Inferior Temporal Lesions Research Articles

Reading Strategy for Japanese Kana in a Case of Alexia with Agraphia after a Left Posterior Inferior Temporal Lesion

Reading Strategy for Japanese Kana in a Case of Alexia with Agraphia after a Left Posterior Inferior Temporal Lesion

Lexical retrieval and semantic knowledge in patients with left inferior temporal lobe lesions

Background: It has been proposed that anomia following left inferior temporal lobe lesions may have two different underlying mechanisms with distinct neural substrates. Specifically, naming impairment following damage to more posterior regions (BA 37) has been considered to result from a disconnection between preserved semantic knowledge and phonological word forms (pure anomia), whereas anomia following damage to anterior temporal regions (BAs 38, 20/21) has been attributed to the degradation of semantic representations (semantic anomia). However, the integrity of semantic knowledge in patients with pure anomia has not been demonstrated convincingly, nor were lesions in these cases necessarily confined to BA 37. Furthermore, evidence of semantic anomia often comes from individuals with bilateral temporal lobe damage, so it is unclear whether unilateral temporal lobe lesions are sufficient to produce significant semantic impairment. This research was supported by a Graduate Imaging Fellowship from the University of Arizona and by NIH grants RO1DC008286 and RO1DC07464. Scans were funded through Arizona Alzheimer's Research Consortium, Cognition and NeuroImaging Lab, Arizona Department of Health Services HB2354. Many thanks to Jen Parrott, Kristin Boruff, and Cathy West for their time and assistance. The authors thank Mark Borgstrom, statistical consultant at the University of Arizona, for his assistance with this project. We also thank Chris Rorden for advice regarding lesion analyses. Aims: The main goals of this study were to determine whether anomia following unilateral left inferior temporal lobe damage reflected a loss of semantic knowledge or a post‐semantic deficit in lexical retrieval and to identify the neuroanatomical correlates of the naming impairment. Methods & Procedures: Eight individuals who underwent left anterior temporal lobectomy (L ATL) and eight individuals who sustained left posterior cerebral artery strokes (L PCA) completed a battery of language measures that assessed lexical retrieval and semantic processing, and 16 age‐ and education‐matched controls also completed this battery. High‐resolution structural brain scans were collected to conduct lesion analyses. Outcomes & Results: Performance of L ATL and L PCA patients was strikingly similar, with both groups demonstrating naming performance ranging from moderately impaired to unimpaired. Anomia in both groups occurred in the context of mild deficits to semantic knowledge, which manifested primarily as greater difficulty in naming living things than nonliving things and greater difficulty in processing visual/perceptual as opposed to functional/associative semantic attributes. Lesion analyses indicated that both patient groups sustained damage to anterior inferior temporal lobe regions implicated in semantic processing. Conclusions: These results contribute to a better understanding of the cognitive mechanism of naming impairment in patients with temporal lobe damage and support the notion that pure anomia and semantic anomia represent two endpoints along a continuum of semantic impairment. Unilateral left temporal lobe lesions in our patients resulted in relatively mild semantic deficits that were apparent primarily in lexical production tasks, whereas severe semantic impairment likely requires bilateral temporal lobe damage.

Apnea Caused by Mesial Temporal Lobe Mass Lesions in Infants: Report of 3 Cases

Apnea as an isolated manifestation of seizures is well described in neonates but is only occasionally observed in infants. This article reports 3 infants presenting with apneic events as the main manifestation of seizure, documented by video electroencephalogram, all with mesial temporal lobe lesions. The 3 infants, after normal pregnancy and delivery at term, showed the first apnea at the age of 4 to 10 months. Although the interictal electroencephalogram result was often normal, ictal video electroencephalogram in all infants showed focal rhythmic discharges with or without generalization. Magnetic resonance imaging showed an inferior mesial temporal lobe mass lesion in all infants. All patients underwent lesion removal, and they are seizure free with normal psychomotor development.

Category-specific knowledge deficit for animals in a patient with herpes simplex encephalitis

A large number of brain-damaged patients with heterogeneous category-specific deficits have been reported in literature. This has given rise to different theories concerning the processing of semantic knowledge. In this paper we report the case of K.C. who, after a bout of herpes simplex encephalitis, displayed a category-specific impairment restricted to the knowledge of animals, irrespective of input modality. K.C.'s magnetic resonance imaging (MRI) showed multiple bilateral antero-mesial and inferior temporal lesions. Although she was impaired for both the perceptual (visual and auditory) and functional/associative attributes of animals, she performed normally in an object-reality decision task involving pictures of animals and nonanimals. The dissociation between K.C.'s intact structural description system and her impaired semantic knowledge is interpreted according to hierarchical interactive theory (HIT), which assumes that conceptual knowledge is hierarchically organized in separate but interactive multiple knowledge substores. K.C.'s results indicate that her access to a presemantic structural description system was intact so that her impairment on animal semantic knowledge arose later at a conceptual stage of the object recognition system. Furthermore, K.C.'s deficits indicate selective disruption of a special class of animate concepts within the broad category of living things, which seems best explained by the “domain-specific knowledge theory” proposed by Caramazza and Shelton.

