Cerebral Perfusion, Electrical Activity and Effects of Serotonergic Treatment in Obsessive-Compulsive Disorder

Abstract

An abnormally increased glucose metabolism has been described with positron emission tomography (PET) in frontal and caudate regions of obsessive-compulsive patients. Perfusion and electroencephalographic studies have been less conclusive. However, these techniques are, currently, more available than PET and, therefore, deserve further study because of their possible clinical applications. In this article, 13 obsessive-compulsive patients were studied with quantitative EEG and auditory and visual evoked potentials. Six of them were studied also with perfusion single photon emission tomography. A group of 4 patients was studied with both techniques before and after a serotonergic treatment. Increased global, beta, and theta electrical power together with an increased perfusion in frontal regions was observed. The patients also showed a delta power increase over right temporal and frontal regions, together with increased perfusion in the right basal ganglia region as well as a decreased amplitude of the P50 and N100 waves of the auditory evoked potentials over temporal electrodes; these alterations were reduced with treatment. These results are discussed in the context of current data about serotonergic neurotransmission.

Neurocognitive indices of executive hypercontrol in obsessive–compulsive disorder

“…extremely cautious and responsible attitude of the former vs. disinhibited attitude of the latter). Moreover, a hyperactivity of executive control would be consistent with the hyperactivity of the fronto‐striato‐thalamic pathway reported by the majority of brain imaging studies (8, 30–35, 42–45).…”

“…According to Carlsson (41) a cortical hyperactivation in the fronto‐striato‐thalamic circuits could be the mechanism underlying this strategy. This hypothesis is in line with the findings of hyperactivity of the fronto‐subcortical pathways reported by brain imaging investigations (8, 29–33, 42–45) and of a relationship between the slow alpha reduction (suggesting a hyperactivity of the functional circuits involved in the selective attention processes) and the time to perform the Self‐Ordered Pointing Tasks for drawings (SOPT‐D) (46).…”

“…However, such a hypoactivation has seldom been reported in OC subjects (16, 27, 28) and, according to some authors, it might be related to the presence of concomitant depression (29). As a matter of fact, in these patients, most neuroimaging studies reported an increased activity of the circuit involving orbitofrontal cortex, cingulate cortex, head of the caudate nucleus and thalamus (8, 30–35). Furthermore, patients with a hypofunctioning DLPFC show behavioural and cognitive‐emotional characteristics that are very different from those generally exhibited by OCD (e.g.…”

The extended fronto-striatal model of obsessive compulsive disorder: convergence from event-related potentials, neuropsychology and neuroimaging

“…Several studies reported increased metabolism and hyperactivity in several areas in OCD patients, including the BG (Swedo et al, 1989; Baxter et al, 1992; Molina et al, 1995; Perani et al, 1995), OFC (Baxter et al, 1988; Molina et al, 1995; Alptekin et al, 2001), and ACC (Swedo et al, 1989; Molina et al, 1995; Perani et al, 1995) cortices (see Figure 1). Furthermore, there is evidence of decreased activation in the DLPFC and parietal cortex during symptom provocation (Maltby et al, 2005; Van Den Heuvel et al, 2005; Viard et al, 2005; Remijnse et al, 2006).…”

Neurobiologie der Zwangsstörung

“…Im Großen und Ganzen unterstützen die Befunde aus funktionellen Ruhestudien, in denen Patienten mit Kontrollgruppen verglichen wurden, das Konzept der Dysfunktion der kortiko-striato-thalamo-kortikalen Schleife. Es liegen mehrere Studien mit FDG-PET (4-6, 42) und SPECT (37,58,59) Eine für die Diagnose Zwangsstörung relativ spezifische Beobachtung stellen Leistungsdefizite bei der Durchführung von Arbeitsgedächtnisaufgaben dar (47). Diese äußern sich in schlechterer Erinnerungsleistung und niedrigerer Verarbeitungsgeschwindigkeit (Reaktionszeit) im Vergleich zu Gesunden, aber auch zu Patienten mit Depression und Angststörungen (47).…”