Neurological Emergencies by: Dr, Sajid Mumtaz Sodhar

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Neurological Emergencies:

Dr. Sajid Mumtaz Sodhar, Internal Medicine Deptt:, King Khalid Civilian Hospital, Tabuk Neurological Emergencies “Sodhar Courtesy” “A judge should not make a judgement between two persons when he is in anger . ” (Last Prophet of all Muhammad saw) “Any man whom Allah has given the authority of ruling some people and he does not look after them in an honest manner, will never have even the smell of Paradise.’ ” (Last Prophet of all Muhammad saw)

Neurologic Emergency Outline:

Neurologic Emergency Outline Change in Mental Status / Coma Stroke/TIA Syndromes Seizure & Status Epilepticus Infectious Vertigo/Headaches Peripheral Neuropathies (GBS) MG “Sodhar Courtesy”

The Neurologic Exam:

The Neurologic Exam KEY!! Must do a complete thorough neuro exam to properly identify and diagnose any neurologic abnormality. Exam should include 5 parts always!: Mental status, level of alertness ( i-e;GCS) Cranial nerve exam Motor / Sensory exam Reflexes Cerebellar Consider ; MMSE if Psych / AMS components “Sodhar Courtesy”

Change in Mental Status / COMA:

Change in Mental Status / COMA Potential Causes – “AEIOU TIPS” A = Alcohol ( Drugs & Toxins) E = Endocrine, Exocrine, Electrolyte I = Insulin O = Opiates, OD U = Uremia T = Trauma, Temperature I = Infection P = Psychiatric disorder S = Seizure , Stroke, Shock, Space occupying lesion “Sodhar Courtesy”

Change in Mental Status/Coma:

Change in Mental Status/Coma Trauma

Stroke / Space Occupying Lesions:

Stroke / Space Occupying Lesions “Sodhar Courtesy ”

Space Occupying Lesion:

Space Occupying Lesion “Sodhar Courtesy ”

Change in Mental Status/Coma:

Change in Mental Status/Coma Temperature Hypothermia: causes coma when Temp<32.0 C Hyperthermia: causes coma when Temp>42.0C Infection Meningitis, Encephalitis, Sepsis Endo/Exocrine, Electrolyte Hypo/Hyperglycemia Hypo/hyperthyroidism Hypo/hypernatremia Hepatic encephalopathy Opiods/ OD / Alcohol Heroin, Psych Meds (TCA’s, SSRI’s)

AMS / COMA Physical Exam Pearls:

AMS / COMA Physical Exam Pearls Always attempt to get a complete history!! LOOK at your patient! Smell the breath (ketones,alcohol,fetid,uremia) Observe respiratory rate & patterns (Cheyne-Stokes) Look for abnormal posturing. Decorticate (Flexion of UE with Extension of LE) Decerebrate (Extension of all Ext.) Look for needle marks, cyanosis, signs of trauma Obtain GCS Score! E4 V5 M 6 If less than 8, IMMEDIATE airway stabilization FIRST priority!!

Glasgow COMA Scale:

Glasgow COMA Scale Scores range from 3 (Worst) – 15 (Best) Important for classifying degree of alteration. (Head Trauma) GCS < 8 = INTUBATE!! EYE Opening Response 4 = Spontaneous 3 = To Voice 2 = To Pain 1 = None Remember as “4 eyes” “Sodhar Courtesy”

Glasgow COMA Scale:

Glasgow COMA Scale Verbal Response 5 = Oriented and converses 4 = Confused but converses 3 = Inappropriate words 2 = Inappropriate sounds 1= None Remember as “Jackson 5 – sing/voice”

Glasgow COMA Scale:

Glasgow COMA Scale Motor 6 = Obeys commands 5 = Localizes pain 4 = Withdraws to pain 3 = Decorticate (flexes to pain) 2 = Decerebrate (extends to pain) 1 = None Remember as “ 6 Cylinder engine – motor”

AMS / COMA Essential Stabilization & Assessment Measures:

