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BackgroundMelioidosis has become an emerging infection in Sri Lanka; a country which is considered non endemic for it. Paraplegia due to Burkholderia pseudomallei is a very rare entity encountered even in countries where the disease is endemic. There are no reported cases of transverse myelitis due to melioidosis in Sri Lankan population thus we report the first case.Case presentationA 21 year old farmer presented with sudden onset bi lateral lower limb weakness, numbness and urine retention. Examination revealed flaccid areflexic lower limbs with a sensory loss of all modalities and a sensory level at T10 together with sphincter involvement. MRI of the thoracolumbar spine showed extensive myelitis of the thoracic spine complicating left psoas abscess without definite extension to the spinal cord or cord compression. Burkholderia pseudomallei was isolated from the psoas abscess pus cultures and the diagnosis of melioidosis was confirmed with high titers of Burkholderia pseudomallei antibodies and positive PCR. He was treated with high doses of IV ceftazidime and oral cotrimoxazole for one month with a plan to continue cotrimoxazole and doxycycline till one year. Patient’s general condition improved but the residual neurological problems persisted.ConclusionThe exact pathogenesis of spinal cord melioidosis is not quite certain except in the cases where there is direct microbial invasion, which does not appear to be the case in our patient. We postulate our patient’s presentation could be due to ischemia of the spinal cord following septic embolisation or thrombosis of spinal artery due to the abscess nearby. A neurotrophic exotoxin causing myelitis or post infectious immunological demyelination is yet another possibility. This emphasizes the necessity of further studies to elucidate the exact pathogenesis in this type of presentations.Health care professionals in Sri Lanka, where this is an emerging infection, need to improve their knowledge regarding this disease and should have high degree of suspicion to make a correct and a timely diagnosis to reduce the morbidity and mortality due to Burkholderia pseudomallei infection. It is highly likely that this infection is under diagnosed in developing countries where diagnostic facilities are minimal. Therefore strategies to improve the awareness and upgrade the diagnostic facilities need to be implemented in near future.

Contrast-induced encephalopathy is a rare idiosyncratic reaction to contrast material. A 56-year-old woman with hypertension developed a hemiparesis with confusion and disorientation 3 hours after routine coronary angiography. The procedure had been prolonged, and during it she had received 130 mL of iopromide contrast. A metabolic screen was negative, and cerebral angiography and MR scan of brain were normal. She recovered completely by day 5. Contrast-induced encephalopathy should be considered in patients developing focal neurological deficits following coronary angiography. Patients requiring investigations to exclude acute stroke in this setting should not receive additional intravenous or intra-arterial contrast, although MR with gadolinium appears safe. Better awareness of this complication should avoid potentially harmful interventions such as thrombolysis.

Adult onset subacute sclerosing panencephalitis (SSPE) after the third decade of life is rare and the manifestations can mimic disorders such as dysmyelinating and metabolic disorders. This case report presents a patient with acute binocular visual impairment in his fifth decade as the first manifestation of SSPE. This is preventable with immunisation against measles. A prior history of measles infection may not be forthcoming in adult onset SSPE. This should be kept in mind as a differential diagnosis when a patient from endemic area presents with acute visual loss even in the absence of classic features. Periodic generalised discharges on the EEG without myoclonus may be seen in this condition rarely as in this case.

Congenital myasthenic syndromes (CMS) result from genetic mutations that cause aberrations in structure and/or function of proteins involved in neuromuscular transmission. The slow-channel CMS (SCCMS) is an autosomal dominant postsynaptic defect caused by mutations in genes encoding alpha, beta, delta, or epsilon subunits of the acetylcholine receptor resulting in a functional defect which is an increase of the opening time of the receptor. We report a case of SCCMS due to a heterozygous mutation in the M2 domain of the AChR alpha subunit - CHRNA1:ENST00000348749.6:exon7:c.806T>G:p.Val269Gly and corresponding kinetic defect. A substitution of valine with phenylalanine in the same position has been previously described. This is the first reported case of a new CHRNA1 variant in a patient with SCCMS from South Asia. We also highlight the phenotype that would favour a genetic basis over an autoimmune one, in an adult presenting with fatigable weakness.