Central pontine myelinolysis (CPM) can be regarded as one of the demyelinating syndromes. First described by Adams et al. in 1959 in their chronic alcoholic patients, it has now been described in the malnourished, the chronically debilitated, the renal, the hepatic and the transplant patient among others. Pathologically, it is defined as a symmetric area of myelin disruption in the center of the basis pontis, although similar symmetric lesions have also been described occurring with CPM as well as independently in other brain areas (extrapontine myelinolysis or EPM) including the cerebellar and neocortical white/gray junctional areas, thalamus and striatum. Possible mechanisms include a hyperosmotically induced demyelination process resulting from rapid intracellular/ extracellular to intravascular water shifts producing relative glial dehydration and myelin degradation and/or oligodendroglial apoptosis. The process most often occurs during rapid rebalancing of the electrolyte parameters in the hyponatremic patient. Avoidance of CPM/EPM is dependent upon recognizing those patients with conditions pre-disposing them to osmotic myelinolysis and then moderating the rate of normalization of the electrolyte imbalance. The morbidity and mortality of CPM/EPM has been greatly reduced by recognition of pre-disposing conditions, increased understanding of the pathophysiology, intensive treatment, and rapid diagnosis and monitoring with advanced neuroimaging.

Background: Both microvascular and macrovascular complications in diabetes are related to oxidative stress. Zinc which has antioxidant property, delays diabetic complications. The present study was conducted with the objective to study the relationship between serum Zinc level and HbA1C level in newly diagnosed type 2 diabetes mellitus and to compare serum Zinc level with its risk factors. Methods: The present study was a cross sectional study, conducted on 100 patients attending the outpatient department at Rajiv Gandhi Government General Hospital and Madras Medical College, Chennai during the period from May 2015 to October 2015. Of them 50 were newly diagnosed type 2 diabetics and considered as diabetic group and other 50 were considered as controls, who attended the master health check-up. All patients were subjected to thorough general and systemic examination. Under strict aseptic precautions blood sample was collected from all the patients and the serum was investigated for creatinine, urea, zinc, HbA1c, cholesterol, triglycerides and fasting blood glucose. The data obtained were analysed using Microsoft excel software. Correlation was found out in SPSS by using regression equation. Results: The body mass index (BMI) and mean systolic blood pressure (SBP) was significantly higher (p<0.001) in diabetic group as compared to controls. Serum levels of HbA1C and fasting blood glucose (FBG) levels were found to be significantly higher in diabetic group than in controls (p<0.001). Serum zinc levels were significantly higher in control group (p<0.001). Mean zinc value decreases with increase in HbA1c, FBG, BMI, SBP, DBP, triglycerides and cholesterol and the difference was statistically significant (p value <0.01). The relation between Pearson correlation coefficient for zinc and the above parameters were higher in diabetics than controls. Conclusions: Lower serum zinc levels were found to be responsible for the development of macrovascular complications in type-2 diabetics. Hence there is a need for zinc supplementation in diabetic patients to prevent long term complications associated with it.

A 9-year-old girl presented with an acute history of headache, vomiting, abdominal pain, right focal seizures with secondary generalization and altered sensorium. There was a history of fever for a day, at the onset of symptoms. Seizures were focal, involving the right upper limb and angle of the mouth. She had not experienced any visual aura/ hallucination or any other visual problem. On admission, she was found to be drowsy and afebrile, with a blood pressure of 180/140 mmHg. There were no meningeal signs or neurological deficits. Rest of the examination was essentially normal, except for a few papular lesions over her arms and legs, which were ostensibly caused by insect bite allergy. There was no history of oliguria, haematuria or oedema, which proved to be a red herring, and the child was managed as a case of viral meningoencephalitis with raised intracranial tension. She was treated with anti oedema measures, anticonvulsants and supportive measures. The child regained normal sensorium within 12 hours of admission, though the hypertension persisted.At this point, an MRI brain was done [Table/ Fig-1] and it revealed extensive vasogenic oedema involving the parietal, occipital, frontal and temporal areas of the cerebrum. These findings were suggestive of PRES and so, the child was evaluated for hypertension. On probing, we obtained a history of a secondary infection on the skin lesions, two weeks prior to her presentation. Urine microscopy revealed microscopic haematuria and serum C3 levels were significantly low (10 mg/dl, normal range 90 -180), though ASLO was normal. Platelet count and peripheral smears were normal. We also did a lupus work up (ANA, DsDNA), which was negative. Renal artery Doppler, VMA levels and ESR were normal. CSF analysis was not done.The hypertension resolved within 2 days of starting oral nifedipine and frusemide. A repeat MRI which was done after two weeks, [Table/ Fig-2] showed a complete resolution of the oedema. At discharge, the child was off anti hypertensives and she was symptom free. C3 levels normalized after four weeks, further validating the diagnosis of post infectious glomerulonephritis. DisCussionPosterior reversible encephalopathy syndrome (PRES) has been associated with a typical pattern of vasogenic oedema, which involving the white matter and is seen mainly in the parieto occipital areas of the cerebrum. It had been originally described in association with ecclampsia and immunosuppressive therapy. Though this condition has been described earlier under other names, Hinchey et al renamed it as PRES [1].The pathogenesis is still an area of debate, with two diametrically opposite hypotheses. The newer and currently accepted one suggests that when the auto regulatory limit of the blood vessels in the brain are exceeded, as in severe hypertension, then the blood brain barrier breaks down, leading to vasogenic oedema [2,3]. In this case, the significantly high blood pressure (>99th percentile) may have contributed to the extensive vasogenic oedema, which in itself is a poo...

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