neurological emergencies stephen deputy, md
TRANSCRIPT
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Neurological EmergenciesStephen Deputy, MD
Acute Ischemic Stroke Intracranial Hemorrhage Status Epilepticus Guillan-Barre Syndrome Acute Myelopathy Myasthenic Crisis
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Acute Ischemic Stroke
AIS is caused by the sudden loss of blood circulation to an area of the brain resulting in ischemia and corresponding loss of neurological function.
Within seconds to minutes of loss of perfusion, an ischemic cascade is unleashed resulting in a central area of irreversible infarction surrounded by an area of potentially reversible ischemic penumbra.
The goal of treatment for AIS is to preserve the area of oligemia in the ischemic penumbra. This is done by limiting the severity of injury (neuronal protection) and by restoring blood flow to the penumbra.
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Acute Ischemic StrokeIschemic Cascade
Loss of O2 and Glucose delivery to the neuron results in cellular depolarization as ATP is depleted and the Na-K ATP-as pump fails.
The resulting Ca influx results in the release of many excitatory neurotransmitters including glutamate which binds to the NMDA receptor resulting in further Ca influx and further depolarization and release of glutamate.
Massive Ca influx results in activation of various degrative enzymes which damage cellular membranes.
The release of free radicals, arachadonic acid and nitric oxide further damage neurons.
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Acute Ischemic Stroke
Ischemic Cascade Within hours to days, activation of apoptotic
and other genes results in the release of cytokines and further inflammatory molecules, resulting in further inflammation and microcirculatory compromise.
Ultimately, the ischemic penumbra is consumed by these progressive insults, coalescing within the ischemic core, often within hours of the onset of the AIS.
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Acute Ischemic StrokeClinical Presentation
No clinical feature reliably distinguishes AIS from hemorrhagic stroke, though headache, N/V, and altered mental status make hemorrhagic stroke more likely.
Common symptoms of AIS include the abrupt onset of hemiparesis, monocular visual loss, ataxia, vertigo, aphasia, or sudden depressed level of consciousness.
Establishing the onset of symptoms is essential when considering possible thrombolytic therapy.
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Acute Ischemic Stroke
Transient Ischemic Attack TIA’s are defined as a transient ischemic
neurological deficit that resolves within 24 hours
80% resolve within 60 minutes TIA’s precede 30% of AIS Left untreated, 30% of TIA’s progress to AIS
(20% within the first month and 50% within the first year)
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Acute Ischemic StrokePhysical Examination
Goal of PE is to look for extra cranial causes of AIS and to distinguish AIS from stroke mimics (seizures, tumors, toxic-metabolic disturbances, positional vertigo, etc).
HEENT: Look for trauma signs and nuchal rigidity, listen for cranial or cervical bruits, evaluate pulse strength. Fundoscopy to look for emboli, hemorrhage, papilledema.
C/V: Signs of CHF, Atrial fibrillation, arrhythmias. Ext: Signs of venous thrombosis and arterial
emboli.
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Acute Ischemic StrokeNeurological Exam
Goal is to establish baseline for monitoring response to therapy and to determine size and location of AIS
MS, CN, Motor, Coordination, Sensory and Gait need to be covered, however speed is of the essence!
MCA: Contralateral : Hemiparesis, Hemianopsia and Sensory loss
Ipsilateral: Gaze preference. Dominant Hemisphere: Aphasia Non-Dominant Hemisphere: Hemi-neglect
and cortical sensory deficits
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Acute Ischemic StrokeNeurological Exam
ACA: Disinhibition, primitive reflexes, contralateral
hemiparesis (legs>arms), urinary incontinence.
PCA: Contralateral hemianopsia, cortical blindness,
altered mental status, impaired memory.
Vertebrobasilar: Vertigo, nystagmus, ataxia. Crossed findings (ipsilateral cranial
nerve deficits along with contralateral long track signs).
Lacunar Infarcts: Pure motor, pure sensory, ataxia/hemiparesis.