AMS / COMA Essential Stabilization & Assessment Measures Always assess & stabilize ABC’s first Special attention to airway with C-Spine control/ protection. Oxygenate! IV line , fluids, Thiamine 100mg IV, 1 amp D 50, & Narcan (if needed) 0.4mg increments until response. Complete history and physical exam after stabilization Radiographic clearance of C-Spine Labs / CT as indicated

Stroke / TIA Syndromes:

Stroke / TIA Syndromes Anatomy of Cerebral Blood Flow Anterior Circulation: 80% of cerebral blood flow originates from the carotids which supplies the Frontoparietal lobes Anterior temporal lobes Optic nerve and retina Posterior Circulation: 20 % of cerebral blood flow which originates from the vertebrobasilar arteries Thalamus & Brainstem Occipital cortex and Cerebellum Upper Spinal cord & Auditory and Vestibular functions in ear Circle of Willis: connects the Anterior and Posterior circulations

Pathophysiology of Stroke / TIA:

Pathophysiology of Stroke / TIA Ischemic Strokes: (thrombi or emboli) Cerebral Thrombi may result from: Atherosclerosis (#1 cause) Infective arteritis Vasculitis Hypercoaguable states Post traumatic carotid or vertebral artery dissections Cerebral emboli may result from: Mural thrombus from heart (#1 cause) Aortic plaques Endocarditis Long bone or Dysbaric injuries (fat / air emboli ) “Sodhar Courtesy”

Pathophysiology of Stroke/TIA:

Pathophysiology of Stroke/TIA Hemorrhagic Strokes result from Spontaneous rupture of berry aneurysm or AV malformation (Subarachnoid hemorrhage) Rupture of arteriolar aneurysms secondary to: Hypertension Congenital abnormality Blood dyscrasia / Anticoagulant usage Infection Neoplasm Trauma (Epidural / Subdural Hematomas) Hemorrhagic transformation of embolic stroke “Sodhar Courtesy”

Stroke /TIA Syndromes:

Stroke /TIA Syndromes Type of Stroke (rule of 2/3’s) 2/3 of ALL Strokes will be ISCHEMIC 2/3 of these will be thrombotic Therefore thrombotic ischemic strokes most common. Incidence of Stroke Biggest Risk Factors Prior TIA ( 30 % will have stroke in 5 years) HTN Atherosclerosis DM Hyperlipidemia Smoking

Ischemic Stroke Syndromes:

Ischemic Stroke Syndromes Thrombotic Syndromes Usually slow, progressive onset Sx develop shortly after awakening and are progressive Embolic Syndromes Usually abrupt onset with maximal deficit that tends to improve over time as the embolus breaks up.

Occlusive Stroke Syndromes:

Occlusive Stroke Syndromes Middle Cerebral Artery Occlusion (MCA) # 1 type Contralateral hemiplegia, hemianesthesia, and homonymous hemianopsia Upper extremity deficit >> Lower extremity Aphasia (if dominant hemisphere involved) Conjugate gaze impaired in the direction of the lesion

PowerPoint Presentation:

Hyperdense MCA Sign “Sodhar Courtesy”

PowerPoint Presentation:

“Sodhar Courtesy”

Occlusive Stroke Syndromes :

Occlusive Stroke Syndromes Anterior Cerebral Artery Occlusion (ACA ) Contralateral leg, arm, paralysis Lower Extremity deficit >> Upper extremity Loss of frontal lobe control Incontinence Primitive grasp and suck reflexes enacted Posterior Cerebral Artery Occlusion (PCA ) Ipsilateral CN III palsy, visual loss Contralateral hemiparesis and hemisensory loss Memory loss

Occlusive Stroke Syndromes :

Occlusive Stroke Syndromes Vertebrobasilar Artery Occlusion (VBA) Keys: CN AND Cerebellar deficits that affect BOTH sides of the body, with contralateral pain and temperature deficits. Contralateral hemiplegia Ipsilateral CN III palsy with Cerebellar findings. Nausea/Vomiting Vertigo, Nystagmus, Ataxia, Dysarthia Tinnitus, deafness

