Many children, adolescents, and adults with Attention Deficit Disorders report chronic difficulties with falling asleep, awakening and/or maintaining adequate daytime alertness. These problems may be due to a variety of factors, including environment, lifestyle, and psychiatric comorbidities. Impairments in sleep/arousal may also be related more directly to the underlying pathophysiology of ADD. This chapter describes clinical manifestations of sleep/arousal problems often associated with ADD and reviews behavioral and medication options for treatment.

Objectives Memory impairment is one of the most prominent cognitive deficits in temporal lobe epilepsy (TLE). The overall goal of this study was to explore the contribution of cortical and hippocampal (subfield) damage to impairment of auditory immediate recall (AIMrecall), auditory delayed recall (ADMrecall), and auditory delayed recognition (ADMrecog) of the Wechsler Memory Scale III (WMS-III) in TLE with (TLE–MTS) and without hippocampal sclerosis (TLE-no). It was hypothesized that volume loss in different subfields determines memory impairment in TLE–MTS and temporal neocortical thinning in TLE-no. Methods T1 whole brain and T2-weighted hippocampal magnetic resonance imaging and WMS-III were acquired in 22 controls, 18 TLE–MTS, and 25 TLE-no. Hippocampal subfields were determined on the T2 image. Free surfer was used to obtain cortical thickness averages of temporal, frontal, and parietal cortical regions of interest (ROI). MANOVA and stepwise regression analysis were used to identify hippocampal subfields and cortical ROI significantly contributing to AIMrecall, ADMrecall, and ADMrecog. Results In TLE–MTS, AIMrecall was associated with cornu ammonis 3 (CA3) and dentate (CA3&DG) and pars opercularis, ADMrecall with CA1 and pars triangularis, and ADMrecog with CA1. In TLE-no, AIMrecall was associated with CA3&DG and fusiform gyrus (FUSI), and ADMrecall and ADMrecog were associated with FUSI. Conclusion The study provided the evidence for different structural correlates of the verbal memory impairment in TLE–MTS and TLE-no. In TLE–MTS, the memory impairment was mainly associated by subfield-specific hippocampal and inferior frontal cortical damage. In TLE-no, the impairment was associated by mesial–temporal cortical and to a lesser degree hippocampal damage.

Summary:Purpose: To investigate the relation between the number and spatial distribution of language sites and specific patient-and epilepsy-related variables.Methods: Patients with stimulation-induced reading or naming errors from anterior or inferior temporal cortex (i.e., atypical temporal language sites) were compared with those with language sites confined to Wernicke's area (WA) in the posterosuperior temporal and inferior parietal perisylvian area. In a consecutive series of 44 left hemisphere language dominant patients with complex partial seizures before left temporal lobectomy, correlations were compared between cortical language distribution and measures of cognitive function.Results: Patients with atypical temporal language sites (group 1) had significantly fewer years of education that did patients with language sites in WA (group 2). Patients in group 1 had poorer verbal learning and fluency than did patients in group 2. Patients with IQ 4 0 were significantly more likely to have multiple sites where stimulation disrupted language than did patients with normal IQ. Number of language sites had significant negative correlations with full-scale IQ, and measures of confrontation naming, verbal fluency, and immediate verbal memory. Conclusions: Language cortex has a wider spatial distribution in epilepsy surgery patients with lower intelligence, poorer education, and worse verbal and memory skills. Key Words: Epilepsy-Language-Electrical stimulation-Temporal lobe.Primary language functions usually localize to peri-METHODS sylvian regions of the left hemisphere ( I -3). However, cortical-stimulation studies of surgical epilepsy patients suggest that language functions are represented in a broader field outside of immediate perisylvian regions (4,5). Individual differences in language localization result from genetic and environmental factors, lesion variables (e.g., age of onset, time course, etiology, location, and size) and epilepsy-related variables (e.g., age of onset, seizure frequency and type, abundance of interictal epileptiform activity) (1,(4)(5)(6). This study examined these factors relating to atypical language localization in patients with temporal lobe epilepsy undergoing cortical stimulation. SubjectsWe identified all patients with left hemisphere language dominance by Wada testing and left temporal lobe complex partial seizure onsets by scalp/sphenoidal video-EEG recordings who underwent cortical language mapping from 1991 to 1996. Forty-four subjects fulfilled these criteria: 21 men, 23 women with a mean age of 30.6 k 7.2 years (SD). Mean age of chronic seizure onset was 10.5 t-9.5 years; mean education was 13.4 t-2.1 years, and mean full-scale IQ (FSIQ) was 88.6 t-12.8. Seven patients were not right-handed. Thirteen patients had structural lesions other than mesial temporal sclerosis: atrophy, six; low-grade neoplasm, three; focal encephalomalacia after traumatic brain injury, one; vascular malformation, one; periventricular increased signal, 1. Sixteen subjects had a history of febrile...

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