Abstracts

Partial Status Epilepticus Associated with Ketotic Hyperglycemia

Abstract number : 3.176
Submission category :
Year : 2000
Submission ID : 1776
Source : www.aesnet.org
Presentation date : 12/2/2000 12:00:00 AM
Published date : Dec 1, 2000, 06:00 AM

Authors :
Fabio Placidi, Andrea Romigi, Mario Tombini, Francesca Izzi, Francesca Sperli, Elena Baviera, Alessandro Bozzao, Roberto Floris, Maria Grazia Marciani, Universita' degli Study di Rome Tor Vergata, Rome, Italy; Univ degli Study di Rome Tor Vergata, Rome, I

RATIONALE:Seizures may occur in metabolic disorders of which nonketotic hyperglycemia (NKH) is a major example.We report partial status epilepticus (PSE) as manifestation of ketotic hyperglycaemia(KH). METHODS:A 44-year old right-handed man was admitted in our department for recurrent focal motor seizures. He had 10day history of clonic jerks at the right hand with progressive involvement of the upper limb, followed after one week by hypostenia of the same limb. He gave a history of alcohol abuse and chronic pancreatitis.There was no history of diabetes mellitus. RESULTS:Laboratory investigations gave hyperglycaemia, glycosuria, ketonuria and metabolic acidosis. EEG demonstrated a generalised depression of the cerebral activity followed by low-voltage spikes and/or sharp waves localised in the left frontal region spreading to the right hemisphere, syncronously with jerks. Brain MRI 3 days after the admission, showed an hypointensity on FLAIR sequences in the left subcortical prerolandic area. Despite anticonvulsant therapy, seizures persisted. Correction of metabolic derangement by insulin therapy and appropriate fluid replacement induced a gradual disappearance of seizures. Brain MRI repeated after one month displayed a little gliotic area in the site of original lesion. CONCLUSIONS:Hyperglycaemia may reduce seizure threshold, because GABA metabolism is increased in this condition and the GABA levels may be depressed. Seizures are unusual in diabetic ketoacidosis, since GAD needs an acidotic pH and ketone bodies supply energetic substrate avoiding GABA utilisation. We cannot exclude that hyperglycaemia has triggered epileptic discharges in the area of a previous silent lesion however according to clinical history, we believe that the metabolic disorder provoked PSE, which might be responsible for a cerebral cortical injury. PSE may occur also in KH, these seizures are remarkably resistant to antiepileptic drugs, but promptly respond to correction of metabolic disorder similarly to ictal events occurring during NKH.