Hemorrhagic Syndromes (SAH, & Intracerebral):

Hemorrhagic Syndromes (SAH, & Intracerebral ) Subarachnoid Hemorrhage Highest incidence in 35-65 year old. Usually from the rupture of a berry aneurysm Clinically: abrupt onset of “worst headache of life” Nuchal rigidity, photophobia, vomiting, retinal hemorrhages. Diagnosis : CT + LP!!!! CT only 92% sensitive within 24 hours of event, loses sensitivity >24 hours out from headache. 72 hours out CANNOT r/o without LP! Management: ( Stroke Mgmt) Consider adding Nimodipine 60 mg Q6 to reduce vasospasm

TIA’s (Transient Ischemic Attacks):

TIA’s (Transient Ischemic Attacks ) Definition: A temporary loss of neurologic function, that resolves completely <24 hours. Clinically; Arm numbness, weakness, HA Facial droop, slurred speech Sx resolved, or improve over time Main point: These patients at high risk for stroke if: >50 HTN, DM, Smoker, Prior TIA in last month Any prior CVA…… ADMISSION IS THE RULE!! Treat as CVA : Head CT (CVA protocol) ASA 165-325mg po Consider Heparin, after Head CT and Neuro consultation and ONLY if cardiac arrhythymia present.

Hemorrhagic Stroke Syndromes:

Hemorrhagic Stroke Syndromes Intracerebral Hypertensive intracerebral hemorrhage MOST common cause. Traumatic, contusion, coup/contracoup Rupture of small blood vessels with bleeding inside the brain parenchyma Putamen Cerebellar Thalamic Pontine ( 3 P’s – pinpoint pontine pupils)

Intracranial Hemorrhage (non-traumatic):

Intracranial Hemorrhage (non-traumatic) Location of Hemorrhage Intraventricular Hemorrhage Intraparenchymal Hemorrhage Subarachnoid Hemorrhage Subdural Hematoma Epidural Hematoma

Subarachnoid Hemorrhage:

Subarachnoid Hemorrhage “Sodhar Courtesy”

PowerPoint Presentation:

“Sodhar Courtesy ”

Subarachnoid Hemorrhage:

Subarachnoid Hemorrhage

Intracerebral Hemorrhage:

Intracerebral Hemorrhage “Sodhar Courtesy”

Basal Ganglia Intraparenchymal Hemorrhage:

Basal Ganglia Intraparenchymal Hemorrhage “Sodhar Courtesy”

Thalamic Intraparenchymal Hemorrhage:

Thalamic Intraparenchymal Hemorrhage “Sodhar Courtesy”

PowerPoint Presentation:

“Sodhar Courtesy”

Intraparenchymal Cerebellar Hemorrhage:

Intraparenchymal Cerebellar Hemorrhage

Lobar Intraparenchymal Hemorrhage:

Lobar Intraparenchymal Hemorrhage

Treatment of Stroke:

Treatment of Stroke AS ALWAYS – ABC’s FIRST with C-Spine Precautions What’s the FS?? Consider Thiamine 100mg IV, D 50 bolus if hypoglycemic. Treat Hyperglycemia if FS > 300mg/dl Protect the “Penumbra” Keep SBP >90mm ( CPP = MAP – ICP) Goal keep CPP > 60mm Hg Treat Fever ( Mild Hypothermia beneficial) Acetaminophen 650mg po or pr, cooling blanket Oxygenate (Keep Sao2 >95%) Elevate head of bed 30 deg. (Clear c-spine) Frequent repeat Neuro checks!! Reassess GCS!

Treatment of Stroke:

Treatment of Stroke What type of stroke is Present?? Bleed vs Ischemic Any signs of shift herniation? Neurosurgery evaluation or transfer necessary? Other management adjuncts: Ischemic strokes ASA 75-325mg Patients with Systolic BP >220 , Diastolic>130 need BP control with Nitroprusside or Labetolol. DO NOT OVERTREAT BP or risk extending the infarct. Consider Heparin if area of infarct small and neurologist agrees. No bolus, just infusion. Risk of hemorrhagic transformation.

