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Simultanagnosia resulting from dorsal stream dysfunction is an under recognized condition. In this case report we describe the case of a young woman who developed posterior reversible encephalopathy syndrome (PRES), and who recovered visual acuities of 20/20 in each eye, along with normal visual fields and contrast sensitivities, yet experienced persistent symptoms of perceptual dysfunction. Detailed and systematic history taking revealed consistent visual difficulties typical of dorsal stream dysfunction. After a detailed explanation of her symptomatology and training in a range of strategies to cope, the patient experienced a great improvement in her day-to-day functioning., Competing Interests: None

Background/aims: Alzheimer disease (AD) is a neurodegenerative disorder characterized by progressive disconnection of various brain networks leading to neuropsychological impairment. Pathology in the visual association areas has been documented in presymptomatic AD and therefore we aimed at examining the relationship between brain connectivity and visuospatial (VS) cognitive deficits in early AD., Methods: Tests for VS working memory, episodic memory and construction were used to classify patients with AD (n = 48) as having severe VS deficits (n = 12, female = 4) or mild deficits (n = 11, female = 4). Resting-state functional magnetic resonance imaging and structural images were acquired as per the standard protocols. Between-group differences in resting-state functional connectivity (rsFC) were examined by dual regression analysis correcting for age, gender, and total brain volume., Results: Patients with AD having severe VS deficits exhibited significantly reduced rsFC in bilateral lingual gyri of the visual network compared to patients with mild VS deficits., Conclusion: Reduced rsFC in the visual network in patients with more severe VS deficits may be a functional neuroimaging biomarker reflecting hypoconnectivity of the brain with progressive VS deficits during early AD., (© 2017 S. Karger AG, Basel.)

Patients with visual object agnosia fail to recognize the identity of visually presented objects despite preserved semantic knowledge. Object agnosia may result from damage to visual cortex lying close to or overlapping with the lateral occipital complex (LOC), a brain region that exhibits selectivity to the shape of visually presented objects. Despite this anatomical overlap the relationship between shape processing in the LOC and shape representations in object agnosia is unknown. We studied a patient with object agnosia following isolated damage to the left occipito-temporal cortex overlapping with the LOC. The patient showed intact processing of object structure, yet often made identification errors that were mainly based on the global visual similarity between objects. Using functional Magnetic Resonance Imaging (fMRI) we found that the damaged as well as the contralateral, structurally intact right LOC failed to show any object-selective fMRI activity, though the latter retained selectivity for faces. Thus, unilateral damage to the left LOC led to a bilateral breakdown of neural responses to a specific stimulus class (objects and artefacts) while preserving the response to a different stimulus class (faces). These findings indicate that representations of structure necessary for the identification of objects crucially rely on bilateral, distributed coding of shape features., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Patient DF, an extensively-tested woman with visual form agnosia from ventral-stream damage, is able to scale her grip aperture to match a goal object's geometry when reaching out to pick it up, despite being unable to explicitly distinguish amongst objects on the basis of their different geometries. Using evidence from a range of sources, including functional MRI, we have proposed that she does this through a functionally intact visuomotor system housed within the dorsal stream of the posterior parietal lobe. More recently, however, Schenk (2012a). The Journal of Neuroscience, 32(6), 2013-2017; Schenk (2012b). Trends in Cognitive Sciences, 16(5), 258-259. has argued that DF performs well in visually guided grasping, not through spared and functioning visuomotor networks in the dorsal stream, but because haptic feedback about the locations of the edges of the target is available to calibrate her grasps in such tasks, whereas it is not available in standard visual perceptual tasks. We have tested this 'calibration hypothesis' directly, by presenting DF with a grasping task in which the visible width of a target varied from trial to trial while its actual width remained the same. According to the calibration hypothesis, because haptic feedback was completely uninformative, DF should be unable to calibrate her grip aperture in this task. Contrary to this prediction, we found that DF continued to scale her grip aperture to the visual width of the targets and did so well within the range of healthy controls. We also found that DF's inability to distinguish shapes perceptually is not improved by providing haptic feedback. These findings strengthen the notion that DF's spared visuomotor abilities are driven largely by visual feedforward processing of the geometric properties of the target. Crucially, these findings also indicate that simple tactile contact with an object is needed for the visuomotor dorsal stream to be engaged, and accordingly enables DF to execute visually guided grasping successfully. This need for actions to have a tangible endpoint provides an important new modification of the Two Visual Systems theory., (© 2013 Published by Elsevier Ltd.)

