Somatoform dissociation and posttraumatic stress syndrome – two sides of the same medal? A comparison of symptom profiles, trauma history and altered affect regulation between patients with functional neurological symptoms and patients with PTSD

Dissociative disorders (DD), characterized amongst others by loss of sensations and control of bodily movements [1], are often related to traumatic experience like sexual abuse [2, 3], and emotional neglect or abuse [4, 5]. Hence, it has been discussed whether DD can be conceived of as trauma-related syndrome [6‐9]. Posttraumatic stress disorder (PTSD), as a prominent representative of trauma-related disorders, is defined as response to life-threatening events (e.g. war, rape, torture or natural disaster) with symptoms like intrusions, hyperarousal and avoidance. Severe trauma, particularly sexual and here predominantly childhood sexual trauma, has been proposed as important source of somatoform and psychoform dissociation, potentially crucial in the development of DD [10‐13]. Yet, somatoform dissociative symptoms have been reported in PTSD patients as well [14], despite emphasis on psychoform dissociative symptoms [15‐17]. Nijenhuis introduced the concept of somatoform dissociation, referring to dissociative symptoms, that phenomenologically involve the body and comprise reduction up to complete loss of sensory perception and/or loss of motor control (negative somatoform dissociation) as well as involuntary perception of sensory (e.g. prickling), motor (e.g. tremor) and/or pain symptoms (positive somatoform dissociation) [18, 19]. On the contrary, psychoform dissociation describes a form of dissociation, that phenomenologically involves the mind [19] and pertains to disrupted mental processes such as consciousness, memory, identity and emotion, manifest in symptoms of depersonalization, derealisation, dissociative amnesia and/or out-of-body experience [17]. Often only those phenomena that Nijenhuis and other authors describe as “psychoform dissociation/dissociative symptoms” are subsumed under the label of “dissociation” or “dissociative symptoms” [17]. Beyond similarity of dissociative symptoms in PTSD and DD, the impact of dissociation in PTSD is mainly attributed to trauma severity, as peri-traumatic (mainly psychoform) dissociation and physiological components like fainting (see shut-down dissociation below) may foster later PTSD development and diagnosis [17]. Concerning somatoform dissociative symptoms in PTSD and DD, the concept of the defense cascade can explain the relation: Existential threat first prompts excessive physiological arousal (to prepare the organisms for fight/flight responses), which upon lack of escape options turns into a “shutdown” response. Fainting and immobility as manifestations of vagal dominance represent typical symptoms of such “shutdown” [14, 20‐22] and can be described as somatoform dissociation, leading e.g. to functional neurological symptoms [23, 24]. Alexithymia, the deficient ability to perceive and verbally express emotions [25], signifies another correspondence between DD and PTSD. As representative of altered affect regulation alexithymia has been shown in DD patients [26‐29], as well as in PTSD patients [30]. Frewen and colleagues reported positive correlations between alexithymia, PTSD symptom severity, dissociative symptom severity, and childhood abuse and neglect in PTSD patients, while Sondergaard and Theorell [31] determined evolving alexithymia as predictor of self-rated PTSD (but not depressive) symptoms in refugees. A recent study by Terock and colleagues reported alexithymia as predictor of adult psychoform dissociative symptoms independent of the effects of PTSD and childhood trauma [32]. Furthermore, alexithymia was found to predict suicidal attempt in veterans diagnosed with PTSD [33].

In the present study, symptom profiles, trauma histories and alexithymia were compared between the two diagnostic categories DD and PTSD with the hypotheses that (1) a common “trauma-related” syndrome becomes manifest in similar somatoform and psychoform dissociative symptoms and similar trauma histories across the diagnostic groups; (2) the relation of trauma history to symptom expression indicates a common meaning of trauma in the generation of DD and PTSD; (3) correspondence of alexithymia between the two diagnostic groups and its relation to dissociative symptom expression indicates the important role of affect regulation in the development of DD and PTSD.

In the present sample, patients with ICD-10 diagnoses of DD were characterized by dissociative motor disorder, i.e. “loss of ability to move the whole or part of a limb or limbs” (ICD-10, p. 127), dissociative anaesthesia and sensory loss, referring to impaired tactile, auditory or sensory perception, or mixed dissociative disorder integrating both.¹ Patients with ICD-10 diagnosis of PTSD represented trauma-related disorders. Matching symptom profiles, trauma history, and alexithymia in the two diagnostic groups should indicate the correspondence of syndromes, thus clarifying the conception of DD as trauma-related disorder (thereby informing the meaning of trauma in the generation of DD and supporting attuned diagnostics and treatment strategies).

