We report an unusual case of subarachnoid hemorrhage (SAH) due to ruptured aneurysm originating at the caudal loop of posterior inferior cerebellar artery (PICA). The patient was a 77-year-old female presented with a sudden onset of headache and vomiting. Initial CT scan demonstrated a SAH with thick hematoma mainly in the cisterna magna. Vertebral angiogram revealed a saccular aneurysm arising from the tonsillomedullary segment of the left PICA, and communicating artery with supplying a territory of contralateral vermis as an anastmotic vessel. At surgery, no vessel branches were confirmed in the vicinity of the aneurysm, and this aneurysm was successfully clipped. In the fetus, numerous basilar and vertebral arteries are organized in plexiform formations around the brain stem. It has been suggested that the pathogenesis of such aneurysm or communicating artery could be related with a remnant of a primitive vertebrobasilar anastomosis. Based on these considerations, congenital vessel-wall weakness and hemodynamic stress associated with communicating artery may contribute to the development of distal PICA aneurysms.
{"title":"[Ruptured aneurysm of distal posterior inferior cerebellar artery located at caudal loop].","authors":"Shinya Oshiro, Takuma Kawahara, Seisaburo Sakamoto, Hirokazu Ohnishi, Tadahiro Ohmura, Hitoshi Tsugu, Takeo Fukushima","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We report an unusual case of subarachnoid hemorrhage (SAH) due to ruptured aneurysm originating at the caudal loop of posterior inferior cerebellar artery (PICA). The patient was a 77-year-old female presented with a sudden onset of headache and vomiting. Initial CT scan demonstrated a SAH with thick hematoma mainly in the cisterna magna. Vertebral angiogram revealed a saccular aneurysm arising from the tonsillomedullary segment of the left PICA, and communicating artery with supplying a territory of contralateral vermis as an anastmotic vessel. At surgery, no vessel branches were confirmed in the vicinity of the aneurysm, and this aneurysm was successfully clipped. In the fetus, numerous basilar and vertebral arteries are organized in plexiform formations around the brain stem. It has been suggested that the pathogenesis of such aneurysm or communicating artery could be related with a remnant of a primitive vertebrobasilar anastomosis. Based on these considerations, congenital vessel-wall weakness and hemodynamic stress associated with communicating artery may contribute to the development of distal PICA aneurysms.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 2","pages":"173-7"},"PeriodicalIF":0.0,"publicationDate":"2007-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26566683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
"Placebo" is Latin for "I shall please". The placebo effect has been widely documented by randomized placebo-controlled drug studies. One of the best examples of placebo effectiveness is that have been shown in clinical trials of anti-parkinsonian drugs. The placebo effect is observable not only in drug trials but also with deep brain stimulation. Recent advances in research on the placebo effect in Parkinson's disease (PD) have suggested that motor symptoms of PD can be essentially improved by placebo. A recent study using positron emission tomography (PET) with raclopride demonstrated that release of endogeneous dopamine in the dorsal striatum occurs in placebo-responsive patients with PD. This suggests that placebo-induced expectation of clinical improvement may activate endogenous dopamine in the striatum, and that placebo effectiveness is thus achieved by endogenous dopamine supplementation. Indeed, decreased neuronal activities in the subthalamic nucleus (STN), that were recorded during surgery to implant deep brain stimulation electrodes, correlated well with placebo-induced clinical improvement in patients with PD. Although the detailed pathophysiological mechanism underlying the placebo effects remains uncertain, theoretically, the placebo effect has generally been explained by two different mechanisms: one is conditioning theory (pavlovian conditioning), and the other is cognitive theory (expectation of clinical improvement). Although both mechanisms may contribute to placebo effects, the placebo effect in PD may be attributed more to cognitive mechanisms such as expectation of improvement, because the placebo effect can be obtained in de novo PD patients. There have been accumulating findings that suggest a functional relationship between dopamine and the expectation of clinical improvement (reward). Further basic studies are required to clarify the complex link between dopamine and the reward system, but such findings will contribute to a better understanding of the pathophysiological mechanism underlying the placebo effect in PD.
