This often difficult-to-diagnose-and-treat condition can frustrate both physicians and patients, whose treatment involves addressing their worry and fear as well as finding appropriate medications. Dysesthesias of the groin are commonly encountered in dermatologic practice. Complaints range from burning, tenderness, and hypersensitivity to aching, pain and pruritus. The dysesthetic regions often include, but are not limited to, the penis, scrotum, vulva, perianal area and crural folds. Other than prolonged chafing bike rides, irritant or allergic contact reactions, or bacterial or fungal infections, obvious precipitating factors are rarely elicited. Physical examination sometimes reveals primary dermatologic skin disease, but all too often the etiology is cryptic, with symptoms strikingly out of proportion to physical findings. Patients often display a great deal of obvious stress and distress, frequently having already been evaluated by several other physicians including primary care, urology, gynecology, and infectious disease. Cultures and serologies are usually negative, although the occurrences of positive IgG titres for HSV and varicella only further complicate matters. What happens in Vegas stays in Vegas, right? Well, not always. Gonorrhea, syphilis, chlamydia, HIV, scabies and lice travel quite well. Ironically, so do fear, guilt, anxiety and shame.
Etiology of Dysesthesias
Dysesthetic sensations can be initiated by a variety of “insults” to the skin, both endogenous and exogenous. Infection, infestation, allergy, irritation and trauma can cause both functional and structural changes that directly elicit or collectively culminate in skin dysesthesias. Neuropeptide release, histamine release, cell mediated immunity, vasodilation and antimicrobial peptides can all be associated with a subjective dysesthetic sensation.
Identifying Sources, Threats
Dysesthesias rarely exist in isolation. They reside with their co-perpetrators that are responsible for their occurrence and invariably elicit both cognitive and affective responses. An incomplete list of etiologic factors and co-perpetrators is listed in Table 1. Intellectual and cognitive processes are always attempting to explain and interpret bodily sensations. Explanation and interpretation of bodily sensations can be considered an adaptive survival technique that allow us to identify and assess any potential threat to our safety, integrity and viability. Thus, benign dysesthetic symptoms must be differentiated from those that are harbingers of underlying infection, infestation, metabolic derangement, destructive inflammatory or neoplastic process.
A Sensitive Area
There is of course the “real estate” issue — location, location, location — which is particularly resonate with regard to groin dysesthesias. Most of us consider the groin area to be a valuable and cherished asset. Its location literally and metaphorically represents the center of fertility, strength, prowess and sexuality.The orifices that reside within this region provide us pleasure, relief and transfer of genetic material creating the union that begins a new life. They are also the final exit points for the toxic metabolic end products of our cellular biology. Therefore, unexplained sensations without logical explanations for their existence can elicit extreme and deep rooted anxiety that may be associated with haunting thoughts of life threatening proportions. If there were in fact a real or imagined “inappropriate” incident or exposure that could explain these symptoms, the dysesthetic process can become intensified.
Physical Symptoms And Emotional Impact
It is imperative that the clinician precisely understand the nature of the dysesthetic symptom. The approach to symptoms should initially involve characterization of the dysesthetic symptom by duration, quality, diurnal or nocturnal fluctuation and precise location(s). Is it best described as itch, burning, pain, crawling, ache, gnawing, or pulling? Is it localized — eg, ventral aspect of the glans penis, right labia majora — or is it more vague or diffuse? Do the symptoms worsen at night, with exer- tion, friction, intercourse, perspiration, stress or fatigue? Is there anything that has been tried — OTC or prescription — that has afforded any relief? Does rest or avoidance of certain activities ameliorate symptoms? Do the symptoms interfere with sleep, work or play? Is there significant associated anxiety, fear, depression, obsession or compulsive-ritualistic behavior such as rubbing, scratching, washing, etc? In addition, it can be very enlightening to elicit from the patient details about their associated cognitions and fears. What do they think is causing their symptoms and what are their fears regarding what they may represent? The constellation of thoughts, fears and behaviors can be overwhelming. They can lead the affected individual to “over-worry,” “over-wash” and culminate in a deafening “overture” of thoughts, fears, and behaviors that usurp their time, energy and availability to self and others.
