Mood disorders after stroke are common and disabling and can have an impact on rehabilitation outcome: depression, for instance, is associated with longer hospital stays, reduced participation in rehabilitation, increased physical impairment and handicap, as well as increased mortality (Ebrahim et al. 1987; House et al., 2001; Morris et al., 1993; Sinyor et al., 1986).
PSD may be treated by means of both phamacological and non-pharmacological interventions, and the drug therapy for depression is based on the notion that this clinical condition is associated with an imbalance and under-activity of the cerebral noradrenergic and serotonergic systems (Takeuchi et al., 2014). In a meta-analysis of 16 studies, Chen and coll. (2006) reported a significant reduction in depressive symptomatology on all scales used to assess outcome, identifying a relationship between duration and benefit of pharmacological intervention: treatment duration of 3 weeks onward revealed significant positive effects. Likewise, Hackett and coll. (2008), by examining the use of pharmacological interventions for the PSD treatment, concluded that use of pharmacotherapy was associated with a small, but significant, positive treatment effect. However, this should be considered in light of side effects associated with the use of antidepressant medications. Indeed, some studies examined the potential risks associated
63 with the use of antidepressants in older individuals (Coupland et al. 2011; Wu et al. 2011), which demonstrated increased risk for some adverse outcomes as stroke/TIA. In particular, Coupland and coll. (2011) identified a large cohort of individuals with diagnosis of depression with an age higher than 65, where the use of antidepressant drugs was associated with significantly increased risk of adverse outcomes including all-cause mortality, attempted suicide/self-harm, falls, and fractures. The pattern of association with adverse outcomes varied with the class of drug examined: more specifically, the use of Selective Serotonin Reuptake Inhibitors (SSRIs) was associated with the greatest risk for falls and hyponatraemia.
In the retrospective study conducted by Ried and colleagues (2011), the treatment with SSRI antidepressant prior to stroke, was only associated with an increased risk for mortality following stroke, even though the SSRI treatment for depression both before and after the stroke, was found to be protective for mortality when compared to no post-stroke treatment.
Psychostimulants (such as methylphenidate), used for treating attention-deficit disorders, have been revealed to be an effective treatment for PSD. More specifically, methylphenidate has its effects in the cortical and subcortical areas of the brain and, thus, is thought to heighten mood by affecting several neurotransmitter systems, in particular the noradrenergic system. In addition, it blocks the reuptake of serotonin and norepinephrine and has dopaminergic activity and, therefore, it is thought that methylphenidate may affect PSD by correcting the depletion of biogenic amines caused by stroke, and to relieve apathy (Johnson et al. 1992).
As for non-pharmacologic treatments of PSD, there is some evidence that psychological interventions, such as motivational interviewing and problem solving, may prevent depression after stroke (Hackett et al., 2008).
64 The efficacy of Cognitive-Behavioral Therapy (CBT), a psychological approach assessing dysfunctional emotions and thoughts and maladaptive behaviours, and aiming to mitigate psychological disorders (Beck, 1967), is supported by studies on patients with diagnosis of ABI (Stalder-Lüthy et al., 2013; Waldron et al., 2012) and other neurological conditions, such as multiple sclerosis (Hind et al., 2014) and Parkinson’s disease (Armento et al., 2012; Dobkin et al., 2011). Using CBT to treat depression after stroke was first described in a single-case study (Hatcher et al., 1985) as part of a successful multidisciplinary approach.
However, Lincoln and Flannaghan (2003) compared, in post-stroke patients with depression, the CBT intervention (provided up to 10 sessions) with an attention placebo and standard care, and they found no significant difference between the groups, in terms of improvements in depression scores. Different explanations have been provided to describe this result, including the low number of CBT sessions and the fact that those who benefited least had poorer communication skills, suggesting that treatment of PSD requires a modified and tailored approach, able to circumvent the communication disabilities often shown by stroke patients (Lincoln and Flannaghan, 2003). Conversely, Chang and coll. (2011) compared a counseling intervention similar to CBT with an usual care, and found that depressive symptoms improved in the patients group received the CBT intervention. While there is some evidence for CBT efficacy in treating PSD, very little is known about its effects on PSA (Kneebone and Jeffries, 2013). In the same way, much is still unknown regarding the effect of relaxation therapy (a behavioural technique which helps to break the cycle of stress response favouring physiological and psychological relaxation; Anand, 2006) on post-stroke mood disorders and, more specifically on PSA, and further studies are warranted.
Finally, there are few studies also regarding effective interventions on post-stroke pseudobulbar affect, and the most common treatment consists of antidepressant drugs, in
65 particular SSRIs (Takeuchi et al., 2014), which are associated with reduction in the frequency and severity of pathological crying episodes (House et al., 2004). However, as noted by House and coll. (2004), study results about the SSRIs efficacy on post-stroke emotionalism, should be interpreted with caution, since most studies were quite small and used different methods to define and assess the pseudobulbar affect, and to determine frequency and severity of episodes or outbursts. Thus, further investigations are required to better establish the efficacy of antidepressant drugs on pathological crying or laughing.
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