NeuroRehabilitation

Hypoxic-ischemic brain injury is a well known consequence of cardiac arrest. Variable injuries can occur with purely hypoxic or histotoxic insults such as asphyxiation and carbon monoxide poisoning. The injury may happen at the time of the insult, but there may also be continued damage after circulation and oxygenation are reestablished. The nature and extent of the damage appears to depend on the severity, time course and duration of the oxygen deprivation and lack of blood supply, as well as on the underlying mechanism. This review describes the pathophysiological and molecular basis of hypoxic ischemic brain injury, and differentiates between the mechanisms of injury by cardiac arrest, pure respiratory arrest, and arrest secondary to cytotoxicity (e.g. carbon monoxide poisoning).

Hypoxic-ischemic brain injury (HI-BI) is a common cause of neurological morbidity in children and adults. Recent developments in neuroimaging techniques may permit in vivo identification of the structural and functional anatomy of HI-BI, and offer opportunities for the development of neuroimaging-guided prognosis. This article provides an update on the types and possible roles of currently-available neuroimaging techniques. The applications and limitations of these techniques to the study and clinical evaluation of persons with HI-BI are discussed, and the need of further research is highlighted.

Neonatal encephalopathy (NE) from perinatal asphyxia (PA) has long been recognized as an important cause of lasting motor impairment in term newborns. NE has also, more recently, been implicated as an important risk factor for cognitive and behavioral difficulties as these children age. Newborns with mild NE appear to have normal neurocognitive outcomes, while those survivors with severe NE tend to have profound impediments. Yet, newborns with moderate NE seem to exhibit a wide range of cognitive outcomes – regardless of motor function – making prognostication in these children difficult in the newborn period. Since deficits are often subtle and remote from the initial injury, cognitive impairment is likely underdiagnosed in survivors of moderate perinatal NE. Therefore, it is important for ongoing formal neuropsychological evaluation, as well as parental and teacher education, to help aid in the cognitive and behavioral rehabilitation resulting from NE and perinatal hypoxic-ischemic brain injury.

Hypoxic-ischemic brain injury (HI-BI) after cardiac arrest commonly results in neurological injury and long term dysfunction, with outcomes ranging from coma and vegetative states to functional disability with various degrees of dependence. Increased rates of bystander CPR and cardiac defibrillation has led to a rapid increase in successful resuscitations. Patients who reach the hospital after cardiac arrest may develop various neurological deficits or clinical syndromes that may preclude recovery to their premorbid baseline. Consequently, clinicians are faced with not only predicting outcome regarding wakefulness and independence but also with long term therapeutic management. Several neurological syndromes have been reported as consequences of HI-BI. This review will describe some of the more common syndromes seen after HI-BI, including the various levels of arousal, seizures, myoclonus, movement disorders, cognitive impairments, and other specific neurological abnormalities.

Despite improvements in the pre-hospital and critical care management of persons with hypoxic-ischemic brain injury (HI-BI) and the conditions with which it is associated, acute and chronic cognitive impairments remain problems for many survivors of such injuries. Disorders of consciousness, attention, speed of processing, and memory impairments, and executive dysfunction are among the most prominent and common disturbances of cognition after HI-BI. Acute interventions, including therapeutic hypothermia, may improve global outcomes after HI-BI, but their specific effects on post-hypoxic cognitive impairments remain uncertain. Additionally, treatments for cognitive impairments after HI-BI are underdeveloped and are generally arrived at by analogy to the treatment of such problems arising from other neurological conditions, especially traumatic brain injury. In the service of offering a practical approach to the evaluation and care of persons with cognitive impairments after HI-BI, the most common types of post-hypoxic cognitive impairments are reviewed. Cognitive outcomes after HI-BI are discussed and suggestions for the nonpharmacologic and pharmacologic neurorehabilitation of these problems are offered.

Delayed post-hypoxic leukoencephalopathy (DPHL) is a demyelinating syndrome characterized by acute onset of neuropsychiatric symptoms days to weeks following apparent recovery from coma after a period of prolonged cerebral hypo-oxygenation. It is diagnosed, after excluding other potential causes of delirium, with a clinical history of carbon monoxide poisoning, narcotic overdose, myocardial infarction, or another global cerebral hypoxic event. The diagnosis can be supported by neuroimaging evidence of diffuse hemispheric demyelination sparing cerebellar and brainstem tracts, or by an elevated cerebrospinal fluid myelin basic protein. Standard or hyperbaric oxygen following CO poisoning may reduce the likelihood of DPHL or other neurologic sequelae. Bed rest and avoidance of stressful procedures for the first 10 days following any prolonged hypoxic event may also lower the risk. Gradual recovery over a 3 to 12 month period is common, but impaired attention or executive function, parkinsonism, or corticospinal tract signs can persist. Stimulants, amantadine or levodopa may be considered for lasting cognitive or parkinsonian symptoms. Anticipation and recognition of DPHL should lead to earlier and more appropriate utilization of health care services.

As increasing numbers of people live, work, and play at high altitudes, awareness of the neurological consequences of hypobaric hypoxic environments becomes paramount. Despite volumes of studies examining the pathophysiology of altitude sickness, the underlying mechanisms of the spectrum of altitude related illnesses is still elusive. High altitude headache, acute mountain sickness, high altitude cerebral edema and other neurological presentations including sleep disturbances and seizures at high altitude are reviewed. As our knowledge advances in the field of altitude physiology, the clinical and research techniques developed may help our understanding of hypoxic brain injury in general.

Hypoxic-ischemic brain damage often results from a combination of cardiogenic and respiratory failure. Whether or not hypoxia in the absence of ischemia is injurious to the brain has been a topic of research. An example of hypoxia without ischemia is found in obstructive sleep apnea (OSA), which causes recurrent nocturnal oxygen desaturations. Furthermore, it is a pervasive problem in the general population, particularly in people with common disorders such as obesity or diabetes. Mounting evidence in the past decade indicates that cerebrovascular disease, specifically stroke, and neurobehavioral consequences, including excessive daytime sleepiness and cognitive deficits, are prevalent in people with OSA, at great costs to the individual well-being, public health, and the economy. Investigation of the two disease associations poses similar and unique challenges. Predictors of these sequelae need to be better defined. The apnea-hypopnea index, the most common measure of OSA, has proven to be variably related to stroke and cognitive impairment. The role of individual markers, whether they are comorbidities or differences in inherent cognitive reserve, also is incompletely understood. This review discusses the burgeoning literature on the neurological and neurobehavioral sequelae of OSA and highlights the future avenues of research in the field.