Specific Interventions
Offering Reassurance and Understanding of the Condition Perhaps one of the most powerful interventions we can offer patients is our confident assurance that we will diminish or eliminate their dysesthetic symptoms. Initially, it is crucial to address the two most prominent fears that commonly fuel their anxiety and worsen their symptom complex. The first is their pervasive terror that the dysesthetic symptoms are harbingers of a serious, communicable or tragic life-threatening illness. The second is their fear that the dysesthetic symptoms will never improve or remit. Thus, they often envision a relent- less progression or downward spiral culminating in disability or demise. In essence, they are individuals with uncontrolled symptoms who feel increasingly out of control. Psychologically speaking, loss of perceived control over thoughts, sensations, impulses or our immediate environment leads to extreme psycho- logical distress and functional difficulties. Given this context, I cannot overstate the therapeutic importance of enhancing the patient’s sense of self-control by allaying these fears and offering hope. An effective initial strategy is to ex- plain to patients that they have developed a condition that is essentially a hyper-reactivity or hyper-irritability of their skin nerve endings. This condition causes the nerve endings to over-react to the normal skin exposures and “insults” to the integument that occur daily. Friction, perspiration, bacterial and fungal colonization, urination, menstruation, etc., are usually tolerated without substantial awareness or alteration in skin sensation. However, once the skin has been abnormally activated, all of these “normal occurrences” can result in nerve fiber activation leading to abnormal, exaggerated and persistent skin sensations. It is important to point out that the initial event or insult that initiated the hyper-reactivity of the nerve fibers may be “long gone.” In other words, we can reassure them that even if the initiating event causing their dysesthesias were in fact a skin infestation or infection (as they often fear), it is fully possible that no active infection or infestation is present despite their ongoing symptoms. A concept of ongoing skin over-reaction and irritability that is analogous to the irritability and sensitivity we feel emotionally when under prolonged stress or duress is often understood by and palatable to patients. In essence, we are presenting a “biologinized” explanation for the basis of the patients’s symptoms with the concept of “biologic over-reactivity” or “cutaneous hypersensitivity.”Thisprovides a biological explanation for the unexplained persistence and intensity of their dysesthesias. Drawing further analogies to poison ivy id reactions and the cutaneous hyperesthesia that persists after herpes zoster can provide additional examples and logical explanations for symptom persistence that regularly occur in the absence of active infection or infestation. One can suggest that this concrete explanation of the “normalcy” of their dysesthesia is a variation of the “talkesthesia” utilized in medical and cosmetic dermatology to diminish the discomfort associated with procedures.
Vigilance and Healing
A comprehensive “two-pronged” approach of vigilance and healing will be utilized. Further stating that this approach has been utilized with consistent success with other patients can be reassuring. The first “prong” is a promise of ongoing vigilance for underlying or associated organic disease. The second “prong” is the use of medications and techniques that help modulate and normalize their underlying nerve ending hyper-reactivity. Assuring them that the nerve endings will remain fully functional and capable of transmitting “important or essential” messages of true organic problems can allow them to feel it is safe to relinquish their obsessive preoccupation. Many of these patients have a plethora of topical medications that they haphazardly apply. This can complicate matters with the possibility of irritant or allergic contact dermatitis. Sometimes, “don’t just do something, stand there” can stop the therapeutic assault on the integument. Scrub, rub, medicate and lubricate can all aggravate! If your novel concoctions have not been very helpful, asking the patient to stop all topical medications, OTC and herbal creams and lotions can do a world of good.
Topical Treatment
Topical Treatment Options Topical agents can be broadly categorized as antifungals, antibiotics, anti-inflammatories, analgesics, barrier agents and anesthetics. The efficacy of antifungal and antibiotic agents may well be due to the reduction of colonized superantigens and barrier restoration rather than “cure” of infection. Combination products containing iodoquinol/hydrocortisone (Vytone, Alcortin) and iodoquinol/aloe (Aloquin) as well as generic and compounded formulations containing these products can be soothing and efficacious. In general, cream and gel formulations tend to be best for daytime use. Low-potency corticosteroid creams, gels and ointments can be helpful in decreasing dysesthesias and reducing visible redness secondary to their vasoconstrictive properties. Non-steroidal creams and ointments such as pimecromalus (Elidel) and tacrolimus (Protopic) can be helpful and have the advantage of quelling any fears of skin atrophy. Topical analgesia may sometimes be achieved using a topical tricyclic antidepressant agent such as doxepin cream 5% (Zonalon) or topical amitriptyline 10% cream available from compounding pharmacies.There is little data regarding agents such as topical diclofenac gel but personal communications have suggested mixed results. Topical anesthetic agent such as lidocaine and prilocaine can afford some patients with relief for several hours, though other patients may report little or no benefit. In addition, topical application of cold compresses, saline compresses, milk soaks and oatmeal preparations can also be beneficial. Topical Treatment Issues Choosing among the topical agents to ameliorate dysesthetic symptoms should be based on a working hypothesis postulating the major causative factors in the affected individual and also the recognition that the involved dysesthetic skin has usually been rubbed, scratched and otherwise abused and manipulated. These activities often compromise the epidermal barrier and lead to underlying neuropathic changes including increased C fibers and other structural and functional changes that create a biologic mi- lieu for dysesthetic symptoms. Our growing understanding of innate immunity including antimicrobial peptides, Toll-like receptors and other signaling mechanisms for inflammation make preservation and restoration of the epidermal barrier essential. Therefore, it is suggested that the role of topical agents is essential to normalize skin reactivity and restore normal barrier function. Again, the possibility of irritant or contact dermatitis must always be kept in mind when using topical agents.A vicious cycle of transient relief from the active ingredient followed by exacerbation of symptoms by irritant or allergic factors can occur. As suggested in a previous section, sometimes cessation of all topical agents can be instructive and clinically beneficial.
