Significant anoxia may cause a variety of neuropathologic changes as well as cognitive deficits. We have recently seen 3 patients who have suffered severe anoxic episodes all with initial Glasgow Coma Scores (GCS) of 3 with sustained coma for 10–14 d. All 3 patients had extended hospitalizations and rehabilitation therapy. A neuropsychological test battery was administered and volumetric analyses of MRI scans were carried out in each case at least 6 mo postinjury. Two of the patients display distinct residual cognitive and neuropathologic changes while 1 patient made a remarkable recovery without evidence of significant morphological abnormality. These three cases demonstrate, that even with similar admission GCS, the outcome is variable and the degree of neuropsychological impairment appears to match the degree of morphologic abnormalities demonstrated by quantitative MR image analysis. An important finding of this study is that even though subjects with an anoxic insult exhibit severe cognitive and memory impairments along with concomitant morphologic changes, their attention/concentration abilities appear to be preserved. MR morphometry provides an excellent means by which neural structural changes can be quantified and compared to neuropsychological and behavioral outcomes. (JINS, 1995, I, 501–509.)

Hypoxia is known to cause damage to the hippocampus as well as memory impairments in humans. Subjects who have experienced a hypoxic episode and age-, gender-, and education-matched control subjects were tested for memory for spatial and linguistic temporal distance information using sentences and spatial locations. Each test contained a familiar component based on information that is meaningful and is thought to be stored as part of the knowledge system (prior knowledge) as well as a novel component based on new information. Subjects were presented a list of eight-word sentences or eight spatial locations (Xs) on a grid on a Macintosh computer and tested for memory for temporal distances. Temporal distance is defined as the number of items that occur between the two test items, in the study phase. Compared to control subjects, hypoxic subjects were impaired across all temporal distances on the novel spatial and linguistic tasks. As the temporal distance increased, hypoxic subjects showed some improvement in memory performance. In addition, memory of familiar temporal distance information was also assessed. Hypoxic subjects were impaired, compared to control subjects, for familiar temporal distance information. For hypoxic subjects there was a proportionally greater impairment for novel compared to familiar spatial and linguistic temporal distance information. There was a significant difference in their performance on the familiar temporal distance tasks compared to their performance on the novel tasks. Prior knowledge appears to attenuate the deficits seen in the familiar temporal distance tasks. It appears that hypoxia may cause more selective damage to the hippocampus and this damage is sufficient to produce profound memory impairments for primarily novel and less severe memory impairments for familiar spatial and linguistic temporal distance information. (JINS, 1995, I, 454–468.)

Cold water near-drowning is often thought to be neuroprotective in individuals with anoxia of a longer duration than that usually required to produce irreversible neurologic damage. There is a paucity of data in adults with cold water near-drowning that assess neuropsychological outcomes. Information regarding long-term effects of near cold water near-drowning on neuropathology, neuropsychological and neurobehavioral outcomes are uncommon. This paper provides an introduction to two cases of cold water near-drowning reported in this issue of JINS by Sameulson and colleagues and provides background information for interpretation of the findings of these cases in the context of outcomes following anoxia. (JINS, 2008, 14, 656–659.)

Some critically ill patients have dramatic recollections of the intensive care unit (ICU), whereas 23–50% have little or no recollection of their ICU stay. In addition, cognitive impairments are common following critical illness and ICU treatment. Little is known regarding the relationship between cognitive sequelae and ICU recall. We assessed recall of the ICU and its relationship to cognitive functioning at hospital discharge and 1 and 2 years after discharge in 70 consecutive acute respiratory distress syndrome (ARDS) patients. Seventeen patients (24%) had no recall of the ICU. Patients without ICU recall had increased rates of cognitive sequelae at hospital discharge and 1-year follow-up compared with the ICU recall group. Patients without ICU recall had a greater magnitude of cognitive impairments at hospital discharge, but not at 1- or 2-year follow-up. Profile analysis showed significant group differences in general intellectual functioning, executive function, processing speed, and spatial skills at hospital discharge, but not at 1- or 2-year follow-up. Estimated premorbid intelligence scores were inversely related to the magnitude of cognitive sequelae, suggesting greater “cognitive reserve” in patients with fewer cognitive decrements. (JINS, 2007, 13, 595–605.)

