Tuberculosis of skull is a rare disease, but its incidence is on rise in developing countries. Skull tuberculosis can have varied neurological presentations. Seizures are uncommon mode of presentation in these patients. We report a patient who presented with seizures and scalp swelling, which was found to be due to skull tuberculosis. Though uncommon, our patient indicates that any patient from tuberculosis endemic zone with skull swellings and neurological symptoms should be suspected and investigated for tuberculosis.

Cerebral venous thrombosis (CVT) is a rare clinical entity, with clinical presentations extending from headache and seizures to coma and death. For adults developing progressive neurological worsening despite adequate medical management, endovascular thrombolysis and/or mechanical thrombectomy may be considered as treatment options. We present one such patient with CVT who developed seizures and slipped into a coma, despite best medical management. A large-bore aspiration catheter was used as a standalone system for the endovascular procedure. The venous sinuses were successfully re-canalized. The patient was discharged a week later with a modified Rankin scale of 2. Studies show that endovascular thrombolysis used alone or in conjunction with thrombectomy for CVT has a higher risk of hemorrhagic complications. If we were to use mechanical thrombectomy devices (that are specifically designed for intracranial clot retrieval) as a stand-alone system, we would probably have better clinical outcomes with a lower risk of hemorrhagic complications.

Rickets, one of the leading causes of bony deformities and short stature, can be calciopenic (inciting event is defective intestinal calcium absorption) or phosphopenic (inciting event is phosphaturia). Early diagnosis and timely treatment of rickets are crucial for correction of the limb deformities. Guidelines exist for nutritional rickets, but the diagnosis and management of the relatively uncommon forms of rickets are complex. This consensus aims to formulate a simplified diagnostic approach for rickets, especially in resource-limited settings. The consensus statement has been formulated by a 29-member committee from the Endocrine Society of Bengal. The process included forming a working group, conducting a literature review, identifying controversies, drafting, and discussion at a consensus meeting. Participants rated their agreement with the clinical practice points, and a 70% consensus was required. Input integration and further review led to the final consensus statements. Children with suspected rickets should initially be examined for distinctive skeletal deformities. The diagnosis of rickets should be confirmed with characteristic radiographic abnormalities. It is advisable to order tests for serum calcium, inorganic phosphorus (Pi), liver function, 25-hydroxyvitamin D (25OHD), parathyroid hormone, creatinine, and potassium in all patients with rickets. In cases of refractory rickets, it is also recommended that assessments be conducted for spot urine calcium, Pi, creatinine, and, blood gas analysis. In children with rickets and metabolic acidosis, tests for glycosuria, uricosuria, aminoaciduria, low molecular weight proteinuria, and albuminuria should be conducted. In children with resistant calciopenic rickets and sufficient serum 25OHD levels, serum 1,25(OH)2D concentration should be tested. 1,25(OH)2 D and fibroblast growth factor 23 estimation is useful for certain forms of phosphopenic rickets.