- Email: [email protected]
Subcutaneous and cerebral cysticercosis
Subcutaneous and cerebral cysticercosis Ana Maria Uthida-Tanaka, PhD,a Maria Carolina A. Sampaio, MD,a Paulo Eduardo Neves Ferreira Velho, PhD,a Benito P. Damasceno, PhD,b Maria Letı´cia Cintra, PhD,c Aparecida Machado de Moraes, PhD,a and Vero ˆ nica Zanardi, PhDd Campinas, Brazil Cysticercosis is a human infestation, which is considered the most common cause of seizures worldwide. The subcutaneous lesions can help in the diagnosis of neurocysticercosis. We describe a case of a 45-year-old patient with multiple cutaneous nodules first seen 2 years ago that were increasing in number, and normal neurologic and fundoscopic examination. Neurologic symptoms started 3 months before hospital admission as a mild headache and muscular weakness. The imaging examinations showed a massive central nervous system involvement. Physicians must be aware of the importance of subcutaneous nodule examination for the diagnosis of neurocysticercosis. (J Am Acad Dermatol 2004;50:S14-7.)
C
ysticercosis is the infestation of human beings by the larval stage of Taenia solium, the pork tapeworm. It is common in developing countries and is related to poor sanitary condition and hygiene.1 It may affect several organs, but its morbidity is related to the central nervous system (CNS) and ocular involvement. The subcutaneous cysticercosis is important as it can help in the diagnosis of neurocysticercosis, which is considered the most common cause of seizures worldwide.2-5 We report a case of an exuberant neurocysticercosis that was not detectable clinically, but could be diagnosed as a result of the skin manifestations.
CASE REPORT
Fig 1. Subcutaneous cysticercosis: papulonodular lesions observed in deltoideal region.
A 45-year-old man presented to the dermatology clinic with numerous nodules that had been noted for 2 years. The lesions were asymptomatic. The patient also reported having muscular weakness and headache for the past 3 months. He denied eating raw pork. Physical examination revealed multiple, firm, mobile, deepseated nodules, 1 to 2 cm, on the trunk, extremities, and face (Figs 1-3). Some lesions were clustered and some nodules on the arms were fixed to the underlying musculature. The overlying skin was normal. Neurologic and fundoscopic examination produced normal results. Histologic examination of an excised nodule showed a cyst containing fluid with a fully developed cysticercus (Fig 4). This supplement is made possible through an unrestricted educational grant from Stiefel Laboratories to the American Academy of Dermatology. From the Departments of Internal Medicine,a Neurology,b Pathological Anatomy,c and Radiology,d Medical School Sciences, State University of Campinas-FCM/Unicamp. Funding sources: None. Conflicts of interest: None identified. Reprint requests: Paulo Eduardo Neves Ferreira Velho, PhD, Department of Internal Medicine, Medical School Sciences, State University of Campinas-Unicamp, Cidade Universita´ria Zeferino Vaz, s/n, 13.081-970, Campinas SP, Brazil. E-mail: [email protected]. 0190-9622/$30.00 © 2004 by the American Academy of Dermatology, Inc. doi:10:1016/S0190-9622(03)00576-0
S14
Fig 2. Subcutaneous cysticercosis: papulonodular lesions observed in suprascapular region.
Microscopic examination of 3 stool samples revealed cysts of Blastocystis hominis and Endolimax nana, but neither ova nor proglottides of T solium was found. The white blood cell count was 5860 with 8.39% eosinophils. A head computed tomography (CT) scan showed scattered nonspace occupying cysticercal lesions in parenchyma and subarachnoid space. There were hypodense lesions, some with a ringlike enhancement and spotted calcifications. A magnetic resonance imaging scan showed cysts with an isointense point in T1 and T2 corresponding to the scolex (Figs 5 and 6). The patient
J AM ACAD DERMATOL VOLUME 50, NUMBER 2
Fig 3. Subcutaneous cysticercosis: papulonodular lesions observed in dorsal region.
