Elliott L. Mancall

Bio: Elliott L. Mancall is an academic researcher. The author has contributed to research in topics: Pseudobulbar palsy & Neuropathology. The author has an hindex of 1, co-authored 1 publications receiving 712 citations.

Central Pontine Myelinolysis: A Hitherto Undescribed Disease Occurring in Alcoholic and Malnourished Patients

Abstract: In the course of our studies of the neuropathology of alcoholism, which were begun at the Neurological Unit, Boston City Hospital, and have continued in the laboratories of the Neurology Service, Massachusetts General Hospital, two of us (R. D. A. and M. V.) observed three, perhaps four, cases in which the myelin sheaths of all the nerve fibers in the central part of the basis pontis had been destroyed in a single, large, symmetric focus. The nerve cells and axis cylinders were spared for the most part, and the blood vessels were patent and unaffected. There were no signs of inflammation in or near the lesion. The disease had occurred on a background of alcoholism and malnutrition; in the two cases with the largest lesions, it had manifested itself clinically by a pseudobulbar palsy and quadriplegia, leading to death in about 13 and 26 days. In the other two cases

Osmotic demyelination syndrome following correction of hyponatremia

Abstract: The treatment of hyponatremia is controversial: some authorities have cautioned that rapid correction causes central pontine myelinolysis, and others warn that severe hyponatremia has a high mortality rate unless it is corrected rapidly Eight patients treated over a five-year period at our two institutions had a neurologic syndrome with clinical or pathological findings typical of central pontine myelinolysis, which developed after the patients presented with severe hyponatremia Each patient's condition worsened after relatively rapid correction of hyponatremia (greater than 12 mmol of sodium per liter per day)--a phenomenon that we have called the osmotic demyelination syndrome Five of the patients were treated at one hospital, and accounted for all the neurologic complications recorded among 60 patients with serum sodium concentrations below 116 mmol per liter; no patient in whom the sodium level was raised by less than 12 mmol per liter per day had any neurologic sequelae Reviewing published reports on patients with very severe hyponatremia (serum sodium less than 106 mmol per liter) revealed that neurologic sequelae were associated with correction of hyponatremia by more than 12 mmol per liter per day; when correction proceeded more slowly, patients had uneventful recoveries We suggest that the osmotic demyelination syndrome is a preventable complication of overly rapid correction of chronic hyponatremia

Hyponatremia, Convulsions, Respiratory Arrest, and Permanent Brain Damage after Elective Surgery in Healthy Women

Abstract: Severe hyponatremia developed after elective surgery in 15 previously healthy women who subsequently either died or had permanent brain damage. The mean age was 41 years (range, 22 to 66), and the preoperative serum sodium level was 138 mmol per liter. All the patients recovered from anesthesia, but about 49 hours after surgery, when the average plasma sodium level was 108 mmol per liter, grand mal seizures, followed by respiratory arrest requiring intubation, developed in all 15. At that time, the urinary sodium level and the osmolality averaged 68 mmol per liter and 501 mOsm per kilogram, suggesting inappropriate secretion of antidiuretic hormone. In 10 of 15 patients, an acute cerebral vascular disorder was suspected, leading to a delay in treatment and multiple diagnostic studies, including CT scanning, cerebral angiography, and open-brain biopsies. The net postoperative fluid retention was 7.5 liters, and when correction of the serum sodium level was initiated, the rate of correction was less than 0.7 mmol per liter per hour. Histologic studies of the brain in five patients were not diagnostic, and no patient had any evidence of central pontine myelinolysis on the basis of autopsy, brain biopsy, or CT scanning. Seven patients recovered from coma after the serum sodium level was increased to 131 mmol per liter, but coma recurred two to six days later and ended in either death or a persistent vegetative state. Overall, 27 percent of the patients died, 13 percent had limb paralysis, and 60 percent were left in a persistent vegetative state.

Treatment of symptomatic hyponatremia and its relation to brain damage. A prospective study.

Abstract: We studied the effects of replacement therapy in two groups of patients with symptomatic hyponatremia. Thirty-three patients, who were studied prospectively, had no evidence of cerebral demyelinating lesions. Their hyponatremia (mean serum sodium concentration [+/- SE], 108 +/- 1 mmol per liter) was increased to 126 +/- 1 mmol per liter with hypertonic saline (856 mM) delivered at a rate of 1.3 +/- 0.2 mmol per liter per hour. The serum sodium concentration did not rise to normal or hypernatremic levels in the first 48 hours of therapy, and none of these patients had a respiratory arrest or other hypoxic episode. Twelve patients, evaluated retrospectively, had evidence of cerebral demyelinating lesions at autopsy or on computerized axial tomography. The rate of correction of hyponatremia (1 +/- 0.2 mmol per liter per hour) was similar to the rate in the patients in Group I. However, at least one of four characteristics was present: an increase in serum sodium to normal or hypernatremic levels in the first 48 hours, a change in the serum sodium concentration of more than 25 mmol per liter in the first 48 hours, a hypoxic-anoxic episode, and an elevation of serum sodium to hypernatremic levels in patients with hepatic encephalopathy. Although these four features were associated with demyelination, our observations suggest that this complication does not depend on the rate of correction of hyponatremia.

Central pontine and extrapontine myelinolysis: The osmotic demyelination syndromes

Abstract: Central pontine myelinolysis (CPM) was described by Adams and colleagues in 1959 as a disease affecting alcoholics and the malnourished.1 The concept was extended from 1962 with the recognition that lesions can occur outside the pons, so-called extrapontine myelinolysis (EPM). In 1976 a link between these disorders and the rapid correction of sodium in hyponatraemic patients was suggested, and by 1982 substantially established. In this review we discuss the clinical, pathological, and aetiological features of the disease, the dilemma facing clinicians treating patients with severe hyponatraemia, and treatment opportunities. ### Clinical manifestations #### Central pontine myelinolysis (CPM) Nothing has been added to the clinical description of CPM since the original report. The patient has usually gone through a biphasic clinical course, initially encephalopathic or presenting with seizures from hyponatraemia, then recovering rapidly as normonatraemia is restored, only to deteriorate several days later. The initial signs of the CPM, which reflect this second phase, include dysarthria and dysphagia (secondary to corticobulbar fibre involvement), a flaccid quadriparesis (from corticospinal tract involvement) which later becomes spastic, all from involvement of the basis pontis (fig 1); if the lesion extends into the tegmentum of the pons pupillary, oculomotor abnormalities may occur. There may be an apparent change in conscious level reflecting the “locked-in syndrome” that a large lesion in this site is particularly liable to produce. If lesions of EPM are also present the clinical picture may be very confusing, as added to the above, or even preceding, can be a variety of apparently psychiatric and behavioural changes and movement disorders (outlined below). Figure 1 A reminder of the anatomy of the pons; although included to clarify the anatomical terms, a small lesion is in fact present, illustrating how easily such lesions may be missed on cursory pathological examination. To summarise: “…whenever a patient who is gravely ill with alcoholism and malnutrition or …