Treatment of Strokes :

Treatment of Strokes Strokes with Edema, Mass Effect or Shift Load with Dilantin 1 g @ rate no faster than 50mg/min. Acute seizure prophylaxis still of benefit. Mannitol, Decadron?? Recently shown to be of NO benefit, some Neurosurgeons still advocate, so consult first. Hyperventilation?? NOT beneficial and perhaps harmful, don’t do it! Thrombolytics??? Ischemic strokes ONLY with large deficit NOT improving. Time from symptom onset <3 hours No ABSOLUTE Contraindications!! Benefit Questionable “Sodhar Courtesy”

Thrombolytic Therapy for Acute Stroke Checklist:

Thrombolytic Therapy for Acute Stroke Checklist Answer to ALL must be YES : Age 18 or older Clinical diagnosis of Acute Ischemic Stroke causing a measurable NON improving neurologic deficit. NO high clinical suspicion for SAH Time of onset to treatment is <180 minutes.

Acute Ischemic Stroke:

Acute Ischemic Stroke Acute Thrombolysis No evidence of hemorrhage on CT Hypodensity on CT < 1/3 of hemisphere Onset of symptoms within 3 hours of rTPA use SBP < 185 DBP < 110 INR < 1.7, Platelets > 100,000, No ASA or anticoagulation, No trauma or recent surgery rTPA: 0.9 mg/kg IV over 60 minutes with 10% of dose given over the 1 st minute “Sodhar Courtesy”

Thrombolytic Therapy for Acute Ischemic Stroke Checklist:

Thrombolytic Therapy for Acute Ischemic Stroke Checklist Answer to ALL MUST be NO : Evidence of hemorrhage on CT Active internal bleeding (GI/GU) within last 21 days. Known bleeding diasthesis: Platelets<100,000 Heparin within last 48 hours with elevated PTT Warfarin use with PT > 15 seconds Within 3 months of IC injury, prior surgery or prior ischemic stroke. Within 14 days of serious trauma, major surgery Recent AMI, arterial puncture/LP within 7 days History of prior ICH, AVM, tumor,or aneurysm or seizure at stroke Systolic BP >185mmHg, or Diastolic BP >110Hg “Sodhar Courtesy”

Seizures & Status Epilepticus:

Seizures & Status Epilepticus Background: 1 – 2% of the general population has seizures Primary Idiopathic epilepsy: onset ages 10-20 Secondary Precipitated by one of the following: Intracranial pathology Trauma, Mass, Abscess, Infarct Extracranial Pathology Toxic, metabolic, hypertensive, eclampsia “Sodhar Courtesy”

Seizure Types:

Seizure Types Generalized Convulsive Seizures (Grand Mal): Tonic , clonic movements, (+) LOC, apnea, incontinence and a post ictal state Non Convulsive Seizures (Petit Mal) Absence seizures – “blank staring spells” Myoclonic – brief contractions of selected muscle groups Partial Seizures Characterized by presence of hallucinations Simple = somatic complaints + no LOC Complex = somatic complaints + AMS or LOC “Sodhar Courtesy”

Approach for 1st Seizure, New Seizure, or Substance/ Trauma Induced Seizure :

Approach for 1 st Seizure, New Seizure, or Substance/ Trauma Induced Seizure As always ABC’s First with C- Spine precautions IV, O2, Monitor. Send blood for CBC, Chem 20, Tox screen as appropriate Anticonvulsant levels Prolactin levels / Lactate levels CXR / UA/ Head CT Is patient still seizing? Post ictal? Pseudoseizure? More later Complete History and Physical Exam Including detailed Neuro Exam Repeat Neuro evaluations a must! “Sodhar Courtesy”

ACEP Guidelines for Postictal Head CT Scans in the ED:

