Madhulika A. Gupta, MD

Psoriasis, a chronic inflammatory, autoimmune skin disorder that is associated with both genetic (concordance rate of about 60% in monozygotic and 20% in dizygotic twins) and environmental factors, affects about 2% to 4% of the population worldwide.

 Initially considered a primary dermatological disorder, psoriasis is now considered by many to be a systemic disorder of immune regulation that is mediated by T cells and dendritic cells (DCs). Common triggers for psoriasis include infection (streptococcal throat infection, HIV infection), physical trauma (Koebner phenomenon), medications (eg, Î²-blockers, lithium, NSAIDs, antimalarials), and psychological stress (associated with both onset and exacerbation of psoriasis).

The most common form presents as symmetrical, sharply demarcated, erythematous, dry, scaling, pruritic plaques, with a predilection for the scalp, extensor surfaces of the limbs, hands and feet, and sacral and genital regions. The total body surface area affected can vary. Pruritus is one of the most bothersome symptoms of psoriasis. Painful nail changes are also seen in some patients, and many patients have psoriatic arthritis that commonly affects the distal interphalangeal joints. Psoriasis can occur at any age from infancy to the eighth decade of life; the age of onset is before 40 years in most patients. Psoriatic plaques may persist for months to years, and periods of complete remission are possible.

The genetics and immunology of psoriasis have direct implications in the management of the psychiatric patient with psoriasis. The presence of the histocompatibility antigen HLA-Cw6 is the major genetic risk factor for psoriasis and is associated with an early age of onset (age 40 or younger) and positive family history for psoriasis; early-onset psoriasis has been associated with greater severity as well as being more reactive to psychological stress.

 Genome-wide association studies have identified other genetic association signals for psoriasis outside the major histocompatibility complex (MHC)1 that fall into 4 areas that may be interrelated:

• Interferon-Î³ (IFN-Î³)/interleukin (IL)-23)/IL-17 signaling: supported by the efficacy of biologics targeting these cytokines.

• Nuclear factor Îº-light-chain-enhancer of activated B cells (NF-ÎºB) signaling: NF-ÎºB, a transcription factor, is widely implicated in inflammatory and autoimmune diseases. Tumor necrosis factor-Î± (TNF-Î±) is a major activator of NF-ÎºB signaling; this is clinically emphasized by the therapeutic response of psoriasis to the anti– TNF-Î± biologics.

• Inflammatory DC function: inflammatory DCs produce TNF-Î± and nitric oxide in addition to their major function in antigen presentation.

• Keratinocyte differentiation: hyperproliferation and altered differentiation of keratinocytes are prominent features of psoriasis.

Immune regulation, which is mediated by T cells and DCs, plays a primary role in the pathophysiology of psoriasis. Psoriasis is characterized by activation of antigen-presenting DCs and activation and expansion of T-helper (T

17 inflammatory cytokines are elevated in the skin and blood of patients with psoriasis. These inflammatory mediators promote angiogenesis and epidermal hyperplasia and affect diverse processes, such as insulin signaling, lipid metabolism, and adipogenesis. Thus, the metabolic aspects of the chronic T

17 inflammation in psoriasis can affect conditions such as obesity, diabetes, and atherosclerosis.

Medical comorbidities have important treatment implications for patients with psoriasis who have psychiatric disorders (eg, adverse effects of medications) and who may already be at a greater risk for obesity, diabetes, and cardiovascular complications (

). The heightened proinflammatory state associated with psoriasis as well as the patient’s emotional reaction to the effects of psoriasis on quality of life may also contribute to psychiatric comorbidity (eg, PTSD, MDD).

Sleep-related symptoms, such as insomnia, are a core feature of psychiatric disorders. One night of sleep deprivation can inhibit recovery of skin barrier function in humans. Skin barrier function recovery was assessed by measuring transepidermal water loss immediately before and at 2 time points following the stripping of the forearm skin with repeated applications of cellophane tape.

Sleep restriction of 25% to 50% of the normal 8-hour sleep period is associated with an elevation of mediators of inflammation such as IL-1Î² and TNF-Î±. In a mouse model of psoriasis, 48 hours of selective paradoxical sleep deprivation was associated with significant increases in proinflammatory cytokines (IL-1Î², IL-6, and IL-12) and decreases in the anti-inflammatory cytokine IL-10.

