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Tic disorders typically start in early childhood and can be classified into provisional tic disorder (tics last <12 months) and chronic tic disorders (tics last > 12 months). The widely known chronic tic disorder Tourette's syndrome is featuring multiple motor and vocal tics. Tics are typically waxing and waning in frequency and intensity. Concentration and relaxation might decrease tics, whereas stress and excitement might increase tics. Psychiatric comorbidities, like obsessive-compulsive disorder, ADHD, depression and anxiety are common. The etiology is multifactorial with genetic and environmental interactions leading to a dysregulation of cortico-striato-pallido-thalamo-cortical networks.A correct diagnosis and psychoeducation are essential for patients as well as their relatives. Additional therapies are needed for patients with severe tics that cause physical impairment or great psychosocial stress. It is crucial to also treat psychiatric comorbidities. Psychotherapeutic interventions for tics include progressive muscle relaxation, habit reversal training, exposure and response prevention and comprehensive behavioral intervention for tics. First-line psychopharmacological treatment in Europe contains aripiprazole, tiapride and risperidone, which are all used off-label for tic disorders. Haloperidol remains the only approved medication for the pharmacotherapy of tics in Germany, but is rarely used due to its side effects. Cannabinoids gain interest as a new pharmacological option, but are mainly offered within the frame of studies., Competing Interests: Dr. Richard Musil hat Vortragshonorare von Otsuka/Lundbeck erhalten. Die Autoren sind Mitglied in der Europäischen Tourette-Gesellschaft (ESSTS) und sind an klinischen Multicenterstudien im Bereich Tourette beteiligt, die von öffentlichen Trägern (DFG, BMBF, EU) oder pharmazeutischen Unternehmen gefördert werden., (© Georg Thieme Verlag KG Stuttgart · New York.)

The pathophysiological mechanism leading to dopaminergic dysfunction in schizophrenia is still unclear. Inflammation seems to play a key role. A dysfunction in the activation of the type 1 immune response is associated with decreased activity of the key enzyme of the tryptophan/kynurenine metabolism, indolamine-2.3-dioxygenase (IDO), results in a higher production of kynurenine acid (KYNA)--an N-methyl-D-aspartate antagonist--in the central nervous system (CNS) and decreased glutamatergic neurotransmission. The differential activation of microglial cells and astrocytes, which serve as immune cells in the CNS, contributes to the TH1-TH2 immune imbalance. Antipsychotics, all acting as dopamine D2 receptor antagonists show several shortcomings. The immune effects of antipsychotics rebalance partly the imbalance of the type-1/type-2 immune response and the overproduction of KYNA. The inflammation is associated with higher prostaglandin E2 (PGE2) production and higher cyclo-oxygenase-2 (COX-2) expression. Increasing evidence from clinical studies with COX-2 inhibitors points to an advantageous effect of anti-inflammatory therapy in schizophrenia, especially in the early stages of the disease. Further options of immunomodulatory therapy in schizophrenia are discussed., (© Georg Thieme Verlag KG Stuttgart · New York.)