Aa
Peripheral Neuropathy or not
I had cervical neck surgery on 12/3/98 to repair a ruptured disk. Fusion (no hardware) at C6-C7 was performed. Left arm and triceps damage resulted from pressure on nerve. The surgery instantly relieved my pain and I feel it was a success. One notable complication from the surgery was my laryngeal nerve was stretched resulting in paralyzed right vocal fold. I could not speak above a whisper for 10 weeks. While still recovering and still suffering with a paralyzed vocal fold I had an emergency appendectomy in February 1999. A few weeks latter while recovering from both surgeries I noticed my right arm and hand would go numb while walking. This sensation quickly settled into my feet and has predominantly been there since then. Sensations include soreness in ankles and feet, pins and needles, numbness, and burning sensation. Occasionally these symptoms are in all extremities (hands and feet). My neurologist suggested Peripheral Neuropathy (PN)
Dear Monica:
I am not sure what to tell you. It is very unusual that an acute event as you describe is the result of a lower spinal cord problem without a trauma. I think the best thing to do is to go to a neurologist and have a complete neurological exam. Have him/her review the MRI (take the film with you) and begin at this point. I think that your problem may be more than a herniated disc.
Sincerely,
CCF Neuro MD
I am not sure what to tell you. It is very unusual that an acute event as you describe is the result of a lower spinal cord problem without a trauma. I think the best thing to do is to go to a neurologist and have a complete neurological exam. Have him/her review the MRI (take the film with you) and begin at this point. I think that your problem may be more than a herniated disc.
Sincerely,
CCF Neuro MD
about 3 years ago i got out of bed just fine - i went to the bathbathroom and when i got up my legs could not support me and i fell to the floor and i just could not get up - finally after about an hour - i got up ever so slowly and i could barely walk.walk - i finally went to the doctor and after 2 weeks an mri was done - i had a herniated disc lower back - i had surgery. my back stopped hurting, however i still could not feel when i would urinate or do poop or had intercourse. after 3 years - I still cannot feel any of these things - sometimes when i get turned on i pee instead of getting lubricated
Dear Mercedes:
I can't tell you for sure, I haven't examined you or seen the MRI. I would suggest a second opinion with another neurologist.
CCF Neuro MD
I can't tell you for sure, I haven't examined you or seen the MRI. I would suggest a second opinion with another neurologist.
CCF Neuro MD
On 3/23/99 I was in a car accident, driver side hit. I passed out for a short period. That night I had pain in my neck and back, but I also felt displaced, spacey, shaken. I suffered with pain in my back, left arm and leg. Ten days later I woke up , tried to turn my head to the left but had vicious dizzy spells and the feeling of falling off a 30 story building. For three days I sat with my head still, and slept with pillows wrapped around my head. I then developed tremors in my head which spreaded to all extremities within four weeks. The MRI of my brain was normal, and the neurologist concluded that it could not be neurological. The MRI of my cervical spine showed small intrusions of focal disc and slight scoliosis. The tremors were so violent that it was difficult to walk. I saw a chiroprator and a psychiatrist as the neurologist stated the onset of the tremors had to be psychological. Well, the chiropractor lifted the pressure off of my neck and back allowing me to have some days free of pain. However, I can no longer see him. I have severe pain, spasms and tremors all day, every day. If you apply pressure to certain places in my neck and spine it relieves the pain. Can this be a pinched nerve and how should I pursue this?
Dear Tara:
Thanks for the information. I was not sure if there was a direct association with lymphoma and it seems that it is only loosely associated with malignacy. From what you described, I really don't think there would be a direct cause and effect of Grover's and perpherial neuropathy. There might be a bystander effect of a malignancy that can give a peripheral neuropathy and also Grover's but likely not a direct effect as Grover's seems to be limited to dermis.
I would say no concerning Grover's and peripheral neuropathy and certainly MG (antibodies to the acetyl choline receptor).
Sincerely,
CCF Neuro MD
Thanks for the information. I was not sure if there was a direct association with lymphoma and it seems that it is only loosely associated with malignacy. From what you described, I really don't think there would be a direct cause and effect of Grover's and perpherial neuropathy. There might be a bystander effect of a malignancy that can give a peripheral neuropathy and also Grover's but likely not a direct effect as Grover's seems to be limited to dermis.
I would say no concerning Grover's and peripheral neuropathy and certainly MG (antibodies to the acetyl choline receptor).
