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Coma

By- Dr. Kajal (PT)


Neural basis of consciousness
A simple definition of consciousness remains elusive,
a number of components, relevant neurologically, can
be considered to contribute: wakefulness, perceptual
awareness, and concept of self and of experience of
awareness.

At present a distinction of value to the clinical


neurologist is that between the content of
consciousness and the state of consciousness itself.
The content of consciousness depends upon the activities of
the cerebral cortex, the thalamus, and their interrelationship
Lesions of these structures will diminish the content of
consciousness without changing the state of consciousness as
such.

By contrast, the ascending reticular activating system


profoundly influences the state of consciousness or arousal.
The cells of origin of this system occupy a paramedian area in the brainstem,
extending from the lower part of the pons to a rostral level that includes the
posterior hypothalamus, the thalamic intralaminar nuclei, and the septal area.

Destruction of the reticular system does not interfere with the action of the sensory
impulses on a specific projection area, but it eliminates the tonic impulses from the
hypothalamic–reticular system to the cortex as a whole.

The reticular activating system is now seen as a complex system which subsumes
noradrenergic and cholinergic projections to the cortex.

Drugs that tend to produce unconsciousness selectively depress the ascending


reticular activating system, while those that cause wakefulness have the opposite,
facilitatory effect.
Etiology
It may be caused by neuronal dysfunction from many
causes including structural or nonstructural processes
affecting the central nervous system.

Metabolic or infectious etiologies may diffusely affect


the brain and lead to a coma. Common toxic or
metabolic causes of coma include hypoglycemia,
hyperglycemia, excessive alcohol intake, and
medication overdose or illicit drug use.
Other less common metabolic causes include hepatic
encephalopathy, hyponatremia, hypernatremia, hypercalcemia,
endocrine abnormalities, and many others. Primary central
nervous system infections such as meningitis or encephalitis may
lead to coma.

Structural brain diseases such as subdural or epidural traumatic


hematomas, spontaneous intracranial hemorrhages, venous
thrombosis, tumors, acute hydrocephalus, raised intracranial
pressure, anoxic brain injury, or brainstem strokes may all cause
altered mental status or coma.
Common causes of coma include:
Anoxic brain injury
Cerebral infarction
Cerebral hemorrhageSpontaneous
Traumatic
Cerebral neoplasms
Hypertensive encephalopathy
Hypoglycemia
Metabolic encephalopathy
Myxedema
Status epilepticus
Toxic encephalopathy
Investigations
At presentation blood will be taken for determination
of glucose, electrolytes, liver function, calcium,
osmolality, and blood gases.
Following the clinical examination, a broad distinction
between a metabolic cause, with preserved pupillary
responses, or a structural cause of coma is likely to
have been established. Although most patients with
coma will require CT scanning
Glasgow Coma Scale
Eye response Motor response Verbal response
 4 = eyes open spontaneously
 6 = obey commands  5 = oriented

 3 = eye-opening to verbal  5 = localizing pain  4 = confused

command  4 = withdrawal from pain  3 = inappropriate


 2 = eye-opening to pain  3 = flexion response to pain
words
 2 = incomprehensible
 1 = no eye-opening  2 = extension response to pain
sounds
 1 = no motor response  1 = no verbal response
The locked-in state
The de-efferented state or ‘locked-in’ syndrome occurs
with lesions of the medulla or anterior pons, with sparing
of the tegmentum and thus preservation of consciousness.

It is most commonly seen with basilar artery infarcts.

The patient, despite being tetraplegic and anarthric, is


fully aware of his or her surroundings.
Brain death

The diagnosis of brain death is equated with functional


death of the brainstem, and when brainstem death has
occurred, there is no possible chance of recovery.
Criteria for diagnosis
Tests for confirming brain death
All of the following should coexist:
All brainstem reflexes should be
The patient must be deeply
absent, as follows:
comatose. The pupils are fixed in diameter and do
The patient must be maintained not respond to sharp changes in the
intensity of incident light.
on a ventilator because There is no corneal reflex.
spontaneous respiration had The vestibulo-ocular reflexes are absent.
previously become inadequate or No motor responses within the cranial
ceased altogether. nerve distribution.
There should be no doubt that the There is no gag reflex or reflex response
to bronchial stimulation
patient's condition is due to No respiratory movements occur when
irremediable structural brain the patient is disconnected from the
damage mechanical ventilator for long enough

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