Electroencephalographic Abnormalities in Monozygotic Twins with Tourette's Syndrome

Abstract

The association of attentional, neuropsychological, and behavioural abnormalities with Tourette's syndrome (TS) suggests that the abnormal function of the disorder extends beyond the motor circuits of the basal ganglia. To explore this possibility we studied, with conventional 18-channel electroencephalography, monozygotic twins ranging from 8 to 26 years of age, where at least one member of the twin pair suffered from TS. In nine out of the 11 twin pairs that differed in clinical severity of the tic disorder, the twin with the more severe course of illness had a significantly more abnormal electroencephalogram (EEG) by qualitative visual analysis. Most of the differences were due to excessive frontocentral theta activity, suggesting dysfunction outside the basal ganglia. There was also a significant relationship between a lower global neuropsychological testing score and a worse overall EEG. In eight of nine twin sets with different global neuropsychological testing scores, the twin with the lower score had a worse EEG. A similar relationship was found between birth weight and overall EEG quality. In the nine sets that differed in birth weight, the twin with a lower birth weight had a worse EEG in seven of the sets. The EEG findings are unlikely to be unlikely to be a medication effect because the same result was seen in the six twin pairs who had been medication-free for at least six months before entry into the study. The origin of this slowing may relate to the interaction between environmental insults to the central nervous system and the genetic component of TS, an interaction producing damage to the cortex, thalamus, or both.

Prenatal risk factors for Tourette Syndrome: a systematic review

“…After full text review of these 31 articles, 9 were excluded because only case series were studied [31,32,35,37,38], only poster abstract was available [33], or the contents didn’t include pre- or peri-natal adversities [10,34,40]. Because of the extreme diversities among studies, the included 22 articles were further categorized according to the different purpose, study design, investigated factors, and outcome.…”

The Gilles De La Tourette syndrome: the current status

“…Thereafter, Leckman et al 78 investigated PNDs in 31 GTS patients, demonstrating that the severity of maternal life stress during pregnancy, gender of the child and severe nausea and/or vomiting during the first trimester were significantly associated with the current tic severity. Tic severity has to date been associated with or positively correlated with maternal smoking,93 94 low birth weight,50 low birth weight and PNDs,77 95–98 psychosocial stress,94 anxiety,99 stress100 and GABHS infections 101. The only study to examine the phenotype and aetiology in the area of neuroimmunology was that of Martino et al 102 who examined the phenotypic features of ABGA-positive and ABGA-negative patients, among 53 children and 75 adults with GTS: 23% of children and 25% of adults with GTS were ABGA-positive.…”

Neurofeedback Training for Tourette Syndrome: An Uncontrolled Single Case Study

“…The suppression of somatosensory information and reduction in muscle tone induce a change in nVB firing patterns, shifting from non-rhythmic and fast to rhythmic and systematic bursts of discharges, that result in the appearance of SMR brainwaves (Sterman and Egner 2006). Excessive frontal Theta, consistently reported in patients with tics (Hyde et al 1994) and motor hyperactivity (Sterman 2000), is most often associated with deficits in cognitive functions, especially attention and executive functions, and with poor impulse control (Lubar et al 1995;Sterman 2000;Swartwood et al 2003;Hermens et al 2005;Banaschewski and Brandeis 2007).…”

“…An altered pattern of cortical activity has been highlighted in patients with TS, including reduced Sensorimotor Rhythm (SMR, 12-15 Hz) over the sensorimotor strip (Monastra et al 1999) and excessive frontocentral Theta (4-8 Hz; Hyde et al 1994). SMR is initiated by reduction in efferent motor activity and afferent somatosensory input, and is suppressed during movement or imagination of a movement (Sterman and Egner 2006).…”