Use of Oral Agents
Several classes of oral agents can be helpful in reducing the frequency, severity and intrusiveness of dysesthetic symptoms. These agents in- clude antihistamines, antibiotics, antifungals, anti-virals, tricyclic anti-depressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepiephrine reuptake inhibitors (SNRIs), anti-seizure agents and beta blockers. These agents may be used alone or in combination, always with the recognition that known and idiosyncratic side effects and interactions are possible. The therapeutic goal is modification of the occurrence, duration, intensity and the perception of the dysesthetic symptom(s). Antihistamines can be beneficial if there is any histamine mediated component to symptoms. Antibiotics, antifungals and anti-viral medications can eradicate infection if present. More often, their ameliorative effects are probably achieved through reduction or eradication of super-antigens. Candida certainly is a prime candidate and anecdotal communications suggest that short courses of fluconazole 100 mg to 200 mg QD or itraconazole at similar dosing can reduce severity of symptoms. This should be repeated at 2 to 3 week intervals. SSRIs and SNRIs can exert their ameliorative benefits acting both centrally and peripherally. Their central effects are through direct inhibition of neurotransmitter re-uptake allowing for higher neurotransmitter levels at the synapse. Inhibition of neurotransmitter re-uptake has been demonstrated to decrease pain, pruritus, burning, and other dysesthetic symptoms. In addition, they reduce the psychological morbidity that frequently accompanies these chronic sensations, such as anxiety, depression, obsessive compulsive symptoms, and anger. Peripherally, SSRIs and SNRIs have been demonstrated to decrease neuropeptide release thereby directly decreasing local pro-inflammatory- exacerbating factors. The ameliorative benefits of anti- seizure agents for the management of neuropathic symptoms is well described elsewhere. Clinical benefit is probably a combined effect of neuronal normalization, anxiolysis, sedation and placebo effect. The role of beta blockers is interesting and mostly anecdotal. Recent evidence suggests that they may decrease peripheral release of neuropeptides thereby reducing the negative proprioceptive sensations locally. Moreover, it has been suggested that neuropeptides cross the blood brain barrier and enhance reuptake at the synapse. This results in depletion of neurotransmitters which can exacerbate both skin symptoms and psychological distress.
Caveats and Conclusions
Management of the patient with groin dysesthesias requires vigilance for a cryptic primary infectious, autoimmune or neoplastic etiology. Akin to chronic itch or an eczematous process that may represent an evolving collagen vascular process or T cell dyscrasia, groin dysesthesia must be followed closely with similar clinical suspicion. Sometimes, patients’ fears are correct and an STD, other infection, infestation, or neoplastic process is in fact present or evolving. Periodic repeat of appropriate serologies, cultures, and skin biopsy(ies) is strongly encouraged in the setting of unremitting symptoms, lack of clinical improvement, or change in symptom constellation. Finally, don’t forget that what happens in Vegas doesn’t always stay there. Dr. Fried, who is a psychologist as well as a dermatologist, maintains a private practice inYardley, PA. Disclosure: Dr. Fried has no conflicts of interest with the subject discussed in this column.
This often difficult-to-diagnose-and-treat condition can frustrate both physicians and patients, whose treatment involves addressing their worry and fear as well as finding appropriate medications. Dysesthesias of the groin are commonly encountered in dermatologic practice. Complaints range from burning, tenderness, and hypersensitivity to aching, pain and pruritus. The dysesthetic regions often include, but are not limited to, the penis, scrotum, vulva, perianal area and crural folds. Other than prolonged chafing bike rides, irritant or allergic contact reactions, or bacterial or fungal infections, obvious precipitating factors are rarely elicited. Physical examination sometimes reveals primary dermatologic skin disease, but all too often the etiology is cryptic, with symptoms strikingly out of proportion to physical findings. Patients often display a great deal of obvious stress and distress, frequently having already been evaluated by several other physicians including primary care, urology, gynecology, and infectious disease. Cultures and serologies are usually negative, although the occurrences of positive IgG titres for HSV and varicella only further complicate matters. What happens in Vegas stays in Vegas, right? Well, not always. Gonorrhea, syphilis, chlamydia, HIV, scabies and lice travel quite well. Ironically, so do fear, guilt, anxiety and shame.
Etiology of Dysesthesias
Dysesthetic sensations can be initiated by a variety of “insults” to the skin, both endogenous and exogenous. Infection, infestation, allergy, irritation and trauma can cause both functional and structural changes that directly elicit or collectively culminate in skin dysesthesias. Neuropeptide release, histamine release, cell mediated immunity, vasodilation and antimicrobial peptides can all be associated with a subjective dysesthetic sensation.
