Posterior Cerebral Artery Infarction Research Articles

Preserved complex emotion-based learning in amnesia

An important role for emotion in decision-making has recently been highlighted by disruptions in problem solving abilities after lesion to the frontal lobes. Such complex decision-making skills appear to be based on a class of memory ability (emotion-based learning) that may be anatomically independent of hippocampally mediated episodic memory systems. There have long been reports of intact emotion-based learning in amnesia, arguably dating back to the classic report of Claparede. However, all such accounts relate to relatively simple patterns of emotional valence learning, rather than the more complex contingency patterns of emotional experience, which characterise everyday life. A patient, SL, who had a profound anterograde amnesia following posterior cerebral artery infarction, performed a measure of complex emotion-based learning (the Iowa Gambling Task) on three separate occasions. Despite his severe episodic memory impairment, he showed normal levels of performance on the Gambling Task, at levels comparable or better than controls—including learning that persisted across substantial periods of time (weeks). Thus, emotion-based learning systems appear able to encode, and sustain, more sophisticated patterns of valence learning than have previously been reported.

Posterior Cerebral Artery Infarction From Middle Cerebral Artery Infarction

While it is known that posterior cerebral artery (PCA) infarction may simulate middle cerebral artery (MCA) infarction, the frequency and localization of this occurrence are unknown. To determine the frequency of PCA infarction mimicking MCA infarction and the territory of the PCA most commonly involved in this simulation. We studied 202 patients with isolated infarction in the PCA admitted to our stroke center to determine the frequency of PCA infarction simulating MCA infarction, the involved PCA territory, and the patterns of clinical presentation. We found 36 patients (17.8%) with PCA ischemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was the superficial PCA territory (66.7%), followed by the proximal PCA territory (16.7%) and both the proximal and the superficial PCA territories (16.7%). The principal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proximal PCA territory, and undetermined (40.2%) in both the proximal and the superficial territories. Among the 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 patients), and severe hemiparesis (7 patients). Posterior cerebral artery infarction simulating MCA infarction is more common than previously thought. Early recognition of the different stroke subtypes in these 2 arteries may allow specific management.

Incidence of residual intracranial AVMs after surgical resection and efficacy of immediate surgical re-exploration.

The true incidence of residual lesions after surgical resection of AVMs is not well documented in the literature. Partial surgical resection is thought to not confer any improvement over the natural history risk of hemorrhage of AVMs, and in certain cases may actually increase the risk of hemorrhage. Over the past 11 years, we have adopted a policy of immediate postoperative angiography with immediate surgical re-exploration if a residual lesion is seen. The purpose of the present study was to review our experience to determine the incidence of residual lesions and subsequent outcome. From June 1991 to June 2002, 324 patients underwent craniotomy and surgical AVM resection. As per protocol, all patients underwent immediate postoperative angiography. We have a protocol for immediate surgical re-exploration if a residual lesion is seen on postoperative angiographic exam. There were total six patients (1.8% of patients operated with intracranial AVMs) with residual lesions on postoperative angiography. All six patients underwent immediate surgical re-exploration with complete 100% obliteration; two patients required two re-exploration procedures. There was one operative complication: posterior cerebral artery and superior cerebellar artery infarcts after re-exploration of residual lesion after surgical resection of a large occipito-temperal-parietal AVM. There were no other morbidities and no mortalities. The incidence of residual lesions seen on postoperative angiography after AVM surgery at an experienced center is 1.8%. Because of the potential imminent danger of hemorrhage from a residual lesion, we recommend a policy of immediate postoperative angiography (or intraoperative angiography if image quality is satisfactory) for all AVM surgery and early surgical re-exploration if a residual lesion is seen.

Zonal frequency analysis of infarct extent. Part II: anterior and posterior cerebral artery infarctions.

