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In a five-year study, 21 patients with multiple tic disorder intolerant of haloperidol therapy were treated with fluphenazine hydrochloride. Sixteen of these patients had fewer side effects with fluphenazine and had either equivalent (five patients) or better (11 patients) tic control. Fluphenazine can be an effective treatment for multiple tics in patients with dose-limiting side effects related to haloperidol.
We report on 8 patients with adult-onset motor tics and vocalisations. Three had compulsive tendencies in childhood and 3 had a family history of tics or obsessive-compulsive behaviour. In comparison with DSM-classified, younger-onset Gilles de la Tourette syndrome, adult-onset tic disorders are more often associated with severe symptoms, greater social morbidity, a potential trigger event, increased sensitivity, and poorer response to neuroleptic medication.
Over the last years evidence on the overlap between tic-disorders (TD) and obsessive compulsive behavior/disorder (OCB/OCD) has increased. The main focus of research have been the phenomenological and epidemiological similarities and differences in samples of different age, primary diagnosis (TD vs. OCD) including the co-occurrence of both. Unfortunately, only a minority of studies included all three groups (TD, TD + OCD, OCD). Nevertheless, new insight concerning possible subtypes for both TD and OCD has been gained. While some authors concentrated on OCD with/without tics we will summarize the field of TD and OCB/OCD from the viewpoint of tics, since OCB plays an important role in patients with TD. Thereby we will not only sharpen the clinicans' awareness of known differences in phenomenology, epidemiology, genetics and neurobiology, aimed to improve their diagnoses and treatment but also highlight the gaps of knowledge and discuss possibilities for further research in this field.
RATIONALE: Family genetic and phenomenological studies support an interrelationship between Gilles de la Tourette syndrome (GTS) and obsessive-compulsive disorder (OCD). Some authors consider GTS as part of a serotonergically mediated cluster of OCD spectrum disorders. OBJECTIVE: To study serotonergic mechanisms in GTS, the effect of the relatively selective 5-HT2c agonist meta-chlorophenylpiperazine (m-CPP) was assessed. METHODS: We studied the behavioural effects of m-CPP on tics, obsessions, compulsions and impulsions of GTS. Twelve medication-free GTS patients (ten men, two women) were included in a single dose 0.5 mg/kg oral m-CPP challenge study with a double-blinded placebo-controlled cross-over design. Global symptom scores, target symptom scores as well as biochemical measures were followed up to 24 h after baseline. RESULTS: While m-CPP caused a significant rise in plasma cortisol and prolactin levels, no significant effects were found on the tics, obsessions and compulsions. Impulsions showed a trend to ameliorate. CONCLUSIONS: This study does not support a predominant role for 5-HT on the tics in GTS. The trend of impulsions to ameliorate after m-CPP can be interpreted as circumstantial support for impulsivity-related 5-HT hypofunctionality in GTS. However, the large variability of m-CPP plasma concentrations found in this study casts doubts upon the reliability of m-CPP as a probe for challenge studies.
COURSE: A 15-year-old boy who had suffered motor tics since age 9 developed progressive cervical myelopathy involving both his hands and his lower extremities. T2-weighted MRI revealed mild canal stenosis and increased signal intensity in the cervical spinal cord beginning at the C-4 level and continuing upward to the medulla oblongata. TREATMENT: After C-3 to C-7 laminoplasty, the patient's clinical symptoms improved. DISCUSSION: It is possible that movement disorders such as tics may contribute to the development of cervical myelopathy owing to the effects of involuntary movements on the neck. Such an intensity change on a T2-weighted image has never been reported in an adolescent tic disorder. Despite such changes, surgical treatment may bring about clinical improvement.
Ear wiggling tics are a rare disorder and there is no reported satisfactory treatment. We had a patient present with ear wiggling tics, which we treated with injections (totaling 40 units) of botulinum toxin A to the pinna muscle (i.e., the auricularis anterior and superior). The tics completely disappeared within 9 days of injection without any side effects.
