Adult-onset tics associated with peripheral injury

We report the cases of two patients with adult onset, simple, nonvarying tic disorder that commenced after a peripheral (non-CNS) injury. The first patient is a 38-year-old man who suffered a right facial injury when his car fell off its jack while he was working underneath. Bilateral facial twitching began hours after the trauma and was characterized as a sniffinglike gesture. The movements waxed and waned, were suppressible, and were associated with a premonitory sensation. The tics remitted after 9 months but still recur occasionally under stressful situations. The second patient is a 34-year-old man with a 3-year history of abrupt, rapid head-turning movements that began 12 months after a motor vehicle accident in which he injured his neck. The tics continue to wax and wane, are suppressible, and are associated with an urge. Neither patient suffered a head injury or had a family history of Tourette syndrome. Based on the clinical and historical features of these patients, the temporal relationship between the trauma and onset of tics, and the occurrence of tics only in the traumatized region, a causal relationship is possible. These may represent the first reported cases of tic disorder in association with peripheral injury. The mechanism by which the tic disorder resulted from the peripheral injury is unclear, but these patients might have been susceptible individuals and the trauma acted as a trigger.     

Delayed and severe but transient Tourette syndrome after head injury

A previously well and intellectually normal 7(1/2)-year-old girl developed an acute and severe Tourette syndrome 15 months after sustaining a severe head injury. The patient displayed a dramatic response to haloperidol. Twelve months after the onset of Tourette syndrome the haloperidol was withdrawn, and there was no relapse of either her motor or phonic tics. Seven years after the head injury the patient remains tic free but demonstrates significant emotional and behavioral sequelae. The patient's brain magnetic resonance imaging findings were consistent with those reported previously in adults with Tourette syndrome.     

New onset of idiopathic bilateral ear tics in an adult

Tic disorders are commonly considered to be childhood syndromes. Newly presenting tic disorders during adulthood are uncommon and mostly described in relation to an acquired brain lesion or as incidental tics, particularly in context with other neurological or psychiatric diseases. Tic disorder involving the ears is extremely uncommon with only few studies in English literature. In the present case, we describe an adult patient with new-onset idiopathic tics disorder involving both ears, causing social embarrassment. In addition, our patient had recent onset of the tics without any childhood or family history of tic disorders. The single most important component of management is an accurate diagnosis. At the same time, tics should be differentiated from other movement disorders such as chorea, stereotypy, and dystonias.     

Complex phonic tic and disinhibition in Tourette syndrome: case report

Tourette syndrome (TS) is a neuropsychiatric disorder characterized by a combination of multiple motor tics and at least one phonic tic. TS patients often have associated behavioral abnormalities such as obsessive compulsive disorder, attention deficit and hyperactive disorder. Coprolalia, defined as emission of obscenities or swearing, is one type of complex vocal tic, present in 8% to 26% of patients. The pathophysiology of coprolalia and other complex phonic tics remains ill-defined. We report a patient whose complex phonic tic was characterized by repetitively saying "breast cancer" on seeing the son of aunt who suffered from this condition. The patient was unable to suppress the tic and did not meet criteria for obsessive compulsive disorder. The phenomenology herein described supports the theory that complex phonic tics result from disinhibition of the loop connecting the basal ganglia with the limbic cortex.     

Tourette's syndrome following temporal lobectomy for seizure control

Gilles de la Tourette's syndrome (TS) is a neurobehavioral disorder characterized by multiple motor and vocal tics, occurring longer than a year and causing marked distress along with social and occupational impairments in level of functioning. It can be accompanied by obsessive-compulsive behavior and attention deficit disorder. This report discusses the case of a young woman with a simple motor tic disorder and intractable seizures who, after right temporal lobectomy for medically intractable epilepsy, developed TS with complex motor and vocal tics, severe obsessive-compulsive disorder, and paranoia. This neurobehavioral complication has not to our knowledge been previously reported after epilepsy surgery.     

