T2-weighted IDEAL fast spin echo imaging of the brachial plexus: comparison with STIR.

BACKGROUND: Short TI inversion-recovery (STIR) imaging is widely used, but its signal-to-noise-ratio (SNR) is relatively low. Iterative decomposition of water and fat with echo asymmetric and least-squares estimation (IDEAL) imaging has demonstrated promising results in several areas. PURPOSE: To compare T2-weighted fast spin-echo IDEAL (T2W IDEAL-FSE) with STIR to determine which sequence is superior to image the brachial plexus. MATERIAL AND METHODS: The brachial plexus was imaged in 18 patients and six volunteers. The patients' diseases comprised of: suspected chronic inflammatory demyelinating polyneuropathy (CIDP), brachial plexus palsy of unknown origin, and suspected amyotrophic lateral sclerosis. Frontal partial MIP images were acquired. Image quality was qualitatively and independently scored by two radiologists on a three-point grading scale for noise, visibility of the nerve roots, and overall image quality. Inter-observer agreement of the rating by two readers was assessed. The SNR and contrast-to-noise-ratio (CNR) were quantitatively calculated, and differences between T2W IDEAL-FSE and STIR were compared. RESULTS: Qualitatively, each score for T2W IDEAL-FSE was significantly higher (P < 0.01) than that for STIR. Quantitatively, both SNR and CNR for T2W IDEAL-FSE (45.3 ± 12.6 and 27.1 ± 12.1, respectively) were significantly higher (P < 0.001) than those for STIR (17.4 ± 6.1 and 8.2 ± 4.7, respectively). CONCLUSION: T2W IDEAL-FSE could be used to replace STIR for visualization of the brachial plexus.

Aquaporin-4 expression in distal myopathy with rimmed vacuoles.

BACKGROUND: Distal myopathy with rimmed vacuoles/hereditary inclusion body myopathy is clinically characterized by the early involvement of distal leg muscles. The striking pathological features of the myopathy are muscle fibers with rimmed vacuoles. To date, the role of aquaporin-4 water channel in distal myopathy with rimmed vacuoles/hereditary inclusion body myopathy has not been studied. CASE PRESENTATION: Here, we studied the expression of aquaporin-4 in muscle fibers of a patient with distal myopathy with rimmed vacuoles/hereditary inclusion body myopathy. Immunohistochemical and immunofluorescence analyses showed that sarcolemmal aquaporin-4 immunoreactivity was reduced in many muscle fibers of the patient. However, the intensity of aquaporin-4 staining was markedly increased at rimmed vacuoles or its surrounding areas and in some muscle fibers. The fast-twitch type 2 fibers were predominantly involved with the strong aquaporin-4-positive rimmed vacuoles and TAR-DNA-binding protein-43 aggregations. Rimmed vacuoles with strong aquaporin-4 expression seen in the distal myopathy with rimmed vacuoles/hereditary inclusion body myopathy patient were not found in control muscles without evidence of neuromuscular disorders and the other disease-controls. CONCLUSIONS: Aquaporin-4 might be crucial in determining the survival or degeneration of fast-twitch type 2 fibers in distal myopathy with rimmed vacuoles/hereditary inclusion body myopathy.

Severe aquaporin 4-IgG-positive neuromyelitis optica with disseminated herpes zoster in a pregnant woman successfully treated with intravenous immunoglobulin.

A 26-year-old, 17-week pregnant woman developed aquaporin-4-IgG-positive severe longitudinally extensive transverse myelitis during the course of disseminated herpes zoster and became quadriparetic. She was unresponsive to high-dose intravenous methylprednisolone but became able to walk without assistance after intravenous immunoglobulin. One and a half months later, left optic neuritis developed but her vision improved with intravenous immunoglobulin. The only sequela was left T5 girdle sensation, and she delivered a healthy baby. Intravenous immunoglobulin may be a rescue therapy in aquaporin-4-IgG-positive neuromyelitis optica attacks in pregnant women, especially those with severe infections.

[A case of ticlopidine-associated thrombotic thrombocytopenic purpura: special emphasis on diffusion weighted MRI].

