Sudden unexpected death in epilepsy refers to sudden death of an individual with a clinical history of epilepsy, in whom a postmortem examination fails to uncover a gross anatomic, toxicologic, or environmental cause of death. Evidence of terminal seizure activity may not be present. One to two percent of natural deaths certified by the medicolegal death investigator are attributed to epilepsy. Detailed microscopic examination of the brain has increasingly afforded the identification of structural changes representative of epileptogenic foci. The authors present 70 cases of death attributed to sudden unexpected death in epilepsy. These cases were classified as follows: individuals who lacked a gross brain lesion, those who had a brain lesion demonstrable at autopsy, and those who lacked neuropathologic evaluation because of decomposition or because only an external examination was done. All of the subjects had a clinical history of seizures. The authors confirm that various microscopic findings, including neuronal clusters, increased perivascular oligodendroglia, gliosis, cystic gliotic lesions, decreased myelin, cerebellar Bergmann's gliosis, and folial atrophy, are present in a higher percentage of the brains of sudden unexpected death in epilepsy subjects than in the brains of age- and sex-matched control subjects.

In a review of 2,616 consecutive autopsies done at the University of Kentucky Medical Center over a 12-year period, 46 patients with complete postmortem examinations had tissue-verified candidiasis in two distinct patterns, with Candida albicans being most frequently cultured. Superficial candidiasis involving only lining surfaces was observed in 21 patients (46%). Usually, it complicated other lethal problems such as malignancy and bacterial sepsis. Nineteen of these patients (95%) had received antibiotics. No vessel invasion or deep organ involvement was evident in this group. The other pattern of candidiasis was a deep or systemic variety recognized in the remaining 25 patients (54%). It was characterized by deep parenchymal organ lesions usually involving the brain (52%), heart (48%), and kidney (80%), but any tissue seemed susceptible. Vessel invasion was seen in 8 patients (32%); intravenous lines were used in 13 (52%); and major operations were done in 16 (64%). All these patients were hospitalized for either benign or malignant conditions and were treated for bacterial sepsis with antibiotics for seven days or more. This investigation indicates that candidiasis occurs when the host's environment is altered primarily by antibiotic therapy. Candida then can colonize lining surfaces and from there could invade adjacent vessels and disseminate throughout the body.

Circulatory arrest (CA) remains a major unresolved public health problem in the United States; the annual incidence of which is ~0.50 to 0.55 per 1000 population. Despite seminal advances in therapeutic approaches over the past several decades, brain injury continues to be the leading cause of morbidity and mortality after CA. In brief, CA typically results in global cerebral ischemia leading to delayed neuronal death in the hippocampal pyramidal cells as well as in the cortical layers. The dynamic changes occurring in neurons after CA are still unclear, and predicting these neurological changes in the brain still remains a difficult issue. It is hypothesized that the "no-flow" period produces a cytotoxic cascade of membrane depolarization, Ca ion influx, glutamate release, acidosis, and resultant activation of lipases, nucleases, and proteases. Furthermore, during reperfusion injury, neuronal death occurs due to the generation of free radicals by interfering with the mitochondrial respiratory chain. The efficacy of many pharmacological agents for CA patients has often been disappointing, reflecting our incomplete understanding of this enigmatic disease. The primary obstacles to the development of a neuroprotective therapy in CA include uncertainties with regard to the precise cause(s) of neuronal dysfunction and what to target. In this review, we summarize our knowledge of the pathophysiology as well as specific cellular changes in brain after CA and revisit the most important neurofunctional, neuroimaging techniques, and serum biomarkers as potent predictors of neurologic outcome in CA patients.

P53 immunohistochemistry has been used to distinguish between malignant tumors and morphologically similar benign processes. In the central nervous system, a major diagnostic dilemma is caused by overlapping features of benign reactive astrocytic lesions and low-grade astrocytomas, especially with small biopsies. P53 immunoreactivity in astrocytes could be useful in differentiating benign reactive lesions from malignant astrocytomas. An immunohistochemical study on 110 brain lesions from 108 patients using a monoclonal antibody (DO-7) against p53 protein was conducted. Using the modified Ringertz and World Health Organization system, the specimens included 22 astrocytomas, 12 anaplastic astrocytomas, 42 glioblastoma multiforme tumors, three nonglial tumors, and 56 reactive astrocytic lesions to 25 neoplasms, nine infectious processes, six cerebrovascular disorders,one metabolic disorder, two vascular malformations, eleven degenerative/demyelinating lesions, and two unknown primary lesions. Immunoreactive astrocytic tumors included 12 (54%) astrocytomas, nine (75%) anaplastic astrocytomas, and 38 glioblastoma multiforme tumors (90%). Among the reactive astrocytic lesions, only five (9%) cases of progressive multifocal leukoencephalopathy were immunoreactive. These data demonstrate that p53 immunoreactivity in astrogliosis is unusual but is to be expected in astrocytomas and can help to differentiate reactive from neoplastic astrocytic lesions.

Surgical specimens from 100 patients with stage I B cervical cancer undergoing radical hysterectomy and pelvic lymphadenectomy were reviewed with respect to vascular invasion and lymphoplasmacytic infiltration. Lymph nodes from these patients were classified morphologically according to the criteria proposed by Cottier. Vascular invasion was associated with a significant increase in nodal metastases and tumor recurrence particularly to extrapelvic sites. A marked lymphoplasmacytic infiltrate around tumor cells was associated with decreased nodal metastases and tumor recurrence. There was no significant relationship between the degree of lymphoplasmacytic infiltration of the primary tumor and regional lymph node morphology.