Treatment of delayed-onset post-stroke monochorea with stereotactic pallidotomy

Chorea that occurs as a result of a stroke is rare. We report a patient who developed hemiplegia following an acute hemorrhagic stroke in the left cerebral peduncle and subthalamus; although he had recovered gradually from the severe limb weakness, monochorea occurred 6 months later. Pallidotomy eliminated this symptom and we found it is a safe treatment for medically intractable post-stroke chorea after hemiplegia has resolved.     

Acute enlargement,morphological changes,and rupture of intracranial infectious aneurysm in infective endocarditis. Serial imaging

A 72-year-old man received a transcatheter aortic valve implantation (TAVI) 2 years ago for leakage of the degenerative bioprosthesis with Corevalve n°31 implantation, presented infective endocarditis (IE) (streptococcus sanguinis) of the bioprosthetic aortic valve. One month after antibiotic treatment was initiated, he presented a left-sided hemiplegia, a right frontal hematoma. MRI/contrast-enhanced magnetic resonance angiography (CE-MRA) revealed 2 infectious intracranial aneurysms (IIAs) of the right (10 mm) and left middle cerebral artery (MCA) (M2 segment, 5 mm). The right MCA IIA was treated within 1 day by glue-embolization. Seven days later, the patient acutely developed motor aphasia. CE-MRA showed significant enlargement (15 mm) and morphologic change of the ruptured left MCA IIA. This IIA was treated with Onyx-embolization.This case adds additional evidence that IIAs, during IE, can show rapid growth and morphological change over a 7 day course and emphasizes the imperative need of close imaging follow-up when IIAs are managed by antibiotic therapy.     

A new case of idiopathic hemiplegia hemiconvulsion syndrome

We report a new case of infantile idiopathic hemiconvulsion–hemiplegia syndrome (HH). A prolonged right-sided febrile convulsion was followed 4 days later, by right hemiconvulsive status epilepticus, documented by video-electroencephalogram (EEG) recording. The child developed an ipsilateral hemiplegia, partially improved during the first month of follow-up. Sequential cerebral magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (1H-MRS) at 6, 15, 30 days of follow-up showed a cytotoxic edema in the left hemisphere and a subsequent necrosis. At 1-year of follow-up, we performed MRI control because of febrile convulsion lasting few minutes that confirmed a non-progressive left hemisphere atrophy. After 2 years, the patient was seizure-free, with a mild right hemiplegia and language skills deficit. We discuss the unclear pathogenesis of HH through sequential neuroradiological evaluation.     

Myelin oligodendrocyte glycoprotein antibody-associated disease in a patient with symptoms of aseptic meningitis who achieved spontaneous remission: A case report and review of the literature

BackgroundA few case reports have described patients with myelin oligodendrocyte glycoprotein antibody (MOG-Ab)-associated demyelinating syndrome who presented with symptoms of aseptic meningitis. All such patients required immunotherapy. We report a patient with MOG-Ab-associated disorder (MOGAD) who presented with symptoms of aseptic meningitis and improved without treatment.CaseA 13-year-old girl presented with fever, headache, decreased appetite, and neck stiffness. Cerebrospinal fluid (CSF) analysis revealed pleocytosis and magnetic resonance imaging (MRI) showed leptomeningeal enhancement. The patient was diagnosed with aseptic meningitis at admission. However, there were no signs of recovery 4 days after admission (i.e., 8 days after disease onset). Therefore, we performed extensive investigations to identify the cause of the underlying infection and inflammation. On day 14 after admission, the serum MOG-Ab test performed at admission came back positive (1:128) and she was diagnosed with MOGAD. She was discharged on day 18 after admission, because her symptoms, CSF pleocytosis, and MRI findings had improved. About 6 weeks after discharge, MRI revealed hyperintensity without gadolinium enhancement. However, her serum MOG-Ab test was negative. We did follow-ups for 11 months but found no new neurological symptoms.Discussion and ConclusionTo the best of our knowledge, this is the first ever report of a pediatric patient with MOGAD experiencing spontaneous remission with no demyelinating symptoms during an extended follow-up period.     