Identifying Sources, Threats
Dysesthesias rarely exist in isolation. They reside with their co-perpetrators that are responsible for their occurrence and invariably elicit both cognitive and affective responses. An incomplete list of etiologic factors and co-perpetrators is listed in Table 1. Intellectual and cognitive processes are always attempting to explain and interpret bodily sensations. Explanation and interpretation of bodily sensations can be considered an adaptive survival technique that allow us to identify and assess any potential threat to our safety, integrity and viability. Thus, benign dysesthetic symptoms must be differentiated from those that are harbingers of underlying infection, infestation, metabolic derangement, destructive inflammatory or neoplastic process.
A Sensitive Area
There is of course the “real estate” issue — location, location, location — which is particularly resonate with regard to groin dysesthesias. Most of us consider the groin area to be a valuable and cherished asset. Its location literally and metaphorically represents the center of fertility, strength, prowess and sexuality.The orifices that reside within this region provide us pleasure, relief and transfer of genetic material creating the union that begins a new life. They are also the final exit points for the toxic metabolic end products of our cellular biology. Therefore, unexplained sensations without logical explanations for their existence can elicit extreme and deep rooted anxiety that may be associated with haunting thoughts of life threatening proportions. If there were in fact a real or imagined “inappropriate” incident or exposure that could explain these symptoms, the dysesthetic process can become intensified.
Physical Symptoms And Emotional Impact
It is imperative that the clinician precisely understand the nature of the dysesthetic symptom. The approach to symptoms should initially involve characterization of the dysesthetic symptom by duration, quality, diurnal or nocturnal fluctuation and precise location(s). Is it best described as itch, burning, pain, crawling, ache, gnawing, or pulling? Is it localized — eg, ventral aspect of the glans penis, right labia majora — or is it more vague or diffuse? Do the symptoms worsen at night, with exer- tion, friction, intercourse, perspiration, stress or fatigue? Is there anything that has been tried — OTC or prescription — that has afforded any relief? Does rest or avoidance of certain activities ameliorate symptoms? Do the symptoms interfere with sleep, work or play? Is there significant associated anxiety, fear, depression, obsession or compulsive-ritualistic behavior such as rubbing, scratching, washing, etc? In addition, it can be very enlightening to elicit from the patient details about their associated cognitions and fears. What do they think is causing their symptoms and what are their fears regarding what they may represent? The constellation of thoughts, fears and behaviors can be overwhelming. They can lead the affected individual to “over-worry,” “over-wash” and culminate in a deafening “overture” of thoughts, fears, and behaviors that usurp their time, energy and availability to self and others.
Specific Interventions
Offering Reassurance and Understanding of the Condition Perhaps one of the most powerful interventions we can offer patients is our confident assurance that we will diminish or eliminate their dysesthetic symptoms. Initially, it is crucial to address the two most prominent fears that commonly fuel their anxiety and worsen their symptom complex. The first is their pervasive terror that the dysesthetic symptoms are harbingers of a serious, communicable or tragic life-threatening illness. The second is their fear that the dysesthetic symptoms will never improve or remit. Thus, they often envision a relent- less progression or downward spiral culminating in disability or demise. In essence, they are individuals with uncontrolled symptoms who feel increasingly out of control. Psychologically speaking, loss of perceived control over thoughts, sensations, impulses or our immediate environment leads to extreme psycho- logical distress and functional difficulties. Given this context, I cannot overstate the therapeutic importance of enhancing the patient’s sense of self-control by allaying these fears and offering hope. An effective initial strategy is to ex- plain to patients that they have developed a condition that is essentially a hyper-reactivity or hyper-irritability of their skin nerve endings. This condition causes the nerve endings to over-react to the normal skin exposures and “insults” to the integument that occur daily. Friction, perspiration, bacterial and fungal colonization, urination, menstruation, etc., are usually tolerated without substantial awareness or alteration in skin sensation. However, once the skin has been abnormally activated, all of these “normal occurrences” can result in nerve fiber activation leading to abnormal, exaggerated and persistent skin sensations. It is important to point out that the initial event or insult that initiated the hyper-reactivity of the nerve fibers may be “long gone.” In other words, we can reassure them that even if the initiating event causing their dysesthesias were in fact a skin infestation or infection (as they often fear), it is fully possible that no active infection or infestation is present despite their ongoing symptoms. A concept of ongoing skin over-reaction and irritability that is analogous to the irritability and sensitivity we feel emotionally when under prolonged stress or duress is often understood by and palatable to patients. In essence, we are presenting a “biologinized” explanation for the basis of the patients’s symptoms with the concept of “biologic over-reactivity” or “cutaneous hypersensitivity.”Thisprovides a biological explanation for the unexplained persistence and intensity of their dysesthesias. Drawing further analogies to poison ivy id reactions and the cutaneous hyperesthesia that persists after herpes zoster can provide additional examples and logical explanations for symptom persistence that regularly occur in the absence of active infection or infestation. One can suggest that this concrete explanation of the “normalcy” of their dysesthesia is a variation of the “talkesthesia” utilized in medical and cosmetic dermatology to diminish the discomfort associated with procedures.
