment Unresolved Seizure: Status Epilepticus 30 minutes of persistent seizures or a series of recurrent seizures without complete return to full consciousness between the seizures. Manage airway: oxygen, OPA/NPA, BVM vs. intubation. No IV access: Midazolam 5-10mg Intramuscular / Intranasal IV access 1. Lorazepam 0.1mg/kg IV or alternative dosing of Lorazepam 4mg IV 2. Phenytoin 20mg/kg IV loading dose 3. Levetiracetam 40-60mg/kg IV loading dose 4. Propofol @ induction dose -> intubate.