Sincerely,
CCF Neuro MD
Dear Doctor,
This is the only thing that I found on it. I developed this rash last year, which was a year into my neurological symptoms. It was just bx'd and dx'd last week.
Any thoughts on this would be helpful as my neurologist feels another autoimmune process is going on.
Twenty-six years have passed since Grover first described transient acantholytic dermatosis. Since then, the concept of Grover's disease has been expanded to include persistent acantholytic dermatoses as well. Although its origin remains unknown, it may result from an isomorphic response to excessive heat, sweating, or xerosis. It is currently classified as a nonfamilial, non-immune-mediated, acantholytic disorder. (J
Am Acad Dermatol 1996;35:653-66.)
ASSOCIATION WITH CANCER
Grover's disease has been observed before, during, and after the discovery of internal malignancies. It has been associated with solid tumors, especially those of genitourinary tract origin. It has also been associated with hematologic malignancies, particularly acute myelogenous leukemia. Among the solid tumors were adenocarcinoma of the stomach,lung, prostate,and unknown primary tumors; transitional cell carcinoma of the urinary bladder and renal pelvis; metastatic renal cell carcinoma;
leiomyosarcoma of the urinary bladder; malignant melanoma; anaplastic carcinoma of the colon; metastatic carcinoma of the breast; spinocellular carcinoma of the larynx; squamous cell carcinoma of the salivary duct; and unclassified carcinoma
of the ovary. Among the hematologic malignancies were acute
Transient acantholytic dermatosis (Grover's disease): A global perspective: Twenty-six years have passed since Grover first described transient acantholytic dermatosis. Since then, the concept of Grover's disease has been expanded to include
persistent acantholytic dermatoses as well. Although its origin remains unknown, it may result from an isomorphic response to excessive heat, sweating, or xerosis. It is currently classified as a nonfamilial, non-immune-mediated, acantholytic disorder. (J
Am Acad Dermatol 1996;35:653-66.)
Grover's disease is an acquired, monomorphous, papulovesicular eruption of unknown cause first characterized by Ralph W. Grover in 1970. Witten and Gelfarb described a similar but more persistent dermatosis in 1963 as ``keratosis follicularis of sudden onset.'' After Grover's original description, Fishman [3] reported an additional case in 1975 as ``acute eruptive
Darier disease.''Similarly, Gisslen and Mobacken described two additional cases in 1978 as ``acute adult-onset Darier-like dermatosis.'' In 1976, Heaphy, Tucker, and Winkelmann reported a case retrospectively from 1954 as ``benign papular acantholytic
dermatosis.'' Other authors have recalled their cases from the 1960s. Through the years the concept of Grover's disease has been expanded to include more persistent forms of the
disease.
DEMOGRAPHICS
Grover's disease is a common disorder that has been reported in many countries throughout the world. Most cases have occurred in white men older than 40 years of age. In fact, the
male-to-female ratio is 3:1. It has also been reported in a black female patient. The youngest patient was a 4-year-old girl; the oldest was an 87-year-old man. Although the disease generally has a self-limited course, its ultimate extent and duration are
directly correlated with age. In other words, older patients are more likely to have extensive eruptions of longer duration.
CLINICAL MANIFESTATIONS
Because the clinical features of Grover's disease are often subtle, the diagnosis requires a high index of suspicion. The eruption usually begins with a few, discrete, erythematous, edematous, acneiform, red-brown, or flesh-colored papules; papulovesicles; or keratotic papules. The individual lesions may resemble Darier's disease, tiny seborrheic keratoses, or even
small basal cell carcinomas. Their size usually ranges from 1 to 3 mm in diameter, but they may be as large as 1 cm lesions have been described. In addition, there have been a few patients in
whom erythematous or eczematous plaques developed.
The eruption begins primarily on the trunk around the clavicles, anterior aspect of the chest, lower rib-cage, upper back, and lumbar area. When it becomes disseminated, it may spread to the deltoids, lateral neck, and thighs The palms and soles are usually spared. The scalp is infrequently affected. Localized cases involving only the face, the lateral neck, or the lower
extremities have been reported. Mucous membrane lesions have been rarely seen on the larynx, in the nares,and in the oral cavity; oral lesions resemble aphthae. Cutaneous lesions may resolve with postinflammatory hyperpigmentation or hypopigmentation.
