Development and psychometric properties of the ADHD-SCL-90-R screening scale for adult ADHD.

OBJECTIVE: Adult attention-deficit/hyperactivity disorder (ADHD) is a prevalent disorder with serious impairments, but it often remains undetected. The aim of the study was to develop an ADHD screening scale from the Symptom Check-List-90-R (SCL-90-R) and describe its psychometric properties. The item selection was based on the ADHD-specific Conners' Adult ADHD Rating Scale (CAARS-S:L). METHOD: In total, 412 subjects of an ADHD Special Consultations Unit were investigated, who completed the SCL-90-R, CAARS-S:L, and ADHD Self-Rating Behavior Questionnaire. RESULTS: The ADHD-SCL-90-R Screening Scale consisted of 16 items with a four-factor structure, including Inattention/Memory Problems, Hyperactivity/Restlessness, Impulsivity/Emotional Lability, and Problems with Self-Concept. It showed excellent internal consistency (Cronbachs α = .90) and good convergent validity (r = .57-.59). Sensitivity was 78%, specificity was 56%, and the discriminatory power was acceptable (area under the curve = 0.74). CONCLUSION: The newly developed ADHD-SCL-90-R Screening Scale showed good psychometric properties, and it has a versatile application in clinical practice.

The epilepsy-linked Lgi1 protein assembles into presynaptic Kv1 channels and inhibits inactivation by Kvbeta1.

The voltage-gated potassium (Kv) channel subunit Kv1.1 is a major constituent of presynaptic A-type channels that modulate synaptic transmission in CNS neurons. Here, we show that Kv1.1-containing channels are complexed with Lgi1, the functionally unassigned product of the leucine-rich glioma inactivated gene 1 (LGI1), which is causative for an autosomal dominant form of lateral temporal lobe epilepsy (ADLTE). In the hippocampal formation, both Kv1.1 and Lgi1 are coassembled with Kv1.4 and Kvbeta1 in axonal terminals. In A-type channels composed of these subunits, Lgi1 selectively prevents N-type inactivation mediated by the Kvbeta1 subunit. In contrast, defective Lgi1 molecules identified in ADLTE patients fail to exert this effect resulting in channels with rapid inactivation kinetics. The results establish Lgi1 as a novel subunit of Kv1.1-associated protein complexes and suggest that changes in inactivation gating of presynaptic A-type channels may promote epileptic activity.