 The cytokine levels normalized after 48 hours of sleep rebound, which suggests that sleep loss is a risk factor for psoriasis.

Psoriasis is also associated with a higher prevalence of obstructive sleep apnea, which is possibly related to the heightened proinflammatory state as well as the risk factors for obstructive sleep apnea, such as hypertension and obesity. Obstructive sleep apnea is more commonly encountered in psychiatric disorders such as MDD and PTSD-conditions that are also more frequently associated with psoriasis.

Most studies of neuroendocrine response to stress in psoriasis have demonstrated a blunted hypothalamic-pituitary-adrenal (HPA) axis cortisol response and a heightened sympathetic response to stressors. During a standardized stressor exposure test (eg, forced mental arithmetic), patients with psoriasis reported higher levels of strain than did healthy controls; the patients also had higher levels of urinary adrenalin and lower levels of plasma cortisol.

 Similar findings were seen in patients with psoriasis during a social performance stressor (version of the Trier paradigm).

A 6-month prospective study of 62 patients with psoriasis examined serum cortisol levels (between 9 and 11 am).

 Peak levels of daily stressors predicted an increase in disease severity a month later (

 = 0.28; P < .05); however, they were associated with a lower cortisol level (

 = −0.28; P < .05). The dysregulation of the HPA axis with decreased release of cortisol, along with a heightened sympathetic response, is assumed to be involved in the stress-induced exacerbation of chronic inflammatory diseases by leading to up-regulation of proinflammatory cytokines.

A study of 5604 randomly selected patients with psoriasis and psoriatic arthritis from the National Psoriasis Foundation database (2003-2011) revealed that 52.3% of patients with psoriasis and 45.5% of patients with psoriatic arthritis were dissatisfied with their overall treatment.

 After controlling for clinical characteristics of psoriasis (psoriasis type, disease severity, and location), patients who received biologic therapy were most satisfied and patients who received topical therapy were least satisfied.

 It is possible that some biologics improve mood and other psychological symptoms independent of the clinical improvement in psoriasis, which, in turn, may reflect as a greater satisfaction with treatment.

More than 50% of patients with psoriasis report that psychological stress exacerbated their psoriasis.

 The physical and psychosocial impact of psoriasis on quality of life has been rated as the same as or worse than the impact of conditions such as cancer, ischemic heart disease, arthritis, and diabetes.

 Stress-reactive psoriasis tends to manifest consequent to greater psoriasis- related stress or the daily hassles associated with the cosmetic disfigurement and the associated social stigma. Disfiguring psoriasis or psoriasis in “emotionally charged” body regions, such as the socially visible and genital regions, had a greater impact on the patient’s quality of life and psoriasis-related stress.

The social impact of psoriasis has been studied using functional MRI in 13 men with psoriasis, by employing a covert recognition of faces task.

 Compared with healthy controls, patients with psoriasis had significantly (

 < .005) smaller signal responses to disgusted faces bilaterally in the insular cortex. Both feelings of disgust and observation of disgust in others are known to activate the insular cortex. This apparently contradictory response may be an indication that patients with psoriasis develop a coping mechanism to protect themselves from stressful emotional responses by blocking the processing of disgusted facial expressions.

An increased frequency of psoriasis has been reported with PTSD (DSM-III criteria; 

). PTSD has been associated with higher circulating levels of T lymphocytes and lower cortisol levels with concurrent higher catecholamine levels, a physiological state (similar to that observed in patients with stress exacerbated psoriasis) that increases the risk of autoimmune diseases.

 Baseline depression, measured using the 5-item Mental Health Index of the Short Form 36 health status survey, was associated with a higher incidence of psoriasis.

 Men who had a lifetime history of DSM-IV-TR–diagnosed anxiety disorders also had an increased rate of psoriasis.

 An increased frequency of psoriasis was also seen in patients with schizophrenia.

 However, neither study controlled for psoriasis risk factors, such as cigarette smoking, alcohol use, and body mass index.

