Nonalcoholic Wernicke's Encephalopathy Associated with Unintentional Weight Loss, Cholecystectomy, and Intractable Vomiting: The Role of Dual Thiamine and Corticosteroid Therapy.

A 23-year-old male with one month of intractable vomiting, subsequent cholecystitis status post cholecystectomy, and overall 40-pound weight loss over the last few months presented with altered mental status and seizures. MRI showed signal abnormalities involving the hypothalamus, periaqueductal gray matter, 4th ventricle, and bilateral thalami, indicative of Wernicke's encephalopathy. The patient was started on empiric IV thiamine and methylprednisolone; thiamine levels were subsequently found to be low. Infectious disease workup was negative. Within a few days of this therapy, the patient's neurological status steadily improved with increased responsiveness and communication. Repeat MRI 7 days after admission showed significant resolution of the signal abnormalities. Over the next several weeks the patient became fully conversational, cognitively intact, and increasingly ambulatory. Nonalcoholic Wernicke's encephalopathy is rare; there have been reports relating it separately to vomiting and invasive surgery. In this case report, we associate it with both recurrent vomiting and minimally invasive cholecystectomy. We also discuss combinatorial therapy of thiamine and corticosteroids, which is poorly defined in the literature. Though there is no consensus-based optimal treatment of Wernicke's encephalopathy, this adds to the discussion of using dual therapy and supports that the use of empiric corticosteroids does not harm the patient.

A case of chronic progressive lyme encephalitis as a manifestation of late lyme neuroborreliosis.

A 54-year-old female living in Europe presented with gait ataxia, dizziness, and bilateral hearing loss. Magnetic resonance imaging (MRI) revealed non-specific white matter changes. The patient's condition gradually deteriorated over two years without diagnosis. The patient continued to decline cognitively and neurologically with worsening ataxia and upper motor neuron signs. Repeat MRI showed worsening white matter changes. Lumbar puncture, not previously done, showed positive Lyme testing. Treatment with intravenous ceftriaxone resulted in marked neurological improvement. Four years after symptom, the patient has short-term memory deficits and chronic fatigue, but is otherwise neurologically, cognitively, and functionally intact. Follow up MRI findings remain largely unchanged. Because cases of intraparenchymal or encephalopathic neuroborreliosis in America are lacking, so are treatment options. We present a rare case and discuss our experience with antibiotic treatment. This case lends evidence to define optimal treatment of this disease, imperative for hastening neurological recovery.

Symptom duration and clinical features in painful sensory neuropathy with and without nerve conduction abnormalities.

BACKGROUND: The term "small fiber sensory neuropathy" (SFSN) refers to an axonal sensory polyneuropathy predominantly affecting cutaneous sensory modalities, often associated with pain and with no evidence of large fiber involvement. We hypothesized that, in most patients, SFSN is the earliest manifestation of a nonspecific axonal neuropathy and will usually progress to involve larger, heavily myelinated sensory and motor fibers. We sought indirect evidence of this through an analysis of the correlation between symptom duration and large fiber involvement in patients with painful sensory neuropathy (PSN). METHODS: A clinical diagnosis of PSN was supported by nerve conduction studies or measurement of epidermal nerve fiber (ENF) density in 43 patients. Symptom duration was correlated with the frequency of large fiber loss as measured by nerve conduction abnormalities. The severity and extent of clinical signs and symptoms were also evaluated in subjects with and without electrodiagnostic abnormalities. RESULTS: Patients with large sensory axon involvement had symptoms of longer duration than patients with SFSN. The frequency of electrodiagnostic abnormalities increased in direct proportion to disease duration. Patients with electrodiagnostic abnormalities also had more extensive pinprick sensory deficits, suggesting that small fiber loss was more advanced in this group as well. CONCLUSIONS: In PSN, the incidence of large fiber involvement appears to increase in proportion to symptom duration. This represents indirect evidence that SFSN usually progresses to involve both large and small fibers within 2-10 years.