Coma

■ Consciousness: it is a state of full awareness of
the self and ones relationship to environment.
■ It has 2 components:
Arousal (RAS)
Awareness (Cortex)

Disorders of consciousness
■ Confusion is clouding of consciousness characterized by impaired
capacity to think, understand, respond & remember stimuli.
■ Delirium is a state of confusion that is accompanied by agitation,
hallucination, tremors or illusion.
■ Stupor is unresponsiveness from which the patient can be aroused
only briefly by vigorous repeated stimulation.
■ Coma is a state in which patient is unarousable and unresponsive to
repeated stimuli.

■ Vegetative state is a subacute or chronic condition after severe
brain injury and comprises return of wakefulness accompanied by
total lack of cognitive function.
■ Akinetic mutism refers to partially or fully awake patient who is
able to form impression & think but remains immobile, mute
particularly when stimulated.
■ Locked in syndrome is a awake state in which there is total
paralysis of limbs, lower cranial nerves with intact consciousness
and vertical eye movements.

■ Catatonia: fixed and sustained position that is resistant to change. It
is also known as waxy flexibility.

Anatomy and Physiology of coma
■ Reticular formation: it is a
diffuse ill defined mass of
intermingled neurons and
nerve fibers occupying the
entire core of brainstem
which when stimulated
will produce arousal.

■ It consists reticular
nuclei, these are
arranged into three
longitudinal columns
Median column (Raphe
nuclei)
Medial column
(magnocellular column)
Lateral column
(parvocellular column)

Connections of reticular formation

■ Functional divisions of reticular formation:
Ascending reticular activating system – it is
responsible for maintaining a state of alertness
and consciousness.
Descending reticular activating system – it
connection to autonomic centers in brainstem
for controlling respiratory and cardiac rhythms
and other vital functions.

■ Causes of coma:
1. Lesions that damage the RAS in upper mid brain or its
projections.
2. Destruction of large portions of both cerebral
hemispheres.
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
the pupillary function and eye movements permits clinical
localization of the cause of coma in many cases.
■ Pupillary enlargement with the 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 movement absolves the upper brainstem and indicates
widespread structural lesions or metabolic suppression of the
cerebral hemispheres is responsible for coma.

■ Causes due to cerebral mass
lesions and herniation's:
The cranial cavity is separated
into compartments by
infoldings of the dura.The two
cerebral hemispheres are
separated by the falx cerebri,
and the anterior and posterior
fossae by the tentorium
cerebri.

Herniation refers to displacement of brain tissue into a
compartment that it normally does not occupy.
Types of cerebral herniations:
A. Trans tentorial (Uncal)
B. Trans tentorial (central)
C. Trans falcial
D. Foraminal

 The most common herniations are from the
supratentorial to the infratentorial
compartments through the tentorial opening,
hence transtentorial.
 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.
 Compression of 3rd cranial nerve –
ipsilateral enlargement of pupil.
 Compression of Para hippocampal gyrus -
coma

In some cases, the lateral displacement of the midbrain
causes compression of the opposite cerebral peduncle,
producing a Babinski sign and hemiparesis.
(the Kernohan-Woltman sign).
 In addition to compressing the upper brainstem, it may
compress major blood vessels, particularly the anterior and
posterior cerebral arteries as they pass over the tentorial
reflections, thus producing brain infarctions.
 The distortions may also entrap portions of the ventricular
system, resulting in regional hydrocephalus.

Central transtentorial herniation denotes a symmetric
downward movement of the thalamic medial structures
through the tentorial opening with compression of the upper
midbrain.
 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 and respiratory arrest.

■ Coma due to metabolic disorders:
Systemic metabolic abnormalities that cause coma by
interrupting the delivery of energy substrates (oxygen and
glucose) or by altering neuronal excitability by drugs,
alcohol, epilepsy or by changes in brain volume
(hyponatremia, hypernatremia)
Cerebral neurons are fully dependent on cerebral blood
flow (CBF) and the related delivery of oxygen and glucose.
CBF is ~75 mL per 100 g/min in gray matter and 30 mL per
100 g/min in white matter (mean = 55 mL per 100 g/min);
oxygen consumption is 3.5 mL per 100 g/min, and glucose
utilization is 5 mg per 100 g per min.

 Brain stores of glucose provide energy for ~2 min after blood
flow is interrupted, and oxygen stores last 8–10 s after the
cessation of blood flow.
 Simultaneous hypoxia and ischemia exhaust glucose more
rapidly.
 Coma and seizures are commonly accompany too large shift
in sodium and water balance in brain.
 Sodium levels <125 mmol/lt – confusion
<115 mmol/lt – coma and convulsions
 Some metabolic diseases: DKA, Hypothyroidism, vit B12
deficiency

■ Epileptic coma: generalized electrical seizures
associated with coma, even in absence of motor
convulsions.
■ Toxic coma (Drug induced):
Many drugs are capable in depressing nervous system
function when taken in over doses.
They act on brain stem nuclei, RAS, cerebral cortex to
produce coma.

Coma

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Coma