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1/105. Therapeutic relowering of the serum sodium in a patient after excessive correction of hyponatremia.

    BACKGROUND: Inappropriate correction of chronic hyponatremia could lead to major neuropathological sequelae. In man, the risk of brain myelinolysis increases strikingly when correction of the serum sodium exceeds 10-15 mEq/l/24 h. No treatment is actually available for this iatrogenic brain injury. However, recent experimental data showed that rapid reinduction of the hyponatremia greatly reduces the incidence of brain damage and death in case of serum sodium overshooting. SUBJECTS AND methods: We tested this rescue manoeuver in a 71-year-old woman with nausea, confusion and severe (SNa 106 mEq/l) chronic hyponatremia related to thiazides. It was associated with hypokalemia (SK: 3.2 mEq/l). RESULTS: Treatment with isotonic saline produced inappropriately high SNa correction level of 21 mEq/l after the first 24 h. After initial improvement, the neurological status deteriorated after 72 h. Rapid reinduction of the hyponatremia was then ordered. Administration of hypotonic fluids (by oral and i.v. route) combined with dDAVP induced a prompt decline in the SNa (-16 mEq/l/14 h) with a final gradient of correction of deltaSNa 9 mEq/l. This manoeuver was well tolerated without untoward effects. The natremia then progressively normalized and the patient completely recovered without neurological sequelae. CONCLUSION: Hypotonic fluids may be safely administered to decrease the natremia after excessive correction of hyponatremia for potential prevention of myelinolysis. ( info)

2/105. Neuropsychiatric and neuropsychological manifestations of central pontine myelinolysis.

    A patient with central pontine myelinolysis (CPM) underwent neurological and mental status examination, as well as neuropsychological testing, during the acute stage of the disease. After correction of the hyponatremia, a gross change in his neuropsychiatric status was observed. The patient underwent extensive neurological, psychiatric, and neuropsychological testing during the acute phase of the disease and at follow-up 4 months later. All major neurological and neuropsychiatric symptoms present at onset were fully reversible. Neuropsychological examination revealed deficits in the domains of attention and concentration, short-term memory and memory consolidation, visual motor and fine motor speeds, and learning ability. Although improved, neuropsychological testing still revealed remarkable deficits at follow-up. We conclude that neuropsychological deficits can accompany CPM, and that these deficits do not necessarily diminish simultaneously with the radiological or clinical neurological findings but may persist for a longer period of time, or even become permanent. In his recovery the patient started to manifest new neurological symptoms consisting of a mild resting tremor of both hands and slow choreoathetotic movements of the trunk and the head, which we considered to be late neurological sequelae of CPM. The significance of CPM in the differential diagnosis of acute behavioral changes after correction of hyponatremia is stressed, even if correction is achieved slowly and carefully. ( info)

3/105. Improvement of central pontine myelinolysis as demonstrated by repeated magnetic resonance imaging in a patient without evidence of hyponatremia.

    Central pontine myelinolysis is usually associated with hyponatremia or rapid correction of this condition. In general, this neurological disorder has a fatal prognosis. We observed a 30-year-old woman with a history of chronic alcohol abuse but without evidence of hyponatremia, who developed severe pontine central myelinolysis. The initial magnetic resonance (MR)-imaging showed a marked lesion in the central pontine area, sequential MR-imaging revealed progressive reduction of this defect over the following months. This reduction was accompanied by excellent clinical recovery. This case report demonstrates that central pontine myelinolysis is not always associated with hyponatremia and illustrates that, although in general the prognosis is bad, some patients may recover with improvement of the abnormalities on the MR-images. ( info)

4/105. Extrapontine myelinolysis with involvement of the hippocampus in three children with severe hypernatremia.

    Central pontine myelinolysis is a disorder of unknown etiology linked to overly aggressive correction of hyponatremia. In addition to the typical location of demyelination with preservation of neurons and axon cylinders in the basis pontis, similar lesions have been described in extrapontine locations. Central pontine myelinolysis and extrapontine myelinolysis usually occur together, and are identified at autopsy rather than in life because symptoms of extrapontine myelinolysis are often masked in the critically ill patient. Central pontine myelinolysis is described in children, usually in the clinical setting of hyponatremic dehydration. Extrapontine myelinolysis has not been described in children previously. We report three children with severe hypernatremia and extrapontine myelinolysis involving various combinations of thalamus, basal ganglia, external and extreme capsules, and cerebellar vermis. All three had additional involvement of the hippocampus seen on T2-weighted magnetic resonance imaging. None of the three had detectable pontine lesions. Clinical features of the three cases were dehydration in a 28-month-old girl, respiratory syncytial virus bronchiolitis in a 14-month-old girl, and acute respiratory failure due to anaphylaxis after consumption of walnuts in a 3-year-old boy. Peak sodium values in each child were 195, 168, and 177 mmol/L, respectively; each received aggressive treatment for hypernatremia. We believe this to be the first report of extrapontine myelinolysis in children, the first report of extrapontine myelinolysis without central pontine myelinolysis in children, and the first report in children of hippocampal formation involvement. The pathogenesis of the central and extrapontine myelinolysis complex in children is more complicated than previously believed, and might differ significantly from that of adults. ( info)

5/105. Extrapontine myelinolysis with parkinsonism after rapid correction of hyponatremia: high cerebrospinal fluid level of homovanillic acid and successful dopaminergic treatment.

