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|NI FEATURE: FACING ADVERSITY…TOMORROW IS ANOTHER DAY! - LETTER TO EDITOR
|Year : 2017 | Volume
| Issue : 1 | Page : 167-169
Proximal ulnar artery thrombosis after cysticidal therapy: A rare complication of neurocysticercosis
Rudrarpan Chatterjee1, Krishnarpan Chatterjee2, Chetana Sen3
1 Department of General Medicine, Grant Medical College, Mumbai, India
2 Department of General Medicine, ESI-PGIMSR, Kolkata, India
3 Department of Neurology, Medical college and Hospital, Kolkata, India
|Date of Web Publication||12-Jan-2017|
ESI-PGIMSR, B-7/11, Diamond Park, Diamond Harbour Road, Joka, Kolkata - 700 104
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Chatterjee R, Chatterjee K, Sen C. Proximal ulnar artery thrombosis after cysticidal therapy: A rare complication of neurocysticercosis. Neurol India 2017;65:167-9
|How to cite this URL:|
Chatterjee R, Chatterjee K, Sen C. Proximal ulnar artery thrombosis after cysticidal therapy: A rare complication of neurocysticercosis. Neurol India [serial online] 2017 [cited 2017 Mar 24];65:167-9. Available from: http://www.neurologyindia.com/text.asp?2017/65/1/167/198199
Neurocysticercosis is the most common helminthic infection involving the human central nervous system. Humans can be the definitive or intermediate host for the pork tapeworm Taenia solium. Neurocysticercosis develops in humans by the encysted larval form “cysticercus cellulosae” of T. solium (acting as the intermediate host). The burden of the disease is not known precisely in our country. Estimates of prevalence have ranged from 2% to 3.8% in the general population in different studies from different endemic countries., Seizures are one of the most common clinical manifestations. The diagnosis of neurocysticercosis is currently based on neuroimaging, clinical, serological, and epidemiological criteria., At present, there are no standardized treatment guidelines for neurocysticercosis. Anti-helminthic treatment with anti-inflammatory drugs to reduce the prolonged inflammatory changes due to the degeneration of the cysts is usually prescribed. Albendazole, with better penetration into the central nervous system, is the usual drug of choice and is preferred to praziquantel in this regard. Concomitant antiepileptic therapy is indicated. Reported complications of cysticidal therapy are predominantly neurological. Arterial thrombosis complicating cysticidal therapy has not been previously reported.
A 15-year-old male patient, a resident of New Delhi, was brought to the emergency room with the first episode of generalized tonic clonic convulsions. On examination, he had postictal confusion. General examination was within normal limits. There were no palpable subcutaneous nodules. There was no demonstrable neurological deficit present. A loading dose of phenytoin was given. Noncontrast CT scan of the brain revealed a single, ill-defined, hypoechoic lesion in the left parietal region with perilesional edema and an ectopic focus of calcification, suggestive of neurocysticercosis and demonstrating the scolex [Figure 1]. On further evaluation, there was no evidence of cysticerci in the retina on fundoscopy or on screening of the spine with magnetic resonance imaging. No calcifications were noted on X-ray examination of the thigh. Serology for human immunodeficiency virus was negative. His seizures were controlled with phenytoin. He was started on anti-helminthic therapy with albendazole in recommended doses along with steroid cover in the form of oral prednisolone. On the second day of the cysticidal therapy, the patient developed tingling and numbness of the medial aspect of the left forearm. On examination, the left arm ulnar artery pulsations were found to be absent. Radial and brachial pulses were normal. There were no signs of tissue loss. A ultrasonographic arterial and venous Doppler was done for the left upper limb, which was suggestive of thrombus in the proximal ulnar artery [Figure 2] along with multiple hypoechoic and calcified lesions in the flexor compartment of the forearm likely representing cysticerci [Figure 3]. Cysticidal therapy was withheld and the patient was started on low molecular weight heparin along with increased dosage of oral steroids. Vascular surgery opinion was taken and conservative management continued. The patient improved symptomatically in 2 days. A follow up scan was carried out after 1 week and showed resolution of thrombosis. The patient was shifted to oral anticoagulation with warfarin, which was continued for 3 months. At follow up, he was asymptomatic on anti-epileptics and a tapering dose of steroids. Further cysticidal therapy was not pursued.
|Figure 1: Non-contrast CT head showing a hypodensity with eccentric calcification (scolex) and perilesional edema|
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|Figure 2: USG Doppler showing thrombus in the left proximal ulnar artery with absence of blood flow|
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|Figure 3: USG showing a hypoechoic lesion with calcification in the proximal compartment of forearm suggestive of cysticerci|
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Neurocysticercosis is endemic in India. The diagnosis of the disease is established using a set of absolute, major, minor, and epidemiological criteria, as proposed by Del Brutto et al., An adaptation of the same for the Indian setting was proposed by Garg  in 2004 and included reservations regarding the diagnosis in the presence of immunosuppression and tuberculosis of the central nervous system.
Seizures are the most common clinical manifestations of the disease. However, focal neurological deficits and manifestations of raised intracranial tension are not uncommon., With recent advances in neuroimaging, the diagnosis today rests mainly on radiological findings. On the basis of radiological findings, neurocysticercosis is classified into five stages, namely, noncystic, vesicular, colloidal vesicular, granular nodular, and calcified nodular, with the definitive demonstration of scolex in the colloidal vesicular stage.
Treatment of neurocysticercosis relies mainly on relief of symptoms with antiepileptic therapy. Anti-inflammatory drugs in the form of steroids are frequently used and have a role in the presence of severe clinical disease or as concomitant therapy with anti-parasitic agents. Anti-parasitic agents are indicated only in the active disease after the patient has been stabilized symptomatically. In this regard, albendazole is preferred over praziquantel in view of its better central nervous system penetration.
Cysticidal therapy in conjunction with steroids has reported lower rates of complications. However, depending on the location of the cysts, a wide variety of complications may present during the course of treatment. Persistent seizures are common in intraparenchymal lesions of the central nervous system. Spinal cord lesions may present as arachnoiditis or as severe root pain as a result of edema in response to the release of antigens from the cyst walls. Extraparenchymal lesions have been known to present with a life-threatening rise in intra-cranial tension on initiating cysticidal therapy. Subretinal cysts have been known to cause blindness. Persistent debilitating headaches and psychiatric manifestations have also been reported.
In our case, cysticidal therapy with steroids was initiated in the hospital. The patient had complaints of tingling and numbness on the ulnar aspect of the arm. As an immediate evaluation was possible in the inpatient setting, ulnar artery thrombosis was diagnosed. Anticoagulation treatment was started promptly leading to a good outcome in the patient. The fact that the ulnar artery is not an end artery, was a favorable factor, as its transient thrombosis did not lead to a permanent ischemic sequel. Only one case of right common femoral vein thrombosis in response to cysticidal therapy in a patient suffering from disseminated cysticercosis has been reported previously. Arterial thrombosis in response to cysticidal therapy has not been reported in literature.
Cysticidal therapy is often initiated on an outpatient basis once the diagnosis is established. The risk-to-benefit ratio of cysticidal therapy as opposed to symptomatic treatment must be evaluated in all cases before initiating therapy. The inherent risks involved in initiating this treatment must be explained to the patient. Patients must be encouraged to report any unusual symptoms during cysticidal therapy. Vascular complications require a high degree of clinical suspicion due to their rarity.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]