Uthida-Tanaka et al S15
Fig 4. Typical section through Cysticercus: 2 bladder walls completely surround parenchymatous portion. Narrow band of host tissue forms fibrous capsule around organism. (Hematoxylin-eosin stain; original magnification ⫻100.)
was also submitted to a lumbar puncture and the study of the cerebrospinal fluid (CSF) showed 34 leukocytes, with 3% eosinophils, and a positive enzyme-linked immunosorbent assay for the detection of cysticercosis. A soft-tissue radiograph revealed elliptic calcifications in the thigh musculature. A diagnosis of disseminated cysticercosis was made on the basis of those findings. Dexamethasone was started with a daily dose of 16 mg 7 days before the initiation of albendazole. The patient received albendazole at a daily dose of 800 mg for 21 days. He experienced no adverse reactions. Most subcutaneous nodules disappeared after 6 months and the headache improved, but a hand tremor developed that was investigated and controlled with propranolol at a daily dose of 20 mg. Follow-up head CT scanning showed only calcifications and nonenhancing cysts.
DISCUSSION The pork tapeworm, T solium, can cause taeniasis, cysticercosis, or both. It is common in Latin America, Asia, Africa, and eastern Europe. Taeniasis is the infestation of the small intestine by the adult tapeworm. It is acquired when the human being ingests inadequately cooked pork containing larval cysts. The cysts release the scolex that attach to the mucosa of the small intestine and develop into the adult worm. The adult worm periodically discharges its eggs in feces, which may contaminate food and water. Cysticercosis is the human infestation caused by Cysticercus cellulosae, the larval stage of T solium. It occurs when the human being ingests eggs presented at fecally contaminated food or water, or through fecal-oral autoinfestation. Less commonly, the infection may be acquired by reverse peristalsis. Once in the small intestine, the eggs hatch, penetrate the mucosa, spread hematogeneously throughout the body, and encyst. Taenias are present in only 25% of patients with cysticercosis.6-8 As the adult
Fig 5. Coronal postgadolinium T1 image of brain showing multiple 0.2to 0.5-cm cysts in bilateral gray and white matter. They are isointense to cerebrospinal fluid with associated well-defined mural nodules corresponding to scolex. There is minimal enhancement and no significant mass effect.
worm can live in the intestine for many years, it is supposed that the autoinfestation is not common.9 The most frequent sites of cysticercosis are skeletal muscle, subcutaneous tissue, CNS, and ocular structures.1 Other reported sites are heart, lungs, peritoneum, kidney, liver, and pancreas. Its morbidity is related to the CNS and ocular involvement.10 CNS involvement, the most serious complication of cysticercosis, occurs in 60% to 96% of patients.9 The clinical manifesta-
S16 Uthida-Tanaka et al
Fig 6. Axial postgadolinium T1 image of brain showing multiple 0.2- to 0.5-cm cysts in bilateral gray and white matter. They are isointense to cerebrospinal fluid with associated well-defined mural nodules corresponding to scolex. There is minimal enhancement and no significant mass effect.