Constitutional symptoms are usually absent. Pruritus of variable intensity occurs in most patients. Paroxysms of severe pruritus may precede the onset of the eruption. The pruritus may
be totally out of proportion to the apparent clinical disease. In fact, one patient had pruritus without a rash, adding Grover's disease to the list of invisible dermatoses detectable
only by biopsy. In other cases, the pruritus has been mild or even nonexistent. Lack of pruritus was a feature of 38% of patients with cancer and Grover's disease in one review of the literature. Although most cases of Grover's disease have a duration of only weeks or months, some may be persistent or recurrent. It is not unusual for the dermatosis to last 7 to 17 years. The extent and severity of the eruption may fluctuate spontaneously during that period. Other patients have had recurrent attacks with intervals of complete remission. One patient had his first attack of Grover's disease in 1954 and his second attack in 1972. Other patients have had several attacks per year for 3 to 5 years. Still others have experienced seasonal recurrences every summer or winter for 7 to 10 years
CAUSES
Many factors have been associated with the development of Grover's disease. Frequently, there is a history of initiation or exacerbation (or both) by sunlight, which may occur after regular extensive sun exposure, a vacation in a sunny latitude, or even an inadvertent burn from a sunlamp. Both the timing and the distribution of the lesions clearly indicate the importance of UV radiation as a trigger factor. Nevertheless, the condition is uncommon when compared with most other manifestations of solar damage, which suggests that other environmental or constitutional factors may be involved. Furthermore,attempts to reproduce the eruption with sunlight or high doses of artificial UVA and UVB light have been unsuccessful.
Grover's disease is often a reaction to excessive heat or sweating. * Many cases have occurred on the backs of febrile or postoperative patients who were bedridden. Others have occurred
after the use of a steambath, hot tub, hot water bottle, or polyester jogging suit. speculated that obstruction of sweat ducts leads to the escape of pooled sweat urea into
the epidermis (internal sweating) with resulting acantholysis. However, immunohistochemical evaluations have shown no evidence of leakage of carcinoembryonic antigen and epithelial
mucin, two large molecules that are commonly found in sweat. Furthermore, intraepidermal sweat ducts were intact in all histologic sections, and the areas of focal acantholysis frequently appeared to be between sweat ducts. Thus, although the pathogenesis of Grover's disease is still unknown, it appears unlikely that leakage occurred from the acrosyringeal duct. However, the possibility still exists that smaller molecules may seep through the ductal epithelium and cause epidermal acantholysis. In addition, heat may directly cause acantholysis through the release of an unknown enzymatic factor after mild
thermal injury. The administration of ionizing radiation has also been associated with the development of Grover's disease. Although several patients with cancer have had transient
acantholytic dermatosis after radiotherapy, lesions confined to the port of radiation developed in only two. These patients had not been febrile and had not received chemotherapy. Perhaps the
role of ionizing radiation as a provocative factor in these cases is analogous to that of UV radiation in previous cases. Only two medications have been associated with the development of Grover's disease: sulfadoxine-pyrimethamine (Fansidar) and recombinant human interleukin-4 (IL-4).
Sulfadoxine-pyrimethamine, administered as an antimalarial agent, induced persistent acantholytic dermatosis of 6 years' duration in one patient. Once the drug was discontinued, the eruption completely cleared and remained clear during an 18-month follow-up period. The author demonstrated that the
sulfadoxine-pyrimethamine reduced the patient's erythema threshold for UVB radiation. The threshold returned to normal once the medication was discontinued. IL-4 has induced transient
acantholytic dermatosis in three patients being treated for advanced metastatic renal cell carcinoma or malignant melanoma. The eruption resolved after discontinuation of the IL-4
therapy only to reappear once the therapy was restarted. The authors speculated that the IL-4 may have produced acantholysis through the activation of the plasminogen/plasmin system.