ACEP Guidelines for Postictal Head CT Scans in the ED Status Epilepticus ( a true emergency) Abnormal Neuro findings No return to GCS 15 Prolonged HA History of malignancy HIV infection of high risk for HIV Anticoagulant use Age > 40 “Sodhar Courtesy”

Approach to Breakthrough Seizure:

Approach to Breakthrough Seizure As Before, But History, History, History!! Main causes of Breakthrough Seizure: Noncompliance with anticonvulsant regimen Start of new medication (level alteration) Antibiotics, OCP’s Infection Fever Changes in body habitus, eating patterns Supratherapeutic level “Sodhar Courtesy”

Status Epilepticus:

Status Epilepticus Definition : operationally defined as seizure lasting greater than 5 minutes OR two seizures between which there is incomplete recovery of consciousness. Treatment algorhythm : As before ABC’s IV, O2, Monitor Consider ALL potential causes INH Eclampsia Alcoholic B-6 deficiency Other Tox ingestion (TCA’s, sulfonylurea OD) Trauma “Sodhar Courtesy”

Status Epilepticus Treatment:

Status Epilepticus Treatment FIRST LINE TREATMENT Lorazepam (Ativan) 2mg/min IV up to 10 mg max. OR Diazepam(Valium) 5mg/min IV or PR up to 20mg SECOND LINE TREATMENT Phenytoin or Fosphenytoin: 20mg/kg IV at rate of 50mg/min THIRD LINE TREATMENT Get Ready to intubate at this point!! Phenobarbitol 10-20mg/kg @ 60 mg/min “Sodhar Courtesy”

Status Epilepticus Treatment:

Status Epilepticus Treatment FINAL TREATMENT Barbiturate Coma Pentobarbitol 5mg/kg @ 25 mg/min Stat Neurology consult for evaluation and EEG Pentobarbitol titrated to EEG response. Always get a through HISTORY Possible trauma Medications in house Others sick, symptomatic Overall appearance of patient

Status Epilepticus Adjunctive Treatment by History:

Status Epilepticus Adjunctive Treatment by History Thiamine 100mg IV, 1-2 amps D 50 If suspect alcoholic, malnourished, hypoglycemia Magnesium Sulfate 20cc of 10% solution As above of if eclampsia (BP does NOT have to be 200/120!!) Pyridoxine 5 gms IV INH or B-6 deficiency

Subdural Hematoma:

Subdural Hematoma Occurs secondary to acceleration/decelleration injury with resultant tearing of the bridging veins that extend from the subarachnoid space to the dural sinuses. Blood dissects over the cerebral cortex and collects under the dura overlying the brain. Patients at risk: Alcoholics Elderly Anticoagulant users Appears as “sickle shape” and does not extend across the midline “Sodhar Courtesy”

Subdural Hematoma:

Subdural Hematoma “Sodhar Courtesy”

Epidural hematoma:

Epidural hematoma Occurs from blunt trauma to head especially over the parietal/temporal area. Presents as LOC which then patient has lucid interval then progressive deterioration, coma , death. ( Patient talks to you & dies!) Commonly associated with linear skull fracture Mechanism of bleed is due to tear of artery, usually middle meningeal. PE reveals ipsilateral pupillary dilitation with contralateral hemiparesis. CT Scan : a BICONVEX (lens) density which can extend across the midline “Sodhar Courtesy”

Epidural Hematoma:

Epidural Hematoma “Sodhar Courtesy”

Signs of Herniation / Increased ICP:

Signs of Herniation / Increased ICP Headache, nausea, vomiting Decreasing LOC Sixth nerve paresis (one or both eyes adducted) Decreased respiratory rate Cushing reflex (hypertension/bradycardia/bradynpea) Papilledema Development of signs of herniation Fixed and dilated pupil Contralateral hemiparesis Posturing “Sodhar Courtesy”

Herniation Syndromes:

Herniation Syndromes CPP = MAP – ICP: Must keep CPP >60 mm Hg Uncal Herniation: Occurs when unilateral mass pushes the uncus (temporal lobe) through the tentorial incisa, prersenting as: Ipsilateral pupil dilatation Contralateral hemiparesis Deepening coma Decorticate posturing Apnea and death “Sodhar Courtesy”

