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Auditory Agnosia With Anosognosia
Abstract
A 66-year-old female medical doctor suffered two consecutive cardioembolic strokes, initially affecting the right frontal lobe and the right insula, followed by a lesion in the left temporal lobe. The patient presented with distinctive phenomenology of general auditory agnosia with anosognosia for the deficit. She did not understand verbal commands and her answers to oral questions were fluent but unrelated to the topic. However, she was able to correctly answer written questions, name objects, and fluently describe their purpose, which is characteristic for verbal auditory agnosia. She was also unable to recognise environmental sounds or to recognise and repeat any melody. This inability is suggestive of environmental sound agnosia and amusia, respectively. Surprisingly, she was not aware of the problems, not asking any questions regarding her symptoms, and avoiding discussing her inability to understand spoken language, which is indicative of anosognosia. The deficits in our patient evolved from generalized AA with distinct pattern of recovery. The verbal auditory agnosia was the first to resolve, followed by environmental sound agnosia. Amusia persisted the longest. The patient was clinically assessed from the first day of symptom onset and the evolution of symptoms was video documented. We give a detailed account of the patient’s behaviour and provide results of audiological and neuropsychological evaluations. We discuss the anatomy of auditory agnosia and anosognosia relevant to the case. This case study may serve to better understand auditory agnosia in clinical settings. It is important to distinguish AA from Wernicke’s aphasia, because use of written language may enable normal communication.
... [2,8,12,[15][16][17][18][19]29,[33][34][35]37,43,46,48], while others evolved to pure word deafness (11/36.6%) [7,[9][10][11]13,18,21,22,24,31,36,39,41,42]. Oral conversation was regained in six (20%) of the patients [7,20,25,27,28,32,42,43]. ...
... [7,[9][10][11]13,18,21,22,24,31,36,39,41,42]. Oral conversation was regained in six (20%) of the patients [7,20,25,27,28,32,42,43]. In two patients, CD was transient, one following a bilateral middle cerebral vasospasm secondary to an aneurysm rupture [30] and the other two after a unilateral ischemic stroke [38,40]. ...
Background: Stroke is the leading cause of cortical deafness (CD), the most severe form of central hearing impairment. CD remains poorly characterized and perhaps underdiagnosed. We perform a systematic review to describe the clinical and radiological features of stroke-associated CD.
Methods: PubMed and the Web of Science databases were used to identify relevant publications up to 30 June 2021 using the MeSH terms: “deafness” and “stroke”, or “hearing loss” and “stroke” or “auditory agnosia” and “stroke”. Results: We found 46 cases, caused by bilateral lesions within the central auditory pathway, mostly located within or surrounding the superior temporal lobe gyri and/or the Heschl’s gyri (30/81%). In five (13.51%) patients, CD was caused by the subcortical hemispheric and in two (0.05%) in brainstem lesions. Sensorineural hearing loss was universal. Occasionally, a misdiagnosis by peripheral or psychiatric disorders occurred. A few (20%) had clinical improvement, with a regained oral conversation or evolution to pure word deafness (36.6%). A persistent inability of oral communication occurred in 43.3%. A full recovery of conversation was restricted to patients with subcortical lesions.
Conclusions: Stroke-associated CD is rare, severe and results from combinations of cortical and subcortical lesions within the central auditory pathway. The recovery of functional hearing occurs, essentially, when caused by subcortical lesions.
... Cortical deafness can be the presenting sign of an auditory processing disorder, but often evolves toward less severe forms (gAA, vAA, and nvAA) [57,68,69]. Intriguingly, in several bilateral cases with persistent cortical deafness, right hemisphere damage involved structures critical for attentional mechanisms [28,[70][71][72], and in a recent case, anosognosia has been reported in a patient with severe AA [73]. In addition, right-sided damage to temporal, but also parietal and frontal regions, can cause auditory neglect [74] whose presence may enhance auditory processing difficulties. ...
Purpose of Review
To investigate the neurofunctional correlates of pure auditory agnosia and its varieties (global, verbal, and nonverbal), based on 116 anatomoclinical reports published between 1893 and 2022, with emphasis on hemispheric lateralization, intrahemispheric lesion site, underlying cognitive impairments.
Recent Findings
Pure auditory agnosia is rare, and observations accumulate slowly. Recent patient reports and neuroimaging studies on neurotypical subjects offer insights into the putative mechanisms underlying auditory agnosia, while challenging traditional accounts.
Summary
Global auditory agnosia frequently results from bilateral temporal damage. Verbal auditory agnosia strictly correlates with language-dominant hemisphere lesions. Damage involves the auditory pathways, but the critical lesion site is unclear. Both the auditory cortex and associative areas are reasonable candidates, but cases resulting from brainstem damage are on record. The hemispheric correlates of nonverbal auditory input disorders are less clear. They correlate with unilateral damage to either hemisphere, but evidence is scarce. Based on published cases, pure auditory agnosias are neurologically and functionally heterogeneous. Phenotypes are influenced by co-occurring cognitive impairments. Future studies should start from these facts and integrate patient data and studies in neurotypical individuals.
... Unauthorized reproduction of this article is prohibited brainstem response (ABR) at 60 dB HL was normal. The patient displayed normal perception of man-made, natural, and music sounds.1,2 Although hearing aids improved thresholds to 30 dB HL, single-syllable word recognition remained poor. ...
Chromosome 9 open reading frame 72 ( C9orf72 ) gene mutations have been typically associated with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), but recent studies suggest their involvement in other disorders. This report describes a family with an autosomal dominant pattern of inheritance of progressive verbal auditory agnosia due to GGGGCC repeat expansion in C9orf72. A 60-year-old right-handed male truck driver presented with slowly progressive poor speech perception for 8 years, which became most troublesome when receiving verbal orders over the phone. He had difficulty recognizing single-syllable spoken words beyond his hearing loss, but had no problem understanding complex written language. He had a heterozygous pathogenic variant carrying 160 hexanucleotide repeats in the C9orf72 gene. His family history included his deceased mother with similar symptoms that had progressed over 30 years, as well as his older brother and youngest sister who experienced speech perception difficulty beginning in their early fifties. His asymptomatic younger brother had a heterozygous 2 repeat in the C9orf72 gene, while his symptomatic youngest sister had a heterozygous 159 repeat. The patient and his sister exhibited more pronounced cortical thinning in the frontotemporoparietal areas. The discrepancy observed between the distribution of atrophy and the presentation of symptoms in patients with C9orf72 pathogenic repeat expansion may be attributable to the slow progression of their clinical course over time. The variable symptom presentation of C9orf72 pathogenic repeat expansion highlights the importance of considering this mutation as a potential cause of autosomal dominant degenerative brain diseases beyond FTD and ALS.
