Dialysis encephalopathy syndrome (also called dialysis dementia) occurs in patients on chronic hemodialysis. Some cases are due to toxicity from aluminum in the dialysis bath,19 so the incidence of the disease has decreased with the use of aluminum-free water.7
Within 1 to 15 months, the disease usually progresses to apneic spells and death from sepsis or suicide.3,16,19,24 In some patients, however, the disease is transient, and others have a variable course lasting several years.24
The EEG shows changes similar to those in aluminum encephalopathy syndrome.13 The bursts of sharp and slow activity and clinical symptoms sometimes are suppressed by oral or intravenous diazepam early in the disease.25 Seizures can be distinguished from nonepileptic movements by combined EEG recordings and electromyography (EMG).
Control of secondary hypoparathyroidism, iron deficiency anemia, and hyperphosphatemia will reduce aluminum absorption by the gastrointestinal tract.3 The concentration of aluminum in the dialysate should be monitored periodically.3
Pyridoxine supplementation must be given when pyridoxine deficiency is present.27
Benzodiazepines such as clonazepam and diazepam are effective in controlling the myoclonus. Benzodiazepines may temporarily control the bursts of sharp and slow activity on the EEG and may temporarily reduce the clinical symptoms of the syndrome.25
Phenytoin usually is used for tonic-clonic seizures because relatively little is removed by hemodialysis and it can be given intravenously in loading doses to maintain a desired plasma concentration. (See Correction for drug loss during hemodialysis)
Adapted from: Browne TR. Renal disorders. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;49-62. With permission from Elsevier (www.elsevier.com).
Reviewed and revised February 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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