Anomia in patients with left inferior temporal lobe lesions

Background: Damage to left inferior temporal cortex has been associated with naming deficits resulting either from impaired access to phonological word forms (pure anomia) or from degraded semantic knowledge (semantic anomia). Neuropsychological evidence indicates that pure anomia may follow damage to posterior inferior temporal cortex (BA 37), whereas semantic anomia is associated with damage to more anterior temporal lobe regions (BA 20, 21, 38). By contrast, some investigators have suggested that it is the overall severity of anomia, rather than the nature of the underlying cognitive impairment, that is affected by the anterior extent of the lesion.Aims: To examine the naming performance of patients with left inferior temporal lobe damage and determine whether anterior extension of the lesion influences the nature and/or the severity of the naming impairment.Methods & Procedures: Eight participants with focal damage to left inferior temporal cortex completed a battery of language measures that included confrontation naming, semantic processing, and single‐word reading and spelling. Degree and type of anomia was examined relative to anterior lesion extension using both visual inspection and statistical analyses.Outcomes & Results: Naming performance ranged from unimpaired to severely defective, with only two participants demonstrating an additional mild impairment of semantic knowledge. The underlying mechanism of anomia seemed to be degraded access to phonological word forms in all participants, regardless of lesion configuration. The severity of the naming impairment was positively correlated with anterior extension of the lesion towards the temporal pole, although additional analyses suggested that these findings were significantly influenced by participant age. Naming was not correlated with performance on the nonverbal semantic task or any other demographic variable.Conclusions: The behavioural and neuroanatomical findings provide modest support for the hypothesis that a relationship exists between anterior lesion extension and the severity of concomitant anomia in patients with left inferior temporal lobe damage. The data suggest that such lesions may disconnect relatively preserved semantic knowledge from regions critical for access to phonological word forms. However, additional research is needed to discern to what extent age and individual variability temper these effects.

Alexia caused by a fusiform or posterior inferior temporal lesion

We evaluated the alexia and agraphia of three patients with different lesions using Japanese kanji (morphograms) and kana (phonograms) and made a lesion-to-symptom analysis. Patient 1 (pure alexia for both kanji and kana and minor agraphia for kanji after a fusiform lesion) made more paragraphic errors for kanji, whereas patient 2 (alexia with agraphia for kanji after a posterior inferior temporal lesion) showed severe reading and writing disturbances and more agraphic errors for kanji. Brodmann Area 37 was affected in both patients, but in patient 2 the lesion was located lateral to that in patient 1. Patient 3 showed agraphia without alexia after restricted lesion to the angular gyrus. We believe that pure alexia (patient 1) results from a disconnection between the medial fusiform gyrus and posterior inferior temporal area (the lateral fusiform and inferior temporal gyri), whereas alexia with agraphia for kanji (patient 2), corresponding to lexical agraphia in Western countries, results from damage to the posterior inferior temporal area, in which whole-word images of words are thought to be stored. Furthermore, restricted lesion in the angular gyrus (patient 3) does not produce alexia; the alexic symptom of “angular” alexia with agraphia may be the result of damage to the adjacent lateral occipital gyri.

Dissociation of visual and auditory pattern discrimination functions within the cat's temporal cortex.

In ablation-behavior experiments performed in adult cats, a double dissociation was demonstrated between ventral posterior suprasylvian cortex (vPS) and temporo-insular cortex (TI) lesions on complex visual and auditory tasks. Lesions of the vPS cortex resulted in deficits at visual pattern discrimination, but not at a difficult auditory discrimination. By contrast, TI lesions resulted in profound deficits at discriminating complex sounds, but not at discriminating visual patterns. This pattern of dissociation of deficits in cats parallels the dissociation of deficits after inferior temporal versus superior temporal lesions in monkeys and humans.