{"title":"[Placebo effect in Parkinson's disease].","authors":"Hideto Miwa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>\"Placebo\" is Latin for \"I shall please\". The placebo effect has been widely documented by randomized placebo-controlled drug studies. One of the best examples of placebo effectiveness is that have been shown in clinical trials of anti-parkinsonian drugs. The placebo effect is observable not only in drug trials but also with deep brain stimulation. Recent advances in research on the placebo effect in Parkinson's disease (PD) have suggested that motor symptoms of PD can be essentially improved by placebo. A recent study using positron emission tomography (PET) with raclopride demonstrated that release of endogeneous dopamine in the dorsal striatum occurs in placebo-responsive patients with PD. This suggests that placebo-induced expectation of clinical improvement may activate endogenous dopamine in the striatum, and that placebo effectiveness is thus achieved by endogenous dopamine supplementation. Indeed, decreased neuronal activities in the subthalamic nucleus (STN), that were recorded during surgery to implant deep brain stimulation electrodes, correlated well with placebo-induced clinical improvement in patients with PD. Although the detailed pathophysiological mechanism underlying the placebo effects remains uncertain, theoretically, the placebo effect has generally been explained by two different mechanisms: one is conditioning theory (pavlovian conditioning), and the other is cognitive theory (expectation of clinical improvement). Although both mechanisms may contribute to placebo effects, the placebo effect in PD may be attributed more to cognitive mechanisms such as expectation of improvement, because the placebo effect can be obtained in de novo PD patients. There have been accumulating findings that suggest a functional relationship between dopamine and the expectation of clinical improvement (reward). Further basic studies are required to clarify the complex link between dopamine and the reward system, but such findings will contribute to a better understanding of the pathophysiological mechanism underlying the placebo effect in PD.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 2","pages":"139-46"},"PeriodicalIF":0.0,"publicationDate":"2007-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26565606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JC virus (JCV) is a causative agent of progressive multifocal leukoencephalopathy and belongs to Polyomavirus. In this article we describe our recent research relating to this virus. First, JCV's major capsid protein VP1 possesses a nuclear localization signal (NLS) and has the ability to construct a virus-like particle (VLP). We have investigated the mechanism of nuclear entry of JCV using VLP, and clarified the role of NLS. In vitro transport assay revealed that wild type VLP (wtVLP), but not deltaNLSVLP, entered the nuclei of cells. The nuclear transport of wtVLP was dependent on the addition of importins alpha and beta and was prevented by antibodies to nuclear pore complex (NPC). These results suggested that JCV VLP binds to cellular importins via the NLS of VP1 and is transported into the nucleus through the NPC. Second, a yeast two-hybrid screen of a human brain cDNA library demonstrated that the fasciculation and elongation protein zeta 1 (FEZ1) and the heterochromatin protein lalpha (HPla) are proteins that interacted with JCV agnoprotein (Agno). In vitro binding assay showed that Agno interacts directly with FEZ1 and HPlalpha. We have also shown that Agno induces the dissociation of FEZ1 from microtubules and dissociates the interaction between HPlalpha and lamin B receptor. We have demonstrated that interaction between Agno and these host proteins inhibited nuclear egress of JCV. Third, in order to inhibit JCV infection in infected cells, we synthesized siRNA which is specific for JCV Agno. Immunoblotting and immunocytochemical analysis demonstrated that expression levels of agnoprotein and VP1 were significantly inhibited by specific siRNA. In addition, levels of viral mRNAs and viral production were decreased in the cells transfected with Agno siRNA. Furthermore, viral production of cell treated with Agno siRNA was significantly inhibited. These results indicate that post-infection treatment with siRNAs, that targets JCV Agno suppresses virus production in JCV infected cells. Thus, siRNA directed against JCV encoding genes may provide a useful tool for suppression of JCV infection.