Psoriasis has been consistently associated with an increased frequency of suicidal ideation in several studies, including a recently published multicenter study.

 Among individuals with a wide range of dermatological diagnoses, only psoriasis had a significant association with suicidal ideation (adjusted odds ratio [OR] = 1.94; 95% confidence interval [CI], 1.33-2.82). In a UK database of Hospital Episode Statistics for 1999-2011, individuals with both psychiatric and medical disorders were examined for hospital episodes of self-harm. The relative risk of self-harm was greater for all years in patients with psoriasis (1.6; 95% CI, 1.5-1.7) than in those in the reference group.

Effective management of psychiatric factors in psoriasis requires an integrated, multidisciplinary approach that treats both cutaneous and systemic inflammation (which in part involves treatment of the psychiatric disorder in which psoriasis may be more frequent, such as MDD or PTSD). Because patients with psoriasis (independent of psychiatric morbidity) tend to experience a greater frequency of suicidal ideation and self-harm, carefully evaluate suicide risk in these patients.

Even mild psoriasis that affects a small percentage of total body surface in socially visible body regions or the genital area can carry a significant psychosocial burden. In such cases, the psoriasis should be treated aggressively because the psoriasis-related stress can adversely affect the course of the disorder.

Obesity, diabetes, metabolic syndrome, and greater cardiovascular morbidity (stroke, hypertension, myocardial infarction) are often present in patients with psychiatric disorders such as MDD and PTSD. Comorbidity with psoriasis, especially severe psoriasis, may further increase the prevalence and risk of these comorbidities in the psychiatric patient. Take such comorbidities into consideration when choosing psychotropics based on their adverse-effect profiles.

Educate patients about the effects of tobacco and alcohol on psoriasis. Tobacco smoking is associated with a 70% increase in the risk of developing psoriasis.

 In addition, the use of alcohol and tobacco is associated with worsening symptoms and less treatment-related improvement.

Obstructive sleep apnea and insomnia are prevalent in patients with psoriasis and psychiatric disorders such as MDD and PTSD (conditions that are also more frequently associated with psoriasis). Remember to screen for sleep disorders because they can heighten the proinflammatory state. Pruritus in psoriasis can be associated with insomnia, which may have to be managed in conjunction with the psoriasis.

Lithium can precipitate or exacerbate psoriasis; lithium-induced psoriasis usually occurs within the first few years of treatment but it can occur within a few months, and it is typically resistant to standard antipsoriatic treatments. If psoriasis becomes intractable, discontinue lithium; psoriasis symptoms will usually remit within a few months. Î²-Blockers such as propranolol that are used to treat lithium-induced tremors may also be associated with psoriasis.

Cyclosporine, an immunosuppressant that is used to treat psoriasis, can interact with psychiatric medications by its action on cytochrome P-450 3A4 (CYP3A4), of which it is both a substrate and an inhibitor. Cyclosporine can dramatically increase blood levels of drugs that are CYP3A4 substrates, such as carbamazepine, antidepressants (doxepin, amitriptyline, and imipramine), benzodiazepines (alprazolam, triazolam, and diazepam), and the antipsychotic pimozide. There are no significant drug-drug interactions reported between psychiatric medications and the biologics used in psoriasis.

Psoriasis is a systemic autoimmune disorder in which immune regulation by T cells and DCs plays a primary role. The comorbidity of psoriasis with certain psychiatric disorders (such as anxiety disorders, including PTSD, and depressive illness) most likely has a multifactorial basis that includes a heightened proinflammatory state underlying both disorders and the impact of a chronic, cosmetically disfiguring condition (eg, psoriasis) on the patient’s quality of life and the resultant stress, mainly as a result of the social stigma associated with psoriasis.

Several studies have reported a blunted HPA axis cortisol response in conjunction with a heightened sympathetic response to psychological stressors in psoriasis; this may be the basis for the stress-induced up-regulation of proinflammatory cytokines. Patients with HLA-Cw6, which is a major genetic risk factor for psoriasis, generally present with early onset (40 years or younger) and with psoriasis that is more reactive to psychological stress.