Herniation Syndromes:

Herniation Syndromes Cerebellar Herniation Downward displacement of cerebellar tonsils through the foramen magnum. Presents as : Medullary compression Pinpoint pupils Flaccid quadriplegia Apnea and circulatory collapse “Sodhar Courtesy”

Infectious Emergencies:

Infectious Emergencies Meningococcemia “Sodhar Courtesy”

Infectious Neurologic Emergencies:

Infectious Neurologic Emergencies Meningitis: inflammation of the meninges History: Acute Bacterial Meningitis: Rapid onset of symptoms <24 hours Fever, Headache, Photophobia Stiff neck, Confusion Etiology By Age: 0-4 weeks: E. Coli, Group B Strep, Listeria 4-12 weeks: neotatal patoogens, S. pneumo, N. meningitides, H. flu 3mos – 18 years: S.pneumo, N. menin.,H. flu >50/ alcholics: S. pneumo, Listeria, N. menin., Gram(-) bacilli “Sodhar Courtesy”


Meningitis Lymphocytic Meningitis (Aseptic/Viral) Gradual onset of symptoms as previously listed over 1-7 days. Etiology: Viral Atypical Meningitis History (medical/social/environmental) crucial Insidious onset of symptoms over 1-2 weeks Etiology: TB(#1) Coccidiomycosis, crytococcus “Sodhar Courtesy”


Meningitis Physical Exam Pearls Infants and the elderly lack the usual signs and symptoms, only clue may be AMS. Look for papilledema, focal neurologic signs, ophthalmoplegia and rashes As always full exam Checking for above Brudzinski’s sign Kernigs sign KEY POINT: If you suspect meningococcemia do NOT delay antibiotic therapy, MUST start within 20 minutes of arrival !!!!! “Sodhar Courtesy”


Meningitis Emergent CT Prior to LP Those with profoundly depressed MS Seizure Head Injury Focal Neurologic signs Immunocompromised with CD4 count <500 DO NOT DELAY ANTIBIOTIC THERAPY !! “Sodhar Courtesy”


Meningitis Lumbar Puncture Results TEST NORMAL BACTERIAL VIRAL Pressure <170 >300 200 Protein <50 >200 <200 Glucose >40 <40 >40 WBC’s <5 >1000 <1000 Cell type Monos >50% PMN’s Monos Gram Stain Neg Pos Neg “Sodhar Courtesy”

Meningitis Management:

Meningitis Management Antibiotics By Age Group Neonates(<1month) = Ampicillin + Gent. or Cefotaxime + Gent Infants (1-3mos) = Cefotaxime or Ceftriaxone + Ampicillin Children (3mos-18yrs) = Ceftriaxone Adults (18yr-up) = Ceftriaxone + Vancomycin Elderly/Immunocomp = Ceftriaxone +Ampicillin + Vancomycin “Sodhar Courtesy”

Meningitis Management:

Meningitis Management Steroids In children, dexamethasone has been shown to be of benefit in reducing sensiorneural hearing loss, when given before the first dose of antibiotic. Indications: Children> 6 weeks with meningitis due to H. flu or S. pneumo. Adults with positive CSF gram stain Dose: 0.15mg/kg IV “Sodhar Courtesy”


Encephalitis Always think of in the young/elderly or immunocompromised with FEVER + AMS Common Etiologies: Viral West Nile Herpes Simplex Virus (HSV) Varicella Zoster Virus (VZV) Arboviruses Eastern Equine viruses St. Louis Encephalitis “Sodhar Courtesy”


Encephalitis Defined as: inflammation of the brain itself Most cases are self limited, and unless virulent strain, or immunocompromised, will resolve. The ONLY treatable forms of encephalitis are: HSV Zoster “Sodhar Courtesy”


Encephalitis Management: Emergent CT : As indicated for meningitis ABC’s with supportive care. Lumbar puncture: Send for ELISA and PCR Acyclovir 10 mg/kg Q 8 hours IV for HSV and Zoster Steroids not shown to be of benefit. “Sodhar Courtesy”