A 69-year-old man of thrombotic thrombocytopenic purpura (TTP) associated with ticlopidine was reported. The patient initially complained of dysarthria and left hemiparesis one month after oral administration of ticlopidine. These motor symptoms were followed by gradual deline in level of consciousness. On admission, he was in apallic state with focal cerebral signs, accompanied by low-grade fever, and purpuric eruptions. Laboratory findings showed remarkable thrombocytopenia, hemolytic anemia, and renal dysfunction. The patient received diagnosis of TTP based on Moschcowitzs criteria. Prompt initiation of plasma exchange dramatically improved the patient's clinical symptoms. In this case, decreased activities of a disintegrin and metallo proteinase with thrombospondin type 1 motifs 13 (ADAMTS13) in plasma and anti-ADAMTS13 IgG antibodies were detected. Serial diffusion weighted MRI with six-day interval starting from the onset showed two interesting findings. First, appearance and disappearance of scattered high intensity areas were observed in the cerebellum, corpus callosum, cerebral white matter, and neocortex. Second, these lesions roughly corresponded to border-zone infarct in distribution. Cranial MRI findings of TTP in the literature could be classified into the following four groups: 1) multiple infarction caused by microthrombi; 2) infarction caused by occulusion of an intracranial main artery; 3) reversible edema involving the cerebral white matter; and 4) unremarkable finding without specific abnormality. This case could be classified into the group 1. Based on the diffusion weighted MRI findings of this case, a previous pathological report and recent elucidations of clinical conditions, it is hypothesized that TTP is a predisposition for resembling the border-zone infarction in group 1. The border-zone distribution of transient high intensity areas in diffusion weighted MRI in this case could be explained by either high resistant vascules zone or impaired clearance of emboli, taking an autopsy case report into consideration.

Increased neuronal and astroglial aquaporin-1 immunoreactivity in rat striatum by chemical preconditioning with 3-nitropropionic acid.

Aquaporin-1 (AQP1) is a water channel expressed in the choroid plexus and participates in forming cerebrospinal fluid. Interestingly, reactive astrocytes also express AQP1 in the central nervous system under some pathological conditions. On the other hand, 3-nitropropionic acid (3NP) is a mitochondrial toxin that causes selective degeneration of striatum; however, its chemical preconditioning is neuroprotective against cerebral ischemia. We previously reported that mild 3NP application is accompanied with numerous reactive astrocytes in rat striatum devoid of typical necrotic lesions. Therefore, we studied whether AQP1 in the rat striatum could be upregulated with reactive astrocytosis using the 3NP model. Immunohistochemical or immunofluorescence analysis showed that reactive astrocytosis in the striatum, which upregulates glial fibrillary acidic protein and glutamine synthetase, was induced by mild doses of 3NP administration. Intriguingly, after 3NP treatment, AQP1 was intensely expressed not only by the subpopulation of astroglia but also by neurons. The AQP1 immunoreactivity became more intensified at the early-subtoxic stage (ES: 24-48h), but not as much in the delayed-subtoxic stage (DS: 96-120h). In contrast, AQP4 expression in the striatum was downregulated after 3NP treatment, in particular during the ES stage. AQP1 upregulation/AQP4 downregulation induced under subtoxic 3NP treatment may play a pivotal role in water homeostasis and cell viability in the striatum.

[NMDA-GluR Subunit Antibody-Positive Encephalitis: A Clinical Analysis of Five Cases].

Five consecutive cases of anti-NMDA-receptor encephalitis that we encountered were marked by a rapidly fluctuating level of consciousness associated with psychotic and delirious mental states. Opisthotonus, catatonia, and rhythmic and non-rhythmic involuntary movements of the mouth and jaw were also characteristic features of these particular cases. Serious and potentially fatal problems included epilepsia partialis continua, partial and generalized seizures, and respiratory depression, resembling the symptoms of encephalitis lethargica. An epidemic of encephalitis lethargica, also known of Economo encephalitis, occurred around 1917. Magnetic resonance imaging revealed edema of the neocortex in two cases and electroencephalography showed polymorphic and monomorphic delta slowing in the acute stage, although electroencephalographic seizure activity were not apparent. Routine cerebrospinal fluid analyses revealed lymphocyte-dominant pleocytosis in three cases, but antibodies against the NMDA-GluR subunit, GluN2B N-terminal, were at a high level in the fluid. All patients recovered without apparent sequelae. Two patients found to have ovarian teratoma underwent surgery for tumor removal. Treatments included pulse intravenous methylprednisolone, high-dose immunoglobulin, and plasma exchange together with seizure control and respiratory support. However, rituximab and or cyclophosphamide pulse therapy should also be considered for intractable cases, as indicated by recent reports. (Received February 16, 2016; Accepted May 2, 2016; Published September 1, 2016).

The critical threshold of 3-nitropropionic acid-induced ischemic tolerance in the rat.