Visual-imitative dissociation apraxia

Liepmann posited that, in right handers, the left parietal lobe contains movement formulas or representations. Therefore, performance failures may be induced by degraded representations, a failure of these representations to influence motor systems or a failure of stimuli to fully access these representations. Imitation may help the performance of subjects with degraded representations. However, patients who have impaired visual access to movement representations may perform more poorly with imitation than to verbal command. Trajectories of repetitive ‘slicing’ gestures made by a previously reported subject (Raymer et al.) with an infarction in the left visual association cortex (left occipital and inferior temporal lobe) that spared the parietal lobe were contrasted with those of three apraxic subjects with lesions that included the left parietal lobe and four non-brain-damaged control subjects. All subjects were asked to produce the gesture to verbal command and to imitation. Movements of the left hand, wrist, elbow and shoulder were digitized from neighboring views, reconstructed in three dimensions, and analysed graphically and numerically. The apraxic subjects with left parietal damage were unable to maintain the proper linearity and spatiotemporal attributes of their wrist motions and showed interjoint coordination deficits. Their deficits were most pronounced to verbal command, with their movements improving though remaining poorly performed when they imitated. The subject with the left occipital and inferior temporal lesion that spared parietal cortex, however, showed an opposite pattern. This subject exhibited close to normal performance when producing the movement to verbal command, but significant deficits when imitating.

The effects of visual cortex lesions on the perception of rotated shapes

Monkeys with inferior temporal cortex lesions cannot discriminate between different shapes (e.g., + vs. 0) but can discriminate between shapes that differ only in orientation (e.g., 6 vs. 9). Lesions of the parietal cortex, on the other hand, impair the discrimination of rotated shapes but spare the ability to discriminate between different shapes. A similar dissociation is found between some visual agnosics who can match but not identify rotated views of objects and other patients who can identify and discriminate objects only if the view is conventional; any change in orientation disrupts performance. In this paper we argue that two mechanisms may be available for the perception of rotated shapes. Which mechanism is used depends on the degree of rotation. It is suggested that the different effects of parietal and temporal lesions reflect the relative contributions of the two areas to the task and disrupt different stages of the two strategies used. A framework for the cortical processing of rotated shapes in the non-human primate is presented.

Lesions of the Superior Temporal Cortical Motion Areas Impair Speed Discrimination in the Macaque Monkey

The effects of circumscribed lesions of the superior temporal cortical motion areas on speed discrimination were tested in three macaque monkeys using both moving random-textured patterns and moving bars. The lesions, which included the middle temporal visual area, the adjacent medial superior temporal visual area and the fundus superior temporal visual area, produced a severe and lasting deficit in speed discrimination when tested with the random patterns. In contrast, deficits were smaller when tested with moving bars. Control lesions of the inferior temporal cortex in two monkeys had little effect on speed discrimination. There was no clear deficit following inferior temporal or superior temporal sulcus lesions on a vernier acuity task. These experiments indicate that the middle temporal and adjacent areas play a crucial role in speed discrimination and that lesion effects depend on the cues available to the animals.

Naming difficulties in alexia with agraphia for kanji after a left posterior inferior temporal lesion

Naming difficulties in alexia with agraphia for kanji after a left posterior inferior temporal lesion

Naming difficulties in alexia with agraphia for kanji after a left posterior inferior temporal lesion.

The case is described of a patient with alexia and agraphia for kanji, and severe anomia after a subcortical haemorrhage in the left posterior inferior temporal area. Magnetic resonance imaging at four months after onset showed a lesion in the inferior temporal and fusiform gyri, extending from the temporo-occipital junction toward the anterior third of the temporal lobe. Comparison with other reported cases of alexia with agraphia and anomia made it clear that when accompanied by severe anomia, the lesions extended either forward to the anterior part of the middle temporal gyrus or medially to the parahippocampal gyrus. It is suggested that the disconnection of association fibres between the parahippocampal, fusiform, middle, and inferior temporal gyri, especially between the parahippocampal gyrus and the other temporal gyri, or the cortical damage to the posterior part of these gyri is essential for the production of anomia.

The effects of inferior temporal and dorsolateral frontal lesions on serial-order behavior and visual imagery in monkeys

Four monkeys were trained preoperatively on a serial-order task to respond to a set of five visual stimuli in a fixed sequence independent of their location. They were then given a test of visual imagery in which only two of the five stimuli appeared at a time, and the animals were required to respond to them in the order in which they appeared in the original sequence. The monkeys then received bilateral lesions of either inferior temporal cortex or dorsolateral frontal cortex. Dorsolateral frontal lesions had no effect on either serial-order behavior or visual imagery. In contrast, inferior temporal lesions severely impaired serial-order behavior. Once the serial-order task was relearned, however, the inferior temporal animals were completely normal on the test of visual imagery.

