Cerebrospinal fluid B-cell activating factor levels as a novel biomarker in patients with neurosarcoidosis.

OBJECTIVES: Neurosarcoidosis (NS) is a severe complication of sarcoidosis. Patients with NS often have poor outcomes. To improve both the quality of life and prognosis in patients with NS, accurate and reliable methods for early diagnosis and determining the efficacy of treatment are needed. This study aims to investigate B-cell-activating factor of the tumor necrosis factor family (BAFF) in cerebrospinal fluid (CSF) and elucidate the relationship between CSF BAFF levels and various parameters of NS. METHODS: We studied 20 patients with NS and 14 control subjects. We measured CSF BAFF levels in all subjects and investigated the relationship with clinical findings, serum and CSF measures, and magnetic resonance imaging (MRI) findings. RESULTS: CSF BAFF levels were significantly increased in patients with NS compared with controls (median 0.089 vs 0.04 ng/mL, p = 0.0005). CSF BAFF values were correlated with CSF findings-cell count, protein, angiotensin-converting enzyme, lysozyme, soluble interleukin-2 receptor, and immunoglobulin G-but not with serum parameters. CSF BAFF levels were especially higher in patients with abnormal intraparenchymal lesions of the brain and abnormal spinal MRI findings. CSF BAFF levels decreased significantly after immunosuppressive therapy. CONCLUSION: CSF BAFF may aid the quantitative evaluation of NS and may serve as a biomarker for this disease.

Cerebrospinal Fluid Interleukin-6 in Immune Checkpoint Inhibitor-Induced Autoimmune Meningoencephalitis.

Immune checkpoint inhibitors (ICIs) have proven clinical benefits in various advanced cancers. However, despite their significant therapeutic efficacy, ICIs induce immune-related adverse events. Among these events, autoimmune meningoencephalitis often has severe effects on patients' outcomes, but its specific clinical features are still unclear. Here, we report two cases of ICI-associated meningoencephalitis with elevated interleukin-6 (IL-6) levels in the cerebrospinal fluid (CSF). A 47-year-old woman (Case 1) with renal cell carcinoma developed severe headache after a seventh nivolumab administration. A neurological examination revealed jolt accentuation signs and hyperreflexia in all extremities. CSF analysis revealed a high IL-6 value (6,620 pg/mL) with marked pleocytosis. A 70-year-old woman (Case 2) who received an initial administration of nivolumab plus ipilimumab for renal cell carcinoma developed alterations of consciousness. She presented with impaired consciousness, neck stiffness, and hyperreflexia in all extremities. CSF analysis demonstrated a high IL-6 value (49.3 pg/mL) with mild pleocytosis. Both patients were treated with steroid pulse therapy (methylprednisolone 1,000 mg/day, 3 days), followed by the administration of oral predonisolone. The symptoms and laboratory findings improved in both cases. CSF IL-6 values were proportional to the severity of meningoencephalitis and other clinical parameters. These findings may help elucidate the mechanisms of central nervous system complications that are caused by ICIs.

Novel Serum Biomarkers of Neurovascular Unit Associated with Cortical Amyloid Deposition.

BACKGROUND: Whether blood biomarkers of neurovascular unit are associated with cortical amyloid deposition on positron emission tomography (PET) imaging remains unclear. OBJECTIVE: To investigate the association between novel serum biomarkers of neurovascular unit, such as protein tyrosine phosphatase receptor type B (PTPRB), gap junction protein alpha-5 (GJA5), adenosine triphosphate-sensitive inward rectifier potassium channel-8 (KCNJ8), and von Willebrand factor (vWF), and cortical amyloid deposition. METHODS: Between 2012 and 2018, 68 elderly individuals with amnestic mild cognitive impairment (32 men and 36 women; mean age 75.2 years) were enrolled. All participants underwent 11C-Pittsburgh compound-B (PiB)-PET, 18F-fluorodeoxyglucose-PET, and measurement of serum PTPRB, GJA5, KCNJ8, and vWF levels using commercially available human enzyme-linked immunosorbent assay kits. Based on the mean cortical standardized uptake value ratio, the participants were divided into two groups: PiB-negative group and PiB-positive group. Serum levels of PTPRB, GJA5, KCNJ8, and vWF were compared between the two groups. Multiple linear regression analysis was performed to investigate the relationship between serum PTPRB, GJA5, KCNJ8, and vWF levels and cortical amyloid deposition. RESULTS: PTPRB and GJA5 levels were significantly lower and KCNJ8 and vWF levels were significantly higher in the PiB-positive group than in the PiB-negative group. PTPRB and GJA5 levels inversely correlated with mean PiB uptake, whereas KCNJ8 and vWF levels positively correlated with mean PiB uptake. CONCLUSION: Serum levels of PTPRB, GJA5, KCNJ8, and vWF correlate with cortical amyloid deposition. These novel blood biomarkers of neurovascular unit are useful for identifying elderly individuals at risk of developing Alzheimer's disease.