3-Nitropropionic acid (3-NPA) is a suicide inactivator of succinate dehydrogenase (SDH), commonly used as a pharmacological model of Huntington's disease in rodents. Several studies have shown that a single administration of 3-NPA given systemically provides subsequent ischemic tolerance. The present study has tested the hypothesis that 3-NPA is capable of inducing tolerance in a model of permanent focal cerebral ischemia and whether 3-NPA can be truly applicable as a tolerance-inducer to ischemia. Rats given 3-NPA intraperitoneally revealed that the mortality of 3-NPA of 15, 20, and 25 mg/kg groups was 20.5, 38.8, and 83.3%, respectively. All rats survived without behavioral sequelae at smaller doses. Three days after 3-NPA preconditioning, the rats showing no behavioral changes underwent the permanent middle cerebral artery occlusion. The groups treated with 10 and 15 mg/kg of 3-NPA showed significantly reduced neurological deficits and infarction volumes in comparison with the control group, whereas the groups treated with 5 and 20 mg/kg of 3-NPA revealed no tolerance effects. When the regional SDH activity (% of control) was photometrically semi-quantified, it was observed that the activity was reduced to 90.8, 76.1, 67.8, and 64.3% in the outer layers of the cerebral cortex, and to 79.4, 67.5, 63.2, and 62.9% in the striatum 1 h after 3-NPA application (5, 10, 15, 20 mg/kg), respectively. In conclusion, although the preconditioning with 3-NPA is clearly shown in the setting of permanent ischemia, the preconditioning with this mitochondrial toxin demonstrated a rather narrow safety margin (critical threshold).

[Distigmine bromide induced Parkinsonism. A case report].

A 74-year-old man became unable to walk two days following the initiation of administration of oral distigmine bromide, 10 mg per day, for his constipation. Neurological examination revealed bradykinesia, rigidity and fine postural tremor without laterality. T2 weighted MRI showed mild front-temporal atrophy and multiple hyperintensities in both deep white matters. His symptoms fully improved one week after discontinuance of distigmine bromide. This is the first case report of distigmine bromide induced Parkinsonism.

[Evaluation of neurosonography for a case of brainstem transient ischemic attack (TIA) due to proximal subclavian artery stenosis, with favorable outcome after axillo-axillary bypass grafting].

We report an 82-year-old man with crescendo brainstem TIA and left upper-limb ischemia due to the left proximal subclavian artery stenosis. Angiography revealed that the left proximal subclavian artery was stenotic. The right vertebral artery was considered to be aplastic or occlusive. Neurosonography, especially the echo-Doppler study of the left vertebral artery, showed that the subclavian artery steal phenomenon did not occur. This study has enabled us to opt for axillo-axillary bypass. We preferred to avoid percutaneous transluminal angioplasty in order to avoid the risk of embolization. The patient received the axillo-axillary bypass operation. He has been free of TIAs and the left upper-limb ischemia since the surgery. We have evaluated his blood circulation fully, by comparing his state before and after the axillo-axillary bypass grafting.

"Anoikis" of oligodendrocytes induced by Wallerian degeneration: ultrastructural observations.

Oligodendrocytes undergo apoptosis in the white matter tracts remote from the experimental cord injury, although its significance is not understood. Our ultrastructural study, however, enabled us to speculate on its neurobiological implications. The spinal cords of male Wistar rats (4 week-old) were transected at Th11 level. At 4, 5, and 7 days after surgery the animals were transcardially perfusion-fixed. The removed cord was embedded in epoxy resin and examined by electron microscopy. Post-embedding terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL) method was also performed. In the degenerative dorsal column above the transection, profiles of apoptotic oligodendrocytes were always found, embedded in a space formed by dilated degenerative myelin lamellae. Often, the dilated space in the myelin sheath lacked any apparent background proteinaceous matrix. In the electron microscopic TUNEL method, these apoptotic cells were electron dense in accordance with nuclear heterochromatinization. In conclusion, in the process of Wallerian degeneration, we observed the apoptosis of oligodendrocytes in a space formed by the split myelin sheath. These degenerative cells, which were enclosed in an ultrafiltrate-filled space formed by split myelin lamellae, were reminiscent of "anoikis."

Lifecorder: a new device for the long-term monitoring of motor activities for Parkinson's disease.

