Purpose of review
This review presents a critical appraisal of current therapeutic strategies for tics in patients with Tourette syndrome (TS) and other chronic tic disorders. We discuss the most ...recent evidence to support behavioural/psychosocial, pharmacological and surgical interventions in patients with tics and summarize existing recommendations about treatment selection. We also indicate the main knowledge gaps regarding efficacy, safety and prioritization of interventions and provide a summary of the emerging therapeutic approaches.
Recent findings
During the past few years, high-quality randomized controlled trials have documented the efficacy and safety of the Comprehensive Behavioural Intervention for Tics (CBIT), based on the habit reversal training strategy. Preliminary data encourage larger trials of the online, remotely delivered, therapist-supported format of CBIT and exposure response prevention. Antipsychotic medications, with recent evidence supporting in particular the use of aripiprazole, and alpha agonists remain the main pharmacological options, alongside botulinum toxin injections for the treatment of simple motor tics. Emerging pharmacological options include ecopipam, a D1-selective dopamine agonist, and endocannabinoid modulators. Increasing experience with thalamic and pallidal deep brain stimulation is paving the way to the development of closed loop approaches and an anticipation of the age limit for consideration of this surgical treatment in otherwise refractory and disabled patients.
Summary
Behavioural therapy should be considered as a first line of active intervention for tics, given its demonstrated efficacy and high tolerability. Pharmacological options (antipsychotics, alpha agonists, topiramate) should be considered if a rapid effect is sought or there is poor feasibility or adherence to behavioural treatments. Deep brain stimulation of the centromedian/parafascicularis thalamic nuclei or globus pallidus internus should be considered for patients refractory to less active interventions, but more evidence is required to support target selection and identify predictors of response to this invasive approach.
Full text
Available for:
EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
In the afternoon of 2 August 1618, a fire broke out in the Weimar Residenzschloss. In a matter of hours, the flames ravaged the church of St Martin, the princely apartments, and the reception rooms ...located in the east and north Wing Of the castle. The conflagration seems to have been caused by an explosion in the workshop of Samuel Kluge, a Bohemian alchemist.' Duke Johann Ernst 'der Jungere' (the Younger) von Sachsen-Weimar (1594 — 1626)' had hoped that the fruits of Kluge's experiments might supplement his revenue; instead, he had to find additional funds to finance the reconstruction Of his castle. The assembled estates of Sachsen-Weimar agreed to an extraordinary tax to pay for the building in March 1619; works began shortly thereafter.' A ground plan of the new Weimar Residenz- schloss is kept in the Graphische Sammlungen of the Klassik Stiftung Weimar (fig. Only a portion of the planned building - the south-eastern pavilion, containing the new church — was effectively constructed, between 1619 and 1630. Anonymous and undated, the ground plan has been attributed to Giovanni Bonalino (c. 1575 — c. 1633), a master-builder from Roveredo, in the Grisons, who directed the reconstruction works of the Weimar Residenzschloss from 1619 to 1623.' As the present article shows, the author of the ground plan, and mastermind of the whole reconstruction project, was actually the Florentine polymath Costantino de' Servi (1554— 1622), whose presence in Weimar in 1618 — 1619 has so far been overlooked.
•We review the relationship between core, social and moral disgust in clinical models.•Abnormal insula activity affects all the three domains of disgust processing.•5-HT alterations predict core and ...moral disgust in clinical models.
Disgust is a multifaceted experience that might affect several aspects of life. Here, we reviewed research on neurological and psychiatric disorders that are characterized by abnormal disgust processing to test the hypothesis of a shared neurocognitive architecture in the representation of three disgust domains: i) personal experience of ‘core disgust’; ii) social disgust, i.e., sensitivity to others’ expressions of disgust; iii) moral disgust, i.e., sensitivity to ethical violations. Our review provides some support to the shared neurocognitive hypothesis and suggests that the insula might be the “hub” structure linking the three domains of disgust sensitivity, while other brain regions may subserve specific facets of the multidimensional experience. Our review also suggests a role of serotonin core and moral disgust, supporting “neo-sentimentalist” theories of morality, which posit a causal role of affect in moral judgment.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Functional neurological disorder (FND) is a common cause of persistent and disabling neurological symptoms. These symptoms are varied and include abnormal control of movement, episodes of altered ...awareness resembling epileptic seizures and abnormal sensation and are often comorbid with chronic pain, fatigue and cognitive symptoms. There is increasing evidence for the role of neurologists in both the assessment and management of FND. The aim of this review is to discuss strategies for the management of FND by focusing on the diagnostic discussion and general principles, as well as specific treatment strategies for various FND symptoms, highlighting the role of the neurologist and proposing a structure for an interdisciplinary FND service.