Background: Olfactory dysfunction has an incidence of 5-10% after head injury. Several objective and subjective tests had been proposed. Recent studies showed that brain single photon emission computed tomography (SPECT) and brain magnetic resonance imaging (MRI) have good diagnostic value in this era in which the most common sites of involvement were olfactory bulb and olfactory nerve in MRI and frontal lobe in SPECT. This study aimed to estimate the sensitivity and specificity of brain MRI and brain SPECT in the diagnosis of traumatic hyposmia and anosmia., Methods: From February 2009 to March 2011, 63 patients with head injury and smell complaint were selected for this study. Using an identification test and a threshold smell test, 28 were anosmic and 27 had hyposmia and the remaining 8 were normosmic. All of them underwent brain MRI and SPECT., Results: The sensitivity of SPECT was 81.5 and 85.7% in hyposmia and anosmia, respectively. Its specificity was 87.5% in anosmia and 87.7% in anosmia. MRI sensitivity was 66.7% in hyposmia but 82.1% in anosmia. Its specificity was 85.7% in anosmia and 87.7% in anosmia. If MRI and SPECT were considered together, the sensitivity was 92.3% in hyposmia and 92% in anosmia, but the specificity was 87% in both cases., Conclusion: According to our study, both brain MRI and SPECT have high sensitivity and specificity in the diagnosis of traumatic anosmia, although brain SPECT is slightly superior to MRI. If the two techniques are applied together, the accuracy will be increased.

We investigated whether a self-rated anosognosia score can be an indicator for progression of brain atrophy in patients with amyotrophic lateral sclerosis (ALS). Scores for 16 patients were compared with the ventricular areas of the bilateral anterior and inferior horns measured on x-ray computed tomography. Longitudinal enlargement was expressed as a monthly increase in size: (ventricular size at the initial scan - ventricular size at the follow-up scan)/scan interval (months). The anosognosia scores ranged from -4 to 3 and 3-18 in patients with and without frontotemporal lobar degeneration (FTLD), respectively (p = 0.0011). Anosognosia scores were significantly correlated with sizes of anterior (r = 0.704, p = 0.0016) and inferior (r = 0.898, p < 0.0001) horns. In non-demented patients for whom follow-up CT scans were available (n = 7), the scores were significantly correlated with the longitudinal increase in inferior horn size (r = 0.754, p = 0.0496), but not with that of anterior horn size (r = -0.166, p = 0.7111). In conclusion, anosognosia in ALS is associated with greater anterior and inferior horn sizes, reflecting frontotemporal lobar atrophy. Moreover, mild anosognosia in ALS patients without FTLD may predict impending inferior horn enlargement, reflecting medial temporal atrophy., (Copyright © 2012 S. Karger AG, Basel.)

Background: The correlation of clinical presentation to pathology in dementia syndromes is important to correctly classify and ultimately treat these conditions. However, despite careful clinical characterization, it remains difficult to accurately predict an underlying causative pathology in some cases. Alzheimer disease is a well-defined clinical entity having established diagnostic criteria and characteristic neuropathologic findings. Alzheimer pathology, however, can cause varying clinical syndromes, including both atypical motor and behavioral presentations., Review Summary: Atypical clinical presentations of Alzheimer disease are reviewed in a case-based format. Corticobasal syndrome, with asymmetric Parkinsonism, dystonia, and apraxia, is increasingly recognized as a presentation of Alzheimer pathology. Frontal variant Alzheimer, clinically indistinguishable from behavioral variant frontotemporal dementia (bv-FTD), can present with difficulties in executive function, poor attention, and behavioral issues. Posterior cortical atrophy (the "visual variant" of Alzheimer) has predominant visuospatial dysfunction and can be an Alzheimer presentation. Finally, Alzheimer can present as logopenic progressive aphasia with word-finding difficulty., Conclusions: Clinicopathologic correlation may be more complex than previously realized, and the location of the microscopic changes may have as much to do with the clinical presentation as the nature of the changes themselves. Recognizing these clinical syndromes can lead to greater accuracy in diagnosis and treatment.

