It has been reported in some studies that there is a connection between childhood trauma and obsessive-compulsive symptoms. More research is needed to understand this relationship better. Mechanisms
Neuroimaging
Functional neuroimaging during symptom provocation has observed abnormal activity in the orbitofrontal cortex (OFC), left dorsolateral prefrontal cortex (dlPFC), right premotor cortex, left superior temporal gyrus, globus pallidus externus, hippocampus, and right uncus. Weaker foci of abnormal activity were found in the left caudate, posterior cingulate cortex, and superior parietal lobule. However, an older meta-analysis of functional neuroimaging in OCD reported that the only consistent functional neuroimaging finding was increased activity in the orbital gyrus and head of the caudate nucleus, while anterior cingulate cortex (ACC) activation abnormalities were too inconsistent.A meta-analysis comparing affective and nonaffective tasks observed differences with controls in regions implicated in salience, habit, goal-directed behavior, self-referential thinking, and cognitive control. For nonaffective tasks, hyperactivity was observed in the insula, ACC, and head of the caudate/putamen, while hypoactivity was observed in the medial prefrontal cortex (mPFC) and posterior caudate. Affective tasks were observed to relate to increased activation in the precuneus and posterior cingulate cortex, while decreased activation was found in the pallidum, ventral anterior thalamus, and posterior caudate. The involvement of the cortico-striato-thalamo-cortical loop in OCD, as well as the high rates of comorbidity between OCD and ADHD, have led some to draw a link in their mechanism. Observed similarities include dysfunction of the anterior cingulate cortex and prefrontal cortex, as well as shared deficits in executive functions.
Skin usually regrows over two to three weeks; however, recovery can take months and most are left with chronic problems. Signs and symptoms
Prodrome
TEN ultimately results in extensive skin involvement with redness, necrosis, and detachment of the top (epidermal) layer of the skin and mucosa. Before these severe findings develop, people often have a flu-like prodrome, with a cough, runny nose, fever, decreased appetite and malaise. A history of drug exposure exists on average 14 days (ranging from 1–4 weeks) prior to the onset of symptoms, but may result as early as 48 hours if it is a reexposure. Skin findings
Initial skin findings include red-purple, dusky, flat spots known as macules that start on the trunk and spread out from there. These skin lesions then transform into large blisters. The affected skin can then become necrotic or sag from the body and peel off in great swaths. Mucosal findings
Nearly all people with TEN have oral, eye and genital involvement as well. Painful crusts and erosions may develop on any mucosal surface. The mouth becomes blistered and eroded, making eating difficult and sometimes necessitating feeding through a nasogastric tube through the nose or a gastric tube directly into the stomach. The eyes can become swollen, crusted, and ulcerated, leading to potential blindness. The most common problem with the eyes is severe conjunctivitis. Complications
Those who survive the acute phase of TEN often develop long-term complications affecting the skin and eyes. Skin manifestations can include scarring, eruptive melanocytic nevi, vulvovaginal stenosis, and dyspareunia.