Cerebellar edema

Abstract: Rotavirus, one of the major causes of severe gastroenteritis in children, occasionally causes central nervous system complications. Recently several patients with acute encephalitis/encephalopathy due to rotavirus associated with cerebellar signs and symptoms have been reported. The condition is characterized by disturbances of consciousness at onset and cerebellar signs and symptoms such as hypotonia, ataxia, dysmetria, and speech disorders, including mutism, slow speech, and dysarthria at convalescence. We report two patients (3-year-old girl, 2-year-old boy) who developed acute encephalitis due to rotavirus and showed cerebellar signs and symptoms. Both patients had characteristic history of consciousness disturbances subsequent to several days of diarrhea, vomiting and fever, and cerebellar symptoms such as hypotonia, ataxia, dysmetria, and speech disorders during the recovery period. Electroencephalography showed diffuse high-voltage delta wave activity in each patient. Brain magnetic resonance imaging showed cerebellar edema in the acute phase followed by cerebellar atrophy on follow-up images in both patients. In the first patient, diffusion-weighted images (DWI) revealed high signals at the left cerebellar peduncle region and apparent diffusion coefficient (ADC) maps showed decreased ADC values of the lesion in the acute phase. The first patient had dysmetria at 1-year follow-up. However, she had normal motor and cognitive functions and could lead her daily life without impairment. In the second patient, no further symptoms were apparent at 1-year follow-up. Acute encephalitis/encephalopathy due to rotavirus with cerebellar signs and symptoms might be diagnosed on DWI, by demonstrating decreased ADC values in acute phase.

Abstract: Abnormal restricted diffusion on magnetic resonance imaging is often associated with ischemic stroke or anoxic injury, but other conditions can present similarly. We present six cases of an unusual but consistent pattern of restricted diffusion in bilateral hippocampi and cerebellar cortices. This pattern of injury is distinct from typical imaging findings in ischemic, anoxic, or toxic injury, suggesting it may represent an under-recognized clinicoradiographic syndrome. Despite initial presentation with stupor or coma in the context of obstructive hydrocephalus, patients may have acceptable outcomes if offered early intervention. We identified an ad hoc series of patients at our two institutions between years 2014 and 2017 who presented to the neurocritical care unit with severe, otherwise unexplained cerebellar edema and retrospectively identified several commonalities in history, presentation, and imaging. Between two institutions, we identified six patients—ages 33–59 years, four male—with similar presentations of decreased level of consciousness in the context of intoxicant exposure, with acute cytotoxic edema of the cerebellar cortex, hippocampi, and aspects of the basal nuclei. All patients presented with severe cerebellar edema which led to obstructive hydrocephalus requiring aggressive medical and/or surgical management. The five patients who survived to discharge demonstrated variable degrees of physical and memory impairment on discharge and at follow-up. We present findings of a potentially novel syndrome involving a distinct pattern of cerebellar and hippocampal restricted diffusion, with imaging and clinical characteristics distinct from ischemic stroke, hypoxic injury, and known toxidromes and leukoencephalopathies. Given the potential for favorable outcome despite early obstructive hydrocephalus, early identification and treatment of this syndrome are critical.

Abstract: The purpose of this study was to determine the maturational period during which the rat pup becomes resistant to the toxic effects of lead on the brain. Pups were fed lead, as lead acetate, by esophageal catheter for 14 days beginning at various ages between 14-24 days. The daily lead doses, which produced a hemorrhagic cerebellar encephalopathy in at least 50% of pups, were 400 micrograms Pb/g body weight for animals fed from 14 days of age, 800 micrograms/g for animals fed from 16 days, and 1600 micrograms/g for animals fed from 18 days. In contrast, pups fed even higher lead doses beginning at 20 days showed only a patchy cerebellar edema by light microscopy while pups fed from 24 days had normal cerebellums by light microscopy. The encephalopathic lead doses in the younger pups resulted in the same cerebellar lead concentrations (about 30 micrograms/g protein) as the higher lead doses fed pups beginning at 20 ot 24 days. When corrected for blood lead concentrations, the cerebellar lead concentrations were 20-25% higher in the encephalopathic compared to the older encephalopathy-resistant animals. This difference may be accounted for by cerebellar hemorrhages in the younger animals. Polarographic studies showed inhibition of respiration in cerebellar slices from animals fed lead from 14 days of age but not in animals fed from 20 or 24 days of age. Our results that, during the encephalopathy-sensitive age period, a critical cerebellar concentration of lead is associated with the encephalopathy. Resistance to lead encephalopathy in older animals, with similar cerebellar lead concentrations, may be related to a capacity to sequester lead in new cellular locations away from its site of action on aerobic energy metabolism.