Correction: Generalized Tetanus Initially Presenting with Dysmasesis.

[This corrects the article DOI: 10.7759/cureus.644.].

Generalized Tetanus Initially Presenting with Dysmasesis.

A 58-year-old male farmer, with no significant history of any chronic morbidity, was admitted via the Emergency Department of SMHS Hospital, Srinagar, with a history of an injury to the hand 20 days earlier followed by a three-day history of dysmasesis (difficulty chewing), progressing to trismus and generalized stiffness interfering with his daily activities. The patient was clinically managed as tetanus on grounds of high clinical suspicion. The patient was treated for a week and discharged without any sequelae to follow-up in the Neurology Outpatient Department of the SMHS Hospital and is currently doing well. After a week of successful management, we received the blood and wound culture reports of the patient that had been sent at the time of his admission to the hospital, which overwhelmingly tested positive for Clostridium tetani. Tetanus is a disease to be suspected post-trauma in patients, especially in developing countries like India. Despite active and passive immunization, it continues to be a significant public health problem in developing countries and should be readily suspected and treated. Although prevention is important for tetanus, the outcomes can be improved by early clinical diagnosis and treatment.

Extra pontine osmotic demyelination syndrome.

The osmotic demyelination syndrome (ODS) has been identified as a complication of the rapid correction of hyponatremia for decades. However, in recent years, a variety of other medical conditions have been associated with the development of ODS, independent of changes in serum sodium which cause a rapid changes in osmolality of the interstitial (extracellular) compartment of the brain leading to dehydration of energy-depleted cells with subsequent axonal damage that occurs in characteristic areas. Slow correction of the serum sodium concentration and additional administration of corticosteroids seems to be a major prevention step in ODS patients. In the current report we aimed to share a rare case which we observed in our hospital. A 65 year old female admitted as altered sensorium with history of vomiting, diarrhea was managed with intravenous fluids for 2 days at a peripheral health centre. Patient was referred to our centre with encephalopathy, evaluated and found to have hyponatremia and hypokalemia rest of biochemical parameters and septic profile were normal. Patient's electrolyte disturbances were managed as per guidelines but encephalopathy persisted. Supportive treatment was continued and patient was discharged after 2 wks of stay in hospital after gaining full sensorium and neurological functions.

Non-Hyperammonemic valproate encephalopathy.

A 21-year-old male known case of primary hypothyroidism, Seizure disorder sequelae of an old trauma receiving sodium valproate, clobazam and phenobarbitone for control of Generalized tonic clonic seizures reported to neurology OPD with history of altered sensorium and gait unsteadiness for 1 week with history of hike in valproate dose 2 weeks before. On examination he was drowsy. Neurological examination was unremarkable except for gait unsteadiness and ataxia. Patient was admitted and evaluated for acute worsening. All (the) biochemical parameters including complete blood count, liver function tests, kidney function tests, routine urine examination, arterial blood gas analysis, blood and urine culture tests were normal. CSF analysis was also normal. Repeat MRI brain was also done which depicted all old changes with no fresh changes which will account for worsening of his sensorium. EEG was suggestive of diffuse encephalopathy. Thyroid function tests were also normal. Valproate encephalopathy was suspected and Valproate was empirically stopped and he was put on levetiracetam and phenytoin. His sensorium improved rapidly after stoppage of valproate with normalization of EEG. Serum valproate Levels were high with serum ammonia levels were in the normal range. We made the inference of nonhyperammoneamic valproate encephalopathy. This case highlights the existence of non-hyperammonemic valproate induced encephalopathy, suggesting mechanisms other than hyperammonemia responsible for this encephalopathy.