De La Tourette's Disease Research Articles

Development of clinical somnology (Contibution of I.G. Karmanova)

Based on her studies of sleep disorders in patients with cataleptic schizophrenia syndrome, narcolepsy and Gille de la Tourette disease, I.G. Karmanova proposed an evolutionary-dissolution approach to sleep analysis. It helps not only identify the type of sleep–wake cycle abnormalities, but also analyze pathogenetic mechanisms of CNS disorders.

Cavum Septi Pellucidi as a Marker of the Neuropsychiatric Diseases: A Pointer or Mislead? A Cadaveric–Clinical Observation

Cavum Septi pellucid (CSP), a cavity between the laminae of the septum pellucidum, for a longer period has been reported as an anomaly of the brain midline, associated with neuropsychiatric diseases, mostly schizophrenia, but also posttraumatic stress disorder, De la Tourette disease, and persons who survived a repeated a serious head trauma, boxers on the first place. Our investigation has been performed on 479 unfixed frozen brains, of the autopsied individuals of both genders, and MRI scans of 250 examinees, out of which 110 had neuropsychiatric illness. In our sample, the prevalence of CSP was 22.96% among the autopsied individuals and 9.2% in examinees who underwent MRI scan. The cause of the death among schizophrenia suffering persons was suicide (18 out of 25 patients). Obviously, CSP is more frequently associated with neuropsychiatric diseases, but a dilemma still exists, did we make a bias in brain suitability for the examination or we did the same mistake in observing clinical cases. A large CSP, though, is an almost certain sign for an underlying neuropsychiatric impairment, especially schizophrenia. The CSP among alcoholics and persons with the priory sustained head blows is probably of the same cause and represents an aftermath of the diffuse axonal injuries, i.e. brain trauma.

Spectre du trouble obsessionnel-compulsif revisité à travers un bipôle impulsion-compulsion

The so-called obsessive-compulsive spectrum disorder (OCD spectrum) is represented by a large variety of clinical entities. There are in general obsessive-compulsive disorder, trichotillomania or Gilles de la Tourette disease among the impulse control disorders, body dysmorphic disorder and hypochondriasis among the somatoform disorders. Updated overview of the OCD spectrum through a bipolar configuration with the impulsion-compulsion (I-C) spectrum, characterized by a failure to resist and control intrusive thoughts associated with repetitive behaviors that seem to be uncontrollable or require considerable efforts to suppress their execution. There are several disrupted processes in the I-C spectrum, including cognitive control, flexibility and behavioural inhibition. All these psychiatric affections demonstrated to share apparent similarities regarding clinical symptomatology, demographic considerations, comorbidity and course pattern, and responses to the serotonine reuptake inhibitors and cognitive behavioural therapy. The concept of I-C spectrum pleads for less categorical and more dimensional approach that seems to be consistently adapted to clinical, genetic, pathophysiology and therapeutic realities.

Tics et syndrome de Gilles de la Tourette : diagnostic, évolution et principes de traitement

The term "Tourette syndrome" designates the combination of tics with other symptoms. Gilles de la Tourette disease is one of its most frequent causes. It combines motor and vocal tics, with no identifiable cause, with self-mutilation and variable psychiatric comorbidity that may include obsessive-compulsive disorder (OCD) and other anxiety disorders, mood and personality disorders, and a syndrome of hyperactivity with attention disorders. The prevalence of Tourette syndrome is estimated at 0.1-1% of the general population. The condition begins during childhood and develops in a succession of periods of relative aggravation and remission of the tics. Most patients show improvement at the end of adolescence, but symptoms can persist into adulthood in approximately one third of patients. The cause of Gilles de la Tourette disease is unknown, but the role of genetic susceptibility has been suggested together with dysfunctions of the dopaminergic system and of neuron networks in associative and limbic areas of the basal ganglia and the prefrontal cortex. Treatment of Tourette syndrome and severe tics is often difficult and requires a multidisciplinary approach (neurologist, psychiatrist, psychologist and social workers). In mild forms, information and psychological management are usually recommended. Drug treatments--including neuroleptics--are essential in the moderate to severe forms of the disease. Psychiatric comorbidities, when present, often justify specific treatment. For the most severe forms of Gilles de la Tourette disease, preliminary results of treatment by deep brain stimulation of the associative and limb areas of the thalamus or pallidum have produced real hope of treatment, but nonetheless require confirmation.

Les récepteurs dopaminergiques centraux (Partie II): Implications physiopathologiques et thérapeutiques

The five subtypes of dopaminergic receptors exhibit different transduction, cerebral localization, regulation, pharmacological, and physiological roles, explaining their multiple pathophysiological implications in different neuropsychiatric conditions which result, at least in part from anomalous dopaminergic neurotransmission: Parkinson's disease, schizophrenia, addiction, migraine, mode disorders, Gilles de la Tourette disease, hyperactivity syndrome with attention deficit. The wide range of pharmacological implications explains the diversity of the therapeutic approaches perspectives for development of new drugs for these neuropsychiatric conditions.