The functional and neural organisation of auditory knowledge is relatively poorly understood. The breakdown of conceptual knowledge in semantic dementia has revealed that pre-morbid expertise influences the extent to which knowledge is differentiated. Whether this principle applies to a similar extent in the auditory domain is not yet known. Previous reports of patients with impaired auditory vs. intact visual expert knowledge suggest that expertise may have differential effects upon the organisation of auditory and visual knowledge. An equally plausible alternative, however, is that auditory knowledge is simply more vulnerable to deterioration. Thus, expertise effects in the auditory domain may not yet have been observed because knowledge of auditory expert vs. non-expert knowledge has yet to be compared. We had the opportunity to address this issue by studying SA, a patient with semantic dementia and extensive pre-morbid knowledge of birds. We undertook a systematic investigation of SA's auditory vs. visual knowledge from matched expert vs. non-expert categories. Relative to a group of 10 age, education and IQ matched bird experts, SA showed impaired auditory vs. intact visual avian knowledge, despite intact basic auditory perceptual abilities. This was explained by independent effects of modality and expertise. Thus, he was also disproportionately impaired for auditory vs. visual knowledge of items from non-expert categories. In both auditory and visual modalities, his performance was relatively more impaired on tests of non-expert vs. expert knowledge. These findings suggest that, while auditory knowledge may be more vulnerable to deterioration, expertise modulates visual and auditory knowledge to a similar extent.
Rationale:
Verbal auditory agnosia is the selective inability to recognize verbal sounds. Patients with this disorder lose the ability to understand language, write from dictation, and repeat words with reserved ability to identify nonverbal sounds. However, to the best of our knowledge, there was no report about verbal auditory agnosia in adult patient with traumatic brain injury.
Patient concerns:
He was able to clearly distinguish between language and nonverbal sounds, and he did not have any difficulty in identifying the environmental sounds. However, he did not follow oral commands and could not repeat and dictate words. On the other hand, he had fluent and comprehensible speech, and was able to read and understand written words and sentences.
Diagnosis:
Verbal auditory agnosia INTERVENTION:: He received speech therapy and cognitive rehabilitation during his hospitalization, and he practiced understanding of verbal language by providing written sentences together.
Outcomes:
Two months after hospitalization, he regained his ability to understand some verbal words. Six months after hospitalization, his ability to understand verbal language was improved to an understandable level when speaking slowly in front of his eyes, but his comprehension of verbal sound language was still word level, not sentence level.
Lessons:
This case gives us the lesson that the evaluation of auditory functions as well as cognition and language functions important for accurate diagnosis and appropriate treatment, because the verbal auditory agnosia tends to be easily misdiagnosed as hearing impairment, cognitive dysfunction and sensory aphasia.
Today’s audiological functional diagnostics is based on a variety of hearing tests, whose large number takes account of the variety of malfunctions of a complex sensory organ system and the necessity to examine it in a differentiated manner and at any age of life. The objective is to identify nature and origin of the hearing loss and to quantify its extent as far as necessary to dispose of the information needed to initiate the adequate medical (conservative or operational) treatment or the provision with technical hearing aids or prostheses. Moreover, audiometry provides the basis for the assessment of impairment and handicap as well as for the calculation of the degree of disability. In the present overview, the current state of the method inventory available for practical use is described, starting from basic diagnostics over to complex special techniques. The presentation is systematically grouped in subjective procedures, based on psychoacoustic exploration, and objective methods, based on physical measurements: preliminary hearing tests, pure tone threshold, suprathreshold processing of sound intensity, directional hearing, speech understanding in quiet and in noise, dichotic hearing, tympanogram, acoustic reflex, otoacoustic emissions and auditory evoked potentials. Apart from a few still existing gaps, this method inventory covers the whole spectrum of all clinically relevant functional deficits of the auditory system.
Pure Word Deafness (PWD) is a rare disorder, characterized by selective loss of speech input processing. Its most common cause is temporal damage to the primary auditory cortex of both hemispheres, but it has been reported also following unilateral lesions. In unilateral cases, PWD has been attributed to the disconnection of Wernicke's area from both right and left primary auditory cortex. Here we report behavioral and neuroimaging evidence from a new case of left unilateral PWD with both cortical and white matter damage due to a relatively small stroke lesion in the left temporal gyrus. Selective impairment in auditory language processing was accompanied by intact processing of nonspeech sounds and normal speech, reading and writing. Performance on dichotic listening was characterized by a reversal of the right-ear advantage typically observed in healthy subjects. Cortical thickness and gyral volume were severely reduced in the left superior temporal gyrus (STG), although abnormalities were not uniformly distributed and residual intact cortical areas were detected, for example in the medial portion of the Heschl's gyrus. Diffusion tractography documented partial damage to the acoustic radiations (AR), callosal temporal connections and intralobar tracts dedicated to single words comprehension. Behavioral and neuroimaging results in this case are difficult to integrate in a pure cortical or disconnection framework, as damage to primary auditory cortex in the left STG was only partial and Wernicke's area was not completely isolated from left or right-hemisphere input. On the basis of our findings we suggest that in this case of PWD, concurrent partial topological (cortical) and disconnection mechanisms have contributed to a selective impairment of speech sounds. The discrepancy between speech and non-speech sounds suggests selective damage to a language-specific left lateralized network involved in phoneme processing.
Although, acquired amusia is a common deficit following stroke, relatively little is still known about its precise neural basis, let alone to its recovery. Recently, we performed a voxel-based lesion-symptom mapping (VLSM) and morphometry (VBM) study which revealed a right lateralized lesion pattern, and longitudinal gray matter volume (GMV) and white matter volume (WMV) changes that were specifically associated with acquired amusia after stroke. In the present study, using a larger sample of stroke patients (N = 90), we aimed to replicate and extend the previous structural findings as well as to determine the lesion patterns and volumetric changes associated with amusia recovery. Structural MRIs were acquired at acute and 6-month post-stroke stages. Music perception was behaviorally assessed at acute and 3-month post-stroke stages using the Scale and Rhythm subtests of the Montreal Battery of Evaluation of Amusia (MBEA). Using these scores, the patients were classified as non-amusic, recovered amusic, and non-recovered amusic. The results of the acute stage VLSM analyses and the longitudinal VBM analyses converged to show that more severe and persistent (non-recovered) amusia was associated with an extensive pattern of lesions and GMV/WMV decrease in right temporal, frontal, parietal, striatal, and limbic areas. In contrast, less severe and transient (recovered) amusia was linked to lesions specifically in left inferior frontal gyrus as well as to a GMV decrease in right parietal areas. Separate continuous analyses of MBEA Scale and Rhythm scores showed extensively overlapping lesion pattern in right temporal, frontal, and subcortical structures as well as in the right insula. Interestingly, the recovered pitch amusia was related to smaller GMV decreases in the temporoparietal junction whereas the recovered rhythm amusia was associated to smaller GMV decreases in the inferior temporal pole. Overall, the results provide a more comprehensive picture of the lesions and longitudinal structural changes associated with different recovery trajectories of acquired amusia.
