Cerebral Anoxia

Anoxic brain injury occurs when the human brain is denied a sufficient degree of oxygen to meet its energy demands.  When the brain is denied oxygen a series of cerebral events is activated which are directed toward maintaining oxygen supply.  Because the brain is unable to store oxygen it is dependent upon a constant supply in order to function effectively.  Studies have determined that a period of longer than 4 to 8 minutes is usually sufficient to produce cell death and subsequent brain damage.  Anoxia is a term which refers to a reduction or cessation in the supply or utilization of oxygen to the brain regardless of the cause.  Following an anoxic event of sufficient duration the neurons are subject to an influx of sodium causing cell swelling and injury, an influx of calcium, and the formation of oxygen free radicals.  Oxygen free radicals are extremely reactive and cause cellular injury by transforming the molecular components of the cell.  A secondary mechanism of injury in anoxic conditions involves recirculation of cerebral blood flow.  While larger caliber vessels are thought to respond effectively to reciruclation.  The capillaries and smaller vessels may be so affected that they are unable to resume normal blood flow, resulting in neuronal death, typically in the cerebral cortex.  Thus, portions of the brain which lie at the outer most areas of major cerebral arteries are the first to experience reductions in blood flow.  Furthermore it has been found that the higher a given brain region demand for oxygen the more likely that area is to be affected by oxygen deprivation.  Thus, the brain is subject to selective vulnerability due to anoxic events.  Nevertheless, there is a high degree of variability in areas of brain damage among anoxic patients.

Traditionally, damage to the hippocampus resulting in significant memory deficits was considered the primary area of damage following an anoxic event.  A review of 9 different studies has found that the hippocampus was the sole affected structure in only 18% of those cases.  More frequently, memory disturbances were noted most often within the context of other cognitive changes.  Other consequences of anoxic events included changes in personality and behavior or some other aspect of executive functioning, visual spatial deficits and disturbed language.

Memory disturbances were more likely related to anterograde rather than retrograde memory impairment.  Personality changes most typically involved emotional lability and impulsivity, lack of emotional expression, and lack of concern.  Some individuals have been found to exhibit emotional shallowness, irritability, and a tendency toward emotional lability.  Executive function deficits was typically related to distractibility and difficulty with multiple tracking, impaired planning, and poor abstraction skills.  Induced attention ability and difficulty modifying responses were often found.  Visual spatial deficits were associated with complex perceptual deficits due to legions in the lateral occipitoprietal cortex bilaterally.  Such deficits frequently occur in the context of more wide spread cognitive change.  While language has typically been considered to be preserved in anoxic events a number of studies have found that expressive language problems are not uncommon.

Anoxic events, even of relatively short duration, can result in profound cognitive changes.  While memory deficits have been suggested as the most common result of such events or recent research has documented that a broad distribution of brain damage is a more likely occurrence following cerebral anoxia.  Comprehensive neuropsychological evaluations in such cases is imperative in order to provide the most effective treatment planning and rehabilitation for the patient.

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