Decreased dopamine uptake into platelet storage granules in Gilles de la Tourette disease

The movement disorder of Gilles de la Tourette (GdlT) disease may reflect hyperactivity of the basal ganglionic dopamine system. Since platelets have been suggested as peripheral models for the study of catecholamine neurons, we developed a method to measure the uptake of [3H]-DA into platelet storage granules (PSG). In the present report, PSG were incubated with [3H] DA, and Vmax and Km values were calculated by linear regression analysis (Lineweaver Burke plot). The uptake of DA (0.5-5 microM) by PSG from 18 GdlT patients was significantly lower (p < .0001) compared to 15 controls (Vmax mean +/- SD, 107.5 +/- 42.5 and 265.3 +/- 66.5 fmole/mg protein resp.). The decrease of DA uptake in GdlT may reflect compensatory presynaptic changes that reduce DA activity.

Behavioral and clinical profiles of Tourette's disease: a comprehensive overview

A breif review of Gules de la Tourette's disease is presented. The initial part gives an overview of major signs, symptoms displayed, and diagnosis in addition to certain minor concomitant features. The latter conditions included appetite, adaptive function, learning disorders, sexual behavior, sleep disturbances, speech pathology, and tic-related injury. Neurological manifestations, infectious etiology, and genetics were discussed. Treatment modalities are outlined and description of various drug therapy is given in conjunction with rationale of pharmacotherapy and possible underlying mechanism of action. Drug-induced Tourette's-like syndrome was also summarized.

Effects of Dopamine Agonists and Antagonists in Tourette's Disease

The actions of haloperidol, dextroamphetamine sulfate, levamfetamine succinate, apomorphine, and piribedil were studied in two patients with Giles de la Tourette's disease in an attempt to clarify the catecholamine mechanisms involved in this condition. Both dextroamphetamine and levamfetamine increased the severity of the symptoms; dextroamphetamine was more potent. Haloperidol controlled the symptoms and also antagonized the effect of dextroamphetamine. Apomorphine injections reduced the severity of symptoms, even in the presence of dextroamphetamine. We conclude that dopamine rather than norepinephrine is the principal catecholamine responsible for the symptoms. The effect of apomorphine may be understood through its action on postulated presynaptic inhibitory dopamine receptors, or other presynaptic mechanisms of action.

SINGLE CASE STUDY: Neuroendocrine Effects of Haloperidol in an Adolescent with Gilles de la Tourette??s Disease and Delayed Onset of Puberty

The effects of haloperidol on the release of prolactin, growth hormone, and luteinizing hormone during sleep were studied in an adolescent male who had Gilles de la Tourette's disease and delayed onset of puberty. At doses of 5 and 2 mg, haloperidol led to an increase of prolactin secretion and a suppression of luteinizing hormone release. Growth hormone was unaffected. Despite these changes, the patient had normal secondary sexual development consistent with puberty.

Chronic, Multiple Tics of Gilles de la Tourette's Disease

Central nervous system metabolism in six children and one adult with the syndrome of chronic multiple tics was studied by measuring the accumulation of acid metabolites of dopamine and serotonin (homovanillic acid [HVA] and 5-hydroxyindole-acetic acid [5-HIAA], respectively) in the CSF following probenecid administration. The accumulation of 5-HIAA was reduced in patients with multiple tics in contrast with other pediatric patients (N = 27). The degree of reduction in 5-HIAA relative to HVA appeared to be associated with the severity of the tic disorder. With dextroamphetamine, tic symptoms worsened, CSF HVA level decreased, and CSF 5-HIAA concentration increased. These findings suggest an association in Gilles de la Tourette's disease of reduced functioning of inhibitory serotonergic mechanisms and functional dopaminergic overactivity.

Emerging Treatments: Replacement Therapy with Choline or Lecithin in Neurological Diseases

This review evaluates the theoretical background and experimental data behind a new development: the replacement therapy of deficient central cholinergic systems with the dietary precursors choline or lecithin. Cholinergic deficiency states are possibly present in five neurological entities: Huntington's chorea, Tardive Dyskinesia, Gilles de la Tourette's disease, Friedreich's ataxia and pre-senile dementia. Preliminary data from various laboratories, including our own, in each of these disorders indicate that some clinical improvement can occasionally be seen, and that this approach deserves further investigation.

