-
Cureus Apr 2024Hyponatremia is an adverse effect of many antiseizure medications (ASMs). It occurs with interference with the normal balance of electrolytes within the body. Various... (Review)
Review
Hyponatremia is an adverse effect of many antiseizure medications (ASMs). It occurs with interference with the normal balance of electrolytes within the body. Various risk factors associated with the development of hyponatremia in patients taking these medications include age, gender, dosage, and combinations with other drugs. ASMs such as carbamazepine (CBZ), oxcarbazepine (OXC), and valproic acid have a higher risk of hyponatremia. Hyponatremia induced by an antiseizure medication can occur through various mechanisms depending on the drug's specific mechanism of action. Hyponatremia can be a potentially fatal side effect. Patients taking these medications need to be monitored closely for the signs and symptoms of hyponatremia. Acute hyponatremia, defined as developing in <48 hours, is more likely to show symptoms than chronic hyponatremia. Signs of acute hyponatremia include delirium, seizures, decerebrate posturing, and cerebral edema with uncal herniation. Chronic hyponatremia, defined as developing in >48 hours, can cause lethargy, dizziness, weakness, headache, nausea, and confusion. Hyponatremia is associated with longer hospital stays and increased mortality. Treatment varies based on the degree of severity of hyponatremia. Choosing a treatment option should include consideration of the drug causing the electrolyte disturbance, the patient's risk factor profile, and the severity of symptoms as they present in the individual patient. Healthcare providers should be aware of hyponatremia as a potential side effect of ASMs, the signs and symptoms of hyponatremia, the different treatment options available, and the potential complications associated with rapid correction of hyponatremia.
PubMed: 38707045
DOI: 10.7759/cureus.57535 -
IDCases 2023We report a case of a 32-year-old male with a history of type 1 diabetes, inhaled drug use, and alcohol use disorder, who presented with encephalopathy, holocranial...
We report a case of a 32-year-old male with a history of type 1 diabetes, inhaled drug use, and alcohol use disorder, who presented with encephalopathy, holocranial headaches, neck pain, confusion, and generalized tonic-clonic seizures. The patient initially presented at a rural community hospital with a fever and was found to be in diabetic ketoacidosis (DKA). He was also hemodynamically stable but stuporous, prompting intubation to protect his airway. Despite initial treatment measures, his neurological condition worsened and he remained ventilator-dependent. Key findings include a high glucose level, presence of ketones, and evidence of drug use. Blood cultures showed no growth, but his febrile state persisted. Cerebrospinal fluid (CSF) analysis revealed mild pleocytosis, hyperglycorrhachia but normal protein, with no growth. Neuroimaging showed right hemispheric slowing on EEG and diffusion restriction in the right frontal lobe on MRI. The patient's neurological status worsened on the second day of admission, manifesting as sluggish pupillary reflexes, right third nerve palsy, and decerebrate posturing. Emergent MRI suggested cerebral edema, leading to initiation of hypertonic saline. This case highlights the diagnostic challenges and critical management considerations in a patient with multiple comorbidities presenting with unexplained neurological deterioration, emphasizing the importance of a comprehensive and timely approach to diagnosis and treatment.
PubMed: 37415782
DOI: 10.1016/j.idcr.2023.e01821 -
Scientific Reports Apr 2024Several neurologic diseases including spinal cord injury, Parkinson's disease or multiple sclerosis are accompanied by disturbances of the lower urinary tract functions....
Several neurologic diseases including spinal cord injury, Parkinson's disease or multiple sclerosis are accompanied by disturbances of the lower urinary tract functions. Clinical data indicates that chronic spinal cord stimulation can improve not only motor function but also ability to store urine and control micturition. Decoding the spinal mechanisms that regulate the functioning of detrusor (Detr) and external urethral sphincter (EUS) muscles is essential for effective neuromodulation therapy in patients with disturbances of micturition. In the present work we performed a mapping of Detr and EUS activity by applying epidural electrical stimulation (EES) at different levels of the spinal cord in decerebrated cat model. The study was performed in 5 adult male cats, evoked potentials were generated by EES aiming to recruit various spinal pathways responsible for LUT and hindlimbs control. Recruitment of Detr occurred mainly with stimulation of the lower thoracic and upper lumbar spinal cord (T13-L1 spinal segments). Responses in the EUS, in general, occurred with stimulation of all the studied sites of the spinal cord, however, a pronounced specificity was noted for the lower lumbar/upper sacral sections (L7-S1 spinal segments). These features were confirmed by comparing the normalized values of the slope angles used to approximate the recruitment curve data by the linear regression method. Thus, these findings are in accordance with our previous data obtained in rats and could be used for development of novel site-specific neuromodulation therapeutic approaches.
Topics: Animals; Cats; Male; Spinal Cord; Electric Stimulation; Spinal Cord Stimulation; Urinary Bladder; Decerebrate State; Urinary Tract; Urethra; Urination; Epidural Space
PubMed: 38670988
DOI: 10.1038/s41598-024-54209-3