Because plasminogen has been detected in the basal buds and acantholytic cells in Grover's disease, it is possible that the activation of plasminogen and the resulting breakdown of
desmosomes contributed to the acantholysis seen in this condition. Infection is another possible cause of Grover's disease. Up to now, no scientific evidence has been found to support a bacterial or a viral origin. However, the coexistence of tinea versicolor and transient acantholytic dermatosis in one patient led to speculation that Malassezia furfur, a yeastlike fungus, could induce Grover's disease. Treatment with selenium
sulfide lotion rapidly resolved both conditions. Infestation with Demodex folliculorum, the human follicle mite, has been associated with an eruption that mimicked both granulomatous rosacea and transient acantholytic dermatosis. Biopsy specimens from the face and trunk showed features of Grover's disease in addition to numerous follicle mites. The authors speculated that the mite was able to produce an enzymelike substance that destroyed the walls of the follicle and induced acantholytic changes in the epidermis. Ironically, Grover and Rosenbaum found a significant negative correlation between acne rosacea and transient acantholytic dermatosis in a large retrospective study. Thus the role of the human follicle mite in the development of Grover's disease and rosacea remains highly speculative at this point. contact dermatitis, atopic dermatitis, and irritation from adhesive tape.Furthermore, the overzealous use of UV light and anthralin therapies has been associated with the simultaneous
development of eruptive psoriasis and transient acantholytic dermatosis.The Koebner phenomenon or isomorphic response appears to account for most of these associations. The idea that nonspecific irritation may cause the appearance of new lesions suggests that the patient's skin responds in a genetically predetermined fashion. Although a genetic basis for
Grover's disease has not been proved, the demonstration of identical dermatoglyphic patterns on the palms and soles of patients with this disease is further support for its hereditary nature.
ASSOCIATION WITH CANCER
Grover's disease has been observed before, during, and after the discovery of internal malignancies. It has been associated with solid tumors, especially those of genitourinary tract origin. It has also been associated with hematologic malignancies, particularly acute myelogenous leukemia. Among the solid tumors were adenocarcinoma of the stomach, lung, prostate, and unknown primary tumors; transitional cell carcinoma of the urinary bladder and renal pelvis; metastatic renal cell carcinoma;
leiomyosarcoma of the urinary bladder; malignant melanoma; anaplastic carcinoma of the colon; metastatic carcinoma of the breast; spinocellular carcinoma of the larynx; squamous cell carcinoma of the salivary duct; and unclassified carcinoma
of the ovary. Among the hematologic malignancies were acute myelogenous leukemia,chronic myelogenous leukemia, acute lymphocytic leukemia, chronic lymphocytic leukemia, multiple myeloma, myelodysplastic syndrome,lymphosarcoma, peripheral T-cell lymphoma,* and angioimmunoblastic lymphadenopathy with dysproteinemia-like T-cell lymphoma. Although the majority of cases were not attributed to the underlying malignancy, the reappearance or onset of Grover's disease (or both) temporally coincided with the discovery of a previously asymptomatic malignancy or the detection of an unsuspected tumor recurrence in a few cases. Although it is conceivable that Grover's disease may be a paraneoplastic phenomenon, the number of known cases associated with neoplasms is negligible even when one considers the many cases for which no tumor testing was conducted. Furthermore, Grover's disease occurs most frequently in the same age group as most malignancies occur. Therefore, although some
authors consider it to be loosely associated with cancer, others believe that the association is a coincidence.
SSOCIATIONS WITH OTHER MEDICAL CONDITIONS
Grover's disease has been associated with a variety of dermatologic diseases. However, only the associations with asteatotic eczema, atopic dermatitis, and allergic contact
dermatitis were both statistically significant and clinically relevant. Other associations included bullous pemphigoid, [13] lichen planus, parapsoriasis en plaques,pemphigus foliaceus, psoriasis, pyoderma gangrenosum, and seborrheic dermatitis.With the possible exception of bullous pemphigoid, the coexistence of Grover's disease with these other cutaneous disorders appears to be a coincidence. Grover's disease has also been associated with certain medical conditions; these include benign thymoma, * benign monoclonal gammopathy, membranous glomerulonephritis, chronic gastritis, rheumatoid arthritis, pregnancy, and infection with HIV and poliomyelitis virus. Future case reports may clarify the significance of these associations.
HISTOLOGIC FEATURES
Microscopically, Grover's disease is an acantholytic process that often displays dyskeratosis, such as is seen in Darier's disease. Not infrequently, there may be an admixture of spongiotic
change; this occurs most often when there is an associated eczematous component, such as nummular eczema. Rarely, and possibly when the process is hyperacute, the histologic features
may resemble pemphigus or Hailey-Hailey disease. Hyperkeratosis, acanthosis, and parakeratosis are other common epidermal changes. There may be alternating vertical orthokeratosis and parakeratosis, and solar elastosis may be present. The papillary dermis may be edematous and contain a perivascular lymphohistiocytic infiltrate. A variable number of eosinophils may be present.*
This is the only thing that I found on it. I developed this rash last year, which was a year into my neurological symptoms. It was just bx'd and dx'd last week.