The proinflammatory state in psoriasis is associated with a higher prevalence of metabolic syndrome, obesity, diabetes, and cardiovascular morbidity. This has important treatment implications for certain patients with psychiatric disorders who may already be at increased risk for comorbidities and more serious adverse effects. Sleep disorders as well as tobacco and alcohol use, which are more common in certain psychiatric populations, have been associated with onset and treatment resistance. Psoriasis is independently associated with increased suicidal ideation and self-harm.

Dr M A Gupta is Professor in the department of psychiatry, Schulich School of Medicine and Dentistry at Western University in London, Ontario, where she is also in private practice. Dr A K Gupta is Professor in the division of dermatology, department of medicine, at the University of Toronto; he is also in private practice (dermatology) in London and Toronto, Ontario. They report no conflicts of interest concerning the subject matter of this article.

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Articles

Psoriasis, a chronic inflammatory, autoimmune skin disorder, is associated with both genetic and environmental factors. It has important treatment implications for patients who have psychiatric disorders. 

Treating Psychiatric Patients With Psoriasis: Clinical Considerations


Sponsored by CME LLC for 1.5 Category 1 credits.
Original release date 12/06. Approved for CME credit through November 2007.

After reading this article, you will be familiar with:

The recent findings in the basic science and clinical aspects of the skin-brain connection.

The association between dermatologic disorders and psychiatric symptoms.

The dermatologic disorders seen in psychiatric patients.

Who will benefit from reading this article?

Psychiatrists, primary care physicians, dermatologists, neurologists, nurse practitioners, psychiatric nurses, and other mental health care professionals. Continuing medical education credit is available for most specialties. To determine whether this article meets the CE requirements for your specialty, please contact your state licensing board.

Dr Gupta is professor in the department of psychiatry at the Schulich School of Medicine and Dentistry, University of Western Ontario in London, Ontario. She reports that she has no conflicts of interest concerning the subject matter of this article.

The skin is the largest organ of the body and functions as a social, psychological, and metabolically active biologic interface between the individual and the environment. Recent studies have demonstrated that as the biologic interface, the skin plays an important role in the multidirectional communication between the endocrine, immune, and central nervous systems; in addition to acting as an effector organ, the skin is also a producer of humoral and neural signals that act both locally and centrally.

Biologically, the skin is an active barrier that separates the organism's internal homeostatic milieu from the stresses and "insults" of the external environment. The skin is therefore equipped to respond to continuous stresses and insults, eg, from solar radiation, mechanical trauma, changes in humidity, and infectious agents, and it has the capability to "fine-tune" itself so that it can differentiate between "environmental noise" and biologically relevant stimuli and stresses. It is possible that this important and somewhat unique role of the skin is also the basis for its sensitivity to psychological stressors; from an evolutionary perspective, physical stressors such as mechanical trauma and infections often have an important psychological component. This article reviews some of the recent findings in the basic science and clinical aspects of the skin-brain connection. The article also reviews some of the major dermatologic associations of psychiatric disorders and the psychiatric disorders encountered in patients with dermatologic disorders.

Recent research indicates that the skin and its appendages are both a target of key stress mediators (such as corticotropin releasing hormone [CRH], cortisol, catecholamines, prolactin, substance P, and nerve growth factor) and a source of these classic immunomodulatory mediators of the response to psychologic stress.

The skin-brain connection may be the basis for the observation that a wide range of inflammatory skin conditions such as atopic dermatitis and psoriasis are exacerbated by psychological stress. Clinically, the importance of psychosomatic factors in dermatologic disorders is well recognized; psychosomatic factors are important in at least one third of all dermatology patients. Furthermore, the placebo response in certain dermatologic disorders is greater than 30%, which further emphasizes the importance of psychosomatic mechanisms in dermatology.

The skin is a powerful organ of communication starting at birth-on the social, psychological, and biologic levels. The skin and its appendages are well innervated with a dense network of afferent sensory nerves and efferent autonomic nerves. The afferent sensory nerves convey sensations of touch, pain, itch, temperature, and other physical stimuli. The efferent autonomic nerves play a role in maintaining cutaneous homeostasis by regulating vasomotor and pilomotor functions and the activity of the apocrine and eccrine sweat glands. The apocrine sweat glands, which produce the protein equivalent of pheromones in humans, become functional at puberty and respond to catecholamines (and not acetylcholine) as do the eccrine sweat glands.