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Acute Ischemic Stroke
Work Up Labs: CBC with platelets, CMP, PT, PTT,
cardiac biomarkers, EKG. Imaging: Emergent non-contrast CT
Distinguishes hemorrhagic from ischemic stroke Defines age and anatomic distribution of stroke Large hypodense area seen within 3 hours brings
into question of timing of AIS and may predict poor outcome
Hyperdense MCA sign, insular ribbon sign, obscuration of lentiform nucleus, loss of gray-white junction
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Hyperdense MCA Sign
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Large Cortical Hypodensity
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Acute Ischemic StrokeOther Imaging Studies
CT Angiography MRI:
Diffusion-Perfusion mismatch (correlates to the core area of infarction and surrounding area of the ischemic penumbra)
More sensitive than CT to early ischemic changes MR Angiography Conventional Cerebral Angiography Echocardiography: (CHF, akinetic wall,
vegetation/clots, septal defects, PFO) Carotid Doppler Ultrasound: Carotid stenosis
evaluation
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Acute Ischemic Stroke
Treatment ABCD’s
Airway: Intubation for GCS < 9 or lack of airway protective reflexes
Breathing: O2 if hypoxic. Keep PCO2 32-36 mmHg
Circulation: Maintain adequate CPP (MAP-ICP). Do not treat HTN unless > 200/120
D = Dextrose. Maintain normoglycemia (even if insulin is needed) as hyperglycemia worsens neurological outcome
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Acute Ischemic Stroke
Treatment Fever: Hyperthermia worsens ischemic injury Cerebral edema: Peaks 72-96 hours.
Hyperventilation can decrease CPP. Mannitol may leak across compromised BBB. No evidence of benefit for steroids. Decompressive craniectomy and resection
of necrotic tissue may be indicated, especially in the setting of hemorrhagic transformation.
Seizure control: Prophylactic AED is not indicated unless malignant elevated ICP is present
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Acute Ischemic StrokeAcute Thrombolysis
Balance restoration of blood flow and hemorrhage risk
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 1st minute
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Acute Ischemic Stroke
Strategies for Reducing Future Strokes Anti-Platelet Therapy Warfarin: (Atrial Fibrillation, Arterial
Dissection) Carotid Endarterctomy / Stent Placement PFO Closure Reducing Stroke Risk Factors
(Hypercholesterolemia, Hypertension, Diabetes, Obesity, Lack of Exercise, Smoking, OCP’s)
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Intracranial Hemorrhage(non-traumatic)
Location of Hemorrhage Intraventricular Hemorrhage Intraparenchymal Hemorrhage Subarachnoid Hemorrhage Subdural Hematoma Epidural Hematoma
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Intracranial Hemorrhage
Intraventricular Hemorrhage Accounts for 3% of all non-traumatic ICH Hypertension is the most common etiology Often results from an intraparenchymal
hemorrhage that extends into the ventricular system
S/S: Headache, N/V, Progressive deterioration of consciousness, raised ICP, Nuchal rigidity
Survivors may develop post-hemorrhagic hydrocephalus
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Intracranial Hemorrhage
Intraparenchymal Hemorrhage Basal Ganglia Hemorrhage
Contralateral hemiparesis, hemichorea, hemisensory loss, and hemi-neglect are common neurological deficits
Putaminal Hemorrhage is the most common location of intraparenchymal hemorrhage secondary to HTN
Putaminal Hemorrhage, if massive, will result in Uncal Herniation(Ipsilateral blown pupil, contralateral hemiparesis, depressed LOC
Caudate Hemorrhage is most likely to rupture into ventricles
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Basal Ganglia Intraparenchymal Hemorrhage
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Intracranial Hemorrhage
Intraparenchymal Hemorrhage Thalamic Hemorrhage
Contralateral hemiparesis, hemisensory loss and depressed LOC (wake center) are common deficits
Extension into ventricular system common resulting in obstructive hydrocephalus with 3rd ventricular enlargement => Parinaud’s Syndrome (Paralysis of voluntary upward gaze, light-near dissociation, convergence-retraction nystagmus, eyelid retraction)
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Thalamic Intraparenchymal Hemorrhage
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Intracranial Hemorrhage
Intraparenchymal Hemorrhage Pontine Hemorrhage
Abrupt onset of coma, pinpoint pupils, autonomic instability, horizontal gaze paralysis, and quadriparesis
The miotic pupils and depressed LOC may mimic opiate overdose
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Pontine Intraparenchymal Hemorrhage
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Intracranial Hemorrhage
Cerebellar Hemorrhage Sudden onset of vertigo, severe N/V, and
ataxia leading to altered mental status and coma over a few hours
Obstructive hydrocephalus can contribute to brainstem herniation
Urgent posterior fossa decompression is essential for survival
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Intraparenchymal Cerebellar Hemorrhage
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Intracranial Hemorrhage
Lobar Intraparenchymal Hemorrhage This is often a clinically silent lesion S/S depend on location of hemorrhage,
though hemiparesis, aphasia, hemianopsia, and hemisensory loss common
Mimics lobar AIS
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Lobar Intraparenchymal Hemorrhage
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Intraparenchymal HemorrhageEtiology
Hypertension is the #1 cause in adults Hyalinization of small penetrating arteries
(replacement of smooth muscle by collagen => increased friability of vessels
Cerebral Amyloid Angiopathy Elderly with dementia and multiple bleeds
