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Anorexia Nervosa/Bulimia and Central Pontine Myelinolysis Central pontine myelinolysis is typically an acute disorder presenting with severe motor disturbances, usually involving dysarthria, dysphagia, and paraparesis or quadriparesis, which may progress to a “locked-in” syndrome. The characteristic neuropathological lesion comprises destruction of oligodendrocytes and disruption of myelin architecture in the ventral pons (neurons and axon cylinders relatively spared), interfering with functioning of local corticospinal, corticobulbar, corticopontine, and pontocerebellar tracts [l]. Cases of central pontine myelinolysis have been reported worldwide over the last three decades, usually in patients with histories of alcoholism or nutritional deficiencies, and/or in association with electrolyte abnormalities [l-3]. This syndrome appears unexpectedly, is frequently unfamiliar to psychiatrists, and often has a fatal outcome. We report a case of a woman with a long-standing severe eating disorder with episodes of hospitalization for electrolyte disturbances, who, during one admission, developed this serious complication.

Case Report Ms. A was a 32-year-old woman who came to the county general hospital emergency room after serum chemistries at an outside laboratory were reported on that day to include a serum sodium of 90.1 mmol/L and a serum potassium of 1.74 mmol/ L, associated with recent excessive water intake, laxative abuse, and vomiting. On admission, serum chemistries determined by the hospital laboratory included sodium 101 mmol/L, potassium 1.5 mmol/L, chloride 60 mmol/L, bicarbonate 41 mmol/L, blood urea nitrogen (BUN) 5 mg/dl, glucose 107 mg/dl, creatinine 0.4 mgidl, and hemoglobin concentration (Hgb) 12.4 g/dl. Ms. A was a nonsmoking, nonalcoholic, nonpsychotic woman, with a history of an eating disorder Gcwmf

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beginning at age 13, when she and a girl friend made a pact to lose weight. The patient developed anorexia nervosa, later complicated by episodes of bulimia, frequent laxative abuse, and excessive water intake. She had eight previous hospitalizations for treatment of her eating disorder and/ or correction of serious electrolyte disturbances, and also received outpatient psychotherapy and trials of anxiolytics, lithium, chlorpromazine, and sedative-hypnotics. At the time of this admission she was receiving lorazepam 6 mglday and phenobarbital 60 mgiday, the latter prescribed for the previous 5 years for a history of seizures, which may have been limited to hyponatremic episodes. On three similar admissions over the preceding 13 months, the patient had presented with serum sodiums of 115-124 mmol/L, and serum potassiums of 2.6-4.7 mmol/L. On this admission she weighed 71 pounds (she was 5 feet tall), and had a phenobarbital level of 16.9 ugiml. Using intravenous dextrose 5% in halfnormal saline with potassium, she was corrected to a serum sodium of 114 and potassium of 3.1 mmol/L within 9 hours, and to a serum sodium of 126 and potassium of 3.8 mmol/L within 34 hours of admission. She was discharged 6 days after admission with normalized electrolytes, but readmitted 4 days later with dizziness, weakness, shortness of breath, and anemia (Hgb 8.4 g/dl), but normal electrolytes. Over the next several days worsening motor difficulties, including quadriparesis, inability to cough or articulate, and absent gag reflex, manifested as the prominent problem. A computed tomography scan 2 days after admission showed only moderate cortical atrophy, but a magnetic resonance imaging scan with gadolinium enhancement 8 days after admission revealed a low density, nonenhancing 2.1 x 2.0 x 1.8 cm pontine lesion consistent with myelinolysis. Over the next 2 months the patient achieved good motor

