Coma

States of impaired consciousness

Delirium – state characterized by agitation and disorientation – acute dementia

Stupor – a state in which the patient can only be aroused by vigorous stimulation (e.g. pain)

Coma – state in which eyes are closed and there is an absence of appropriate response to any form of stimulation

Structural basis for Coma

Coma results from compromises of the function of the reticular formation bilaterally, at the level of the mid-pons (or cephalad), the thalamus, or the cerebral hemispheres.

When the pontine or mesecephalic reticular formation (specifically the reticular activating system) is damaged bilaterally, the reticular formation cannot activate the cortex Þ always synchronous

Bilateral damage to the thalamic relay nuclei of the reticular formation (intralaminar nuclei) disrupts the pathway for activation of cortex by the reticular activating system.

Bilateral damage to cerebral hemispheres prevents the hemispheres from responding to activation by reticular formation.

Structural damage must be bilateral to produce coma

Causes of Coma

Structural damage – damage treated by relieving primary cause before it results in permanent damage

Cerebral hemispheres – from CO or global hypoxia
Diencephalon – from hemorrhage or tumor
Brainstem (reticular formation) – from an infarct

Toxic or Metabolic – treated by supporting the patient (ventilation, hydration) until the toxic or metabolic insult has passed

Distinguishing between structural or metabolic/toxic causes of coma

Toxic/metabolic Coma	Structural Lesions Causing Coma
Diffuse, multifocal deficits	Signs point to a single locus (focal findings)
Signs can fluctuate	May deteriorate in a rostralÞ caudal progression
Oculo-vestibular responses may be lost	Eye movements are comprimised with brainstem injury
Pupil response to light is usually preserved	Pupil responses can be impaired with brainstem injury
Treat with support and correction of metabolic disorder	May require neurosurgical decompression

Initial management of the comatose patient

Assure oxygenation

Maintain BP and CO

Give Glucose and Thiamine

Restore acid-base and electrolyte balance

Maintain normal body temp

Control seizures

Treat infections

Consider antidotes or dialysis of toxins

Clinical Features

Rostral-Caudal progression – suggests a unilateral lesion in the cerebrum that leads to uncal herniation which puts pressure on one side of the brainstem. (mass effect because of limited space in the skull and the tentorium bordering the midbrain)

Signs include asymmetric pupils, one eye won’t adduct. As pressure gets worse responses get more asymmetrical
parasympathetic knocked out 1^st (big pupil), then later sym gets knocked out (both gone = middle, fixed pupil)

Pupil

Damage to parasympathetic (limited to midbrain) Þ BIG PUPILS

Damage to sympathetic (pathways extends over a large area) Þ small pupils

Damage to both sym and parasym Þ middle, fixed (pupil doesn’t respond)

Caloric response

Cold water in the ear initially causes eye to look to the ipsilateral side then induces nystagmus with the fast phase beating away from the cold water

Doll’s response

When passively moving the head the eyes move in the opposite direction because of aVOR.
These responses are lost in low brainstem lesions

Faking it (a.k.a. psychogenic unresponsiveness)

Eyes tightly closed, in a real coma eyes are closed but not tightly
Bell’s phenomenon (eyes roll up in head under tightly closed eyes), will be looking at you in real coma
Hand falling to the side of face when the arm is held over the patient’s head and released, voluntary movement