How do we use electroencephalography in child epileptology?

How do we use electroencephalography in child epileptology?

Clinical Neurophysiology Society of Serbia and Montenegro / Clinical Neurophysiology 118 (2007) e117–e127 Methods: We describe the clinical and elect...

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Clinical Neurophysiology Society of Serbia and Montenegro / Clinical Neurophysiology 118 (2007) e117–e127

Methods: We describe the clinical and electroencephalographic features of three female infants diagnosed as early-onset absence seizures (onset of absences as the only seizure type before age 3). Results: The age at onset of the seizures ranged between 7 and 22 months. Ictal EEG revealed a normal background and generalised spike-and-wave complexes at 3–3.5 Hz accompanied by disruption of ongoing activity in keeping with absence seizures. The duration of seizures ranged from 5 to 20 s. Clinical and electroencephalographic follow-up ranged from 10 months to 3 years. Two children were on treatment with valproate and in one case, the combination of valproate and ethosuximide and clonazepam was necessary. Control of absence seizures was achieved in all our cases. Neurological evaluation was normal in all patients. At the follow-up, two patients showed mild mental retardation. Conclusions: Early-onset of absences is uncommon, and multicenter studies should help clarify the nosology and prognosis. A video–electroencephalogram is the method of choice in the diagnostic evaluation and syndromic classification of these paroxysmal events. doi:10.1016/j.clinph.2006.11.296

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Methods: A case of acute intermittent porphyria in a 20-yearold male with epilepsy is reported. The diagnosis was made only after the third hospitalisation, with the measurement of enzyme activity. Results: First symptoms (abdominal pain, nausea, and vomiting) lasting one week occurred when patient was 15-year-old. They were followed by generalized tonic-clonic seizures (GTSs). Afterward, abdominal pains were frequent, so the patient consulted a gastroenterologist. One year later, high blood tension and tachycardia were found and antihypertensive drugs were prescribed. Two years ago, appendectomy was performed and holecystectomy one year ago. GTCs were rare at first but became more frequent when carbamazepine was prescribed, 6 months ago. Computerized tomography scan was normal, Excretion of 5-aminolevulinic acid (ALA) in the urine was increased (96.13 lmol/d, normal range up to 76.3 lmol/d). After the definite diagnosis, clonazepam was prescribed, instead of carbamazepine, and epileptic seizures were reduced. Conclusions: Refractory epilepsy could be caused by metabolic disturbance. Porphyria should be suspected, especially if frequent epileptic seizures and abdominal pain coexist in the same patient. doi:10.1016/j.clinph.2006.11.298

How do we use electroencephalography in child epileptology?—M. Knezˇevic´ Pogancˇev (Child and Youth Health Care Institute, Novi Sad, Serbia) Electroencephalography as the most commonly used diagnostic method in child neurology is used after any consciousness disorder in children; nevertheless, it is not of the primary importance in making a diagnosis. The aim of this study was to show that the electroencephalography (EEG) has been applied too often in the process of getting the information it cannot obtain. Study was conduced in period from 1993 to 2003 year in Institute for Child and Youth Health Care in Novi Sad in 2000 first time hospitalized children after any consciousness disorder. Starting from the fact that EEG is expected to confirm the presence of epileptic electrographic activity, and having in mind that its absence does not exclude epilepsy it has been found that 75% of the EEG findings do not meet paediatrics expectations. The dominance of the normal EEG findings is the result of the fact that a large number of EEG is ordered to ‘‘exclude epilepsy’’. The EEG has been applied too often in the process of getting the information it cannot obtain. The EEG without precise anamnestic data and clinical observations is not enough – neither to diagnose epilepsy nor to deny its existence. doi:10.1016/j.clinph.2006.11.297

Refractory epilepsy and porphyria—R. Sujic´, S. Kostic´, S. Kazˇic´ (Clinic Centre Zvezdara, Belgrade, Serbia) Purpose: To report a patient with frequent epileptic seizures, poorly responding to antiepileptic therapy, with 5-year evolution before conforming the diagnosis of porphyria.

Epileptic seizures as first manifestation of limbic encephalitis in patient with small cell carcinoma of the lung—Lj. Stancˇetic´-Bacˇvanin (Neurology unit, Health Center, Sremska Mitrovica, Serbia) Purpose: To present limbic encephalitis as a possible cause of late onset seizures. A 59-year-old man, presented a year ago with generalized tonic clonic seizures (GTCS), severe shortmemory loss, agitated behavior and confusion. His father died from lung carcinoma. A month prior to admission he had five generalized tonic clonic jerks first time in his life. On admission, patient was conscious, incoherent, agitated and was talking irrelevantly. Methods and results: EEG recorded excessive bitemporal spikes and slow wave discharges two weeks after first GTCS. CSF revealed 180 cells/mm3, mostly lymphocytes without malignant cells. The levels of protein in the CSF were within normal limits, but with oligoclonal bands. The viral screening was negative. Magnetic resonance imaging revealed bilateral symmetrical hyperintensities on T2WI. Chest computerized tomography revealed left hilar nodular lesion, diagnosed as small cell carcinoma of the lung on histology. Over the following 6 weeks, seizures ceased but patient’s mental state progressively deteriorated. An EEG showed diffuse theta activity. Ten weeks after admission he was demented. A year after admission he has residual amnestic disturbance with no seizure. Conclusions: Seizures can be seen at the onset or during well developed clinical picture of limbic encephalitis. doi:10.1016/j.clinph.2006.11.299