The prevalence of DAA/HCD or ADHD in young adult prison inmates is significantly elevated when compared to nondelinquent controls. Generally the population of young adult male prison inmates exhibits a considerable psychiatric morbidity. Of the total sample, 64% suffered from at least 2 disorders. Only 8.5% had no psychiatric diagnoses. This indicates the urgent need for more psychiatric expertise in young offender facilities.

We report on the development of a German self-rating behaviour questionnaire (ADHD-SR) and diagnostic checklist (ADHD-DC) for the diagnosis of attention-deficit/hyperactivity disorder in adults according to DSM IV and ICD 10 research criteria. When comparing self-rating with expert rating, we found good concordance measured by intraclass coefficients on the level of single symptoms and syndrome scores. High retest reliability of the ADHD-SR demonstrated the ability to assess time-stable behaviour traits. Evaluation of the psychometric properties revealed good internal consistency and adequate convergent and divergent validity measured by the "big five" derived from the NEO-FFI and the constructs impulsivity, venturesomeness, and empathy of Eysenck's impulsiveness questionnaire. We detected a remarkable correlation with the Wender Utah Rating Scale, which targets the detection of childhood ADHD symptoms. Diagnostic sensitivity for different cutoff points was calculated by ROC analysis at 65--88%. Specificity was 67% to 92%.

There is evidence that disturbances in central serotonin (5-HT) function have a role in impulsive aggression, violence, and criminality. A deletion/insertion polymorphism within the 5-HT transporter (5-HTT) promoter gene (5-HTT gene-linked polymorphic region, 5-HTTLPR) is thought to be associated with several psychopathological phenotypes related to disturbed impulse control, anxiety and depression. This study examined the association of the 5-HTTLPR with violent behavior in a sample of 153 male Caucasians referred for a forensic psychiatric examination. We found a significant excess of the short (s) allele and the s/s genotype in patients characterized by recurrent and overt physical violent behavior. This genetic variance explained 5% of the variance of violent behavior. When controlled for the impact of several psychopathologies related to violent behavior, this association was observed in individuals with a history of childhood attention deficit/hyperactivity disorder (ADHD)-related symptoms, but not presenting with personality disorder or increased impulsiveness. In conclusion, the results (i). suggest an association between serotonergic dysfunction and violent behavior, (ii). provide evidence for an-at least partial-genetic regulation of violent behavior in a subgroup of male offenders, and (iii). suggest a significant role for 5-HT transporter functionality for violent behavior.

Recent studies using transcranial sonography (TCS) have provided evidence of alterations in the mesencephalic midline structures in patients with unipolar depression and depression in Parkinson's disease (PD), suggesting an involvement of the basal limbic system in primary and secondary mood disorders. This study tested the hypothesis of brainstem midline abnormality in depression and investigated 31 PD patients by magnetic resonance imaging (MRI) and TCS. Signal intensity of the pontine and mesencephalic brainstem midline was rated on T2-weighted images and measured by relaxometry. In addition, two blinded investigators assessed the echogenicity of the brainstem midline by TCS. The severity of motor symptoms and depression were graded independently using standard research scales. Rating of signal intensity and T2 relaxometry of the pontomesencephalic midline structures revealed significant difference between depressed and nondepressed PD patients (P < 0.05). This corresponded to a significant reduction in mesencephalic midline echogenicity of depressed PD patients on TCS images. No correlation was found between raphe signal intensity, T2 relaxation times, or TCS echogenicity and the severity of motor symptoms or depression. This study is the first to show changes in signal intensity and T2 relaxation time of the pontomesencephalic midline structures on MRI in depressed PD patients confirming previous TCS findings. As these midline structures comprise fiber tracts and nuclei of the basal limbic system, the findings may support the hypothesis of an alteration in the basal limbic system in mood disorders.

We report the transcranial sonography (TCS) findings of the basal ganglia in 86 patients with dystonic disorders including idiopathic dystonia (facial, cervical, upper limb, and generalized dystonia), drug-induced tardive dystonia, dopa-responsive dystonia, and kinesigenic dystonia. The TCS was focused on alterations of the lenticular, caudate, raphe nuclei, and the thalamus. Seventy-five percent of patient with idiopathic cervical and 83% of those with idiopathic upper limb dystonia had a hyperechogenic lesion of the middle segment of the lenticular nucleus on the side opposite to the clinical dystonic symptoms. The ipsilateral side was also affected in 20%. In facial dystonia, only one-third of the patients revealed lenticular nucleus lesions. The mean area of the lenticular nucleus lesion opposite to the clinically affected side was 30 mm2 in cervical dystonia, 17 mm2 in upper limb dystonia, and 7.5 mm2 in facial dystonia. These lenticular abnormalities were significantly more frequent (p < 0.001) and their areas were significantly greater (p < 0.001) compared with a control group of 50 patients afflicted with radiculopathy. There was a significant correlation of the severity of symptoms with the intensity of lenticular nucleus hyperechogenicity in patients with cervical and upper limb dystonia (p < 0.05). Increased caudate nucleus echogenicity was present in 20% of patients with cervical and upper limb dystonia, mostly contralateral to the clinically affected side and raphe abnormalities were present in 7% of all patients with idiopathic dystonia. In contrast, there were no abnormalities of the lenticular nucleus or thalamus in nonidiopathic dystonias. We conclude that idiopathic dystonia is associated with lesions in the basal ganglia, particularly the lenticular nucleus, that can be visualized by TCS. An alteration of the basal ganglia matrix may be the pathologic basis of idiopathic dystonia with secondary affliction of striatopallidothalamic pathways.