Temporal Changes in Brain Perfusion in Neuronal Intranuclear Inclusion Disease.

We herein report a patient with neuronal intranuclear inclusion disease (NIID) who presented with encephalitis-like episodes. A neurological examination revealed a disturbance of consciousness without any evidence of encephalitis or epilepsy on laboratory tests. Brain perfusion single-photon emission computed tomography revealed an elevated cerebral blood flow during the encephalitis-like episode and reduced cerebral blood flow in the chronic phase with clinical recovery. This report suggests that the cerebral blood flow of patients with NIID can change over the clinical course. Encephalitis-like episodes of NIID should thus be considered in the differential diagnosis of acute disturbance of consciousness.

A case of myelin oligodendrocyte glycoprotein-antibody-associated disease presenting with tumefactive demyelinating lesion.

We report the case of a patient with myelin oligodendrocyte glycoprotein (MOG)- antibody-associated disease presenting with tumefactive demyelinating lesion. Neurological examination showed aphasia, acalculia, agraphia, alexia, left-right disorientation, and right hemiplegia. Brain magnetic resonance imaging revealed a large monofocal lesion with mild brain edema and ring enhancement. Stereotactic brain biopsy was performed, and neuropathological findings showed inflammatory demyelination and preserved axons without tumor cells. A cell-based assay detected anti-MOG antibody in the cerebrospinal fluid. Neurological symptoms gradually improved after steroid pulse therapy. MOG-antibody-associated diseases should be considered in the differential diagnosis of tumefactive demyelinating lesion.

Multiple ulcerations and perforation in the small intestine after steroid treatment in eosinophilic granulomatosis with polyangiitis: a case report and literature review.

Eosinophilic granulomatosis with polyangiitis (EGPA), formerly called Churg-Strauss syndrome, is an uncommon disease with pathological features consisting of systemic necrotizing vasculitis, eosinophilic infiltration, and granulomatous or nongranulomatous extravascular eosinophilic inflammation. EGPA preferentially affects certain organ systems, including the airways, peripheral nerves, heart, kidney, and gastrointestinal tract. Although gastrointestinal involvement, such as ulcerations, is common in EGPA, gastrointestinal perforation is relatively uncommon and is associated with a poor prognosis. Ulceration, perforation, and stenosis of the gastrointestinal tract are assumed to be the result of ischemia caused by vasculitis. The histological finding in the biopsy specimens of EGPA is generally only eosinophil infiltration, and vasculitis is not often seen. Therefore, in biopsy specimens, it is difficult to distinguish eosinophilic gastroenteritis from the gastrointestinal involvement of EGPA. In addition, in general, steroid therapy is the first-choice treatment for EGPA, but some reports have described the frequent occurrence of acute ulcer or perforation of the gastrointestinal tract in association with steroid treatment. We herein report an EGPA patient who was treated with steroid therapy and subsequently developed perforation of the small intestine.

A New Serum Biomarker Set to Detect Mild Cognitive Impairment and Alzheimer's Disease by Peptidome Technology.