Selective involvement of temporal regions in a case of flavivirus encephalitis

Clinical manifestations of flavivirus infection may be various, from unapparent to severe meningoencephalitis. Our patient, 2 weeks after returning home from a holiday at Elba Island, developed biphasic fever, later associated with nausea and vomiting and followed by incoming seizures responsive to thiopental sodium only. Brain MRI showed bilateral hyperintensity (T2) in amygdale, hippocampus, left insular and temporal inferior cortex. Standard and microbiological CSF examination was normal, but microbiological serum analysis showed seroconversion for flavivirus. The patient came to our observation 6 months after disease onset and at that time he was affected by frequent seizures and severe cognitive impairment with behavioural disturbances; the patient also showed distal weakness with footstepping. EEG showed bitemporal epileptic foci. During the following months, seizures greatly decreased and cognitive status improved in response to a complex antiepileptic therapy. Flavivirus encephalitis should be taken into account in the differential diagnosis of encephalitis selectively involving temporal lobes.     

Kernohan's notch phenomenon demonstrated by diffusion tensor imaging and transcranial magnetic stimulation

Kernohan's notch phenomenon is the ipsilateral hemiplegia caused by compression of the contralateral cerebral peduncle against the tentorial edge by a supratentorial mass. Diffusion tensor imaging (DTI) and transcranial magnetic stimulation (TMS) could be useful for exploring the state of the corticospinal tract (CST). This report attempts to demonstrate Kernohan's notch phenomenon in a patient with subdural haematoma by using DTI and TMS. One patient and six normal control subjects were recruited. The patient showed severe right hemiplegia even though the subdural haematoma was located in the right hemisphere. Brain CT at the time of onset showed right transtentorial herniation, and T2 weighted images at 6 weeks after onset showed a leucomalacic lesion on the left cerebral peduncle. DTI and TMS were performed at 6 weeks after onset. The fractional anisotrophy value of the left midbrain and medulla of the patient was found to be decreased in comparison with that of the control subjects. On fibre tractography for the CST, an interruption was observed in the left midbrain and medulla. The motor evoked potential obtained from the right hand muscle showed delayed latency, low amplitude and a higher excitatory threshold, thus indicating that the CST of the left hemisphere had been damaged. It seems that the CST had been damaged at the left midbrain, although subdural haematoma and transtentorial herniation had occurred in the right hemisphere in this patient. This report demonstrates Kernohan's notch phenomenon in this patient using DTI and TMS.     

An autopsied case of MM1 + MM2‐cortical with thalamic‐type sporadic Creutzfeldt‐Jakob disease presenting with hyperintensities on diffusion‐weighted MRI before clinical onset

A 78‐year‐old Japanese man presented with rapidly progressive dementia and gait disturbances. Eight months before the onset of clinical symptoms, diffusion‐weighted magnetic resonance imaging (DWI) demonstrated hyperintensities in the right temporal, right parietal and left medial occipital cortices. Two weeks after symptom onset, DWI showed extensive hyperintensity in the bilateral cerebral cortex, with regions of higher brightness that existed prior to symptom onset still present. Four weeks after clinical onset, periodic sharp wave complexes were identified on an electroencephalogram. Myoclonus was observed 8 weeks after clinical onset. The patient reached an akinetic mutism state and died 5 months after onset. Neuropathological examination showed widespread cerebral neocortical involvement of fine vacuole‐type spongiform changes with large confluent vacuole‐type spongiform changes. Spongiform degeneration with neuron loss and hypertrophic astrocytosis was also observed in the striatum and medial thalamus. The inferior olivary nucleus showed severe neuron loss with hypertrophic astrocytosis. Prion protein (PrP) immunostaining showed widespread synaptic‐type PrP deposition with perivacuolar‐type PrP deposition in the cerebral neocortex. Mild to moderate PrP deposition was also observed extensively in the basal ganglia, thalamus, cerebellum and brainstem, but it was not apparent in the inferior olivary nucleus. PrP gene analysis showed no mutations, and polymorphic codon 129 showed methionine homozygosity. Western blot analysis of protease‐resistant PrP showed both type 1 scrapie type PrP (PrP^Sc) and type 2 PrP^Sc. Based on the relationship between the neuroimaging and pathological findings, we speculated that cerebral cortical lesions with large confluent vacuoles and type 2 PrP^Sc would show higher brightness and continuous hyperintensity on DWI than those with fine vacuoles and type 1 PrP^Sc. We believe the present patient had a combined form of MM1 + MM2‐cortical with thalamic‐type sporadic Creutzfeldt‐Jakob disease (sCJD), which suggests a broader spectrum of sCJD clinicopathological findings.     

