Coma

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• coma, defined as a deep sleep like state from which
the patient cannot be aroused. Stupor refers to a
higher degree of arousability in which the patient can
be transiently awakened only by vigorous stimuli,
accompanied by motor behavior that leads to
avoidance of uncomfortable or aggravating stimuli.
• Drowsiness, which is familiar to all persons, simulates
light sleep and is characterized by easy arousal and
the persistence of alertness for brief periods.
• Vegetative signifies an awake but
nonresponsive state in a patient who has
emerged from coma. In the vegetative state,
the eyelids may open, giving the appearance
of wakefulness. Respiratory and autonomic
functions are retained. Cardiac arrest with
cerebral hypoperfusion and head injuries are
the most common causes of the vegetative
• Akinetic mutism refers to a partially or fully awake state in
which the patient is able to form impressions and think, but
remains virtually immobile and mute. The condition results
from damage in the regions of the medial thalamic nuclei or
the frontal lobes (particularly lesions situated deeply or on
the orbitofrontal surfaces) or from extreme hydrocephalus.
• The term abulia describes a milder form of akinetic mutism
characterized by mental and physical slowness and
diminished ability to initiate activity. It is also usually the
result of damage to the frontal lobes and its connections
• The locked-in state describes an awake patient
has no means of producing speech or
volitional movement but retains voluntary
vertical eye movements and lid elevation, thus
allowing the patient to signal with a clear
mind. The pupils are normally reactive. The
usual cause is an infarction or hemorrhage of
the ventral pons.
• The reticular activating system (RAS), its ascending
projections to the cortex, and the cortex itself are
required to maintain alertness and coherence of
thought. It follows that the principal causes of coma
are (1) lesions that damage the RAS in the upper
midbrain or its projections; (2) destruction of large
portions of both cerebral hemispheres; and (3)
suppression of reticulocerebral function by drugs,
toxins, or metabolic derangements such as
hypoglycemia, anoxia, uremia, and hepatic failure.
• The proximity of the RAS to midbrain structures that
control pupillary function and eye movements permits
clinical localization of the cause of coma in many cases.
Pupillary enlargement with loss of light reaction and loss
of vertical and adduction movements of the eyes suggests
that the lesion is in the upper brainstem.
• Conversely, preservation of pupillary light reactivity and of
eye movements absolves the upper brainstem and
indicates that widespread structural lesions or metabolic
suppression of the cerebral hemispheres is responsible for
coma
 Coma Due to Cerebral Mass Lesions and
Herniations
• The cranial cavity is separated into
compartments by infoldings of the dura. The
two cerebral hemispheres are separated by
the falx, and the anterior and posterior fossae
by the tentorium.
• Herniation refers to displacement of brain
tissue into a compartment that it normally
does not occupy.
• The most common herniations are those in which a part of
the brain is displaced from the supratentorial to the
infratentorial compartment through the tentorial opening;
this is referred to as transtentorial herniation.
• Uncal transtentorial herniation refers to impaction of the
anterior medial temporal gyrus (the uncus) into the
tentorial opening just anterior to and adjacent to the
midbrain.
• The uncus compresses the third nerve as it traverses the
subarachnoid space, causing enlargement of the ipsilateral
pupil (parasympathetic).
• The coma that follows is due to compression of the
midbrain against the opposite tentorial edge by the
displaced parahippocampal gyrus.Lateral displacement of
the midbrain may compress the opposite cerebral
peduncle, producing a Babinski's sign and hemiparesis
contralateral to the original hemiparesis (the Kernohan-
Woltman sign). Herniation may also compress the
anterior and posterior cerebral arteries as they pass over
the tentorial reflections, with resultant brain infarction.
The distortions may also entrap portions of the ventricular
system, resulting in hydrocephalus
• Central transtentorial herniation denotes a
symmetric downward movement of the
thalamic medial structures through the
tentorial opening with compression of the
upper midbrain. Miotic pupils and drowsiness
are the heralding signs.
• transfalcial herniation (displacement of the
cingulate gyrus under the falx and across the
midline
• foraminal herniation (downward forcing of the
cerebellar tonsils into the foramen magnum,
which causes compression of the medulla,
respiratory arrest, and death
 Coma Due to Metabolic Disorders
• by interrupting the delivery of energy
substrates (e.g., hypoxia, ischemia,
hypoglycemia) or by altering neuronal
excitability (drug and alcohol intoxication,
anesthesia, and epilepsy).
• Cerebral neurons are fully dependent on
cerebral blood flow (CBF) and the delivery of
oxygen and glucose. The EEG rhythm diffusely
slowed, typical of metabolic
encephalopathies, and as conditions of
substrate delivery worsen, eventually brain
electrical activity ceases.
• The causes of the reversible effects of these
conditions on the brain are not understood
but may result from impaired energy supplies,
changes in ion fluxes across neuronal
membranes, and neurotransmitter
abnormalities,toxicity, increased permeability
of the blood-brain barrier to toxic substances
such as organic acids and an increase in brain
calcium and CSF phosphate content
• Sodium levels <125 mmol/L induce confusion,
and <115 mmol/L are associated with coma
and convulsions. In hyperosmolar coma, the
serum osmolarity is generally >350 mosmol/L.
Hypercapnia depresses the level of
consciousness in proportion to the rise in
carbon dioxide (co2) tension in the blood.
 Epileptic Coma
• Generalized electrical discharges of the cortex
(seizures) are associated with coma . The self-
limited coma that follows a seizure, the
postictal state, may be due to exhaustion of
energy reserves or effects of locally toxic
molecules that are the by-product of seizures.
 Toxic (Including Drug–Induced) Coma
• Produce coma by affecting both the brainstem
nuclei, including the RAS, and the cerebral cortex.
The combination of cortical and brainstem signs,
which occurs in certain drug overdoses, may lead
to an incorrect diagnosis of structural brainstem
disease. Overdose of medications that have
atropinic actions produces signs such as dilated
pupils, tachycardia, and dry skin; opiate overdose
produces pinpoint pupils <1 mm in diameter.