Anticoagulation and Anti-Platelet Meds Systemic anticoagulated states (eg. DIC) Sympathomimetic Drugs Aneurysms, AVM’s, Cavernous Angiomas Brain Tumors
Metastatic (renal cell CA, malignant melanoma, prostate, and lung CA) GBM and Hemangioblastoma
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Intraparenchymal HemorrhageTreatment
ABCD’s Intubation Treat Hypertension to keep SBP < 160 mmHg
Fluid and Electrolyte Management Use Normal Saline, avoid Dextrose Watch for SIADH and Cerebral Salt Wasting
Prevent Hyperthermia Seizure Prophylaxis Correct Underlying Coagulopathy
FFP, platelet Infusions, Vitamin K
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Intraparenchymal HemorrhageTreatment
Recombinant Factor VII Dosing ranges between 40 and 160 micrograms Beneficial if given within 4 hours of onset Risk of myocardial infarction and AIS
Management of ICP Hyperventilate to keep PaCO2 around 30 mmHg Avoid Mannitol (can leak into hematoma) External Ventricular Drain (if hydrocep0halus present) Surgical Evacuation of Hematoma (controversial)
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Subarachnoid Hemorrhage(non-traumatic)
Aneurysmal rupture accounts for 80% of cases Risk Factors
Advancing age, Smoking, HTN, Cocaine use, Hypertension, Heavy Alcohol use, Connective Tissue Disorders, Sickle Cell Disease, First Degree Relatives with Aneurysms
Fatality rate is 50% within 2 weeks 30% of survivors require lifelong care 15% of patients will have > 1 aneurysm Outcome largely dependent on clinical
presentation and CT findings
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Subarachnoid Hemorrhage
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Subarachnoid Hemorrhage
Clinical presenting signs Sudden-Onset “Thunderclap Headache” “Worst Headache of my life” CN III palsy (p. comm aneurysm) CN VI palsy (raised ICP) Retinal Hemorrhages Altered Mental Status Nuchal Rigidity
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Subarachnoid Hemorrhage
Diagnostic Work Up CT Imaging
Will pick up > 90% SAH (get thin cuts through skull base)
Sensitivity drops to < 50% after 2 weeks Carefully evaluate basilar cisterns for
hemorrhage
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Subarachnoid Hemorrhage
Diagnostic Work Up Lumbar Puncture
Perform if high index of suspicion and negative CT
Elevated Opening Pressure Increased RBC count that does not
“clear” between tubes one and tube four Xanthochromia (rule of 2’s)
Starts at 2 hours, Peaks at 2 days, Clears by 2 weeks
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Subarachnoid Hemorrhage
Diagnostic Work Up Angiography
Digital Subtraction Angiography is gold standard
CT Angiography MR Angiography Look for Multiple Aneurysms
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ConventionalAngiogram
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CT Angiogram
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MR Angiogram
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Subarachnoid HemorrhageTreatment
General Measures ABCD’s
Intubation for GCS < 9 Treat HTN: SBP 90-140 prior to aneurysm treatment, < 200
mmHg after Rx Glucose between 80 and 120 mg/dl Euvolemia (CVP 5-8 mmHg unless vasospasm, then CVP 8-12
mmHg) Temperature Quiet Room / Sedation GI (H2 blocker, stool softener, NPO) Vasospasm
Nimodipine 60 mg po q 4 hrs for 21 days Seizures (Phenobarbital or Lorazepam)
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Subarachnoid Hemorrhage
Treating the Aneurysm Surgical Intervention Endovascular Coiling
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Status Epilepticus
Definitions A single seizure or back-to-back
seizures without return of consciousness lasting > 45 minutes (primate studies) >30 minutes (WHO definition) >10 minutes (working definition)
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Status Epilepticus
Epidemiology 10% of all individuals with epilepsy will
have at least one episode of SE in their lifetime
10% of patients experiencing a first unprovoked seizure will present in SE
Risk of recurrent SE: Greatest for those with remote symptomatic
etiologies Not any higher in those with idiopathic or
febrile etiologies
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Status EpilepticusEtiologies
Idiopathic (24%) No precipitating event, pt is neurologically and developmentally normal
Febrile (24%) Includes “febrile seizures” and seizures in the setting of a febrile illness
Remote Symptomatic (23%) Prior neurological insult or developmental brain malformation
Acute symptomatic (23%) Progressive Degenerative (6%)
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Status EpilepticusAcute Symptomatic Etiologies
Vascular Stroke (Hemorrhagic > Ischemic) Subarachnoid Hemorrhage Hypoxic Ischemic Encephalopathy
Toxic Cocaine and other sympathomimetics Alcohol withdrawal Various Medications (Isoniazid, TCA’s,
various chemotherapy agents) AED non-compliance or withdrawal
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Status EpilepticusAcute Symptomatic Etiologies
Metabolic Hyper or Hypo-Natremia Hypoglycemia Hypocalcemia Liver or Renal failure
Infectious Meningoencephalitis Brain Abscess
Trauma Neoplastic
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Status Epilepticus
Treatment ABCD’s
Airway: Risk of aspiration, suction to bedside
Breathing: Give supplemental O2 C/V: Initial tachycardia giving way to
hypotension (especially when Benzos or Barbiturates are given)
Dextrose: Symptomatic hypoglycemia is causing irreversible brain injury until corrected
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Status Epilepticus History
Fever, pre-existing epilepsy, trauma, baseline AED’s and their dosing
Physical Exam Signs of trauma, nuchal rigidity, end
organ injury Subtle signs of seizures (tachycardia,
pupil dilation and hippus, nystagmus, irregular respirations)
Work Up Lytes, glucose, AED levels, CPK, LFT’s,
ABG, NH3 CT of brain LP (when stable) if indicated. Empiric
antibiotics.