Vigilance and Healing
A comprehensive “two-pronged” approach of vigilance and healing will be utilized. Further stating that this approach has been utilized with consistent success with other patients can be reassuring. The first “prong” is a promise of ongoing vigilance for underlying or associated organic disease. The second “prong” is the use of medications and techniques that help modulate and normalize their underlying nerve ending hyper-reactivity. Assuring them that the nerve endings will remain fully functional and capable of transmitting “important or essential” messages of true organic problems can allow them to feel it is safe to relinquish their obsessive preoccupation. Many of these patients have a plethora of topical medications that they haphazardly apply. This can complicate matters with the possibility of irritant or allergic contact dermatitis. Sometimes, “don’t just do something, stand there” can stop the therapeutic assault on the integument. Scrub, rub, medicate and lubricate can all aggravate! If your novel concoctions have not been very helpful, asking the patient to stop all topical medications, OTC and herbal creams and lotions can do a world of good.
Topical Treatment
Topical Treatment Options Topical agents can be broadly categorized as antifungals, antibiotics, anti-inflammatories, analgesics, barrier agents and anesthetics. The efficacy of antifungal and antibiotic agents may well be due to the reduction of colonized superantigens and barrier restoration rather than “cure” of infection. Combination products containing iodoquinol/hydrocortisone (Vytone, Alcortin) and iodoquinol/aloe (Aloquin) as well as generic and compounded formulations containing these products can be soothing and efficacious. In general, cream and gel formulations tend to be best for daytime use. Low-potency corticosteroid creams, gels and ointments can be helpful in decreasing dysesthesias and reducing visible redness secondary to their vasoconstrictive properties. Non-steroidal creams and ointments such as pimecromalus (Elidel) and tacrolimus (Protopic) can be helpful and have the advantage of quelling any fears of skin atrophy. Topical analgesia may sometimes be achieved using a topical tricyclic antidepressant agent such as doxepin cream 5% (Zonalon) or topical amitriptyline 10% cream available from compounding pharmacies.There is little data regarding agents such as topical diclofenac gel but personal communications have suggested mixed results. Topical anesthetic agent such as lidocaine and prilocaine can afford some patients with relief for several hours, though other patients may report little or no benefit. In addition, topical application of cold compresses, saline compresses, milk soaks and oatmeal preparations can also be beneficial. Topical Treatment Issues Choosing among the topical agents to ameliorate dysesthetic symptoms should be based on a working hypothesis postulating the major causative factors in the affected individual and also the recognition that the involved dysesthetic skin has usually been rubbed, scratched and otherwise abused and manipulated. These activities often compromise the epidermal barrier and lead to underlying neuropathic changes including increased C fibers and other structural and functional changes that create a biologic mi- lieu for dysesthetic symptoms. Our growing understanding of innate immunity including antimicrobial peptides, Toll-like receptors and other signaling mechanisms for inflammation make preservation and restoration of the epidermal barrier essential. Therefore, it is suggested that the role of topical agents is essential to normalize skin reactivity and restore normal barrier function. Again, the possibility of irritant or contact dermatitis must always be kept in mind when using topical agents.A vicious cycle of transient relief from the active ingredient followed by exacerbation of symptoms by irritant or allergic factors can occur. As suggested in a previous section, sometimes cessation of all topical agents can be instructive and clinically beneficial.
Use of Oral Agents
Several classes of oral agents can be helpful in reducing the frequency, severity and intrusiveness of dysesthetic symptoms. These agents in- clude antihistamines, antibiotics, antifungals, anti-virals, tricyclic anti-depressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepiephrine reuptake inhibitors (SNRIs), anti-seizure agents and beta blockers. These agents may be used alone or in combination, always with the recognition that known and idiosyncratic side effects and interactions are possible. The therapeutic goal is modification of the occurrence, duration, intensity and the perception of the dysesthetic symptom(s). Antihistamines can be beneficial if there is any histamine mediated component to symptoms. Antibiotics, antifungals and anti-viral medications can eradicate infection if present. More often, their ameliorative effects are probably achieved through reduction or eradication of super-antigens. Candida certainly is a prime candidate and anecdotal communications suggest that short courses of fluconazole 100 mg to 200 mg QD or itraconazole at similar dosing can reduce severity of symptoms. This should be repeated at 2 to 3 week intervals. SSRIs and SNRIs can exert their ameliorative benefits acting both centrally and peripherally. Their central effects are through direct inhibition of neurotransmitter re-uptake allowing for higher neurotransmitter levels at the synapse. Inhibition of neurotransmitter re-uptake has been demonstrated to decrease pain, pruritus, burning, and other dysesthetic symptoms. In addition, they reduce the psychological morbidity that frequently accompanies these chronic sensations, such as anxiety, depression, obsessive compulsive symptoms, and anger. Peripherally, SSRIs and SNRIs have been demonstrated to decrease neuropeptide release thereby directly decreasing local pro-inflammatory- exacerbating factors. The ameliorative benefits of anti- seizure agents for the management of neuropathic symptoms is well described elsewhere. Clinical benefit is probably a combined effect of neuronal normalization, anxiolysis, sedation and placebo effect. The role of beta blockers is interesting and mostly anecdotal. Recent evidence suggests that they may decrease peripheral release of neuropeptides thereby reducing the negative proprioceptive sensations locally. Moreover, it has been suggested that neuropeptides cross the blood brain barrier and enhance reuptake at the synapse. This results in depletion of neurotransmitters which can exacerbate both skin symptoms and psychological distress.