Aberrant pyramidal tract in a patient with corona radiata infarct A diffusion tensor tractography study

The aberrant pyramidal tract refers to the collateral pathway of the pyramidal tract through the medial lemniscus in the brainstem.A 63-year-old male patient presented with severe paralysis of the left extremities due to a right corona radiata infarct.He was able to extend the affected fingers against resistance at 2 months after stroke onset.At 6 months after stroke onset,he was able to perform some fine motor activities,as well as to walk with a nearly normal gait.Functional MRI,which was performed at 6 months after onset,showed that the contralateral primary sensorimotor cortex was activated during affected(left) hand movements.Diffusion tensor tractography results showed that at 2 weeks after stroke onset,pyramidal tracts of the affected hemisphere originated from the primary motor cortex and descended along the known pathway of the pyramidal tract with an aberrant pyramidal tract,which was bypassed through the medial lemniscus from the midbrain to the lower pons.However,the pyramidal tract from midbrain to pons in the affected hemisphere could not be depicted by diffusion tensor tractography at 6 months after stroke onset;instead,only the aberrant pyramidal tract existed for the course of the disappeared pyramidal tract.Results from this study indicate that the main motor functions of the affected extremities appeared to be controlled via the aberrant pyramidal tract with degeneration of the pyramidal tract in the brainstem of the affected hemisphere.     

Rendu-Osler-Weber syndrome presented paramedian thalamic and midbrain infarcts and primary medullary hemorrhage: a case report

We reported a 41-year-old male with paramedian thalamic and midbrain infarcts due to cerebral embolism from bilateral pulmonary arterio-venous fistula and primary medullary hemorrhage. The patient had an episode of sudden onset consciousness disturbance with left Weber's syndrome (right hemiplegia and left oculomotor palsy) and vertical gaze palsy at age of 23. He noticed numbness in the left hand and the left half body under clavicular when he had got up in a morning at age 41. He had headache and left tinnitus on second and third days, and on the 3rd and 4th days, he experienced nausea. He had severe hiccup persisting from the 6th to the 13th days. The 23rd days he was admitted to our hospital. He showed dysesthesia and paresthesia in left half body under clavicular, dysesthesia in left hand and vertical gaze palsy and convergence disturbance. MRI performed on the 18th and 24th days, disclosed hyperdense mass in T1 and T2-weighted images in dorsal site of medulla, but the 70th days MRI showed no abnormal lesions. Therefore we diagnosed the high intensity mass as primary medullary hemorrhage. Cerebral angiography showed no abnormal vasculature. Many members of his family had history of sever nasal bleeding. He had skin hemangioma and mucosal hemangioma in esophagus, stomach, colon and rectum, and bilateral pulmonary arterio-venous fistula which had been operated at age 39. His mother also had skin hemangioma and pulmonary arterio-venous fistula. Therefore this family was diagnosed Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasia). MRI also disclosed multiple cerebral infarctions in bilateral thalamus, left cerebral peduncle and left cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)     

核磁共振弥散张量纤维素成像对脑血管病患者预后的判定

目的观察急性脑血管病患者皮质脊髓束的损伤状况,分析运动功能变化并对临床预后进行判定。方法对18例脑卒中患者(其中脑梗死患者16例,脑出血患者2例)进行磁共振弥散张量纤维素成像(DTI)检查纤维束的连续性及破坏情况。于患者入院时、发病后2周、1月及2月分别进行肌力判定和神经功能评分。结果皮质脊髓束受累情况分为2级,1级:皮质脊髓束完整,共5例;2级:皮质脊髓束中断,共13例。16例脑梗死患者不同时期肌力及NIHSS评分与皮质脊髓束级别明显相关(P<0.05),发病后2月NIHSS评分转归情况与皮质脊髓束级别有显著性差异(P=0.0202)。2例脑出血患者入院时肌力均为0级但DTI显示皮质脊髓束完整的其预后也较好。18例受试者均进入结果分析,不同时期NIHSS评分与皮质脊髓束级别明显相关(P<0.05),发病后2月NIHSS评分转归情况与皮质脊髓束级别有显著性差异(P=0.0269)。结论三维纤维束示踪成像图可以更立体直观的显示皮质脊髓束状况,并在脑血管病初期即可对其损伤情况进行判定,同时可以提示脑血管病患者的预后。     

