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Cranial Neuropathies I, V, and VII–XII
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Brainstem (pontomedullary junction): Infarct or hemorrhage.MS.Tumor.Central pontine myelinolysis.
Endocrine surgery
Published in Alexander Trevatt, Richard Boulton, Daren Francis, Nishanthan Mahesan, Take Charge! General Surgery and Urology, 2020
Ross M. Warner, Richard Boulton
Addisonian crisis = acute illness due to adrenal failureAetiology: Often precipitated by an acute illness (sepsis) or trauma, but also seen following withdrawal of steroid medication.Signs and symptoms: Severe hypotension and dehydration with low sodium and glucose and elevated potassium levels.Management: If suspected, assess and treat the patient in an ABCDE (airway, breathing, circulation, disability, exposure) manner with early ITU and senior medical involvement. The mainstay of treatment, however, is IV hydrocortisone (100 mg) given immediately with IV saline (0.9% NaCl) to resuscitate the patient before the confirmation of the diagnosis is made (but send serum cortisol levels). Remember to check and correct glucose levels, and request an ECG due to electrolyte imbalances. Severe hyponatraemia should not be corrected too quickly due to the risk of central pontine myelinolysis.
Clinical Theory and Skills EMIs
Published in Michael Reilly, Bangaru Raju, Extended Matching Items for the MRCPsych Part 1, 2018
Alcohol-induced amnesia.Alcohol-induced psychosis.Alcoholic hallucinosis.Central pontine myelinolysis.Korsakoff syndrome.Hepatocerebral degeneration.Marchiafava-Bignami syndrome.Wernicke’s encephalopathy.
Evaluation of knowledge and practices about administration and regulations of high alert medications among hospital pharmacists in Pakistan: findings and implications
Published in Current Medical Research and Opinion, 2022
Muhammad Salman, Zia Ul Mustafa, Naureen Shehzadi, Tauqeer Hussain Mallhi, Noman Asif, Yusra Habib Khan, Tahir Mehmood Khan, Khalid Hussain
Hypertonic saline is a promising therapeutic modality for patients with severe symptomatic hyponatremia, cerebral edema and increased intracranial pressure32. For treatment of severe hyponatremia, 3% saline is either infused at a rate of 1–2 mL/kg/hour to elevate the serum sodium concentration by 6–8 mEq/L (not to exceed 10–12 mEq/L in the first 24 h or 18 mEq/L in 48 h) or infusing one dose of 100–150 mL 3% saline over 10–20 min with aim of increasing serum sodium level by 2–3 mEq/L; may repeat bolus twice if symptoms do not resolve33–39. Although common adverse effects are related to the route of administration and include infection at the IV site, thrombophlebitis, infiltration, extravasation, and hypervolemia but rapid correction of severe hyponatremia can result in osmotic demyelination syndrome/central pontine myelinolysis32,39. Other possible adverse reaction includes hyperchloremic metabolic acidosis. Administration of hypertonic saline through peripheral intravenous access is acceptable if no other access is available, but the central venous site is the preferred route. In our study, around 71% of pharmacists were aware of the correct way of hypertonic saline administration. However, inappropriate awareness among 29% of pharmacists is also a point of concern.
Hyperammonemia in the setting of Roux-en-Y gastric bypass presenting with osmotic demyelination syndrome
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Carly Rosenberg, Michael Rhodes
The question we ask ourselves now is can hyperammonemia cause osmotic demyelination syndrome? A case report by Langer et al. [5] described a pediatric patient with carbamoyl phosphate synthetase deficiency who developed osmotic demyelination and transient cortical blindness after rapid correction of hyperammonemia. The hypothesized underlying mechanism was due to disruption of the blood–brain barrier and re-equilibration of osmolytes, in particular glutamine. Similarly, another case had been reported earlier by Mattson et al. [6] of a child with ornithine carbamoyl transferase deficiency who presented with hyperammonemic encephalopathy with a maximum ammonia level of 376 mmcol/L. Her ammonia was corrected with hydration and protein restriction; however, 5 days after correction of her hyperammonemia, she developed seizures and fell into a coma. MRI brain imaging ultimately revealed characteristic findings of central pontine myelinolysis.
Clinical implications of myelin regeneration in the central nervous system
Published in Expert Review of Neurotherapeutics, 2018
Christopher E McMurran, Srikirti Kodali, Adam Young, Robin JM Franklin
Besides these autoimmune disorders, a number of other pathological states can damage myelin. Rapid electrolyte disturbances can cause central pontine myelinolysis, classically with an iatrogenic cause due to rapid correction of hyponatremia. It is thought that oligodendrocytes in the pons are particularly vulnerable to resultant changes in cell volume, which triggers apoptosis [20]. This is an unusual example of demyelination occurring in the relative absence of an inflammatory infiltrate, and again shows a wide range of prognostic outcomes, which can be difficult to predict. Exposure to various toxins can cause clinical demyelination, presumably by selective toxicity to oligodendrocytes. This includes carbon monoxide which is thought to kill oligodendrocytes by hypoxia and damage myelin through lipid peroxidation [21]. The disinfectant hexachlorophene, once widely used, became heavily regulated in the 1970s after being shown to alter the ultrastructure of myelin and cause demyelination [22]. Dietary deficiency can also lead to CNS demyelination, for example of vitamin B12, which is an essential cofactor for maintaining a myelin sheath [23]. The JC virus is a direct infective cause of multifocal primary demyelination [24], while several other pathogens are possible triggers for autoimmune demyelination through molecular mimicry [25].