Objectives
To determine the incidence of brain edema after ischaemic stroke and its impact on the outcome of patients in the acute phase of ischaemic stroke.
Patients and Methods
We retrospectively analyzed 114 patients. Ischaemic stroke and brain edema are verified by computed tomography. The severity of stroke was determined by National Institutes of Health Stroke Scale. Laboratory findings were made during the first four days of hospitalization, and complications were verified by clinical examination and additional tests.
Results
In 9 (7.9%) patients developed brain edema. Pneumonia was the most common complication (12.3%). Brain edema had a higher incidence in women, patients with hypertension and elevated serum creatinine values, and patients who are suffering from diabetes. There was no significant correlation between brain edema and survival in patients after acute ischaemic stroke. Patients with brain edema had a significantly higher degree of neurological deficit as at admission, and at discharge (p = 0.04, p = 0.004).
Conclusion
The cerebral edema is common after acute ischaemic stroke and no effect on survival in the acute phase. The existence of brain edema in acute ischaemic stroke significantly influence the degree of neurological deficit.
Healthy volunteers engaged in self-referential tasks such as reflecting on their personality traits exhibit mostly left lateralized brain activation, yet patients with lack of awareness of their deficit suffer from predominantly right hemisphere damage. How can the same basic process of self-awareness be associated with opposite sides of the brain? Anosognosia and self-awareness substantially differ on important dimensions and thus should not be equated. It is proposed that (1) anosognosia does not actually result from uniquely right hemisphere damage; (2) self-awareness and anosognosia do not constitute unitary concepts and encompass multiple other related processes, most likely associated with activity in distinct anatomical networks; and (3) impaired awareness of deficit is mostly caused by problems with self-monitoring, pre-/post-brain damage comparisons of performance, and episodic memory, and is more passive, unintentional, and about the body. Self-awareness produced by inviting participants to intentionally and actively think about more mental aspects of the self relies on judgements, inferential reasoning, imagination, and semantic memory. Consequently, the "self-awareness-anosognosia" paradox is only apparent. Furthermore, the claim that healthy self-awareness is located in the right hemisphere because anosognosia results from damage to this side of the brain must be fallacious.
Cerebral activation was measured with positron emission tomography in ten human volunteers. The primary auditory cortex showed increased activity in response to noise bursts, whereas acoustically matched speech syllables activated secondary auditory cortices bilaterally. Instructions to make judgments about different attributes of the same speech signal resulted in activation of specific lateralized neural systems. Discrimination of phonetic structure led to increased activity in part of Broca's area of the left hemisphere, suggesting a role for articulatory recoding in phonetic perception. Processing changes in pitch produced activation of the right prefrontal cortex, consistent with the importance of right-hemisphere mechanisms in pitch perception.
Objective: To use functional magnetic resonance imaging to map the auditory cortical fields that are activated, or nonreactive, to sounds in patient M.L., who has auditory agnosia caused by trauma to the inferior colliculi. Background: The patient cannot recognize speech or environmental sounds. Her discrimination is greatly facilitated by context and visibility of the speaker's facial movements, and under forcedchoice testing. Her auditory temporal resolution is severely compromised. Her discrimination is more impaired for words differing in voice onset time than place of articulation. Words presented to her right ear are extinguished with dichotic presentation; auditory stimuli in the right hemifield are mislocalized to the left. Methods: We used functional magnetic resonance imaging to examine cortical activations to different categories of meaningful sounds embedded in a block design. Results: Sounds activated the caudal sub-area of M.L.'s primary auditory cortex (hA1) bilaterally and her right posterior superior temporal gyrus (auditory dorsal stream), but not the rostral subarea (hR) of her primary auditory cortex or the anterior superior temporal gyrus in either hemisphere (auditory ventral stream). Conclusions: Auditory agnosia reflects dysfunction of the auditory ventral stream. The ventral and dorsal auditory streams are already segregated as early as the primary auditory cortex, with the ventral stream projecting from hR and the dorsal stream from hA1. M.L.'s leftward localization bias, preserved audiovisual integration, and phoneme perception are explained by preserved processing in her right auditory dorsal stream.
The auditory efferent system originates in the auditory cortex and projects to the medial geniculate body (MGB), inferior colliculus (IC), cochlear nucleus (CN) and superior olivary complex (SOC) reaching the cochlea through olivocochlear (OC) fibers. This unique neuronal network is organized in several afferent-efferent feedback loops including: the (i) colliculo-thalamic-cortico-collicular; (ii) cortico-(collicular)-OC; and (iii) cortico-(collicular)-CN pathways. Recent experiments demonstrate that blocking ongoing auditory-cortex activity with pharmacological and physical methods modulates the amplitude of cochlear potentials. In addition, auditory-cortex microstimulation independently modulates cochlear sensitivity and the strength of the OC reflex. In this mini-review, anatomical and physiological evidence supporting the presence of a functional efferent network from the auditory cortex to the cochlear receptor is presented. Special emphasis is given to the corticofugal effects on initial auditory processing, that is, on CN, auditory nerve and cochlear responses. A working model of three parallel pathways from the auditory cortex to the cochlea and auditory nerve is proposed.
Disorders of audition stand at a crossroads between neurology, audiology, psychiatry and ENT. It is not uncommon for patients to ‘fall between the cracks’ of the referral pathway, and to become increasingly frustrated when specialties cannot decide who is responsible for them. The aim of this ‘How to understand it’ article is to demystify central auditory disorders for neurologists, and to show that they can be assessed like any other neurological symptom, based on a consideration of the anatomy and physiology of the auditory pathway. To illustrate this we describe the case history of a patient who had lost the ability to recognise and appreciate music who presented to an audiology clinician (DMB), who then sought neurology support (TEC, TDG). We elucidated the nature of the deficit in the analysis of sound patterns using psychophysics, but the deficits could have been predicted by a consideration of the anatomy and physiology of the auditory system.