The object of the study was to test the hypotheses that analysis of the anatomic zones affected by single anterior (A), posterior (P), and middle (M) cerebral artery (CA) infarcts, and by dual- and triple-vessel infarcts, will disclose (i) sites most frequently involved by each infarct type (peak sites), (ii) sites most frequently injured by multiple different infarct types (vulnerable zones), and (iii) anatomically overlapping sites in which the relative infarct frequency becomes equal for two or more different infarct types and/or in which infarct frequency shifts greatly between single and multivessel infarcts (potential border zones). Precise definitions of each vascular territory were adopted. CT and MRI studies from 20 ACA, 20 PCA, three dual ACA-PCA, and four triple ACA-PCA-MCA infarcts were mapped onto a standard template (Part I). Relative infarct frequencies in each zone were analyzed within and across infarct types to identify the centers and peripheries of each infarct type, the zones most frequently affected by multiple different infarct types, the zones where relative infarct frequency was equal for different infarcts, and the zones where infarct frequency shifted markedly from single- to multiple-vessel infarcts. Zonal frequency analysis provided quantitative data on the relative infarct frequency in each anatomic zone for each infarct type. It displayed zones of peak infarct frequency for each infarct, zones more vulnerable to diverse types of infarct, peripheral "overlap" zones of equal infarct frequency, and zones where infarct frequency shifted markedly between single- and multiple-vessel infarcts. It is concluded that the hypotheses are correct.

GENETIC AND ENVIRONMENTAL INFLUENCES ON THE ORGANISATION OF SEMANTIC MEMORY IN THE BRAIN:IS “LIVING THINGS” AN INNATE CATEGORY?

The organisation of semantic memory into separately lesionable or imageable components must be determined by some combination of genetic and environmental factors. Little is known about the relative contributions of these two factors in establishing the functional architecture of semantic memory. By assessing the semantic memory impairment of an individual who sustained brain damage as a newborn, it is possible to place an upper bound on the contribution of post-natal experience. The present case study demonstrates a profound and enduring impairment in knowledge of “living things” following posterior cerebral artery infarctions at approximately 1 day of age. The design of the two experiments reported here allows us to characterise the subject's semantic memory impairment in terms of its scope and selectivity. The impairment affects both the naming of pictures of living things and the retrieval of verbal information about living things. It cannot be accounted for by differences in the difficulty of retrieving knowledge of living and nonliving things, as the living and nonliving items were equated for difficulty in each experiment. When visual and nonvisual information were queried separately for living and nonliving things, the impairment was manifest for both kinds of information about living things, but for neither kind of information about nonliving things. Because this impairment resulted from brain damage sustained too early for experience to have contributed to the organisation of semantic memory, this case study supports a genetic basis for the living-nonliving distinction in semantic memory.

Ischemic stroke and depression

P219 Objective: To investigate the frequency and clinical determinants of depression after ischemic stroke. Methods: We administered the Structured Interview Guide for the Hamilton Depression Rating Scale (SIGH-D) and neurological, neuropsychological, and functional assessments to 421 patients (age = 71.5 ± 8.0 years) three months after ischemic stroke and 249 stroke-free control subjects. We required a SIGH-D total score > 11 for the identification of clinically significant depression. Results: We identified clinically significant depression in 47 of the 421 patients (11.2%) and 13 of the 249 control subjects (5.2%), yielding an unadjusted odds ratio (OR) of 2.3 (95% confidence interval, 1.2 to 4.3) for depression associated with stroke. Logistic regression suggested that depression was independently associated with dementia (OR, 3.2), a major hemispheral stroke syndrome (OR, 1.7), infarcts in the anterior and posterior cerebral artery territories vs. infarcts in other vascular territories (OR, 1.6), and female sex (OR, 1.7). When present, depression tended to be mild and typically remitted in follow-up examinations. Somatic SIGH-D items but not depressed mood best distinguished stroke patients from control subjects and demented from nondemented stroke patients. Conclusions: Depression was less frequent, less severe, and less persistent in our stroke cohort than previously reported, possibly due to the underrepresentation of patients with a premorbid history of affective illness. It was associated with more severe stroke, particularly in vascular territories that supply limbic structures, and it was more frequent among patients with dementia and women. Somatic symptoms but not depressed mood best distinguished stroke patients from control subjects and demented from nondemented stroke patients, however, suggesting that stroke is more likely to be associated with a “pseudo-depression of dementia” than a “pseudo-dementia of depression.”