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Discussion Myelinolysis, generally pontine but occasionally also extrapontine, appears to be a relatively recent disorder, recognized syndromally only since 1959, when the first four cases were reported [l]. It has usually been associated with chronic alcoholism, electrolyte disturbances secondary to the use of diuretics or the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or other causes, malnutrition accompanying malignancies or other serious illnesses, pulmonary infections, hepatic dysfunction, and burns [2,3]. After initially focusing on alcoholism, and then on the frequent association with severe inanition and/or hyponatremic presentations, most clinicians now believe that this syndrome is usually iatrogenic, resulting from too-rapid correction of hyponatremia [4]. Several case reports suggest hypokalemia may also be a risk factor [5], and others cogently argue for a more general stressing of the significance of rapid shifts in extracellular osmolarity [6]. One widely accepted recommendation is that severe hyponatremia should be corrected at a rate no greater than 12 mmol/L/day [4]. Myelinolysis has been frequently noted to occur in the context of malnutrition and electrolyte disturbances, including otherwise healthy young patients with hyperemesis gravidarum [7,8]. We were surprised, therefore, to find only one reported case occurring in an individual with a known eating disorder: a 35-year-old woman with anorexia nervosa and marked abuse of furosemide [9]. As with our patient, this individual presented with severe hyponatremia and hypokalemia, and her serum sodium was rapidly corrected. by focusing narrowly on Early observers, biomedical descriptions, may have failed to uncover and/or report eating disorders in their patients with myelinolysis. We would not expect that eating disorders per se would predispose to myelinolysis, but it would certainly seem that patients with serious eating disorders, who frequently are malnourished, who self-induce vomiting, and who may abuse laxatives, diuretics, and drink water excessively, have multiple risk factors for this syndrome. Psychiatrists and other physicians should be alert not only to the possibility of dangerous electrolyte disturbances in this population [lo], but

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to the great risk of iatrogenic morbidity and mortality attendant upon too-rapid correction, a risk still sometimes underappreciated in the medical community. As serum electrolytes may be dangerously out of balance at presentation, as in our patient, one may be forced to warily navigate between the Scylla of too-rapid and Charybdis of too-slow correction. Although intravenous correction using only half-normal saline has been reasonably recommended to try to prevent myelinolysis, it does not warrant success in this regard, as evidenced by our patient. Slow correction guided by very frequent monitoring of serum electrolytes would appear prudent. William M. Greenberg, M.D.* Pritesh J. Shah, M.D.t Mahaveer Vakharia, M.D.* *Bergen Pines County Hospital Paramus, New Jersey tElmhurst Hospital Queens, New York

References 1. Adams RD, Victor M, Mancall EL: Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients. Arch Neurol Psychiatry 81:154-172, 1959 2. Messert B, Orrison WW, Hawkins MJ, Quaglieri CE: Central pontine myelinolysis: considerations on and treatment. Neurology etiology, diagnosis, 29(2):147-160, 1979 3. Berlit P: Die zentrale pontine myelinolyse. Nervenarzt 57(11):624-633, 1986 4. Sterns RH, Riggs JE, Schochet SS Jr: Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med 314(21):1535-1542, 1986 5. Bahr M, Sommer N, Petersen D, Wietholter H, Dichgans J: Central pontine myelinolysis associated with low potassium levels in alcoholism. J Neurol 237(4): 275-276, 1990 6. Norenberg MD: A hypothesis of osmotic endothelial injury: a pathogenetic mechanism in central pontine myelinolysis. Arch Neurol 40(2):66-69, 1983 7. Fraser D: Central pontine myelinolysis as a result of treatment of hyperemesis gravidarum. Case report. Br J Obstet Gynaecol 95(6):621-623, 1988 8. Castillo RA, Ray RA, Yaghmai F: Central pontine myelinolysis and pregnancy. Obstet Gynecol73(3 Pt 2):459-461, 1989 9. Copeland PM: Diuretic abuse and central pontine myelinolysis. Psychother Psychosom 52:101-105, 1989 10. Silber TJ: Seizures, water intoxication in anorexia nervosa (letter). Psychosomatics 25(9):705-706, 1984

bulimia and central pontine myelinolysis.

Letters to the Editor Letters to the Editor are invited for comment on a topic of current interest or on material published in GENERAL HOSPITAL PSYC!H...
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