Any thoughts on this would be helpful as my neurologist feels another autoimmune process is going on.
Twenty-six years have passed since Grover first described transient acantholytic dermatosis. Since then, the concept of Grover's disease has been expanded to include persistent acantholytic dermatoses as well. Although its origin remains unknown, it may result from an isomorphic response to excessive heat, sweating, or xerosis. It is currently classified as a nonfamilial, non-immune-mediated, acantholytic disorder. (J
Am Acad Dermatol 1996;35:653-66.)
ASSOCIATION WITH CANCER
Grover's disease has been observed before, during, and after the discovery of internal malignancies. It has been associated with solid tumors, especially those of genitourinary tract origin. It has also been associated with hematologic malignancies, particularly acute myelogenous leukemia. Among the solid tumors were adenocarcinoma of the stomach,lung, prostate,and unknown primary tumors; transitional cell carcinoma of the urinary bladder and renal pelvis; metastatic renal cell carcinoma;
leiomyosarcoma of the urinary bladder; malignant melanoma; anaplastic carcinoma of the colon; metastatic carcinoma of the breast; spinocellular carcinoma of the larynx; squamous cell carcinoma of the salivary duct; and unclassified carcinoma
of the ovary. Among the hematologic malignancies were acute
Transient acantholytic dermatosis (Grover's disease): A global perspective: Twenty-six years have passed since Grover first described transient acantholytic dermatosis. Since then, the concept of Grover's disease has been expanded to include
persistent acantholytic dermatoses as well. Although its origin remains unknown, it may result from an isomorphic response to excessive heat, sweating, or xerosis. It is currently classified as a nonfamilial, non-immune-mediated, acantholytic disorder. (J
Am Acad Dermatol 1996;35:653-66.)
Grover's disease is an acquired, monomorphous, papulovesicular eruption of unknown cause first characterized by Ralph W. Grover in 1970. Witten and Gelfarb described a similar but more persistent dermatosis in 1963 as ``keratosis follicularis of sudden onset.'' After Grover's original description, Fishman [3] reported an additional case in 1975 as ``acute eruptive
Darier disease.''Similarly, Gisslen and Mobacken described two additional cases in 1978 as ``acute adult-onset Darier-like dermatosis.'' In 1976, Heaphy, Tucker, and Winkelmann reported a case retrospectively from 1954 as ``benign papular acantholytic
dermatosis.'' Other authors have recalled their cases from the 1960s. Through the years the concept of Grover's disease has been expanded to include more persistent forms of the
disease.
DEMOGRAPHICS
Grover's disease is a common disorder that has been reported in many countries throughout the world. Most cases have occurred in white men older than 40 years of age. In fact, the
male-to-female ratio is 3:1. It has also been reported in a black female patient. The youngest patient was a 4-year-old girl; the oldest was an 87-year-old man. Although the disease generally has a self-limited course, its ultimate extent and duration are
directly correlated with age. In other words, older patients are more likely to have extensive eruptions of longer duration.
CLINICAL MANIFESTATIONS
Because the clinical features of Grover's disease are often subtle, the diagnosis requires a high index of suspicion. The eruption usually begins with a few, discrete, erythematous, edematous, acneiform, red-brown, or flesh-colored papules; papulovesicles; or keratotic papules. The individual lesions may resemble Darier's disease, tiny seborrheic keratoses, or even
small basal cell carcinomas. Their size usually ranges from 1 to 3 mm in diameter, but they may be as large as 1 cm lesions have been described. In addition, there have been a few patients in
whom erythematous or eczematous plaques developed.
The eruption begins primarily on the trunk around the clavicles, anterior aspect of the chest, lower rib-cage, upper back, and lumbar area. When it becomes disseminated, it may spread to the deltoids, lateral neck, and thighs The palms and soles are usually spared. The scalp is infrequently affected. Localized cases involving only the face, the lateral neck, or the lower
extremities have been reported. Mucous membrane lesions have been rarely seen on the larynx, in the nares,and in the oral cavity; oral lesions resemble aphthae. Cutaneous lesions may resolve with postinflammatory hyperpigmentation or hypopigmentation.
