الکتروشوک درمانی و نشانگرهای زیستی آسیب عصبی و شکل پذیری: سطح سرمی نورون های خاص و پروتئین S-100B
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|34497||2010||4 صفحه PDF||سفارش دهید||4074 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research, Volume 177, Issues 1–2, 15 May 2010, Pages 97–100
Electroconvulsive therapy (ECT) is considered an effective and safe treatment in major depressive disorders. However, the possibility that it may induce cognitive adverse effects observed in selected patients has raised a concern that ECT may induce neuronal damage. The biomarkers of brain damage, neuron-specific enolase (NSE) and S-100b protein (S-100b), were measured in serum before and after ECT to determine whether this treatment induces neuronal injury or glial activation. ECT was administered to 10 patients with major depressive disorder. The serum samples were analyzed before (baseline) and after ECT at 1 h, 2 h, 6 h, 24 h and 48 h. The severity of depression was scored with the Montgomery-Åsberg Depression Rating Scale (MADRS) and Beck Depression Inventory (BDI) pre-to-post ECT. There were no statistically significant changes in the median concentrations of NSE or S-100b at various time points before or after ECT. However, there were substantial elevations in the levels of S-100b in four patients. High levels of S-100 at 2 and 6 h correlated with the response to the treatment. These results suggest that ECT does not produce neuronal injury. The transient increase in the levels of S-100b reflecting activation of glial cells may play a part in mediating the antidepressant effects of ECT.
Electroconvulsive therapy (ECT) is regarded as an effective treatment in major depressive disorders, especially in medication-resistant patients (American Psychiatric Association, 2001 and Wahlund and von Rosen, 2003). Although ECT is considered safe, it may induce reversible memory deficits, i.e. acute postictal disorientation and anterograde or retrograde amnesia (Calev et al., 1991, Sackeim, 1992, Sackeim et al., 1993 and Rose et al., 2003). Persistent cognitive adverse effects observed in selected patients have raised a concern that ECT may induce neuronal damage (Sackeim et al., 2007). However, no evidence of structural brain damage due to ECT has been found in brain imaging studies (Devanand et al., 1994, Puri et al., 1998, Anghelescu et al., 2001 and Szabo et al., 2007). Neuron-specific enolase (NSE) and S-100b protein (S-100b) are specific markers of brain damage. NSE, the γ-subunit of enolase, originates predominantly from the cytoplasm of neurons and neuroendocrine cells. S-100b is present in high concentrations in glial cells and Schwann cells and plays a regulatory role in the cytoskeleton and cell cycle (Donato, 2001). The serum levels of these proteins are elevated after different types of brain damage such as focal and global ischemia (Büttner et al., 1997, Missler et al., 1997 and Rosén et al., 1998), head injury (Savola et al., 2004) and hemorrhagic brain damage (Persson et al., 1987). Increased levels of NSE have been reported in a subset of epileptic patients after seizures (Pitkänen and Sutula, 2002), but no postictal elevation of S-100b after single seizures has been observed (Büttner et al., 1999, Palmio et al., 2001 and Leutmezer et al., 2002). Serum levels of NSE or S-100b after ECT at different time points have not been increased compared with the baseline in the majority of previous ECT studies (Greffe et al., 1996, Berrouschot et al., 1997, Zachrisson et al., 2000 and Agelink et al., 2001). However, Arts et al. found a small rise in S-100b at 1 h after ECT (Arts et al., 2006). Only one study has used both NSE and S-100b as marker of brain damage after ECT, but the first samples after ECT were taken after 6 h (Agelink et al., 2001). Given the short half-life of S-100b, possible changes may not have been detected. On the other hand, in the chronic electroconvulsive shock (ECS) model astrocytic responses have been interpreted as representing plastic reactions in rat brains. With the absence of evident neuronal injury the observed elevations of S-100b levels suggest that ECS-induced astrocytic activation may also be neuroprotective (Busnello et al., 2006). Thus S-100b changes in ECT may not necessarily reflect neuronal damage but, rather, transient activation of glial cells associated with therapeutic responses of the treatment. In the present study we measured NSE and S-100b levels in serum before and after ECT to determine whether this treatment is associated with either neuronal injury or glial activation.