Case Reports in Medicine 3 Figure 4: Axial postcontrast T1-weighted brain MRI shows a contrast-enhanced left-sided lesion in the periventricular white matter. Figure 5: Sagittal T2-weighted spinal MRI 2 months later shows complete resolution of the lesion. a 2-year-old child with Toxocara encephalomyelitis has been reported, pointing out the possible resemblance to acute disseminated encephalomyelitis [6]. The enzyme-linked immunosorbent assay (ELISA), that uses antigens secreted by the second-stage larvae, is the best indirect test for diagnosing infection. The ELISA has a reasonably high sensitivity of approximately 78% at a titer greater than 1 : 32 [2]. A disadvantage of this test is that anti-Toxocara antibodies measured by ELISA were found to persist for up to 2.8 years in infected adults so that the presence of these antibodies alone does not distinguish between current and past infections [1]. In northern industrialized countries, the seroprevalence of this infection is 5% in urban adults and up to 40% in children and rural farmers. In the West Indies and Bali, seroprevalence Figure 6: Axial T2-weighted brain MRI 2 months later shows complete resolution of the occipital lesion. rates approach 80% [1, 4]. Therefore, one should also take into account blood eosinophilia, which is considered to be a reliable indicator of active helminthiasis, serum IgE, and nonspeciﬁc tests such as erythrocyte sedimentation rate and C-reactive protein in case of VLM. Neurological syndromes with Toxocara infection of the central nervous system are generally nonspeciﬁc, and peripheral eosinophilia is often lacking. MRI can detect granulomas located cortically and subcortically, and these may appear as hyperintense foci on T2-weighted and proton density images. When associated with eosinophilia in the CSF, such images suggest a Toxocara infection. The presence of Toxocara larvae in cerebrospinal ﬂuid, in brain tissue or in the meninges, and/or a positive anti-Toxocara antibody titre in CSF, can conﬁrm the diagno- sis [1]. In cases of cerebral and spinal parenchymal lesions in combination with eosinophilia in blood and CSF, one should also consider neurocysticercosis, especially in endemic areas. Neurocysticercosis typically presents with epileptic seizures and one or multiple cystic brain lesions. Although very rare, cases of extramedullary and intramedullary spinal neurocysticercosis have been described [8, 9]. Acute VLM should be treated. Diﬀerent treatment regi- mens exist. Diethylcarbamazine (DEC), if available, is often considered the most eﬀective treatment [1, 4]. It is given in a dosage of 3 to 4 mg/kg body weight in 3 divided doses daily for 21 days. DEC should not be given together with corti- costeriods because of being antagonism of corticosteriods, which partially inhibit DEC’s mechanism of action. There- fore, DEC and corticosteriods must be given sequentially. The drug has been associated with a high rate (28%) of neu- rological side eﬀects (especially dizziness and headache) and (in 10%) a Mazzotti-like reaction (itching, urticaria, and/or oedema). Mebendazole (MBZ) is available in many countries and would appear to be a good alternative to DEC, for example, if the occurrence of major DEC-related side eﬀects is feared. Dosage is 20 to 25 mg/kg body weight (in a single dose) daily for 3 to 4 weeks. The drug is practically insoluble in water and should be taken with a fatty meal [1, 4].