Pathophysiology of Tourette’s syndrome Anatomical studies The development of surgical strategies for medically recalcitrant TS was enabled by efforts to localize an anatomical source of the symptoms. Psychodynamic theories prior to the 1970s sought to explain tics as resulting from suppressed aggression and “impaired functioning of the ‘motility controlling function of the ego’ ” (Mahler and Luke 1946;Flinn et al 1983). Autopsy findings from patients with TS that demonstrated no specific anatomical pathologies or only subtle changes in the striatum seemed to support conceptions that tics had a psychogenic origin ( DeWulf and van Bogaert 1941; Balthasar 1957). The search for an anatomical basis for TS using autopsy material is thought to be problematic, however, both because few post-mortem brains have been studied and most of those available have come from patients with long-standing disease and treatment that might confound the histological analyses ( Mink et al 2001; Frey et al 2006). Nevertheless, more recent studies have found abnormalities particularly in the basal ganglia and frontal cortex. For example, studies have reported decreased levels of dynorphin-like immunoreactivity in the striatum and globus pallidus ( Haber et al 1986; Haber and Wolfer 1992), decreased subcortical levels of serotonin ( Anderson et al 1992), increased numbers of neurons expressing parvalbumin in the globus pallidus pars internus (GPi) and decreased numbers of neurons expressing parvalbumin in the caudate nucleus and globus pallidus pars externus (GPe) ( Kalanithi et al 2005). Interestingly, Itard had speculated that the symptoms of TS had a cerebral origin in his 1825 case report: What is the nature of these strange convulsions, or to pose the question in a clearer manner, the seat of the irritation which provokes them? Considering that the muscles which move against the will belong to different motor apparatuses which are not managed by the same nerves, this irritation is not caused by any of them but at their common centre which is the brain.
Neuroimaging studies Modern imaging studies lend further evidence for a neuroanatomic basis of TS. Asymmetric striatal volumes have been observed in magnetic resonance images (MRI) of patients with TS, with smaller striatal volumes suggesting abnormalities in striatal development or the loss of GABAergic interneurons that are thought to play a role in gating sensory information ( Peterson et al 1993; Singer et al 1993). Abnormally smaller caudate volumes are thought to be predictive of the development of more severe tics in early adulthood ( Bloch et al 2005) and have been associated with more severe symptoms in twin studies ( Hyde et al 1995). Abnormalities of volume also have been observed in the lenticular nuclei ( Peterson et al 1993; Singer et al 1993). These findings are inconsistent, however, since other studies have found no significant differences in basal ganglia nuclei volumes compared to those of normal control patients ( Moriarty et al 1997; Zimmerman et al 2000), or have found increased caudate volumes in children with TS ( Denkla et al 1991). Functional MRI has revealed activity in the neocortex, striatum, thalamus, parietal operculum, supplementary motor area, insular cortex, and cerebellum in association with tic generation ( Peterson 2001; Bohlhalter et al 2006; Lerner et al 2007), while increased activity in the caudate and frontal and temporal cortices and decreased activity in the ventral GP, putamen and thalamus have been observed during tic suppression ( Peterson 2001). Increased activation of the substantia nigra, ventral tegmental area, and basal ganglia structures of the direct pathway has also been associated with increased tic severity in nonmedicated children with TS ( Baym et al 2008). Positron emission tomography (PET) studies using 18F-fluorodeoxyglucose in patients with TS demonstrate increased metabolic activity in the premotor and supplementary cortices and midbrain and concomitant decreased activity in the caudate and thalamus ( Stoetter et al 1992; Eidelberg et al 1997) while in those studies using 15O-water found increased activity in cerebral regions associated with sensorimotor, language, executive and paralimbic functions, which was temporally related to both the expression of motor and phonic tics and their premonitory urges ( Stern et al 2000). Finally, consistent with PET findings of decreased glucose utilization, single photon emission tomography (SPECT) has revealed decreased regional blood perfusion of the basal ganglia, thalamus, and frontal and temporal cortices in TS ( Peterson et al 1993). Anatomic localization of TS symptom generation to the basal ganglia is consistent with current understanding of basal ganglia physiology. In a general sense, disordered cortico-striato-pallido-thalamo-cortical circuitry is thought to be etiologically-related to TS, although the