tion depends on the number of parasites, its anatomic location, and the host-immune response.1,11 The clinical onset occurs months to years after infestation and the most frequent manifestation is epilepsy.4 Other manifestations include raised intracranial pressure, obstructive hydrocephalus, headache, encephalitis, meningitis, focal neurologic deficits, and dementia. Neurocysticercosis is asymptomatic in 50% of patients and represents the main cause of epilepsy worldwide.3,5,8 Seizures are more often focal than generalized.1,9,11 Neurologic symptoms in our patient were absent, except for headache and muscular weakness. CT scanning is important in the diagnosis of neurocysticercosis and has been used for classification on the basis of the presence of calcified lesions and enhancing or nonenhancing cysts. Magnetic resonance imaging is indicated when CT scanning is inconclusive, because it has advantages such as better visualization of parenchymal lesions and identification of developmental stages of the larval cysts.11,12 However, small calcifications are frequently not detected. Immunologic diagnosis to detect Cysticercus antibodies in both serum and CSF has also been used. The enzyme-linked immunoelectrotransfer blot assay is the best for the diagnosis of cysticercosis. It has shown better sensitivity and specificity than enzyme-linked immunosorbent assay as demonstrated in a recent study: 94% versus 65% and 100% versus 63%, respectively, when tested in serum. Moreover, antibodies have been found in serum more often than in CSF. Sensitivity in CSF was 86% by enzyme-linked immunoelectrotransfer blot.13 The ocular cysticercosis occurs in 3% to 7% of patients and its diagnosis is made on the basis of fundoscopic examination.5,11 The cysticerci may be located at subretinal space, vitreous, and conjuntiva. Common manifestations include severe pain, and blurring or loss of vision. In ocular cysticercosis, anticysticercal drugs should be avoided and operation is indicated to remove the cysts.4,6,11 Muscular cysticercosis is often associated with neurocysticercosis. Most cases are asymptomatic, but an evident acute myositis can occur.8,11 The soft-tissue radiograph shows eliptic calcifications that are seen 5 years after infestation.8 The subcutaneous cysticercosis occurs months to decades
J AM ACAD DERMATOL FEBRUARY 2004
after the initial infestation. It is characterized by multiple, mobile, firm, subcutaneous nodules, a few millimeters to several centimeters in size (average: 1-2 cm), with normal overlying skin. The number of nodules varies from a few to more than 1000. They are usually asymptomatic, but can be painful in up to 20% of cases.2,7 The trunk is twice more affected than the face.3,14 Diagnosis is made by an excisional biopsy specimen of a nodule that will show the cysticercus. Subcutaneous involvement can occur in about 54% of cases and can be used as a marker of neurocysticercosis in such cases.4,7,15 The differential diagnosis includes lipomas, epidermoid cysts, neurofibromas, and ganglia. The treatment with anticysticercal drugs–albendazole or praziquantel–is indicated when there are active cysticerci in brain parenchyma.11,16,17 It should be started early to avoid the natural course to calcification. However, long-term prognosis of neurocysticercosis is not satisfactory.16 To date there are no sufficient data to determine the real benefit of cysticidal therapy to patients with neurocysticercosis. A great number of patients remain with seizures and headaches, and some have new seizures develop after treatment.18-20 Albendazole is more effective than praziquantel.16,17 A recent study showed that albendazole caused a reduction in the number of cysts in 85% of patients versus 60% with praziquantel.16 Moreover, albendazole can be administered for only 8 days (15 mg/kg/d), increasing the compliance, although it can be extended up to 30 days.1,7,16 By contrast, praziquantel should be administered for 15 days (50 mg/kg/d) as a shorter course decreases its efficiency.17 Some authors recommend simultaneous use of dexamethasone and anticysticercal drugs to prevent adverse reactions that, however, are usually mild and transient.1,16,21,22 Other authors recommend simultaneous use of dexamethasone only in patients harboring several cysts.17 Surgical treatment is required in most cases of spinal cysticercosis, presence of intraventricular cysts, and to relieve intracranial pressure in obstructive hydrocephalus.1,2,11 Our patient received dexamethasone before albendazole, and no adverse reactions were seen. Most subcutaneous nodules disappeared, and nonenhancing cysts were demonstrated on CT scaning. The anticysticercal drugs can also be used in the treatment of subcutaneous cysticercosis, although it is unnecessary in asymptomatic forms. It has been observed that most of the nodules disappear months after treatment. If only few nodules are present, they are best treated surgically.2 Nonetheless, the best measure is to prevent infestation by means of education about personal hygiene, improvement of public sanitation, and meat inspection.1,5 Vaccination of pigs at risk of infection is another strategy that has been studied.23 Physicians also must be aware of the importance of subcutaneous nodule examination for the diagnosis of neurocysticercosis, which may be asymptomatic for a long time.9 The case reported here presents massive CNS involvement, without symptoms, except muscular weakness and headache for the last 3 months. REFERENCES 1. Veronese R, Franc¸a Netto AS, Focaccia R. Cisticercose. In: Veronesi R, Focaccia R, Dietze R, editors. Doenc¸as infecciosas e Parasita´rias. Rio de Janeiro: Guanabara Koogan; 1991. p. 820-6. 2. Wortman P. Subcutaneous cysticercosis. J Am Acad Dermatol 1991;25: 409-14. 3. Falanga V, Kapoor W. Cerebral cysticercosis: diagnostic value of subcutaneous nodules. J Am Acad Dermatol 1985;12:304-7. 4. King DT, Gilbert DJ, Guievitch AW, Mok MW, Hirese FM. Subcutaneous cysticercosis [letter]. Arch Dermatol 1979;115:236.
