Focal inhibitory seizures: a cause of recurrent transient weakness Fahmida A Chowdhury, 1 Steve Connor, 2 Rosalie Ferner, 3 Guy Leschziner 3 1 Department of Neurology, St Thomas’ Hospital, London, UK 2 Department of Radiology, St Thomas’ Hospital, London, UK 3 Department of Neurology, Guy’s Hospital, London, UK Correspondence to Fahmida A Chowdhury, Department of Neurology, St Thomas’ Hospital, Westminster Bridge Road, London SE1 7EH, UK; fahmidachowdhury@hotmail. com Accepted 13 July 2015 Published Online First 5 August 2015 To cite: Chowdhury FA, Connor S, Ferner R, et al. Pract Neurol 2015;15: 460–462. ABSTRACT Focal seizures are usually manifest with stereotyped positive phenomena. However, seizures may also give negative phenomena, such as paralysis, speech arrest, neglect, atonia and numbness. We report a 39-year-old man with neurofibromatosis 2 who had recurrent stereotyped episodes of weakness affecting his right leg and right arm. His MR scan of brain showed numerous meningiomas, the largest of which was near the vertex, adjacent to the left side of the falx. Interictal electroencephalogram, MR cerebral angiogram and Doppler carotid artery ultrasound scan were normal. He was diagnosed with epilepsy and started on levetiracetam, with no subsequent attacks. We postulate his negative motor seizures related to a meningioma overlying the supplementary negative motor area in the mesial superior frontal gyrus, and discuss diagnostic criteria for inhibitory seizures. INTRODUCTION Seizures are usually stereotyped positive phenomena, such as clonic, myoclonic or tonic motor activity, automatisms, paraes- thesias or hallucinations. However, sei- zures may also cause negative phenomena, such as paralysis, ictal blindness, speech arrest, neglect, atonia and numbness. 1 We report a man with transient hemiparesis that we believe were focal negative motor seizures, and we discuss the likely mechanisms. CASE REPORT A 39-year-old man with neurofibroma- tosis 2 (NF2) was reviewed at our special- ist clinic. He had a frameshift mutation in the NF2 gene, bilateral vestibular schwan- nomas, multiple cranial and spinal men- ingiomas and schwannomas. The MRI of the entire neuro-axis had shown numer- ous meningiomas, the largest of which was near the vertex, adjacent to the left side of the falx, measuring 3.3×2.5 cm, with underlying T2 and fluid-attenuated inversion recovery signal hyperintensity within the surrounding brain parenchyma within the left frontal/anterior parietal lobes ( figure 1). He reported recurrent stereotyped epi- sodes of weakness affecting his right leg, with sudden onset of weakness and numbness of the whole leg, reaching a maximum over 30 s, and lasting for 30 min, followed by almost complete and rapid resolution over a minute. There was a residual abnormal feeling for about 24 h but he would feel otherwise well. During these episodes, his right arm felt slightly weak and uncoordinated. On one occasion, he was woken from sleep by momentary cramping in the right leg before the onset of weakness and numb- ness. There had been three such episodes over 6 months but before his clinic appointment, there had been a cluster of four attacks within 24 h, requiring admis- sion to another hospital. He was then started on levetiracetam 500 mg daily, without further investigations, and his attacks stopped. Subsequent interictal electroencephalogram (EEG), MR cere- bral angiogram and Doppler ultrasound scan of the carotid arteries were all normal. DISCUSSION NF2 is a rare autosomal dominant condi- tion caused by an abnormal tumour sup- pressor gene, and characterised by bilateral vestibular schwannomas and mul- tiple cranial and spinal schwannomas and meningiomas. 2 Meningiomas are the most common cause of its morbidity and mor- tality and frequently cause focal epilepsy. This patient experienced stereotyped negative motor events that we postulate were focal inhibitory seizures, on the basis of clinical history, the dramatic response to antiepileptic medication, and the anatomical location of one of his meningiomas. The abolition of events NEUROLOGICAL RARITIES 460 Chowdhury FA, et al. Pract Neurol 2015;15:460–462. doi:10.1136/practneurol-2014-001017