As an organ of communication, the skin plays a vital role in attachment starting in infancy. Freud observed that during early development, the ego is rooted in the body, especially the skin. Bodily sensations and experiences, both internal and from the surface of the body, form the core around which the ego develops. The skin remains a very important organ of communication throughout a person's lifetime. It may react to emotional states such as extreme fear, anxiety and stress, and embarrassment with blanching, increased perspiration, flushing, and blushing reactions.

In addition, the overall appearance of the skin, even when minimally flawed, can have a profound effect on the body image of the person, especially in adolescence, and can result in body image pathology. As an organ of communication, the skin continues to play an important role in later life, when the appearance of the skin projects socially important attributes such as chronologic age and social status. The idea that chronologic age does not necessarily signal the beginning of old age is becoming increasingly widespread, and an attempt to reverse some of the aging-related bodily changes frequently involves medical and surgical procedures on the skin.


Histologically, the skin is composed of 2 main structures-the epidermis and the dermis. The skin and the nervous system share some common embryologic origins. The keratinocytes, hair follicle and sebum-forming sebaceous glands, and apocrine and eccrine sweat glands originate from the embryonic ectoderm. The Merkel cells and melanocytes that migrate to the epidermis from the neural crest are also of ectodermal origin. The dermal components, with the exception of nerves and specialized receptors, are of mesodermal origin.


One of the main adaptive responses to systemic stress is mediated by the central hypothalamic-pituitary- adrenal (HPA) axis. Activation of the HPA axis centrally starts with the hypothalamic production of corticotropin-releasing hormone (CRH), which activates the CRH type 1 (CRH-1) receptor in the anterior pituitary and induces the release of proopiomelanocortin (POMC)-derived peptides adrenocorticotropin (ACTH), Î±-melanocyte stimulating hormone (a-MSH), and Ã-endorphin. ACTH stimulates the production and secretion of cortisol in humans by the adrenal cortex.

It has been demonstrated that the skin expresses a neuroendocrine system involving CRH, urocortin (a CRH-like neuropeptide that has been identified in the brain and has a high affinity for the CRH-2 receptor in addition to the CRH-1 receptor), and the POMC-derived peptides ACTH, Î±-MSH, and Ã-endorphin. Skin cells also express functional receptors activated by these neuropeptides.

It has been proposed that the central HPA axis acts as a coordinator of the local cutaneous response to stress, and the local cutaneous effectors of the HPA axis (ie, CRH, urocortin, and the POMC-derived peptides like ACTH and a-MSH) regulate the skin pigmentary, immune, epidermal, adnexal, and dermal systems. In addition, local cholinergic, catecholaminergic, and serotoninergic/ melatoninergic systems and some elements of the pituitary-thyroid axis have been demonstrated in the skin.

Neuroendocrine-immune circuitry and stress-mediated skin disorders


Stress-mediated production of glucocorticoids may induce the suppression of T helper 1 (T

1)-mediated cellular immunity and create a shift towards T helper 2 (T

2)-mediated humoral immunity. Neurohormonal responses to stress also involve the activation of the sympathetic nervous system (SNS) with a subsequent increase of catecholamines. The SNS has been shown to directly participate in cutaneous inflammation. Sympathetic nerve fibers travel with sensory nerves and innervate the dermis and epidermis, where they release norepinephrine.

Catecholamines have a suppressive effect on cutaneous Langerhans cells, which anatomically are associated with cutaneous nerves. The bone marrow-derived Langerhans cells participate in the cutaneous immune response and migrate from skin to lymph nodes. They possess surface receptors common to macrophages and function as antigen-presenting cells to T or B lymphocytes.

The skin responds differently to acute versus chronic stress. Skin responses to acute stress include an enhanced skin immune function with increased intracutaneous migration of immunocompetent cells, while chronic stress may suppress cutaneous immunity. Lymphocytes express adrenergic receptors and respond to increased levels of catecholamines with the development of stress-induced lymphocytosis, changes in lymphocyte trafficking, circulation, proliferation, and cytokine production.

