Wernicke's encephalopathy after gastroplasty for morbid obesity

A young woman developed Wernicke's encephalopathy after gastroplasty for morbid obesity. Her clinical presentation of nystagmus and ocular gaze palsies, ataxia, and a sensorimotor neuropathy is described. A small number of previously described patients are compared with respect to clinical features, response to treatment, and investigative procedures.     

Wernicke's encephalopathy following gastroplasty for morbid obesity

BACKGROUND: The syndrome of Wernicke's encephalopathy consists of two of four features of (1) dietary deficiency; (2) oculomotor abnormality; (3) cerebellar dysfunction; and (4) confusion or mild memory impairment. Predisposing risk factors include alcoholism, hyperemesis gravidarum and prolonged intravenous feeding. METHODS: A 35-year-old female developed refractory emesis, severe weight loss, and hypokalemia following banded gastroplasty for morbid obesity. Reversal of gastroplasty was performed four months following initial surgery. Following reversal, the patient developed confusion, ataxia, leg weakness and nystagmus. RESULTS: Examination of the patient demonstrated disorientation with confusion, vertical nystagmus worse on downgaze, diffuse weakness of the lower extremities, and bilateral dysmetria. Magnetic resonance imaging of the brain demonstrated symmetrical areas of increased T2 signal present bilaterally in the medial thalamic nuclei. The patient did not demonstrate any initial improvement with intravenous thiamine but improved over two months of follow-up. CONCLUSION: Wernicke's encephalopathy has been reported in the European literature as a complication of gastroplasty, with rare recognition of this clinical entity in the North American literature. This potential complication of gastroplasty may be preventable by nutritional intervention in subjects experiencing severe weight loss and emesis following surgery.     

Wernicke-korsakoff encephalopathy and polyneuropathy after gastroplasty for morbid obesity: report of a case

BACKGROUND: Gastric partitioning is a surgical procedure for the treatment of morbid obesity that may engender neurological complications, such as Wernicke encephalopathy and polyneuropathy. SETTING: A specialist hospital. PATIENT: A 36-year-old woman developed Wernicke-Korsakoff encephalopathy and polyneuropathy 3 months after gastroplasty for morbid obesity. A magnetic resonance scan documented the diagnosis, and a clear improvement occurred after parenteral thiamine treatment. In our patient and in previously described cases of the literature, postsurgical vomiting is a constant finding that seems to be the precipitating factor of neurological complications of gastric partitioning. CONCLUSION: Persistent vomiting after gastroplasty for morbid obesity should be considered an alarming symptom to treat immediately with appropriate measures.     

Wernicke-Korsakoff syndrome after subtotal gastrectomy

A case of Wernicke-Korsakoff syndrome in a nonalcoholic patient after gastric surgery provides support for the theory that nutritional deficiencies play an important part in the pathogenesis of the disease.

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Sommario Viene descritto un caso di sindrome di Wernicke-Korsakoff in un paziente non alcolista dopo gastrectomia subtotale. È sottolineato il ruolo fondamentale svolto dal deficit nutrizionale nella patogenesi della malattia.

     

Neurologic complications after gastric restriction surgery for morbid obesity

We report the occurrence of neurologic complications in 23 patients who underwent gastric restriction surgery for the treatment of morbid obesity. Complications occurred 3 to 20 months after surgery. All the patients had had protracted vomiting for the first 3 months after the operation. The following syndromes were found: chronic or subacute symmetric polyneuropathy (12 patients), acute severe polyneuropathy (1 patient), burning feet syndrome (2 patients), meralgia paresthetica (3 patients), myotonic syndrome (1 patient), posterolateral myelopathy (2 patients), and Wernicke-Korsakoff encephalopathy (2 patients). The patients suffering from burning feet syndrome and those with Wernicke-Korsakoff encephalopathy showed a clear improvement after parenteral thiamine treatment. As to the rest of the patients, the occurrence of the complications seems to be linked to nutritional causes, although no such deficiencies were detected.     