Caveats and Conclusions
Management of the patient with groin dysesthesias requires vigilance for a cryptic primary infectious, autoimmune or neoplastic etiology. Akin to chronic itch or an eczematous process that may represent an evolving collagen vascular process or T cell dyscrasia, groin dysesthesia must be followed closely with similar clinical suspicion. Sometimes, patients’ fears are correct and an STD, other infection, infestation, or neoplastic process is in fact present or evolving. Periodic repeat of appropriate serologies, cultures, and skin biopsy(ies) is strongly encouraged in the setting of unremitting symptoms, lack of clinical improvement, or change in symptom constellation. Finally, don’t forget that what happens in Vegas doesn’t always stay there. Dr. Fried, who is a psychologist as well as a dermatologist, maintains a private practice inYardley, PA. Disclosure: Dr. Fried has no conflicts of interest with the subject discussed in this column.
This often difficult-to-diagnose-and-treat condition can frustrate both physicians and patients, whose treatment involves addressing their worry and fear as well as finding appropriate medications. Dysesthesias of the groin are commonly encountered in dermatologic practice. Complaints range from burning, tenderness, and hypersensitivity to aching, pain and pruritus. The dysesthetic regions often include, but are not limited to, the penis, scrotum, vulva, perianal area and crural folds. Other than prolonged chafing bike rides, irritant or allergic contact reactions, or bacterial or fungal infections, obvious precipitating factors are rarely elicited. Physical examination sometimes reveals primary dermatologic skin disease, but all too often the etiology is cryptic, with symptoms strikingly out of proportion to physical findings. Patients often display a great deal of obvious stress and distress, frequently having already been evaluated by several other physicians including primary care, urology, gynecology, and infectious disease. Cultures and serologies are usually negative, although the occurrences of positive IgG titres for HSV and varicella only further complicate matters. What happens in Vegas stays in Vegas, right? Well, not always. Gonorrhea, syphilis, chlamydia, HIV, scabies and lice travel quite well. Ironically, so do fear, guilt, anxiety and shame.
Etiology of Dysesthesias
Dysesthetic sensations can be initiated by a variety of “insults” to the skin, both endogenous and exogenous. Infection, infestation, allergy, irritation and trauma can cause both functional and structural changes that directly elicit or collectively culminate in skin dysesthesias. Neuropeptide release, histamine release, cell mediated immunity, vasodilation and antimicrobial peptides can all be associated with a subjective dysesthetic sensation.
Identifying Sources, Threats
Dysesthesias rarely exist in isolation. They reside with their co-perpetrators that are responsible for their occurrence and invariably elicit both cognitive and affective responses. An incomplete list of etiologic factors and co-perpetrators is listed in Table 1. Intellectual and cognitive processes are always attempting to explain and interpret bodily sensations. Explanation and interpretation of bodily sensations can be considered an adaptive survival technique that allow us to identify and assess any potential threat to our safety, integrity and viability. Thus, benign dysesthetic symptoms must be differentiated from those that are harbingers of underlying infection, infestation, metabolic derangement, destructive inflammatory or neoplastic process.
A Sensitive Area
There is of course the “real estate” issue — location, location, location — which is particularly resonate with regard to groin dysesthesias. Most of us consider the groin area to be a valuable and cherished asset. Its location literally and metaphorically represents the center of fertility, strength, prowess and sexuality.The orifices that reside within this region provide us pleasure, relief and transfer of genetic material creating the union that begins a new life. They are also the final exit points for the toxic metabolic end products of our cellular biology. Therefore, unexplained sensations without logical explanations for their existence can elicit extreme and deep rooted anxiety that may be associated with haunting thoughts of life threatening proportions. If there were in fact a real or imagined “inappropriate” incident or exposure that could explain these symptoms, the dysesthetic process can become intensified.
