{'fraction_non_alphanumeric': 0.03492786636294609, 'fraction_numerical': 0.02050113895216401, 'mean_word_length': 5.367149758454106, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Disseminated intracranial lesions of toxoplasmic encephalitis in a healthy elderly patient

A 75-year-old man was admitted for disturbance of consciousness. Three months earlier, he had been found to have cognitive dysfunction and gait disturbance. Magnetic resonance imaging of the brain showed disseminated hyperintense lesions in fluid-attenuated inversion recovery and diffusion weighted images, which were enhanced with gadolinium (Fig. 1a–e). Laboratory results showed a white blood cell count of 5200/lL (neutrophils 55.1%, lymphocytes 33.6% and monocytes 8.2%), and CD4 T cells of 943/lL. Cerebral spinal fluid was normal. He had no history of malignancy or HIV infection, and was not taking immunosuppressive medications. Immunoglobulin G and immunoglobulin M antibodies to Toxoplasma gondii measured by enzyme-linked immunosorbent assay were 42.0 IU/L and 1.0 IU/L respectively, suggesting acute toxoplasmosis, although polymerase chain reaction (PCR) analysis for T. gondii tested at day 8 after the administration of the medicine was negative. Treatment with trimethoprim/sulfamethoxazole was continued, and the patient showed significant improvement of the symptoms and the enhancing lesions diminished within 8 months (Fig. 1f–i). The positive response to antiprotozoal agents supported the diagnosis of