The role of monkey inferior parietal cortex in visual discrimination of identity and orientation of shapes

Three cynomolgus monkeys (Macaca fascicularis) were tested for their visual learning ability following bilateral lesions to the inferior parietal cortex. In discrimination learning with patterns differing from each other in form and colour their performance was normal. In discriminating monochromatic patterns their performance depended on the nature of the pattern discrimination; when the discriminanda were different shapes (e.g. x,v) they performed well, while with discriminanda which differed only in the orientation of the shape (e.g. p,d) they performed relatively badly. These results were compared to the previously reported results of normal animals and animals with inferior temporal lesions performing the same task. The ratio of errors in orientation discrimination to errors in shape discrimination was significantly higher than normal in the group with parietal lesions, and significantly lower than normal in the group with inferior temporal lesions. These results suggest that the roles of inferior temporal and inferior parietal cortex in the discrimination of shape and orientation are complementary.

Visual impairments in macaques following inferior temporal lesions are exacerbated selectively by additional damage to superior temporal sulcus

The present study examined the behavioural effects of removing the inferior temporal cortex (area TE) either on its own or in combination with the adjacent fundus and upper bank of the superior temporal sulcus (area STP). Comparisons with preoperative behaviour showed that the addition of superior temporal sulcal damage led to an increase in visual components of the Klüver-Bucy syndrome, i.e. an increased tendency to touch and examine objects coupled with a decrease in emotional reactivity, but no excessive orality, changes in food preference, or coprophagia. No group differences were found in the learning of 3 pattern discriminations, but the animals with additional superior temporal sulcal lesions were more impaired than the others on 3 colour discriminations, successive reversals of an object discrimination, and a learning-set task. These findings indicate that STP provides an important route, independent of the route via TE, by which visual information can reach limbic structures to evoke affective responses and contribute to visual learning.

Alexia with agraphia due to the left posterior inferior temporal lobe lesion—Neuropsychological analysis and its pathogenetic mechanisms

We report three cases of alexia with agraphia due to the left posterior inferior temporal lesions. In Case 1, the reading disability was more prominent in the use of Kana than in the use of Kanji, which is similar to previously reported cases of alexia with agraphia due to angular gyrus lesion. In Cases 2 and 3, by contrast, the reading disability was more prominent in the use of Kanji than in the use of Kana. In spontaneous writing and dictation, the disability was more pronounced in the use of Kanji compared with the use of Kana. In each of the three cases, the CT scan and positron emission tomography showed a localized lesion in the lower part of the left posterior temporal lobe. A typical form of an alexia with agraphia could be caused not only by the left angular lesion but also by the left posterior inferior temporal lesion. We discuss the neuropsychological analysis and pathogenetic mechanisms of alexia with agraphia due to the left posterior inferior temporal lesion in the comparison of alexia with agraphia caused by the left angular lesion.

Dissociation of the effects of inferior temporal and limbic lesions on object discrimination learning with 24-h intertrial intervals

Monkeys with bilateral ablations of the inferior temporal cortical area TE were trained on a visual discrimination task thought to measure non-cognitive habit formation. The task consisted of 20 object discriminations presented concurrently, but at the rate of only one trial on each per day; successive trials on a given discrimination were thus separated by 24-h intertrial intervals. Performance on this task by the animals with TE lesions was compared to that of both normal control monkeys and monkeys that had sustained bilateral removals of the amygdala and hippocampus. In contrast to the latter animals, which learned the 24-h intertrial interval task about as quickly as the normal controls, monkeys with area TE removals were markedly impaired. Taken together with earlier findings demonstrating that ablation of area TE impairs visual recognition memory, the present results suggest that area TE contributes not only, like limbic structures, to a cognitive memory system, but also, unlike limbic structures, to a non-cognitive habit system. Evidence is reviewed suggesting that this latter system may involve a corticostriatal circuit.

Effects of inferior temporal lesions on discrimination of stimuli differing in orientation

Monkeys with inferior temporal (IT) cortex lesions were compared with normal and operated control monkeys on a series of two-choice visual discrimination problems. In some problems, the discriminanda were different patterns or objects whereas, in other problems, the discriminanda were identical patterns or objects presented in different orientations. The animals with IT lesions were significantly impaired in learning to discriminate the different patterns and objects; however, they were not impaired in learning to discriminate stimuli which differed only in orientation by 60 degrees or more. These results help to specify further the role of the IT cortex in visual associative learning by demonstrating that there are some types of visual discriminations which are not sensitive to IT lesions.

Stimulus equivalence after inferior temporal lesions in monkeys.

Monkeys with inferior temporal cortex lesions and unoperated monkeys were trained to discriminate pairs of objects and then tested for transfer after the original discriminanda were made larger or smaller, rotated, or presented as two-dimensional projections. The two groups of monkeys transferred equally well to the discriminanda altered in size or orientation, but only the unoperated animals transferred to the two-dimensional representation.

Effects of inferior temporal lesions on visual discrimination performance in monkeys with complete and incomplete striate cortex ablations.

Effects of inferior temporal lesions on visual discrimination performance in monkeys with complete and incomplete striate cortex ablations.