Headache & Vertigo:

Headache & Vertigo Headache Types of Headache: Migraine With aura Without aura Cluster Headache Subarachnoid hemorrhage Temporal arteritis “Sodhar Courtesy”


Headache Migraine Now thought to be due to neurogenic inflammation and abnormalities of serotonergic transmission. Symptoms: Severe headache either preceeded by a visual “aura”(scintillating scotoma or VF cut) or motor disturbance. Nausea, vomiting, light sensitivity, sound sensitivity Factors that may provoke an attack include: Menstruation, Sleep/food deprivation Physical activity or certain foods (chocolate) Contraceptive estrogens “Sodhar Courtesy”


Migraines History & PE CRUCIAL to obtain HA history from patient Is this HA similar to others or is it “worst HA of life” Prior workups Medications Foods Menses FULL PE including Neuro and Skin “Sodhar Courtesy”


Migraines Management Place patient in cool quiet, dark environment IV fluids if dehydrated Abortive therapy: Proclorperazine(compazine) 10 mg IV DHE + antiemetic Sumatriptan Opiods as LAST RESORT!! “Sodhar Courtesy”


Headaches Cluster Headaches Classically as boring headache on one side of face behind the eye. May be signs of facial flushing, tearing, nasal stuffiness TX: 100% O2 by N/C at 6-8 l/min - If no relief, Sumatriptan “Sodhar Courtesy”


Headaches Subarachnoid hemorrhage Clinically: Abrupt onset of severe thunderclap “worst HA of life”. Usually associated nausea and vomiting Nonfocal neurologic exam (usually) Etiology: usually due to leaking berry aneurysm. DX: CT +LP A MUST If CT (-), MUST perform LP LP (+) if (+) xanthrochromia OR failure of CSF to clear RBC’s by tube #4 “Sodhar Courtesy”


Headaches Subarachnoid Hemorrhage Management ABC’s as always IV, O2, Monitor Head of bed @ 30 degress Prophylax patient for seizures with Dilantin load. Ca Channel blocker (nimlodipine) 60 mg Q6 h to prevent vasospasm, and rebleed. “Sodhar Courtesy”


Headaches Temporal Arteritis Etiology: a granulomatous inflammation of one or more of the branches of the ext. carotid artery Clinically presents as: Severe unilateral HA over Temporal area Usually in middle aged females. PE reveals: a tender, warm, frequently pulseless temporal artery, with decreased visual acuity on the affected side. “Sodhar Courtesy”


Headaches Temporal Arteritis DX: Clinically + ESR elevation, usually>50mm/hr Confirm with biopsy of artery TX: HIGH dose steroids are VISION SAVING! Start on prednisone IMMEDIATELY once suspected Prednisone 60 – 80 mg Q day Stat Neurology Consult “Sodhar Courtesy”


Vertigo History and PE exam again CRUCIAL!! History: Truly a vertiginous complaint? r/o syncope / near syncope?? Acute onset of severe symptoms or more gradual course PE: Full exam paying particular attention to: HEENT : Eyes, TM’s Neuro : Cerebellar function “Sodhar Courtesy”


Vertigo Peripheral Vertigo History: Acute onset of severe dizziness, nausea, vomiting. May be a positional worsening of symptoms Recent history of URI or similar episodes in past which resolved. PE Pearls: Horizontal nystagmus which fatigues Possible TM abnormality Normal Neuro exam with normal cerebellar function and gait. Reproduction of symptoms with Hallpike maneuver “Sodhar Courtesy”


Vertigo Peripheral Common Causes: Labrynthitis Cerumen Impaction OM OE URI Menieres Disease (tinnitus,hearing loss, vertigo) TX: Symptomatic and treat underlying cause: Antivert 25 mg Q6h Neurology / ENT follow up “Sodhar Courtesy”


