A 61-year-old woman presented to our department with a 3-week history of progressive bilateral weakness of her lower limbs. She had severe walking impairment with associated dizziness, headache, nausea, and vomiting. Although in good spirits, she reported anorexia, insomnia, and urinary and fecal incontinence, with a recent 5-kg weight loss. The patient denied a history of hypertensive disease, diabetes mellitus, and infectious diseases, such as hepatitis and tuberculosis. She also denied a history of respiratory symptoms such as fever, dyspnea, cough, and sputum. She had no food or drug allergies and no familial genetic disorders. She denied tobacco or alcohol use and had no history of surgery or trauma.
On the first admission, the patient's vital signs were stable, body temperature was normal (37.0 C), blood pressure was 153/92 mmHg, heart rate was 86 beats per minute, and the breath sounds and respiratory rate were normal. Her speech was initially fluent. Her pupils were equal in size, 3-mm diameter, and reacted appropriately to light. No apparent ocular muscle weakness was present, although she had horizontal nystagmus. There was no facial muscle weakness, and her tongue extension was centered. The muscle strength of both upper limbs was normal. Kernig's sign was negative.
At the presentation, the examination was notable for movement disorders having grade -1 muscle strength in both her lower limbs, with active tendon reflexes. The swelling was observed in her left lower limb. The Babinski and Chaddock reflexes were positive bilaterally. There was a profound sensory disturbance with hypoesthesia at the T6 level and below with reduced vibration sense. The bilateral finger-nose and rapidly alternating tests were normal when testing for cerebellar dysfunction, but she could not perform the bilateral heel-knee-shin test.
On the 2nd day after admission, the patient developed severe chest pain with intermittent nausea and vomiting, chest tightness, and dyspnea. After the blood test and imaging results were available, she was diagnosed with PE. During hospitalization, about 2 weeks after the admission, the patient developed a progressively worsening speech disturbance. The patient can understand others but is not fluent in her speech. Before discharge, that patient was in poor condition. She was indifferent to answering any questions. Her vital signs and other physical examinations were the same as her admission.
The patient tested arterial oxygen saturation at the time of the dyspnea and chest pain, indicating a partial oxygen pressure of 63 mmHg. The D-dimer blood level was elevated, 11.26 mug/ml (normal range: 0-1 mug/ml). The cerebrospinal fluid (CSF) was yellow with elevated pressure, >400 mmH2O. CSF examination showed elevated protein level 30.81 g/l (normal range: 0.15-0.45 g/l), but low levels of glucose, 1.6 mmol/l (normal range: 2.3-4.1 mmol/l), and chloride, 110 mmol/l (normal range: 119-129 mmol/l). Moreover, for the white cell count (WBC-BF: 34.00 x 106/l), 96.0% of the content comprised lymphocytes and 4.0% monocytes; however, the red blood cell count was 0/L.
Brain 3T MRI [ Figure 1A  (1-4)] showed lesions in the corpus callosum and the left lateral periventricular area. Combined with the MR spectroscopy results, the lesions were considered tumors. Spectroscopic metabolite analysis at the corpus callosum lesion showed a low N-acetyl aspartate peak and increased choline. Cervical-spine MRI [ Figure 1B  (1-2)] showed high-intensity signaling in the spinal cord at the C2-C7 vertebra levels and abnormal enhancement in the spinal cord at the C5-T4 vertebrae. Positron emission tomography-computed whole-body imaging showed limited hypermetabolic foci in the corpus callosum and diffused metabolic increases in the spinal cord cervicothoracic and lumbosacral regions, which were suggestive of malignancy. No hypermetabolic changes were observed in other organs, including the lungs. Ultrasound scanning of the lower extremities suggested the presence of thrombosis in the left common femoral vein and bilateral intermuscular veins (acute stage, complete type). A pulmonary computed tomography angiogram ( Figures 2A, B ) showed multiple bilateral pulmonary-artery embolisms.
Biopsy showed that the pathological diagnosis was grade IV glioblastoma with necrosis not otherwise specified. Immunohistochemistry staining ( Figure 3 ) results were CD20(-), CD3(-), CD79a (-), PAX-5(-), LCA (-), Ki-67(>40%), GFAP (+), Olig-2(+), ATRX (+), MAP2(+), P53(+30%), IDH1R132H mutation (-), MGMT (+30%), MBP (-), NeuN (-), Syn (+), vimentin (+), nestin (+), CD56(+), H3K27me3(+), and H3K27M mutation (+). According to the 2016 World Health Organization Classification of Tumors of the Central Nervous System, this case lacked molecular test results; there was insufficient evidence to classify this case as a distinct disease entity.
The biopsy tissues were obtained from the corpus callosum, and the lesions are shown in brain MRI (in  Figure 1 , lesions marked with arrows). The family and patient decided that palliative care was the best option for the brain and spinal cord gliomas because she felt severely unwell and had non-operable multicentric midline GBM lesions. The patient developed deep vein thrombosis (VTE) and PE during hospitalization. Therefore, she was administered rivaroxaban 15 mg orally twice daily for the first 3 weeks. After the follow-up, we learned that the patient gradually became unconscious at home, and his respiratory and cardiac functions gradually worsened. The patient died 42 days after hospital discharge. The time from symptom onset to death was approximately 3 months.