|Year : 2014 | Volume
| Issue : 2 | Page : 87-89
Corpus callosal infarction due to disseminated cysticercosis
Sampath Sai1, Anil Kumar Tatikonda1, Ravikiran Padala1, Umamaheswara Reddy Venati2, Amit Agrawal3
1 Department of Neurology, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
2 Department of Radiology, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
3 Department of Neurosurgery, Narayana Medical College Hospital, Nellore, Andhra Pradesh, India
|Date of Web Publication||29-Dec-2014|
Department of Neurosurgery, Narayana Medical College Hospital, Chinthareddypalem, Nellore - 524 003, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Disseminated cysticercosis (DCC) is the widespread dissemination of cysticercus cellulosae (larva of pork tapeworm). CNS complications of DCC include encephalitis, obstructive hydrocephalus, raised intracranial pressure, ischemic infarctions, hemorrhage, and rarely subarachnoid hemorrhage. Here, we report a case of young male who developed corpus callosal infarction following cysticercal angitis.
Keywords: Arteritis, disseminated cysticercosis, neurocysticercosis
|How to cite this article:|
Sai S, Tatikonda AK, Padala R, Venati UR, Agrawal A. Corpus callosal infarction due to disseminated cysticercosis. Int J Adv Med Health Res 2014;1:87-9
| Introduction|| |
Disseminated cysticercosis (DCC) is the widespread dissemination of cysticercus cellulosae (larva of pork tapeworm) with brain, lungs, muscles, subcutaneous tissues, thyroid, pancreas, and eyeball being the commonly involved sites of this helminthic larval infestation. ,,,, Characteristic features of DCC include seizures, cognitive impairment, pseudo-hypertrophied muscles giving Herculean appearance, subcutaneous palpable nodules, and inguinal lymphadenopathy. ,,,, Another hallmark is relative absence of focal neurological signs until late stage of disease. Approximately 50 cases of DCC were reported worldwide and the majority of them were from India. CNS complications of DCC include encephalitis, obstructive hydrocephalus, raised intracranial pressure, ischemic infarctions, hemorrhage, and rarely subarachnoid hemorrhage. ,,, Here, we report a case of DCC which presented to us with seizures and ischemic infarction of the corpus callosum.
| Case report|| |
A 40-year-old male patient was brought to the emergency department in altered sensorium state as he was found unconscious on bed with frothing from mouth. He had no preceding history of fever, headache, vomiting, or trauma. Patient was a chronic smoker, alcoholic, and pork eater. He had no past and family history of convulsions. Examination gave the following findings: pulse: 64/min, BP: 160/100 mmHg, respiratory rate (RR) 18/min, and SPO2: 96% at room air. Patient was drowsy, but arousable with ill-sustained attention, and was obeying commands occasionally; E3 M6 V4 and lateral tongue bite was noted. Extraocular movements were full; bilateraly pupil was normal sized reacting to light; fundus was normal. There was no facial palsy and he was moving all limbs equally. Tone was normal; deep tendon reflexes were brisk in the both upper and lower limbs; bilateral plantars reflex was flexor; there were no meningeal signs and no subcutaneous nodules. On systemic examination, no abnormality was detected. Investigations such as hemogram, random blood sugar, and renal function tests and liver function tests were normal. Retroviral tests were negative; X-ray chest, thigh, and both lower limbs showed soft tissue rice grain calcifications [Figure 1] and [Figure 2]. MRI brain imaging revealed acute infarcts in genu, body, and splenium of corpus callosum, and cystic lesions with scolex in the left external capsule, left parieto-occipital, and right frontal areas [Figure 3]. Diffusion-weighted images showed areas' restriction [Figure 4]. CSF examination revealed lymphocytic pleocytosis with protein and sugar within normal limits, and serum anticysticercal antibody was negative. Patient was treated with antiepileptic drugs, steroids, albendazole, and other supportive measures and got discharged without any sequelae.
|Figure 1: Plain radiograph of chest and abdomen showing radiopaque lesions in the muscles and subcutaneous tissues giving rice grain appearance|
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|Figure 2: Plain radiograph of both thighs, anteroposterior and lateral views, showing linear calcifi ed lesions giving typical rice grain appearance|
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|Figure 3: MRI fluid-attenuated inversion recovery sequence showing cystic lesions in the left frontal and parieto-occipital regions with visible scolices|
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|Figure 4: MRI diffusion-weighted sequence and corresponding ADC showing diffusion restriction areas seen in genu, body, and splenium of corpus callosum suggestive of infarcts|
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| Discussion|| |
Cysticercus larva disseminates from the gastrointestinal tract via portal system into the blood stream and these eggs then migrate to various organs and form cysts. , Clinical presentation depends upon the size, location, number of cysts, and host immunity.  Cerebrovascular complications (hemorrhage, infarction, subarachnoid hemorrhage) following neurocysticercosis infection are rare and are usually caused by inflammation of arteries at the base of the brain secondary to chronic cysticercotic arachnoiditis. ,,, Incidence of cerebrovascular complications is higher with focal neurocysticercosis than the diffuse form. In majority of cases, small penetrating arteries are involved leading to lacunar infarction. However, large infarcts related to the occlusion of the middle cerebral or internal carotid artery can also occur.  MRI is extremely useful in diagnosing cysticercal cerebrovascular complications. Prognosis is usually better for focal form of neurocysticercosis than the diffuse form.  Management of DCC includes antiepileptics, steroids, and antiparasitic treatment. Surgical removal of the cysts and ventriculoperitoneal shunting are performed in cases where the cysts are causing obstructive hydrocephalus and raised intracranial tension (ICT) features. Medical management consists of cysticidal drugs praziquantel (50 mg/kg/day for 6-21 days) and albendazole (15 mg/kg/day for 30 days), which cause the death of the cysts. Medical treatment may be associated with severe anaphylactic reactions. Before starting the cysticidal drug, priming with corticosteroids reduces the incidence of such complications. Steroids also play an important role in treating cysticercal angitis. , There is no role of antiparasitic drugs in calcified cysts as the parasite is dead. ,
| Conclusion|| |
Clinical presentation of DCC depends upon severity of the organ affected, host immune reaction, and the size, shape, and number of disseminated parasites. Cerebrovascular complications are rare in disseminated form as compared to the focal form, and are the result of chronic arachnoiditis and cysticercal angitis. As far as our knowledge is concerned, this is the first report of a case having corpus callosal infarction following cysticercal angitis. Diagnosis of neurocysticerosis/DCC should be considered in young patients from endemic regions. Prognosis is bad for the diffuse form of neurocysticercosis as compared to the focal form.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]