Constitutional symptoms are usually absent. Pruritus of variable intensity occurs in most patients. Paroxysms of severe pruritus may precede the onset of the eruption. The pruritus may
be totally out of proportion to the apparent clinical disease. In fact, one patient had pruritus without a rash, adding Grover's disease to the list of invisible dermatoses detectable
only by biopsy. In other cases, the pruritus has been mild or even nonexistent. Lack of pruritus was a feature of 38% of patients with cancer and Grover's disease in one review of the literature. Although most cases of Grover's disease have a duration of only weeks or months, some may be persistent or recurrent. It is not unusual for the dermatosis to last 7 to 17 years. The extent and severity of the eruption may fluctuate spontaneously during that period. Other patients have had recurrent attacks with intervals of complete remission. One patient had his first attack of Grover's disease in 1954 and his second attack in 1972. Other patients have had several attacks per year for 3 to 5 years. Still others have experienced seasonal recurrences every summer or winter for 7 to 10 years
CAUSES
Many factors have been associated with the development of Grover's disease. Frequently, there is a history of initiation or exacerbation (or both) by sunlight, which may occur after regular extensive sun exposure, a vacation in a sunny latitude, or even an inadvertent burn from a sunlamp. Both the timing and the distribution of the lesions clearly indicate the importance of UV radiation as a trigger factor. Nevertheless, the condition is uncommon when compared with most other manifestations of solar damage, which suggests that other environmental or constitutional factors may be involved. Furthermore,attempts to reproduce the eruption with sunlight or high doses of artificial UVA and UVB light have been unsuccessful.
Grover's disease is often a reaction to excessive heat or sweating. * Many cases have occurred on the backs of febrile or postoperative patients who were bedridden. Others have occurred
after the use of a steambath, hot tub, hot water bottle, or polyester jogging suit. speculated that obstruction of sweat ducts leads to the escape of pooled sweat urea into
the epidermis (internal sweating) with resulting acantholysis. However, immunohistochemical evaluations have shown no evidence of leakage of carcinoembryonic antigen and epithelial
mucin, two large molecules that are commonly found in sweat. Furthermore, intraepidermal sweat ducts were intact in all histologic sections, and the areas of focal acantholysis frequently appeared to be between sweat ducts. Thus, although the pathogenesis of Grover's disease is still unknown, it appears unlikely that leakage occurred from the acrosyringeal duct. However, the possibility still exists that smaller molecules may seep through the ductal epithelium and cause epidermal acantholysis. In addition, heat may directly cause acantholysis through the release of an unknown enzymatic factor after mild
thermal injury. The administration of ionizing radiation has also been associated with the development of Grover's disease. Although several patients with cancer have had transient
acantholytic dermatosis after radiotherapy, lesions confined to the port of radiation developed in only two. These patients had not been febrile and had not received chemotherapy. Perhaps the
role of ionizing radiation as a provocative factor in these cases is analogous to that of UV radiation in previous cases. Only two medications have been associated with the development of Grover's disease: sulfadoxine-pyrimethamine (Fansidar) and recombinant human interleukin-4 (IL-4).
Sulfadoxine-pyrimethamine, administered as an antimalarial agent, induced persistent acantholytic dermatosis of 6 years' duration in one patient. Once the drug was discontinued, the eruption completely cleared and remained clear during an 18-month follow-up period. The author demonstrated that the
sulfadoxine-pyrimethamine reduced the patient's erythema threshold for UVB radiation. The threshold returned to normal once the medication was discontinued. IL-4 has induced transient
acantholytic dermatosis in three patients being treated for advanced metastatic renal cell carcinoma or malignant melanoma. The eruption resolved after discontinuation of the IL-4
therapy only to reappear once the therapy was restarted. The authors speculated that the IL-4 may have produced acantholysis through the activation of the plasminogen/plasmin system.