The patient was a 48-year-old, right-handed salesman who was a keen listener to popular music. He had no previous symptoms relating to environmental sound or speech perception.
He suffered two low-speed road traffic accidents in a single journey on the way to work. The first was nose-to-tail, as he failed to see the car in front stop in traffic, and the second was nose-to-nose with a parked car. After the second incident, he pulled over and called an ambulance, as he felt ‘disorientated’. The ambulance crew found him to be confused and complaining of headache and nausea, so brought him to hospital. Initial physical examination showed no injuries but his blood pressure was 230/120 mm Hg. Neurological examination identified a left upper motor neurone facial palsy with preserved limb power, left-sided sensory and visual neglect, left-sided hyper-reflexia and left extensor plantar response. Immediate unenhanced CT of the head …
Hypoacusis is the most prevalent sensory disability in the world and consequently, it can lead to impede speech in human beings. One best approach to tackle this issue is to conduct early and effective hearing screening test using Electroencephalogram (EEG). EEG based hearing threshold level determination is most suitable for persons who lack verbal communication and behavioral response to sound stimulation. Auditory evoked potential (AEP) is a type of EEG signal emanated from the brain scalp by an acoustical stimulus. The goal of this review is to assess the current state of knowledge in estimating the hearing threshold levels based on AEP response. AEP response reflects the auditory ability level of an individual. An intelligent hearing perception level system enables to examine and determine the functional integrity of the auditory system. Systematic evaluation of EEG based hearing perception level system predicting the hearing loss in newborns, infants and multiple handicaps will be a priority of interest for future research.
Word-deafness (verbal auditory agnosia, agnosia for speech, agnosia for acoustic language) is the most devastating of all the disorders of the central auditory pathway in children, whether the disorder is present from infancy (dysphasia) or is acquired (aphasia). Typically, word-deaf children are mute and understand little or nothing of what is said to them; they resemble deaf children in this respect, except that it is their brains that are abnormal rather than their ears. Judging from personal experience and from the literature, there are many more word-deaf children than adults. The literature on adults consists entirely of isolated case reports. While there are now over a hundred descriptions of children with so-called epileptic aphasia, these have been summarized in several recent reports (e.g., Holmes, McKeever, & Saunders, 1981; Dugas et al., 1982; Dulac, Billard, & Arthuis, 1983; Aicardi, in press). Epileptic aphasia produces the most dramatic form of word-deafness in the pediatric age-group, yet it may not be the most frequent since there are no data on the prevalence of word-deafness among autistic and congenitally dysphasic children. The ability to hear, process, and comprehend speech is indispensable for normal language acquisition. Sustained speech input is also required for the maintenance of speech during the preschool years. Most congenitally deaf children fail to acquire speech (and language) unless educated through the visual channel; the same is true of word-deaf infants. Preschool children who are deafened suddenly by meningitis become mute immediately or within days; so do preschool children with acute epileptic aphasia. Abrupt onset of deafness or word-deafness may result in a dramatic decrease in verbal output, even in older children, despite the advantage provided by better practiced speech and by a sparing of the ability to process language through the visual modality (reading and writing). Adolescents and adults with acquired deafness do not lose their speech, although its acoustic properties will eventually deteriorate somewhat through lack of feedback. Word-deaf adults speak but complain that they don't know what they are saying. There is controversy as to whether word-deafness, in both its developmental and acquired forms, should be considered an auditory disorder or a linguistic disorder specific to the decoding of acoustic language (phonol-ogy). This controversy exists not only for word-deafness in children but also for the acquired syndrome in adults; pure syndromes of "cortical" deafness, auditory agnosia, and verbal auditory agnosia are exceedingly rare, if they exist at all. The reason for this lack of "pure" cases is that the cerebral insults responsible for these syndromes are not selective (damage may be cortical or subcortical in either hemisphere or both). Pathology often involves areas adjacent to the auditory pathway, so that most patients have associated deficits, especially during the acute phase of the illness. These concomitant signs may complicate the interpretation of the language deficit. Occasional word-deaf adults may be "cortically" deaf, most have an auditory agnosia, and they may have a hemiparesis or a transient aphasia as well. Children with congenital or acquired word-deafness almost never have a demonstrable structural lesion on computerized tomography (CT); at best, evidence for localization of dysfunction is an abnormal EEG. Word-deaf children are difficult to test behaviorally because of their age, lack of comprehension of speech, and frequent behavior disorders. In order to gain an understanding of the children's deficits, it has been necessary to consider evidence from adults in whom word-deafness was the result of a stroke and in whom the extent of cerebral infarction was demonstrable on CT or at autopsy. Adults with word-deafness can be alert and cooperative, making detailed testing possible. Furthermore, they can describe what they are experiencing.
Previous research has demonstrated that altered auditory feedback (AAF) disrupts music performance and causes disruptions in both action planning and the perception of feedback events. It has been proposed that this disruption occurs because of interference within a shared representation for perception and action (Pfordresher, 2006). Studies reported here address this claim from the standpoint of error monitoring. In Experiment 1 participants performed short melodies on a keyboard while hearing no auditory feedback, normal auditory feedback, or alterations to feedback pitch on some subset of events. Participants overestimated error frequency when AAF was present but not for normal feedback. Experiment 2 introduced a concurrent load task to determine whether error monitoring requires executive resources. Although the concurrent task enhanced the effect of AAF, it did not alter participants’ tendency to overestimate errors when AAF was present. A third correlational study addressed whether effects of AAF are reduced for a subset of the population who may lack the kind of perception/action associations that lead to AAF disruption: poor-pitch singers. Effects of manipulations similar to those presented in Experiments 1 and 2 were reduced for these individuals. We propose that these results are consistent with the notion that AAF interference is based on associations between perception and action within a forward internal model of auditory-motor relationships.
Singing provides a unique opportunity to examine music performance—the musical instrument is contained wholly within the body, thus eliminating the need for creating artificial instruments or tasks in neuroimaging experiments. Here, more than two decades of voice and singing research will be reviewed to give an overview of the sensory-motor control of the singing voice, starting from the vocal tract and leading up to the brain regions involved in singing. Additionally, to demonstrate how sensory feedback is integrated with vocal motor control, recent functional magnetic resonance imaging (fMRI) research on somatosensory and auditory feedback processing during singing will be presented. The relationship between the brain and singing behavior will be explored also by examining: (1) neuroplasticity as a function of various lengths and types of training, (2) vocal amusia due to a compromised singing network, and (3) singing performance in individuals with congenital amusia. Finally, the auditory-motor control network for singing will be considered alongside dual-stream models of auditory processing in music and speech to refine both these theoretical models and the singing network itself.
