| Contributed by Mel B Feany1, MD, PhD, Douglas C Anthony1, MD, PhD, Matthew P Frosch1, MD, PhD, William Zane2, MD, and Umberto De Girolami, MD1|
1Departments of Pathology (Neuropathology), Brigham and Women's Hospital and Children's Hospital, Boston, MA, and 2Office of the Chief Medical Examiner, Boston, MA Hospital, Boston, MA, and 2Office of the Chief Medical Examiner, Boston, MA
|Published on line in August 2000|
A 51 year old woman and a friend went into the family recreational vehicle to have a few drinks. They used water from the vehicle's tap to mix with their alcohol. The patient's husband had not flushed out the water system as he usually did in the early spring. Two days later, the patient became delirious and short of breath. She was admitted to the hospital, and remained unconscious until her death, seven days after the initial exposure. The friend was hospitalized for four days, and survived following treatment.
External examination revealed moderate cerebral edema, but no evidence of herniation. Coronal sections of the brain showed softening and acute hemorrhage in the putamen (Figs. 1 and 2). The remainder of the central gray matter, including the globus pallidus, hypothalamus, and thalamus, was unremarkable. The brainstem and cerebellum were also well-preserved. Softening of the subcortical white matter was evident in the frontal, parietal, and occipital lobes.
Microscopic examination showed acute hemorrhage and necrosis of the lateral putamen. Acute necrosis was also evident in subcortical white matter (Fig. 3, note myelin pallor), but white matter hemorrhage was minimal.
A 26 year old woman was admitted to the hospital with severe acidosis and vomiting. Two days prior to admission she attended a party where she drank a presumed gin and tonic. After the party she became sick and vomited during the night. The next day, she experienced more episodes of vomiting with headache and blurred vision. On the day of hospital admission, the headaches were persistent, and there was intermittent loss of vision. Physical examination on admission revealed normal vital signs. Pupils were 7 mm and nonreactive bilaterally. Fundi were normal. Despite treatment, the patient died after three weeks of hospitalization.
External examination revealed massive cerebral edema with prominent cuffing of the medulla with cerebellar tonsillar tissue. Horizontal sections of the cerebrum and brainstem showed widespread, multifocal hemorrhagic necrosis of the white matter, involving predominantly subcortical white matter, but also extending into the centrum semiovale (Fig. 4 [macroscopic]). Cavitation was evident grossly. The corpus callosum was spared. Smaller areas of hemorrhage were noted in the lateral and posterior aspects of the putamen.
Microscopic examination showed hemorrhagic necrosis, cavitation, and extensive macrophage infiltration in the subcortical white matter and lateral putamen (Fig. 5).
What is the most likely etiology for the putamen and white matter lesions in these two cases?