Search

This is a rare side effect of amisulpride-induced phonic and motor tics that completely resolved within 2 weeks of stopping the drug. Naranjo adverse drug effect probability scale is eight, suggests that it's a probable causation of the tics.

This overview on Volkameria inermis (Lamiaceae) is the first in updating information on the chemical constituents and pharmacological properties of the species, notably on its unique ability in ameliorating motor tics. The information was procured from Google, Google Scholar, PubMed, PubMed Central, Science Direct, J-Stage, and PubChem. Previously named Clerodendrum inerme (Verbenaceae), V. inermis is a scrambling or scandent coastal shrub in the tropics and sub-tropics. From different parts of the plant, compounds such as flavonoids, diterpenes/diterpenoids, sterols, triterpenes/triterpenoids, iridoid glycosides, phenolic glycosides, phenylethanoid glycosides (PEGs), phenylpropanoid glycosides (PPGs), chalcones, and sesquiterpenes have been reported. Major pharmacological properties of V. inermis include anti-cancer, anti-inflammatory, antioxidant, hepatoprotective, analgesic, and antibacterial activities. Other properties include anti-tyrosinase, antifungal, neuroprotective, hypotensive, hypoglycemic, amyloid-β aggregation, wound healing, antipyretic, and larvicidal activities. A unique pharmacological property of V. inermis leaf extract, discovered by scientists from Taiwan, is the amelioration of motor tic disorders, a spectrum of Tourette syndrome. This property included a case report, three in vivo studies, and one patent. Areas of further research of V. inermis are suggested.

Cholinergic interneurons in the striatum, also known as tonically active interneurons or TANs, are thought to have a strong effect on corticostriatal plasticity and on striatal activity and outputs, which in turn play a critical role in modulating downstream basal ganglia activity and movement. Striatal TANs can exhibit a variety of firing patterns and responses to synaptic inputs; furthermore, they have been found to display various surges and pauses in activity associated with sensory cues and reward delivery in learning as well as with motor tic production. To help explain the factors that contribute to TAN activity patterns and to provide a resource for future studies, we present a novel conductance-based computational model of a striatal TAN. We show that this model produces the various characteristic firing patterns observed in recordings of TANs. With a single baseline tuning associated with tonic firing, the model also captures a wide range of TAN behaviors found in previous experiments involving a variety of manipulations. In addition to demonstrating these results, we explain how various ionic currents in the model contribute to them. Finally, we use this model to explore the contributions of the acetylcholine released by TANs to the production of surges and pauses in TAN activity in response to strong excitatory inputs. These results provide predictions for future experimental testing that may help with efforts to advance our understanding of the role of TANs in reinforcement learning and in motor disorders such as Tourette's syndrome. [ABSTRACT FROM AUTHOR]

Background Experimental findings and theoretical models have associated Tourette syndrome with abnormal striatal inhibition. The expression of tics, the hallmark symptom of this disorder, has been transiently induced in non-human primates and rodents by the injection of GABA A antagonists into the striatum, leading to temporary disinhibition. New method The novel chronic model of tic expression utilizes mini-osmotic pumps implanted subcutaneously in the rat’s back for prolonged infusion of bicuculline into the dorsolateral striatum. Results Tics were expressed on the contralateral side to the infusion over a period of multiple days. Tic expression was stable, and maintained similar properties throughout the infusion period. Electrophysiological recordings revealed the existence of tic-related local field potential spikes and individual neuron activity changes that remained stable throughout the infusion period. Comparison with existing methods The striatal disinhibition model provides a unique combination of face validity (tic expression) and construct validity (abnormal striatal inhibition) but is limited to sub-hour periods. The new chronic model extends the period of tic expression to multiple days and thus enables the study of tic dynamics and the effects of behavior and pharmacological agents on tic expression. Conclusions The chronic model provides similar behavioral and neuronal correlates of tics as the acute striatal disinhibition model but over prolonged periods of time, thus providing a unique, basal ganglia initiated model of tic expression. Chronic expression of symptoms is the key to studying the time varying properties of Tourette syndrome and the effects of multiple internal and external factors on this disorder. [ABSTRACT FROM AUTHOR]

