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Psychosis and lack of efficacy: case report A woman [exact age not stated] experienced lack of efficacy following treatment with carbamazepine, clobazam, clonazepam, lamotrigine, zotepine and risperidone. Additionally, she developed psychosis during treatment with levetiracetam at the approximate age of 42 years [not all routes stated]. The woman was admitted in 2015 (i.e. at the age of 45 years) with auditory verbal and cenesthetic hallucinations, persecutory and mystic delusions and behavioural disturbance. She had been diagnosed with epilepsy secondary to bilateral parieto-occipital and perirolandic lesions of ulegyria at the age of 5 years. She had been followed up by different neurologists since the diagnosis of epilepsy was made and had tried many antiepileptics (she cannot recall the names). In 2007, levetiracetam 1000 mg/day had been added to carbamazepine 1200 mg/day and clobazam 20 mg/day. In 2009, the dose of levetiracetam was increased to 4000 mg/day. The dose of clobazam was increased to 40 mg/day in 2010 and the dose of carbamazepine was increased to 1800 mg/day in 2011. In 2014, she reduced the dosage of carbamazepine to 1200 mg/day on her own. Despite many therapeutic adjustments over the years, she continued having seizures, mostly during catamenia (2–3 seizures/month). At the current hospitalisation, her antiepileptic medication included levetiracetam 4000 mg/day, carbamazepine 1200 mg/day, clobazam 40 mg/day and clonazepam 4 mg/day. She had no psychiatric history until 2012. In 2012, she had her first psychiatric hospitalisation, as she was experiencing persecutory delusion. At that time, she received oral risperidone 6 mg/day. She was then discharged and was followed up at the outpatient department. However, she continued to have residual persecutory delusion. Electroencephalogram revealed no alterations and a brain MRI showed high-intensity signal at the perirolandic and parieto-occipital areas and atrophy with ulegyric pattern in the parieto-occipital area. The Raven’s Progressive Matrices test revealed a middle inferior level of intelligence. Addenbrooke’s cognitive examination showed memory compromise as the only cognitive function affected (16/26). Brief symptom inventory revealed an above-average level of paranoid ideation. In 2013, due to functional disability, she was awarded a disability pension. Despite many therapeutic adjustments, including administration of long-acting IM injection of risperidone 37.5 mg/mL fortnightly on suspicion of non-adherence to oral therapy, her psychosis did not improve and she was hospitalised. By the time of her inpatient admission, physical examination and analytical tests showed no relevant alterations. Long-acting injectable risperidone was increased to 50 mg/mL; however, no improvement was noted in her psychosis. Zotepine was added, up to 300 mg/day; however, no improvement was noted in her psychosis. Due to disabling extrapyramidal symptoms, risperidone was suspended and dose of zotepine was decreased. Following consultation with the neurology de