Tic exacerbation and precipitation during atomoxetine treatment in two children with attention-deficit hyperactivity disorder

Stimulants have been the mainstay of treatment for children with Attention-deficit/hyperactivity Disorder (ADHD). However, stimulants have been controversially purported to precipitate and exacerbate tics. Atomoxetine, a selective norepinephrine inhibitor, was introduced as a safe non-stimulant alternative treatment for ADHD children with comorbid tics or TS. We are presenting two children with ADHD, in which atomoxetine, at relatively low doses, exacerbated and precipitated tics. The diagnoses of ADHD and tic disorder were based on clinical observations and standardized rating scales. Case 1, an 8-year-old boy, had history of stimulant-induced tics. This child was placed on atomoxetine reported to be safe for patients with tics. This patient's tic control was adequate prior to atomoxetine treatment. However, while on atomoxetine, the patient promptly experienced tic exacerbation. Case 2, a 6-year-old boy, had no previous history of stimulant therapy and was receiving citalopram due to a comorbid anxiety disorder. Atomoxetine was initiated for the treatment of ADHD with improvement in the ADHD symptoms. But, upon a mild dose increase, the patient presented tic precipitation consisting primarily of neck twitches. Both cases experienced a decrease in tic activity when atomoxetine was discontinued, but tics did not fully resolve, causing psychosocial disturbance. Atypical neuroleptics were used with good results. Periodic assessments of the need for continued neuroleptic treatment were emphasized. These two children exemplify atomoxetine's potential to exacerbate and precipitate tics in children with ADHD. Independent controlled studies are needed to determine if atomoxetine should be used in children with ADHD and comorbid tic disorders or TS.     

Tic syndrome

A tic is an involuntary, sudden, rapid, recurrent, nonrrhythmic, stereotyped, motor movement or vocalization. This paper reviews clinical, pathophysiological, epidemiological and treatment issues of tic disorders. The clinical presentation of tic disorders with simple and complex motor or vocal tics is reviewed in detail. The most common psychiatric comorbid conditions, such as personality disorder (PD), Obsessive-Compulsive Disorder (OCD), Self-Destructive Behavior (SDB) and Attention Deficit Hyperactivity Disorder (ADHD) are presented too. All forms of tics may be exacerbated by anger or stress, but they are usually markedly diminished during sleep. Premonitory feelings or "sensory experiences", which are distinct from the actual motor or phonic tics and precede the tics, occur in over 80% of tic-patients and in 95% of patients with Gilles de la Tourette Syndrome (GTS). The American Psychiatric Association recognizes three types of tic disorders on the basis of clinical criteria: Transient Tic Disorder, Chronic Motor or Vocal Tic Disorder and GTS. The diagnostic criteria for these types are described. According to epidemiological data, up to 10% of children have at least somewhere a transient tic disorder. The onset of tics, whether simple or multiple, occurs at approximately 7 years of age. The accepted prevalence figure for GTS is 0.05-3%. Although tics can appear as the result of brain injury, Huntington chorea or encephalitis, they are most commonly idiopathic. Genetic factors appear to be present in many but not in all cases of tic disorders. Autosomal dominant, sex-linked models or semirecessive-semidominant-oligogenic models have been considered. Based on the review of the literature we believe that tic disorders are related to altered neurotransmitter function within the CNS, especially that the functional abnormality is somehow related to dopaminergic mechanism. Several authors have recently investigated the possible role of autoimmune response to streptococcal infection in the pathogenesis of tics. The differential diagnosis of tics is reviewed in detail. Above all tics represent a social disability. The ability to tolerate tics varies greatly from one individual to another, and the need for treatment is better defined by the patient than by the physician. Mild cases do not need be treated. Ideally, management should be multidisciplinary and can range from educative to supportive means or to intricate pharmacological interventions. The major form of treatment of the motor or vocal symptoms continues to be based on high-potency "typical" neuroleptics (tiaprid, pimozide, haloperidol), which induce a wide range of potentially serious side effects. In everyday practice we prefer to start with an "atypical" neuroleptic drug--for example, olanzapin (5-10 mg/day), risperidone or clozapine. Other drugs, such as clonidin or pergolid are widely used but their efficiency is still questionable. SSRIs (sertaline, citalopram, fluoxetin, fluvoxamine) or other antidepressants (clomipramine) have been used in treatment of psychiatric comorbid conditions, too. Botulinum toxin injections have proved useful in tics, targeting at the symptoms of blepharospasm, in neck and facial muscles.     

Tourettism and dystonia after subcortical stroke.

The term "tourettism" has been used to describe Tourette syndrome (TS)-like symptoms secondary to some specific cause. Tics associated with attention deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD), or both, are commonly present in TS, but this constellation of symptoms has been rarely attributed to stroke. We describe two boys who suffered a subcortical stroke and subsequently developed hemidystonia, tics, and behavioral comorbidities. Both had right hemispheric stroke involving the basal ganglia at 8 years of age, and in both the latency from the stroke to the onset of left hemidystonia was 2 weeks. In addition to ADHD and OCD, both exhibited cranial-cervical motor tics but no phonic tics. The temporal relationship between the stroke and subsequent TS-like symptoms, as well as the absence of phonic tics and family history of TS symptoms in our patients, argues in favor of a cause and effect relationship, and the observed association provides evidence for an anatomic substrate for TS and related symptoms.     

