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Lack of efficacy: case report A 28-year-old woman exhibited lack of efficacy with desflurane, flunarizine, ketamine, lacosamide, levetiracetam, lidocaine, magnesium, midazolam, perampanel, phenobarbital, phenytoin, propofol, thiopental sodium, topiramate, valproate, valproic acid and zonisamide for new-onset refractory status epilepticus (NORSE) [not all routes stated; dosages not stated]. The woman, who had Axenfeld-Rieger syndrome, developed fever and generalised seizures. After detailed evaluation, NORSE was suspected. She was treated with IV levetiracetam and IV valproate; however, the seizures continued. Based on suspicious diagnosis, she was started on an unspecified high-dose steroid pulse therapy. She was admitted to the neurointensive care unit and was started on continuous IV anaesthetic drugs comprising propofol and ketamine followed by thiopental. Her seizures recurred in spite of repeated attempts to decrease the depth of anaesthesia. Additionally, IV immune globulin [immunoglobulin] therapy, plasmapheresis and hypothermia were ineffective for seizures. An EEG revealed an iatrogenic burst-suppression pattern, with isoelectric activity intercalated by epileptic bursts of prolonged, bilateral high-voltage polyspikes. Based on the depth of anaesthesia, electroclinical seizures arising from the right hemisphere were noted. An MRI of the brain revealed abnormal T2/fluid-attenuated inversion recovery (FLAIR) signal in the cortex of both frontotemporal regions. Various investigations for neoplasms, ovarian teratoma and tuberous sclerosis were negative. A muscle biopsy ruled out mitochondrial disease. Focal seizures recurred following each attempt to lower the anaesthetic or the serum phenytoin dosage. A repeat MRI without gadolinium enhancement revealed T2/ FLAIR hyperintensity in the left temporoparietal cortical and subcortical regions and in the bilateral thalamic pulvinar. An [18F]fluorodeoxyglucose PET brain scans revealed hypermetabolism in the same regions. Surgical treatment was not opted due to bilateral epileptic foci. Cerebral biopsy of the left parietal cortex demonstrated unspecific macroglial and microglial activation. There were no other signs of massive inflammatory response. The possibility of neuronal storage diseases was ruled out. Then an anaesthetic regimen was changed to a combination of thiopental sodium and midazolam along with magnesium infusion. She was treated with valproic acid, levetiracetam, lacosamide, zonisamide, topiramate, phenytoin, pyridoxine, perampanel, lidocaine, phenobarbital, flunarizine and inhaled desflurane; however, no effect was noted. Transcranial direct current stimulation was performed, which showed a temporary effect. Four months later, modifications in the antiepileptic regimen were done. The modified regimen comprised of valproate, phenytoin, clobazam, lamotrigine, perampanel and topiramate, on which an improvement in the EEG was noted. Despite continuing midazolam infusion, she regained contact. She was not following commands but was awake. She still h