Anosognosia for hemiplegia (AH) is characterized by a lack of awareness of motor disorders and appears associated with fronto-temporal-parietal damage. Neuropsychological evidence indicates that behavioral indices of residual forms of motor awareness may co-exist with explicit denial of impairment. Here we explore whether the attempt by AH patients to perform an action may disclose residual forms of motor awareness and whether such forms are underpinned by different neural structures. Twelve hemiplegic patients affected by AH were tested in tasks assessing: (i) implicit awareness (IA), indexed by discrepancies between verbal reports and actual motor behavior; (ii) emergent awareness (EA), indexed by increased verbal awareness induced by the attempt to perform actions. IA and EA were found in five and three patients, respectively. Lesion analysis indicates that while the lack of IA is associated with damage to subcortical white matter anterior to the basal ganglia, lack of EA is linked to damage to cortical regions including insulo-frontal, temporal and parietal structures. Our results indicate that deficits in explicit and implicit awareness are associated with lesions involving different cortico-subcortical structures. Moreover, the results show that the attempt to perform an action may ameliorate body awareness deficits and have implications for rehabilitation., (Copyright © 2011 Elsevier B.V. All rights reserved.)

After a cerebral infarction, some patients acutely demonstrate contralateral hemiplegia, or aphasia. Those are the obvious symptoms of a cerebral infarction. However, less visible but burdensome consequences may go unnoticed without closer investigation. The importance of a thorough clinical examination is exemplified by a single case study of a 72-year-old, right-handed male. Two years before he had suffered from an ischemic stroke in the territory of the left posterior cerebral artery, with right homonymous hemianopia and global alexia (i.e., impairment in letter recognition and profound impairment of reading) without agraphia. Naming was impaired on visual presentation (20%-39% correct), but improved significantly after tactile presentation (87% correct) or verbal definition (89%). Pre-semantic visual processing was normal (correct matching of different views of the same object), as was his access to structural knowledge from vision (he reliably distinguished real objects from non-objects). On a colour decision task he reliably indicated which of two items was coloured correctly. Though he was unable to mime how visually presented objects were used, he more reliably matched pictures of objects with pictures of a mime artist gesturing the use of the object. He obtained normal scores on word definition (WAIS-III), synonym judgment and word-picture matching tasks with perceptual and semantic distractors. He however failed when he had to match physically dissimilar specimens of the same object or when he had to decide which two of five objects were related associatively (Pyramids and Palm Trees Test). The patient thus showed a striking contrast in his intact ability to access knowledge of object shape or colour from vision and impaired functional and associative knowledge. As a result, he could not access a complete semantic representation, required for activating phonological representations to name visually presented objects. The pattern of impairments and preserved abilities is considered to be a specific difficulty to access a full semantic representation from an intact structural representation of visually presented objects, i.e., a form of visual object agnosia.

Impaired awareness may be associated with increased neuropsychiatric symptoms in moderate to severe Alzheimer's disease, but relatively little is known about the association in early Alzheimer's disease. The aim of this study was to investigate if impaired awareness was associated with a higher frequency of neuropsychiatric symptoms in early Alzheimer's disease. In a Danish multicenter study, 321 patients with MMSE score > or =20 were evaluated. Patients with poor insight had significantly more neuropsychiatric symptoms than patients with full insight. When patients had increasing neuropsychiatric symptoms, caregivers reported higher levels of distress.