Full text
Available for:
EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Treatment Recommendations for Tardive Dyskinesia Ricciardi, Lucia; Pringsheim, Tamara; Barnes, Thomas R.E. ...
Canadian journal of psychiatry,
06/2019, Volume:
64, Issue:
6
Book Review, Journal Article
Peer reviewed
Open access
Background:
Tardive dyskinesia is a movement disorder characterised by irregular, stereotyped, and choreiform movements associated with the use of antipsychotic medication. We aim to provide ...recommendations on the treatment of tardive dyskinesia.
Methods:
We performed a systematic review of studies of the treatment of tardive dyskinesia. Studies were rated for methodological quality using the American Academy of Neurology Risk of Bias Classification system. Overall level of evidence classifications and grades of recommendation were made using the Scottish Intercollegiate Guidelines Network framework.
Results:
Preventing tardive dyskinesia is of primary importance, and clinicians should follow best practice for prescribing antipsychotic medication, including limiting the prescription for specific indications, using the minimum effective dose, and minimising the duration of therapy. The first-line management of tardive dyskinesia is the withdrawal of antipsychotic medication if clinically feasible. Yet, for many patients with serious mental illness, the discontinuation of antipsychotics is not possible due to disease relapse. Switching from a first-generation to a second-generation antipsychotic with a lower D2 affinity, such as clozapine or quetiapine, may be effective in reducing tardive dyskinesia symptoms. The strongest evidence for a suitable co-intervention to treat tardive dyskinesia comes from tests with the new VMAT inhibitors, deutetrabenazine and valbenazine. These medications have not been approved for use in Canada.
Conclusion:
Data on tardive dyskinesia treatment are limited, and the best management strategy remains prevention. More long-term safety and efficacy data are needed for deutetrabenazine and valbenazine, and their routine availability to patients outside of the USA remains in question.
Full text
Available for:
NUK, OILJ, SAZU, UKNU, UL, UM, UPUK
In 2011 a working group of the European Society for the Study of Tourette Syndrome (ESSTS) has developed the first European assessment guidelines for Tourette syndrome (TS). Now, we present an ...updated version 2.0 of these European clinical guidelines for Tourette syndrome and other tic disorders, part I: assessment. Therefore, the available literature has been thoroughly screened, supplemented with national guidelines across countries and discussions among ESSTS experts. Diagnostic changes between DSM-IV and DSM-5 classifications were taken into account and new information has been added regarding differential diagnoses, with an emphasis on functional movement disorders in both children and adults. Further, recommendations regarding rating scales to evaluate tics, comorbidities, and neuropsychological status are provided. Finally, results from a recently performed survey among ESSTS members on assessment in TS are described. We acknowledge that the Yale Global Tic Severity Scale (YGTSS) is still the gold standard for assessing tics. Recommendations are provided for scales for the assessment of tics and psychiatric comorbidities in patients with TS not only in routine clinical practice, but also in the context of clinical research. Furthermore, assessments supporting the differential diagnosis process are given as well as tests to analyse cognitive abilities, emotional functions and motor skills.
Full text
Available for:
DOBA, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, MFDPS, NLZOH, NUK, ODKLJ, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, SIK, UILJ, UKNU, UL, UM, UPUK, VKSCE, VSZLJ, ZAGLJ
The purpose of this study was to examine associations between physical activity, sleep and symptom severity in children with tic disorders. Children with tic disorders wore the GeneActiv device, a ...wrist-worn accelerometer that measures physical activity intensity and sleep/wake parameters continuously for seven days, and completed questionnaires on sleep quality, exercise and severity of tics, ADHD, obsessive–compulsive behaviours, anxiety and depression. 110 children participated in the study. Children with more severe tics had significantly more frequent comorbid diagnoses, greater impairment in subjective sleep measures, greater sedentary activity time and less light, moderate and vigorous activity time (all
p
< 0.05). There was a significant negative correlation between light, moderate and vigorous physical activity and the severity of tics (− 0.22,
p
= 0.04), obsessive compulsive behaviours (− 0.22,
p
= 0.03), anxiety (− 0.35,
p
= 0.0005) and depression (− 0.23,
p
= 0.03). There was no correlation between objective sleep time, sleep efficiency and symptom severity. Subjective sleep quality was positively correlated with all symptom severity measures, with the strongest correlation with ADHD severity (0.42,
p
< 0.00001). The results of this observational study indicate a small, but significant relationship between activity and sleep measures and the severity of the main symptom domains present in tic disorders.