{"title":"[Recent research on the JC virus].","authors":"Hirofumi Sawa, Tadaki Suzuki, Yasuko Orba, Yuji Sunden, Kazuo Nagashima","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>JC virus (JCV) is a causative agent of progressive multifocal leukoencephalopathy and belongs to Polyomavirus. In this article we describe our recent research relating to this virus. First, JCV's major capsid protein VP1 possesses a nuclear localization signal (NLS) and has the ability to construct a virus-like particle (VLP). We have investigated the mechanism of nuclear entry of JCV using VLP, and clarified the role of NLS. In vitro transport assay revealed that wild type VLP (wtVLP), but not deltaNLSVLP, entered the nuclei of cells. The nuclear transport of wtVLP was dependent on the addition of importins alpha and beta and was prevented by antibodies to nuclear pore complex (NPC). These results suggested that JCV VLP binds to cellular importins via the NLS of VP1 and is transported into the nucleus through the NPC. Second, a yeast two-hybrid screen of a human brain cDNA library demonstrated that the fasciculation and elongation protein zeta 1 (FEZ1) and the heterochromatin protein lalpha (HPla) are proteins that interacted with JCV agnoprotein (Agno). In vitro binding assay showed that Agno interacts directly with FEZ1 and HPlalpha. We have also shown that Agno induces the dissociation of FEZ1 from microtubules and dissociates the interaction between HPlalpha and lamin B receptor. We have demonstrated that interaction between Agno and these host proteins inhibited nuclear egress of JCV. Third, in order to inhibit JCV infection in infected cells, we synthesized siRNA which is specific for JCV Agno. Immunoblotting and immunocytochemical analysis demonstrated that expression levels of agnoprotein and VP1 were significantly inhibited by specific siRNA. In addition, levels of viral mRNAs and viral production were decreased in the cells transfected with Agno siRNA. Furthermore, viral production of cell treated with Agno siRNA was significantly inhibited. These results indicate that post-infection treatment with siRNAs, that targets JCV Agno suppresses virus production in JCV infected cells. Thus, siRNA directed against JCV encoding genes may provide a useful tool for suppression of JCV infection.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 2","pages":"101-8"},"PeriodicalIF":0.0,"publicationDate":"2007-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26566318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ten newer antiepileptic drugs have been developed since 1990s. These drugs have wider therapeutic spectra, fewer side-effects, and lesser drug-to-drug interactions compared with the older typical antiepileptic drugs. Among them, zonisamide was developed in Japan and has been used from 1989. Gabapentin was at length approved in 2006. The other newer antiepileptic drugs are not approved yet in Japan. Felbamate can not be used in Europe because it may induce lethal hepatic toxicity and aplastic anemia. Vigabatrin is not approved in USA because it may induce permanent visual field deficit. The USA guideline for epilepsy treatment recommends that patients with newly diagnosed epilepsy can be treated with gabapentin, lamotrigine, topiramate, and oxcarbazepine. In contrast, based on epilepsy treatment guideline in England, newer antiepileptic drugs are considered only when patients with newly diagnosed epilepsy are unable to use the older antiepileptic drugs for some reasons. All newer antiepileptic drugs are used for intractable partial epilepsies, and lamotrigine and topiramate can also be used for idiopathic generalized epilepsies. The response rate (seizure reduction rate with 50% or more) and drop-out rate are overlapping among all newer antiepileptic drugs. Gabapentin, levetiracetam, and pregabalin are eliminated from kidney, and they had no drug-to-drug interactions and can be titrated rapidly. The serum concentration of lamotrigine is decreased with co-administration of hepatic enzyme inducing drugs and is increased with co-administration of valproic acid. Hypersensitivity reactions are rare with gavapentin, levetiracetam, topiramate, and tiagabin. Psychoses are reported to be induced with zonisamide, however, they can be induced with the other newer drugs (topiramate, levetiracetam, etc.). Drug-induced psychiatric symptoms, especially depression, may be often underdiagnosed. Many of these newer drugs (gabapentine, lamotrigine, levetiracetam, oxycarbazepine, etc.) have effects on chronic neuropathic pain. Some newer drugs show mood stabilizing effects (lamotrigine, oxycarbazepine, etc.), or antianxiety effect (gabapentin, topiramate, levetiracetam, pregavalin, etc.). Wide range of action to central nervous system of these newer antiepileptic drugs may serve not only for clinical seizure suppression, but also for neuroprotection.