A history of traumatic experience and corresponding symptoms in affected patients have encouraged the association of dissociative and posttraumatic stress disorders. However, conceiving of both diagnoses as the same syndrome asks for conformity on all levels. The present comparison of characteristic symptoms, trauma and maltreatment history between patients diagnosed with DD or PTSD (per hypothesis 1) demonstrated group differences in symptom prominence (e.g., psychoform vs. somatoform symptoms) and trauma profiles (e.g. emotional vs. sexual abuse) that challenge a global assignment of DD to the category of trauma-related disorders. Rather, the conformity of DD patients with co-occuring PTSD and PTSD patients on several measures (number of lifetime traumata, amount of physical and emotional abuse in childhood, PTSD symptom severity and severity of somatoform dissociation) suggests the portrayal of a “trauma-related DD syndrome”. While accumulated traumatic experience may add to symptom severity, they are not critical for the generation of DD (compare also research by Stone and colleagues [47]). Distinction of syndromes per symptom and trauma profile does not render the association between trauma and dissociation obsolete (hypothesis 2). Indeed, the variation of severity of posttraumatic stress symptoms and dissociative symptoms with traumata and childhood maltreatment, illustrated in Figs. 1, 2 and 3, suggests an impact of coping with such experience on augmented somatoform dissociation and the development of DD. Moreover, chronic dissociative symptoms in DD and PTSD may be explained as a conditioned response upon repeated adverse experience [14, 20‐22]. It is conceivable, that the individual post-traumatic learning and coping history shapes development and type of dissociative symptom (psychoform or somatoform) upon later confrontation with adverse and traumatic events [20]. For instance a learning history of early coping with the emotional consequences of trauma and maltreatment with somatic symptoms and somatoform dissociation may favour the development of DD. Alexithymia as an expression of altered emotion processing was expected to be increased in patient groups and related to symptom expression. The present diagnostic groups differed in alexithymia, in that DD patients had lower TAS scores than PTSD patients. This suggests that DD patients were able to perceive and express their emotions, although less efficiently than HC. In line with the hypothesis of modulation by learning history, and the literature [29], the positive relation between alexithymia and somatoform symptom severity might reflect the learned attribution of feelings to somatic sensations. A further factor to explain the evolution of trauma-related and dissociation-related disorders (PTSD and DD in the present example) might be the dose: The coincidence of higher trauma load (childhood adversities and lifetime traumata) and higher symptom scores in PTSD patients and DD patients with comorbid PTSD may indicate a “dose effect”, i.e., higher trauma load results in the more severe disorder as characterized by comorbidity and symptom severity [48]. Commonly, higher trauma load in patients with PTSD as well as in DD patients is described to be related to more sexual traumata. In contrast, in the present data this relation was replicated for the PTSD group only, while both DD groups report similar sexual traumata as HC. Interestingly, emotional adverse experience do differentiate between both DD groups, which may point towards emotional neglect/abuse as a distinguishing factor. Potential influences of comorbid conditions also have to be taken into account here: Depression is a frequent comorbid disorder in PTSD [49] and DD [50] also in the present groups (Table 5). Recent research found evidence for a depressive subtype of PTSD that is associated with greater dissociative experience [51]. Since 38.5% of the current sample of PTSD patients suffered from a comorbid depressive disorder or depressive episode, this may explain the high amount of dissociative symptoms. Frequency of comorbid depressive and anxiety disorders (identified as further comorbid conditions across groups) did not significantly differ between the current patient groups, so that a major impact of this comorbidity on the between-group differences of interest seems unlikely. Current group-specific comorbidities, i.e. comorbid somatoform disorder in DD patients and comorbid borderline personality disorder in PTSD patients are comparable to results from previous studies [3, 52‐54] and indicate common contributions to dissociative symptoms. Dissociative disorders are characterized by somatoform dissociative symptoms independent of comorbid PTSD diagnosis – as reflected by the amount of comorbid somatoform disorder diagnoses, which was significantly higher in patients diagnosed with DD compared to patients diagnosed with PTSD.

Limitations of the present study have to be noted: (1) Different syndromes of PTSD and DD were concluded from different symptom profiles. However, as patient samples were recruited in different institutions, differences in treatment settings between the two patient groups are likely. It cannot be ruled out, that these differences may have influenced the results. (2) Many DD patients showed substantial signs of severe somatoform dissociative symptoms (like sitting in a wheelchair) parallel to low self-evaluation of somatoform dissociation (lower SDQ-20 scores than PTSD patients). This suggests, that the SDQ-20 may not properly mirror severity of functional neurological symptoms in DD patients. For each symptom the SDQ-20 evaluated the frequency of experience, while symptom duration was not assessed. Somatoform dissociative symptoms are long lasting or permanent in DD, while they may last for minutes or hours in PTSD. Thus, including symptom duration in the measurement of dissociative symptoms seems mandatory for the specification of DD syndrome and its distinction from PTSD. (3) Involving PTSD as an example of trauma-related syndrome in the present study does not justify the generalization of the present results and conclusions. Further studies should consider other trauma-related syndromes, such as acute stress disorder, adjustment disorder etc. However, complex PTSD was chosen as an example for trauma-related disorders in the present study, since it is associated with high levels of dissociation – which is especially documented in manifold studies reporting psychoform dissociative symptoms in PTSD patients [15‐17] and multiple trauma experience in patients with conversion or other dissociative disorders [12, 23, 55].

The present comparison of symptoms and trauma history between DD and PTSD revealed a clear distinction between the diagnostic groups, disconfirming hypothesis (1) of a common syndrome. Still, results indicate an important role of adverse/traumatic experiences and the experience of posttraumatic stress symptoms in the development of dissociative symptoms (per hypothesis 2). This specification matches the diagnostic descriptions in DSM-V, in that a relevant psychological stressor preceding the onset of functional neurological symptom disorder, earlier required as diagnostic criterion, is now labelled as a specification feature. Moreover, distinct sub-groups of DD patients with and without PTSD are also reflected in the specification of a dissociative subtype of PTSD in DSM-5 [56]. The results have important clinical implications: Adopting a context of linking dissociative and trauma-related disorders asks to consider a broad range of dissociative symptoms, not only psychoform derealization or depersonalization phenomena but also somatoform dissociative symptoms [14, 20, 21, 57]. Present results further direct attention to individual maltreatment and coping/learning history to be considered in diagnostics and treatment: While the number of traumatic events may determine the severity of distress, the individual coping history with adversities and traumata may modulate, how symptoms develop and accentuate in patients diagnosed with DD, and potentially overlap with those of individuals diagnosed with PTSD. This advocates the careful assessment of trauma history and its consequences in diagnostics and treatment of DD.