Full text
Available for:
DOBA, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, MFDPS, NLZOH, NUK, ODKLJ, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, SIK, UILJ, UKNU, UL, UM, UPUK, VKSCE, VSZLJ, ZAGLJ
Gilles de la Tourette syndrome is a common neuropsychiatric disorder spectrum with tics as the defining feature. Comorbidities such as attention-deficit/hyperactivity disorder, obsessive-compulsive ...disorder, and autism spectrum disorder often complicate clinical presentation. Their recognition is paramount for the introduction of efficient treatment strategies to promote healthy development and good quality of life. Here, knowledge on the movement disorder of tics, the spectrum of associated comorbidities, and the list of differential diagnoses of tic disorders are summarized. Also, an account of the prevailing pathophysiologic models of tic generation is provided, and a concise update on contemporary treatment strategies is presented.
Background:
Akathisia is a common and distressing neuropsychiatric syndrome associated with antipsychotic medication, characterised by subjective and objective psychomotor restlessness. The goal of ...this guideline is to provide clinicians with recommendations on the assessment and treatment of akathisia.
Methods:
We performed a systematic review of therapeutic studies assessing the treatment of antipsychotic-induced extrapyramidal symptoms. Forty studies on akathisia and 4 systematic reviews evaluating the adverse effects of antipsychotics were used in the formulation of recommendations. Studies were rated for methodological quality using the American Academy of Neurology Risk of Bias Classification system. The overall level of evidence classifications and grades of recommendation were made using the Scottish Intercollegiate Guidelines Network framework.
Results:
As a good practice point, clinicians should systematically assess akathisia with a validated scale before starting antipsychotics and during antipsychotic dosage titration. For the management of akathisia, there was adequate evidence to allow recommendations regarding antipsychotic dose reduction, antipsychotic polypharmacy, switching antipsychotic medication, and the use of adjuvant medications including beta-blockers, anticholinergics, 5HT2A antagonists, benzodiazepines, and vitamin B6.
Conclusion:
The treatment of antipsychotic-induced akathisia should be personalised, with consideration of antipsychotic dose reduction, cessation of antipsychotic polypharmacy, and switching to an antipsychotic with a perceived lower liability for akathisia, before the use of adjuvant medications. The choice of adjuvant medications should favour the more established treatments, with careful consideration of contraindications and side effects. Limitations in the evidence should be acknowledged and prompt cautious prescribing, particularly with respect to the duration of use of adjuvant medications, is warranted.
Full text
Available for:
NUK, OILJ, SAZU, UKNU, UL, UM, UPUK
The goal of this article is to review the past decade's literature and provide a critical commentary on the involvement of immunological mechanisms in normal brain development, as well as its role in ...the pathophysiology of Tourette syndrome, other Chronic tic disorders (CTD), and related neuropsychiatric disorders including Obsessive-compulsive disorder (OCD) and Attention deficit hyperactivity disorder (ADHD).
We conducted a literature search using the Medline/PubMed and EMBASE electronic databases to locate relevant articles and abstracts published between 2009 and 2020, using a comprehensive list of search terms related to immune mechanisms and the diseases of interest, including both clinical and animal model studies.
The cellular and molecular processes that constitute our "immune system" are crucial to normal brain development and the formation and maintenance of neural circuits. It is also increasingly evident that innate and adaptive systemic immune pathways, as well as neuroinflammatory mechanisms, play an important role in the pathobiology of at least a subset of individuals with Tourette syndrome and related neuropsychiatric disorders In the conceptual framework of the holobiont theory, emerging evidence points also to the importance of the "microbiota-gut-brain axis" in the pathobiology of these neurodevelopmental disorders.
Neural development is an enormously complex and dynamic process. Immunological pathways are implicated in several early neurodevelopmental processes including the formation and refinement of neural circuits. Hyper-reactivity of systemic immune pathways and neuroinflammation may contribute to the natural fluctuations of the core behavioral features of CTD, OCD, and ADHD. There is still limited knowledge of the efficacy of direct and indirect (i.e., through environmental modifications) immune-modulatory interventions in the treatment of these disorders. Future research also needs to focus on the key molecular pathways through which dysbiosis of different tissue microbiota influence neuroimmune interactions in these disorders, and how microbiota modification could modify their natural history. It is also possible that valid biomarkers will emerge that will guide a more personalized approach to the treatment of these disorders.
PDF