The control of vocalization is critically dependent on auditory feedback. Here, we determined the human peri-Sylvian speech network that mediates feedback control of pitch using direct cortical recordings. Subjects phonated while a real-time signal processor briefly perturbed their output pitch (speak condition). Subjects later heard the same recordings of their auditory feedback (listen condition). In posterior superior temporal gyrus, a proportion of sites had suppressed responses to normal feedback, whereas other spatially independent sites had enhanced responses to altered feedback. Behaviorally, speakers compensated for perturbations by changing their pitch. Single-trial analyses revealed that compensatory vocal changes were predicted by the magnitude of both auditory and subsequent ventral premotor responses to perturbations. Furthermore, sites whose responses to perturbation were enhanced in the speaking condition exhibited stronger correlations with behavior. This sensorimotor cortical network appears to underlie auditory feedback-based control of vocal pitch in humans.
The mechanisms and functional anatomy underlying the early stages of speech perception are still not well understood. Auditory agnosia is a deficit of auditory object processing defined as a disability to recognize spoken languages and/or nonverbal environmental sounds and music despite adequate hearing while spontaneous speech, reading and writing are preserved. Usually, either the bilateral or unilateral temporal lobe, especially the transverse gyral lesions, are responsible for auditory agnosia. Subcortical lesions without cortical damage rarely causes auditory agnosia. We present a 73-year-old right-handed male with generalized auditory agnosia caused by a unilateral subcortical lesion. He was not able to repeat or dictate but to perform fluent and comprehensible speech. He could understand and read written words and phrases. His auditory brainstem evoked potential and audiometry were intact. This case suggested that the subcortical lesion involving unilateral acoustic radiation could cause generalized auditory agnosia.
Pure word deafness (PWD) is a rare neurological syndrome characterized by severe difficulties in understanding and reproducing spoken language, with sparing of written language comprehension and speech production. The pathognomonic disturbance of auditory comprehension appears to be associated with a breakdown in processes involved in mapping auditory input to,lexical representations of words, but the functional locus of this disturbance and the localization of the responsible lesion have long been disputed. We report here on a woman with PWD resulting from a circumscribed unilateral infarct involving the left superior temporal lobe who demonstrated significant problems processing transitional spectrotemporal cues in both speech and nonspeech sounds. OD speech discrimination tasks, she exhibited poor differentiation of stop consonant-vowel syllables distinguished by voicing onset and brief formant frequency transitions. Isolated formant transitions could be reliably discriminated only at very long durations (> 200 ms). By contrast, click fusion threshold, which depends on millisecond-level resolution of brief auditory events, was normal. These results suggest that the problems with speech analysis in this case were not secondary to general constraints on auditory temporal resolution. Rather, they point to a disturbance of left hemisphere auditory mechanisms that preferentially analyze rapid spectrotemporal variations in frequency. The findings have important implications for our conceptualization of PWD and its subtypes.
Pure word deafness (PWD) is a rare disorder characterized by impaired verbal comprehension sparing discrimination and recognition of nonverbal sounds with relatively normal spontaneous speech, writing, and reading comprehension. Etiologies of this syndrome are varied, and there are rare reports about brain tumor with PWD in children. We report a case of medulloblastoma presented with PWD in a 7-year-old girl. She visited our outpatient clinic because of English dictation performance deterioration. PWD was diagnosed by the otolaryngologist after examinations. Posterior fossa tumor and obstructive hydrocephalus were shown in the magnetic resonance imaging of the brain. The diagnosis of medulloblastoma was then made by pathology.
Introduction
The study of the neural networks involved in music processing has received less attention than work researching the brain's language networks. For the last two decades there has been a growing interest in discovering the functional mechanisms of the musical brain and understanding those disorders in which brain regions linked with perception and production of music are damaged.
Discussion
Congenital and acquired musical deficits in their various forms (perception, execution, music-memory) are grouped together under the generic term amusia. In this selective review we present the “cutting edge” studies on the cognitive and neural processes implicated in music and the various forms of amusia.
Conclusions
Musical processing requires a large cortico-subcortical network which is distributed throughout both cerebral hemispheres and the cerebellum. The analysis of healthy subjects using functional neuroimaging and examination of selective deficits (e.g., tone, rhythm, timbre, melodic contours) in patients will improve our knowledge of the mechanisms involved in musical processing and the latter's relationship with other cognitive processes.
Confabulation denotes the recitation of memories about events and experiences that never happened. Based on multiple case examples, The Confabulating Mind provides an in-depth review of the presentations, the causative diseases, and the mechanisms of this phenomenon and compares confabulation with normal false memories, as they occur in healthy adults and children. Memory-related confabulations are compared with false statements made by patients who confuse people, places, or their own health status, as this happens in disorders like déjà vu, paramnesic misidentification, and anosognosia. One form of confabulation called behaviourally spontaneous confabulation receives particular attention. It is characterized by a confusion of reality evident from disorientation and acts according to the confabulations. Recent studies revealed a specific mechanism-orbitofrontal reality filtering-which attributes a critical role to the orbitofrontal cortex for the ability to keep thought and behaviour in phase with reality. The book concludes with an overview of current interpretations of confabulations and recommendations for future study.
A 55-year-old right-handed man with a history of hypertension suddenly fell and developed right hemiparesis. Neurological examination revealed that he was alert, but did not appropriately respond to verbal questions and commands. Detailed examination revealed that he could correctly respond to written commands. His speech was almost fluent, showing no paraphasia and normal articulation. His written sentences were legible. Pure tone audiometry showed that his auditory acuity was relatively preserved. His brainstem auditory evoked potential components from I to V were recorded bilaterally with normal latency. Cerebral CT demonstrated fresh bleeding in the left putamen and an old haemorrhage on the opposite side. He was treated by antihypertensive therapy and rehabilitation. Although there remained mild sensory deficit on his right extremities and he felt a slight noise during conversation, he had little difficulty with verbal communication when he was transferred to another hospital on day 38.