Because plasminogen has been detected in the basal buds and acantholytic cells in Grover's disease, it is possible that the activation of plasminogen and the resulting breakdown of
desmosomes contributed to the acantholysis seen in this condition. Infection is another possible cause of Grover's disease. Up to now, no scientific evidence has been found to support a bacterial or a viral origin. However, the coexistence of tinea versicolor and transient acantholytic dermatosis in one patient led to speculation that Malassezia furfur, a yeastlike fungus, could induce Grover's disease. Treatment with selenium
sulfide lotion rapidly resolved both conditions. Infestation with Demodex folliculorum, the human follicle mite, has been associated with an eruption that mimicked both granulomatous rosacea and transient acantholytic dermatosis. Biopsy specimens from the face and trunk showed features of Grover's disease in addition to numerous follicle mites. The authors speculated that the mite was able to produce an enzymelike substance that destroyed the walls of the follicle and induced acantholytic changes in the epidermis. Ironically, Grover and Rosenbaum found a significant negative correlation between acne rosacea and transient acantholytic dermatosis in a large retrospective study. Thus the role of the human follicle mite in the development of Grover's disease and rosacea remains highly speculative at this point. contact dermatitis, atopic dermatitis, and irritation from adhesive tape.Furthermore, the overzealous use of UV light and anthralin therapies has been associated with the simultaneous
development of eruptive psoriasis and transient acantholytic dermatosis.The Koebner phenomenon or isomorphic response appears to account for most of these associations. The idea that nonspecific irritation may cause the appearance of new lesions suggests that the patient's skin responds in a genetically predetermined fashion. Although a genetic basis for
Grover's disease has not been proved, the demonstration of identical dermatoglyphic patterns on the palms and soles of patients with this disease is further support for its hereditary nature.
ASSOCIATION WITH CANCER
Grover's disease has been observed before, during, and after the discovery of internal malignancies. It has been associated with solid tumors, especially those of genitourinary tract origin. It has also been associated with hematologic malignancies, particularly acute myelogenous leukemia. Among the solid tumors were adenocarcinoma of the stomach, lung, prostate, and unknown primary tumors; transitional cell carcinoma of the urinary bladder and renal pelvis; metastatic renal cell carcinoma;
leiomyosarcoma of the urinary bladder; malignant melanoma; anaplastic carcinoma of the colon; metastatic carcinoma of the breast; spinocellular carcinoma of the larynx; squamous cell carcinoma of the salivary duct; and unclassified carcinoma
of the ovary. Among the hematologic malignancies were acute myelogenous leukemia,chronic myelogenous leukemia, acute lymphocytic leukemia, chronic lymphocytic leukemia, multiple myeloma, myelodysplastic syndrome,lymphosarcoma, peripheral T-cell lymphoma,* and angioimmunoblastic lymphadenopathy with dysproteinemia-like T-cell lymphoma. Although the majority of cases were not attributed to the underlying malignancy, the reappearance or onset of Grover's disease (or both) temporally coincided with the discovery of a previously asymptomatic malignancy or the detection of an unsuspected tumor recurrence in a few cases. Although it is conceivable that Grover's disease may be a paraneoplastic phenomenon, the number of known cases associated with neoplasms is negligible even when one considers the many cases for which no tumor testing was conducted. Furthermore, Grover's disease occurs most frequently in the same age group as most malignancies occur. Therefore, although some
authors consider it to be loosely associated with cancer, others believe that the association is a coincidence.
SSOCIATIONS WITH OTHER MEDICAL CONDITIONS
Grover's disease has been associated with a variety of dermatologic diseases. However, only the associations with asteatotic eczema, atopic dermatitis, and allergic contact
dermatitis were both statistically significant and clinically relevant. Other associations included bullous pemphigoid, [13] lichen planus, parapsoriasis en plaques,pemphigus foliaceus, psoriasis, pyoderma gangrenosum, and seborrheic dermatitis.With the possible exception of bullous pemphigoid, the coexistence of Grover's disease with these other cutaneous disorders appears to be a coincidence. Grover's disease has also been associated with certain medical conditions; these include benign thymoma, * benign monoclonal gammopathy, membranous glomerulonephritis, chronic gastritis, rheumatoid arthritis, pregnancy, and infection with HIV and poliomyelitis virus. Future case reports may clarify the significance of these associations.
HISTOLOGIC FEATURES
Microscopically, Grover's disease is an acantholytic process that often displays dyskeratosis, such as is seen in Darier's disease. Not infrequently, there may be an admixture of spongiotic
change; this occurs most often when there is an associated eczematous component, such as nummular eczema. Rarely, and possibly when the process is hyperacute, the histologic features
may resemble pemphigus or Hailey-Hailey disease. Hyperkeratosis, acanthosis, and parakeratosis are other common epidermal changes. There may be alternating vertical orthokeratosis and parakeratosis, and solar elastosis may be present. The papillary dermis may be edematous and contain a perivascular lymphohistiocytic infiltrate. A variable number of eosinophils may be present.*
Der Tara:
Could you please tell me something about Grover's disease (?) I am not aware of this entity being associated with MG or neuropathy.
CCF Neuro MD
Could you please tell me something about Grover's disease (?) I am not aware of this entity being associated with MG or neuropathy.