J AM ACAD DERMATOL VOLUME 50, NUMBER 2 5. Grisolia JS, Wiederholt WC. Central nervous system cysticercosis. Arch Neurol 1982;39:540-4. 6. Manson-Bahr PEC, Wilcocks C. Cestode infections: taeniasis. In: Manson-Bahr PEC, Wilcocks C, editors. Manso’s tropical diseases. London: Barlliere Tindall; 1972. p. 337-41. 7. Jordan HF, Schneider JW, Cilliers J. Cerebral and subcutaneous cysticercosis treated with albendazole. Int J Dermatol 1995;34:574-9. 8. Yamashita P, Kelsey J, Hendeerson SO. Subcutaneous cysticercosis [clinical communications]. J Emerg Med 1998;16:583-6. 9. McCornick GF, Zee CS, Heiden J. Cysticercosis cerebri–review of 127 cases. Arch Neurol 1982;39:534-9. 10. Jones TC. Cestodes (tapeworms). In: Mandell GL, Douglas RG Jr, Bennet JE, editors. Principles and practice of infectious diseases. New York: Churchill Livinstone Inc; 1999. p. 2183-5. 11. Botero D, Tanowitz HB, Weiss LM, Wittner M. Parasitic diseases: taeniasis and cysticercosis. In: Maguire JH, Keystone JS, editors. Infectious disease clinics of North America. Philadelphia: WB Saunders; 1993. p. 683-97. 12. Jena A, Sanchetee PC, Gupta RK, Khushu S, Chandra R, Lakshmipathi N. Cysticercosis of the brain shown by magnetic resonance imaging. Clin Radiol 1988;39:542-6. 13. Diaz JF, Verastegui M, Gilman RH, Tsang VC, Pilcher JB, Gallo C, et al. Immunodiagnosis of human cysticercosis (Taenia solium): a field comparison of an antibody-enzyme-linked immunosorbent assay (ELISA), an antigen-ELISA, and an enzyme-linked immunoelectrotransfer blot (EITB) assay in Peru. Am J Trop Med Hyg 1992;46:610-5.
Uthida-Tanaka et al S17 14. Tschen E, Tschen EA, Smith EB. Cutaneous cysticercosis treated with metrifonate. Arch Dermatol 1981;117:507-9. 15. Dixon HBF, Lipscomb FM. Cysticercosis: an analysis and follow up of 450 cases. Med Res Spec Rep (Lond) 1961;299:1-58. 16. Takanagui OM, Jardim E. Therapy for neurocysticercosis: comparison between albendazole and praziquantel. Arch Neurol 1992;49:290-4. 17. Sotelo J, Brutto OH, Penagos P, Escobeto F, Torres B, Rodriguez-Carbajal L, et al. Comparison of therapeutic regimen of anticysticercal drugs of parenchymal brain cysticercosis. J Neurol 1990;237:69-72. 18. Kim SK, Wang KC, Paek SH, Hong KS, Cho BK. Outcomes of medical treatment of neurocysticercosis: a study of cases in Cheju Island, Korea. Surg Neurol 1999;52:563-9. 19. Salinas R, Counsell C, Prasad K, Gelband H, Garner P. Treating neurocysticercosis medically: a systematic review of randomized, controlled trials. Trop Med Int Health 1999;4:713-8. 20. Moodley M, Moosa A. Treatment of neurocysticercosis: is praziquantel the new hope? Lancet 1989;4:262-3. 21. Alarcon F, Perez Y, Banda H. Praziquantel and dexamethasone [letter]. Neurology 1988;38:997-9. 22. Robles C, Sedano AM, Vargas-Tentori N, Galindo-Virgen S. Long-term results of praziquantel therapy in neurocysticercosis. J Neurosurg 1987; 66:359-63. 23. Lightowlers MW. Erradication of Taenia solium cysticercosis: a role for vaccination of pigs. Int J Parasitol 1992;29:811-7.