Acquired amusia provides a unique opportunity to investigate the fundamental neural architectures of musical processing due to the transition from a functioning to defective music processing system. Yet, the white matter (WM) deficits in amusia remain systematically unexplored. To evaluate which WM structures form the neural basis for acquired amusia and its recovery, we studied 42 stroke patients longitudinally at acute, 3-month, and 6-month post-stroke stages using DTI [tract-based spatial statistics (TBSS) and deterministic tractography (DT)] and the Scale and Rhythm subtests of the Montreal Battery of Evaluation of Amusia (MBEA). Non-recovered amusia was associated with structural damage and subsequent degeneration in multiple WM tracts including the right inferior fronto-occipital fasciculus (IFOF), arcuate fasciculus (AF), inferior longitudinal fasciculus (ILF), uncinate fasciculus (UF), and frontal aslant tract (FAT), as well as in the corpus callosum (CC) and its posterior part (tapetum). In a linear regression analysis, the volume of the right IFOF was the main predictor of MBEA performance across time. Overall, our results provide a comprehensive picture of the large-scale deficits in intra- and interhemispheric structural connectivity underlying amusia, and conversely highlight which pathways are crucial for normal music perception.
A 45-year-old right-handed man with a past history (10 years) of putaminal hemorrage presented with auditory agnosia associated with left putaminal hemorrhage. It was suspected that the auditory agnosia was due to bilateral damage in the acoustic radiations. Generalized auditory agnosia, verbal and non-verbal (music and environmental), was diagnosed by neuropsychological examinations. It improved 4 months after the onset. However, the clinical assessment of attention remained poor. The cognition for speech sounds improved slowly, but once it started to improve, the progress of improvement was rapid. Subsequently, the cognition for music sounds also improved, while the recovery of the cognition for environmental sounds remained delayed. There was a dissociation in recovery between these cognitions. He was able to return to work a year after the onset. We also reviewed the literature for cases with auditory agnosia and discuss their course of recovery in this report.
The insular cortex, or "Island of Reil," is hidden deep within the lateral sulcus of the brain. Subdivisions within the insula have been identified on the basis of cytoarchitectonics, sulcal landmarks, and connectivity. Depending on the parcellation technique used, the insula can be divided into anywhere between 2 and 13 distinct subdivisions. The insula subserves a wide variety of functions in humans ranging from sensory and affective processing to high-level cognition. Here, we provide a concise summary of known structural and functional features of the human insular cortex with a focus on lesion case studies and recent neuroimaging evidence for considerable functional heterogeneity of this brain region.
Unlabelled:
Although acquired amusia is a relatively common disorder after stroke, its precise neuroanatomical basis is still unknown. To evaluate which brain regions form the neural substrate for acquired amusia and its recovery, we performed a voxel-based lesion-symptom mapping (VLSM) and morphometry (VBM) study with 77 human stroke subjects. Structural MRIs were acquired at acute and 6 month poststroke stages. Amusia and aphasia were behaviorally assessed at acute and 3 month poststroke stages using the Scale and Rhythm subtests of the Montreal Battery of Evaluation of Amusia (MBEA) and language tests. VLSM analyses indicated that amusia was associated with a lesion area comprising the superior temporal gyrus, Heschl's gyrus, insula, and striatum in the right hemisphere, clearly different from the lesion pattern associated with aphasia. Parametric analyses of MBEA Pitch and Rhythm scores showed extensive lesion overlap in the right striatum, as well as in the right Heschl's gyrus and superior temporal gyrus. Lesions associated with Rhythm scores extended more superiorly and posterolaterally. VBM analysis of volume changes from the acute to the 6 month stage showed a clear decrease in gray matter volume in the right superior and middle temporal gyri in nonrecovered amusic patients compared with nonamusic patients. This increased atrophy was more evident in anterior temporal areas in rhythm amusia and in posterior temporal and temporoparietal areas in pitch amusia. Overall, the results implicate right temporal and subcortical regions as the crucial neural substrate for acquired amusia and highlight the importance of different temporal lobe regions for the recovery of amusia after stroke.
Significance statement:
Lesion studies are essential in uncovering the brain regions causally linked to a given behavior or skill. For music perception ability, previous lesion studies of amusia have been methodologically limited in both spatial accuracy and time domain as well as by small sample sizes, providing coarse and equivocal information about which brain areas underlie amusia. By using longitudinal MRI and behavioral data from a large sample of stroke patients coupled with modern voxel-based analyses methods, we were able provide the first systematic evidence for the causal role of right temporal and striatal areas in music perception. Clinically, these results have important implications for the diagnosis and prognosis of amusia after stroke and for rehabilitation planning.
Auditory training (AT) is an important component of rehabilitation for patients with central auditory processing disorder (CAPD). The present article identifies and describes aspects of AT as they relate to applications in this population. A description of the types of auditory processes along with information on relevant AT protocols that can be used to address these specific deficits is included. Characteristics and principles of effective AT procedures also are detailed in light of research that reflects on their value. Finally, research investigating AT in populations who show CAPD or present with auditory complaints is reported. Although efficacy data in this area are still emerging, current findings support the use of AT for treatment of auditory difficulties.
We report a clinical case of a 19-year-old male patient who developed pure word deafness due to the local compressive effect of a pineal germinoma on the inferior colliculi of the quadrigeminal plate. After percutaneous radiation therapy the size of the tumor decreased significantly, while audiometry demonstrated a complete regression of the auditory deficit. Since pure word deafness is commonly attributed to temporal lesions, the inferior colliculi represent an exceptional site for these symptoms. The pathophysiological background and the scarce literature on pure word deafness, especially the one related to neoplasms of the tectal region, are briefly discussed.
Based on results from functional imaging, cortex along the superior temporal sulcus (STS) has been suggested to subserve phoneme and pre-lexical speech perception. For vowel classification, both superior temporal plane (STP) and STS areas have been suggested relevant. Lesion of bilateral STS may conversely be expected to cause pure word deafness and possibly also impaired vowel classification. Here we studied a patient with bilateral STS lesions caused by ischemic strokes and relatively intact medial STPs to characterize the behavioral consequences of STS loss. The patient showed severe deficits in auditory speech perception, whereas his speech production was fluent and communication by written speech was grossly intact. Auditory-evoked fields in the STP were within normal limits on both sides, suggesting that major parts of the auditory cortex were functionally intact. Further studies showed that the patient had normal hearing thresholds and only mild disability in tests for telencephalic hearing disorder. Prominent deficits were discovered in an auditory-object classification task, where the patient performed four standard deviations below the control group. In marked contrast, performance in a vowel-classification task was intact. Auditory evoked fields showed enhanced responses for vowels compared to matched non-vowels within normal limits. Our results are consistent with the notion that cortex along STS is important for auditory speech perception, although it does not appear to be entirely speech specific. Formant analysis and single vowel classification, however, appear to be already implemented in auditory cortex on the STP.