Effects of high-frequency repetitive transcranial magnetic stimulation over the contralesional motor cortex on motor recovery in severe hemiplegic stroke: A randomized clinical trial

BackgroundThe contralesional hemisphere compensation may play a critical role in the recovery of stroke when there is extensive damage to one hemisphere. There is little research on the treatment of hemiplegia by high-frequency repetitive transcranial magnetic stimulation (rTMS) delivered to the contralesional cortex.ObjectiveWe conducted a 2-week randomized, sham-controlled, single-blind trial to determine whether high-frequency rTMS (HF-rTMS) over the contralesional motor cortex can improve motor function in severe stroke patients.MethodsForty-five patients with ischemic or hemorrhagic stroke in the middle cerebral artery territory were randomly assigned to treatment with 10 Hz rTMS (HF group), 1 Hz rTMS (LF group) or sham rTMS (sham group) applied over the contralesional motor cortex (M1) before physiotherapy daily for two weeks. The primary outcome was the change in the Fugl-Meyer Motor Assessment (FMA) Scale score from baseline to 2 weeks. The secondary endpoints included root mean square of surface electromyography (RMS-SEMG), Barthel Index (BI), and contralesional hemisphere cortical excitability.ResultsThe HF group showed a more significant improvement in FMA score (p < 0.05), BI (p < 0.005), contralesional hemisphere cortical excitability and conductivity (p < 0.05), and RMS-SEMG of the key muscles (p < 0.05) compared with the LF group and sham group. There were no significant differences between the LF group and sham group. There was a positive correlation between cortical conductivity of the uninjured hemisphere and recovery of motor impairment (p = 0.039).ConclusionsHF-rTMS over the contralesional cortex was superior to low-frequency rTMS and sham stimulation in promoting motor recovery in patients with severe hemiplegic stroke by acting on contralesional cortex plasticity.Trial registrationClinical trial registered with the Chinese Clinical Trial Registry at http://www.chictr.org.cn/showproj.aspx?proj=23264 (ChiCTR-IPR-17013580).     

Kernohan-Woltman notch phenomenon caused by an acute subdural hematoma

Uncal herniation through the tentorial notch is occasionally associated with false localizing ipsilateral hemiparesis, known as the Kernohan-Woltman notch phenomenon (KWNP). We report an 81-year-old female who presented with a decreased level of consciousness, a right mydriasis and an ipsilateral motor deficit caused by a large right hemispheric subdural hematoma that was immediately evacuated. The patient recovered well, although her right hemiplegia persisted. A follow-up MRI showed a residual lesion in the left cerebral peduncle, corresponding to KWNP. The presence of such a structural lesion suggests a poor prognosis for recovery from the initial motor deficit.     

Abdominal epilepsia partialis continua in neurocysticercosis

Epilepsia partialis continua (EPC) of abdominal muscles is a rare entity with variable clinical localization and aetiology. A 25‐year‐old man presented with sudden onset of intermittent focal myoclonic movements involving the abdominal muscles on the right side exclusively, lasting from 20 minutes to an hour. Brain MRI revealed a ring‐enhancing lesion, suggestive of cysticercal granuloma over the left precentral gyrus. The patient fulfilled the revised diagnostic criteria for definitive diagnosis of neurocysticercosis. EEG did not show focal abnormalities during the events. Episodes of EPC were controlled with difficulty using 600 mg oxcarbazepine, 200 mg lacosamide, and 2,000 mg levetiracetam. The patient received antiparasitic therapy with albendazole (15 mg/kg for two weeks) and oral dexamethasone (0.1 mg/kg) for two weeks which was then tapered. The involvement of the primary motor cortex during ictal propagation may account for this curious phenomenon. This is the first report of abdominal EPC in a patient with inflammatory granuloma as a result of neurocysticercosis.     

Cerebral embolism associated with Becker muscular dystrophy-related dilated cardiomyopathy]

A 65-year-old man with previous history of congestive heart failure and genetically proven Becker muscular dystrophy (BMD) was suddenly suffered from aphasia and right hemiplegia. Physical examination showed severe motor aphasia, right hemiplegia, and signs of left heart failure. An echocardiogram before the onset of aphasia showed markedly dilated left ventricle and decreased ventricular contraction. Intracardiac thrombus was not detected. Although his electrocardiogram on admission showed sinus rhythm, atrial fibrillation was noted at the time of neurological deterioration. MRI of the brain revealed acute infarction in the territory of the left middle cerebral artery and the left anterior inferior cerebellar artery. MR angiography showed vascular occlusion at the left M2 segment. Cerebral embolism due to atrial fibrillation associated with BMD-related DCM was diagnosed. While an administration of anti-coagulant, diuretics, and dopamine relieved his respiratory distress and right hemiplegia, severe motor aphasia persisted. Cerebral embolism may be a notable complication in patients with BMD presenting with late-life expression of skeletal muscular weakness and antecedent cardiac involvement.     