C
ysticercosis is the infestation of human beings by the larval stage of Taenia solium, the pork tapeworm. It is common in developing countries and is related to poor sanitary condition and hygiene.1 It may affect several organs, but its morbidity is related to the central nervous system (CNS) and ocular involvement. The subcutaneous cysticercosis is important as it can help in the diagnosis of neurocysticercosis, which is considered the most common cause of seizures worldwide.2-5 We report a case of an exuberant neurocysticercosis that was not detectable clinically, but could be diagnosed as a result of the skin manifestations.
CASE REPORT
Fig 1. Subcutaneous cysticercosis: papulonodular lesions observed in deltoideal region.
A 45-year-old man presented to the dermatology clinic with numerous nodules that had been noted for 2 years. The lesions were asymptomatic. The patient also reported having muscular weakness and headache for the past 3 months. He denied eating raw pork. Physical examination revealed multiple, firm, mobile, deepseated nodules, 1 to 2 cm, on the trunk, extremities, and face (Figs 1-3). Some lesions were clustered and some nodules on the arms were fixed to the underlying musculature. The overlying skin was normal. Neurologic and fundoscopic examination produced normal results. Histologic examination of an excised nodule showed a cyst containing fluid with a fully developed cysticercus (Fig 4). This supplement is made possible through an unrestricted educational grant from Stiefel Laboratories to the American Academy of Dermatology. From the Departments of Internal Medicine,a Neurology,b Pathological Anatomy,c and Radiology,d Medical School Sciences, State University of Campinas-FCM/Unicamp. Funding sources: None. Conflicts of interest: None identified. Reprint requests: Paulo Eduardo Neves Ferreira Velho, PhD, Department of Internal Medicine, Medical School Sciences, State University of Campinas-Unicamp, Cidade Universita´ria Zeferino Vaz, s/n, 13.081-970, Campinas SP, Brazil. E-mail: [email protected]. 0190-9622/$30.00 © 2004 by the American Academy of Dermatology, Inc. doi:10:1016/S0190-9622(03)00576-0
S14
Fig 2. Subcutaneous cysticercosis: papulonodular lesions observed in suprascapular region.
Microscopic examination of 3 stool samples revealed cysts of Blastocystis hominis and Endolimax nana, but neither ova nor proglottides of T solium was found. The white blood cell count was 5860 with 8.39% eosinophils. A head computed tomography (CT) scan showed scattered nonspace occupying cysticercal lesions in parenchyma and subarachnoid space. There were hypodense lesions, some with a ringlike enhancement and spotted calcifications. A magnetic resonance imaging scan showed cysts with an isointense point in T1 and T2 corresponding to the scolex (Figs 5 and 6). The patient
J AM ACAD DERMATOL VOLUME 50, NUMBER 2
Fig 3. Subcutaneous cysticercosis: papulonodular lesions observed in dorsal region.
Uthida-Tanaka et al S15
Fig 4. Typical section through Cysticercus: 2 bladder walls completely surround parenchymatous portion. Narrow band of host tissue forms fibrous capsule around organism. (Hematoxylin-eosin stain; original magnification ⫻100.)
was also submitted to a lumbar puncture and the study of the cerebrospinal fluid (CSF) showed 34 leukocytes, with 3% eosinophils, and a positive enzyme-linked immunosorbent assay for the detection of cysticercosis. A soft-tissue radiograph revealed elliptic calcifications in the thigh musculature. A diagnosis of disseminated cysticercosis was made on the basis of those findings. Dexamethasone was started with a daily dose of 16 mg 7 days before the initiation of albendazole. The patient received albendazole at a daily dose of 800 mg for 21 days. He experienced no adverse reactions. Most subcutaneous nodules disappeared after 6 months and the headache improved, but a hand tremor developed that was investigated and controlled with propranolol at a daily dose of 20 mg. Follow-up head CT scanning showed only calcifications and nonenhancing cysts.