BACKGROUND: Because dementia is an emerging problem in the world, biochemical markers of cerebrospinal fluid (CSF) and radio-isotopic analyses are helpful for diagnosing Alzheimer's disease (AD). Although blood sample is more feasible and plausible than CSF or radiological biomarkers for screening potential AD, measurements of serum amyloid- ß (Aß), plasma tau, and serum antibodies for Aß1 - 42 are not yet well established. OBJECTIVE: We aimed to identify a new serum biomarker to detect mild cognitive impairment (MCI) and AD in comparison to cognitively healthy control by a new peptidome technology. METHODS: With only 1.5µl of serum, we examined a new target plate "BLOTCHIP®" plus a matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF/MS) to discriminate control (n = 100), MCI (n = 60), and AD (n = 99). In some subjects, cognitive Mini-Mental State Examination (MMSE) were compared to positron emission tomography (PET) with Pittsburgh compound B (PiB) and the serum probability of dementia (SPD). The mother proteins of candidate serum peptides were examined in autopsied AD brains. RESULTS: Apart from Aß or tau, the present study discovered a new diagnostic 4-peptides-set biomarker for discriminating control, MCI, and AD with 87% of sensitivity and 65% of specificity between control and AD (***p < 0.001). MMSE score was well correlated to brain Aß deposition and to SPD of AD. The mother proteins of the four peptides were upregulated for coagulation, complement, and plasticity (three proteins), and was downregulated for anti-inflammation (one protein) in AD brains. CONCLUSION: The present serum biomarker set provides a new, rapid, non-invasive, highly quantitative and low-cost clinical application for dementia screening, and also suggests an alternative pathomechanism of AD for neuroinflammation and neurovascular unit damage.

"Recurrent multiple cerebral infarctions related to the progression of adenomyosis: a case report".

BACKGROUND: Benign gynecologic tumor, such as uterine adenomyosis, has been suggested to develop hypercoagulability. Although some cases of cerebral infarction associated with adenomyosis have been reported, the mechanism of hypercoagulation initiated by adenomyosis is still not clear, and the therapeutic strategy is uncertain. CASE PRESENTATION: A 44-year-old woman was presented to our department with headache, left hand weakness, and gait disturbance during her menstrual phase. She had a history of adenomyosis and infertility treatment for 18 years and heavy menstrual bleeding. Magnetic resonance imaging on admission showed multiple hyperintense lesions in cortical and subcortical areas in the cerebrum and cerebellum on diffusion-weighted imaging. Transesophageal echocardiography showed neither embolic sources nor existence of foramen ovale. Her laboratory data revealed anemia, a high D-dimer level, and elevated levels of a mucinous tumor marker. She had adenomyosis and no malignancy was detected. Anticoagulation therapy with intravenous heparin followed by rivaroxaban did not prevent recurrence of cerebral infarction. We discontinued rivaroxaban, and started warfarin therapy with pseudomenopause treatment, which prevented recurrence for 6 months. Five months after her last pseudomenopause treatment, multiple cerebral infarctions occurred. Total hysterectomy was performed, which prevented recurrence of the multiple cerebral infarctions for 2 years without anticoagulation therapy. CONCLUSIONS: Our findings reveal for the first time that anticoagulation therapy, including novel oral anticoagulants, had no preventive effect against cerebral infarctions associated with adenomyosis in a middle-aged woman. Although pseudomenopause treatment temporarily prevented recurrence, resection of the adenomyosis might be the most effective therapy in these cases.

Effects of white matter lesions on brain perfusion in patients with mild cognitive impairment.

OBJECTIVE: To evaluate the effects of white matter lesions on regional cerebral blood flow in subjects with amnestic mild cognitive impairment. PATIENTS AND METHODS: Seventy-five subjects with mild cognitive impairment (36 men and 39 women; mean age, 78.1 years) were included in the study. We used the Mini-Mental State Examination to assess cognitive function. All subjects underwent brain magnetic resonance imaging and 99mTc ethylcysteinate dimer single photon emission computed tomography. Subjects were stratified based on the presence or absence of white matter lesions on magnetic resonance imaging. Statistical parametric mapping of differences in regional cerebral blood flow between the two groups were assessed by voxel-by-voxel group analysis using SPM8. RESULTS: Of all 75 subjects with mild cognitive impairment, 46 (61.3%) had mild to moderate white matter lesions. The prevalence of hypertension tended to be higher in subjects with white matter lesions than in those without white matter lesions. Mini-Mental State Examination scores were significantly lower in subjects with white matter lesions than in those without white matter lesions. Subjects with white matter lesions had decreased regional cerebral blood flow mainly in the frontal, parietal, and medial temporal lobes, as well as the putamen, compared to those without white matter lesions. CONCLUSION: In subjects with mild cognitive impairment, white matter lesions were associated with cognitive impairment and mainly frontal lobe brain function.

Induction of Genes Expressed in Endothelial Cells of the Corpus Callosum in the Chronic Cerebral Hypoperfusion Rat Model.