    Extrapontine myelinolysis (EPM) is a demyelinating process of the brain. We report the case of an 11-year-old girl who developed EPM with parkinsonism. magnetic resonance imaging revealed demyelinating patterns in the basal ganglia without central pontine lesions. The cerebrospinal fluid levels of homovanillic acid and 5-hydroxyindoleacetic acid were high at the time of onset and normalized upon complete recovery from extrapyramidal symptoms after a dopaminergic treatment. We speculated that demyelination of nerve fibers containing dopamine receptors in the striatum might be a main cause of these symptoms. ( info)

6/105. Acute intermittent porphyria with central pontine myelinolysis and cortical laminar necrosis.

    Acute intermittent porphyria (AIP) is an autosomal-dominant disease caused by a deficiency of porphobilinogen (PBG) deaminase. patients with AIP present with neurological syndromes such as autonomic neuropathy, peripheral axonal neuropathy or central nervous system dysfunction. We report serial MRI of a patient with AIP who had cortical and subcortical cerebral changes. A 29-year-old woman with a 6-month history of AIP had an attack with severe hyponatraemia and generalised convulsions, treated with haem arginate and supportive therapy. MRI showed central pontine and extrapontine myelinolysis and cortical laminar necrosis. These are not common in AIP, but are likely to have been caused by rapid correction of hyponatraemia and by vasospasm, which could be induced by AIP. ( info)

7/105. Severe hyponatraemia secondary to beer potomania complicated by central pontine myelinolysis.

    A case of severe hyponatraemia in a 56-year-old male alcohol misuser secondary to beer potomania is presented. In view of severe volume depletion and the patient's inability to drink, normal saline was cautiously infused. Despite initial improvement, he subsequently deteriorated neurologically. magnetic resonance imaging demonstrated the classical lesion of central pontine myelinolysis (CPM). The rate of correction of plasma sodium was within limits normally considered safe. beer potomania should be considered as a cause of hyponatraemia in alcohol misusers. Recognition is important as the electrolyte imbalance repairs simply with cessation of alcohol intake and institution of normal diet. Correction of chronic hyponatraemia by infusion of normal or hypertonic saline should not be attempted unless life-threatening neurological complications supervene. When the balance of risks favours correction, caution should be exercised, as CPM may occur. Although a rate of correction of plasma sodium of up to 10 mM per 24-hour period has been associated with a low risk of precipitating CPM, this case illustrates that a completely safe rate of correction probably cannot be defined. ( info)

8/105. "Deaf hearing": unacknowledged detection of auditory stimuli in a patient with cerebral deafness.

    We describe a patient with the rare disorder of total deafness caused by a bilateral lesion in the temporal lobes and lesions in the central pontine area. Although she displayed no voluntary ability to detect or localize or identify sounds and denied hearing them when asked in writing, she retained some ability to respond reflexively to sounds. When attempts were made to restore awareness of sounds and/or voluntary responses to sounds by drawing her attention to her appropriate orienting head movements her performance improved and she began to respond successfully in a "forced-choice" paradigm. However, even when she became confident at detecting and localizing sounds she remained densely agnosic to their meaning. Her condition of deaf-hearing bears many similarities to that of blindsight. ( info)

9/105. Central pontine myelinolysis.

    A 9 year old boy presented with fever, drowsiness, quadriparesis and facial myokymia. MRI showed demyelination in the pontine region. A diagnosis of central pontine myelinolysis was made. literature review revealed the rarity of uneventful recovery as has been seen in our case. ( info)

10/105. Clinics in diagnostic imaging (45). Osmotic myelinolysis ( central potine myelinolysis).

    A 65-year-old woman developed progressive neurological deterioration following rapid correction of hyponatremia. magnetic resonance imaging showed T2 hyperintense areas in the central pons, basal ganglia and deep white matter, typical of osmotic myelinolysis (OM). Previously thought to be uniformly fatal, there are increasing reports of non-fatal cases of OM. The recognition and understanding of this entity is important to prevent or reduce the incidence of its occurrence, as there is no specific treatment once it develops. The clinical and radiological features of OM are reviewed. ( info)
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