Stroke and status epilepticus: stroke type, type of status epilepticus, and prognosis

Even though stroke is known to be a common cause of status epilepticus (SE), the types of stroke or SE that may be associated are not yet clearly defined. The aims of this study were to assess the timing and type of SE in stroke patients and to observe the effects of stroke and the type of SE on the response to treatment and mortality. From May 1998 to May 2001 a total of 121 patients were admitted with SE. Among these, 30 cases (24.8%) of poststroke SE were identified and evaluated. There were 20 early-onset, and 10 late-onset SE. All stroke types were evenly distributed within the early-onset group, whereas only ischaemic stroke was found in the late-onset group. Posterior cerebral artery (PCA) infarcts were significantly more common within the latter ( P: 0.0017). Nonconvulsive SE (NCS) was more frequent than convulsive SE (CS) in the early-onset group ( P: 0.0352). There was a delay in the time-to-treatment for NCS compared to CS ( P: 0.0007). Without, however any effect on the rate of response to first step treatment (intravenous diazepam and phenytoin; P: 0.6334). Thirteen patients died (43.3%) during hospitalisation. Disability was significantly associated with higher mortality in the early-onset group ( P: 0.0201). As a conclusion, NCS seems to be an important issue in stroke, thus requiring a high degree of suspicion in an acute stroke setting to avoid further neuronal injury and morbidity.

Single stroke dementia: Insights from 12 cases in Singapore

Background: Vascular dementia (VaD) is occasionally caused by a single, strategically located stroke. In this report, we describe the clinical and anatomical features of 12 cases of strategic single infarct dementia (SSID) from Singapore. Methods: Each patient completed a standardized diagnostic evaluation including history, neurological and neuropsychological examination, laboratory testing, and brain imaging. Dementia was diagnosed using the Diagnostic and Statistical Manual, 3rd edition, revised (DSM-III-R) criteria, and VaD was diagnosed using the National Institute of Neurologic Disorders and Stroke and the Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS–AIREN) criteria. VaD patients whose brain imaging study revealed a single cerebrovascular event were diagnosed with SSID. Results: We identified 12 cases of SSID among 125 VaD patients (9.6%). Stroke mechanism was lacunar infarction in five cases, embolism in four cases, large vessel thrombosis in two cases, and parenchymal hemorrhage in one case. The most commonly impaired cognitive domains on neuropsychological testing were visual memory, visuoconstruction, and language. In 11 of the 12 SSID cases, the stroke was located in the left hemisphere. The thalamus, either alone or as the proximal portion of a posterior cerebral artery infarction, was involved in 8 of the 12 cases. Stroke locations in the nonthalamic SSID cases included left angular gyrus, subcortical left frontal lobe including minor forceps, left basal forebrain and medial frontal lobe plus anterior corpus callosum (proximal anterior cerebral artery infarction), and anterior corpus callosum alone. Conclusions: Various stroke mechanisms may produce SSID. In our SSID cases, vascular damage almost always involved the left hemisphere and frequently involved the thalamus and major interhemispheric or intrahemispheric white matter pathways.

Masking of Vertebral Artery Dissection by Severe Trauma to the Cervical Spine

A prospective case study was performed. To illustrate the association of cervical trauma with vertebral artery dissection, and to propose a diagnostic and therapeutic algorithm for suspected traumatic vertebral artery dissection. Vertebral artery dissection is a recognized but underdiagnosed complication of trauma to the cervical spine. Symptoms of spinal cord injury, however, may obscure those of vertebral artery dissection, presumably causing gross underdiagnosis of this complication. All patients with vertebral artery dissection admitted to the authors' facility between 1992 and 1997 were screened for cervical trauma. This article presents four patients with severe trauma to the cervical spine, defined as luxation, subluxation, or fracture, in whom symptoms of vertebral artery dissection developed after a delay ranging from several hours to weeks. The traumatic vertebral artery dissection typically was located at the site of vertebral injury or cranial to it. One patient with fracture of the odontoid process survived symptom free without ischemic brain infarctions. Another patient survived with traumatic quadriplegia in addition to large cerebellar and posterior cerebral artery infarctions. Two patients died as a result of fulminant vertebrobasilar infarctions, both with only moderate impairment from the primary spinal cord injury. Early signs of vertebral artery dissection include head and neck pain, often localized to the site of intimal disruption, which may be disguised by the signs of the spinal injury. Early Doppler ultrasound and duplex sonography as a noninvasive screening method should be performed for patients with severe trauma to the cervical spine. In cases of vertebral artery dissection, immediate anticoagulation should be initiated. Traumatologists should be aware of this complication in evaluating patients with severe trauma of the cervical spine, and also for a variety of forensic reasons.