BACKGROUND: Cerebrovascular white matter lesions (WMLs) are associated with cognitive impairment in patients with subcortical vascular dementia. We performed a comprehensive gene expression analysis to elucidate genes associated with WML development in a chronic cerebral hypoperfusion rat model. METHODS: Brains of rats with bilateral carotid ligation (2VO, n = 10) and sham-operated rats (n = 5-10/group) were removed on days 1, 7, or 28 after surgery. Total RNA isolated from the corpus callosum was evaluated by microarray analysis and quantitative reverse transcription-polymerase chain reaction. RESULTS: On days 7 and 28, WMLs exhibited histologic changes. On day 7, 16 genes were differentially expressed between groups. mRNA levels of Ptprb, Kcnj8, Crispld2, Bcl6b, and Gja5 were differentially expressed in 2VO rats on day 7, but then returned to normal, whereas mRNA levels of Vwf and Trappc6a were upregulated after day 7. Immunohistochemistry showed that GJA5 and vWF were detected in endothelial cells, KCNJ8 in endothelial cells and astrocytes, CRISPLD2 in neurons and astrocytes, and TRAPPC6A in neurons. CONCLUSION: Our findings indicate novel genes that may be associated with WML development in the chronic cerebral hypoperfusion rat model, and suggest an important role of neurovascular dysfunction in the pathophysiology.

Brain perfusion SPECT in limbic encephalitis associated with autoantibody against the glutamate receptor epsilon 2.

OBJECTIVES: The aim of this study was to elucidate the single-photon emission computed tomography (SPECT) pattern at the acute stage of disease in non-herpetic limbic encephalitis (NHLE) patients associated with the N-methyl-D-aspartate-type glutamate receptor epsilon 2 (GluR ϵ2) autoantibody using Z-score imaging system (eZIS) analyses. METHODS: Brain magnetic resonance imaging (MRI) and brain perfusion SPECT using technetium-99 ethyl cysteinate dimer ((99m)Tc-ECD) were performed in eight patients with NHLE (5 men and 3 women; mean age 48.8±22 years) within 20days after clinical onset. RESULTS: All patients had various clinical limbic-associated symptoms and no evidence of herpes simplex infection or systemic malignancies. Two of eight patients showed abnormally hyperintense lesions on diffusion-weighted images and significant hyperperfusion in ipsilateral cerebral cortex on eZIS analysis, whereas other patients showed normal MRI findings and significant hypoperfusion in one or both sides of the limbic and paralimbic areas. CONCLUSION: We suggest that (99m)Tc-ECD SPECT study using eZIS analyses may be helpful to detect the neuronal dysfunction, particularly in NHLE patients without abnormal MRI findings.

Effect of white matter lesions on brain perfusion in Alzheimer's disease.

BACKGROUND: This study examined the effect of white matter lesions (WMLs) on regional cerebral blood flow (rCBF) in patients with Alzheimer's disease (AD). METHODS: Ninety-eight patients with AD were included in the study (40 men and 58 women; mean age, 78.1 years). Cognitive function was assessed using the Mini-Mental State Examination. Brain magnetic resonance imaging (MRI) and (99m)Tc ethyl cysteinate dimer single photon emission computed tomography were performed in all subjects. AD patients were divided into two subgroups according to the presence of WMLs on MRI. A voxel-by-voxel group analysis using Statistical Parametric Mapping 8 was used to detect the differences in rCBF between the two groups. RESULTS: Fifty-seven of 98 AD patients (58%) showed mild to moderate WMLs on MRI. The prevalence of hypertension was significantly higher in AD patients with WMLs than in those without WMLs. AD patients with WMLs exhibited a significantly decreased rCBF in the anterior cingulate gyrus and insula, compared to AD patients without WMLs. CONCLUSION: We suggest that WMLs might influence brain regions associated with the limbic system in patients with AD.

[A case of neurosarcoidosis with swelling and gadolinium enhancement of spinal nerve roots on magnetic resonance imaging].