Aims: We previously reported that minocycline attenuates acute brain injury and inflammation after focal cerebral ischemia, and this is partly mediated by inhibition of 5-lipoxygenase (5-LOX) expression. Here, we determined the protective effect of minocycline on chronic ischemic brain injury and its relation with the inhibition of 5-LOX expression after focal cerebral ischemia., Main Methods: Focal cerebral ischemia was induced by 90 min of middle cerebral artery occlusion followed by reperfusion for 36 days. Minocycline (45 mg/kg) was administered intraperitoneally 2h and 12h after ischemia and then every 12h for 5 days. Sensorimotor function was evaluated 1-28 days after ischemia and cognitive function was determined 30-35 days after ischemia. Thereafter, infarct volume, neuron density, astrogliosis, and 5-LOX expression in the brain were determined., Key Findings: Minocycline accelerated the recovery of sensorimotor and cognitive functions, attenuated the loss of neuron density, and inhibited astrogliosis in the boundary zone around the ischemic core, but did not affect infarct volume. Minocycline significantly inhibited the increased 5-LOX expression in the proliferated astrocytes in the boundary zone, and in the macrophages/microglia in the ischemic core., Significance: Minocycline accelerates functional recovery in the chronic phase of focal cerebral ischemia, which may be partly associated with the reduction of 5-LOX expression., (Copyright 2009 Elsevier Inc. All rights reserved.)

Ocular dipping refers to a slow downward deviation of both eyes followed by a quick return to the midposition after a brief delay. Two patients with rapid neurologic deterioration in Creutzfeldt-Jakob disease (CJD) displayed ocular dipping, which quickly evolved into sustained downgaze deviation. Ocular dipping may thus be a transitional sign in a vertical gaze disturbance.

The purpose of this study was to determine the brain regions associated with anosognosia in Alzheimer's disease (AD). Anosognosia for memory disturbance was assessed in 29 probable AD patients, based on the discrepancy between questionnaire scores of the patients and their caregivers. In I-123-IMP single photon emission computed tomography (SPECT), a significant association was found between anosognosia and decreased perfusion in the orbitofrontal cortex, using regression analysis. This result is consistent with the previous studies that have reported an association between frontal dysfunction and anosognosia, and further suggests that the orbitofrontal cortex specifically associates with anosognosia in AD within the frontal cortex.

Objective: To search for specular disorders of body representations in right hemisphere stroke., Background: Mirror self-misidentification, asomatognosia, and personal confabulation are similar to body illusions or changes in sensorial or sensorimotor perceptions generated by mirror in right brain damage patients with body image disorders., Method: Prospective study. Ten consecutive right-handed patients (1) performed body part naming and localization tasks and (2) were examined for asomatognosia at the acute phase of stroke, then at least 3 months after stroke, under 3 test conditions: without a mirror, with a conventional mirror, and with an inverted mirror. Video recordings of the tests were analyzed to assess performance., Results: Analysis of variance of the data confirmed that the interaction of mirror's conditions (specifically without a mirror vs. an inverted mirror) with subtest type was significant. The errors are symmetrically distributed. Asomatognosia was "reactivated" in 10 patients who experienced asomatognosia during the acute phase. No particular pattern characterized the clinical manifestations of asomatognosia., Conclusions: A causal conflict of sensorial input is proposed. The specific symptoms observed would suggest the existence of an incomplete specular Gerstmann syndrome and/or Anton Babinski syndrome. These results emphasize the role of specular input in the generation of body representations and self-awareness.

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system causing severe disability via the progressive damage of white matter. Beyond physical signs cognitive dysfunction might be present as well. The aim of this study was to investigate the frequency and characteristics of brain atrophy and cognitive alterations. Significant cortical and subcortical atrophy was found on brain MRI of 30 MS patients included in this study comparing to healthy controls. Abnormal findings were detected in more than 60% of patients using a cognitive test battery. Generally, verbal abstraction, visuospatial orientation, attention, short-term memory was impaired and the psychomotor speed was decreased, even in the early stage of the disease. Depression-related complaints were found in 57% of this population. The Kurtzke scale, the atrophy of corpus callosum and widening of 3rd ventricle and Sylvian fissures were related to impaired cognitive performances. The authors would like to call attention to the early cognitive deficit and the need of treatment in MS.

