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10 out of 10

Anterograde amnesia is characteristic of (AIIMS Nov 2010)

A Post traumatic head injury

B Stroke

C Spinal cord injury

D Traumatic paraplegia

Ans. A

Post traumatic head injury

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 - Harrison 16th / 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 has a neuroprotective role. "Hypothermia is sometimes used for refractory elevated Intracranial pressure". Harrison 16th / 1634

3). 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: (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.

Brain death

1). Definition. Death is recognized as occurring when there is irreversible cessation of all brain function. A brain insult sufficient to cause complete loss of cerebral function should be docu­mented, if possible.

2). Approach to the patient

a. Physical examination.

i. Pupillary responses are absent,

ii. Eye movements cannot be elicited by the vestibulo ocular reflex or by irrigating the ears with cold water.

iii. The corneal reflex is absent

iv. Gag reflex is absent, and there is no facial or tongue movement.

b. Apnea test. Patients have no respiratory function. An apnea test should be performed to ascertain that no respirations occur at a PaCO2 level of at least 60 mm Hg. The oxygenation should be maintained as the PaCO2 is allowed to rise. The inability to develop respiration is consistent with medullary failure.

c. Exclusionary criteria. A diagnosis of brain death cannot be made in the setting of drug intoxication, hypothermia (defined as a core temperature of <32°C), or severe hypotension (i.e., shock).

d. Confirmatory tests. These tests are usually not necessary to diagnose brain death but can be used if doubt exists or if local statutes require them.

3). An EEG does not demonstrate any physiologic brain activity.

4). Tests to assess cerebral blood flow fail to show cerebral perfusion.

a. Period of observation. Periodic evaluation is necessary before a diagnosis of brain death can be made, unless there is gross evidence of a no survivable insult to the brain.

b. Two evaluations (6 to 12 hours apart) are usually sufficient to support a diagnosis of brain death declaring brain death

FIGURE 274- 3. Examination of brainstem reflexes in coma. Midbrain and third nerve function are tested by pupillary reaction to light, pontine function by spontaneous and reflex eye movements and corneal responses, and medullary function by respiratory and pharyngeal responses. Reflex conjugate, horizontal eye movements are dependent on the medial longitudinal fasciculus (MLF) interconnecting the sixth and contralateral third nerve nuclei. Head rotation (oculocephalic reflex) or caloric stimulation of the labyrinths (oculovestibular reflex) elicits controversies eye movements (Ref. Hari-18th ed., pg- 2250)

Extra Edge: (Ref. Hari-18th ed., pg- 2250)

1). Decorticate rigidity and decerebrate rigidity, or "posturing," describe stereotyped arm and leg movements occurring spontaneously or elicited by sensory stimulation.

2). Flexion of the elbows and wrists and supination of the arm (decortication) suggests bilateral damage rostral to the midbrain, whereas extension of the elbows and wrists with pronation (decerebration) indicates damage to motor tracts in the midbrain or caudal diencephalon.