Topisch-neuropsychologische Diagnostik sprachlicher Gedächtnisdefizite nach kortikalen Durchblutungsstörungen

In recent years a consensus has been reached about the neuroanatomical substrate of verbal memory, but this state of knowledge has not yet been implemented in clinical practice. One reason for this may be that most of the neuroscientific studies on verbal memory used different neuropsychological instruments and that only a small set of patient groups with the same etiology but different lesion sites were analysed. Returning to three earlier studies, we analyse the possibility to make differential judgements on the verbal memory impairments of four different patient groups by using the California Verbal Learning Test (CVLT). We compare patients with left-sided (n = 16) and right-sided (n = 10) posterior cerebral artery infarcts and patients with infarcts of the left (n = 10) or right (n = 21) frontal lobe, and we integrated data about their retention errors that had not been analysed so far. Our findings reveal significant differences between these patient groups, concerning the quantitative aspects of impairments, and also the profiles of memory errors (recall, interference and perseverations). Our study documents a relation between the site of the lesion and the type of verbal memory impairment, agreeing with some of the most recent neuroscientific findings. Starting from this observation we try to define a neuropsychological pattern of memory impairment which enables differential clinical diagnoses using the CVLT as a memory test.

Ischemic stroke and depression

P219 Objective: To investigate the frequency and clinical determinants of depression after ischemic stroke. Methods: We administered the Structured Interview Guide for the Hamilton Depression Rating Scale (SIGH-D) and neurological, neuropsychological, and functional assessments to 421 patients (age = 71.5 ± 8.0 years) three months after ischemic stroke and 249 stroke-free control subjects. We required a SIGH-D total score > 11 for the identification of clinically significant depression. Results: We identified clinically significant depression in 47 of the 421 patients (11.2%) and 13 of the 249 control subjects (5.2%), yielding an unadjusted odds ratio (OR) of 2.3 (95% confidence interval, 1.2 to 4.3) for depression associated with stroke. Logistic regression suggested that depression was independently associated with dementia (OR, 3.2), a major hemispheral stroke syndrome (OR, 1.7), infarcts in the anterior and posterior cerebral artery territories vs. infarcts in other vascular territories (OR, 1.6), and female sex (OR, 1.7). When present, depression tended to be mild and typically remitted in follow-up examinations. Somatic SIGH-D items but not depressed mood best distinguished stroke patients from control subjects and demented from nondemented stroke patients. Conclusions: Depression was less frequent, less severe, and less persistent in our stroke cohort than previously reported, possibly due to the underrepresentation of patients with a premorbid history of affective illness. It was associated with more severe stroke, particularly in vascular territories that supply limbic structures, and it was more frequent among patients with dementia and women. Somatic symptoms but not depressed mood best distinguished stroke patients from control subjects and demented from nondemented stroke patients, however, suggesting that stroke is more likely to be associated with a “pseudo-depression of dementia” than a “pseudo-dementia of depression.”

Is decompressive craniectomy for acute cerebral infarction of any benefit?

BACKGROUND Acute occlusion of the major cerebral arteries results in ischaemic changes to the brain, without time for reperfusion by the collateral circulation. The subsequent cellular events lead to a breakdown of the blood-brain barrier, causing malignant cerebral edema manifested clinically by a rapid neurological deterioration. The aim of this study was to determine the value of surgical decompression in patients who present with acute cerebral infarction. METHODS Retrospective review of patients with deteriorating consciousness level from massive cerebral ischemia and secondary edema, treated by decompressive craniectomy. RESULTS There were 10 patients over a 2-year period from 1997–99, consisting of seven male and three female patients (mean age 47.56 years) with a mean preoperative Glasgow Coma Scale (GCS) score of 6/15. Three patients had dominant middle cerebral artery (MCA) infarction, four had nondominant MCA infarction, one had posterior cerebral artery infarction, and the remaining two had cerebellar infarction. At a mean follow-up period of 7 months, two patients had died (20% mortality), four patients (40%) were vegetative or severely disabled, and the remaining four patients (40%) had mild disability or good outcome. Favorable prognostic factors were younger age (less than 50 years) and good initial GCS score (14 or better). CONCLUSION Decompressive craniectomy in the setting of acute brain swelling from cerebral infarction is a life-saving procedure and should be considered in younger patients who have a rapidly deteriorating neurologic status.