Physical Symptoms And Emotional Impact
It is imperative that the clinician precisely understand the nature of the dysesthetic symptom. The approach to symptoms should initially involve characterization of the dysesthetic symptom by duration, quality, diurnal or nocturnal fluctuation and precise location(s). Is it best described as itch, burning, pain, crawling, ache, gnawing, or pulling? Is it localized — eg, ventral aspect of the glans penis, right labia majora — or is it more vague or diffuse? Do the symptoms worsen at night, with exer- tion, friction, intercourse, perspiration, stress or fatigue? Is there anything that has been tried — OTC or prescription — that has afforded any relief? Does rest or avoidance of certain activities ameliorate symptoms? Do the symptoms interfere with sleep, work or play? Is there significant associated anxiety, fear, depression, obsession or compulsive-ritualistic behavior such as rubbing, scratching, washing, etc? In addition, it can be very enlightening to elicit from the patient details about their associated cognitions and fears. What do they think is causing their symptoms and what are their fears regarding what they may represent? The constellation of thoughts, fears and behaviors can be overwhelming. They can lead the affected individual to “over-worry,” “over-wash” and culminate in a deafening “overture” of thoughts, fears, and behaviors that usurp their time, energy and availability to self and others.
Specific Interventions
Offering Reassurance and Understanding of the Condition Perhaps one of the most powerful interventions we can offer patients is our confident assurance that we will diminish or eliminate their dysesthetic symptoms. Initially, it is crucial to address the two most prominent fears that commonly fuel their anxiety and worsen their symptom complex. The first is their pervasive terror that the dysesthetic symptoms are harbingers of a serious, communicable or tragic life-threatening illness. The second is their fear that the dysesthetic symptoms will never improve or remit. Thus, they often envision a relent- less progression or downward spiral culminating in disability or demise. In essence, they are individuals with uncontrolled symptoms who feel increasingly out of control. Psychologically speaking, loss of perceived control over thoughts, sensations, impulses or our immediate environment leads to extreme psycho- logical distress and functional difficulties. Given this context, I cannot overstate the therapeutic importance of enhancing the patient’s sense of self-control by allaying these fears and offering hope. An effective initial strategy is to ex- plain to patients that they have developed a condition that is essentially a hyper-reactivity or hyper-irritability of their skin nerve endings. This condition causes the nerve endings to over-react to the normal skin exposures and “insults” to the integument that occur daily. Friction, perspiration, bacterial and fungal colonization, urination, menstruation, etc., are usually tolerated without substantial awareness or alteration in skin sensation. However, once the skin has been abnormally activated, all of these “normal occurrences” can result in nerve fiber activation leading to abnormal, exaggerated and persistent skin sensations. It is important to point out that the initial event or insult that initiated the hyper-reactivity of the nerve fibers may be “long gone.” In other words, we can reassure them that even if the initiating event causing their dysesthesias were in fact a skin infestation or infection (as they often fear), it is fully possible that no active infection or infestation is present despite their ongoing symptoms. A concept of ongoing skin over-reaction and irritability that is analogous to the irritability and sensitivity we feel emotionally when under prolonged stress or duress is often understood by and palatable to patients. In essence, we are presenting a “biologinized” explanation for the basis of the patients’s symptoms with the concept of “biologic over-reactivity” or “cutaneous hypersensitivity.”Thisprovides a biological explanation for the unexplained persistence and intensity of their dysesthesias. Drawing further analogies to poison ivy id reactions and the cutaneous hyperesthesia that persists after herpes zoster can provide additional examples and logical explanations for symptom persistence that regularly occur in the absence of active infection or infestation. One can suggest that this concrete explanation of the “normalcy” of their dysesthesia is a variation of the “talkesthesia” utilized in medical and cosmetic dermatology to diminish the discomfort associated with procedures.
Vigilance and Healing
A comprehensive “two-pronged” approach of vigilance and healing will be utilized. Further stating that this approach has been utilized with consistent success with other patients can be reassuring. The first “prong” is a promise of ongoing vigilance for underlying or associated organic disease. The second “prong” is the use of medications and techniques that help modulate and normalize their underlying nerve ending hyper-reactivity. Assuring them that the nerve endings will remain fully functional and capable of transmitting “important or essential” messages of true organic problems can allow them to feel it is safe to relinquish their obsessive preoccupation. Many of these patients have a plethora of topical medications that they haphazardly apply. This can complicate matters with the possibility of irritant or allergic contact dermatitis. Sometimes, “don’t just do something, stand there” can stop the therapeutic assault on the integument. Scrub, rub, medicate and lubricate can all aggravate! If your novel concoctions have not been very helpful, asking the patient to stop all topical medications, OTC and herbal creams and lotions can do a world of good.