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Status Epilepticus
Anticonvulsant Therapy Benzodiazepine Therapy (10
minutes) Long-Acting AED Therapy (10 to 30
minutes) Refractory Status Therapy (>30
minutes)
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Status EpilepticusBenzodiazepine Therapy
Lorazepam 0.1 mg/kg max: 4 mg/dose Has 8 hour effective t½
Diazepam 0.3 to 0.5 mg/kg max: 10 mg/dose Fat-soluble so pr dosing possible Diastat (Dosing about double that of IV)
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Status EpilepticusLong-Acting Anticonvulsant Therapy
Phenytoin 20 mg/kg over 20 minutes (regardless of
weight) C/R monitor during load No dextrose in line Extravasation injuries are severe Cerebyx
20 mgPE/kg over 8 minutes No precipitation in dextrose Less severe extravasation injury (more
neutral pH)
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Status Epilepticus
Long-Acting Anticonvulsant Therapy Phenobarbital
20 mg/kg over 20 minutes Watch for respiratory suppression
(especially if the patient has received Benzodiazepines)
Watch for hypotension Good for Febrile Status Epilepticus
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Status EpilepticusRefractory Status
Secure airway Transfer to ICU Extra lines for hypotension treatment EEG Monitoring (electrical-clinical
dissociation) Medications
Pentobarbital Other agents (Midazolam drip, Propofol,
Lidocaine, inhalation anesthetics, other AED’s)
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Guillan-Barre´SyndromeDefinition
Progressive ascending weakness along with various cranial neuropathies
Areflexia Minimal sensory deficits (though radicular
pain is common) Progression over days to 4 weeks Preceding infection or Immunization: 1 to
4 weeks prior to onset of weakness (C. jejuni, CMV, Mycoplasma, dT, OPV, VZV)
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Guillan-Barre´Syndrome
GBS Variants Acute Inflammatory Demyelinating
Polyneuropathy Acute Motor Axonal Neuropathy Acute Motor Sensory Axonal Neuropathy Miller Fisher Syndrome Chronic Inflammatory Demyelinating
Polyneuropathy(> 4weeks of progression or future
relapses)
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Guillan-Barre´SyndromePhysical Exam
Look for the Tick! Bulbar and Respiratory Compromise Relatively Symmetric Ascending
Weakness Diminished/Absent DTR’s No Sensory Level Radicular Pain/Paresthesias Autonomic Dysfunction: Increased or
Decreased SNS or PNS Function (tachy-brady arrhythmias, hyper/hypotension, urinary retention, decreased GI mobility)
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Guillan-Barre´SyndromeLaboratory Support
CSF: Albuminocytological Dissociation Elevated Protein without Pleocytosis
Nerve Conduction: Multifocal, asymmetrical demyelination
with secondary axonal degeneration Slowing of Nerve Conduction Velocities Temporal Dispersion and Conduction
Block
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Guillan-Barre´SyndromeTreatment
ABC’s Airway/Breathing: (Serial Examinations)
Forced Vital Capacity: (want > 15 ml/kg) Negative Inspiratory Force (want > - 40
mmHg) ABG’s : Look for rising Pa CO2 Clinical Exam (accessory muscles, SOB,
diminished exhalation strength) Elective Intubation if Respiratory
Insufficiency or significant Bulbar Weakness
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Guillan-Barre´Syndrome
Treatment ABC’s
Cardiovascular C/R and BP Monitoring Careful when treating hypo or
hypertension Excessive Vagal Response with GI pain,
Intubation, Tracheal Suctioning and other Procedures
ICU Monitoring Until Patient Reaches Nadir of Weakness
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Guillan-Barre´Syndrome
Treatment IVIG
5 day infusion of 0.4 g/kg per day Plasmapharesis
5 exchanges (40-50 ml/kg) given on alternate days using saline and albumin as replacement fluid
No Role for Steroids
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Guillan-Barre´Syndrome
Outcome 10% to 20% require mechanical
ventilation Mortality 2% to 5% After nadir, plateau phase lasts 2-4
weeks 70% complete recovery within 1 yr,