Training-induced brain plasticity in aphasia.

It has long been a matter of debate whether recovery from aphasia after left perisylvian lesions is mediated by the preserved left hemispheric language zones or by the homologous right hemisphere regions. Using PET, we investigated the short-term changes in the cortical network involved in language comprehension during recovery from aphasia. In 12 consecutive measurements of regional cerebral blood flow (rCBF), four patients with Wernicke's aphasia, caused by a posterior left middle cerebral artery infarction, were tested with a language comprehension task. Comprehension was estimated directly after each scan with a modified version of the Token Test. In the interval between the scans, the patients participated in brief, intense language comprehension training. A significant improvement in performance was observed in all patients. We correlated changes in blood flow measured during the language comprehension task with the scores achieved in the Token Test. The regions which best correlated with the training-induced improvement in verbal comprehension were the posterior part of the right superior temporal gyrus and the left precuneus. This study supports the role of the right hemisphere in recovery from aphasia and demonstrates that the improvement in auditory comprehension induced by specific training is associated with functional brain reorganization.

Exaggeration of Neuropsychological Deficit in Competency to Stand Trial

Abstract We discuss exaggeration of neuropsychological deficit in the context of pretrial competency evaluation, and present a case of verified symptom exaggeration to examine the validity of techniques commonly used to detect malingering but typically developed in other contexts. The defendant was diabetic, had stenosis of both internal carotid arteries, and experienced a large right posterior cerebral artery infarct while awaiting trial. He presented with severe cognitive deficits, including remarkable retrograde and anterograde amnesia, and by appearances was not competent to stand trial, nor did he appear restorable to competency. His performance on measures designed to detect response bias strongly suggested exaggeration of cognitive deficits. He was diagnosed as malingering, and the diagnosis was confirmed by surveillance. The opinion was rendered, and affirmed in court, that the defendant was competent to stand trial. Implications for the assessment of symptom exaggeration are discussed.

Cerebrospinal fluid spinal lumbar drainage: indications, technical tips, and pitfalls.

Since the publication by F. Vourc'h in 1963 [Br J Anaesth (1963) 35:118-120] describing the use of a plastic catheter inserted percutaneously for the drainage of lumbar cerebrospinal fluid (CSF) the indications for spinal drainage are numerous, but not very well systematized. The bibliographical review shows few recent papers concerning the techniques, indications, complications and pitfalls. The authors considered it interesting to analyze nine papers, in particular those dedicated to the use of spinal drainage in skull base surgery and in the prevention and/or treatment of CSF fistulas. Two papers describe for the first time pachymeningeal gadolinium enhancement associated with orthostatic headaches, owing to CSF hypotension mimicking an inflammatory or infiltrative disease. The results of the treatment of CSF fistulas are good with a high success rate, avoiding direct surgical repair. The use of a specially designed subarachnoid catheter is clearly superior to the epidural catheter, with good flow of CSF and minimal complications. The main problems are deficient flow and infections. Overdrainage is potentially dangerous, with acute pneumocephalus, brain collapse and neurological deterioration. Infrequent but possible is Chiari II-like syndrome with vocal cord paralysis and life-threatening aspiration, or temporal downward herniation with kinking of the posterior cerebral artery and acute brain infarct. The key to success lies in a rigid protocol, intermittent CSF drainage with a closed circuit, and daily biochemical and microbiological monitoring. Highly qualified medical and nursing staff are essential.

Quadruple sectoranopia caused by posterior cerebral artery infarction

Quadruple sectoranopia (QSA) has been attributed to anterior choroidal artery infarction affecting the lateral geniculate body. We report a case of QSA caused by posterior cerebral artery infarction in a patient having migraine without aura and suggest that QSA is not always diagnostic of a lesion in the lateral geniculate body in the territory of anterior choroidal artery.

