11 BINGE DRINKING AS AN UNUSUAL CAUSE OF CENTRAL PONTINE MYLELINOLYSIS. Issue 1 (1st January 2007)

• Record Type: Journal Article
• Authors: Haq, S.; Saghier, S.
• Is Part Of: Journal of investigative medicine. Volume 55:Issue 1(2007)
• Page Start: S248
• Page End: S248
• Publication Date: 2007-01-01
• Subjects: Clinical medicine -- Periodicals; Medicine -- Research -- Periodicals; Medicine; Research -- United States; Clinical medicine; Medicine -- Research; Periodicals; 616.075
• Languages: English
• ISSNs: 1081-5589

Abstract

Abstract : Introduction: Central pontine myelinolysis (CPM) is a symmetric acquired demyelination of the basis pontis. Although hyponatremia and its acute correction have been postulated as causative factors, the etiology remains obscure. We describe an unusual case of alcoholic female who suffered CPM after an episode of binge drinking. Case Presentation: A 34-year-old white female with a history of alcoholism had an alcoholic binge for a 2-week period 1 month ago. Initially, the patient had severe nausea and vomiting, limiting her food and water intake; and once she began to recover she began experiencing incoordination and truncal ataxia, which worsened progressively over a 3-week period. Later she developed slurring of speech and dysphagia, which made her ultimately seek medical attention. Patient denied any sensory loss, memory deficits, fever, chills, pain, or weight loss. Laboratory investigations reported Na 142 mmol/L, K 2.3 mmol/L, HCO3 33 mmol/L, total protein 5.1 g/dL, albumin 3.0 g/dL, normal LFTS; negative serum/urine drug screen and heavy metal screen. Lumbar puncture findings were nonspecific. CT scan of the head was unremarkable. MRI of the head demonstrated symmetric high intensity in the central portion of the pontine base, which was further confirmed with the magnetic resonance spectroscopy to be consistent with CPM. Patient was treated supportively with motor function rehabilitation. She had a favorable prognosis and her neurologic symptoms regressed completely in 6 months. Discussion: This case highlights an interesting cause of CPM related to binge drinking without any acute iatrogenic correction of hyponatremia. Various pathophysiologic mechanisms can be proposed, including direct toxicity of alcohol on pons; the possibility of an undocumented rapid rise in the serum sodium (as her symptoms occurred during the late stages of binge drinking when the intake of food and water increased and ethanol intake decreased), potentially causing an osmotic injury to the endothelium, resulting in the release of myelinotoxic factors or production of vasogenic edema in the central pons. This case demonstrates that central pontine myelinosis should be considered in the differential diagnosis of a patient with a history of binge drinking presenting with acute neurologic symptoms. It also illustrates that although, in general, the prognosis is unfavorable, some patients may recover favorably.