“…Either the patient developed LMND as a consequence of the infection with T. canis or neurotoxocariasis and LMND were causally unrelated and occurred coincidentally in a time-related manner. Arguments for a causal relation are that myelitis and polyradiculitis have been reported as manifestations of an infection with T. canis [2][3][4][5][6][7][8][9][10][11][12][13][14] , that there are human and animal studies indicating that larvae of T. canis also migrate to the spinal cord 9,15 , that antibodies against T. canis persisted in the CSF during clinical deterioration, and that neurotoxocariasis and neurotoxocariasis mimicking motor neuron disease -J. Finsterer et al LMND were time-related. Arguments against a causal relation are that serial MRIs did not show swelling, enhancing structures, or granuloma in the spinal cord or surrounding meningeas, that the patient did not develop upper motor neuron signs, as has been previously reported 10 ; that there was no eosinophilia, neither in the serum nor CSF, although acute myelitis could have passed already and LMND and antibodies against T. canis in the CSF may have been the only remains of the disease, and that albendazole did not resolve the clinical manifestations.…”