Showing papers on "Tourette syndrome published in 1981"

Simple tics in Gilles de la Tourette's syndrome are not prefaced by a normal premovement EEG potential.

Abstract: EEG events prior to simple tics have been examined in six patients with Gilles de la Tourette's syndrome, and compared to EEG changes occurring when the same subjects voluntarily mimicked their own tics. Voluntary jerks were prefaced by a premovement negative potential commencing about 500 ms prior to the muscle EMG discharge and reaching an amplitude of about 7 muV. No such premovement potential was evident in the EEG prior to spontaneous tics in five of the six patients; a very small event was seen in the sixth patient but it was only about one-tenth of the size of the premovement potential seen prefacing voluntary jerks in the same subject. These data indicate that simple tics in Gilles de la Tourette's syndrome are physiologically distinct from normal self-paced willed movements.

Familial pattern and transmission of Gilles de la Tourette syndrome and multiple tics.

Abstract: Fifty-two patients with Gilles de la Tourette syndrome (TS) diagnosed according to DSM-lll criteria and/or their parents were interviewed regarding symptoms among family members. Occurrences of TS and multiple tics (MT) among first-degree relatives were distinguished to determine the familial patterns of the two diagnoses. comparing these data with family data collected on a random national sample of patients with TS, we found no differences between the two samples. Each separately and both combined showed that (1) MT seems to be a mild form of TS; (2) both MT and TS are transmitted in the same families; (3) the sex difference is real and not an artifact of ascertainment; and (4) the sex difference is related the the transmitted susceptibility as a threshold effect. A specific genetic mechanism has not been identified.

Genetic analysis of Tourette syndrome suggesting major gene effect

Abstract: Data on Gilles de la Tourette syndrome are analyzed by multiple threshold models in inheritance that incorporate sex effect. The polygenic-multifactorial model is rejected. Single major locus inheritance can account for the data, although many of the occurrences of Tourette are due to nongenetic phenocopies. In both models, males and females share a common genetic environmental liability, but the less prevalent sex, that is, females, has a higher genetic loading for the disorder. The predicted population prevalences in the single major locus model are 2.3% for males and 0.8% for females. The implications for genetic and biological research in Tourette syndrome are discussed.

Neuropsychological functioning in gilles de la Tourette's syndrome

Abstract: Thirteen diagnosed Tourette Syndrome males, aged 10 through 13 years, were administered the Halstead Neuropsychological Test Battery for Children, the WISC-R, the Wide Range Achievement Test, and the Bender-Gestalt Test The norms utilized for the Halstead Neuropsychological Battery for Children were those of Selz and Reitan (1979) When such criteria were employed, overall level of performance was normal for 11 of the 13 subjects However, analysis of the results of the additional tests administered demonstrated consistent impairment of circumscribed functions Significant impairment in visual-motor copying was noted on the Bender-Gestalt Test and on the Coding subtest of the WISC-R Impairment in arithmetic ability emerged only when a visual-motor component was added to the task This relevant and interesting cluster of deficits is considered to represent a dysfunction of nonconstructional visuopractic abilities

Increased body movements during sleep in gilles de la tourette syndrome

Abstract: Overnight sleep polygrams were recorded from 9 patients with Gilles de la Tourette syndrome (GTS). Six of 9 patients had abnormal electroencephalograms, but no specific abnormalities were detected. Body movements and twitch movements during sleep were analyzed. At all stages of sleep, body movements during sleep were more frequent in cases of GTS than those in normal controls. Twitch movements in stage REM of sleep were significantly increased in GTS. These results are consistent with the idea that GTS is due to an imbalance between the central neurotransmitters, catecholamine and serotonin.

Huntington disease and Tourette syndrome. I. Electron spin resonance of bed ghosts.

Abstract: Abnormalities in the electron spin resonance (ESR) of nitroxide-labeled red blood cell membranes have been reported in Huntington disease (HD). Because of the importance of verifying a general membrane defect in this disease, we have examined 13 unmedicated HD patients of all grades of severity, with a duration of symptoms from 3 to 20 years and including juvenile and rigid cases. No significance differences in the ESR of controls, HD patients, and three Tourette syndrome patients were found.

