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Coma & Brain Death

Definition. Coma is a state in which a patient is unresponsive to environmental stimuli and unable to communicate in any manner. Coma is associated with extensive structural or physio­logic damage to both cerebral hemispheres or to the ascending RAS in the diencephalon, mesen­cephalon, or pons.

Causes of coma



  1. Drugs, poisoning, eg carbon monoxide, alcohol.
  2. Hypoglycemia, hyperglycemia (ketoacidotic, or HONK)
  3. Hypoxia, CO2 narcosis
  4. Septicaemia
  5. Hypothermia
  6. Myxoedema, Addisonian crisis
  7. Hepatic/uraemic encephalopathy      

Neurological: Trauma

  1. Infection meningitis; encephalitis, eg Herpes simplex: malaria, typhoid, rabies, trypanosomiasis
  2. Tumour: cerebral/meningeal tumour
  3. Vascular, subdural/subarachnoid haemorrhage, stroke, hypertensive encephalopathy
  4. Epilepsy: non-convulsive status or post-ictal state


Extra Edge: Highest score of Glasgow coma scale is 15 and the least score is 3 (LQ 2012).

Physical examination

  1. Pupils. Pupillary size
    1. Large, nonreactive pupils result from the disruption of the parasympathetic portion of the third cranial nerve, but may also be seen with barbiturate overdose.
    2. Pinpoint pupils that are nonreactive to light may be seen with narcotic overdose.
  2. Ocular motility.
    1. If the eyes are immobile, movement can be elicited through the vestibulo-ocular reflex by moving the patient's head side to side (the "doll's eyes" or oculocephalic maneuver)
      1. Failure of an eye to abduct in response to these maneuvers implies dysfunction of pontine structures or sixth nerve compromise.
      2. Failure of an eye to adduct implies dysfunction of the medial longitudinal fasciculus or oculomotor nucleus or nerve.

Extra Edge   (Ref. Hari. 18th ed., Pg -2251) 

  1. Spontaneous eye movements in coma often take the form of conjugate horizontal roving.
  2. This finding alone exonerates damage in the midbrain and pons and has the same significance as normal reflex eye movements.
  3. Conjugate horizontal ocular deviation to one side indicates damage to the pons on the opposite side or alternatively, to the frontal lobe on the same side.
  4. This phenomenon is summarized by the following maxim: The eyes look toward a hemispheral lesion and away from a brainstem lesion.
  5. The eyes may occasionally turn paradoxically away from the side of a deep hemispheral lesion ("wrong-way eyes"). The eyes turn down and inward with thalamic and upper midbrain lesions, typically thalamic hemorrhage.
  6. "Ocular bobbing" describes brisk downward and slow upward movements of the eyes associated with loss of horizontal eye movements and is diagnostic of bilateral pontine damage, usually from thrombosis of the basilar artery.
  7. "Ocular dipping" is a slower, arrhythmic downward movement followed by a faster upward movement in patients with normal reflex horizontal gaze; it indicates diffuse cortical anoxic damage.
  8. Thermal, or "caloric," stimulation of the vestibular apparatus (oculovestibular response) provides a more intense stimulus for the oculocephalic reflex but provides essentially the same information.
  9. The test is performed by irrigating the external auditory canal with cool water in order to induce convection currents in the labyrinths. After a brief latency, the result is tonic deviation of both eyes to the side of cool-water irrigation and nystagmus in the opposite direction. (The acronym "COWS" has been used to remind generations of medical students of the direction of nystagmus—"cold water opposite, warm water same.")
  10. The loss of induced conjugate ocular movements indicates brainstem damage. The presence of corrective nystagmus indicates that the frontal lobes are functioning and connected to the brainstem; thus functional or hysterical coma is likely.
  1. Motor functions.
    1. Quadriparesis and flaccidity suggests pontine or medullary compromise or a high cervical spinal cord insult.
    2. Decorticate posturing (i.e., leg extension with flexion of the arm, wrist, and fingers) can be unilateral or bilateral and suggests a hemisphere or diencephalic lesion.
    3. Decerebrate posturing (i.e., leg and arm extension) also can be unilateral or bilateral and suggests midbrain or pontine compromise.

Glasgow coma scale is the best prognostic factor head injury.

Other poor prognosis indicators:


Older age

Increase ICP

Hypoxia & Hypotension

CT evidence of compression of cisterns / midline shift

Delayed evacuation of large intracerebral hemorrhage

Carrier status for apolipoprotein E-4 allele

Secondary Insult to Injured Brain: Secondary Ischemia

  1. Hypotension                        
  2. Hypoxia                       
  3. Hyperthermia (Fever)
  4. Hyperglycemia                            
  5. Hypercapnia

Hypotension and Hypoxia initiate the 'ischaemic cascade' by reducing delivery of substrates principally oxygen and glucose there by interfering with cellular function.

Hypercapnia causes cerebral vasodilatation, increases cerebral blood flow and intracranial pressure and worsens cerebral perfusion and hence contributes to the ischemic cascade - (Ref. Hari. 18th ed., pg - 1632)

Hyperthermia (fever) and hyperglycemia

  1. Contribute to secondary insult by increasing cellular metabolism and hence the requirement of essential substrates outstripping the compensatory process.       
  2. Hypothermia is known to have neuro protective effects and may even be used as a modality of management of refractory elevated intracranial pressure.
Post traumatic amnesia
(Ref. Hari. 18th ed., Pg - 209)
  1. Post-traumatic amnesia is generally due to a head injury (e.g., a fall, a knock on the head).
  2. Traumatic amnesia is often transient, but may be permanent of either anterograde, retrograde, or mixed type.
  3. The extent of the period covered by the amnesia is related to the degree of injury and may give an indication of the prognosis for recovery of other functions. 
  4. Mild trauma, such as a car accident that results in no more than mild whiplash, might cause the occupant of a car to have no memory of the moments just before the accident due to a brief interruption in the short/long-term memory transfer mechanism.
  5. The sufferer may also lose knowledge of who people are, they may remember events, but will not remember faces of them.

Extra Edge: Many patients do not lose consciousness after a minor head injury but instead are dazed or confused, or feel stunned or "star struck." Severe concussion may precipitate a brief convulsion or autonomic signs such as facial pallor, bradycardia, faintness with mild hypotension, or sluggish pupillary reaction, but most patients are quickly neurologically normal. (Ref. Hari. 18th ed., pg - 3377)

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