Stupor & Coma

Question 1

Lethargy

Answer 1

sleepy but easily aroused

Question 2

Hypersomnia

Answer 2

-excessively sleepy but normal cognition when awakened

Question 3

Obtundation

Answer 3

mental blunting, dec. alertness

Question 4

Stupor

Answer 4

eyes open only briefly after vigorous stimulation before returning to deep sleep
-cognition impaired

Question 5

Coma

Answer 5

eyes remain closed after vigorous stimulation

Question 6

Delirium

Answer 6

• disoriented, misperception of sensory stimuli, hallucinations
• vacillates b/w quite, sleepy periods & hyper-vigilance/agitation

Question 7

Abulia

Answer 7

• awake but apathetic, no spontaneity

- with vigorous stimulation, cognitive function may be normal (bilateral frontal lobe disease, lobotomized)

Question 8

Akinetic Mutism

Answer 8

• silent, alert-appearing immobility

- no mental activity with vigorous stimulation (disease of frontal lobes & hypothalamus)

Question 9

Minimally Conscious State

Answer 9

-fragments of awareness

Question 10

Vegetative State

Answer 10

-awake, no awareness or meaningful interaction with the environment

Question 11

Consciousness

Answer 11

1. Arousal: sleep-wake cycles
   - ascending arousal system of the rostral brainstem
   - disease causes stupor & coma
2. Content: awareness of: oneself, environment
   - Corrtical circuits - cognition, purposeful interaction with world
   - Disease causes dementia

Question 12

Cataplexy

Answer 12

-sudden involentary loss of muscle tone during emotional excitement

Question 13

Primary Lesions that Cause Coma

Answer 13

1. extensive, acute bihemispheric disease
2. lesions of diencephalon (thalamus & hypothalamus)
3. Lesions of midbrain peri-aqueductal grey
4. Involvement of upper 1/3 of pontine tegmentum

Question 14

Causes of Coma

Answer 14

1. Structural Cause: supratentorial mass lesions, acute obstructive hydrocephalus, infratentorilal mass lesion
2. Metabolic (non-structural): reversible injury (sedative overdose), irreversible injury (hypoxia in cardiac arrest)

**always rule out psychogenic coma

Question 15

Oculomotor nerve is near the?

Answer 15

tentorium

Question 16

Central Herniation

Answer 16

• Rostral-Caudal deterioration
• Diencephalon (thalamus & hypothalamus) to midbrain failure
  
  • reduced consciousness
  • small reactive pupils (1-3mm)
  • decorticate postruing
  • Cheyne-Stokes respirations
  • Midbrain failure follows (fixed mid-postiion pupils, decerebration)

Question 17

Infratentorial Lesions

Answer 17

1. Intrinsic brainstem lesions:
   - top of basilar artery ischemic stroke
   - pontine hemorrhage
2. Extrinsic lesions compress & distory the brainstem
   - cerebellar hemorrhage
   - cerebellar infarction
   - cerebellar brian tumor

Question 18

Primary Brainstem Lesions cause:

Answer 18

• Segmental cranial nerve deficits
• ascending (spinothalamic) tract dysfunction
• descending (corticospinal, central sympathetic) tract dysfunction
• early cerebellar signs

Question 19

Pontine Hemorrhage Clinical Syndrome

Answer 19

• coma abrupt
• pupils are pinpoint
• decerebrate rigidity or flacid quadriplegia
• horizontal gaze paresis
• ocular bobbing

Question 20

Metabolic Encephalopathy (toxic-metabolic coma)

Answer 20

• Non-cerebral disease may interfere w/metabolism of the cerebral cortex & rostral brainstem AAS
• Endogenous toxins in uremia & hepatic failure
• Exogenous toxins in drug overdose, poisons, & sepsis
• Hypoxia, hypoglycemia, hypo & hyper-osmolality
• Electrolyte & acid-base imbalances
• Metabolic insult to brain is global, diffuse, symmetric
• Neuro-exam is “non-focal”
• Head CT is neg.
• Pupils stay reactive even as other reflexes are lost
• Asterixes, multifocal myoclonus & tremor
• Stupor & coma are reversible with metabolic correction & ICU support

Question 21

Causes of Metabolic Encephalopathy

Answer 21

• hypoxia, CO2 narosis, Hypoglycemia, Hyperglycemia, Hyperosmolar, Hyponatremia, Dehydration, Uremia, Liver failure, Hyperthermia, Hypotheria, Acidosis
• Drug intox, toxins, sepsis, Wernicke’s, Post-ictal state, DIC, TTP, Sever anemia, Lupus

Question 22

Coma: Immediate Management

Answer 22

• Stablilize vital signs (ABC’s first): secure ariway, cardiac monitor, IV access & blood drawing
• Stabilize neck (trauma)
• Determine the circumstances in which coma occurred
• Rapidly examine patient
• Empirical D50, thiamine, naloxone (opiate OD)
• tasks performed simulaneously by ED team

Question 23

Respiratory Patterns in Coma

Answer 23

-Cheyne Stokes respirations can be an early sign of herniation, both central & transtentorial

Question 24

Noxious stimuli to arouse patients who do not respond to voice command?

Answer 24

• supraorbital pressure
• nailbed pinch
• sternal rub

Question 25

Glasgow coma scale

Answer 25

-prognosis in head trauma -highest 15 12 or better is excellent prognosis -scores of 7 or below: nursing home care -3 means death

Question 26

Flexor response to Pain

Answer 26

(decorticate posturing) | -due to loss of cortical control of brainstem

Question 27

Extensor response

Answer 27

(decerebrate posturing) | -arises with loss of red nucleus & rubrospinal tract in the midbrain

Question 28

Coma: Diagnostic Testing

Answer 28

-STAT Head CT (or MRI if available) -CXR -Tests: EEG (status epilepticus, brain death) Spinal tap (CNS infection, subarachnoid hemorrhage) Cervical Spine X-ray (trauma) Stat toxicology: cocaine, opiates, phencyclidine, barbiturates, anticonvulsants, & sedatives, ethanol, methanol, ethylene glycol, acetaminophen, salixylates, tricyclics

Question 29

Treatment of Coma

Answer 29

- Ensure Oxgenation - Maintain circulation - Control glucose - Lower Intracranial pressure - Stop Seizures - Treat Infection - Restore acid-base balance & electrolytes - Adjust body temperature - Give thiamine - Consider specific antidotes (naloxone, flumazenil) - Control agitation

Question 30

Coma Prognosis

Answer 30

- Non-traumatic coma: absence of pupillary light & comeal reflex of 3 days carries poor prognosis - In hypoxic coma, absence of purposeful motor movements at 3 days also carries a poor prognosis