Wants Talk Psychotherapy but Cannot Talk

In three years has your hospital decided that this might be worth a try?

Do you prefer your  incompetence NOT KNOWING? OR NOT DOING?

Wants Talk Psychotherapy but Cannot Talk

Innov Clin Neurosci. 2018 Feb 1; 15(1-2): 45–48.

Published online Jan-Feb 2018.

 

Jeffrey Guina, MD and Cathryn Guina, BSN, RN, CNRN

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Abstract

While post-stroke depression (PSD) is a common sequelae of stroke, many stroke survivors also have expressive aphasia (i.e., the inability to produce spoken or written language), which limits or prevents treating depression with talk psychotherapy. Unlike most psychotherapy modalities, eye movement desensitization and reprocessing (EMDR) does not require extensive verbal communication to therapists, which might make EMDR an ideal treatment modality for aphasic patients with mental health concerns. The authors present the first known case reporting EMDR in aphasia, describing the treatment of a 50-year-old woman with a history of depression following a left middle cerebral artery stroke. Left frontal lobe strokes are independently associated with both PSD and expressive aphasia. EMDR began two years following the stroke, at which point the patient continued to have persistent expressive aphasia despite previously completing more than a year of speech therapy. Using the Blind to Therapist Protocol, EMDR successfully led to improvement in depressive symptoms and, surprisingly, improvement in aphasia. This case report suggests that EMDR might be beneficial for those with mental health concerns who have expressive communication impairments that might prevent treatment with other psychotherapy modalities. We discuss potential challenges and technical workarounds with EMDR in aphasia, we speculate about potential biopsychosocial explanations for our results, and we recommend future research on EMDR for PSD and other mental health concerns in the context of aphasia, as well as possibly for aphasia itself.

Keywords: Stroke, aphasia, depression, EMDR, psychotherapy

Among stroke survivors, 35 percent develop expressive and/or receptive aphasia, 30 percent develop post-stroke depression (PSD), and seven percent complete suicide.^1,2 Treating PSD is important because of increased risks for all-cause mortality, suicide, recurrent stroke, and worse neurological recovery.^2–7 While studies have indicated that antidepressants and psychotherapy are effective for PSD,^2,3,8 psychotherapy options are very limited for those with comorbid aphasia. Only a few studies/cases have been reported demonstrating positive results with behavioral therapy,⁹ counseling¹⁰ and family therapy.¹¹ Although the ability to communicate is generally considered a prerequisite for psychotherapy, verbal expression of information is not necessary for eye movement desensitization and reprocessing (EMDR) to be successful.¹²

EMDR is a psychotherapy that uses, among other techniques, alternating bilateral stimulation (BLS; e.g., eye movement, auditory, tactile) while patients internally attend to memories, emotions, cognitions, images, and bodily sensations. The blind to therapist (B2T) protocol¹³ was developed for those unwilling/unable to describe memories during EMDR due to control, shame/embarrassment, cultural reasons, or language barriers. Though EMDR is effective for depression,^14–16 PubMed, PsycINFO, EMDRIA, and Ingenta Connect searches did not reveal any articles about EMDR in those with comorbid aphasia. We aimed to determine if our patient with PSD could benefit from EMDR despite severe expressive aphasia.

 Case report at link.

EMDR therapy for PTSD after motor vehicle accidents: meta-analytic evidence for specific treatment

Would this be useful for the 23% chance of PTSD following stroke?
http://journal.frontiersin.org/article/10.3389/fnhum.2015.00213/full? 
Maddalena Boccia^1,2, Laura Piccardi^2,3*, Pierluigi Cordellieri¹, Cecilia Guariglia^1,2 and Anna Maria Giannini¹

• ¹Department of Psychology, “Sapienza” University of Rome, Rome, Italy
• ²Neuropsychology Unit, IRCCS Fondazione Santa Lucia of Rome, Rome, Italy
• ³Department of Life, Health and Environmental Sciences, L’Aquila University, L’Aquila, Italy

Motor vehicle accident (MVA) victims may suffer both acute and post-traumatic stress disorders (PTSD). With PTSD affecting social, interpersonal and occupational functioning, clinicians as well as the National Institute of Health are very interested in identifying the most effective psychological treatment to reduce PTSD. From research findings, eye movement desensitization and reprocessing (EMDR) therapy is considered as one of the effective treatment of PTSD. In this paper, we present the results of a meta-analysis of fMRI studies on PTSD after MVA through activation likelihood estimation. We found that PTSD following MVA is characterized by neural modifications in the anterior cingulate cortex (ACC), a cerebral structure involved in fear-conditioning mechanisms. Basing on previous findings in both humans and animals, which demonstrate that desensitization techniques and extinction protocols act on the limbic system, the effectiveness of EMDR and of cognitive behavioral therapies (CBT) may be related to the fact that during these therapies the ACC is stimulated by desensitization.