Acute Respiratory Distress Syndrome (ARDS) is characterized by lung injury and hypoxemia, has a high mortality rate, and is associated with significant morbidity including cognitive and emotional sequelae and decreased quality of life. There is limited information regarding which of these factors are associated with decreased quality of life. This study assessed the relationships between quality of life, cognitive and emotional function in ARDS survivors at 1-year post-hospital discharge. Sixty-six ARDS survivors were administered a battery of neuropsychological tests, measures of emotional function and quality of life 1 year post-hospital discharge. At 1 year 45% of the ARDS patients had cognitive sequelae and 29% had mild to moderate symptoms of depression and anxiety. Depression, anxiety, and intensive care unit length of stay were significantly correlated with decreased quality of life. Cognitive impairments did not correlate with decreased quality of life. Illness severity and emotional function, but not cognitive sequelae, are associated with decreased quality of life 1 year following ARDS. ARDS is common and may result in significant cognitive and emotional morbidity and decreased quality of life. (JINS, 2004, 10, 1005–1017.)

In recent years there has been extensive research in neuropsychological sequelae of a variety of etiologies, including traumatic brain injury, dementia, stroke, Parkinson's disease, schizophrenia, and cardiac surgery. With the exception of stroke and cardiac surgery, significantly fewer studies have been published regarding neuropsychological outcome in adults with disorders associated with anoxia or ischemia. Outcomes research in anoxic or ischemic disorders in pediatric patient populations are even more limited.

Hypoxia damages multiple organ systems especially those with high oxygen utilization such as the central nervous system. The purpose of this study was to compare the neuropathological and neuropsychological effects of hypoxia in patients with either carbon monoxide poisoning or obstructive sleep apnea. Neuroimaging revealed evidence of hippocampal atrophy in both groups although a linear relationship between hippocampal volume and memory performance was found only for selected tests and only in the sleep apnea group. There were significant correlations between hippocampal volume and performance on measures related to nonverbal/information processing. Generalized brain atrophy, as measured by the ventricle-to-brain ratio, was more common in the carbon monoxide poisoning group compared to the obstructive sleep apnea group. Performance on tests of executive function improved following treatment with nasal continuous positive airway pressure treatment in the obstructive sleep apnea group but there was no associated improvement in general intellectual function. We found that hypoxia due to obstructive sleep apnea and CO poisoning resulted in neuropathological changes and neuropsychological impairments. The observed group differences provide insight into the relationship between etiology of injury, neuropathological changes, and clinical presentation. (JINS, 2004, 10, 60–71.)

Magnetic resonance (MR) images and neuropsychological testing data of 69 carbon monoxide (CO) poisoned patients were prospectively obtained within 1 day of CO poisoning, two weeks and six months. CO patients' Day 1 cross-sectional fornix surface area measurements, corrected for head size by using a fornix-to-brain ratio (FBR), were compared to normal age and gender-matched controls. Additionally, a within-subjects analysis was performed comparing the mean areas between CO patients' Day 1, 2 weeks and 6-month FBR. The FBR was correlated with patients' neuropsychological data. There were no significant differences between CO patients' Day 1 fornix measurements compared to normal control subjects. However, significant atrophic changes in the fornix of CO poisoned patients occurred at two weeks with no progressive atrophy at 6 months. By 6 months, CO patients showed significant decline on tests of verbal memory (when practice effects were taken into account), whereas visual memory, processing speed and attention/concentration did not decline. This study indicates that CO results in brain damage and cognitive impairments in the absence of lesions and other neuroanatomic markers. (JINS, 2001, 7, 640–646.)

Recently an outbreak of acute respiratory infection associated with the hantavirus occurred in the southwestern United States. Hantavirus pulmonary syndrome (HPS) is a life threatening illness that carries with it a high mortality rate. Patients with HPS experience prolonged periods of hypoxemia requiring mechanical ventilation and treatment in intensive care units. We have recently seen 2 survivors of HPS. A neuropsychological test battery was administered immediately following their acute hospitalization and at 1 year postrecovery from HPS. Both patients exhibited cognitive impairments immediately following HPS as well as persistent cognitive impairments at 1 year. The cognitive impairments seen in these two HPS survivors are similar to those seen in other patients who have experienced brain anoxia, including memory impairments. It is also possible that hantavirus may directly cause brain injury with concomitant cognitive impairments. Additional research needs to be carried out in order to determine the extent and severity of the cognitive impairments in survivors of HPS. (JINS, 1998, 4, 190–196.)