Ighodaro Eseosa T., Maini Kushagra, Arya Kapil, Sharma Sandeep
Emory University Hospital
Augusta University
A focal onset seizure refers to abnormal neural activity in only one brain area within one brain hemisphere with a fixed focal or localized onset. Focal onset seizures are divided into 2 subtypes: motor onset and nonmotor onset. Both focal motor and focal nonmotor onset seizures can be further classified based on level of awareness: aware, impaired, and unknown awareness. The motor manifestations of focal motor onset seizures can be characterized as automatism, atonic, clonic, epileptic spasms, hyperkinetic, myoclonic, or tonic movements. The behavioral manifestations of focal nonmotor onset seizures can be described by autonomic, behavioral arrest, cognitive, emotional, or sensory symptoms. Some focal onset seizures can be preceded by an "aura," which refers to symptoms and signs that occur before the onset of seizure activity. These symptoms may include vision changes, dyspepsia, déjà vu, paresthesias, hearing disturbances, and sensation of abnormal taste or smell. A seizure is a sign that refers to a transient occurrence of signs and symptoms due to episodic, excessive, and disorderly neuronal activity within the brain. Epilepsy is a brain disorder "characterized by an enduring predisposition to generate epileptic seizures and by this condition's neurobiological, cognitive, psychological, and social consequences. The definition of epilepsy requires the occurrence of at least one epileptic seizure." These events have traditionally been classified into partial and generalized seizures. However, the International League Against Epilepsy (ILAE) in 2017 reclassified seizures into 3 types: generalized onset seizures (formerly known as grand-mal seizures), focal onset seizures (formerly known as simple partial seizures or complex partial seizures), and unknown onset seizures. Focal motor seizures occur due to an epileptogenic lesion on the contralateral frontal lobe. They usually originate from the supplementary motor area. The excitatory focus is generally around the rolandic (motor) cortex. Temporal lobe seizures can also have motor symptoms. These symptoms include turning the head and neck to the opposite side and sometimes tonic contractions of the limbs and trunk. The motor manifestations of focal motor onset seizures can be characterized by tonic, clonic, atonic, myoclonic, hyperkinetic, epileptic spasms, and automatisms. Motor manifestations of focal motor onset seizures include the following: Abnormal sustained contractions and posturing of the limbs characterize tonic movements. Clonic movements are characterized by repeated, short contractions of various muscle groups characterized by twitching movements or rhythmic jerking. Atonic movements are characterized by loss of tone in a limb. Myoclonic movements are characterized by irregular, nonrhythmic jerking of the limbs. Abnormal regular or irregular excess involuntary movements of the limbs characterize hyperkinetic movements. Epileptic spasms are characterized by repetitive flexion of the waist and flexion or extension of the arms. Automatisms are characterized by coordinated, repetitive motor activities such as lip-smacking, tapping, or swallowing. Following focal motor seizures, patients may have transient, functional, and localized paralysis of the affected muscles, known as Toddparalysis. This paralysis can last minutes to hours, usually in proportion to the duration of the focal motor seizure. This postepileptic paralysis occurs due to persistent focal dysfunction of the affected epileptogenic area and is the signature of a focal seizure. The significant clinical value lies in lateralizing the hemisphere of seizure onset, and it is often mistaken for a stroke. The clinical manifestations of focal nonmotor seizure include autonomic, behavioral arrest, cognitive, emotional, or sensory symptoms. Autonomic seizures are characterized by changes in blood pressure, heart rate, sweating, skin color, or gastrointestinal upset. Behavioral arrest seizures are characterized by cessation of movement. Cognitive seizures are characterized by abnormal language or thinking, eg, jamais vu, déjà vu, hallucinations, and visualization of illusions. Emotional seizures are characterized by emotional changes such as fear, dread, anxiety, or pleasure. Nonmotor seizures that manifest as laughing are called gelastic, and those that manifest as crying are called dacrystic. Sensory seizures are characterized by changes in sensation, such as abnormal sensations of vision, paresthesias, hearing, smell, or pain. At times, focal motor and focal nonmotor seizures can evolve into bilateral tonic-clonic seizures.