Purpose: Tics can be considered hyperkinetic movements akin to restless leg syndrome (RLS). Drawing the analogy of iron deficiency as an etiology of RLS, it is conceivable that iron deficiency may underlie or worsen tics in Tourette syndrome (TS). The purpose of this study was to evaluate the relationship between serum ferritin levels and tic severity, as well as consequent impact on life, in children with TS. Methods: Children <18 years, diagnosed with TS during 2009-2015, were reviewed. Only those with serum ferritin testing were included. The following data were collected: tic severity, impact on life, medication, comorbidities, blood count, and serum ferritin at diagnosis and follow-up. Results: In fifty-seven patients, M:F = 2:1, serum ferritin was 48.0 ± 33.28 ng/mL, tic severity score 2.3 ± 0.80, impact on life score 2.2 ± 0.93, and composite score 4.57 ± 1.6. Serum ferritin was not influenced by comorbid obsessive compulsive disorder (OCD), attention deficit hyperactive disorder (ADHD), or anxiety ( P > 0.16). Thirty-eight percent with low serum ferritin (≤50 ng/mL) ( n = 37) had severe tics (>5 composite score), compared with 25% in normal ferritin group ( n = 20). Over 6-12 months, tic severity score improved in both iron treated groups, deficient (2.70 to 1.90) and sufficient (2.40 to 1.95), whereas tics worsened or remained the same when not treated with iron. Conclusions: Our data suggest iron deficiency may be associated with more severe tics with higher impact on TS children, independent of the presence of OCD, ADHD, or anxiety. Iron supplementation showed a trend towards improvement of tic severity upon follow-up. We suggest a double-blind, placebo-controlled prospective study to reach a definite conclusion. [ABSTRACT FROM AUTHOR]

Background: Tics and Tourette syndrome are common problems evaluated by both the general pediatrician and pediatric neurologist. The common comorbidities of tics are well known, but the severe neurological complications are rare and may not be appreciated.Methods: This is a retrospective case series and literature review.Results: We present here four adolescents with Tourette syndrome who had severe neurological complications secondary to motor tics. We provide the history, neurological examination, and radiological findings in addition to a review of previously reported cases of vascular and cervical cord complications associated with violent motor tics.Conclusions: We highlight the importance of recognizing the presenting signs of these complications early and the need to vigorously treat violent motor tics to prevent significant neurological complications. [ABSTRACT FROM AUTHOR]

Background Since its first application in 1999, the potential benefit of deep brain stimulation (DBS) in reducing symptoms of otherwise treatment-refractory Tourette syndrome (TS) has been documented in several publications. However, uncertainty regarding the ideal neural targets remains, and the eventuality of so far undocumented but possible negative long-term effects on personality fuels the debate about the ethical implications of DBS. Methods In this prospective open-label trial, eight patients (three female, five male) 19–56 years old with severe and medically intractable TS were treated with high-frequency DBS of the ventral anterior and ventrolateral motor part of the thalamus. To assess the course of TS, its clinical comorbidities, personality parameters, and self-perceived quality of life, patients underwent repeated psychiatric assessments at baseline and 6 and 12 months after DBS onset. Results Analysis indicated a strongly significant and beneficial effect of DBS on TS symptoms, trait anxiety, quality of life, and global functioning with an apparently low side-effect profile. In addition, presurgical compulsivity, anxiety, emotional dysregulation, and inhibition appeared to be significant predictors of surgery outcome. Conclusions Trading off motor effects and desirable side effects against surgery-related risks and negative implications, stimulation of the ventral anterior and ventrolateral motor part of the thalamus seems to be a valuable option when considering DBS for TS. [ABSTRACT FROM AUTHOR]

Tourette syndrome (TS) is a common childhood-onset disorder characterized by motor and vocal tics that are typically accompanied by a multitude of comorbid symptoms. Pharmacological treatment options are limited, which has led to the exploration of deep brain stimulation (DBS) as a possible treatment for severe cases. Multiple lines of evidence have linked TS with abnormalities in the motor and limbic cortico-basal ganglia (CBG) pathways. Neurophysiological data have only recently started to slowly accumulate from multiple sources: noninvasive imaging and electrophysiological techniques, invasive electrophysiological recordings in TS patients undergoing DBS implantation surgery, and animal models of the disorder. These converging sources point to system-level physiological changes throughout the CBG pathway, including both general altered baseline neuronal activity patterns and specific tic-related activity. DBS has been applied to different regions along the motor and limbic pathways, primarily to the globus pallidus internus, thalamic nuclei, and nucleus accumbens. In line with the findings that also draw on the more abundant application of DBS to Parkinson's disease, this stimulation is assumed to result in changes in the neuronal firing patterns and the passage of information through the stimulated nuclei. We present an overview of recent experimental findings on abnormal neuronal activity associated with TS and the changes in this activity following DBS. These findings are then discussed in the context of current models of CBG function in the normal state, during TS, and finally in the wider context of DBS in CBG-related disorders. [ABSTRACT FROM AUTHOR]

