RESUMO
Quality and quantity of the human stress response are highly individual. Not only are there differences in terms of psychological and physiological stress reactivity, but also with regard to facial muscle stress reactivity. In a first correlative pilot study to decipher the signature of stress as it presents in the physiognomy of a stressed individual, we investigated how stress-induced muscle movement activity in the face is associated with stress marker activation during a standardized laboratory stress test. Female and male participants (N = 62) completed the Trier Social Stress Test and provided multiple measurements of salivary cortisol, subjective experience, heart rate, and high-frequency heart rate variability. In addition, participants were filmed during stress induction to derive the activation of 13 individual muscles or muscle groups, also termed action units (AU). Mean AU intensity and occurrence rates were measured using the opensource software OpenDBM. We found that facial AU activity correlated with different aspects of the psychosocial stress response. Higher stress-induced cortisol release was associated with more frequent upper eyelid raiser (AU05) and upper lip raiser (AU10) occurrences, while more lip corner pulling (AU12) went along with lower cortisol reactivity. More frequent eyelid tightener (AU07) occurrences were linked to higher subjective stress reactivity but decreased heart rate and HF-HRV reactivity. Last, women showed greater stress-induced smiling intensity and occurrence rates than men. We conclude that psychosocial stress reactivity is systematically linked to facial muscle activity, with distinct facial stress profiles emerging for different stress markers. From all the AUs studied, eyelid tightening (AU07) seems to provide the strongest potential for future attempts of diagnosing phases of acute stress via facial activity.
RESUMO
Exposure to excessive and long-term stress may result in dysregulation of the stress system, including the acute stress response. In particular, failure to downregulate stress-related reactivity may lead to prolonged stress responses and the accumulation of allostatic load. However, the contribution of altered acute cortisol recovery to chronic stress and associated health impairments has often been neglected. Addressing this lack of research, we explored whether recovery from - more so than reactivity to - acute stress captures the basal stress load of an individual. Using Piecewise Growth Curve Models with Landmark Registration, we analyzed cortisol reactivity and recovery slopes of 130 healthy participants exposed to a standardized psychosocial laboratory stressor. Reactivity and recovery were predicted by measures indicative of long-term stress and its downstream effects, including self-report questionnaires, diurnal cortisol indices [cortisol awakening response (CAR); diurnal cortisol slope], markers of pro-inflammatory activity (interleukin-6; high-sensitive C-reactive protein), and hippocampal volume (HCV). Among these measures, only an increased CAR was specifically and consistently associated with relatively impaired recovery. Since the CAR represents the physiological enhancement needed to meet the anticipated demands of the forthcoming day, this finding may highlight the contribution of cognitive processes in determining both CAR and acute stress recovery. Furthermore, greater cortisol reactivity covaried with smaller HCV, showing that increased acute reactivity translates to health-relevant downstream effects. The lack of further associations between long-term and acute stress measures may arise from biases in self-reported chronic stress and the rigorously health-screened study sample. Overall, our findings suggest that while cortisol stress recovery might not supersede reactivity as an indicator of the long-term stress load or associated health effects, recovery and reactivity have differential utility in describing individuals' allostatic states.
RESUMO
BACKGROUND: Anti-NMDA receptor encephalitis (NMDAR-E) is an autoimmune encephalitis (AE) mainly affecting young females. It typically presents with isolated psychiatric symptoms (e.g. depressed mood) at first and neurological abnormalities (e.g. seizures, movement disorders) only develop later. Thus, there is a high risk of overlooking NMDAR-E in patients with preexisting psychiatric illness due to symptom overlap in the prodromal period of the disease when treatment is most effective. Although rare, concomitant or sequential development of a demyelinating disorder is increasingly recognized as an associated disease entity (overlap syndrome), with immediate diagnostic and therapeutic implications. CASE PRESENTATION: We report a patient with a borderline personality disorder (BPD), which developed NMDAR-E and an overlapping demyelinating disorder with anti-Myelin oligodendrocyte glycoprotein (MOG) -IgG positivity. The initial clinical presentation with predominantly affective symptoms (e.g. mood lability, anxiety, depressed mood) lead us to suspect an exacerbation of the BPD at first. However, acute changes in premorbid behavior, newly developed psychotic symptoms and memory deficits lead us to the correct diagnosis of an AE, which was further complicated by the development of a demyelinating disorder. As a result of impaired illness awareness and psychosis, diagnostic and treatment was difficult to carry out. The symptoms completely remitted after treatment with methylprednisolone 1 g daily for 5 days and 5 cycles of plasma exchange. CONCLUSIONS: Continuous awareness for neuropsychiatric clinical warning signs in patients with a pre-diagnosed psychiatric disorder is important for a timely diagnosis. Therefore, we believe that the diagnostic and therapeutic algorithm provided here, for the first time specifically addressing patients with preexisting psychiatric illness and integrating overlap syndromes, can be a useful tool. Moreover, in order to timely perform diagnostics and treatment, judicial approval should be obtained rapidly.
