Correlation Between Medically Diagnosed Anxiety and Depression Disorder and Self-Reported Breast Implant Illness.

BACKGROUND: Anxiety disorders, both with and without comorbid depression, are widespread globally. This study investigates the intersection of anxiety, depression, and self-reported Breast Implant Illness (BII) in women undergoing aesthetic breast surgery. OBJECTIVES: The objective of our research is to enhance understanding about mental health history, psychotropic medication use, and its relation to BII symptoms. METHODS: A cohort of 240 consecutive female patients undergoing elective breast surgery was studied. The study categorized patients into groups based on the presence of self-reported BII symptoms and the type of breast surgery performed. Mental health history, psychotropic medication use, and time spent in treatment for mental illness were scrutinized. Statistical analyses were conducted, including multiple regression analysis. RESULTS: Results reveal that patients with self-reported BII symptoms often have a pre-existing anxiety/depression disorder treated medically before obtaining breast implants, and this disorder predicts the occurrence of BII symptoms. These patients tend to be diagnosed with anxiety and depression at a younger age, initiate medication therapy earlier, take more medications for their condition, and spend more time in therapy compared to others undergoing elective breast surgery. CONCLUSIONS: Implications of this study highlight the need for comprehensive counseling between plastic surgeons and patients with self-reported BII symptoms. Understanding the role of anxiety/depression in the pathogenesis of self-reported BII is crucial, and collaboration with psychiatrists and other mental health professionals can ensure improved supportive care. The findings contribute to a better understanding of the psychological aspects surrounding breast implant surgery and self-reported BII and emphasize the importance of preoperative mental health assessments in appropriate patient selection for elective breast surgery.

Deterioration of vitiligo and new onset of halo naevi observed in two patients receiving adalimumab.

Two patients with a long-standing history of recalcitrant ankylosing spondylitis were commenced on adalimumab as monotherapy. Case 1 developed marked rapid deterioration in his previously stable vitiligo within 3 months of commencing treatment. This was attributed to anti-tumor necrosis factor (TNF) therapy, and a marked improvement was noted following withdrawal of adalimumab. Case 2 developed multiple new halo naevi over the trunk and limbs. They did not show dysplastic features and have remained unchanged despite continuation of treatment. Possible mechanisms and implications of the paradoxical occurrence of immune-mediated skin lesions seen in patients receiving anti-TNF therapies are discussed.

Segmentally arranged somatotopy within the face representation of human primary somatosensory cortex.

Though somatotypic representation within the face in human primary somatosensory cortex (S1) to innocuous stimuli is controversial; previous work suggests that painful heat is represented based on an "onion-skin" or segmental pattern on the face. The aim of this study was to determine if face somatotopy for brush stimuli in S1 also follows this segmental representation model. Twelve healthy subjects (nine men: three women) underwent functional magnetic resonance imaging to measure blood oxygen level dependent signals during brush (1 Hz, 15 s) applied to their faces. Separate functional scans were collected for brush stimuli repetitively applied to each of five separate stimulation sites on the right side of the face. These sites were arranged in a vertical, horizontal, and circular manner encompassing the three divisions of the trigeminal nerve. To minimize inter-individual morphological differences in the post-central gyrus across subjects, cortical surface-based registration was implemented before group statistical image analysis. Based on activation foci, somatotopic activation in the post-central gyrus was detected for brush, consistent with the segmental face representation model.

Comparison of evoked vs. spontaneous tics in a patient with trigeminal neuralgia (tic doloureux).