OBJECTIVE: To quantitatively evaluate motor activity, its fluctuations, and drug effects in patients with Parkinson's disease (PD), the Lifecorder, a new monitoring device, was attached to a group of patients for several weeks. This enabled the continuous recording of motor activity in ten scaled magnitudes at two-minute intervals for 6 weeks. PATIENTS AND METHODS: Thirteen patients with PD who required dopamine receptor agonist therapy were monitored with Lifecorder, and seven healthy subjects served as the control group. The data obtained with this device correlated well with the Unified Parkinson's Disease Rating Scale (UPDRS) and Hoehn-Yahr grading. The dose of cabergoline, a D2-receptor agonist, was increased every 2 weeks, until optimum improvement was achieved. RESULTS: By adding cabergoline, the mean UPDRS improved from 40.5 to 28.4, which was significant. In parallel, the mean daily walking count (WC) also increased from 2,459 to 3,315 steps (p < 0.01) and movement-related calorie consumption (MCC) increased from 56 to 74 kcal (p < 0.05). UPDRS thus correlated well with WC and MCC (p < 0.05) obtained with this device. The improvement ratio of WC and MCC of each individual patient was compared with that of UPDRS. WC, and MCC shifted in parallel with UPDRS with one exception. The daily time-dependent fluctuation of motor activity was clearly shown by the Excel-generated graphs to improve with D-agonist therapy. In contrast to enhanced daytime activities, nocturnal restfulness was also clearly documented with this device. CONCLUSION: The unique properties of Lifecorder make this device a useful adjunct to the UPDRS for the objective evaluation of Parkinsonian motor activity. The device has a significant advantage over conventional clinical scales, as daytime as well as nocturnal motor activity can be objectively evaluated over long time periods ranging from one hour to one month, and the magnitude of motor activity is quantifiable in relation to the time-course.

[Problems in neurologic specialty training in Japan; a personal view].

Since started as a newly established department in a medical school fourteen years ago, my role as a clinician and teacher/investigator has been hampered by several problems; one is only five full-time faculty members available, simply too small in number, the lack of specialists in neurophysiology, neuropathology and neuroimaging diagnosis in the school, and regularly irregular annual enrollment of residents. Those problems, yet not fully solved, have been in part overcome by the intradepartmental efforts; that is, to run all the electrophysiology works by us, to have the neuropath lab of our own and to read all the neuro-images in our own conferences. It is certainly ideal and efficient, if the persons specialized to the fields teach residents how to run and read. In my experience, however, I had no chance of performing a needle EMG when a resident. In contrast, our approach to let all the residents expose to necessary procedures, of course under the supervision, may have a great impact on the resident's learning experience. It is my recommendation, if I can, that in-training examination be done 2-3 years prior to the neurology board, the subspecialty training course needs to be more comprehensive, covering the entire basic and clinical subjects in one full week or so, and our Neurology Association eases the passing rate of neurology board exam (currently between 30-60%), when the association figures out the number of neurologists necessary in Japan for next 10-20 years. The tough exam has certainly served a role of producing well-qualified neurologists, which we are proud of. However, our young trainees in neurology require something else, that is, to touch and feel the patients, electrodes, specimens and neuro-images by themselves. Then, one will be able to perform the role of a fully practice-oriented neurologist, wherever he has to work.

[A case of childhood multiple sclerosis presented with meningitis and multiple silent plaques].

A 13-year-old girl presented herself with right optic neuritis and pleocytosis in the cerebrospinal fluid (CSF) in May 2000. Although her vision gradually improved after steroid therapy, the right optic neuritis relapsed a month later, and MRIs of the brain showed multiple high-signal intensity areas in the white matter of the right frontal and parietal lobes on T2-weighted and FLAIR images. She developed nuchal pain, low-grade fever, and general malaise in January 2002. Mononuclear pleocytosis and an elevation of myelin basic protein level were noted in CSF (33/microliter, 17.7 ng/ml, respectively). In addition to the plaque-like lesions seen in June 2000, MRI at this time showed an increase in the number of plaques in the medulla, pons, bilateral cerebellar peduncles and cerebellum. We thus considered this case as MS presenting with no focal neurological deficits but meningitis and asymptomatic MRI lesions. The past history of relapsed optic neuritis is supportive and compatible with that diagnosis. One might assume that the case belongs to that of relapsed type acute disseminated encephalomyelitis (ADEM). However, the cardinal pictures of the case are those of relapsing optic neuritis and multiple asymptomatic plaques despite clinical remission. Some atypical features like meningitis may predominate in clinical presentations of child MS, since immune response in child may differ from that of adult.

[Postpartum cerebral angiopathy--a case report the vasculopathy associated with co-administration of two vasoconstrictives, methylergometrine maleate and sumatriptan].