Nonverbal environmental sound recognition was investigated in 24 subjects with unilateral subcortical lesions and 20 age-matched normal controls. All patients incurred putaminal hemorrhage at least three months before examination, and had a cystic lesion under the insula on CT or MRI at the time of evaluation. A mild impairment was found in association with extensive damage to the lateral and ventral portions of the putamen and the adjacent white matter in either the right or left hemisphere. Degree of impairment and type of error did not differ significantly between the sides of lesions. These observations and a review of literature suggest that the impairment of environmental sound recognition may arise with a unilateral subcortical lesion disrupting the geniculo-auditory association cortex projection fibers.

To study the selectivity of visual perceptual impairment in children with early brain injury, eight visual perceptual tasks (L94), were administered to congenitally disabled children both with and without risk for cerebral visual impairment (CVI). The battery comprised six object-recognition and two visuoconstructive tasks. Seven tasks were newly designed. For these normative data are presented (age 2.75-6.50 years). Because the recognition tasks required object naming, each item included a canonical control drawing and visual perceptual ability was evaluated relative to the non-verbal intelligence level, instead of chronological age. In 22 multiple disabled children with no indications of CVI, the frequency of impairment did not exceed that in the reference sample for any L94 task. In contrast, in 57 5-year-old children who were at risk for CVI due to pre-maturity or birth asphyxia, a significant increase in the frequency of impairment was seen on six L94 tasks (range 12-38%). However, only five children had more than two impairments, indicating that the deficits were selective, not pervasive. We conclude that early brain lesions interfere with the functioning of particular visual subsystems, yet leave other subsystems intact and functioning within the normal range.

Unilateral cerebrovascular lesions occurring during adulthood have been reported to be accompanied by high-amplitude somatosensory evoked potentials over the nonaffected hemisphere; however, the mechanisms by which somatosensory evoked potential amplitude increases over the nonaffected hemisphere are still unclear. To investigate the eventual presence of similar amplitude abnormalities in children, we recorded somatosensory evoked potentials in three groups of patients: one with unilateral cerebrovascular lesions that occurred during the perinatal period and another two with unilateral cerebrovascular lesions occurring during late adulthood or old age. Group 1 was comprised of 12 children and young adults (age range 2 3/12-31 years, 6 males and 6 females) who suffered from unilateral cerebrovascular lesion with perinatal onset. Four control groups were arranged with age matched to that of the patients. Adult patients were subdivided into two subgroups (group 2: n = 10, all males; group 3: n = 18, 12 males and 6 females) on the basis of the presence or absence of sensory impairment over the hemiplegic side. In group 1, the four youngest subjects, aged less than 6 years, were found to show somatosensory evoked potentials of abnormally high amplitude over the nonaffected hemisphere, with a "giant" main negative wave at around 45 ms (range 38.7-49.2), strictly localized over the central areas contralateral to the lesion; in normal controls, there was no such wave. All patients in group 2 were found to be affected by large infarctions in the territory of the middle cerebral artery, whereas patients in group 3 presented with subcortical lesions of the internal capsule isolated or in association with an involvement of the frontal and/or temporal cortex. Regarding somatosensory evoked potential parameters measured over the nonaffected hemisphere in adult/elderly subjects, a significant difference was observed for N20 and P22 latency, which was longer in both groups of patients than in controls. There is a significant difference in the neurophysiologic consequences of unilateral cerebrovascular lesion, as well as over the nonaffected hemisphere, if it occurs during early infancy or during adulthood. Our findings show a new type of "giant" somatosensory evoked potentials in some children affected by unilateral cerebrovascular lesion with perinatal onset.

How do we detect a target in a cluttered environment? Here we present neuropsychological evidence that detection can be based on the action afforded by a target. A patient showing symptoms of unilateral neglect following damage to the right fronto-temporal-parietal region was slow and sometimes unable to find targets when they were defined by their name or even by a salient visual property (such as their color). In contrast, he was relatively efficient at finding a target defined by the action it afforded. Two other patients with neglect showed an opposite pattern; they were better at finding a target defined by its name. The data suggest that affordances can be effective even when a brain lesion limits the use of other properties in search tasks. The findings give evidence for a direct pragmatic route from vision to action in the brain.