The use of methylphenidate and imipramine in Gilles de la Tourette's disease in children

The authors treated two children with Gilles de la Tourette's disease and one child with a probable combination of Gilles de la Tourette's disease and minimal brain dysfunction with methylphenidate, which resulted in exacerbation of symptoms. One child was briefly treated with imipramine, with similar results. The authors suggest that these pharmacologic agents should be used cautiously in treating patients with possible movement disorders (tics) and conclude that their findings lend support to the catecholamine hypothesis of the etiology of Gilles de la Tourette's disease.

Gilles de la Tourette's disease--a review.

The author describes Gilles de la Tourette's disease, noting that it is characterized by sudden involuntary movements, explosive involuntarty utterances, and imitative phenomena; the pathognomonic feature is the sudden, uncontrolled repetitive utterance of obscenities. The general progression of symptoms is cephalocaudad, with frequent waxing and waning; symptoms become worse during affective arousal and improve with relaxation. Etiology is unclear, with recent evidence suggesting catecholaminergic overactivity. Although this disease and schizophrenia are clearly two separate entities, the author suggests that Gilles de la Tourette's disease may be behaviorally related to schizophrenia and biochemically related to the amphetamine psychosis. The treatment of choice is haloperidol.

Familial Incidence of Gilles de la Tourette's Disease, with Observations on Aetiology and Treatment

Gilles de la Tourette's disease is a relatively rare condition characterized by multiple motor tics and an irresistible compulsion to swear. It was first described by Itard in 1825. Many years later, at the Salpêtrière under the tutelage of Charcot and Brissaud, Georges Gilles de la Tourette made a study of nine cases, including Itard's original one, and published his account of the disorder in 1885. He defined it as a nervous affliction characterized by motor incoordination accompanied by echolalia and coprolalia. He distinguished it from the large number of conditions which previously had been grouped under the heading of chorea. He pointed out similarities between this syndrome and the ‘jumping Frenchmen of Maine’ described by Beard in 1880 and the ‘myriachit’ of Siberia described by Hammond in 1884. Other authors however, question whether these conditions are really part of the same disorder.

Report of Gilles de la Tourette's disease in two succeeding generations

Report of Gilles de la Tourette's disease in two succeeding generations

Gilles de la Tourette's disease and minimal brain dysfunction: amphetamine isomers reveal catecholamine correlates in an affected patient.

Graduated doses of d- and l-isomers of amphetamine were administered on several occasions in double blind fashion to a patient with symptoms of both Gilles de la Tourettes disease and minimal brain dysfunction. d-Amphetamine markedly increased the frequency of ticking while l-amphetamine did not alter the tics. By contrast both isomers decreased the patient's hyperactivity to a similar extent. Based on the known differential influence of amphetamine isomers upon brain norepinephrine and dopamine, these findings suggest that aggravation of the tics is mediated by brain norepinephrine, while brain dopamine plays a major role in the alleviation of the symptoms of minimal brain dysfunction.

Familial Incidence of Gilles de la Tourette's Disease, with Observations on Aetiology and Treatment

Familial Incidence of Gilles de la Tourette's Disease, with Observations on Aetiology and Treatment

Gilles de la Tourette's disease.

Back to table of contents Previous article Next article ArticleNo AccessGilles de la Tourette's DiseaseARTHUR K. SHAPIROARTHUR K. SHAPIROSearch for more papers by this authorPublished Online:1 Apr 2006https://doi.org/10.1176/ajp.129.1.99AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail "Gilles de la Tourette's Disease." American Journal of Psychiatry, 129(1), p. 99 Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - American Journal of Psychiatry $35.00 Add to cart PPV Articles - American Journal of Psychiatry Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited ByThe Indian Journal of Pediatrics, Vol. 40, No. 12 Volume 129Issue 1 July 1972Pages 99-99 Metrics PDF download History Published online 1 April 2006 Published in print 1 July 1972

Haloperidol therapy in tourette's syndrome: Neurophysiological, biochemical and behavioral correlates

A longitudinal, controlled, double-blind, single-case study of Gilles de la Tourette's disease treated with gradually increasing dosage of haloperidol is reported. Neurophysiological measurements, observations of behavior and quantitative determinations of the urinary catecholamine, norepinephrine and dopamine and their respective major metabolites, vanillylmandelic acid and homovanillic acid have been made. Dopamine excretion was above normal during placebo and during the initial phase of drug theraphy. Prolonged haloperidol treatment resulted in a decrease in dopamine excretion toward normal levels, corresponding to the observed decrease in tics per minute. The extent of pupillary contraction was decreased from normal during the placebo phase, and increased to normal during the first week of treatment. During the first week of theraphy homovanillic acid excretion decreased while the extent of pupillary contraction increased as compared to the placebo period. The results are discussed with reference to the possible role of dopamine in Tourette's disease.

Results of psychological testing on a child with Gilles de la Tourette's disease.

Results of psychological testing on a child with Gilles de la Tourette's disease.