{"title":"[Newer antiepileptic drugs].","authors":"Masato Matsuura","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Ten newer antiepileptic drugs have been developed since 1990s. These drugs have wider therapeutic spectra, fewer side-effects, and lesser drug-to-drug interactions compared with the older typical antiepileptic drugs. Among them, zonisamide was developed in Japan and has been used from 1989. Gabapentin was at length approved in 2006. The other newer antiepileptic drugs are not approved yet in Japan. Felbamate can not be used in Europe because it may induce lethal hepatic toxicity and aplastic anemia. Vigabatrin is not approved in USA because it may induce permanent visual field deficit. The USA guideline for epilepsy treatment recommends that patients with newly diagnosed epilepsy can be treated with gabapentin, lamotrigine, topiramate, and oxcarbazepine. In contrast, based on epilepsy treatment guideline in England, newer antiepileptic drugs are considered only when patients with newly diagnosed epilepsy are unable to use the older antiepileptic drugs for some reasons. All newer antiepileptic drugs are used for intractable partial epilepsies, and lamotrigine and topiramate can also be used for idiopathic generalized epilepsies. The response rate (seizure reduction rate with 50% or more) and drop-out rate are overlapping among all newer antiepileptic drugs. Gabapentin, levetiracetam, and pregabalin are eliminated from kidney, and they had no drug-to-drug interactions and can be titrated rapidly. The serum concentration of lamotrigine is decreased with co-administration of hepatic enzyme inducing drugs and is increased with co-administration of valproic acid. Hypersensitivity reactions are rare with gavapentin, levetiracetam, topiramate, and tiagabin. Psychoses are reported to be induced with zonisamide, however, they can be induced with the other newer drugs (topiramate, levetiracetam, etc.). Drug-induced psychiatric symptoms, especially depression, may be often underdiagnosed. Many of these newer drugs (gabapentine, lamotrigine, levetiracetam, oxycarbazepine, etc.) have effects on chronic neuropathic pain. Some newer drugs show mood stabilizing effects (lamotrigine, oxycarbazepine, etc.), or antianxiety effect (gabapentin, topiramate, levetiracetam, pregavalin, etc.). Wide range of action to central nervous system of these newer antiepileptic drugs may serve not only for clinical seizure suppression, but also for neuroprotection.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 2","pages":"147-56"},"PeriodicalIF":0.0,"publicationDate":"2007-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26565607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The authors herein report a case of a ruptured dissection of the superior cerebellar artery (SCA). A 68-year-old man presented with symptons of sudden headache and nausea. The CT scan revealed the presence of both a subarachnoid hemorrhage (SAH) and acute hydrocephalus. The left vertebral angiogram showed an fusiform dilatation in the cerebellomesencephalic segment of the left SCA. Endovascular embolization of the aneurysm and SCA was successfully performed using Guglielmi detachable coils (GDCs). No delayed ischemic deficits were observed after the treatment. A dissection of the distal segment of the SCA is a very rare occurrence. We believe endovascular embolization using GDCs to be an effective and less invasive therapy for the treatment of an SCA dissection with SAH.
