title: Tiagabine-induced generalised non convulsive status epilepticus in patients with lesional focal epilepsy.
abstract: OBJECTIVE
  To report 3 cases with focal lesional epilepsy that had non-convulsive status epilepticus (NCSE) induced by treatment with tiagabine (TGB) and review the previously published cases. Drugs that enhance GABAnergic transmission are recognised to promote absence seizures in patients with generalised epilepsy syndromes and may on occasions even induce NCSE. However, that TGB can also induce NCSE in focal lesional epilepsy is not widely recognised in clinical practice.
  
  
  METHODS
  The clinical history, EEG and MRI findings were reviewed in 3 patients with lesional focal epilepsy who presented to our epilepsy programs over a 12 month period with TGB-induced NCSE. All previously reported cases in the English medical literature were reviewed.
  
  
  RESULTS
  The three patients had longstanding complex partial and secondarily generalised seizures refractory to multiple different anti-epileptic drugs. In two cases, MRI demonstrated a focal malformation of cortical development in the left parieto-occipital region and in the third left mesial temporal sclerosis. Following commencement of TGB in one patient and dose escalation in two, prolonged episodes of confusion and poor responsiveness were noted. Prolonged EEG monitoring demonstrated continuous high amplitude, generalised, 2-4 Hz delta activity with intermingled spikes during the episodes of unresponsiveness, consistent with NCSE. The clinical and EEG activity normalised following the administration of IV clonazepam followed by dose reduction or withdrawal of the TGB. Eleven previously reported cases of patients with partial epilepsy and a focal underlying lesion on MRI were identified, all of whom had similar features to that seen in our cases.
  
  
  CONCLUSIONS
  These cases illustrate that TGB may induce generalised NCSE in patients with focal lesional epilepsy, in addition to those with generalised syndromes. We hypothesise that patients may have developed an acquired alteration in the sensitivity of their thalamocortical circuitry that renders them more sensitive to the effects of drugs that enhance GABAnergic activity.
authors.affiliation: Department of Neurology, The Royal Melbourne Hospital, The University of Melbourne, Parkville, Vic., Australia.
authors.forename: Anita
authors.initials: A
authors.lastname: Vinton
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Kornberg
authors.forename: Max
authors.initials: M
authors.lastname: Cowley
authors.forename: Zelko
authors.initials: Z
authors.lastname: Matkovic
authors.forename: Christine
authors.initials: C
authors.lastname: Kilpatrick
authors.forename: Terence J
authors.initials: TJ
authors.lastname: O'Brien
mesh_terms: D000293:Adolescent; D000328:Adult; D000927:Anticonvulsants / Q000009:adverse effects*; D002998:Clonazepam / Q000627:therapeutic use; D004569:Electroencephalography; D004827:Epilepsy / Q000188:drug therapy* / Q000473:pathology; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D009557:Nipecotic Acids / Q000009:adverse effects*; D013226:Status Epilepticus / Q000139:chemically induced* / Q000188:drug therapy; D000078308:Tiagabine
chemical_list: D000927:Anticonvulsants; D009557:Nipecotic Acids; D002998:Clonazepam; D000078308:Tiagabine