An 80-year-old woman was admitted to our hospital because of developed sense of constriction in the trunk and gradually progressive numbness and muscle weakness in the upper and lower extremities. Cerebrospinal fluid analysis showed increased cell count and protein level. Gadolinium enhanced magnetic resonance imaging (MRI) of spine showed the enhancement and swelling of bilateral nerve root in the cervical and lumbar segments. Although chest computed tomography showed neither bilateral hilar lymphoadenopathy nor lung lesions and serum angiotensin converting enzyme and lysozyme (ACE) were normal, tuberculin skin test was negative and cell count and CD4/CD8 elevated in bronchoalveolar lavage fluid. Biopsy specimen of scalene lymph node showed noncaseating granuloma. The patient was treated with oral predonisolone, which improved her symptoms and abnormalities on MRI. It is important to consider neurosarcoidosis in the differential diagnosis of polyradiculopathy with swelling and gadolinium enhancement of spinal nerve roots.

[A case of limbic encephalitis repeated aphasic status epilepticus with periodic lateralized epileptiform discharges].

We report a case of limbic encephalitis repeated aphasic status epilepticus with periodic lateralized epileptiform discharges (PLEDs). A 51-year-old man developed convulsions, psychiatric symptoms such as anxiety, phobia and ease of anger, and Wernicke's aphasia. Analysis of the cerebrospinal fluid (CSF) showed increase of leukocyte count (148/microl, mononuclear cells). Brain magnetic resonance imaging (MRI) showed hyperintensity lesions in the left medial temporal area and basal frontal area on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images. The electroencephalography (EEG) showed PLEDs over the left hemisphere, occurring at intervals of 0.5-1 Hz. Although his limbic symptoms improved, Wernicke's aphasia occurred periodically with PLEDs appearance. After the administration of antiepileptic drugs, his language performance improved, and PLEDs were completely disappeared. We diagnosed him limbic encephalitis with non-convulsive repeated aphasic status epilepticus with periodic lateralized epileptiform discharges. Aphasic status epilepticus should be considered in the patients with limbic encephalitis, and careful evaluation of aphasia and EEG should be necessary to diagnose of aphasic status epilepticus.

Cerebral vasculitis associated with amyloid angiopathy: case report.

A 78-year-old female presented with coexisting primary angiitis of the central nervous system (CNS) and cerebral amyloid angiopathy (CAA) manifesting as motor aphasia caused by a left frontal lobe lesion. Magnetic resonance imaging revealed an enhanced lesion with moderate surrounding edema.Technetium-99m propylene amine oxime single-photon emission computed tomography showed decreased cerebral blood flow (CBF) in the lesions, and high serum soluble-interleukin-2 level was detected, suggesting intravascular lymphoma of the CNS. Cerebral biopsy revealed CAA with secondary florid vasculitic appearance. The CBF and neurological symptoms, such as aphasia and dementia, recovered following steroid treatment. Cerebral vasculitis associated with CAA should be included in the differential diagnosis of an unusually enhanced lesion, because timely diagnosis and aggressive treatment are critical to successful recovery in such elderly patients.

[Case of Vogt-Koyanagi-Harada disease associated with non-herpetic acute limbic encephalitis with autoantibodies against glutamate receptor epsilon2 in the cerebrospinal fluid].

We report a case of Vogt-Koyanagi-Harada (VKH) disease associated with non-herpetic acute limbic encephalitis with autoantibodies against glutamate receptor epsilon2 in the cerebrospinal fluid. A 42-year-old woman developed a complaint of visual distortion, visual disturbance, headache and mild psychiatric symptoms, such as anxiety and depression. She was diagnosed as VKH through the fidings of fluorescein fundus angiography, which revealed patchy hypofluorescence associated with delayed choroidal filling at early fluorescein angiographic phase, and spotted choroidal hyperfluorescence and pooling of dye at late phase. Analysis of the cerebrospinal fluid (CSF) showed slight increase of leukocyte count (49/microl, mononuclear cells) and immunoglobulin (Ig) G index. An anti-GluRepsilon2 IgM antibody was positive in CSF. Brain magnetic resonance imaging (MRI) showed a monofocal hyperintensity lesion in the left parahippocampal gyrus on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images. We diagnosed her VKH disease associated with non-herpetic acute limbic encephalitis. She was treated with oral prednisone, 70 mg day and her symptoms have gradually improved. To our knowledge, meningoencephalitis in VKH disease is extremely rare and the analysis of anti-GluRepsilon2 IgM antibody in CSF has not been reported. We speculate that a certain immunologic mechanism, including the anti-GluRepsilon2 IgM antibody, contributes to the pathogenesis of the VKH disease with non-herpetic acute limbic encephalitis.