{"title":"[Case of ruptured superior cerebellar artery dissection treated by endovascular embolization].","authors":"Minoru Iko, Kiyoshi Kazekawa, Hiroshi Aikawa, Masanari Onizuka, Akira Tanaka","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The authors herein report a case of a ruptured dissection of the superior cerebellar artery (SCA). A 68-year-old man presented with symptons of sudden headache and nausea. The CT scan revealed the presence of both a subarachnoid hemorrhage (SAH) and acute hydrocephalus. The left vertebral angiogram showed an fusiform dilatation in the cerebellomesencephalic segment of the left SCA. Endovascular embolization of the aneurysm and SCA was successfully performed using Guglielmi detachable coils (GDCs). No delayed ischemic deficits were observed after the treatment. A dissection of the distal segment of the SCA is a very rare occurrence. We believe endovascular embolization using GDCs to be an effective and less invasive therapy for the treatment of an SCA dissection with SAH.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 1","pages":"72-5"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26551170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shoji Tsuji, Tadashi Isa, Tadafumi Kato, Hidehiro Mizusawa, Takao Takahashi, Yoko Kato, Tomoki Todo
{"title":"[Roundtable discussion: advances in neuroscience and therapeutic research on neurological diseases--the present status and future prospects].","authors":"Shoji Tsuji, Tadashi Isa, Tadafumi Kato, Hidehiro Mizusawa, Takao Takahashi, Yoko Kato, Tomoki Todo","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 1","pages":"6-22"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26493978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The patients with cardioembolic stroke sometimes suffer from severe neurological deficit and from recurrent strokes. Since atrial fibrillation, especially non-valvular atrial fibrillation (NVAF) is associated with over half of the cardioembolic strokes, the prevention of cardioembolic stroke in patients with NVAF is important. There have been some reports about how to prevent stroke. They have indicated that the best medication for preventing from stroke was anticoagulation by warfarin. Therefore, the guidelines recommended the patients with NVAF to take warfarin. In case with the older patients under 70 years, prothrombin international normalized ratio (PT-INR) should be kept from 2.0 to 3.0. On the other hand, if the patients with NVAF are over 70 years, PT-INR has to be controlled from 1.6 to 2.6. Before extraction of a tooth, anticoagulation should not be call off.
{"title":"[Prevention of brain infarction in patients with atrial fibrillation].","authors":"Toshiyasu Ogata, Masahiro Yasaka","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The patients with cardioembolic stroke sometimes suffer from severe neurological deficit and from recurrent strokes. Since atrial fibrillation, especially non-valvular atrial fibrillation (NVAF) is associated with over half of the cardioembolic strokes, the prevention of cardioembolic stroke in patients with NVAF is important. There have been some reports about how to prevent stroke. They have indicated that the best medication for preventing from stroke was anticoagulation by warfarin. Therefore, the guidelines recommended the patients with NVAF to take warfarin. In case with the older patients under 70 years, prothrombin international normalized ratio (PT-INR) should be kept from 2.0 to 3.0. On the other hand, if the patients with NVAF are over 70 years, PT-INR has to be controlled from 1.6 to 2.6. Before extraction of a tooth, anticoagulation should not be call off.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 1","pages":"53-8"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26493981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In recent years, population of elder people has increased in Japan, following augmentation of the number of people with dementia in Japan. Then it is important to detect cognitive impairment in early stage for adequate treatment, care and prevention. We studied 135 subjects, 49 patients with Alzheimer's disease (AD) and 86 healthy controls using Telephone Interview for Cognitive Status (TICS), and developing Japanese version of the TICS (TICS-J). The sensitivity and the specificity of the TICS-J to differentiate AD patients from healthy controls was 98.0% and 90.7%, respectively. Pearson's correlation coefficiency between the TICS-J and Mini-Mental State Examination (MMSE) was 0.858 (p < 0.001). On the receiver operating curves, the area under the curve for the TICS-J was 98.7% (95% CI: 97.5%-100%). These results indicate that TICS-J is sensitive and specific instrument for differentiating AD patients from healthy controls.
