Neuropsychological and neuropathological sequelae of cerebral anoxia: A critical review

Abstract

Fifty-eight studies of the neuropathological and neuropsychological outcomes of cerebral anoxia were reviewed. Neuropathological reports were examined for the variety, extent, and specificity of lesions resulting from an anoxic event. While most attention has focused on damage to the hippocampus following anoxic brain injury, the review indicated that watershed cerebral cortex and the basal ganglia were both more frequently damaged than the hippocampus. The hippocampus was the sole affected structure in only 18% of reported cases. Neurological, neuropsychological and psychiatric studies were analyzed. Of 67 individual case reports, a memory disturbance was documented in 36 (54%), but a memory disturbance without report of additional cognitive deficits occurred in only 13 (19.4%). Changes in personality and behavior were noted in 31 (46.2%). Visuospatial or, less frequently, visual recognition problems were noted in 21 individual cases (31.3%) reviewed. Memory deficits were found in all 14 group studies reviewed, while in 9 papers changes in behavior or personality were also documented. Six studies also reported visuospatial deficits. Careful reading of the literature reveals a range of cognitive and behavioral changes that reflect very well the neuropathological outcomes of anoxic episodes. (JINS, 2000, 6, 86-99.)

Mild hypoxia disrupts recollection, not familiarity

“…By another account, both recollection and familiarity reflect forms of declarative memory and are equally dependent on a single medial temporal lobe system (e.g., Squire, 1994;Squire & Zola, 1998). Critical in testing these opposing views are recent results from studies of hypoxic patients, because imaging and histological research have suggested that damage in these patients can have occurred primarily in the hippocampus (e.g., Gadian et al, 2000;Rempel-Clower, Zola, Squire, & Amaral, 1996; but see Caine & Watson, 2000).…”

Neurobehavioral Grand Rounds Introduction: Does near drowning in ice water prevent anoxic induced brain injury?

“…Generalized brain volume loss leading to ventricular enlargement and sulcal widening (Caine & Watson, 2000) and hippocampal atrophy are also common (Hopkins et al, 1995b;Press et al, 1989). A review of anoxic brain injury (N 5 90) found that 44% of individuals had cortical edema or atrophy, 33% had cerebellar lesions, 22% had basal ganglia lesions, 21% had hippocampal atrophy, and 3% had thalamic lesions (Caine & Watson, 2000). & Bond, 1975), cognitive sequelae, and development of new psychiatric disorders (Bachevalier & Meunier, 1996;Caine & Watson, 2000).…”

“…A review of anoxic brain injury (N 5 90) found that 44% of individuals had cortical edema or atrophy, 33% had cerebellar lesions, 22% had basal ganglia lesions, 21% had hippocampal atrophy, and 3% had thalamic lesions (Caine & Watson, 2000). & Bond, 1975), cognitive sequelae, and development of new psychiatric disorders (Bachevalier & Meunier, 1996;Caine & Watson, 2000). Neuropsychological deficits after anoxia or ischemia are heterogeneous and include agnosia (Farah, 1990), impaired memory (Hopkins et al, 2004;Manns et al, 2003a;Zola-Morgan et al, 1986), executive dysfunction (Hopkins et al, 1995a;Lezak, 1995), impaired visual-spatial skills (Barat et al, 1989), generalized cognitive impairments (Wilson, 1996), and motor disturbances (Lishman, 1998).…”

“…However, brain imaging findings in near-drowning survivors are heterogeneous with abnormalities ranging from hemorrhageic infarctions to global atrophy (Fitch et al, 1985). Similarly, brain MRI findings in anoxic patients who were not near-drowning accidents include lesions in gray (e.g., basal ganglia, hippocampus, etc) and white matter, and global and focal atrophy (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Hopkins et al, 2004;Manns et al, 2003a;Zola-Morgan et al, 1986). Whereas braining imaging was normal by radiologic report in Case 1, quantitative neuroimaging was not carried out (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Gale et al, 1999;Hopkins et al, 1995b).…”

“…Similarly, brain MRI findings in anoxic patients who were not near-drowning accidents include lesions in gray (e.g., basal ganglia, hippocampus, etc) and white matter, and global and focal atrophy (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Hopkins et al, 2004;Manns et al, 2003a;Zola-Morgan et al, 1986). Whereas braining imaging was normal by radiologic report in Case 1, quantitative neuroimaging was not carried out (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Gale et al, 1999;Hopkins et al, 1995b). Nonspecific brain damage may result in general volume reduction manifested by reduced gyral volume, increased sulcal space, passive increase in ventricular volume (i.e., hydrocephalus ex vacuo), increase in whole brain cerebral spinal fluid (CSF; Graham et al, 2002), and structural atrophy (e.g.…”