Focal seizures in the older child and adolescent are usually similar in presentation to the adult. However, children with profound developmental delay may still display an immature seizure semiology. Stereotyped seizure patterns suggesting focal origin apart from benign epilepsy syndromes should prompt a search for a structural lesion. If seizures persist despite aggressive AED treatment, referral for presurgical evaluation is appropriate.1
In this age group, semiology can be informative not only with regard to lobe of seizure origin but also as in the case of the frontal lobe, the particular region of involvement (see Table 19–1). The seizure semiology may also indicate lateralization (see Table 19–2). Frontal lobe seizures are typically brief (<30 seconds), and rapid in onset and offset with almost immediate recovery. They typically occur in clusters, and often occur out of sleep. Seizures arising from rolandic and primary motor cortex typically involve clonic movement of one side of the body. Supplementary motor area seizures involve sudden onset of an asymmetric “fencing” posture of the upper limbs. Hypermotor activity and ictal hallucinations are reported in orbitofrontal seizures, and fear/laughter in seizures arising from the cingulate gyrus. Mesial temporal lobe seizures classically present with an aura, most commonly of fear or epigastric sensation (rising feeling from the abdomen). Some degree of behaviural arrest may follow with or without impaired awareness, or confusion with ictal or postictal dysphasia. Automatisms, most commonly oroalimentary (e.g., swallowing, lip smacking) or motor (picking) may also occur. Seizures typically last 60–90 seconds, followed by a period of recovery, with or without confusion. Lateral or posterior temporal onset seizures often have similar characteristics, although the aura typically differs, for example, auditory or complex visual changes.
Frontal lobe seizures Opercular Orbitofrontal Perirolandic Supplementary motor area Dorsolateral frontal Cingulate gyrus | Sudden offset/onset, short duration, nocturnal, clusters, brief or absent postictal confusion2,3 Profuse salivation, oral facial apraxia, and possibly some focal facial clonic activity Autonomic changes and heightened motor activity (hypermotor seizures) Typically motor with unilateral clonic jerking contralateral face and limbs Speech arrest and “fencing” posture, with asymmetric motor movements and contralateral head and eye version Contralateral head and eye tonic elevation and contralateral clonic movements arms and face Intense fright, facial expression of fear, incomplete loss of awareness |
Temporal lobe seizures Mesial Lateral neocortical Posterior basal | Aura, longer duration, postictal confusion Abdominal aura or fear, oroalimentary/motor automatisms Auditory, vertiginous and complex visual aurae, early contralateral dystonic posturing in the absence of oral alimentary automatisms, early loss of contact, shorter seizure duration Behavioral arrest followed by motor manifestations (mainly contralateral head version and contralateral arm tonic stiffening)4 |
Parietal lobe seizures | Somatosensory aura, or relatively silent until anterior propagation5 |
Occipital lobe seizures | Elementary visual hallucinations, ictal amaurosis, rapid eye blinking, sensations of eye movement6 |
Contralateral signs
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Ipsilateral signs
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Dominant hemisphere
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Nondominant hemisphere
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Occipital seizures present with an aura of an elementary visual hallucination that can often be described in detail (see Fig. 19–1). The aura is then variably followed by contralateral eye deviation. Ictal vomiting or retching (ictus emeticus) may or may not be prominent. Ictal nystagmus is observed more commonly with involvement of the temporal parietal occipital junction. Aurae are reported in 80%–90% of children with occipital or temporal lobe seizure onset. Parietal seizure onset is associated with nonspecific features. Sensory aura may be apparent, but other features such as atonic attacks result from rapid spread to motor cortex.

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