Topical Treatment
Topical Treatment Options Topical agents can be broadly categorized as antifungals, antibiotics, anti-inflammatories, analgesics, barrier agents and anesthetics. The efficacy of antifungal and antibiotic agents may well be due to the reduction of colonized superantigens and barrier restoration rather than “cure” of infection. Combination products containing iodoquinol/hydrocortisone (Vytone, Alcortin) and iodoquinol/aloe (Aloquin) as well as generic and compounded formulations containing these products can be soothing and efficacious. In general, cream and gel formulations tend to be best for daytime use. Low-potency corticosteroid creams, gels and ointments can be helpful in decreasing dysesthesias and reducing visible redness secondary to their vasoconstrictive properties. Non-steroidal creams and ointments such as pimecromalus (Elidel) and tacrolimus (Protopic) can be helpful and have the advantage of quelling any fears of skin atrophy. Topical analgesia may sometimes be achieved using a topical tricyclic antidepressant agent such as doxepin cream 5% (Zonalon) or topical amitriptyline 10% cream available from compounding pharmacies.There is little data regarding agents such as topical diclofenac gel but personal communications have suggested mixed results. Topical anesthetic agent such as lidocaine and prilocaine can afford some patients with relief for several hours, though other patients may report little or no benefit. In addition, topical application of cold compresses, saline compresses, milk soaks and oatmeal preparations can also be beneficial. Topical Treatment Issues Choosing among the topical agents to ameliorate dysesthetic symptoms should be based on a working hypothesis postulating the major causative factors in the affected individual and also the recognition that the involved dysesthetic skin has usually been rubbed, scratched and otherwise abused and manipulated. These activities often compromise the epidermal barrier and lead to underlying neuropathic changes including increased C fibers and other structural and functional changes that create a biologic mi- lieu for dysesthetic symptoms. Our growing understanding of innate immunity including antimicrobial peptides, Toll-like receptors and other signaling mechanisms for inflammation make preservation and restoration of the epidermal barrier essential. Therefore, it is suggested that the role of topical agents is essential to normalize skin reactivity and restore normal barrier function. Again, the possibility of irritant or contact dermatitis must always be kept in mind when using topical agents.A vicious cycle of transient relief from the active ingredient followed by exacerbation of symptoms by irritant or allergic factors can occur. As suggested in a previous section, sometimes cessation of all topical agents can be instructive and clinically beneficial.
Use of Oral Agents
Several classes of oral agents can be helpful in reducing the frequency, severity and intrusiveness of dysesthetic symptoms. These agents in- clude antihistamines, antibiotics, antifungals, anti-virals, tricyclic anti-depressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepiephrine reuptake inhibitors (SNRIs), anti-seizure agents and beta blockers. These agents may be used alone or in combination, always with the recognition that known and idiosyncratic side effects and interactions are possible. The therapeutic goal is modification of the occurrence, duration, intensity and the perception of the dysesthetic symptom(s). Antihistamines can be beneficial if there is any histamine mediated component to symptoms. Antibiotics, antifungals and anti-viral medications can eradicate infection if present. More often, their ameliorative effects are probably achieved through reduction or eradication of super-antigens. Candida certainly is a prime candidate and anecdotal communications suggest that short courses of fluconazole 100 mg to 200 mg QD or itraconazole at similar dosing can reduce severity of symptoms. This should be repeated at 2 to 3 week intervals. SSRIs and SNRIs can exert their ameliorative benefits acting both centrally and peripherally. Their central effects are through direct inhibition of neurotransmitter re-uptake allowing for higher neurotransmitter levels at the synapse. Inhibition of neurotransmitter re-uptake has been demonstrated to decrease pain, pruritus, burning, and other dysesthetic symptoms. In addition, they reduce the psychological morbidity that frequently accompanies these chronic sensations, such as anxiety, depression, obsessive compulsive symptoms, and anger. Peripherally, SSRIs and SNRIs have been demonstrated to decrease neuropeptide release thereby directly decreasing local pro-inflammatory- exacerbating factors. The ameliorative benefits of anti- seizure agents for the management of neuropathic symptoms is well described elsewhere. Clinical benefit is probably a combined effect of neuronal normalization, anxiolysis, sedation and placebo effect. The role of beta blockers is interesting and mostly anecdotal. Recent evidence suggests that they may decrease peripheral release of neuropeptides thereby reducing the negative proprioceptive sensations locally. Moreover, it has been suggested that neuropeptides cross the blood brain barrier and enhance reuptake at the synapse. This results in depletion of neurotransmitters which can exacerbate both skin symptoms and psychological distress.
Caveats and Conclusions
Management of the patient with groin dysesthesias requires vigilance for a cryptic primary infectious, autoimmune or neoplastic etiology. Akin to chronic itch or an eczematous process that may represent an evolving collagen vascular process or T cell dyscrasia, groin dysesthesia must be followed closely with similar clinical suspicion. Sometimes, patients’ fears are correct and an STD, other infection, infestation, or neoplastic process is in fact present or evolving. Periodic repeat of appropriate serologies, cultures, and skin biopsy(ies) is strongly encouraged in the setting of unremitting symptoms, lack of clinical improvement, or change in symptom constellation. Finally, don’t forget that what happens in Vegas doesn’t always stay there. Dr. Fried, who is a psychologist as well as a dermatologist, maintains a private practice inYardley, PA. Disclosure: Dr. Fried has no conflicts of interest with the subject discussed in this column.