Tardive Dyskinesia in Persons With Gilles de la Tourette's Disease

Abstract: To the Editor.— The note by Mizrahi et al (Archives1980;37:780) describing tardive dyskinesia in a child with Gilles de la Tourette's disease (TD) prompts us to report three other cases that we have observed, in addition to one that we reported previously.1 Report of Cases.— Case1.—An 8-year-old boy first received treatment with haloperidol after referral for the sudden onset of incessant coprolalia. Prior to that time, he had eye tics that began six months after beginning treatment with methylphenidate for symptoms of hyperactivity. His haloperidol dosage was gradually increased to 5 to 6 mg/day, which provided beneficial (but not complete) suppression of tics. Performance in school was unaffected by this dosage, although his family noted increased appetite and weight gain. He was followed up for two years, with regular monitoring of his TD symptoms as well as repeated dosage reduction to evaluate the possible emergence of drug-induced

Familial aspects of Gilles de la Tourette syndrome.

Abstract: The authors present two cases in which Gilles de la Tourette syndrome was present in at least two family members: the first case is a mother and her son and the second an uncle and his nephew. the increasing severity of the syndrome from one generation to the next and some similar clinical features in the two cases are noted. The authors also speculate that the incidence of family cases of Tourette syndrome may be underestimated because of the painstaking efforts required to obtain this kind of history.

Clonidine and Haloperidol in Gilles de la Tourette Syndrome

Abstract: To the Editor.— The article describing clinical experience with clonidine hydrochloride as an alternative to haloperidol for the treatment of Gilles de la Tourette syndrome (TS) (Archives 1980;37:1350-1357), as well as the genetic and biochemical studies emanating from the Yale group, is a substantial contribution to the literature. However, we believe that several issues raised in this article warrant discussion. Gilles de la Tourette syndrome is defined by the authors as a "severe neuropsychiatric syndrome of childhood onset and lifelong duration that consists of multiform motor and phonic tics and other behavioral and psychological symptoms." It is conceptualized as a neuropsychiatric dysfunction that affects the regulation of impulses, thoughts, motor activities, speech, and complex actions... a disorder of psychomotor inhibition with a more or less pervasive impact and with varied and individualistic symptom profiles ranging from chronic tics through disabling compulsions, irritability, and attentional and learning difficulties, as well as

Clonidine and Haloperidol in Gilles de la Tourette Syndrome-Reply

Abstract: In Reply.— The letter of Drs A. and E. Shapiro offers the opportunity for clarifying our findings concerning TS. Diagnosis.— Each of the patients in our report satisfied the following DSM-III criteria for TS: multiple motor and phonic symptoms of over one year's duration, temporary suppressibility, and waxing and waning severity. In addition, the patients demonstrated characteristics of TS that have been highlighted since the first descriptions in the 19th century, including complex behaviors, echo phenomena, compulsions, obsessions, impulsivity, coprolalia, poor frustration tolerance, attentional difficulties, as well as school and learning proplems. 1-4 For example, the Shapiros and colleagues found that 58% of their patients had minimal brain dysfunction and 57% had marked behavioral maladjustment. 5 In the current letter, they state that the mental disorders of patients with TS are not statistically distinguishable from those of psychiatric outpatients, again suggesting the range and severity of psychiatric difficulties in patients with TS.

Neuroleptic-induced ‘tardive Tourrette’s syndrome’ and neurotoxicity

Abstract: Neurological side effects have been associated with neuroleptic drugs since these drugs were introduced in the treatment of psychiatric disorders. Acute dystonia and parkinsonism may be seen in the initial phases of treatment while a hyperkinetic syndrome may develop later. Fauerby et al. (1964) named this late syndrome tardive dyskinesia. The frequent irreversibility of the syndrome may be regarded as a sign of a potential neurotoxic effect of neuroleptic drugs (Gerlach, 1979).

Huntington Disease andTourette Syndrome. 1.Electron SpinResonance ofRedBlood Cell Ghosts

Abstract: SUMMARY Abnormalities intheelectron spinresonance (ESR)ofnitroxide-labeled redbloodcell membranes havebeenreported inHuntington disease (HD).Because oftheimportance ofverifying ageneral membrane defect inthis disease, wehaveexamined 13unmedicated HD patients ofall grades ofseverity, withaduration ofsymptoms from3to20years and including juvenile andrigid cases. Nosignificant differences intheESRof controls, HD patients, andthree Tourette syndrome patients werefound.