局灶性发作是指仅在一个脑半球内的一个脑区出现异常神经活动,发作起始固定于局灶或局部。局灶性发作分为2个亚型:运动性发作和非运动性发作。局灶性运动性发作和局灶性非运动性发作均可根据意识水平进一步分类为:意识清楚、意识障碍和意识情况不明。局灶性运动性发作的运动表现可特征化为自动症、失张力、阵挛、癫痫性痉挛、运动过多、肌阵挛或强直运动。局灶性非运动性发作的行为表现可用自主神经、行为停止、认知、情感或感觉症状来描述。一些局灶性发作之前可能有“先兆”,先兆是指在癫痫发作活动开始之前出现的症状和体征。这些症状可能包括视力变化、消化不良、似曾相识感、感觉异常、听力障碍以及异常的味觉或嗅觉。发作是指由于脑内神经元活动阵发性、过度且无序而导致的症状和体征的短暂出现。癫痫是一种脑部疾病,“其特征为具有产生癫痫发作的持久倾向以及这种情况所导致的神经生物学、认知、心理和社会后果。癫痫的定义要求至少发生一次癫痫发作。” 这些发作传统上分为部分性发作和全身性发作。然而,国际抗癫痫联盟(ILAE)在2017年将发作重新分类为3种类型:全身性发作(以前称为大发作)、局灶性发作(以前称为单纯部分性发作或复杂部分性发作)和发作起始不明的发作。局灶性运动性发作是由于对侧额叶的致痫性病变引起的。它们通常起源于辅助运动区。兴奋灶一般在中央前回(运动)皮质周围。颞叶发作也可能有运动症状。这些症状包括头和颈转向对侧,有时还有肢体和躯干的强直收缩。局灶性运动性发作的运动表现可特征化为强直、阵挛、失张力、肌阵挛、运动过多、癫痫性痉挛和自动症。局灶性运动性发作的运动表现包括以下方面:强直运动的特征是肢体异常持续收缩和姿势异常。阵挛运动的特征是各种肌肉群反复短暂收缩,表现为抽搐运动或有节律的 jerking。失张力运动的特征是肢体张力丧失。肌阵挛运动的特征是肢体不规则、无节律的 jerking。运动过多运动的特征是肢体异常规则或不规则的过度不自主运动。癫痫性痉挛的特征是腰部反复屈曲以及手臂屈曲或伸展。自动症的特征是协调的、重复性的运动活动,如咂嘴、轻拍或吞咽。局灶性运动性发作后,患者可能出现受累肌肉的短暂、功能性和局限性麻痹,称为托德麻痹。这种麻痹可持续数分钟至数小时,通常与局灶性运动性发作的持续时间成比例。这种癫痫后麻痹是由于受累致痫区持续的局灶性功能障碍引起的,是局灶性发作的特征。其重要的临床价值在于确定发作起始半球的位置,且常被误诊为中风。局灶性非运动性发作的临床表现包括自主神经、行为停止、认知、情感或感觉症状。自主神经发作的特征是血压、心率、出汗、皮肤颜色变化或胃肠道不适。行为停止发作的特征是运动停止。认知发作的特征是语言或思维异常,如似不相识感、似曾相识感、幻觉和错觉的视觉化。情感发作的特征是情感变化,如恐惧、 dread、焦虑或愉悦。表现为发笑的非运动性发作称为痴笑性发作,表现为哭泣的称为哭性发作。感觉发作的特征是感觉变化,如视觉、感觉异常、听力、嗅觉或疼痛的异常感觉。有时,局灶性运动性发作和局灶性非运动性发作可演变为双侧强直阵挛发作。
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