Ethnopharmacological relevance Previously, we found a patient with an intractable motor tic disorder that could be ameliorated by the ground leaf juice of Clerodendrum inerme ( CI ). Furthermore, the ethanol extract of CI leaves effectively ameliorated methamphetamine-induced hyperlocomotion (MIH) in mice, an animal model mimicking the hyper-dopaminergic status of tic disorders/Tourette syndrome, schizophrenia, or obsessive–compulsive disorder. Here, we for the first time identified a constituent able to reduce MIH from the CI ethanol extract that might represent a novel lead for the treatment of such disorders. Materials and methods The ethanol extract of CI was sub-divided into n -hexane, dichloromethane, n -butanol and water fractions. Using MIH alleviation as a bioassay, active compounds were identified in these fractions using silica gel chromatography, recrystallization and proton NMR spectroscopy. Results The dichloromethane and n -hexane fractions were active in the bioassay. Further subfractionation and re-crystallization resulted in an active compound that was identified to be hispidulin by proton NMR spectroscopy. Hispidulin significantly alleviated MIH in mice at doses that did not affect their spontaneous locomotor activity or performance in the rotarod test, a measure for motor coordination. Conclusions Hispidulin is a flavonoid that has been isolated from several plants and reported to have anti-oxidative, anti-inflammatory and anti-cancer activities. Here, we for the very first time found that hispidulin can also alleviate MIH at doses that did not impair motor activity, suggesting a therapeutic potential of hispidulin in hyper-dopaminergic disorders. [ABSTRACT FROM AUTHOR]

The problem of comorbid disorders in attention deficit hyperactivity disorder (ADHD) is considered, which occur in at least 60% of patients and lead to additional difficulties in intra-family, school and social adaptation. Children and adolescents with ADHD have a wide range of neurological and somatic disorders caused by complex polygenic pathogenetic mechanisms. Among the pathologies associated with ADHD in this cohort of children, neurotic and anxiety manifestations, motor disorders: dyspraxia, discoordination, impaired gross and fine motor skills, tics, behavioral disorders, enuresis, tension cephalgia are common disorders. Treatment of ADHD should be pathogenetic, taking into account the main symptoms of ADHD and manifestations of comorbid disorders, since it is quite long. When choosing pharmacotherapy, it is preferable to use drugs with verified efficacy not only in the correction of ADHD, but also concomitant behavioral, motor and emotional disorders. Also an important aspect in the pediatric clinic is the use of drugs with a reliable safety profile.

Abstract: Pharmacological animal models of Tourette syndrome (TS) are an important tool for studying the neural mechanisms underlying this disorder. Dysfunction of the cortico-basal ganglia (CBG) system has been widely implicated in TS but the exact nature of this dysfunction is unknown. Pharmacological treatments of TS have prompted multiple hypotheses regarding the involvement of different neuromodulators in the disorder. Pharmacological manipulations in animal models were used to investigate the relationships between these neuromodulators and different symptoms of TS, including motor (tics) and non-motor (sensorimotor gating deficits) phenomena. Models initially focused on the direct effects of pharmacology on behavior, and only recently have begun providing neurophysiological data reflecting the neuronal mechanism linking the two. Animal models support the notion of CBG dysfunction as the neural mechanism underlying TS, and suggest that it may be derived from either direct deficits of local striatal GABAergic networks or a dysfunction of the neuromodulator systems controlling them. These findings can provide the much- needed conceptual construct for the TS etiology and point to new therapeutic targets. [Copyright &y& Elsevier]