Introduction

Traumatic events (including not only large-scale disasters but also common day-to-day events, such as Motor vehicle accidents (MVAs) are an important cause of psychological distress and psychiatric disorders. Harvey and Bryant (1998) reports the presence of acute stress disorders (ASD) in 13% of MVA survivors, and according to Mayou et al. (1993) one year after a MVA a quarter of those followed up showed psychiatric disorders, with 11% affected by post-traumatic stress disorders (PTSD).

PTSD is a relatively common psychiatric disorder occurring as a consequence of a major traumatic event. It is clinically characterized by the following symptoms: involuntarily re-experiencing phenomena (e.g., nightmares, flashbacks, intrusive images as well as recurrent distressing thoughts of the event); avoidance of talking about or being reminded of the traumatic event, negative alterations in thoughts and mood, emotional numbing and hyperarousal symptoms (e.g., sleep disturbance, difficulty in concentrating, increased irritability and hypervigilance) (DSM-IV; American Psychiatric Association, 2000, 2004).

Different types of psychological therapies have been proposed in the treatment of PTSD, including exposure therapy (Creamer et al., 2004), cognitive therapy (Resick and Schnicke, 1992; Ehlers et al., 2005), psychodynamic psychotherapy (Brom et al., 1989) and eye movement desensitization and reprocessing (EMDR; Shapiro, 1989). EMDR is currently an effective psychological treatment, recognized and recommended as a firstline treatment for trauma in numerous international guidelines (Bisson and Andrew, 2007). According to the review by Ponniah and Hollon (2009) EMDR ameliorates PTSD symptoms significantly more than waiting list, standard care, and pill placebo. They also reported that a number of studies found that EMDR was superior to trauma-focused cognitive behavioral therapies (CBT) on some measures of PTSD symptoms. However, all of these studies had mixed trauma samples. Another data coming from this review is that between 77 and 90% of EMDR patients no longer met diagnostic criteria for PTSD at the end of treatment. Ponniah and Hollon findings provide support for the use of EMDR for all patients with PTSD.

EMDR is a supplementary trauma-focused therapy that includes elements from other effective psychotherapies in a structured protocol drawn from an information processing model of PTSD (Bisson et al., 2013). It requires the individual suffering from PTSD to focus attention on a traumatic memory whilst simultaneously visually tracking the therapist’s finger as it moves across his/her visual field, and then to engage in a restructuring of the memory (Shapiro, 1995). Eye movements are the most common form of bilateral stimulation, but stimulation might also be auditory (alternating tones) or sensory (finger tapping). It acts by using dual attention tasks to help the patient process the traumatic event while focusing on negative trauma-related memories, emotions and thoughts during the performance of a task that requires a bilateral stimulation (e.g., eye movements; hand tapping; tones) until a growth in more positive trauma-related thoughts (Jensen, 1994; Shepherd et al., 2000; Marcus et al., 2004).