Our patient was first diagnosed with auditory agnosia following his second cerebral vascular accident (CVA) in 1975 when he was 37 years old. Comprehensive follow-up examinations of auditory function were periodically conducted until his sudden death 15 years later. His brain was studied postmortem for neuropathology. Initial pure-tone audiometry revealed moderate sensorineural hearing loss in the right ear and mild sensorineural hearing loss in the left ear. However, repeated pure-tone audiometry revealed that thresholds became progressively poorer over time, bilaterally. Speech audiometry of both ears consistently revealed that the patient was unable to discriminate any monosyllabic words (i.e. speech intelligibility scores were 0%, bilaterally). In general, speech and hearing tests demonstrated that he could not comprehend spoken words, but could comprehend written commands and gestures. Postmortem neuropathological study of the left hemisphere revealed total defect and neuronal loss of the superior te...
Auditory agnosia refers to impairments in sound perception and identification despite intact hearing, cognitive functioning, and language abilities (reading, writing, and speaking). Auditory agnosia can be general, affecting all types of sound perception, or can be (relatively) specific to a particular domain. Verbal auditory agnosia (also known as (pure) word deafness) refers to deficits specific to speech processing, environmental sound agnosia refers to difficulties confined to non-speech environmental sounds, and amusia refers to deficits confined to music. These deficits can be apperceptive, affecting basic perceptual processes, or associative, affecting the relation of a perceived auditory object to its meaning. This chapter discusses what is known about the behavioral symptoms and lesion correlates of these different types of auditory agnosia (focusing especially on verbal auditory agnosia), evidence for the role of a rapid temporal processing deficit in some aspects of auditory agnosia, and the few attempts to treat the perceptual deficits associated with auditory agnosia. A clear picture of auditory agnosia has been slow to emerge, hampered by the considerable heterogeneity in behavioral deficits, associated brain damage, and variable assessments across cases. Despite this lack of clarity, these striking deficits in complex sound processing continue to inform our understanding of auditory perception and cognition.
© 2015 Elsevier B.V. All rights reserved.
Historically, anosognosia referred to under-report of striking symptoms of acquired brain injury (e.g., hemiplegia) with debilitating functional consequences and was linked with anosodiaphoria, an emotional reaction of indifference. It was later extended to include under-report of all manner of symptoms of acquired brain injury by the patient compared to clinicians, family members, or functional performance. Anosognosia is related to time since onset of brain injury but not consistently to demographic variables, lesion location (except that it is more common after unilateral right than left hemispheric injury), or specific neuropsychological test scores. This review considers all manifestations of anosognosia as a unitary phenomenon with differing clinical characteristics dictated by variability in linked cognitive impairments. It is concluded that anosognosia has three chief contributing factors: (1) procedural: measurement differences across studies in terms of symptom selection and the designation of a "gold standard" of patient symptomatology; (2) psychological: a tendency towards positive self-evaluation and the avoidance of adverse information, that also occurs in neurologically intact individuals; and (3) neuropathological: an increased likelihood of error recognition failure from disconnections that disrupt feedback between injured brain regions governing specific behaviours (symptoms) and anterior cingulate/insular cortex. Anosodiaphoria is considered as an associated symptom, resulting from the same psychological and neuropathological factors.
Awareness of cognitive and motor impairments was evaluated in 100 patients with cerebral infarction, dementia, or head trauma, using a standardized interview which elicited subjects' descriptions of their condition. “Unawareness” was operationally defined as a discrepancy between the subject's description of abilities, and measurement of those abilities with neuropsychological and neurological evaluations. In all three neuropathologic groups, subjects frequently demonstrated unawareness of acquired impairments. Unawareness was associated with unilateral right-hemisphere damage, impaired performance on IQ tests, and temporal disorientation. All subjects with unawareness of hemiparesis also had unawareness of cognitive defects. It is evident that unawareness of cognitive defects is an important and common manifestation of brain disease, and systematic evaluation of this problem may aid in patient management and rehabilitation planning.
Introduction:
Music perception involves processing of melodic, temporal and emotional dimensions that have been found to dissociate in healthy individuals and after brain injury. Two components of the temporal dimension have been distinguished, namely rhythm and metre. We describe an 18 year old male musician 'JM' who showed apperceptive music agnosia with selectively preserved metre perception, and impaired recognition of sad and peaceful music relative to age and music experience matched controls after resection of a right temporoparietal tumour.
Method:
Two months post-surgery JM underwent a comprehensive neuropsychological evaluation including assessment of his music perception abilities using the Montreal Battery for Evaluation of Amusia (MBEA, Peretz, Champod, & Hyde, 2003). He also completed several experimental tasks to explore his ability to recognise famous songs and melodies, emotions portrayed by music and a broader range of environmental sounds. Five age-, gender-, education- and musical experienced-matched controls were administered the same experimental tasks.
Results:
JM showed selective preservation of metre perception, with impaired performances compared to controls and scoring below the 5% cut-off on all MBEA subtests, except for the metric condition. He could identify his favourite songs and environmental sounds. He showed impaired recognition of sad and peaceful emotions portrayed in music relative to controls but intact ability to identify happy and scary music.
Conclusion:
This case study contributes to the scarce literature documenting a dissociation between rhythmic and metric processing, and the rare observation of selectively preserved metric interpretation in the context of apperceptive music agnosia. It supports the notion that the anterior portion of the superior temporal gyrus (STG) plays a role in metric processing and provides the novel observation that selectively preserved metre is sufficient to identify happy and scary, but not sad or peaceful emotions portrayed in music.
OBJECTIVE:
To review the literature regarding cortical hearing loss and document a case of cortical hearing loss including its presentation, diagnosis, and evolution over 32 months of follow-up.
PATIENT:
A 56-year-old woman with profound bilateral sensorineural hearing loss secondary to sequential hemorrhagic, temporal lobe infarctions separated in time by 8 months.
INTERVENTION:
Diagnostic.
RESULTS:
Sequential infarctions affecting the patient's auditory radiations and primary auditory cortices bilaterally combined to cause cortical hearing loss. At presentation, audiogram revealed a bilateral profound sensorineural hearing loss with no reliable responses to pure-tone or speech audiometry. She has subsequently recovered the ability to distinguish environmental sounds. At her 32-month follow-up, she had a pure-tone average (PTA) of 62 dB on the right and 70 dB on the left but continued to display a poor word recognition score (0%). A literature review was performed from the year 1891 until the present.