Recurrence of childhood multiple tic in late adult life

In contrast to the lifelong persistence of symptoms characteristic of Gilles de la Tourette's syndrome, multiple tic of childhood is considered to be a self-limited disorder that remits by early adulthood. We describe four patients who had a history of multiple tic of childhood, complete absence of tics throughout most of their adult lives, and recurrence of tics in late adult life. All four had multiple tics that began before the age of 9 years and included both motor and vocal tics that changed in location and severity over time. None of the patients exhibited coprolalia. All tics subsided before the age of 20 years, only to recur after the age of 60 years, once again including both motor and vocal tics that changed in location and severity slowly over time. The one patient who was severely bothered by the recurrence of motor and vocal tics responded well to haloperidol. Although they do not fit into any accepted diagnostic category for multiple tic, these patients suggest that multiple tic of childhood can recur in adult life. This suggests that Gilles de la Tourette's syndrome may be a continuum for chronic multiple tic of childhood to full-blown classic Gilles de la Tourette's syndrome.     

Transient tic disorder following carbon monoxide poisoning

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.     

Adult onset tic disorders

BACKGROUND: Tic disorders presenting during adulthood have infrequently been described in the medical literature. Most reports depict adult onset secondary tic disorders caused by trauma, encephalitis, and other acquired conditions. Only rare reports describe idiopathic adult onset tic disorders, and most of these cases represent recurrent childhood tic disorders. OBJECTIVE: To describe a large series of patients with tic disorders presenting during adulthood, to compare clinical characteristics between groups of patients, and to call attention to this potentially disabling and underrecognised neurological disorder. METHODS: Using a computerised database, all patients with tic disorders who presented between 1988 and 1998 to the movement disorders clinic at Columbia-Presbyterian Medical Center after the age of 21 were identified. Patients' charts were retrospectively reviewed for demographic information, age of onset of tics, tic phenomenology, distribution, the presence of premonitory sensory symptoms and tic suppressibility, family history, and associated psychiatric features. These patients' videotapes were reviewed for diagnostic confirmation and information was obtained about disability, course, and response to treatment in a structured follow up interview. RESULTS: Of 411 patients with tic disorders in the database, 22 patients presented for the first time with tic disorders after the age of 21. In nine patients, detailed questioning disclosed a history of previous childhood transient tic disorder, but in 13 patients, the adult onset tic disorder was new. Among the new onset cases, six patients developed tics in relation to an external trigger, and could be considered to have secondary tic disorders. The remaining patients had idiopathic tic disorders. Comparing adult patients with recurrent childhood tics and those with new onset adult tics, the appearance of the tic disorder, the course and prognosis, the family history of tic disorder, and the prevalence of obsessive-compulsive disorder were found to be similar. Adults with new onset tics were more likely to have a symptomatic or secondary tic disorder, which in this series was caused by infection, trauma, cocaine use, and neuroleptic exposure. CONCLUSIONS: Adult onset tic disorders represent an underrecognised condition that is more common than generally appreciated or reported. The clinical characteristics of adults newly presenting to a movement disorder clinic with tic disorders are reviewed, analysed, and discussed in detail. Clinical evidence supports the concept that tic disorders in adults are part of a range that includes childhood onset tic disorders and Tourette's syndrome.     

New-onset tic disorder following acute hemorrhage of an arteriovenous malformation

The etiology of tic disorder includes idiopathic, postencephalitic, head injury, carbon monoxide poisoning, stroke, and developmental syndromes. We report a case of new-onset complex motor and vocal tics that began after hemorrhage of an arteriovenous malformation located in the left frontal lobe. We have found no reported cases of new-onset tics related to arteriovenous malformations or hemorrhage into the frontal lobes. The patient is a 16-year-old right-hand-dominant boy who presented with generalized tonic-clonic seizures. Evaluation, including magnetic resonance imaging, revealed a left frontal arteriovenous malformation, confirmed by angiogram. Following resection, there was an intraparenchymal hemorrhage of the left frontal lobe with intraventricular hemorrhage, noted most prominently in the left lateral and IIIrd ventricles, and a subdural hematoma caudal to the craniotomy. The postoperative course was complicated by hemiparesis and global aphasia. During recovery, the patient developed what was thought to be a complex partial seizure evidenced by head turning to the right with vocalization and left upper extremity clonic jerks. These were brief and occurred multiple times per day. A trial of carbamazepine was given with no improvement. It was noted that the spells occurred more frequently under stress, as when the patient was frustrated with communication. The diagnosis was changed to complex motor tics and the therapy changed to clonidine. The tics subsequently improved by 80%, although they were still present. We believe the development of complex motor tics due to frontal hemorrhage represents a unique etiology and could complicate postsurgical recovery in similar cases.     