Acute stress experienced prior to the exposure to a novel antigen has been shown to increase memory T-cell formation, and acute stress experienced during antigen reexposure may enhance the secondary immune response. Alternatively, chronic stress may reduce the immune response to vaccines, slow wound healing (since the cellular immune response plays a key role in the early phase of wound healing), and reactivate latent viral infections such as herpesviruses.


Acute stress is associated with increased mast cell activation and degranulation.

 The mast cell is a key player in the skin-brain connection and an important regulator of neurogenic inflammation during the stress response. A wide range of stress-related mediators such as CRH, ACTH, cytokines, and substance P are triggers for mast cell activation, which, in turn, results in the synthesis and/or release of prestored mediators that may lead to the onset or exacerbation of a wide range of dermatologic disorders that are known to be exacerbated by psychological stress.

The skin mast cell is not only triggered by classic stress mediators such as ACTH and CRH, it is also a generator of stress hormones such as CRH. The skin mast cell is one of the richest sources of CRH outside the brain.

 Some of the dermatologic disorders in which mast cells play an important role include urticaria and angioedema, alopecia areata, atopic dermatitis, psoriasis, contact dermatitis, acne vulgaris, and various pruritic states that may be associated with mast cell activation and histamine release.

Acute psychological stress and skin barrier function


Some recent studies have demonstrated that acute psychological stress, which is associated with increased glucocorticoid levels, adversely affects skin barrier function recovery induced by tape stripping; in contrast, chronic psychological stress, which may be a feature of chronic posttraumatic stress disorder (PTSD), is often associated with an attenuated HPA axis response and has been associated with an enhancement in skin barrier function recovery. Glucocorticoids most likely act by inhibiting epidermal cell proliferation and lipid synthesis.


Psychodermatologic disorders have generally been classified into 2 major categories

Cutaneous associations of psychiatric disorders.

Psychiatric associations of cutaneous disorders.

Some of the dermatologic presentations of primary psychiatric symptoms are summarized in Table 1. The self-induced dermatoses represent the fact that stimulation of the skin, which is richly innervated and has bilateral communication with the CNS, serves as a means of regulating affect and coping with intense emotional states. In some instances the self-induced cutaneous lesions also communicate emotional distress.

Table 2 highlights some of the psychiatric associations of primary dermatologic disorders; this group can be further divided into 3 subcategories.

Disorders that have a primary dermatopathologic basis but may be influenced by psychosomatic factors, eg, psoriasis, atopic dermatitis, urticaria and angioedema, lichen planus, acne, and alopecia areata.

Disorders that represent an accentuated physiologic response, eg, hyperhidrosis and blushing.

Disorders that result in an emotional reaction primarily as a result of cosmetic disfigurement, social stigma, and the overall impact of the disorder on the quality of life of the patient.

These 3 subcategories are not mutually exclusive. Most of the disorders in the first category, such as psoriasis, atopic dermatitis, chronic urticaria, lichen planus, and alopecia areata, have an immunologic component. Second, most of these primary dermatologic disorders have been associated with both psychiatric comorbidity,

 (most frequently depressive disease and anxiety disorders) and with psychosocial stress, which typically is reported to exacerbate the skin disorder.

In up to 70% of cases of psoriasis, atopic dermatitis, chronic urticaria, and acne, psychological stress has been identified as an exacerbating factor. Some reports suggest that psoriasis is one of the most stress-reactive dermatoses. The association between stress and exacerbations of alopecia areata and lichen planus is less robust. A wide range of other dermatologic disorders, such as viral infections of the skin, and a range of other skin disorders that may also be immunologically mediated, such as vitiligo, may be exacerbated by psychological stress and have a psychosomatic component. However, an exhaustive review of these disorders is outside the scope of this paper. In some disorders, such as psoriasis, a significant component of the psychosocial stress arises from the impact of the skin disorder on quality of life and the daily hassles associated with having to cope with a chronic disfiguring disorder.

