Notes on “Neurologic Emergencies” Pupillary Causes

Lecturer: Dr. Johnny Lokin March changes

12, 2007 Equally reactive, Metabolic or toxic
Overview: small
Stupor & Coma Small but reactive Diencephalic
Increase ICP Anisocoria (larger Cranial nerve
Herniation pupil: site of lesion
Myasthenic Crisis and Guillain Large fixed pupils Tectum
Barre Syndrome Pinpoint pupils Pons
Stroke Midposition & fixed Midbrain
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 Definition
Confuse Bewildered but
attentive
Delirium Irritable
Obtundation Reduced alertness
Stupor Responsive only to
vigorous stimulus
Vegetative Return of alertness but
State without cognitive
function
Apallic Similar to vegetative
Syndrome state
Akinetic Minimal motor response
mutism to noxious stimulus
Locked-in Paralyzed but alert &
syndrome aware of his
surroundings (Victor &
Ropper, 2002)

Neurologic Pattern & Location

Breathing
Cheyne-Stokes Periods of deep
breathing breathing alternate w/
periods of apnea
Cerebral hemispheres
or diencephalon
Ataxic Unpredictable
Breathing irregularity; Cerebellum
& Medullary level
Apneustic Pons
Breathing
Oculocephalic Reflex or Doll’s Eye • Depressed level of consciousness
Maneuver (Lethargy, stupor, coma)
Looking for conjugate movement of the • HTN with or without bradycardia
eye Sometimes present:
Normal response: movement of the eyes • Headache
opposite the movement of the head
• Nausea & vomiting
Alteratio Posture Pathology • Papilledema
n in • Bilateral CN VI palsy
moveme
nt ICP Monitoring
Decorticat UE: flexed Brainstem is not
e LE: inhibited by
posturing externally motor function
rotated & of cortex;
extended Lesion in cortex
Decerebra UE: flexed Extensive BS
te LE: flexed 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: d. Hyperthermia produces
1. Cerebral ischemia; Cushing’s reflex deleterious effects on neuronal
2. Systemic vasoconstriction recovery & blood-brain barrier
3. Response to increase BP: slow-heart integrity
rate low CO2 Indications for ICP Monitoring:
4. From accelerated circulation, 1. Signs of transtentorial herniation
decrease RR 2. Progressive neurologic
5. … deterioration

Visual Signs: Clinical Sequelae of ↑ ICP:

1. Change in eye • Compression
2. Pressure on CN III: size & response of • Herniation
pupils • Destruction of brain tissues
• Ipsilateral pupil become fixed &
dilated: sign of an impending
uncal herniation

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 Pathol Poly NMJ
Uncal hernation: ogy radiculoneurop Immune-
• Unilateral mass pushes uncus athy mediated
(temporal lobe) through tentorial Axonal
incise degeneration
• Ipsilateral pupil dilation &
• Contralateral hemiparesis demyelination
Lab Albuminocytol EMG-NCV
• Deepening coma
ogic (+)
• Decorticate posture dissocation in Cholinesterase
• Apnea & death CSF after 7-10 Ab titer
days
Cerebellar herniation: Mgt DOC: IVIg DOC: Mestinon
• Cerebellar tonsil through foramen 0.4g/kg/day for Plasmapharesi
magnum 5 days s: 5x for 2
• Medullary compression  respiratory Respiratory consecutive
arrest support days
• Pinpoint pupils No steroids Corticosteroids
• Flaccid quadriplegia Notes by: Jobern Hipol IIIB ‘08
Wisdom denotes the pursuing of the best ends by the
• Apnea & circulatory collapse best means. – Frances Hutcheson

Rostrocaudal herniation
Early Late Later Latest
dienceph
alic
Respi Cheyne Cheyn Sustain Slow
-Stokes e- ed irregula
Stokes tachypn r
ea
Pupil Pinpoin Pinpoin Midsize, Fixed
t t midposi
tion
Oculo Normal (+) (+) (-)
-
vesti
b&
ceph
alic
Motor (N) Decortic Decerebr Motionl
ate ate ess &
flaccid

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