Gilles de la Tourette Syndrome in a child with congenital deafness

We present the case of a 10-year-old boy, Sam, with congenital deafness and Gilles de la Tourette Syndrome (GTS). GTS is characterised by multiple motor tics and one or more vocal tics that wax and wane. Due to his deafness Sam never developed vocal language but instead used sign language from the age of four. His tic disorder rapidly accelerated from the age of seven over a six-month period and soon sign language was incorporated into tics as complex “vocal” tics. Bursting out “words”in sign language would also occur in front of people unfamiliar with sign language and often with an obscene content although this was not evident to someone not trained in sign language. To our knowledge this is the first reported case of a congenital deaf child with GTS. The case presented here supports previously published work that the intentional share of the tics in GTS is very small. This case also questions former theories on which regions and circuits of the brain are involved in GTS. Accepted: 16 May 2001     

Altered cortical excitability in obsessive-compulsive disorder

OBJECTIVE: To assess cortical inhibitory and excitatory mechanisms in obsessive-compulsive disorder (OCD). BACKGROUND: Transcranial magnetic stimulation (TMS) studies have found decreased neuronal inhibition and a reduced cortical silent period in the primary motor area in Tourette's syndrome, focal dystonia, and other disorders believed to involve dysfunction of subcortical structures, including the basal ganglia. Dysfunction of the basal ganglia and linked regions also has been implicated in OCD, which has significant clinical and familial overlap with tic disorders. METHODS: We applied the TMS techniques previously used in Tourette's syndrome to a group of 16 OCD patients (seven unmedicated) and 11 age-matched healthy volunteers extensively screened for psychopathology. Measures of motor cortex excitability included resting and active motor threshold, cortical silent period duration, and intracortical inhibition and facilitation using a paired-pulse TMS technique with a subthreshold conditioning stimulus. RESULTS: Similar to recent findings in Tourette's syndrome and focal dystonia, this study reports significantly decreased intracortical inhibition (ICI) relative to the volunteers at interstimulus intervals from 2 to 5 msec. We also found decreased active and resting motor evoked potential threshold in the OCD patients, another indication of increased cortical excitability. Neither abnormality appeared medication related. The decreases in ICI and motor threshold were greatest in OCD patients with comorbid tics, but remained significant in patients without tics. CONCLUSIONS: The data suggest abnormal cortical excitability in obsessive-compulsive disorder. These findings are congruent with the hypothesis that Tourette's syndrome and obsessive-compulsive disorder (OCD) are analogous disorders with overlapping dysfunction in corticobasal circuits. Patients with tic-related OCD may have more abnormal motor cortex excitability than OCD patients without tics.     

High-frequency pallidal stimulation eliminates tic-related neuronal activity in a nonhuman primate model of Tourette syndrome

High-frequency deep brain stimulation targeting the output nucleus of the basal ganglia, the globus pallidus internus, has been suggested as a treatment modality for intractable Tourette syndrome and basal-ganglia-mediated motor tics. Recent studies on the modeling of motor tics induced by focal injections of bicuculline to the striatum, a putative model of Tourette syndrome, have shown that tics induce a widespread modulation within both segments of the globus pallidus. The purpose of this study was to investigate, using the bicuculline-induced Tourette syndrome model, whether and how high-frequency deep brain stimulation targeted to the globus pallidus internus could modulate tic-related activity in the pallidum. The perievent rate changes coinciding with tic expression under the on-stimulation and off-stimulation conditions were examined to determine the effect of high-frequency stimulation on pallidal activity. The results showed that the stimulation blocked tic-related phasic changes in the firing pattern of pallidal cells in parallel with a reduction of the peak amplitude of tic events in the electromyography record. This finding supports the premise that deep brain stimulation targeted to the globus pallidus internus could be a viable treatment option for Tourette syndrome, and the use of pallidal stimulation for motor tics warrants further study.     

