Pyridoxine Toxicity Small Fiber Neuropathy With Dysautonomia: A Case Report.

Pyridoxine (vitamin B6) toxicity is a well-known cause of primary sensory, length-dependent, axonal polyneuropathy. Although sensory symptoms predominate, autonomic symptoms have also been reported in some cases. To date, there is no objective evidence of autonomic dysfunction reported in the literature. We present the case of a 41-year-old woman with 2 years of progressive burning pain, numbness, tingling, and weakness in a stocking-glove distribution who was found to have severe pyridoxine toxicity. Concurrent presence of large and small fiber nerve dysfunction was noted in the form of abnormal electromyography/nerve conduction study demonstrating a chronic sensory polyneuropathy and autonomic testing demonstrating abnormal responses to quantitative sweat testing and cardiovagal function testing. This case highlights the need for consideration of small fiber nerve damage by obtaining autonomic testing in cases of pyridoxine toxicity.

Looks like a stroke, acts like a stroke, but it's more than a stroke: a case of cerebral mucormycosis.

Mucormycosis is a fungus that exhibits angiocentric growth and can cause a thrombotic arteritis. Infection with this organism is uncommon and cerebral involvement is most often secondary to direct invasion through the paranasal sinuses. Here, we present a case of mucormycosis with cerebral involvement without sinus disease, which resulted in ischemic stroke with rapid progression resulting in death.

Atorvastatin as novel treatment for neuropathic pain: a case report.

INTRODUCTION: Managing neuropathic pain can be very challenging, with standard medical therapies often providing inadequate relief. It has recently been reported in the literature that statins alleviate neuropathic pain in the rat model. We present a case report in which an above-the-knee amputee achieved relief of his neuropathic stump pain with atorvastatin. CASE REPORT: We describe the case of a 50-year-old man with a 12-year history of chronic neuropathic stump pain and sporadic phantom limb pain following an above-the-knee amputation. For 11 years the pain was managed with gabapentin 300 mg 3 times daily plus oxycodone 10 mg twice daily. He autonomously weaned himself to gabapentin 300 mg once daily and oxycodone 10 mg once daily, exacerbating his stump pain in the process. After starting atorvastatin 20 mg once daily for hypercholesterolemia, he immediately experienced decreased intensity of his stump pain, but his phantom pain persisted at its usual intensity. CONCLUSIONS: More studies are needed to characterize the analgesic effects of statins better. In patients who have neuropathic pain refractory to traditional treatment options or, rather, decline traditional treatment options, statin therapy may be helpful.

Chronic non-exertional myalgia and myoadenylate deaminase deficiency: a possible association.

UNLABELLED: Myoadenylate deaminase deficiency is noted in skeletal muscles. It generally presents with exertional myalgias, fatigue and weakness. We present a patient who complained of constant pain unrelated to activity with biopsy finding consistent of myoadenylate deaminase deficiency. KEYWORDS: Myoadenylate deaminase deficiency; Myalgia; Pain.

Familial Creutzfeldt-Jakob disease presenting as epilepsia partialis continua.

Creutzfeldt-Jakob disease (CJD) is a rare disorder caused by prions that can affect any part of the central nervous system. It is characterized by a long incubation period, but once symptoms start there is a progressive neurological decline. Clinical features include dementia, ataxia and myoclonus (startle), among others. We report a biopsy-proven case of familial CJD (fCJD) presenting with continuous focal seizures, epilepsia partialis continua (EPC), as the initial presentation. CJD is an unusual neurological disorder with an incidence of approximately one case per million population (Prusiner 2001). The disorder is due to neuronal degeneration resulting from the accumulation of a pathological isoform (PrP) of the prion protein (PrPc). Patients with fCJD have mutations in the gene encoding PrPc (PRNP) (Vercueil 2006, Collins et al. 2004). This fCJD represents 10-15% of CJD cases making the sporadic form more common 85-95% (Parry et al. 2001). During the course of the disease myoclonus has been reported in 88% of cases, and epileptic seizures (partial seizures, generalized status epilepticus) in 8% (Vercueil 2006). Periodic sharp wave complexes (PSWC) are uncommon in fCJD and occur in about 10% of patients (Wieser et al. 2006).