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We investigated primary motor cortex and brain stem plasticity in patients with Gilles de la Tourette syndrome. The study group comprised 12 patients with Gilles de la Tourette syndrome and 24 healthy subjects. Patients were clinically evaluated using the Yale Global Tic Severity Scale. We tested cortical plasticity by conditioning left primary motor cortex with intermittent or continuous theta-burst stimulation in 2 separate sessions. Test stimulation consisted of 20 motor-evoked potentials recorded from right first interosseous muscle before and after theta-burst stimulation. We also tested brain stem plasticity by conditioning the right supraorbital nerve with facilitatory electric high-frequency stimulation delivered at the same time as the late response of the blink reflex or inhibitory high-frequency stimulation delivered before the late response on 2 separate sessions. Test stimulation consisted of 10 blink reflexes from the right orbicularis oculi muscle before and after high-frequency stimulation. After intermittent theta-burst stimulation, motor-evoked potential amplitudes in healthy subjects increased significantly but remained unchanged in patients. Similarly, after continuous theta-burst stimulation, motor-evoked potential amplitudes decreased significantly in healthy subjects but did not in patients. After facilitatory high-frequency stimulation, the blink reflex late response area in healthy subjects increased, whereas after inhibitory high-frequency stimulation, it decreased. Conversely, in patients, both interventions left the blink reflex late response area unchanged. The lack of the expected inhibitory and facilitatory changes in motor-evoked potential amplitudes and blink reflex late response area suggests that abnormal plasticity in the primary motor cortex and brain stem play a role in the pathophysiology of Gilles de la Tourette syndrome.
The term Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infections (PANDAS) was coined by Swedo et al. in 1998 to describe a subset of childhood obsessive-compulsive disorders (OCD) and tic disorders triggered by group-A beta-hemolytic Streptococcus pyogenes infection. Like adult OCD, PANDAS is associated with basal ganglia dysfunction. Other putative pathogenetic mechanisms of PANDAS include molecular mimicry and autoimmune-mediated altered neuronal signaling, involving calcium-calmodulin dependent protein (CaM) kinase II activity. Nonetheless the contrasting results from numerous studies provide no consensus on whether PANDAS should be considered as a specific nosological entity or simply a useful research framework. Herein we discuss available data that could provide insight into pathophysiology of adult OCD, or might explain cases of treatment-resistance. We also review the latest research findings on diagnostic and treatment.
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Deep brain stimulation (DBS) has proved useful for several movement disorders (Parkinson’s disease, essential tremor, dystonia), in which first and/or second line pharmacological treatments were inefficacious. Initial evidence of DBS efficacy exists for refractory obsessive-compulsive disorder, treatment-resistant major depressive disorder, and impulse control disorders. Ethical concerns have been raised about the use of an invasive surgical approach involving the central nervous system in patients with possible impairment in cognitive functioning and decision-making capacity. Most of the disorders in which DBS has been used might present with alterations in memory, attention, and executive functioning, which may have an impact on the mental capacity to give informed consent to neurosurgery. Depression, anxiety, and compulsivity are also common in DBS candidate disorders, and could also be associated with an impaired capacity to consent to treatment or clinical research. Despite these issues, there is limited empirical knowledge on the decision-making levels of these patients. The possible informed consent issues of DBS will be discussed by focusing on the specific treatable diseases.
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