Chapter 17 - Depression of consciousness

Questions

Define the following terms:

stupor, coma, delerium, encephalopathy, reticular activating system, decorticate posture, decerebrate posture, "locked-in", Cheyne-Stokes respirations, central neurogenic hyperventilation, ataxic respiration, vestibulo-ocular reflex, diencephalic pupils.
Stupor is a nonsleep depression of consciousness where normal reactions to the environment are blunted.
Coma is a nonsleep loss of consciousness where normal reactions to the environment are lost.
Delerium is a nonsleep depression of consciousness where normal reactions to the environment are blunted and replaced by agitated responses.
Encephalopathy is diffuse suppression of normal cerebral cortical function that often results in stupor or coma.
The reticular activating system is the reticular system connecting the rostral pontine and midbrain through the thalamus to the cerebral cortex.
Decorticate posture is a posture in which the lower limbs are extended and the upper limbs flexed in response to noxious stimuli.
Decerebrate posture is a posture in which the lower and upper limbs are extended in response to noxious stimuli.
"Locked-in" refers to damage to the base of the pons with preservation of consciousness and vertical eye movements, but loss of all other voluntary movements.
Cheyne-Stokes respiration is a pattern of breathing characterized by waxing and waning amplitude of respiration with preserved respriatory frequency.
Central neurogenic hyperventilation typically occurs with pontine lesions, with increased depth of respiration.
Ataxic respiration is a pattern of respiration with irregular depth and frequency of respirations with pauses.
The vestibulo-ocular reflex is the reflex that keeps eyes directed on a target during head movements. It can be elicited by head movments or caloric tests.
Diencephalic pupils refer to bilaterally small pupils with lesions of the thalamus.

17-1. What are the two potential causes of coma?

Answer 17-1. Coma may result from diffuse dysfunction of cerebral hemispheres or from damage to reticular activating system in brain stem (especially midbrain).

17-2. What are the causes of diffuse cerebral cortical suppression?

Answer 17-2. This may be due to direct cerebral effects of sedative drugs, systemic electrolyte disturbances, various severe metabolic upsets, trauma, diffuse ischemic damage,may be observed in the period after seizure (postictal). In these cases of toxic or metabolic encephalopathy, brainstem function is usually preserved until last - may see Cheyne-Stokes respirations.

17-3. What physical findings would indicate that coma was due to diffuse cerebral cortical dysfunction rather that to brain stem damage?

Answer 17-3. With diffuse cerebral cortical dysfunction you would expect to find normal dysinhibited oculovestibulor reflex eye movement to caloric testing. Motor findings and responses would be the same on both sides of the body (symmetrical). It is critical to be sure that there is no structural damage to the reticular formation. This is accomplished by determining whether eye movements are affected (extraocular nuclei are close to reticular formation).

17-4. What are key physical exam findings in patients with coma?

Answer 17-4. The vestibuloocular reflexes (oculocephalic testing or caloric testing) is critical to this assessment. Pupillary reactions may also be important.

17-5. What is transtentorial herniation?

Answer 17-5. Transtentorial herniation occurs with lateralized, supratentorial masses with displacement of the brain away from the expanding lesion. This produces stupor and coma by damaging the midbrain and reticular activating system. The uncus of the temporal lobe is usually the structure that herniates.

17-6. What are common symptoms of transtentorial herniation?

Answer 17-6. The third cranial nerve is often involved early in transtentorial herniation (with pupillary constrictor fibers usually damaged first). This is usually ipsilateral to the side of expanding lesion. The corticospinal tract is often involved next with contralateral weakness. Occasionally, with large shifts of the brain stem, this may be reversed (false localizing sign: Kernohan's notch).

17-7. What is the "locked-in" syndrome?

Answer 17-7. Locked-in syndrome usually results from damage at the level of the pons. Consciousness is preserved.

17-8. How can you recognize "locked-in" syndrome?

Answer 17-8. In the "locked-in" syndrome, vertical gaze and convergence is usually preserved. Eye opening may be preserved (eye closure is passive only). Other voluntary motions (including horizontal gaze included) are abolished.