Tics are involuntary movements that can affect one or more muscles producing simple or complex movements. Blink reflex and startle reflex studies disclose an increased excitability of brainstem interneurons. Analysis of voluntary movement shows that when advance visual information is reduced, patients with tics and Tourette syndrome become progressively slower in completing motor sequences. Sensorimotor integration is abnormally processed. Studies of the contingent negative variation demonstrate abnormalities of movement preparation and the investigation of premotor potentials shows that in some patients tics are not preceded by a normal premotor potential. Magnetic stimulation studies demonstrate an increased excitability of cortical motor cortex. Functional MRI, PET and SPECT studies show abnormal activation of cortical and subcortical areas. Dysfunction of basal ganglia-thalamo-cortical projections affects sensorimotor, language and limbic cortical circuits, and may explain why patients with Tourette syndrome have difficulty in inhibiting unwanted behaviors and impulses.
Tics are the essential component of a variety of disorders, notably Tourette syndrome. Because the mere presence of tics does not require therapeutic intervention, criteria are essential for determining a functional disability. Suggested tic-suppressing treatments have been extremely diverse, including hydrotherapy, behavioral treatments, pharmacotherapy, botulinum toxin, immunomodulatory therapy, and surgery. This manuscript reviews each of these approaches with emphasis on more recent pharmacologic trials.
The effectiveness of awareness training alone in treating multiple tics in a young adult was assessed using a multiple baseline across behaviors design. The results showed that the awareness training was very effective in suppressing both head and facial tics and that the treatment effects generalized to a nonclinic situation. Follow-up data showed that both tics were still at low levels one, two, four and eight months after treatment. Treatment satisfaction ratings by the subject and social validation ratings by independent observers are also reported.
A brief history of the competing response practice treatment for motor and phonic tic reduction is presented, as well as a basic explanation of the procedure. A table defining the competing responses of various tics that have been systematically studied over the past twenty years is also presented. This table is designed to be a reference tool for clinicians and researchers in the treatment of Tourette syndrome and tic disorders.
The objective of the present work was to study the effects of tic disorder (TD) and hyperactivity (HA) on slow cortical potentials in children with combined TD + HA symptoms. Being related to different processes of frontal lobe control over preparatory cortical activity, early and late components of the slow negative potentials (eSNP, ISNP) were examined. SNP amplitude was analyzed as reflecting the sufficiency of preparatory cortical activation; scalp distribution of SNP and relationships to reaction times were studied as revealing the efficiency of task-related region-specific activation. It was hypothesized that if the effects of TD and HA were independent, additive effects on SNP amplitudes would be observed in children with coexisting TD and HA symptoms (TD + HA). Differences in SNP scalp distribution between control and patient groups were predicted to occur mainly over the frontal brain areas. Four groups of children (n = 10/11 in each group) were studied: healthy controls, pure TD, pure attention deficit hyperactivity disorder (ADHD), and combined tic and hyperactivity symptoms. SNPs were recorded in an auditory warned reaction time task (S1-S2-RT) from 8 electrode locations. According to the results, the effects of TD and HA on the sufficiency of task-dependent cortical activation were different, with only the TD factor related to lower SNP amplitudes. Nevertheless, deviant patterns of scalp distribution were found for pure ADHD patients, which suggested an inefficiency in involving the adequate task-related areas. For TD + HA children, like pure TD, lower SNP amplitudes and similar distribution and correlation patterns were present. Thus, according to amplitude, topography, and correlation criteria, TD + HA does not appear to be a subgroup of HA disorder but seems more similar to pure tic disorder.
Developmental stuttering and tics share many clinical and therapeutical aspects. Dopaminergic neurotransmission seems to be involved in the pathophysiology of both, tics and stuttering. We report on a patient with severe stuttering and mild facial tics which were dramatically improved by cocaine, challenging previous reports.
