Accidental intrathecal administration of vincristine.

We describe a case of accidental intrathecal administration of vincristine in a 33-year-old man with clinical diagnosis of acute lymphocytic leukemia. The patient died 20 days after receiving the drug. Clinically, the patient developed acute ascending paralysis with motor and sensory dysfunctions, and respiratory failure. Neuropathological investigation revealed lesions in spinal cord, roots, and cerebellum characterized by rarefaction of the neuropil, axonal, and myelin degeneration, accompanied by macrophagic infiltration.

Resistance to Alzheimer's pathology is associated with nuclear hypertrophy in neurons.

This study focuses on the morphometric changes of neurons in asymptomatic Alzheimer's disease (AD), a state characterized by the presence of AD lesions in subjects without cognitive impairment. In autopsy brains, we used stereological methods to compare the cell body and nuclear volumes of anterior cingulate gyrus (ACG) and CA1 hippocampal neurons in asymptomatic AD subjects (n=9), subjects with AD dementia (AD, n=8), mild cognitive impairment (MCI, n=9), and age-matched controls (controls, n=9). In ACG, we observed a significant decrease in the neuronal volume of MCI and AD compared to controls; by contrast, no atrophy was present in asymptomatic AD. Moreover, we found a significant increase in nuclear volume in asymptomatic AD compared to controls (P<0.001), MCI (P<0.01) and AD (P<0.001) brains. Similar results were found in the CA1 region of the hippocampus. This nuclear hypertrophy may represent an early neuronal reaction to Abeta or Tau, or a compensatory mechanism which forestalls the progression of AD and allows the brain to resist the development of dementia.

Causes of unexpected death in patients with multiple sclerosis: a forensic study of 50 cases.

To determine the cause of death (as a result of neurologic or nonneurologic complications or accidents) in patients with multiple sclerosis (MS), we reviewed the autopsies of 50 subjects with MS from the Office of the Chief Medical Examiner of Maryland (OCME) between 1982 and 2004. The series included 32 females and 18 males (mean age, 45.8 years; range, 25-69 years) and the causes of death were classified into 3 categories: (A) neurologic complication directly related to MS; (B) nonneurologic complications or other medical causes; and (C) accidents, etc. Of the 50 cases, in 43 there was a history of MS, but in 7 subjects there was not, and the diagnosis was established by neuropathologic examination. In Group A, 21 (42%) cases, deaths were directly related to a neurologic complication; in Group B, 14 (28%) cases were related to the following nonneurologic and medical causes: ASCVD 9 (18%), metabolic disorder 1 (2%), pulmonary embolism 3 (6%), and bronchopneumonia 1 (2%); and in Group C, 15 (30%) cases, deaths were due to trauma, 9 (18%); intoxication, 5 (10%); and thermal injury, 1 (2%). Thus, among the 50 subjects, in 26, deaths occurred naturally; and in 24, from accidents, homicides, suicides, or undetermined causes. Pathologically, the majority of cases showed either chronic inactive (66.7%) or chronic active (15.6%) demyelinating lesions, mainly in the cerebral hemispheres. In some cases, it appears that demyelinating lesions, involving brain regions that regulate cardiorespiratory activity, could be considered as the immediate cause of death, but a large proportion appears to be due to other causes such as accidents and trauma. Thus, it seems likely that taking specific precautions could prevent some deaths in MS.

Pseudolaminar necrosis in cyanide intoxication: a neuropathology case report.

We describe the gross and microscopic neuropathological changes in the brain of a 17-year-old male who died 4 days after being poisoned with cyanide. Previous reports indicate that following cyanide intoxication, the brain develops diffuse hypoxic/ischemic changes, predominantly of the basal ganglia. The case we describe here had similar features but in addition showed striking laminar necrosis of the cerebral cortex. This finding in cyanide poisoning has been previously demonstrated by neuroimaging, but not pathologically.