Wernicke encephalopathy and Creutzfeldt-Jakob disease

We assessed the prevalence of Wernicke encephalopathy (WE) in all 657 cases suspected of Creutzfeldt-Jakob (CJD) referred from 2001 to 2006 to the French Neuropathology Network of CJD. Clinical, biological and imaging data were reviewed when the diagnosis of WE was made at autopsy. No CJD was found in five cases suspected of sporadic CJD. In these five cases, myoclonus had been observed in four, CSF 14-3-3 protein in two. In 14 other cases, WE was combined with CJD, 13 of which were sporadic. These belonged mainly to the molecular variants of sporadic CJD associated with a long duration of disease. This stresses the necessity of remaining alert to the diagnosis of WE when CJD is suspected.     

Wernicke encephalopathy after gastrointestinal surgery for cancer: causes of diagnostic failure or delay

Wernicke encephalopathy (WE) is a neurological emergency due to thiamine deficiency. We aimed to identify clinical course and causes of diagnostic delay or failure of WE in a group of patients who underwent surgery for gastrointestinal tumors. A retrospective review of clinical, laboratory, neuroimaging, and therapeutic features of 10 patients with WE following abdominal surgery for cancer was carried out. Four patients died; in these subjects, diagnosis was delayed and supplementation of vitamin was absent or likely inadequate. Diagnostic delay or failure was also related to the coexistence of several medical complications at presentation masking typical symptoms of WE. In the surviving patients, outcome was influenced by promptness and type of therapy. Postoperative abdominal bleeding and number of subsequent operations may also had an effect. Postsurgical patients with gastrointestinal tumors may develop a subtle WE. The number of subsequent operations and the severity of postoperative complications may increase the risk of unrecognized WE. The disease should be suspected in postsurgical patients who have unexpected mental status changes, even under prophylactic treatment with vitamins. We suggest that prophylaxis with high doses of thiamine should be undertaken in patients with gastrointestinal tumors before surgery.     

Jakob-Creutzfeldt disease associated with Wernicke encephalopathy

Wernicke disease (WD) is a complication of alcoholism and malnutrition and usually presents acutely and is characterized by disturbances of consciousness, paralysis of the external ocular muscles, and ataxia. The disease results from deficiency of vitamin B 1, or thiamine, an essential coenzyme in intermediate carbohydrate metabolism. On the other hand, Jakob-Creutzfeldt disease (J-C) results from infection with an unconventional agent with a long incubation period and is characterized by a rapidly progressive dementia and histologically by a spongiform encephalopathy associated with neuronal destruction and pronounced astrogliosis. Combination of both diseases has not been reported in the literature previously and their relationship is uncertain. We present 3 cases with this interesting association and consider their relationship.     

Anti-Ma encephalitis masquerading as Wernicke encephalopathy

BackgroundAnti-Ma encephalitis is a disease usually associated with testicular cancer in young male patients. Anti-Ma encephalitis presented as Wernicke encephalopathy-like symptoms and with gastric cancer is rare. Here, we report a case of anti-Ma encephalitis with gastric cancer in an elderly patient, which has been misdiagnosed of Wernicke encephalopathy.Case reportA 71-year old male with a history of alcohol abuse was admitted to the hospital because of progressive dizziness, diplopia and anorexia lasted for 1 month. He was initially diagnosed as Wernicke encephalopathy. However, this patient failed in the treatment of VitB1. The blood and cerebrospinal fluid examination found the presence of anti-Ma1/2 antibodies. ¹⁸F-FDG PET-MR showed symmetrical hypermetabolic changes on the bilateral hypothalamus, basal ganglion and brainstem, as well as gastric neoplasms with liver metastasis. The patient was finally diagnosed with anti-Ma encephalitis.ConclusionAnti-Ma encephalitis should be suspected in patient with Wernicke encephalopathy-like symptoms but failed VitB1 treatment.     

Hypothermia, Wernicke encephalopathy and multiple sclerosis

Neurological exacerbation observed in MS patients is usually related to a demyelinating process. We report two patients where hypothermia (32.4 degrees C and 32.5 degrees C) and neurological exacerbation were probably due to a Wernicke encephalopathy (WE). The clinical features and the rapid efficiency of parenteral thiamine were suggestive of WE. Hypothermia is an exceptional symptom observed in MS and has been considered as resulting from hypothalamic demyelination; these two cases showed that WE which is another cause of reversible hypothermia, can be associated with MS.