Tourette syndrome, a condition first recognized in 1825, is characterized by the presence of multiple motor tics and one or more phonic tics. Individuals with Tourette syndrome may also demonstrate fluency failures in their speech. This study investigated the disfluencies and phonic tics in an 18-year-old affected male before and after a three week period of speech therapy. It was found that the speech pattern displayed by this subject did not completely conform to the classic pattern of stuttering but did bear more resemblance to cluttering. A limited number of therapy sessions resulted in a significant improvement of speech.
We report a 12-year-old male patient who developed transient motor and vocal tics twelve days after carbon monoxide (CO) poisoning. Cranial magnetic resonance image (MRI) of the patient showed bilateral symmetric hyperintensity in the caudate nucleus and putamen. Tic disorder was successfully treated with haloperidol. Thirty-three months after CO poisoning, the patient was asymptomatic and MRI revealed atrophy in caudate nucleus and putamen. The mechanism of tic disorder in CO intoxication is discussed.
In tic disorders, increased seroreactivity against neuronal antigens has been demonstrated, without performing molecular characterization of antigens. Here, unselected patients with a tic disorder were compared with healthy controls, autistic disorder (AD), and obsessive-compulsive disorder (OCD) patients. Seroreactivity against neuroblastoma cells was analyzed by Western blot. Anti-60 kDa binding occurred significantly more frequently in tic disorder patients (67.1%) than in AD (40.0%), OCD (40.0%) and healthy controls (41.9%). Sequence analysis of the 60 kDa protein band identified this as a ubiquitous heat shock protein. However, the involvement of other autoantigens with a molecular weight of 60 kDa cannot be excluded.
On gray-scale transfontanel sonography, the small arteries supplying the basal ganglia are indistinct from the brain parenchyma in normal infants. Bright linear 'branched candlestick' stripes in these regions, suggesting sonographic lenticulostriate vasculopathy, were reported in more than 200 infants in the English literature; including 34 our own patients. To identify its long-term outcome, a prospective study was accomplished on our 34 infants with sonographic lenticulostriate vasculopathy which included 13 cryptogenic cases and 21 with distinct etiologies. At the age of 7 to 9 years in the cryptogenic group, 7 in 13 patients developed tics, attention deficits, hyperactivity, and/or obsession/compulsion; while in the symptomatic group only 2 of 21 patients had tics. The rate of mortality (33% vs. 0%), developmental delay (24% vs. 8%), mental retardation (24% vs. 0%), and neurologic deficits (29% vs. 0%) were significantly higher in the symptomatic group than the cryptogenic group. Comparatively, the occurrence rate of attention deficit-hyperactivity disorder (10% vs. 54%), tics (10% vs. 38%), and obsessive-compulsive disorder (5% vs. 13%) were significantly lower in the symptomatic group than the cryptogenic group. The rates of these neuropsychiatric disorders were 10% in the symptomatic group and 54% in the cryptogenic group. We concluded that idiopathic sonographic lenticulostriate vasculopathy in infancy may predict development of neuropsychiatric disorders later in childhood.
Tourette syndrome (TS) is familial neuropsychiatric disorder that is characterized by motor and phonic tics that begin in childhood. Once thought of as a rare and debilitating disorder, in the last decade new scientific knowledge suggests that TS and related tic disorders are more common and less debilitating for the majority of individuals. Evidence points toward a spectrum of TS symptomatology that extends beyond the tics disorder to probably include obsessive-compulsive disorder, attention deficit hyperactivity disorder, and mood disorders. Tourette syndrome and its differential diagnosis are discussed in this article with a focus on new developments in classification, etiology, epidemiology, genetics, pathophysiology, and clinical management.
The putative relationship between a variety of neurologic and neuropsychiatric disorders, which have been reported in association with tics, is reviewed. Tics also may be increased or exacerbated by drugs affecting a variety of neurotransmitter systems. Recognition and study of these secondary tic disorders may further our understanding of basal ganglia physiology and the pathogenesis of Tourette syndrome.