Clonazepam-induced liver dysfunction, severe hyperlipidaemia, and hyperglycaemic crisis: A case report.

In this study, we report a case of a 50-year-old Japanese man who had chronic whiplash-associated disorder, hyperlipidaemia, hyperuricacidaemia, and mild liver dysfunction due to excessive alcohol intake. Recently, he developed mild tremor in his left hand. Initiation of clonazepam (0.5 mg once daily before bedtime) helped to gradually ameliorate the tremor. However, 13 days after clonazepam initiation, his liver function and lipid profiles aggravated, and his postprandial glucose level increased to 400 mg/dL. Clonazepam was stopped promptly, and at 7 days after discontinuation, the abnormal triglyceride levels, liver dysfunction, and glycometabolism improved without any other medical intervention. This case may provide information on cautious use of clonazepam. When clonazepam is used for patients with existing hyperlipidaemia and liver dysfunction, it may cause abnormal lipid profile, aggravate liver dysfunction, and lead to remarkable glucose elevation.

[A 26-year-old woman of interval form of acute carbon monoxide intoxication with cerebrospinal fluid abnormalities].

A 26-year-old woman was admitted to our hospital for the treatment of hyperbaric oxygen therapy to acute carbon monoxide intoxication. The consciousness disturbance improved and she was discharged after 23 times of the hyperbaric oxygen therapy. However, she was readmitted because of dementia and urinary incontinence after 22 days. Diffusion-weighted images showed bright high signal intensities in the periventicular white matter and corpus callosum. The condition was considered to be an interval form of carbon monoxide intoxication. She was treated by 38 times of the hyperbaric oxygen therapy with cytochrome C and fully recovered. MRI images and cerebrospinal fluid abnormality (high protein content and IgG index) became normalized somewhat later than the improvement of the symptoms. By an investigation utilizing diffusion-weighted images, we thought that not only the demyelination which mentioned formerly, but the vasogenic edema was involving in the mechanism of these high signal intensities in the periventicular white matter of the interval form. And in the range which we searched, this is the first report which mentioned the abnormal findings of cerebrospinal fluid in an interval form of carbon monoxide intoxication. So we believe this case is very important for telling us suspected the mechanism and some indications about the treatment of an interval form.

Acute disseminated encephalomyelitis following Plasmodium vivax malaria.

A 24-year-old Japanese man showed neurological disturbances 2 weeks after complete recovery from Plasmodium vivax infection. Magnetic resonance (MR) images of the brain showed multiple high-intensity spotty lesions in the left cerebral cortex and subcortex. Cerebrospinal fluid examination, including polymerase chain reaction analysis for viruses, revealed no sign of active infection. Repeated blood smears were negative for malaria. We diagnosed acute disseminated encephalomyelitis (ADEM) following Plasmodium vivax malaria from the clinical course and MR images. ADEM should be regarded as one of the neurological complications after malarial infection.

Acute disseminated encephalomyelitis following dengue fever.

A58-year-old man suffered from acute disseminated encephalomyelitis (ADEM) after dengue fever. ADEM has not been described as the cause of neurological complications in dengue fever. However, the increasing use of magnetic resonance imaging in endemic areas may help to identify ADEM as being responsible for neurological complications in dengue fever.