Since its discovery, EMDR has been considered one of the treatments of choice for PTSD, even though studies on its effectiveness are often hindered by methodological problems (see for a critical review Cahill et al., 1999), and in the view of some authors “what is effective in EMDR (imaginal exposure) is not new, and what is new (eye movements) is not effective” (McNally, 1999, p. 2). Although bilateral stimulation is discussed controversially (Cahill et al., 1999), growing evidence has demonstrated the effectiveness of EMDR in treating both PTSD in victims and mourning in survivors (Sprang, 2001; Solomon and Rando, 2007; see also meta-analysis studies: Bisson et al., 2013; Lee and Cuijpers, 2013; Watts et al., 2013). Lee and Cuijpers (2013) performed a meta-analysis in which 15 clinical and 11 experimental studies demonstrated different effects of bilateral stimulation through eye movements compared with those produced by other exposure therapies. Possible explanations for the effectiveness of alternating bilateral stimulation are: stimulation acts specifically on disintegrated information related to the traumatic event, or boosts the processing of emotionally memories or, last but not least, may enhance emotional processing in general (Sprang, 2001; Korn and Leeds, 2002). Herkt et al. (2014) recently observed in healthy subjects without post-traumatic symptoms increased activation in the right amygdala during alternating auditory bilateral stimulation, as used in EMDR, while processing emotionally negative stimuli. These authors suggested that the increase in limbic processing along with decreased frontal activation is in line with theoretical models (Shapiro, 1989, 2002) of how alternating bilateral stimulation might help with the therapeutic reintegration of information. Specifically, Shapiro (1989) suggests two possible interpretations for the effects of alternating bilateral stimulation: (i) it may boost the processing of any emotionally laden material in general; or (ii) it may have a specific effect just on disintegrated information related to the traumatic episode. Clinicians also observe a decrease in vividness and arousal related to trauma-associated stimuli after EMDR, and neuroimaging studies show that after EMDR there is a decreased activation in limbic areas and increased activation in prefrontal brain regions known to be responsible for cognitive control after the completion of successful treatments (Lansing et al., 2005; Pagani et al., 2007). Clinical trials suggest that different traumatic events interact with individual factors (such as personality, gender and genetic factors) and lead to different physical and behavioral outcomes as well as a different prevalence of PTSD (Ditlevsen and Elklit, 2012; Santiago et al., 2013; Husarewycz et al., 2014; Perrin et al., 2014). Even if altered brain areas after PTSD are common and play complementary roles in maintaining the PTSD symptomatology, such as fear conditioning of trauma-related stimuli and failing to recall fear extinction (Pitman et al., 2012). However, specific network of areas could be observed due to specific trauma. In details, PTSD after physical or sexual abuse modifies specific brain structures including the middle and anterior cingulate cortex (MCC; ACC), precuneus (pCU) and middle frontal gyrus (see Shin et al., 1999; Lanius et al., 2002, 2005). These brain regions are involved in pain processing, fear, sadness and proprioceptive information. Differently, in the PTSD after combat-related trauma alterations have been found in a network of areas including the bilateral insula, inferior frontal gyrus (IFG), posterior cingulate cortex (PCC), superior parietal lobe (SPL) and hippocampus (Pissiota et al., 2002; Britton et al., 2005; Geuze et al., 2007; Morey et al., 2008). Also these structures are known to be involved in emotional processing, especially of sadness (Vogt, 2005), and in monitoring internal body states, but they are also involved in a wide range of cognitive functions, including episodic memory, spatial navigation, imagining and planning for the future (Hassabis and Maguire, 2007; Vann et al., 2009; Boccia et al., 2014). A specific network of areas is present also in PTSD after catastrophe and includes the bilateral parahippocampal gyrus (PHG), right superior temporal gyrus (STG) and superior frontal gyrus (SFG; Hou et al., 2007; Chen et al., 2009; Mazza et al., 2012). Specifically, the PHG has a crucial role in spatial navigation and in scene perception (Epstein and Morgan, 2012) and it is reported only in this kind of trauma, likely due to the fact that the natural disasters mostly involved the surrounding environment and familiar places. Taking together these fMRI studies seem suggest that PTSD due to different kind of trauma can be different from a neurological and cognitive point of view. As a consequence also the variability in the psychological therapies effectiveness could be partially explained by the existence of different neural substrates underpinning the main disorder.

In view of this evidence, the main aim of the present study is to examine the extent to which neurobiological evidence supports the specific treatment of PTSD after MVA with EMDR. To pursue this aim we first reviewed previous neuroimaging studies about PTSD after MVA and those about neural correlates of EMDR. We hypothesized that by modulating the dysfunctional network of PTSD-MVA, EMDR may be the treatment of choice for patients who develop PTSD after a MVA. To test this hypothesis, we performed a meta-analysis of fMRI studies on PTSD after MVA to assess neural network functional changes in people suffering from PTSD following a MVA, using activation likelihood estimation (ALE; Eickhoff et al., 2009). Results have been discussed in light of current evidence about the neural underpinnings of EMDR, which suggests a specific and biologically-based approach to PTSD after MVA.