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Biomedical subjects

Masumi Ito

Publications and source records attributed to Masumi Ito.

7 recordsLinked to original sources
PubMed2006

Déjà vu experiences in patients with schizophrenia.

To investigate whether déjà vu experiences are psychopathologic phenomena, we studied the frequency and characteristics of déjà vu experiences in patients with schizophrenia. One hundred thirteen patients with schizophrenia and 386 nonclinical control subjects were evaluated with the Inventory of Déjà vu Experiences Assessment. The frequency and features of déjà vu experiences were compared between the 2 groups. The patients with schizophrenia had déjà vu experiences less frequently (53.1%) than did the nonclinical subjects (76.2%). The frequency of déjà vu experiences did not correlate significantly with age at evaluation or education level among the patients with schizophrenia. Most characteristics of déjà vu experiences of the patients were comparable with those of the control subjects. However, the experiences of the patients tended to be longer and more monotonous. The patients often felt alert, oppressed, and disturbed by the experiences. They appeared to have the experiences under unpleasant mental or physical states. Their déjà vu experiences are not primarily different in nature from those of the nonclinical subjects. The decreased frequency of the experiences in the patients may suggest déjà vu experiences as nonpathologic phenomena.

Adult↗
PubMed2005

Prolonged postictal psychosis with forced normalization (Landolt) in temporal lobe epilepsy.

We report two patients with temporal lobe epilepsy who developed prolonged episodes of postictal psychosis (12 weeks) following a bout of seizures and a lucid interval. No drug toxicity was noted, and no recurrent or continuous seizures were observed during their prolonged psychotic episodes. Repeated EEGs during the period of psychosis showed that their habitual focal epileptiform abnormalities had disappeared. Responses to neuroleptic treatments were not remarkable. Their psychotic symptoms gradually dispelled after their epileptiform abnormalities reappeared. These observations may suggest possible overlapping mechanisms between a prolongation of psychosis and suppression of epileptiform discharges on a scalp EEG.

Adult↗
PubMed2005

Intellectual prognosis of status epilepticus in adult epilepsy patients: analysis with Wechsler Adult Intelligence Scale-revised.

PURPOSE: Status epilepticus (SE) appears to cause cognitive dysfunction as well as other serious neurologic sequelae. To confirm whether SE produces a subsequent intellectual decline, we evaluated intellectual function prospectively in adult epilepsy patients with and without SE. METHODS: Of 1,685 patients with epilepsy who underwent comprehensive neuropsychological testing in two national hospitals in Japan, 15 patients experienced an episode of SE afterward and underwent the second neuropsychological examination after the SE episode. Forty clinically matched patients with epilepsy, but without an episode of SE since their initial neuropsychological examination, were also reevaluated. We compared IQs and subscores from the Wechsler Adult Intelligence Scale-Revised between the two groups by repeated measures analysis of variance. In the patients who experienced an SE episode, SE-related variables (i.e., age at the SE episode and type and duration of SE) and epilepsy-related variables such as epilepsy type, lateralization of EEG abnormalities, the presence of mesial temporal sclerosis, and previous history of SE, were evaluated in relation to intellectual outcome. RESULTS: Patients with SE, in comparison to those without SE, failed to show any significant post-SE intellectual decline. Furthermore, neither the SE-related variables nor the clinical characteristics were correlated with intellectual outcome. CONCLUSIONS: Our findings suggest that SE does not lead to a significant intellectual decline in adult patients receiving treatment for epilepsy.

Adult↗
PubMed2003

Multi-center study on post-ictal headache in patients with localization-related epilepsy.

The nature of post-ictal headache (PIH) remains unclear. A multicenter study was conducted in order to evaluate frequency and risk factors for PIH. The subjects consisted of 97 patients with temporal lobe epilepsy (TLE), 65 patients with frontal lobe epilepsy (FLE) and 37 patients with occipital lobe epilepsy (OLE). The subjects were asked about PIH at each institute. Clinical factors of epilepsy were reviewed for each patient and correlated with PIH. Post-ictal headache occurred in 41% of TLE patients, 40% of FLE patients and 59% of OLE patients. Logistic regression analysis revealed that the risk of PIH was significantly higher in OLE than in FLE. In contrast, there were no significant differences in the incidence of PIH between TLE and either OLE or FLE patients. Post-ictal headache occurred significantly more frequently in subjects with generalized tonic-clonic seizure (GTCS) than in those without GTCS. Other clinical factors, such as sex, age, age at onset, duration of illness, seizure frequency, family history of headache and interictal headache were found to have no associations with PIH. A difference was found in the incidence of PIH depending on classification of epilepsy, but only to a relatively slight extent. It was also found that GTCS was significantly related to PIH. These results suggest that both the location of epileptogenic focus and the involvement of certain cerebral areas in the spread of seizure discharges may be closely related to PIH.

Adult↗
PubMed2002

An autoantibody inhibitory to glutamic acid decarboxylase in the neurodegenerative disorder Batten disease.

Mutations in the CLN3 gene are responsible for the neurodegenerative disorder Batten disease; however, the molecular basis of this disease remains unknown. In studying a mouse model for Batten disease, we report the presence of an autoantibody to glutamic acid decarboxylase (GAD65) in cln3-knockout mice serum that associates with brain tissue but is not present in sera or brain of normal mice. The autoantibody to GAD65 has the ability to inhibit the activity of glutamic acid decarboxylase. Furthermore, brains from cln3-knockout mice have decreased activity of glutamic acid decarboxylase as a result of the inhibition of this enzyme by the autoantibody, resulting in brain samples from cln3-knockout mice having elevated levels of glutamate as compared with normal. This elevated glutamate in the brain of cln3-knockout mice co-localizes with presynaptic markers. The decreased activity of GAD65 and increased levels of glutamate may have a causative role in astrocytic hypertrophy evident in cln3-knockout mice, and in altered expression of genes involved in the synthesis and utilization of glutamate that underlie a shift from synthesis to utilization of glutamate. An autoantibody to GAD65 is also present in sera of 20 out of 20 individuals tested who have Batten disease. Postmortem tissue shows decreased reactivity to an anti-GAD65 antibody that may be due to loss of GAD65-positive neurons or due to the reactive epitope being blocked by the presence of the autoantibody. We propose that an autoimmune response to GAD65 may contribute to a preferential loss of GABAergic neurons associated with Batten disease.

Adult↗