A case of bilateral limbic and recurrent unilateral cortical encephalitis with anti-myelin oligodendrocyte glycoprotein antibody positivity

BackgroundAnti-myelin oligodendrocyte glycoprotein (MOG) antibody can be detected not only in acute disseminated encephalomyelitis or optic neuritis but also in limbic or cortical encephalitis. However, no previous reports have demonstrated a relapsing case of these two types of encephalitis.Case reportAn 11-year-old girl presented with fever, headache, abnormal behavior, focal impaired awareness seizures (FIAS) on the left side, and MRI hyperintensities in the bilateral amygdala, hippocampus, and right posterior temporal cortex. The symptoms were alleviated with two courses of intravenous methylprednisolone (IVMP) and one course of immunoglobulin. At 16 years of age, the patient returned with left-sided headache and MRI hyperintensities in the left temporal, parietal, and insular cortices, which improved after 3 courses of IVMP. Oral prednisolone (PSL) was tapered over 6 months, when FIAS reappeared on the right side of the body. MRI showed recurrence in the same regions as in the second episode. She received 3 courses of IVMP, followed by gradually tapered PSL without relapse for 1.5 year. Anti-MOG antibodies were positive in both serum and the cerebrospinal fluid prior to treatment in all three episodes.ConclusionOur results revealed that anti-MOG antibody-related bilateral limbic and unilateral cortical encephalitis can manifest with a variety of phenotypes over time in the same patient.     

A case of cardiogenic cerebral embolism with successful recanalization: apparent diffusion coefficient analysis for prediction of reversible cerebral ischemia]

A 54-year-old woman complaining of left hemiplegia was transferred to our hospital. Computed tomography on admission demonstrated normal. Electrocardiogram showed atrial fibrillation. Cerebral blood flow (CBF) was decreased in both the cortex and the perforator territory of the right middle cerebral artery (MCA), whereas the apparent diffusion coefficient (ADC) in the cortex was normal. Digital subtraction angiography (DSA) revealed an occlusion of the right MCA (M 1 proximal) with collateral flow from the right anterior cerebral artery (ACA) to the territory of the right MCA. After intra-arterial injection of tissue-plasminogen activator (t-PA), DSA showed partial recanalization, and the symptoms of the patient improved considerably. Five days after that, the patient deteriorated again and showed disturbance of consciousness and left hemiplegia. In this episode, both CBF and ADC in the cortex of the right MCA were decreased. DSA revealed an occlusion of the right internal carotid artery (ICA) and collateral flow from the right ACA to the territory of the right MCA disappeared. After intra-arterial injection of t-PA, DSA showed partial recanalization with collateral flow from the right ACA, and the symptoms of the patient improved. DSA 5 weeks after onset showed complete recanalization of both the right MCA and the ICA. The patient was diagnosed as both mitral and aortic stenosis and regurgitation (MSR + ASR) and underwent an operation for both mitral and aortic value replacement. She was discharged with no neurological deficit 4 months after onset. ADC analysis is especially useful for the prediction of reversible ischemic damage and the prevention of hemorrhagic transformation and fatal edema in acute ischemic stroke.     

Anosognosia for hemiplegia with pontine infarction

INTRODUCTION: Anosognosia for hemiplegia (AHP) is unawareness of unilateral motor deficit. This syndrome usually is reported in association with large lesions of the nondominant frontal and parietal lobes, the perithalamic lesions or their connexions with cortical or subcortical structures. Little is known about AHP in patients with brainstem's infarctions. CASE REPORT: A 79-year-old right handed woman, without history of intellectual deterioration or psychiatric diseases, with hypertension and paroxysmal atrial fibrillation, was admitted with acute left hemiplegia, somatosensory left deficit and slurred speech. Cerebral MRI indicated a recent infarct in the right anteromedial pontine territory. The patient had moderate anosognosia for hemiplegia (AHP) during the first week after the onset of stroke. There was no sign of left spatial hemineglect or left hemiasomatognosia, no persistant mental confusion and no associated significant cortical or subcortical lesions. CONCLUSION: We presumed that AHP is compatible with brainstem's lesions, particularly with pontine infarcts. The pathogenesis of AHP in pontine infarcts may result from the functional deactivation of frontal and parietal areas.     

