Howard et al. Journal of Medical Case Reports 2010, 4:409 http://www.jmedicalcasereports.com/content/4/1/409 prior to this presentation. He remained ambulant. Abnormalities on clinical examination included grade 4 power throughout both his lower limbs, absent ankle jerks and glove and stocking distribution reduction in pinprick sensation to his mid forearms and proximal thighs. Initial electromyogram (EMG)/nerve conduction studies (NCS) demonstrated a mild sensory peripheral polyneuropathy (consistent with long standing type 2 DM and chronic alcohol abuse). There were also patchy non-specific EMG abnormalities suggesting a non-speci- fic myopathic process. Clinical course Rapid deterioration occurred over the course of approxi- mately three months, with relatively rapid evolution of tetraparesis. Urgent admission was arranged, by which stage he was unable to walk. He had also developed tin- gling in his legs and arms. On examination, his cranial nerves remained intact but he had marked weakness of upper limbs (grade 3) and lower limbs (grade 2), with absent lower limb and reduced upper limb deep tendon reflexes bilaterally. He also had prominent sensory impairment in his upper and lower limbs, including loss of pain sensation to his waist. At one stage this was sug- gestive of a possible spinal sensory level. Repeat EMG/ NCS four months after the first study showed evidence of a widespread polyneuropathy, with sensory nerve action potentials absent or reduced and evidence of extensive acute and sub-acute denervation in his upper and lower limbs. Although an EMG showed extensive motor denervation suggestive of anterior horn cell dis- ease, this could be ruled out due to the extensive degree of sensory impairment. Other investigations His cerebrospinal fluid was acellular with normal protein and glucose concentrations. Oligoclonal bands were absent. A muscle biopsy of his left quadriceps showed mild non-specific morphological abnormalities with mainly selective type 2-fibre atrophy, possibly associated with an element of neurogenic atrophy. This was thought to correlate with underlying alcohol-related or endocrine myopathy. There were no features of meta- bolic, mitochondrial, inflammatory or necrotising myopathies. A whole body computed tomography (CT)-18fluorodeoxyglucose (FDG) positron emission tomography (PET) scan identified no abnormality other than lobular increased thyroid intake, a lesion for which he had previously undergone a negative fine needle aspiration biopsy. Despite the possible spinal sensory level, magnetic resonance imaging of his spine was not undertaken given the absence of any other myelopathic features coupled with the confirmation of a severe neu- ropathy. Serum immunoglobulins revealed raised immu- noglobulin M (IgM) at 3.65 g/L (normal range, 0.5-2.0 g/L). Electrophoresis identified no monoclonal band. Page 2 of 4 Gamma-glutamyl transferase was elevated at 385 u/L (normal range, 1-71 u/L). No other cause was identified other than excessive alcohol intake prior to admission. A full blood count showed a haemoglobin level of 12.3 g/dL (normal range, 13-18 g/dL) and a mean cell volume of 104.3fL (normal range 82-98fL). Vitamin B12 deficiency (191 ng/L, normal range 200-900 ng/L) had been identified when our patient initially presented with symptoms, and was treated with B12 replacement (insti- tuted by his general practitioner). Other relevant investi- gation results which were negative or did not show significant abnormalities included renal function, the remainder of liver function tests and full blood count, bone profile, coagulation screen, creatine kinase, thyroid function tests, HIV-1, HIV-2, Borrelia burgdorferi serol- ogy, and autoantibody testing for anti-nuclear, extracta- ble nuclear antigen and anti-neutrophil cytoplasmic antibodies. Anti-glycolipid antibody testing revealed an elevated titre of anti-GM1 IgM antibody at 1700 units (normal range, 0-500 units). Glycated hemoglobin (HbA1C) was 5.9%. His vitamin B1 level was measured prior to thiamine supplementation and hypovitaminosis B1 was confirmed (45 nmol/L, reference range 66-200 nmol/L), in keeping with his rapid clinical deterioration being attributable to dry beriberi. Treatment High potency intravenous (iv) multivitamins (Pabrinex) and then oral thiamine (200 mg twice a day) were com- menced shortly after admission. On the basis of his anti-GM1 antibody positivity and the remaining possibi- lity of a primary immune-mediated polyneuropathy, he received a trial of treatment with intravenous immuno- globulin. Anti-GM1 positivity was subsequently regarded to be a probable non-pathogenic epiphenomenon. Our patient also received his usual medications for estab- lished medical co-morbidities (oral hypoglycaemics and anti-hypertensives). He received gabapentin for neuro- pathic symptoms. Progress Within two weeks of treatment with intravenous Pabri- nex and subsequent oral thiamine, our patient started to improve significantly, with dramatic improvement in limb power and reduction in sensory loss. He was dis- charged six weeks after admission. When subsequently followed up as an out-patient, 15-16 months from initial onset of symptoms and approximately six months after the onset of his marked tetraparesis, he was able to stand independently and was gradually gaining confi- dence in walking pending a period of in-patient neuror- ehabilitation. On examination he had grade 5 power throughout his upper limbs, and grade 4+ throughout his lower limbs. Pinprick sensation was only reduced in his legs in stocking distribution. Reflexes remained