Neurologic Emergencies

Notes on “Neurologic Emergencies” Lecturer: Dr. Johnny Lokin March 12, 2007 Overview: Stupor & Coma Increase ICP Herniation Myasthenic Crisis and Guillain Barre Syndrome Stroke STUPOR & COMA Reticular Activating System: wakefulness, attention & concentration Pathology must involve: Bilateral Supratentorial ARAS Infratentorial Diffuse Toxic or Metabolic Level of Arousal : depends on brainstem, especially ARAS Cognitive function : cortical & thalamocortical integrity Five Physiologic Variables 1. State of consciousness 2. Pattern of breathing 3. Size & reactivity of pupils 4. Eye movements & oculovestibular response 5. Skeletal muscle motor responses Terms Confuse Delirium Obtundation Stupor Vegetative State Apallic Syndrome Akinetic mutism Locked-in syndrome

Neurologic Breathing Cheyne-Stokes breathing

Ataxic Breathing Apneustic Breathing

Definition Bewildered but attentive Irritable Reduced alertness Responsive only to vigorous stimulus Return of alertness but without cognitive function Similar to vegetative state Minimal motor response to noxious stimulus Paralyzed but alert & aware of his surroundings (Victor & Ropper, 2002) Pattern & Location Periods of deep breathing alternate w/ periods of apnea Cerebral hemispheres or diencephalon Unpredictable irregularity; Cerebellum & Medullary level Pons

Pupillary changes Equally reactive, small Small but reactive Anisocoria (larger pupil: site of lesion Large fixed pupils Pinpoint pupils Midposition & fixed

Causes Metabolic or toxic Diencephalic Cranial nerve Tectum Pons Midbrain

Oculocephalic Reflex or Doll’s Eye Maneuver Looking for conjugate movement of the eye Normal response: movement of the eyes opposite the movement of the head Alteratio n in moveme nt Decorticat e posturing

Posture

Pathology

•

Depressed level of consciousness (Lethargy, stupor, coma) • HTN with or without bradycardia Sometimes present: • Headache • Nausea & vomiting • Papilledema • Bilateral CN VI palsy ICP Monitoring

UE: flexed LE: externally rotated & extended UE: flexed LE: flexed

Decerebra te

Brainstem is not inhibited by motor function of cortex; Lesion in cortex Extensive BS lesions especially pons & compression of thalamus & midbrain

INCREASE ICP Monro-Kellie Doctrine Brain 80% V1 parenchyma Blood 10% V2 CSF 10% V3 ICP = V1 + V2 + V3 If with tumor: ICP = V1 + V2 + V3 + V tumor

Normal ICP = 5-15 mmHg (3-20 cmH20) Increase ICP: ICP of > 20 mmHg lasting for > 5 mins Increase ICP 1. Early : autoregulation 2. Gradual increase in ICP 3. ~ 30 mmHg (to 50 mmHg): brain losses its compliance & the skull acts like a box thereby producing s/sx of ↑ ICP Causes: Tumour Abscess Hematoma S/sx of ↑ ICP: Headache with nausea & vomiting Deteriorating sensorium Papilledema Sudden HTN Bradycardia Cushing’s Bradypnea reflex Clinical Signs of ↑ ICP: Always present:

VS: 1. Cerebral ischemia; Cushing’s reflex 2. Systemic vasoconstriction 3. Response to increase BP: slow-heart rate low CO2 4. From accelerated circulation, decrease RR 5. …

d. Hyperthermia produces deleterious effects on neuronal recovery & blood-brain barrier integrity Indications for ICP Monitoring: 1. Signs of transtentorial herniation 2. Progressive neurologic deterioration

Visual Signs: 1. Change in eye 2. Pressure on CN III: size & response of pupils • Ipsilateral pupil become fixed & dilated: sign of an impending uncal herniation

Clinical Sequelae of ↑ ICP: • Compression • Herniation • Destruction of brain tissues

Management: 1. Head position • 30° head-elevated position: decreases ICP without deleterious effects on cerebral perfusion pressure or cerebral blood flow • Midline position 2. Mannitol a. Plasma expanding effect ↓ Hematocrit ↓ ↓ blood viscosity ↓ ↓ Cerebral blood volume ↓ ↑ cerebral blood flow ↓ ↑ cerebral O2 delivery •

Effect is immediate (20 mins) & transient • Only operate when pressure autoregulation of CBF is intact b. Osmotic effect • Prolonged due to dehydration • Delayed 15-30 mins, lasts 1.5-6 hours • Excreted in urine • Avoid if osmolarity > 320 mOsm to prevent Acute Tubular Necrosis • Administer in boluses to avoid brain cellular swelling due to mannitol accumulation Intermittent boluses: 0.25 – 1g/kg C/I: plasma osm > 320 mmol/L (risk of renal failure) 3. Hypothermia a. Prevention & aggressive treatment for fever b. Sig benefit: mild hypothermia 32-34 C for 24-48 hours c. Seizure incidence & decrease in ICP

HERNIATION SYNDROMES Uncal hernation: • Unilateral mass pushes uncus (temporal lobe) through tentorial incise • Ipsilateral pupil dilation • Contralateral hemiparesis • Deepening coma • Decorticate posture • Apnea & death

Pathol ogy

Cerebellar herniation: • Cerebellar tonsil through foramen magnum • Medullary compression  respiratory arrest • Pinpoint pupils • Flaccid quadriplegia • Apnea & circulatory collapse

Mgt

Rostrocaudal herniation Early

Late

Later

Latest Slow irregula r

Motionl ess & flaccid

dienceph alic

Respi

Cheyne -Stokes

Cheyn eStokes

Pupil

Pinpoin t

Pinpoin t

Oculo vesti b& ceph alic Motor

Normal

(+)

Sustain ed tachypn ea Midsize, midposi tion (+)

(N)

Decortic ate

Decerebr ate

Fixed (-)

Reducing ICP: 1. Mannitol 20% infusion for 3 days 2. Hypertonic NaCl: 20-25%, 30 cc every 4 hours 3. Controlled hyperventilation a. Intubate b. pCO2: 25-30mmHg 4. CSF withdrawal a. Ventricular drainage b. ICP monitoring 5. Sedatives 6. Steroids: Dexamethaxone (only for tumors) 7. Others: Trimethamine, Barbital, Lidocaine, Hypothermia, Furosemide GBS & MG GBS MG Motor Progressive Fluctuating weakness weakness Sensor Slightly (N) y affected DTR Decrease or (N) Zero

Lab

Poly radiculoneurop athy Axonal degeneration & demyelination Albuminocytol ogic dissocation in CSF after 7-10 days DOC: IVIg 0.4g/kg/day for 5 days Respiratory support No steroids

NMJ Immunemediated

EMG-NCV (+) Cholinesterase Ab titer DOC: Mestinon Plasmapharesi s: 5x for 2 consecutive days Corticosteroids

Notes by: Jobern Hipol IIIB ‘08 Wisdom denotes the pursuing of the best ends by the best means. – Frances Hutcheson