82% by 2 yrs 3% will go on to have relapse (CIDP)
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Acute Myelopathy
Clinical FindingsThe spinal cord contains closely
approximated ascending and descending tracts that will result in multiple deficits in the setting of injury. Some of the more clinically important tracts include:
Descending Corticospinal Tract Ascending Spinothalamic Tract Ascending Posterior Columns Descending Autonomic Nervous System
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Acute MyelopathyClinical Deficits
Acute Flaccid Paralysis (Ipsilateral to side of lesion) Dropped DTR’s below the level of the lesion Anterior Horn Cell dysfunction at the level of
the lesion Distinguish from dropped DTR’s due to GBS Plantar Responses will be Extensor Superficial Reflexes absent below the level of
the lesion Superficial Abdominal Reflex Cremaster Reflex Bulbocavernosus Reflex
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Acute Myelopathy
Clinical Deficits Sensory Level
Pain and Temperature (Contralateral to side of lesion) Spinothalamic Tract
Vibration and Joint Position Sense (Ipsilateral) Posterior Columns
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Acute MyelopathyClinical Deficits
Autonomic Nervous System Horner’s Sign
Ptosis, Meiosis, Anhydrosis Ipsilateral Descending SNS (C1-T2)
Bladder Dysfunction Sphincter Dysynergy Spastic Bladder with Incontinence
Bowel Dysfunction Constipation or Incontinence Diminished Rectal Tone
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Acute Myelopathy
Etiologies Trauma
High-Dose Methylprednisolone Protocol Spontaneous Epidural or Subdural
Hematoma Neoplastic
Metastatic or Primary Tumors Vascular
Ischemia (Aortic Surgery, Hypotension, Spinal Surgery)
Hemorrhagic (Vascular Malformations, Coagulopathy)
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Acute Myelopathy
Etiologies Demyelinating
Transverse Myelitis (Isolated or as part of MS)
Vasculitis (SLE) Infectious
Epidural/Subdural Abscess Osteomyelitis/Discitis
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Acute MyelopathyEtiologies
Acute Myelopathy should be considered to be caused by a mass lesion compressing the cord until proven otherwise!
Emergent Imaging is warranted MRI of Spine is preferred CT Myelogram is second choice
Emergent Neurosurgical Consultation Time is of the essence!
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Myasthenic CrisisMG is an auto-immune disorder characterized by a humoral-mediated immune attack on Acetylcholine receptors on skeletal muscle
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Myasthenic Crisis
Clinical Features Opthalmoparesis and Ptosis Bulbar Weakness Respiratory Muscle Weakness Key Point: Weakness is Fatigable
Progressive Weakness with Repetitive Testing
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Myasthenic CrisisDiagnosis
Clinical Fatigable weakness Preserved DTR’s Tensilon Test (Acetylcholine Esterase
Inhibitor) Electrophysiology
Decremental CMAP amplitudes with repetitive stim.
Lab Acetylcholine Receptor Antibodies
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Myasthenic Crisis
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Myasthenic Crisis
Treatment of MG Acetylcholine Esterase Inhibitors
(Mestinon) Immunosupression
Steroids IVIg Plasmapharesis
Thymectomy
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Myasthenic CrisisTreatment of Myasthenic Crisis
ABC’s Secure the airway with intubation if there is
any doubt Look for and Rx any underlying infection Remove medications which can
exacerbate MG Gentamycin, steroids, anticholinergics Never increase Mestinon to try and get out
of a myasthenic crisis It may be reasonable to D/C or lower
Mestinon if one cannot exclude a cholinergic crisis (SLUDGE)
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Myasthenic Crisis
Treatment of Myasthenic Crisis High dose Methylprednisolone IVIg Plasmapharesis
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Clinical Neurosciences Clerkship
Now you are ready to go out there and confidently
handle patients presenting with these various
Neurological Emergencies!