CCF Neuro MD
Dear Doctor,
Have you ever heard of Grover's disease ever being associated with neuropathy and MG? I would be thankful for any information you have to offer.
Thank you
Have you ever heard of Grover's disease ever being associated with neuropathy and MG? I would be thankful for any information you have to offer.
Thank you
In December I reported to my doctor that my neck hurt and I also had my first migraine headache shortly before. That same week. He sent me for an MRI which came back normal, I suppose because I never heard from my doctor. A week after my hurt neck I got into a car accident and got whiplash. The day before that I got a flu shot. The following day and night I experienced pins and needles sensation all over my body and it would come and go. At night time it worse for the next 2 months. I would wake up feeling like one side of my body was half a sleep and would shake my arm or leg to wake it up. It would happen almost every night. An arm or a leg. Left arm, right leg. All different places and different sides of my body. Also during this 2 months time I was slipping off my shirt and I felt a pull through both of my arms and a very intense hot kinda like pins and needles painn that went all the way up to my middle fingers. The were numb and prickly for about a week after. Right now it is February. I have my good nights and my bad nights. I still feel sometimes numbness and weakness in certain parts of my body. I do take Vasotec for blood pressure. My blood pressure has been fine since I've been on it for the past 6 years. I also have meniere disease which was diagnosed about 5 years ago. My question is do you think this numbness and pins and needles sensations are from the accident?flu shot after affects? or something else?
In December I reported to my doctor that my neck hurt and I also had my first migraine headache shortly before. That same week. He sent me for an MRI which came back normal, I suppose because I never heard from my doctor. A week after my hurt neck I got into a car accident and got whiplash. The day before that I got a flu shot. The following day and night I experienced pins and needles sensation all over my body and it would come and go. At night time it worse for the next 2 months. I would wake up feeling like one side of my body was half a sleep and would shake my arm or leg to wake it up. It would happen almost every night. An arm or a leg. Left arm, right leg. All different places and different sides of my body. Also during this 2 months time I was slipping off my shirt and I felt a pull through both of my arms and a very intense hot kinda like pins and needles painn that went all the way up to my middle fingers. The were numb and prickly for about a week after. Right now it is February. I have my good nights and my bad nights. I still feel sometimes numbness and weakness in certain parts of my body. I do take Vasotec for blood pressure. My blood pressure has been fine since I've been on it for the past 6 years. I also have meniere disease which was diagnosed about 5 years ago. My question is do you think this numbness and pins and needles sensations are from the accident?flu shot after affects? or something else?
I noticed that you said that the EMG ruled out demyelination. I thought that EMG only tested peripheral nervous system and couldn't rule out demyelination such as MS. Am I wrong? Thanks.
Dear Sandra:
PN is a peripheral neuropathy and not a central disorder. The EMG is used to detect peripheral disorders of nerves and muscle. MS is a central disorder of demyelination and does not affect the periperal nervous system myelination. An EMG would show an upper motor neuron disease of unclear origin.
I hope this helps.
CCF Neuro MD
PN is a peripheral neuropathy and not a central disorder. The EMG is used to detect peripheral disorders of nerves and muscle. MS is a central disorder of demyelination and does not affect the periperal nervous system myelination. An EMG would show an upper motor neuron disease of unclear origin.
I hope this helps.
CCF Neuro MD
Have you ever heard of Grover's disease ever being associated with neuropathy and MG?
Thank you
Thank you
Dear WJB:
Low levels of vitamin B12 can cause a neuropathy. Your level was in the low range and this is one of the likely explanations for your problems. Certainly damage to the spinal column at C6 and C7 can cause a lower extremity problem, but usually it is spasticity (tight muscles) and the new onset R sided arm problems should not have been okay for awhile and then flaired. The EMG being normal is comforting that axonal loss or demyelination has occured. I think the logical explanation is the vitamin B12.
Sincerely,
CCF Neuro MD
Low levels of vitamin B12 can cause a neuropathy. Your level was in the low range and this is one of the likely explanations for your problems. Certainly damage to the spinal column at C6 and C7 can cause a lower extremity problem, but usually it is spasticity (tight muscles) and the new onset R sided arm problems should not have been okay for awhile and then flaired. The EMG being normal is comforting that axonal loss or demyelination has occured. I think the logical explanation is the vitamin B12.
Sincerely,
CCF Neuro MD
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