Behavioral and Movement Disorders due to Long-Lasting Myoclonic Status Epilepticus Misdiagnosed as ADHD in a Patient With Juvenile Myoclonic Epilepsy: Electroclinical Findings and Related Hemodynamic Changes.

Clinical EEG and neuroscience Pub Date : 2016-01-01 Epub Date: 2015-03-01 DOI:10.1177/1550059415574622
Martina Fanella, Marco Carnì, Alessandra Morano, Mariarita Albini, Leonardo Lapenta, Sara Casciato, Jinane Fattouch, Elisabetta Di Castro, Claudio Colonnese, Anna Elisabetta Vaudano, Anna Teresa Giallonardo, Carlo Di Bonaventura
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引用次数: 2

Abstract

Epilepsy and attention-deficit/hyperactivity disorder (ADHD) likely share common underlying neural mechanisms, as often suggested by both the evidence of electroencephalography (EEG) abnormalities in ADHD patients without epilepsy and the coexistence of these 2 conditions. The differential diagnosis between epilepsy and ADHD may consequently be challenging. In this report, we describe a patient presenting with a clinical association of "tics" and behavioral disorders that appeared 6 months before our first observation and had previously been interpreted as ADHD. A video-EEG evaluation documented an electroclinical pattern of myoclonic status epilepticus. On the basis of the revised clinical data, the EEG findings, the good response to valproate, the long-lasting myoclonic status epilepticus, and the enduring epileptic abnormalities likely causing behavioral disturbances, the patient's symptoms were interpreted as being the expression of untreated juvenile myoclonic epilepsy. The EEG-functional magnetic resonance imaging study revealed, during clinical generalized spike-and-wave and polyspike-and-wave discharges, positive blood oxygen level-dependent (BOLD) signal changes bilaterally in the thalamus, the prefrontal cortex (Brodmann area 6, supplementary motor area) and the cerebellum, and negative BOLD signal changes in the regions of the default mode network. Such findings, which are typical of BOLD changes observed in idiopathic generalized epilepsy, may also shed light on the anatomofunctional network underlying ADHD.

青少年肌阵挛性癫痫患者因长期肌阵挛性癫痫持续状态被误诊为ADHD而导致的行为和运动障碍:电临床表现和相关血流动力学改变。
癫痫和注意力缺陷/多动障碍(ADHD)可能具有共同的潜在神经机制,这通常由ADHD患者无癫痫的脑电图(EEG)异常以及这两种情况共存的证据所提示。因此,癫痫和ADHD的鉴别诊断可能具有挑战性。在这篇报告中,我们描述了一个在我们第一次观察前6个月就出现了“抽搐”和行为障碍的临床关联的病人,之前被解释为多动症。视频脑电图评估记录了肌阵挛性癫痫持续状态的电临床模式。根据修改后的临床资料、脑电图结果、丙戊酸钠的良好反应、持续的肌阵挛性癫痫持续状态,以及持续的可能引起行为障碍的癫痫异常,将患者的症状解释为未经治疗的青少年肌阵挛性癫痫的表现。脑电图功能磁共振成像研究显示,在临床广泛性峰波放电和多峰波放电时,丘脑、前额叶皮层(Brodmann区6、辅助运动区)和小脑双侧的血氧水平依赖(BOLD)阳性信号发生变化,默认模式网络区域的BOLD负信号发生变化。这些发现是特发性广泛性癫痫中观察到的典型的BOLD变化,也可能揭示ADHD背后的解剖功能网络。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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