{"title":"[Development of the Telephone Interview for Cognitive Status (TICS) in Japanese].","authors":"Yoko Konagaya, Tomoyuki Watanabe, Yukihiko Washimi, Hideyuki Hattori, Akinori Takeda, Yoshiko Aihara, Ryoko Suzuki, Toshiki Ohta","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In recent years, population of elder people has increased in Japan, following augmentation of the number of people with dementia in Japan. Then it is important to detect cognitive impairment in early stage for adequate treatment, care and prevention. We studied 135 subjects, 49 patients with Alzheimer's disease (AD) and 86 healthy controls using Telephone Interview for Cognitive Status (TICS), and developing Japanese version of the TICS (TICS-J). The sensitivity and the specificity of the TICS-J to differentiate AD patients from healthy controls was 98.0% and 90.7%, respectively. Pearson's correlation coefficiency between the TICS-J and Mini-Mental State Examination (MMSE) was 0.858 (p < 0.001). On the receiver operating curves, the area under the curve for the TICS-J was 98.7% (95% CI: 97.5%-100%). These results indicate that TICS-J is sensitive and specific instrument for differentiating AD patients from healthy controls.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 1","pages":"67-71"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26550705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We review recent researches in neural mechanisms of facial recognition in the light of three aspects: facial discrimination and identification, recognition of facial expressions, and face perception in itself. First, it has been demonstrated that the fusiform gyrus has a main role of facial discrimination and identification. However, whether the FFA (fusiform face area) is really a special area for facial processing or not is controversial; some researchers insist that the FFA is related to 'becoming an expert' for some kinds of visual objects, including faces. Neural mechanisms of prosopagnosia would be deeply concerned to this issue. Second, the amygdala seems to be very concerned to recognition of facial expressions, especially fear. The amygdala, connected with the superior temporal sulcus and the orbitofrontal cortex, appears to operate the cortical function. The amygdala and the superior temporal sulcus are related to gaze recognition, which explains why a patient with bilateral amygdala damage could not recognize only a fear expression; the information from eyes is necessary for fear recognition. Finally, even a newborn infant can recognize a face as a face, which is congruent with the innate hypothesis of facial recognition. Some researchers speculate that the neural basis of such face perception is the subcortical network, comprised of the amygdala, the superior colliculus, and the pulvinar. This network would relate to covert recognition that prosopagnosic patients have.
{"title":"[Neural mechanisms of facial recognition].","authors":"Chiyoko Nagai","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We review recent researches in neural mechanisms of facial recognition in the light of three aspects: facial discrimination and identification, recognition of facial expressions, and face perception in itself. First, it has been demonstrated that the fusiform gyrus has a main role of facial discrimination and identification. However, whether the FFA (fusiform face area) is really a special area for facial processing or not is controversial; some researchers insist that the FFA is related to 'becoming an expert' for some kinds of visual objects, including faces. Neural mechanisms of prosopagnosia would be deeply concerned to this issue. Second, the amygdala seems to be very concerned to recognition of facial expressions, especially fear. The amygdala, connected with the superior temporal sulcus and the orbitofrontal cortex, appears to operate the cortical function. The amygdala and the superior temporal sulcus are related to gaze recognition, which explains why a patient with bilateral amygdala damage could not recognize only a fear expression; the information from eyes is necessary for fear recognition. Finally, even a newborn infant can recognize a face as a face, which is congruent with the innate hypothesis of facial recognition. Some researchers speculate that the neural basis of such face perception is the subcortical network, comprised of the amygdala, the superior colliculus, and the pulvinar. This network would relate to covert recognition that prosopagnosic patients have.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 1","pages":"45-51"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26493980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We reported double-dissociation between the visual processing of the edges and the surfaces of objects. Patients with lateral occipital damage showed selective impairment in the perception of edges whereas those with medial ventral occipital damage showed selective impairment in the perception of the 3D structure of the surface. Patients with medial ventral occipital damage also exhibited impaired perception of color, which is also a surface property. Those results were consistent with those from neuroimaging studies. Taken together, those studies suggest that objects may be processed in two separate pathways in the ventral occipital cortex: the edges of objects are processed in the lateral pathway and the surface of objects are processed in the medial pathway. Both edges and surfaces play important roles in object recognition, and both types of perception should be evaluated in patients with visual agnosia.
{"title":"[Neural mechanisms for object and color recognition].","authors":"Shinichi Koyama, Mitsuru Kawamura","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We reported double-dissociation between the visual processing of the edges and the surfaces of objects. Patients with lateral occipital damage showed selective impairment in the perception of edges whereas those with medial ventral occipital damage showed selective impairment in the perception of the 3D structure of the surface. Patients with medial ventral occipital damage also exhibited impaired perception of color, which is also a surface property. Those results were consistent with those from neuroimaging studies. Taken together, those studies suggest that objects may be processed in two separate pathways in the ventral occipital cortex: the edges of objects are processed in the lateral pathway and the surface of objects are processed in the medial pathway. Both edges and surfaces play important roles in object recognition, and both types of perception should be evaluated in patients with visual agnosia.</p>","PeriodicalId":19163,"journal":{"name":"No to shinkei = Brain and nerve","volume":"59 1","pages":"31-6"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26493977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}