specific nuclei and circuits responsible for the various symptoms remain a matter of continued investigation ( Müller-Vahl 2002; Mink et al 2006). It has been suggested, for example, that simple motor tics could be due to abnormal activation of the motor cortex via thalamocortical pathways while involvement of premotor, supplementary motor, and cingulate cortices may be related to more complex motor tics ( Stern et al 2000; Mink et al 2001). Inappropriate activity in Broca’s area, the frontal operculum, and the caudate nucleus could elicit vocal tics ( Stern et al 2000; Mink et al 2001). Abnormal activation of the orbitofrontal region, which has been observed in obsessive compulsive disorder, may underlie the compulsions and urges that patients with TS experience ( Stern et al 2000; Mink et al 2001). Alternatively, tics in TS may be due to abnormal activity within subsets of neurons within the caudate and putamen ( Graybiel et al 1994; Mink et al 2001); indeed, microstimulation of discrete areas of the putamen in monkeys induces stereotypic movements akin to tics ( Alexander et al 1985). Neurotransmitter studies Given the diversity of nuclei and circuits that may be involved in TS pathogenesis, the variety of neurotransmitter systems that are also implicated is not surprising ( Jankovic 2001). In the frontal subcortical circuits alone, abnormalities in glutamate, dopamine, serotonin, GABA, acetylcholine, noradrenaline, opioid, and cannabinoid receptors are thought to be involved ( Lavenstein et al 2003). The serotonergic system has been studied in particular: patients with TS have been found to have decreased levels of serotonin and its metabolite 5-hydroxyindoleacetic acid in their serum ( Comings 1990) and cerebrospinal fluid ( Butler et al 1979), respectively, and post-mortem studies have found decreased serotonin levels in the brain stem ( Swerdlow and Young 2001). This latter finding is particularly relevant since serotonergic projections from the medial raphe nucleus are known to project to regions implicated in tic generation, such as the prefrontal cortex, substantia nigra pars compacta, ventral tegmental area, striatum, and nucleus accumbens ( Alex et al 2005; Pehek et al 2006). These target structures are components of the dopaminergic system and, thus, it has been hypothesized that it is not serotonergic dysfunction, per se, that induces tics, but rather its effects on the dopaminergic system ( Harris et al 2006). Serotonin influences dopaminergic release via a number of receptors, including serotonin heteroreceptors and inhibitory and stimulatory somatodendritic receptors, and is involved in dopamine reuptake ( Sershen et al 2000; Alex et al 2005; Pehek et al 2006; Carta et al 2007). Indeed, the most widely purported hypothesis to explain the etiology of TS concerns dopaminergic circuitry dysfunction. The ability of dopaminergic antagonists to suppress tics suggests that the dopaminergic system is hyperactive in TS ( Jankovic 2001). The direct dopaminergic basal ganglia pathway is thus facilitated, and the indirect pathway inhibited, which results in thalamocortical over-activity ( Visser-Vandewalle 2007; Figure 1). Dopaminergic hyperactivity could arise due to alterations in dopamine release ( Snyder et al 1970; Singer et al 1982; Harris et al 2006). Imaging studies In TS suggest an “overactive DAT [dopamine transporter] system” ( Harris et al 2006): for example, SPECT has demonstrated increased dopamine transporter binding in the striatum in patients with TS ( Cheon et al 2004; Serra-Mestres et al 2004), suggesting an elevated density of presynaptic dopamine terminals and postsynaptic D2 dopamine receptors, particularly in the ventral striatum ( Wong et al 1989; Ernst et al 1999; Wolf et al 1996; Albin et al 2003). In further study of D2 receptors using 11C raclopride PET, amphetamine challenge caused a 21% increase in intrasynaptic dopamine levels that was not observed in control patients ( Singer et al 2002). Although D2 receptor density has correlated with TS symptom intensity in monozygotic twins ( Wolf et al 1996), this has not been consistently observed ( Wong et al 1997). The net result of increased DAT density is decreased tonic extracellular levels of dopamine, increased dopamine levels in the axon terminal, and dopamine receptor supersensitivity (reviewed in Harris et al 2006). Alternatively, TS may result not from abnormalities of dopaminergic transmission but from changes in the resting membrane potentials of striatal neurons whose response to dopamine is consequently affected ( Mink et al 2001). | Figure 1Schematic representation of basal ganglia circuitry (modified from Visser-Vandewalle et al 1997), with excitatory (glutamatergic) projections
and inhibitory (GAB-Aergic) projections →. Normally, dopamine, acting via D1 dopamine receptors, has (more ...) |
|
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