Vertigo Central Vertigo Due to lesions of brainstem or cerebellum 10 – 15% of cases Signs & Symptoms : Gradual onset of mild disequilibrium Mild nausea and vomiting Nonfatigable any direction nystagmus Associated neurological abnormalities: Ptosis Facial palsy, dysarthria Cerebellar findings, ataxia “Sodhar Courtesy”


Vertigo Central Causes: Brainstem ischemia or infarction Cerebellar hemorrhage Vertebrobasilar insufficiency MS Diagnosis: Thorough Neurologic exam Head CT with Posterior fossa thin cuts Management: Neuro consult Admit and workup depending on etiology “Sodhar Courtesy”

Emergent Peripheral Neuropathies:

Emergent Peripheral Neuropathies Acute Toxic Neuropathies Diptheria (Cornybacterium diptheriae) Acutely ill patient with fever, in a dPT deficient patient. Membranous pharyngitis that bleeds Powerful exotoxin produces widespread organ damage. Myocarditis/AV Block,Nephritis, Hepatitis. Neuritis with bulbar and peripheral paralysis. (ptosis, strabismus, loss of DTR’s) TX: Parenteral PCN or Erythromycin Horse Serum antitoxin Respiratory isolation and admission the rule.

Emergent Peripheral Neuropathies:

Emergent Peripheral Neuropathies Botulism (Clostridium botulinum toxin) Earliest finding(90%)= Blurred vision, diplopia, ophthalmoplegia, ptosis Neurologic abnormalities descend and will lastly involve the respiratory musculature and cause respiratory paralysis and death with 6 hours if not treated! Mentation and sensation are normal. Remember in infants with FTT Raw honey contains C. botulinum Tx: Aggressive airway stabilization! Trivalent serum antitoxin Lastly some reported cases of hypersensitivity from “Bo-tox” So ……..

Emergent Peripheral Neuropathies:

Emergent Peripheral Neuropathies Tetanu s Symptoms 4 “T”’s Trismus, Tetany, Twitching, Tightness Risus sardonicus Signs of sympathetic overstimulation. Tachycardia, hyperpyrexia, diaphoresis. Management: Human Tetanus Immunoglobulin (HTIG) dT Toxoid Metronidazole

Emergent Peripheral Neuropathies:

Emergent Peripheral Neuropathies Guillain-Barre Syndrome Most common acute polyneuropathy. 2/3’s of patients will have preceeding URI or gastroenteritis 1-3 weeks prior to onset. Presents as: paresthesias followed by ascending paralysis starting in legs and moving upwards. Remember Miller-Fischer variant: has minimal weakness and presents with ataxia, arreflexia, and ophthalmoiplegia. DX: LP will show cytochemical dissociation. Normal cells with HIGH protein. TX: Self limiting, Early and aggressive airway stabilization.

Emergent Peripheral Neuropathies:

Emergent Peripheral Neuropathies Myasthenia Gravis Most common disorder of neuromuscular transmission. An autoimmune disease that destroys acetylcholine receptors which leads to poor neurotransmission and weakness. Commonly will present as: Muscle weakness exacerbated by activity, and is relieved by rest Clinically: ptosis, diplopia and blurred vision are the most common complaints. Pupil is spared! “Sodhar Courtesy”

Emergent Peripheral Neuropathies:

Emergent Peripheral Neuropathies Myasthenia Gravis Myasthenic crisis = A true emergency!! Occurs in undiagnosed or untreated patients Due to Ach deficiency Patients present with profound weakness and impending respiratory failure TX: Stabilize and manage airway Look for chloinergic signs”SLUDGE” If cholinergic give atropine 1mg IV prn Consider edrophonium 1 -2 mg IV “Sodhar Courtesy”

New Emerging Treatments:

New Emerging Treatments Stroke/ TIA’s Hypothermia units with cooling . Lasers, cerebral angioplasty and clot retrieval. “Sodhar Courtesy”

PowerPoint Presentation:

ANY QUESTIONS???? Jasakallah khairan Now you are ready to go out there and confidently handle patients presenting with these various Neurological Emergencies! “Sodhar Courtesy”