A 53-year old woman with tic doloureaux, affecting her right maxillary division of the trigeminal nerve (V2), could elicit shooting pains by slightly tapping her teeth when off medication. The pains, which she normally rated as > 6/10 on a visual analog scale (VAS), were electric shock-like in nature. She had no other spontaneous or ongoing background pain affecting the region. Based on her ability to elicit these tics, functional magnetic resonance imaging (fMRI) was performed while she produced brief shocks every 2 minutes on cue (evoked pain) over a 20 min period. In addition, she had 1-2 spontaneous shocks manifested between these evoked pains over the course of functional image acquisition. Increased fMRI activation for both evoked and spontaneous tics was observed throughout cortical and subcortical structures commonly observed in experimental pain studies with healthy subjects; including the primary somatosensory cortex, insula, anterior cingulate, and thalamus. Spontaneous tics produced more decrease in signals in a number of regions including the posterior cingulate cortex and amygdala, suggesting that regions known to be involved in expectation/anticipation may have been activated for the evoked, but not spontaneous, tics. In this patient there were large increases in activation observed in the frontal regions, including the anterior cingulate cortex and the basal ganglia. Spontaneous tics showed increased activation in classic aversion circuitry that may contribute to increased levels of anxiety. We believe that this is the first report of functional imaging of brain changes in tic-doloureaux.

Capsaicin-induced thermal hyperalgesia and sensitization in the human trigeminal nociceptive pathway: an fMRI study.

The aim of this study was to differentiate the processing of nociceptive information, matched for pain intensity, from capsaicin-induced hyperalgesic vs. control skin at multiple levels in the trigeminal nociceptive pathway. Using an event-related fMRI approach, 12 male subjects underwent three functional scans beginning 1 h after topical application of capsaicin to a defined location on the maxillary skin, when pain from capsaicin application had completely subsided. Brush and two levels of painful heat (low-Thermal-1 and high-Thermal-2) were applied to the site of capsaicin application and to the mirror image region on the opposite side. Temperatures for each side were set to evoke perceptually matched pain (mean temperatures [capsaicin/control]: Thermal-1=38.4/42.8 degrees C; Thermal-2=44.9/47.8 degrees C). We found differences in activation patterns following stimuli to treated and untreated sides in sensory circuits across all stimulus conditions. Across the trigeminal nociceptive pathway, Thermal-2 stimulation of hyperalgesic skin evoked greater activation in trigeminal ganglion and nucleus, thalamus, and somatosensory cortex than the control side. Thus, trigeminal nociceptive regions showed increased activation in the context of perceptually equal pain levels. Beyond these regions, contrast analyses of capsaicin vs. control skin stimulation indicated significant changes in bilateral dorsolateral prefrontal cortex and amygdala. The involvement of these emotion-related regions suggests that they may be highly sensitive to context, such as prior experience (application of capsaicin) and the specific pain mechanism (hyperalgesic vs. normal skin).

Trigeminal neuropathic pain alters responses in CNS circuits to mechanical (brush) and thermal (cold and heat) stimuli.

Functional magnetic resonance imaging was used to study patients with chronic neuropathic pain involving the maxillary region (V2) of the trigeminal nerve in patients with spontaneous pain and evoked pain to brush (allodynia). Patients underwent two functional scans (2-3 months apart) with mechanical and thermal stimuli applied to the affected region of V2 and to the mirror site in the unaffected contralateral V2 region, as well as bilaterally to the mandibular (V3) division. Patients were stimulated with brush, noxious cold, and noxious heat. Significant changes were observed in regions within and outside the primary trigeminal sensory pathway. Stimulation to the affected (neuropathic) side resulted in predominantly frontal region and basal ganglia activation compared with the control side. The differences were consistent with the allodynia to brush and cold. A region of interest-based analysis of the trigeminal sensory pathway revealed patterns of activation that differentiated between the affected and unaffected sides and that were particular to each stimulus. Activation in the spinal trigeminal nucleus was constant in location for all pain stimuli. Activation in other brainstem nuclei also showed differences in the blood oxygenation level-dependent signal for the affected versus the unaffected side. Thus, sensory processing in patients with trigeminal neuropathic pain is associated with distinct activation patterns consistent with sensitization within and outside of the primary sensory pathway.