The neuropsychiatry of Gilles de la Tourette syndrome: The état de l’art

Gilles de la Tourette syndrome (GTS) is a chronic tic disorder characterised by the presence of multiple motor and vocal tics with onset during development. Tics are the most common hyperkinetic symptoms in childhood and co-morbid behavioural conditions (especially obsessive-compulsive disorder, attention-deficit and hyperactivity disorder, affective symptoms, and impulsivity) are present in the majority of patients. Although GTS is no longer considered a rare medical curiosity, its exact pathophysiology remains elusive. Recent research on the brain correlates of the subjective ‘urge to tic’ has highlighted the role of extra-motor pathways within the brain mechanisms of tic generation. Advances in our understanding of the pathophysiology of GTS can pave the way to the implementation of more effective treatment strategies for this heterogeneous neurobehavioral condition. Finally, the development of GTS-specific instruments for the assessment of health-related quality of life has allowed more standardised assessments across the lifespan, capturing the impact of both tics and behavioural co-morbidities.     

Secondary tics after osmotic demyelination syndrome involving both the striatum and the cerebral cortex

Although some reports have associated parkinsonism, dystonia, and chorea with the extrapontine lesions of osmotic demyelination syndrome (ODS), to our knowledge delayed-onset tic disorder has not been reported. Thus, we report a rare secondary tic associated with ODS involving both the striatum and the cerebral cortex. We can hypothesize that aberrant neuronal plasticity after the initial insult in both basal ganglia and motor cortical areas could be implicated in the pathogenesis of delayed-onset tics.     

Prevalence of tic disorders and Tourette syndrome in a Swedish school population

The aim of the study was to find the epidemiological distribution of tic disorders and Tourette syndrome (TS) in Swedish school children aged 7 to 15 years. A total population of 4,479 children and their parents were asked to fill in a questionnaire covering both motor and vocal tics. A three-stage procedure was used: screening, interview, and clinical investigation. Two hundred and ninety-seven children (190 males, 107 females) were found to have tics. TS, according to DSM-IV criteria, was found in 0.6% of the total population, another 0.8% had chronic motor tics, and 0.5% had chronic vocal tics. Further, 4.8% of the children had transient tics. All together 6.6% of 7- to 15-year-old children currently had or had experienced some kind tic disorder during the last year. Prevalence of different tic disorders was higher among younger children and in males, and was highly associated with school dysfunction. The prevalence of TS was higher than was previously thought but other tic disorders were more common in this childhood population.     

Premonitory sensory phenomenon in Tourette's syndrome.

We administered a questionnaire designed to probe for premonitory sensations associated with motor tics to 50 patients with Tourette's syndrome (TS). Premonitory sensations were reported by 46 (92%) patients, and the most common sensation was an urge to move and an impulse to tic ("had to do it"). Intensification of premonitory sensations, if prevented from performing a motor tic, was reported also in 37 patients (74%), 36 patients (72%) reported relief of premonitory sensations after performing the tic, and 27 of 40 (68%) described a motor tic as a voluntary motor response to an involuntary sensation, rather than a completely involuntary movement. The "just right" sensation correlated with the presence of co-morbid obsessive-compulsive disorder. We conclude that premonitory sensations are an important aspect of motor tics and some patients perceive motor tics as a voluntary movement in response to an involuntary sensation.     

Tourette syndrome: Evolving concepts

Tourette syndrome is a common childhood‐onset neurobehavioral disorder characterized by multiple motor and phonic tics affecting boys more frequently than girls. Premonitory sensory urges prior to tic execution are common, and this phenomenon helps to distinguish tics from other hyperkinetic movement disorders. Tourette syndrome is commonly associated with attention deficit hyperactivity disorder, obsessive‐compulsive disorder, learning difficulties, and impulse control disorder. The pathophysiology of this complex disorder is not well understood. Involvement of basal ganglia–related circuits and dopaminergic system has been suggested by various imaging and postmortem studies. Although it is considered a genetic disorder, possibly modified by environmental factors, an intense search has thus far failed to find causative genes. Symptomatic treatment of tics chiefly utilizes various alpha adrenergic agonists, antidopaminergic drugs, topiramate, botulinum toxin, and deep brain stimulation. Habit reversal therapy and other behavioral approaches may be a reasonable option for some cases. Improved understanding of Tourette syndrome should lead to better symptomatic and more effective pathogenesis‐targeted therapies. © 2011 Movement Disorder Society