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Wernicke encephalopathy (WE) is a neurologic disorder characterized by clinical symptoms, such as nystagmus, ataxia, and mental confusion. Hypothermia in patients with WE is a rare complication, and its pathogenic mechanism and therapy are yet to be ascertained. Herein, we presented a case of a 61-year-old man who was diagnosed with WE 3 months earlier. We investigated the cause of hypothermia (35.0℃) that occurred after an enema (bowel emptying). Brain magnetic resonance imaging revealed mammillary body and hypothalamus atrophy. In the autonomic function test, the sympathetic skin response (SSR) test did not evoke SSR latencies on both hands. In addition, abnormal orthostatic hypotension was observed. Laxative and stool softener medication were administered, and his diet was modified, which led to an improvement in constipation after 2 weeks. Moreover, there was no recurrence of hypothermic episode. This is the first reported case of late-onset hypothermia secondary to WE.
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A 50-year-old man with liver cirrhosis and esophageal varix for 3 years was diagnosed with hematemesis and treated for a bleeding varix. However, bleeding recurred 11 days later, and he developed drowsiness with left hemiparesis. His left upper and lower extremity muscle strengths based on the manual muscle test at the onset were grade 2/5 and 1/5, respectively. The Babinski sign was positive. His serum ammonia level was elevated to 129.9 µg/dL (normal, 20-80 µg/dL). Magnetic resonance imaging revealed restriction on diffusion and T2-hyperintensities with decreased apparent diffusion coefficient values in the bilateral frontoparietooccipital cortex. The effect was more severe in the right hemisphere and right parietooccipital cortices, which were compatible with hepatic encephalopathy. Although the patient's mental status recovered, significant left-sided weakness and sensory deficit persisted even after 6 months. Diffusion tensor tractography (DTT) performed 3 months post-onset showed decreased volume of the right corticospinal tract. We reported a patient with hepatic encephalopathy involving the corticospinal tract by DTT.
Rotavirus encephalopathy (RE) is a benign afebrile seizure associated with acute gastroenteritis caused by rotavirus infection. We investigated the diffusion tensor tractography (DTT) findings of a patient with RE. The patient was a 30-month-old female that had experienced a brief, generalized convulsive seizure. On the day of admission, the patient had vomiting and experienced watery diarrhea. Her stool was positive for rotavirus antigen. At onset, the patient displayed a drowsy and delirious mental status; later, a splenial lesion of the corpus callosum was found on MRI. One week later, the patient's condition improved and the splenial lesion had disappeared by conventional MRI. Initial DTI showed decreased fractional anisotropy (FA) values of fornix, as well as of the corpus callosum. A follow-up DTT showed a restored interrupted right fonical crus and increased FA values of corpus callosum and fornix. These results highlight the implications of the probability of not only a corpus callosum injury, but a fornix injury as well, in this patient with RE.
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Morbid obesity is a curable systemic disease that can cause several complications, including hypertension, diabetes mellitus, and osteoarthritis. However, it is not easy to control solely by conservative management. Bariatric surgeries, such as sleeve gastrectomy and gastric banding, are recently developed treatments that are applied to patients with morbid obesity in Korea. However, gastric surgery can cause surgical or metabolic complications, such as thiamine deficiency, which can lead to Wernicke's encephalopathy. This metabolic complication presents with typical symptoms of confusion, ophthalmoplegia, nystagmus, and ataxia. In this case report, we present a case of Wernicke's encephalopathy, which developed slowly following sleeve gastrectomy in a patient with morbid obesity.
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We report the case of a 40-year-old hypoxic encephalopathy patient who suffered from dry mouth and frequent poor oral hygiene secondary to a prominent nasolabial fold and elevated upper lip, exposing the canine teeth at rest. This expression was confirmed secondary to persistent contraction of the levator labii superioris muscle with electromyography (EMG) study. We have injected 6 units of Botulinum toxin A in levator labii superioris muscle with electromyographic guidance. Elevation of upper lip at rest causing exposure of canine teeth has been nearly disappeared 3 days after the injection. We suggest that chemical weakening of the levator labii superioris muscle using Botulinum toxin A could be possibly responsible for the dramatic reduction of elevated upper lip exposing canine teeth in patients with hypoxic encephalopathy.
Ammonia is a colorless alkaline gas with a sharp pungent odor. It is widely used in industry and there are several case reports on deleterious pulmonary damage. Ammonia is also highly neurotoxic that interferes energy metabolism in the brain even with a small amount and causes encephalopat hy in patients with severe liver disease.
We experienced two patients with toxic encephalopathy and followed- up for 18 months. We assumed that ammonia was supposed to play a major role in the dysfunction of their brains. In our cases, the possible mechanisms of brain damage are as followings: ⸁ ammonia has direct toxic effect on brain by altering the energy metabolism, ⸂ inhalation of ammonia results in severe pulmonary damage and it may aggravate brain injury, and ⸃ besides ammonia itself, relatively hypoxic environment that they were exposed can take part in the brain injury.
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