We report a pediatric patient with auditory agnosia as a sequel of herpes encephalitis. His early development was completely normal. He uttered three words at 12 months old. Disease onset was 1 year and 2 months of age. He was discharged from the hospital seemingly with no sequel; however, he could not recover his intelligible words even at age 2 years. He was diagnosed as having auditory agnosia caused by bilateral temporal lobe injury. We began to train him at once, individually and intensively. Adult patients with pure auditory agnosia followed by two episodes of temporal lobe infarction have impairment in central hearing but not inner language. Therefore, they can communicate by reading and writing. Moreover, impairment in hearing is not always severe and is often transient. However, despite long-term (more than 15 years) energetic education and almost normal intellectual ability (Performance IQ of Wechsler Intelligence Scale for Children-Revised was 91), our patient's language ability was extremely poor. Cerebral plasticity could not work fully on our patient, whose bilateral temporal lobe was severely injured in early childhood. The establishment of a systematic training method in such patients is an urgent objective in this field.

A case of the post-traumatic auditory-and-speech agnosia in a left-handed female patient is presented. The patient (a professional painter) showed satisfactory recovery in painting, speech production, reading and writing, whereas a severe deficit in auditory recognition of speech, melodies and rhythms persisted over time. She was also impaired in some aspects of visual recognition including prosopagnosia. To study this patient comprehensively, a neuropsychological assessment was combined with structural (magnetic resonance imaging-MRI) and metabolic (positron emission tomography--PET) data. Both PET and MRI revealed a large bilateral cortical damage in the medial basal cortex of the frontal, temporal and occipital lobes along with the anterior half of the lateral temporal cortex. In the left hemisphere the damaged area involved the whole temporal lobe, a large part of the occipital lobe and the opercular frontal and parietal regions. The relationship of the symptoms with the brain damage extension is discussed taking into account the left-handedness of the patient.

To determine the relation between developmental dysphasia and EEG anomalies during sleep, we compared 52 subjects with dysphasia with a control group of 20 children by using the ambulatory EEG method. Whereas 50% of the children with dysphasia experienced paroxysmal activity (PA), only two of the control group did. It is likely that paroxysmal abnormalities and language impairment are related to architectural dysplasia and neuron-migration disturbances. PA is frequent in subjects with receptive developmental dysphasia and may be the cause of language deterioration. When the occurrence of paroxysmal abnormalities during sleep is higher than 8% of total sleep time, we suggest the use of antiepileptic drugs.

Verbal auditory agnosia are rare in clinical practice. Clinically, it characterized by impairment of comprehension and repetition of speech but reading, writing, and spontaneous speech are preserved. So it is distinguished from generalized auditory agnosia by the preserved ability to recognize non verbal sounds. We present the clinical picture of a forty-years-old, right handed woman who developed verbal auditory agnosic after an bilateral temporal ischemic infarcts due to atrial fibrillation by dilated cardiomyopathie. Neurophysiological studies by pure tone threshold audiometry: brainstem auditory evoked potentials and cortical auditory evoked potentials showed sparing of peripheral hearing and intact auditory pathway in brainstem but impaired cortical responses. Cranial CT-SCAN revealed two large hypodenses area involving both cortico-subcortical temporal lobes. Cerebral SPECT using 99mTc-HMPAO as radiotracer showed hypoperfusion just posterior in both frontal lobes nect to Roland's fissure and at level of bitemporal lobes just anterior to Sylvian's fissure.

In 25 patients with subacute sclerosing panencephalitis in various phases of the disease CT and NMR imaging of the brain were done at the same times and the findings were related to clinical symptomatology. NMR imaging, in contrast to CT imaging, demonstrated even very small brain changes in the initial stage. The inflammatory-demyelinizing process begins in SSPE as a rule in the white matter of the occipital lobes, and only later in appears in the vicinity of the anterior horns of the lateral ventricles. Spreading of subcortical changes in the occipital lobes and their later penetration into the parietal lobes causes the development of ideatory apraxia frequent in these cases, and involvement of the cortex of the occipital lobes leads to visual agnosia. The paresis of extremities in later stages not always are correlated with greater intensity of changes in the contralateral cerebral with greater intensity of changes in the contralateral cerebral hemisphere. Hydrocephalus developing after longer duration of the disease is an expression of postinflammatory brain atrophy and not of disturbances in cerebrospinal fluid absorption.