DISCUSSION The pork tapeworm, T solium, can cause taeniasis, cysticercosis, or both. It is common in Latin America, Asia, Africa, and eastern Europe. Taeniasis is the infestation of the small intestine by the adult tapeworm. It is acquired when the human being ingests inadequately cooked pork containing larval cysts. The cysts release the scolex that attach to the mucosa of the small intestine and develop into the adult worm. The adult worm periodically discharges its eggs in feces, which may contaminate food and water. Cysticercosis is the human infestation caused by Cysticercus cellulosae, the larval stage of T solium. It occurs when the human being ingests eggs presented at fecally contaminated food or water, or through fecal-oral autoinfestation. Less commonly, the infection may be acquired by reverse peristalsis. Once in the small intestine, the eggs hatch, penetrate the mucosa, spread hematogeneously throughout the body, and encyst. Taenias are present in only 25% of patients with cysticercosis.6-8 As the adult
Fig 5. Coronal postgadolinium T1 image of brain showing multiple 0.2to 0.5-cm cysts in bilateral gray and white matter. They are isointense to cerebrospinal fluid with associated well-defined mural nodules corresponding to scolex. There is minimal enhancement and no significant mass effect.
worm can live in the intestine for many years, it is supposed that the autoinfestation is not common.9 The most frequent sites of cysticercosis are skeletal muscle, subcutaneous tissue, CNS, and ocular structures.1 Other reported sites are heart, lungs, peritoneum, kidney, liver, and pancreas. Its morbidity is related to the CNS and ocular involvement.10 CNS involvement, the most serious complication of cysticercosis, occurs in 60% to 96% of patients.9 The clinical manifesta-
S16 Uthida-Tanaka et al
Fig 6. Axial postgadolinium T1 image of brain showing multiple 0.2- to 0.5-cm cysts in bilateral gray and white matter. They are isointense to cerebrospinal fluid with associated well-defined mural nodules corresponding to scolex. There is minimal enhancement and no significant mass effect.
tion depends on the number of parasites, its anatomic location, and the host-immune response.1,11 The clinical onset occurs months to years after infestation and the most frequent manifestation is epilepsy.4 Other manifestations include raised intracranial pressure, obstructive hydrocephalus, headache, encephalitis, meningitis, focal neurologic deficits, and dementia. Neurocysticercosis is asymptomatic in 50% of patients and represents the main cause of epilepsy worldwide.3,5,8 Seizures are more often focal than generalized.1,9,11 Neurologic symptoms in our patient were absent, except for headache and muscular weakness. CT scanning is important in the diagnosis of neurocysticercosis and has been used for classification on the basis of the presence of calcified lesions and enhancing or nonenhancing cysts. Magnetic resonance imaging is indicated when CT scanning is inconclusive, because it has advantages such as better visualization of parenchymal lesions and identification of developmental stages of the larval cysts.11,12 However, small calcifications are frequently not detected. Immunologic diagnosis to detect Cysticercus antibodies in both serum and CSF has also been used. The enzyme-linked immunoelectrotransfer blot assay is the best for the diagnosis of cysticercosis. It has shown better sensitivity and specificity than enzyme-linked immunosorbent assay as demonstrated in a recent study: 94% versus 65% and 100% versus 63%, respectively, when tested in serum. Moreover, antibodies have been found in serum more often than in CSF. Sensitivity in CSF was 86% by enzyme-linked immunoelectrotransfer blot.13 The ocular cysticercosis occurs in 3% to 7% of patients and its diagnosis is made on the basis of fundoscopic examination.5,11 The cysticerci may be located at subretinal space, vitreous, and conjuntiva. Common manifestations include severe pain, and blurring or loss of vision. In ocular cysticercosis, anticysticercal drugs should be avoided and operation is indicated to remove the cysts.4,6,11 Muscular cysticercosis is often associated with neurocysticercosis. Most cases are asymptomatic, but an evident acute myositis can occur.8,11 The soft-tissue radiograph shows eliptic calcifications that are seen 5 years after infestation.8 The subcutaneous cysticercosis occurs months to decades