Drug-resistant temporal lobe epilepsy due to middle fossa meningoencephalocele in a child: A surgical case report

BackgroundMeningoencephalocele (ME) of the temporal lobe through a bone defect in the middle cranial fossa is a rare known cause of refractory temporal lobe epilepsy (TLE). ME-induced drug-resistant TLE has been described in adults; however, its incidence in children is very rare.Case reportA 7-year-old girl presented at our hospital with brief episodes of impaired consciousness and enuresis. Initial brain MRI results were interpreted as normal. Her seizures could not be controlled even with multiple anti-seizure medications. She was diagnosed with drug-resistant TLE, which presented with prolonged impaired awareness seizures for 30–60 s and secondary bilateral tonic seizures. At 9 years of age, brain MRI revealed a left temporal anteroinferior ME with a congenital bone defect in the left middle cranial fossa. She was referred for presurgical epilepsy evaluation. Long-term video electroencephalography (EEG) failed to reveal regional abnormality in the left temporal lobe; invasive evaluation using stereoelectroencephalography (SEEG) was thus indicated.Ictal onset SEEG was identified in the temporal pole near the ME which was rapidly propagated to the mesial temporal structures and other cortical regions. The left temporal pole including the ME was micro-surgically disconnected while preserving the hippocampus and amygdala. The patient’s seizures have been completely controlled for 1 year and 6 months post-operatively.ConclusionSEEG revealed rapid propagation of ictal activity in this patient’s case, confirming that the ME was epileptogenic. Since the majority of patients with refractory epilepsy caused by ME have favorable postoperative seizure outcomes, it is important to carefully check for ME in drug-resistant TLE patients with apparently normal MRI.     

Progressive necrotic encephalopathy following tacrolimus therapy for liver transplantation

Previously described neurologic damage induced by immunosuppressive treatments includes transient or reversible central nervous system involvement. We describe a 57-year-old man who underwent liver transplantation and was started on immunosuppressive therapy with tacrolimus (FK506). Six months later, he started complaining of a progressive motor and sensory impairment of the left side, together with cognitive impairment. Brain MRI showed an enlarging lesion of the white matter with peripheral contrast enhancement. PET study indicated severe hypometabolism in the right hemisphere and spectroscopic MRI showed a peak of choline and relative reduction of other metabolites. Findings of CSF examinations and cultures, serology, and molecular techniques were normal. Tacrolimus treatment was stopped. A cerebral biopsy of the lesion showed a sub acute necrotizing process. In the following months, cognitive status of the patient tended to improve although he remained hemiplegic, while serial MRI confirmed the tendency to the recovery of the lesion that was still present 1 year after. The present observation describes a progressive encephalopathy associated with immune suppression with an unusual feature and permanent brain damage.     

Thrombosis of the superior cerebral vein with hemorrhagic cerebral infarction--serial MRI and pathological study of a case

We reported an autopsy case of thrombotic occlusion of the superior cerebral vein with hemorrhagic laminar necrosis of the right parietal cortex. A 68-year-old woman was admitted to our hospital because of a severe headache and left hemiplegia of acute onset. There was a past history of hypertension, fever of unknown origin, leukocytopenia and nasal dermatitis. Magnetic resonance images (MRI) disclosed thrombosis of the superior sagittal sinus and of the right parietal cortical vein as well as right parieto-occipital cerebral infarction. Although she improved with mild sequelae, the subsequent MRI showed a recurrent thrombosis of the superior sagittal sinus. Ten months after the onset she died suddenly, presumably due to acute myocardial infarction. Pathologically, thrombotic occlusion of the right parietal cortical vein, recurrent thrombosis of the superior sagittal sinus and old hemorrhagic cortical laminar necrosis of the right parietal region were revealed. Moreover, intracranial arteritis and phlebitis were observed, as well as arteriolitis in the peripheral nerves. In our case, MRI was useful for the diagnosis and following the course of cerebral venous thrombosis. Cerebral noninfective vasculitis may well have caused the venous thrombosis.