The authors report the case of a 66-year-old woman who developed progressive occipital dysfunction and lately a dementing illness. Brain CT revealed posterior cerebral atrophy. Post-mortem examination showed the characteristic features of Alzheimer's disease, mainly in the posterior areas, relatively sparing the amygdala and Ammon's horn. The occurrence of focal signs and lesions in Alzheimer's disease is emphasized.

We measured the severity of left spatial neglect in 29 patients, 2 to 4 weeks after right cerebral infarction. The severity of neglect increased with both the size of the lesion and the degree of premorbid diffuse cortical atrophy. Recovery over 3 to 5 months from an initially moderate to severe neglect was less complete in patients with cortical atrophy. The importance of lesion size shows that spared areas of the right hemisphere limit the severity and duration of left neglect. The importance of premorbid atrophy suggests that the integrity of the left hemisphere is also essential.

The object of the studies were peculiarities of recognizing visual images by patients with local cerebral lesions under conditions of incomplete sets of the image features, disjunction of the latter, distortion of their spatial arrangement, and unusual spatial orientation of the image as a whole. It was found that elimination of even one essential feature sharply hampered the recognition of the image both by healthy individuals (control), and patients with extraoccipital lesions, whereas elimination of several nonessential features only slowed down the process. In distinction from this the difficulties of the recognition of incomplete images by patients with occipital lesions were directly proportional to the number of the eliminated features irrespective of the latters' significance, i.e. these patients were unable to evaluate the hierarchy of the features. The recognition process in these patients were followed the way of scanning individual features. The reaccumulation and summation. The recognition of the fragmental, spatially distorted and unusually oriented images was found to be affected selectively in patients with parietal lobe affections. The patients with occipital lesions recognized such images practically as good as the ordinary ones.

A case is reported of severe agnosia for verbal and nonverbal sounds in a setting of well-preserved intelligence and transient dysphasic symptoms. The lesions responsible for this disorder were bilateral cerebral infarcts, one of which had virtually destroyed the areas of Wernicke and Broca. The relation between lesions and disabilities is discussed and comparisons made with other published cases.

A case of a severe receptive and expressive amusia in a professional musician following a left hemisphere vascular stroke is reported. Recognition and production of single tones and random tone sequences were found to be surprisingly well preserved. In contrast, the recognition and production of simple rhythm patterns were grossly disturbed. It is suggested that amusia is due to the demonstrated rhythm disturbance. Moreover, it has been found that the defect in recognition and reproduction of rhythms was manifested regardless of the modality of perception, i.e. whether rhythm patterns were perceived by audition, vision, or touch. Therefore, the disturbance of rhythm abilities is supramodal in nature, based probably on the perception of time microintervals. Thus, this type of amusia is a result of a non-auditory supramodal defect, i.e., an impairment of temporal pattern recognition.

Clinical observations suggest left hemispheric compensation for prosopagnosia in patients with isolated right posterior lesions. To test this hypothesis we investigated six patients with right posterior lesions, three with and three without prosopagnosia, with a series of tachistoscopic matching experiments. Faces with and without paraphernalia, shapes, objects and words were presented at different exposure durations (unlimited, 1000, 200, 50 and 20 ms). Prosopagnosia patients performed better than non-prosopagnosia patients if pure faces (eyes, nose and mouth only) were presented for an unlimited time, but performed worse than non-prosopagnosia patients if exposure duration was reduced. Patients with prosopagnosia were especially handicapped when required to match emotional expressions. Both patient groups had no difficulty in matching objects and words, even at short exposure durations. The results are discussed with respect to a possible left hemispheric compensation in prosopagnosia patients.