Abstract: The term Tourettism refers to Tourette Syndrome (TS)-like symptoms which appear secondary to a variety of both acquired and congenital neurological and neuropsychiatric disorders or following an exposure to several drugs. The association between Tourettism and Multiple Sclerosis (MS) is very rare. Only two cases of patients affected by MS who also showed a simple phonic tic and complex vocal tics respectively have been reported. The case here described reports of a 30 year-old woman affected by secondary-progressive MS who developed, 7 years after the onset of the disease, TS-like symptoms which were responsive to quetiapine. At that time her brain MRI, when compared with the previous scan, showed an increased lesion burden and an increased atrophy in the regions around Sylvian fissures. Considering recent findings on TS, the increased atrophy in these strategic brain regions could be responsible for the tics onset in our patient. At the same time, the diffuse involvement of the white matter and the progressive brain atrophy which we observed could have impaired the cortico-striato-thalamo-cortical circuits consistently implicated in the pathogenesis of TS. In conclusion, we can hypothesize that in our case Tourettism and MS could be considered causal related more than coincidentally associated. [Copyright &y& Elsevier]

Abstract: Objectives: Paliperidone-associated motor tics. Method: Case report. Results: We report a 30-year-old man with schizophrenia who developed motor tics (eye blinking) after treatment of paliperidone up to 15 mg daily. Conclusion: Tic-like symptoms, from simple eye blinking to complex Tourette-like syndrome, may occur during paliperidone treatment, especially with high dose. [Copyright &y& Elsevier]

Based on their phenomenology, tics can be classified as clonic, dystonic, and tonic. Although tic syndromes are considered to be childhood disorders, there are reports on (clonic) tics developing late in life. Literature on dystonic tics is sparse, and it is unclear whether adult-onset dystonic tics are part of the same disorder spectrum that includes Tourette's syndrome or represent a discrete entity. We describe here 11 patients with adult-onset primary dystonic tics. Ten patients (90.1%) were males. Mean age at onset was 42.2 ± 14.9 years. More than 60% had both motor clonic and dystonic tics. Dystonic tics most frequently involved the cranial-cervical region and the shoulders and, less frequently, the limbs. Psychiatric comorbidities were present in 5 patients. Family history for any movement disorder or for psychiatric disorders was present in 2 cases. One patient showed a sensory geste, which allowed him to partially control his tics, whereas another developed overt dystonia 3 years after his first assessment. The hyperkinesias exhibited by these patients were likely consistent with tics. However, other clinical features would allow us to argue that adult-onset dystonic tics may represent a discrete entity, which is intermediate between tics and dystonia.

This review summarizes animal models of Tourette syndrome (TS) and associated tic disorders that have been developed through pharmacological manipulation. These models provide a useful platform to explore the pathophysiology and the therapeutic interventions available for these disorders. The current pharmacological models, primarily using rodents and nonhuman primates, are classified in this review into two major categories depending on the methodology used for administration, that is, systemic and focal (intracerebral) injection protocols. The systemic protocol primarily targets monoamines such as dopamine and serotonin, whereas the focal protocol mainly manipulates local transmission of gamma-aminobutyric acid (GABA). Each category is capable of inducing behavioral abnormalities that are characteristic of TS spectrum disorders, ranging from sensorimotor to cognitive and emotional symptoms to various degrees. Among a variety of pharmacological models, focal microinjection of GABA antagonists into the sensorimotor striatum has helped identify abnormal neural discharge in the global networks which underlie tourettism, including not only the cerebral cortex and basal ganglia but also the cerebellum, consistent with recent neuroimaging studies for TS subjects. This unique model also provides the opportunity to clarify the effect and mechanisms of therapeutic deep brain stimulation. Continuing efforts to incorporate cutting-edge knowledge into the existing models, as well as to combine different model platforms, will allow further refinement of animal models, thereby leading to a greater understanding of TS and associated tic disorders., (© 2013 Elsevier Inc. All rights reserved.)

Hallervorden-Spatz disease (HSD) is a rare autosomal-recessive hereditary disorder characterized by the early onset of progressive movement alterations, including dystonia, rigidity, choreoathetosis, and mental deterioration. HSD is also associated with a variety of psychiatric symptoms, primarily depression and mental deterioration. However, psychosis has rarely been reported as a major symptom of HSD. We report two siblings who presented psychiatric symptoms as major clinical presentations, accompanied by ataxic and spastic gait, dysarthria, and typical neuroimaging findings of HSD. A 14-year-old girl presented complex motor tics, stereotypic behavior and anxiety symptoms. Her older brother, a 16-year-old boy, presented prominent auditory hallucinations, persecutory delusions and social withdrawal symptoms. Psychiatric symptoms were improved after atypical antipsychotic treatment. HSD is a rare disease but should be carefully considered in the diagnosis of patients with both motor disorder and various psychiatric symptoms.