Some of the major psychiatric disorders (DSM-IV-TR) that are encountered in dermatology include mood disorders: major depressive disorder; anxiety disorders: obsessive-compulsive disorder (OCD), social phobia, anxiety disorder caused by a general medical condition, and PTSD; somatoform disorders: body dysmorphic disorder (BDD); psychotic disorders: delusional disorder, somatic type encountered in delusions of parasitosis, and shared psychotic disorder or folie deux; and eating disorders: anorexia nervosa and bulimia nervosa. The personality disorders, especially borderline, narcissistic, histrionic, and obsessive-compulsive, may be encountered in certain groups of dermatology patients. Among these, the most frequently encountered psychiatric disorders are major depressive disorder, anxiety disorders, and somatoform disorders.


Depressive disease is one of the most commonly encountered psychiatric syndromes in dermatology. A direct correlation has been observed between the severity of depression and pruritus or itch severity in psoriasis, atopic dermatitis, and chronic idiopathic urticaria. Pruritus is one of the most bothersome symptoms in dermatology and has been associated with suicide. The sleep difficulties encountered in depressive disease may lower the threshold for pruritus perception; alternatively, intractable pruritus may further contribute toward disruption of sleep.

The severity of the skin disorder and severity of depression and suicidal ideation are generally correlated in some disorders, such as psoriasis. In other conditions, such as acne, the severity of depression and suicidal ideation are often not related to the severity of the dermatosis. Even mild acne has been associated with depression, suicidal ideation, and completed suicide.

 The high prevalence of psychiatric morbidity among patients with mild to moderate acne is most likely due to the fact that the peak incidence of acne occurs during mid-adolescence, a life stage that is also associated with depressive disease and body image disorders. The association between acne and depression is further confounded by reports of a possible link between isotretinoin (which is used to treat acne) and suicide.


Some of the compulsive scratching and picking of the skin in OCD may exacerbate psoriasis as a result of the Koebner phenomenon, and exacerbate eczema and a wide range of other pruritic conditions, or further contribute to the inflammatory process in acne, and/or lead to scarring that is encountered in acne excorie. OCD may also result in hand dermatitis caused by excessive handwashing. In some instances OCD may manifest as an obsessive preoccupation with some aspect of the skin, and these symptoms may overlap with BDD.


Patients with hyperhidrosis and rosacea often perspire or blush excessively and may develop a social phobia as a result. Social phobia is also encountered in patients with cosmetically disfiguring skin conditions such as acne and psoriasis, and may interfere with normal socialization. Exposure to the feared social situation may trigger a situationally bound panic attack, which in turn can cause flare-ups of the underlying skin condition. Social phobia is typically underdiagnosed because the very nature of the disorder prevents patients from seeking medical help.


The autonomic dysregulation in PTSD can lead to exacerbations of stress-mediated dermatoses such as psoriasis and atopic dermatitis. Urticarial reactions and angioedema have been associated with an acute stress response

; urticarial reactions and angioedema may represent a conditioned response to a stimulus that had been previously associated with a traumatic experience. Patients with PTSD who have dissociative symptoms may present with a wide range of cutaneous sensory complaints and/or self-induced dermatoses such as trichotillomania.


The skin and hair are frequently the focus of excessive body image concerns. BDD often involves excessive concerns about thinning hair, acne, wrinkles, scars, vascular markings, paleness or redness of the complexion, swelling, facial disproportion or asymmetry, or excessive facial hair. BDD may be comorbid with acne and acne excorie. Some associated features include excessive grooming behavior such as excessive hair combing, hair removal, hair picking, or ritualized makeup application.


Some of the recent advances in psychodermatology expand on the traditional concept of psychosomatic medicine because there is increasing evidence that the impact of psychological stress on the skin is not necessarily mediated primarily by the CNS but is mediated by a local stress response system in the skin that is the equivalent of the central HPA axis, and that further interacts with the central HPA axis response. These findings refute the traditional mind-body dichotomy. The local stress response system that has been recently described in the skin

 may be present in other organ systems and therefore may not be unique to the integumentary system; however, the stress response can be observed most easily in the skin. A psychodermatologic evaluation may therefore give the psychiatrist further insights into the mental state of the patient.

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The skin is the largest organ of the body and functions as a social, psychological, and metabolically active biologic interface between the individual and the environment. 