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Chronic kidney disease and seizures often co-exist. When seizures are provoked in patients with kidney disease, their treatment poses a particular challenge. Seizures may be provoked in the context of uremia, and toxic substances associated with uremic encephalopathy. In that case, the mainstay of therapy is to treat the uremia before consideration for anticonvulsant therapy. Treatment of seizures in the setting of chronic kidney disease requires special attention to selection of anticonvulsant medications and knowledge of the altered pharmacokinetics of these medications, which may require special titration schedule in that setting. The purpose of this review is to summarize the current knowledge about inter-relation of seizures and kidney disease. The review will also help practitioners who treat patients with renal failure and coexisting seizures in choosing the best treatment options.

Renal diseases-related metabolic abnormalities cause diverse CNS disturbances, namely uremic encephalopathy, seizures, stroke, movement disorders, sleep alterations, and peripheral nervous system involvement comprising polyneuropathy, mononeuropathies, and myopathy. Some inherited and acquired renal diseases present with concomitant or precedent neurologic syndromes. Several mechanisms involved include toxic metabolic accumulation, hyperkalemia, hypercoagulability, immunologic disturbances, and tubular acido-basic disequilibrium. Clinical symptoms usually indicate severe renal dysfunction, but subtle abnormalities may occur. Judiciously tailored renal replacement therapy may avoid these complications, whereas others may emerge from these very therapies with overlapping clinical pictures. This makes an already complex management of renal patients even more difficult and asks for tight collaboration between nephrologists and neurologists.

The electroencephalographic finding of periodic synchronous discharges (PSDs) is a basic clue for the diagnosis of Creutzfeldt-Jacob disease (CJD). We proposed grading of PSDs. We defined grade A as typical PSDs, grade B as PSDs of relatively longer periodic intervals, grade C as PSDs of relatively rare appearance, grade D as PSDs of rudimentary appearance, and grade E as absent PSDs. The occurrence rate of PSDs in Japanese CJD surveillance was 62% in total CJD (490/794), 72% in sporadic CJD (441/610), 24% in genetic CJD (41/171), and 61% in dura CJD patients (8/13). Among 171 genetic CJD patients, the occurrence rate of PSDs was 0% in P105L mutation CJD (0/2), 3% in V180I mutation CJD (3/90), 14% in P102L mutation CJD (4/29), 70% in E200K mutation CJD (16/23), and 71% in M232R mutation CJD patients (17/24). The occurrence rate of MRI changes in both cortical and basal ganglia was significantly higher in the s-CJD group with PSDs than in the s-CJD group without PSDs. The occurrence rate of PSDs in non-CJD patients who needed differential diagnosis of CJD was 10% (37/355). Non-CJD diseases associated with PSDs were status epilepticus, diffuse Lewy disease, Hashimoto encephalopathy, Wernicke encephalopathy and uremic encephalopathy.

An 85 year old man with a history of chronic renal insufficiency was admitted to the cardiothoracic intensive care unit after aortic valve replacement. His postoperative course was marked by acute oliguric renal failure for high blood urea nitrogen (BUN) and acute hyperactive delirium. At this time he also developed tremors with muscle twitching; he received no other form of sedatives. A neurology consult made the diagnosis of twitch-convulsive syndrome associated with uremic encephalopathy. While the patient was receiving the dexmedetomidine infusion, the signs of the twitch-convulsive syndrome, particularly the twitching and tremors, disappeared. Within 30 minutes of the end of the dexmedetomidine infusion, symptoms of the twitch-convulsive syndrome returned, manifesting as acute tremulousness. After several dialysis treatments, his BUN decreased and the dexmedetomidine was weaned, without return of the symptoms of twitch-convulsive syndrome.

The symptoms which develop in well-managed patients with acute or chronic progressive renal failure comprise the neurobehavioral syndrome, uremic encephalopathy. Interfering with vigilance, cognitive functions, and ultimately consciousness, these symptoms impose significant disability unless dialysis treatment can reverse and suppress them or a successful renal transplant provides the patient with virtually normal renal function, and, consequently, complete symptomatic recovery. This apparent connection between disability as a neurobeha-vioral “encephalic” disorder and its response to dialysis prompted our attempts to apply quantitative electroencephalogram (EEG) measures as indices of the “toxic encephalopathy” of renal failure and of its response to “standard” dialysis regimens and to transplantation. Subsequent work indicates that EEG measures are sensitive to varying amounts or intensity of maintenance dialysis, to changes in modality of dialysis, for example, the shift from conventional prescriptions of maintenance hemodialysis to peritoneal dialysis, CAPD, CCPD, and so forth, or to effects within individual dialysis sessions in cases of dialysis disequilibrium.These findings invite the prospect that one may objectively assess at least the relative adequacy of different levels and modalities of dialysis in individual patients using objective indices which are particularly relevant both to the symptomatic disability of renal failure on one hand, and to the symptomatic improvement evoked by dialysis on the other.Therefore, in this article we describe the use of computer-based methods for the evaluation of uremic encephalopathy and its response to treatment. Examples are given in which such computerized evaluations have guided decisions about treatment, particularly to assure sufficient dialysis to suppress even the milder manifestations of the dialysis-responses, clinical uremic syndrome. The purpose of the article is to dispel the mystique that has surrounded the use of the computer for evaluation of EEGs recorded from renal patients.The methods described below were designed specifically for use with EEGs recorded from renal patients and should not be considered as a replacement for a trained EEG scorer. Visual scoring of the EEG provides a comprehensive examination of an EEG record that is unlikely ever to be matched by any computer program. Hence, the methods described should be viewed simply as a quantitative evaluation tool for a limited range of significant features in EEGs secured from a rather select population.We hope the practical information given can be used to guide physicians as they begin to incorporate the methods described into their everyday practice. A survey of the history of the use of computers in the evaluation of electroencephalograms recorded from patients with renal disorders is given as well as a critical evaluation of computer methods employed in past approaches. The practical consequences of a decision to utilize computerized testing methods will be examined. A prospectus that attempts to highlight possible future directions in this area completes the paper.

It has been demonstrated that anesthesia primarily affects the reticular activating system and psychological studies on patients undergoing anesthesia demonstrated a verbal memory defect. This study was performed in order to determine whether metabolic (uremic) encephalopathy follows the Jacksonian dissolution hypothesis and disrupts cortical function or whether it acts like an anesthetic, causes dysfunction in phylogenetically older systems and thereby produces a memory defect. Twenty-four uremic subjects were tested for memory function, language function, and intellectual function, and compared to 12 control subjects. The greatest difference between the groups was in immediate memory function suggesting that uremia probably acts in a manner similar to anesthesia (by causing dysfunction in the reticular activating system). It is postulated that poor arousal interferes with rehearsal and rehearsal is probably an important component of immediate memory.