Differing mechanisms between posterior and middle cerebral artery infarctions

Cardiac embolism has been thought to be one of the principal causes of posterior cerebral artery territory infarction. To determine stroke mechanisms and stroke risk factors in patients with posterior cerebral artery infarction, we studied 23 consecutive patients with recent infarcts in the posterior cerebral artery distribution (PCA infarcts) and compared these with a case-control group of 46 patients with recent infarcts in the middle cerebral artery distribution (MCA infarcts). All patients were similarly studied, including angiography and echocardiography. Case controls were age- and sex-matched and were randomly chosen from the most recent MCA infarcts seen at our institutions. All subjects were white. PCA infarcts had significantly more cardiac-source emboli (P=.01), less evident atherothrombosis (P=.003), multiplicity of infarctions (P=.05), and documented branch occlusions in the vessel involved (P=.05). MCA infarcts had more preinfarction transient ischemic attacks (P=.03) and evident occlusion of the appropriate extracranial vessel (P=.03). Different stroke mechanisms should lead to different diagnostic and therapeutic decisions.

Posterior Distribution of Infarcts in Strokes Related to Cardiac Operations

Background. Stroke complicates cardiac surgical procedures in a substantial number of patients. The mechanism of stroke is predominantly embolic, although hypoperfusion may play a role. The aim of this study was to determine whether radiologic appearances in this population were consistent with an embolic cause. Methods. We reviewed computed tomographic scans and medical records in 24 patients who suffered stroke after cardiac operation. Stroke was evident at 24 hours in 19 patients (79%). Infarcts were multiple in 16 and single in 3 patients (group 1). The remaining 5 patients suffered stroke beyond 24 hours and had single infarcts on computed tomographic scan (group 2). Results. In group 1, 15 patients (79%) had bilateral cerebellar infarcts, 4 (74%) had posterior cerebral artery infarcts, 10 (53%) had posterior watershed infarcts, and 11 patients (58%) had middle cerebral artery branch infarcts. The mean number of vascular territories involved was 5.1 (range, 1 to 10). Mobile atheromatous plaque was present in the ascending aorta or arch in 5 of 9 patients (56%) in group 1. In group 2, stroke occurred in close association with atrial or ventricular fibrillation in 3 of 5 patients (60%). Conclusions. In patients with radiologic evidence of infarction, perioperative strokes after cardiac operation are typically multiple, and involve the posterior parts of the brain, consistent with atheroembolization. Delayed strokes may be attributable to cardiogenic embolism.

Posterior cerebral artery infarction associated with carotid dissection

Posterior circulation stroke may rarely be associated with occlusive disease in the anterior circulation, such as in the context of a direct (fetal) origin of the posterior cerebral artery (PCA) from the internal carotid artery (ICA), or in the presence of a persistent trigeminal artery. Carotid dissection is an increasingly recognized cause of anterior circulation ischemia. It is possible that in the setting of certain cerebral hemodynamics, embolism from carotid dissection could cause PCA infarction via a patent posterior communicating artery. We report the MR and MR angiography findings of cerebral dynamics whereby a patient presents with posterior circulation symptoms from anterior circulation pathology: left ICA dissection with subsequent left PCA territory infarction. Cerebral hemodynamics may allow PCA infarction from carotid disease even in the absence of a fetal PCA origin. This report also broadens the spectrum of stroke associated with carotid dissection.

左後大脳動脈梗塞例における失読の研究 仮名失読／漢字失読／視覚失語の障害水準について

左後大脳動脈領域の脳梗塞で視覚失語を呈した症例における読みの能力を検討した。漢字，仮名ともに音読はほとんど不能であったが，漢字と絵カードとの matching が比較的良好であった。 (1) 文字の正誤判断， (2) 文字分類テストの成績は良好で，漢字,.仮名ともに文字形態記憶は保たれていた。 (3) 仮名文字列の lexical decision はまったく不能で，仮名文字列を全体として意味的処理を行う経路は障害されていると考えられた。(4) 漢字の odd word out test, (5) 漢字の分類テスト，(6) 漢字の連想テストの結果から，漢字の表す意味のカテゴリーや漢字同士の連合的および統合的関係の把握は良好であると考えられた。(7) 漢字の pointing では，選択枝が同一のカテゴリーに属する場合には成績が不良で，意味的に近縁な漢字の判別には障害があると考えられた。 以上の結果を，純粋失読における音読と読解の解離や視覚失語の視覚性呼称障害の成立機序との関連において考察した。