Evaluation of regional cerebral blood flow in cerebellar variant of multiple system atrophy using FineSRT.

OBJECTIVES: In the present study, we compared the patterns of regional cerebral blood flow (rCBF) between cerebellar variant of multiple system atrophy (MSA-C) and the late-onset cortical cerebellar ataxia (LCCA) using FineSRT. PATIENTS AND METHODS: We performed (99m)Tc ethylcysteinate dimer (ECD) single-photon emission computed tomography in 11 patients with MSA-C (mean age 65.7 years), 7 patients with LCCA (mean age 62.0 years), and 12 age-matched healthy controls (mean age 64.1 years). The rCBF in the region of interest (ROI) was measured by the noninvasive Patlak plot method and calculated using FineSRT, which is a fully automated the ROI technique. RESULTS: All patients with MSA-C had various degrees of atrophy in the brainstem and middle cerebellar peduncles and 4 of 11 patients showed a clear 'hot cross bun' sign in pontine base on T2-weighted MR images. All patients with LCCA showed the various degrees of atrophy in cerebellum without brainstem. FineSRT revealed the significantly decreased rCBF in the caudate tail, fusiform, lingual, cerebellum, midbrain, and pons in MSA-C group compared with controls. Moreover, MSA-C group showed significantly decreased rCBF in the pons compared with LCCA group. CONCLUSION: We suggest that a widespread brain involvement is present in patients with MSA-C and the decreased rCBF in the pons may support the differential diagnosis between MSA-C and LCCA.

Primary central nervous system lymphoma with cortical laminar hemorrhage.

Here we report a case of primary central nervous system (CNS) lymphoma with cortical laminar hemorrhage. The present case showed an acute onset of focal neurologic signs and bilateral cortical lesions surrounded by peripheral white matter edema on magnetic resonance imaging. A part of the left frontal cortical lesion was hyperintense on T1-weighted images and hypointense on T2-weighted and T2-weighted gradient-echo images, suggesting subacute laminar hemorrhage. The patient was initially diagnosed with multiple hemorrhagic infarctions, but a biopsy specimen revealed diffuse large B-cell lymphoma with hemosiderin deposits. Immunohistochemical studies revealed that the tumor cell cytoplasm and membrane stained positively for anti-vascular endothelial growth factor antibody. The present case reconfirms the danger of making a specific lymphoma diagnosis based on magnetic resonance imaging findings alone and that histopathologic examination following brain biopsy is necessary for a correct diagnosis. Vascular endothelial growth factor expression might be associated with the intratumoral hemorrhage.

Monofocal large inflammatory demyelinating lesion, mimicking brain glioma.

Here we report two cases of pathologically confirmed tumor-like demyelinating lesions. In comparison with common primary demyelinating diseases, our cases demonstrated atypical radiologic features, such as a large monofocal lesion with mild brain edema, and open ring-like or focal enhancement on magnetic resonance images, suggesting brain tumors. The clinical manifestations included focal neurologic signs due to the lesions, monophasic episodes without relapse over a long follow-up period, and efficacy of oral corticosteroid therapy. Histological analysis of brain biopsy specimens showed the inflammatory demyelination and preserved axons without tumor cells. The present cases suggest the importance of considering inflammatory demyelinating disease in the different diagnosis of monofocal tumor-like lesion.

[A case of hematomyelia caused by coagulation--fibrinolysis abnormality accompanied with colon cancer and its metastasis].

A 76-year-old woman developed weakness and sensory loss in the lower limbs and urinary disturbance in four days. She had a history of operation for the ascending colon cancer and lung metastasis one year ago. Neurological examination revealed flaccid paraplegia, absent Achilles tendon reflex, severe disturbance of superficial and deep sensation below the L3 level, and vesicorectal abnormality. Magnetic resonance imaging (MRI) studies showed an intramedullary T1-iso, T2-low lesion with Gd-DTPA contrast enhancement in conus medullaris at LI level. The laboratory examination revealed the elevated level of serum FDP. D-dimer and TAT. She was diagnosed as hematomyelia, which may be caused by the activation of coagulation and fibrinolysis system. We suggested that the ascending colon cancer and lung metastasis may contribute to the coagulation-fibrinolysis abnormality.