A 25-year-old woman (gravida 1, para 0) who had no history indicating the toxemia of pregnancy developed hypertension and severe throbbing headache after the delivery of her first child by the cesarean section. Generalized tonic-clonic seizure ensued 5 days after the delivery, after which she did not fully regain her consciousness. Her head T2-weighted and FLAIR MRIs showed areas of multiple high intensities in the basal ganglia and cerebral white matter. Her cerebral MRA revealed the segmental stenosis and irregular wall of the major vessels, in particular of the right MCA trunk. Three weeks later, these abnormalities in the neuroimages disappeared and she was free of any symptoms. The history disclosed that obstetricians had used methylergometrine maleate for uterine contraction after delivery and then sumatriptan for her throbbing headache. We speculate that these vasoconstrictive agents might have induced the postpartum cerebral angiopathy. Postpartum cerebral angiopathy may be distinct from reversible posterior leukoencephalopathy in that the abnormalities are not restricted to the posterior lobes and that the vascular changes are apparent on neuroimagings. However, this entity might have a common underlying physiology, which is the abnormally elevated blood pressure that occurs in the setting of early postpartum period. Caution should be exercised when vasoconstrictives are to be used in postpartum period.

[A case of hypertrophic pachymeningitis, resolved by antimicrobial therapy].

A 65-year-old woman with diabetes mellitus and chronic otitis media developed headache, fever, and hoarseness, all of which did not responded to the oral antibiotics. As stiff neck and lower cranial nerve palsies appeared, bacterial meningitis was suspected. Neurological examination revealed the right hearing disturbance, right recurrent laryngeal nerve palsy, left sternocleidomastoid muscle atrophy and bilateral tongue atrophy. The CSF examination revealed mild pleocytosis and elevated protein, but no bacterial organism was cultured from the CSF. CT scans showed bilateral mastoiditis, and the right mastoid process and a posterior part of the petrous bone were eroded, indicating the exposed bony structures to the posterior fossa. MRI scans demonstrated the thickening of the dura mater of the posterior fossa and the right cerebellar tentorium. This is a rare example of bacterial pachymeningitis of the posterior fossa, the clinical symptoms and MRI findings of which resolved solely by antimicrobial agents without corticosteroid.

[Recurrent multiple cerebral hemorrhages complicated with polyarteritis nodosa].

In January 2001, a 72-year-old woman, who had been treated for polyarteritis nodosa, and vasculitic neuropathy, was admitted in somnolent state. She was monoparetic in her right leg, and disoriented. Neuroimaging studies revealed multiple superficial parenchymal hemorrhages in the bilateral hemispheres with dural Gd enhancement and parenchymal thickenings. No evidence of intracranial vasculitis was seen in visible arterial branches and veins by MRV and helical CTs. While in the hospital, intracerebral hemorrhage recurred three times. In April 2001, the third large intracerebral hemorrhage occurred, for which the removal of hematoma was carried out and brain biopsy was done. The specimens showed an evidence of cerebrovascular amyloidosis, but no inflammation. In view of the absence of angitis in the parenchymal and pial blood vessels, despite the presence of pachymeningitis, the cortical and bridging veins which drained into the venous sinuses, were likely involved in inflammation. Impaired venous drainage due to pachymeningitis might be a mechanism by which recurrent multiple cerebral hemorrhages have taken place in the presence of amyloid angiopathy.

[Marked thickening of the peripheral nerves in chronic inflammatory polyradiculoneuropathy associated with HCV infection].

We report a case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) in a middle-aged patient with hepatitis C virus (HCV) infection. A 49-year-old man presented chronic progressive distal motor weakness and sensory disturbances. Laboratory findings indicated chronic liver dysfunction due to HCV infection, transient positive serum cryoglobulinemia and marked decreased motor and sensory conduction velocities in electrodiagnosis. Lumbar MRI showed marked hypertrophy of the bilateral lumbar radicular nerve roots. Steroid treatment, not IVIg, improved neurological manifestation of this patient, but the serum HCV-RNA level was extremely increased after this treatment. Choice of treatment for patients suffered from CIDP associated with HCV infection is still controversial. Newly discovered patients with HCV infection are increased in Japan in number according to the routine check their anti-HCV antibodies. It is important to monitor carefully the serum HCV-RNA level in CIDP patients associated with HCV infection when steroid treatment is initiated.

[Dramatic but temporary improvements in a case of CNS intravascular malignant lymphomatosis].

