Individuals sustaining cerebral anoxia, hypoxia, or an associated anoxic encephalopathy, often experience a myriad of neurocognitive, neurobehavioral, and adaptive changes/limitations. Cerebral anoxia occurs following oxygen deprivation to the brain. The extent and duration of potential deficits are contingent upon a specific etiology and period of oxygen deprivation.
Most noteworthy causes of cerebral anoxia occur following cardiac arrest (e.g., heart attack), as well as cerebrovascular accidents (e.g., stroke), drug overdose, near drowning, strangulation, electrocution, and adult respiratory distress syndrome (ARDS) are other potential contributing events.
The pathophysiology of cerebral anoxia is such that generalized cognitive deficits occur; this is the result of reduced blood flow and oxygenation to the entire brain and not one specific area. Cerebral anoxia is due to oxygen deprivation and hypoventilation as noted above. Physiological and neurochemical changes occur especially with regard to the cessation of blood flow and results in general circulatory collapse. Immediate loss of consciousness may occur within seconds which is often accompanied by severe brain trauma. Areas of the brain most vulnerable to damage are those that require sustained oxygenation. In part, the hippocampus, cerebellar cortex, parieto-occipital cortex, and bifrontal regions are most susceptible. Clinically, symptoms often manifest with cortical blindness, extrapyramidal involvement, cerebellar ataxia, and profound amnesia (e.g., memory impairment).
Initially, individuals are treated by multi-specialty physicians including, but not limited to cardiologists, neurologists, neurosurgeons, physiatrists, pulmonologists, to name a few. Often patients require both inpatient acute hospitalization and rehabilitation. Inpatient and outpatient rehabilitation is generally provided by a multi-disciplinary team including physical, occupational, speech, and respiratory therapists. Nutritional and psychological support is often part of the rehabilitation team. Furthermore, neuropsychological consultation is required throughout the patient’s treatment to monitor the individuals’ neurocognitive strengths, weaknesses, and overall level of adaptive functioning. Serial neuropsychological evaluations, possibly completed at 3-6 months intervals, is imperative to assist the medical specialists, patient, and family members in developing additional diagnostic impressions and treatment recommendations.
From a neuropsychological perspective, patients, as described above, often demonstrate a myriad of neurocognitive and neurobehavioral difficulties on formal neuropsychological assessment. Primary deficits may include:
· Recent/delayed memory (often profound)
· Sustained levels of attention/concentration
· Executive dysfunction
· Language difficulties
· Slowed processing speed
· Sensorimotor limitations
· Disorientation
Within the realm of neurobehavioral alterations, patients are often described as having noteworthy personality changes including, frustration, impulsivity, restlessness, indifference, amotivation, and emotional lability. Often these individuals experience organically induced depression (organic affective disorder/frontal lobe syndrome) as well as variable levels of anxiety. When diagnosed, psychiatric and psychological consultation and treatment is imperative.
In summary, the effects of cerebral anoxia is multifaceted based on an array of potential causes and clinical manifestations (e.g., physical, neurocognitive, neurobehavioral). Treatment is often prolonged at the acute and post-acute stages, frequently warranting both inpatient and outpatient brain injury rehabilitation. Serial neuropsychological assessment is often recommended to assist in the monitoring of the patient’s overall level of adaptive functioning.
For additional information or a clinical consultation regarding the consequences of cerebral anoxia, please contact our office at 732-988-3441.
Michael J. Raymond, Ph.D., ABN, FACPN
Board Certified Neuropsychologist #232
Licensed Psychologist #35S100252900