J AM ACAD DERMATOL FEBRUARY 2004
after the initial infestation. It is characterized by multiple, mobile, firm, subcutaneous nodules, a few millimeters to several centimeters in size (average: 1-2 cm), with normal overlying skin. The number of nodules varies from a few to more than 1000. They are usually asymptomatic, but can be painful in up to 20% of cases.2,7 The trunk is twice more affected than the face.3,14 Diagnosis is made by an excisional biopsy specimen of a nodule that will show the cysticercus. Subcutaneous involvement can occur in about 54% of cases and can be used as a marker of neurocysticercosis in such cases.4,7,15 The differential diagnosis includes lipomas, epidermoid cysts, neurofibromas, and ganglia. The treatment with anticysticercal drugs–albendazole or praziquantel–is indicated when there are active cysticerci in brain parenchyma.11,16,17 It should be started early to avoid the natural course to calcification. However, long-term prognosis of neurocysticercosis is not satisfactory.16 To date there are no sufficient data to determine the real benefit of cysticidal therapy to patients with neurocysticercosis. A great number of patients remain with seizures and headaches, and some have new seizures develop after treatment.18-20 Albendazole is more effective than praziquantel.16,17 A recent study showed that albendazole caused a reduction in the number of cysts in 85% of patients versus 60% with praziquantel.16 Moreover, albendazole can be administered for only 8 days (15 mg/kg/d), increasing the compliance, although it can be extended up to 30 days.1,7,16 By contrast, praziquantel should be administered for 15 days (50 mg/kg/d) as a shorter course decreases its efficiency.17 Some authors recommend simultaneous use of dexamethasone and anticysticercal drugs to prevent adverse reactions that, however, are usually mild and transient.1,16,21,22 Other authors recommend simultaneous use of dexamethasone only in patients harboring several cysts.17 Surgical treatment is required in most cases of spinal cysticercosis, presence of intraventricular cysts, and to relieve intracranial pressure in obstructive hydrocephalus.1,2,11 Our patient received dexamethasone before albendazole, and no adverse reactions were seen. Most subcutaneous nodules disappeared, and nonenhancing cysts were demonstrated on CT scaning. The anticysticercal drugs can also be used in the treatment of subcutaneous cysticercosis, although it is unnecessary in asymptomatic forms. It has been observed that most of the nodules disappear months after treatment. If only few nodules are present, they are best treated surgically.2 Nonetheless, the best measure is to prevent infestation by means of education about personal hygiene, improvement of public sanitation, and meat inspection.1,5 Vaccination of pigs at risk of infection is another strategy that has been studied.23 Physicians also must be aware of the importance of subcutaneous nodule examination for the diagnosis of neurocysticercosis, which may be asymptomatic for a long time.9 The case reported here presents massive CNS involvement, without symptoms, except muscular weakness and headache for the last 3 months. REFERENCES 1. Veronese R, Franc¸a Netto AS, Focaccia R. Cisticercose. In: Veronesi R, Focaccia R, Dietze R, editors. Doenc¸as infecciosas e Parasita´rias. Rio de Janeiro: Guanabara Koogan; 1991. p. 820-6. 2. Wortman P. Subcutaneous cysticercosis. J Am Acad Dermatol 1991;25: 409-14. 3. Falanga V, Kapoor W. Cerebral cysticercosis: diagnostic value of subcutaneous nodules. J Am Acad Dermatol 1985;12:304-7. 4. King DT, Gilbert DJ, Guievitch AW, Mok MW, Hirese FM. Subcutaneous cysticercosis [letter]. Arch Dermatol 1979;115:236.
