A cross-sectional study was done on 100 consecutive paediatric patients presenting with acute encephalitis syndrome. The clinico-laboratory features of all patients were recorded in a prestructured performa. Cerebrospinal fluid and serum samples were tested for: Japanese encephalitis (JE) virus; Chandipura virus; coxsackie virus; dengue virus; enterovirus 76; and West Nile virus. Twenty-two (22.0%) patients were confirmed JE cases and 17% had parasitic or bacteriological aetiology. The remaining 61 cases (61.0%) in which no viral aetiological agent was found were grouped as non-JE cases. Peripheral vascular failure, splenomegaly and hypotonia were distinguishing clinical features found in the non-JE patients. A high mortality of 26.5% was seen in patients with confirmed or presumptive viral encephalitis (22/83). A fatal outcome was independently associated with peripheral vascular failure and pallor at the time of admission. Early recognition of these signs may help clinicians to manage these cases.

In this study, magnesium alloy (AZ91D) matrix composites reinforced with 1 wt% of nano alumina (n-Al 2 O 3 ) were fabricated using novel Ultrasonic Treatment (UST)assisted squeeze casting method. UST was carried out at four different levels of ultrasonic power namely, 0 W (without UST), 1500 W, 2000 W and 2500 W at constant frequency and time. The composites were heat-treated at T6 condition under argon gas protected environment. Microstructural analysis was done using optical microscopy and high-resolution scanning electron microscopy. Physical, mechanical and tribological properties of the composites were evaluated. A significant refinement in grain structure and improvement in porosity was seen on an increase in UST power. Improvement was seen in microhardness, yield strength, ultimate tensile strength and % of elongation of the composite fabricated at 2500 W by 18%, 48%, 28%, and 10% respectively compared to an untreated composite. The composite fabricated at 2500 W showed less wear rate and coefficient of friction when compared to other composites at all sliding conditions. Scanning electron microscope images of the worn surface of the composite pins revealed that the wear mechanisms dominated were abrasion, adhesion, oxidation and delamination.

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Acute polyneuropathy is a rare manifestation of severe hyperthyroidism. We report a 22-year-old Omani male who presented to the Sohar Hospital, Sohar, Oman, in 2016 with acute-onset rapidly progressive flaccid areflexic paraplegia as the presenting manifestation of thyrotoxicosis. Nerve conduction studies revealed mixed axonal and demyelinating polyneuropathy in both the motor and sensory nerves. Treatment of the hyperthyroidism with β-blockers and carbimazole along with physiotherapy resulted in the patient's full recovery and the alleviation of his symptoms. Besides highlighting this rare association, this report underscores the importance of including thyroid function tests in the evaluation of patients with acute polyneuropathy. 1,2 In contrast to muscles, the involvement of the peripheral nerves in hyperthyroidism has received little attention. 3,4 Even though the association between these two disorders has been questioned, electron microscopic studies of sural nerve biopsies have shown changes compatible with thyrotoxicosis. 5,6 This report describes a case of acute flaccid paraplegia which resolved upon treatment of the underlying hyperthyroidism. Keywords Case ReportA 22-year-old Omani male presented to the Sohar Hospital, Sohar, Oman, in 2016 with a three-day history of progressive weakness in both lower limbs, resulting in him becoming bed-bound. There were no symptoms in the upper limbs or evidence of sphincter dysfunction. On examination, he was anxious, diaphoretic and had bilateral exophthalmos with lid lag. His pulse rate was 110 beats per minute and blood pressure was 130/82 mmHg. Motor weakness and reflex changes were confined to both of the lower extremities. The lower limbs were hypotonic and areflexic with a power grade of 2/5 both proximally and distally; there was no wasting or fasciculations. An examination of the feet revealed normal flexor plantar reflexes.The results of routine blood tests were unremarkable, including serum electrolyte, creatine phosphokinase and antiganglioside antibody tests. A cerebrospinal fluid examination and electrocardiogram were normal. His serum thyroxine (T4) level was >100 pmol/L (normal range: 12-22 pmol/L), his triiodothyronine level was 11.77 pmol/L (normal range: 3.1-6.8 pmol/L) and his thyroid stimulating hormone (TSH) level was <0.005 IU/mL (normal range: 0.27-4.2 IU/mL). Levels of antithyroid peroxidase and TSH receptor antibodies were 16.2 IU/mL (normal range: <6 IU/mL) and 5.9 IU/L (normal range: ≥1.57 IU/L), respectively. Plain and contrast magnetic resonance imaging (MRI) of the brain and spine was essentially normal, although an MRI scan of the lumbosacral plexus was not performed. Tests