Abstract
P.K. Kuruvilla, Mar Thomas Medical Mission Centre, Ranny, Kerala State, India, John Alexander, Neurologist, MGDM Hospital, Kangazha, Kerala State, India:
Ray [1] and Richard [2] have reported non-convulsive seizure activity in patients while on both lithium carbonate and electroconvulsive therapy. We wish to report non-convulsive status epilepticus (NCSE) occuring as a manifestation of lithium toxicity alone.
A 37 year old man was treated for bipolar affective disorder and non-insulin dependent diabetes mellitus with lithium, antipsychotic drugs and oral hypoglycaemic agents. He was discharged on the 29 May 1998 with a serum lithium level of 0.6 mmol/L and serum creatinine of 97.24 mmol/L. Three weeks later, he was readmitted with abscesses on the medical aspects of both thighs and high blood sugars. Incision and drainage of the abscesses was done and antibiotics started. On day six, as the patient developed mild tremors and decreased urinary output, his serum lithium and blood biochemistry were rechecked. The values were suggestive of acute renal dysfunction; serum lithium was 1.9 mmol/L, Random Blood Sugar 15.73 mmol/L, Serum creatinine 203.32 mmol/L, Blood urea 29.63 mmol/L, Na+ 139 mmol/L, K+ 5.9 mmol/L, urine acetone negative. Lithium and all psychotropic medicines were stopped and the patient was started on measures for oliguric renal failure. By day 10, his renal functions and biochemical parameters had returned to normal. At this point, the patient started to show increasing stiffness of the limbs and his level of consciousness had deteriorated. The patient was afebrile and the vital parameters stable. A repeat neurological examination revealed a mute, akinetic patient not responding to commands; his eyes were open, but visual tracking was absent. Cranial nerves including optic fundii were normal. There was generalised rigidity in all four limbs and no withdrawal on painful stimuli. All the deep tendon reflexes were exaggerated and the plantar response was flexor bilaterally.
The investigations repeated were as follows –serum lithium 1.9 mmol/L, serum creatinine 132.6 mmol/L serum CPK 194 IU/L (3.233 m kat/L), serum LDH 415 IU/L (6.918 m kat/L). An EEG taken revealed a background 5-6 Hz theta rhythm, independent sharp discharges were seen over both hemispheres and in addition intermittent bursts of high amplitude generalised electrographic seizure activity was seen bilaterally. With these findings on EEG, a diagnosis of non-convulsive status epilepticus was made. The patient was dilantinised and supportive measures instituted. Over the next week, he showed gradual improvement which correlated with the return of normal background alpha rhythm on serial EEGs. Lithium levels too returned to zero by the 10th day of initiating treatment.
The patient was discharged within a week-ambulant and in normal sensorium Neuroleptic Malignant Syndrome (NMS) and metabolic encephalopathy are ruled out by the clinical picture as well as the laboratory parameters. Lithium neurotoxicity was the most likely diagnosis in view of the close temporal correlation of the clinical profile and the serum lithium levels. Also, this case documents the occurrence of prolonged and total unresponsiveness with no overt convulsive seizures at any time, but the EEG showing typical electrographic seizure activity pointing to a diagnosis of NCSE. In this case there was neither a past history, nor a family history of seizures and the only aetiology which can be implicated is the near toxic levels of lithium, making it a unique case.
An EEG helped us to make a diagnosis of NCSE and to institute appropriate therapeutic measures specifically dilantinisation. Therefore it seems worthwhile to do an EEG on all patients on lithium presenting with altered sensorium.