J AM ACAD DERMATOL VOLUME 50, NUMBER 2 5. Grisolia JS, Wiederholt WC. Central nervous system cysticercosis. Arch Neurol 1982;39:540-4. 6. Manson-Bahr PEC, Wilcocks C. Cestode infections: taeniasis. In: Manson-Bahr PEC, Wilcocks C, editors. Manso’s tropical diseases. London: Barlliere Tindall; 1972. p. 337-41. 7. Jordan HF, Schneider JW, Cilliers J. Cerebral and subcutaneous cysticercosis treated with albendazole. Int J Dermatol 1995;34:574-9. 8. Yamashita P, Kelsey J, Hendeerson SO. Subcutaneous cysticercosis [clinical communications]. J Emerg Med 1998;16:583-6. 9. McCornick GF, Zee CS, Heiden J. Cysticercosis cerebri–review of 127 cases. Arch Neurol 1982;39:534-9. 10. Jones TC. Cestodes (tapeworms). In: Mandell GL, Douglas RG Jr, Bennet JE, editors. Principles and practice of infectious diseases. New York: Churchill Livinstone Inc; 1999. p. 2183-5. 11. Botero D, Tanowitz HB, Weiss LM, Wittner M. Parasitic diseases: taeniasis and cysticercosis. In: Maguire JH, Keystone JS, editors. Infectious disease clinics of North America. Philadelphia: WB Saunders; 1993. p. 683-97. 12. Jena A, Sanchetee PC, Gupta RK, Khushu S, Chandra R, Lakshmipathi N. Cysticercosis of the brain shown by magnetic resonance imaging. Clin Radiol 1988;39:542-6. 13. Diaz JF, Verastegui M, Gilman RH, Tsang VC, Pilcher JB, Gallo C, et al. Immunodiagnosis of human cysticercosis (Taenia solium): a field comparison of an antibody-enzyme-linked immunosorbent assay (ELISA), an antigen-ELISA, and an enzyme-linked immunoelectrotransfer blot (EITB) assay in Peru. Am J Trop Med Hyg 1992;46:610-5.
Uthida-Tanaka et al S17 14. Tschen E, Tschen EA, Smith EB. Cutaneous cysticercosis treated with metrifonate. Arch Dermatol 1981;117:507-9. 15. Dixon HBF, Lipscomb FM. Cysticercosis: an analysis and follow up of 450 cases. Med Res Spec Rep (Lond) 1961;299:1-58. 16. Takanagui OM, Jardim E. Therapy for neurocysticercosis: comparison between albendazole and praziquantel. Arch Neurol 1992;49:290-4. 17. Sotelo J, Brutto OH, Penagos P, Escobeto F, Torres B, Rodriguez-Carbajal L, et al. Comparison of therapeutic regimen of anticysticercal drugs of parenchymal brain cysticercosis. J Neurol 1990;237:69-72. 18. Kim SK, Wang KC, Paek SH, Hong KS, Cho BK. Outcomes of medical treatment of neurocysticercosis: a study of cases in Cheju Island, Korea. Surg Neurol 1999;52:563-9. 19. Salinas R, Counsell C, Prasad K, Gelband H, Garner P. Treating neurocysticercosis medically: a systematic review of randomized, controlled trials. Trop Med Int Health 1999;4:713-8. 20. Moodley M, Moosa A. Treatment of neurocysticercosis: is praziquantel the new hope? Lancet 1989;4:262-3. 21. Alarcon F, Perez Y, Banda H. Praziquantel and dexamethasone [letter]. Neurology 1988;38:997-9. 22. Robles C, Sedano AM, Vargas-Tentori N, Galindo-Virgen S. Long-term results of praziquantel therapy in neurocysticercosis. J Neurosurg 1987; 66:359-63. 23. Lightowlers MW. Erradication of Taenia solium cysticercosis: a role for vaccination of pigs. Int J Parasitol 1992;29:811-7.