CONCLUSION:
Cortical deafness is an exceedingly rare entity. Presentation and recovery of hearing are dependent on the extent of the initial lesions. The majority of patients can expect improvements in pure-tone auditory thresholds over time; however patients should be counseled that recovery of the ability to understand speech is unlikely.
A 29-year-old right-handed human immunodeficiency virus (HIV)–seropositive (CD4 lymphocyte nadir, 7/mm3) woman commenced antiretroviral therapy (emtricitabine, 200 mg; tenofovir, 300 mg; and efavirenz, 600 mg, once a day) in December 2011. In February 2012, she developed headache and hearing impairment, which progressed to complete deafness over 3 weeks. She reported “muffled” and “gibberish” conversational and musical sounds in March 2012. Her communication was confined to lip reading and reading from written language. Her spontaneous speech was normal. She was able to read aloud and comprehend the written speech. She could write spontaneously and copy transcription. Auditory verbal repetition and writing (to auditory dictation) were impossible. Auditory word recognition score using NuChip picture pointing cards showed severe impairment. She could hear and recognize nonverbal sounds such as telephone ringing and her parents’ voices. Her nonverbal gestural, emotional, and prosodic elements in communication appeared intact. Pure tone audiometry and otoacoustic reflexes were intact bilaterally. Brain magnetic resonance imaging showed multiple cerebral lesions including bilateral superior temporal lesions (Figure). A biopsy from the right frontal lesion showed findings suggestive of HIV encephalitis and immune reconstitution inflammatory syndrome1 (data not shown).
Observations on a case of pure auditory agnosia are reported. The patient, aged 57, had pure word deafness, sensory amusia and advanced general auditory agnosia. The ability te read and write was unimpaired. Spontaneous speech was normal and the inner language was intact. Marked alteration of patient 's speaking voice and personal character was noted after the attack. A bilateral, slight perceptive loss of hearing at low frequencies was observed in standard audiometry, while the hearing level according to EEG-audiometry was 10 db b etter in the left ear than in the right. Both thresholds of standard audiometry and of Bekesy tracings varied from test to test. All the Bekesy tracings showed a large amplitude of as much as 10 db to 30 db. The patient's difficulty in estimating the intensity of sounds was revealed by the difference limen t est. A directional preponderance of nystagmus to the left was observed with alternate hot and cold caloric tests.
Objective:
To investigate the impact of objective cognitive impairment, negative affect, and fatigue on cognitive complaint in a postacute (mean=6.64±1.32mo) sample of patients with ischemic stroke.
Design:
Cross-sectional study.
Setting:
Specialized stroke units at major metropolitan hospitals.
Participants:
Patients with first-ever ischemic stroke (N=25) aged between 50 and 85 years with relatively good neurologic recovery (National Institutes of Health Stroke Scale score ≤7) during the postacute period. Participants were excluded from the study if there was a documented history of psychiatric illness, neurologic disease, dementia, or a moderate or severe aphasia.
Interventions:
Not applicable.
Main outcome measures:
Cognitive complaint as measured by the A-B Neuropsychological Assessment Schedule.
Results:
Ninety percent of the patients reported some level of cognitive difficulty in everyday life. Fatigue, cognitive slowing, memory difficulties, and poor concentration were the most frequently reported complaints. More than half of all participants had significant impairment in at least 1 cognitive domain after their stroke. A standard multiple regression was performed to evaluate the relative impact of negative affect, fatigue, and objective cognitive functioning on subjective cognitive complaint. This model accounted for 61% of the variance in total subjective cognitive complaint (R=.78, F3,21=10.96, P<.001), with depression being the only variable to make a significant independent contribution to the prediction of subjective cognitive complaint.
Conclusions:
Cognitive complaints are reported by almost all patients after a stroke. Although 50% of the participants had objective evidence of a cognitive impairment, neither objective cognitive impairment nor fatigue predicted cognitive complaint independently of negative affect. Clinicians who receive reports of cognitive complaints in the postacute period after stroke should be alert to the possibility of psychological distress in their patient.
Although a half century has passed since Babinski1 described anosognosia for hemiplegia, a considerable difference of opinion as to its nature remains. One feature that as yet has not been explained adequately is the great predominance of patients with anosognosia for left hemiplegia over those in whom the right side of the body is involved. In studies where the relative incidence is given, the ratio has ranged from eight to one in the series of Hécaen2 to two to one in the studies of Nathanson, Bergman, and Gordon,3 and Battersby, Bender, Pollack, and Kahn.4
Despite different formulations, there is a fair consensus as to what clinical manifestations are included under the rubric of anosognosia. These are verbal negation of the paralyzed limbs, denial of their existence, and delusions, illusions, and hallucinations concerning the affected side including the phantom of an extra limb, and neglect of, and
After a right temporoparietal stroke, a left-handed man lost the ability to understand speech and environmental sounds but developed greater appreciation for music. The patient had preserved reading and writing but poor verbal comprehension. Slower speech, single syllable words, and minimal written cues greatly facilitated his verbal comprehension. On identifying environmental sounds, he made predominant acoustic errors. Although he failed to name melodies, he could match, describe, and sing them. The patient had normal hearing except for presbyacusis, right-ear dominance for phonemes, and normal discrimination of basic psychoacoustic features and rhythm. Further testing disclosed difficulty distinguishing tone sequences and discriminating two clicks and short-versus-long tones, particularly in the left ear. Together, these findings suggest impairment in a direct route for temporal analysis and auditory word forms in his right hemisphere to Wernicke's area in his left hemisphere. The findings further suggest a separate and possibly rhythm-based mechanism for music recognition.
The analysis of pure word deafness (PWD) suggests that speech perception, construed as the integration of acoustic information to yield representations that enter into the linguistic computational system, (i) is separable in a modular sense from other aspects of auditory cognition and (ii) is mediated by the posterior superior temporal cortex in both hemispheres. PWD data are consistent with neuropsychological and neuroimaging evidence in a manner that suggests that the speech code is analyzed bilaterally. The typical lateralization associated with language processing is a property of the computational system that acts beyond the analysis of the input signal. The hypothesis of the bilateral mediation of the speech code does not imply that both sides execute the same computation. It is proposed that the speech signal is asymmetrically analyzed in the time domain, with left-hemisphere mechanisms preferentially extracting information over shorter (25–50 ms) temporal integration windows and right mechanisms over longer (150–250 ms) windows.