A 54-year-old man with a past history of gastric malignant lymphoma treated by the total gastrectomy and the chemotherapy, developed bilateral sudden deafness one year later. Two years after the gastrectomy he became abruptly paraplegic with sensory impairments of the lower extremities and neurogenic bladder. Serum LDH and soluble IL-2 receptor were high in titers (552 U/l and 1,090 U/l, normal range 145-519). Although the imaging studies of the spinal cord were negative, the myelopathic symptoms resolved dramatically after a course of pulse dose methylprednisolone therapy. However, he soon developed an abnormal behavior and mental deterioration in 3 weeks. The MRIs of the brain revealed abnormal signals compatible with multiple cerebral infarctions. As intravascular malignant lymphomatosis (IML) was suspected because of the laboratory and MRI findings, biopsies of the skin, the bone marrow, the muscle and the lymph node were carried out, without evidence of lymphoma. The brain biopsy ultimately confirmed the presence of IML. The patient remarkably responded to biweekly CHOP (cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in terms of regaining the mental alertness and improved hearing. However, the CHOP therapy was prematurely interrupted prior to completion because of infective arthritis. The relapse soon ensued, and he died 6 months after admission. This case was of interest because a solid gastric lymphoma appears to have transformed into the form of intravascular lymphomatosis without mass formations or leukemic changes. Although the neurological symptoms in association with IML are thought to be the results of ischemic events, this case illustrates a remarkable reversibility of the symptoms. This implies that the cerebral symptoms are not necessarily the results of typical ischemic infarction, but due to relative ischemia because of chiefly capillary-venous occlusion by lymphoma cells. The majority of the symptoms is thus attributable to the functional impairment. Therefore, the therapeutic intervention may dramatically improve the symptoms due to IML.

[A case of recurrent bacterial meningitis by delayed cerebrospinal fluid (CSF) leakage due to a head trauma].

A 42-year-old man was admitted due to recurrent bacterial meningitis, as he had been treated here for bacterial meningitis three years prior to the current event. He had a remote history of head injury that he had almost forgotten, and his laboratory data showed no immunodeficiency state. 111In-DTPA cisternography showed an abnormal radioactive accumulation in the frontal lobe adjacent to the left frontal sinus at 23 hours after intrathecal injection, and MPR CT images revealed the left frontal sinus bone fracture. These findings indicated that he had a head injury by which a delayed CSF fistula has been formed. He was surgically treated for a CSF leakage. Although a combination therapy of ABPC and CTRX was efficacious for this patient, this regimen may not be ideal, as meningitis by PRSP has been increasing in incidence. Pneumococcal meningitis, once not a difficult infection to treat, could be a difficult one, as resistant strains to ABPC and CTRX have been more common.

Risk factors for left atrial thrombus from transesophageal echocardiography findings in ischemic stroke patients.

BACKGROUND: To identify the cause of cerebral embolism, we performed transesophageal echocardiography (TEE) in patients suspected of embolic brain infarction including transient ischemic attack (TIA). We analyzed TEE findings and investigated factors associated with left atrial thrombus (LAT) detected by TEE. METHODS: We enrolled 98 consecutive patients who underwent TEE and had acute brain infarction or TIA that was possibly due to embolism. We assessed age, sex, presence of atrial fibrillation (AF), days from admission to TEE and TEE findings, including the prevalence of LAT, spontaneous echo contrast (SEC), left atrial appendage (LAA) slow flow velocity, patent foramen ovale (PFO), atrial septal aneurysm and aortic plaque (ASA). RESULTS: LAT was detected with TEE in 20 patients (20%). The factors that were significantly associated with the presence of LAT were male sex (unadjusted odds ratio (OR), 3.94; 95% confidence interval (CI), 1.07-14.58; p=0.037), presence of AF (unadjusted OR, 9.58; 95% CI, 2.58-35.50; p< 0.001), SEC (unadjusted OR, 8.48; 95% CI, 2.57-28.00; p< 0.001) and LAA slow flow velocity (unadjusted OR, 5.18; 95% CI, 1.59-16.91; p=0.005). Multivariate logistic regression analysis revealed that male sex (adjusted OR, 5.30; 95% CI, 1.09-25.71; p=0.039), presence of AF (adjusted OR, 8.97; 95% CI, 1.10-73.20; p=0.041) and SEC (adjusted OR, 10.87; 95% CI, 1.001-118.0; p=0.049) were independently associated with LAT, but LAA slow flow velocity was not. CONCLUSION: SEC is an important risk factor associated with LAT in patients suspected of embolic brain infarction that is independent of AF.