Auditory verbal agnosia

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Auditory verbal agnosia (AVA), also known as pure word deafness, is the inability to comprehend speech. Individuals with this disorder lose the ability to understand language, repeat words, and write from dictation. Some patients with AVA describe hearing spoken language as meaningless noise, often as though the person speaking was doing so in a foreign language. [1] However, spontaneous speaking, reading, and writing are preserved. The maintenance of the ability to process non-speech auditory information, including music, also remains relatively more intact than spoken language comprehension. [2] Individuals who exhibit pure word deafness are also still able to recognize non-verbal sounds. [3] The ability to interpret language via lip reading, hand gestures, and context clues is preserved as well. [4] Sometimes, this agnosia is preceded by cortical deafness; however, this is not always the case. Researchers have documented that in most patients exhibiting auditory verbal agnosia, the discrimination of consonants is more difficult than that of vowels, but as with most neurological disorders, there is variation among patients. [5]

Contents

Auditory verbal agnosia (AVA) is not the same as auditory agnosia ; patients with (nonverbal) auditory agnosia have a relatively more intact speech comprehension system despite their impaired recognition of nonspeech sounds. [2]

Presentation

Auditory verbal agnosia can be referred to as a pure aphasia because it has a high degree of specificity. Despite an inability to comprehend speech, patients with auditory verbal agnosia typically retain the ability to hear and process non-speech auditory information, speak, read and write. This specificity suggests that there is a separation between speech perception, non-speech auditory processing, and central language processing. [2] In support of this theory, there are cases in which speech and non-speech processing impairments have responded differentially to treatment. For example, some therapies have improved writing comprehension in patients over time, while speech remained critically impaired in those same patients.

The term "pure word deafness" is something of a misnomer. By definition, individuals with pure word deafness are not deaf – in the absence of other impairments, these individuals have normal hearing for all sounds, including speech. The term "deafness" originates from the fact that individuals with AVA are unable to comprehend speech that they hear. The term "pure word" refers to the fact that comprehension of verbal information is selectively impaired in AVA. For this reason, AVA is distinct from other auditory agnosias in which the recognition of nonspeech sounds is impaired. Classical (or pure) auditory agnosia is an inability to process environmental sounds. Interpretive or receptive agnosia (amusia) is an inability to understand music.

Patients with pure word deafness complain that speech sounds simply do not register, or that they tend not to come up. Other claims include speech sounding as if it were in a foreign language, the words having a tendency to run together, or the feeling that speech was simply not connected to the patient's voice. [2]

Causes

Auditory verbal agnosia has been shown to form as a result of tumor formation, especially in the posterior third ventricle, trauma, lesions, cerebral infarction, encephalitis as a result of herpes simplex, and Landau-Kleffner syndrome. [6] [4] [7] [8] [9] The exact location of damage which results in pure word deafness is still under debate, but the planum temporale, posterior STG, and white matter damage to the acoustic radiations (AR) have all been implicated. [4] [2] [10]

Auditory verbal agnosia is rarely diagnosed in its pure form. Auditory verbal agnosia can both present as the result of acute damage or as chronic, progressive degeneration over time. Cases have been documented that result from severe acute head trauma resulting in bilateral temporal lobe damage. [4] Auditory information enters both hemispheres, so auditory agnosia usually develops from bitemporal damage or lesions. [1] In contrast, auditory verbal agnosia has also been documented to present progressively over several years. In one such case, the patient exhibited progressive word deafness over a 9-year period but did not exhibit any other cognitive of mental deterioration. MRIs showed cortical atrophy in the left superior temporal lobe region. [11]

Auditory verbal agnosia can also occur as a result of traumatic brain injury. In one case, a man fell and developed auditory verbal agnosia. This can be challenging to diagnose because he had fluent speech and could understand written language. However, he was unable to follow oral commands or repeat words. This marks a difference from other aphasias, including Wernike aphasia, because he had fluent speech and was able to understand written language. He explained that verbal language sounded like a buzzing and he could not understand it, but he could differentiate language from environmental sounds. The man underwent speech therapy and his condition improved over time. [12]

In childhood, auditory verbal agnosia can also be caused by Landau-Kleffner syndrome, also called acquired epileptic aphasia. It is often the first symptom of this disease. [13] A review of 45 cases suggested a relationship between prognosis and age of onset with poorer prognosis for those with earlier onset. [14] In extremely rare cases, auditory verbal agnosia has been known to present as a symptom of neurodegenerative disease, such as Alzheimer's disease. [15] In such cases auditory verbal agnosia is a symptom that is typically followed by more severe neurological symptoms typical of Alzheimer's disease.

Diagnosis

There is no uniform performance among patients with auditory verbal agnosia; therefore it is not possible to attribute specific phonetic or phonological deficits to the syndrome. [2] In order to diagnose AVA, two intact abilities need to be established:

If both of these criteria are met and lack of auditory verbal comprehension is apparent, a diagnosis of AVA may follow.

In at least one instance, the Boston Diagnostic Aphasia Examination has been used to profile AVA. This method was able to show that the patient experienced marked difficulty in speech perception with minor to no minor deficits in production, reading, and writing, fitting the profile of AVA. [7] While this provides a well-known example, other verbal-audio test batteries can and have also been used to diagnose pure speech deafness.

Cognitive deficits

Auditory verbal agnosia is the inability to distinguish phonemes. [3] In some patients with unilateral auditory verbal agnosia, there is evidence that the ability to acoustically process speech signals is affected at the prephonemic level, preventing the conversion of these signals into phonemes. [17] There are two predominate hypotheses that address what happens within the language center of the brain in people that have AVA. One of the hypotheses is that an early stage of auditory analysis is impaired. The fact that AVA patients have the ability to read shows that both the semantic system and the speech output lexicon are intact. The second hypotheses suggests that there is either a complete or partial disconnection of the auditory input lexicon from the semantic system. This would suggest that entries in the lexicon can still be activated but they cannot go on to cause subsequent semantic activation. [16] In relation to these two different hypotheses, researchers in one study differentiated between two different types of AVA. [18] According to this study, one form of AVA is a deficit at the prephonemic level and is related to the inability to comprehend rapid changes in sound. This form of AVA is associated with bilateral temporal lobe lesions. Speech perception in patients with this form of AVA has been shown to improve significantly in understanding when the pace of speech is drastically slowed. [2] The second type of AVA that the study discusses is a deficit in linguistic discrimination that does not adhere to a prephonemic pattern. This form is associated with left unilateral temporal lobe lesions and may even be considered a form of Wernicke's aphasia. It is important in clinical settings to distinguish between AVA and Wernicke's aphasia. In auditory agnosia, patients can communicate through written language, but not in Wernike's aphasia. [6] Often individuals diagnosed with auditory verbal agnosia are also incapable of discriminating between non-verbal sounds as well as speech. The underlying problem seems to be temporal in that understanding speech requires the discrimination between specific sounds which are closely spaced in time. [19] Note that this is not unique to speech; studies using non-speech sounds closely spaced in time (dog bark, phone ring, lightning, etc.) have shown that those with auditory verbal agnosia are unable to discriminate between those sounds in the majority of cases, though a few putative examples of speech-specific impairment have been documented in the literature.

Neurological deficits

Auditory verbal agnosia is caused by bilateral damage, often in the form of cerebrovascular accidents which form as a result of an embolism, to the posterior superior temporal lobes or disruption of connections between these areas. [20] A unilateral lesion in the left or right superior temporal lobe can also result in pure word deafness, this being much more common in the left hemisphere than the right. [8] It is often associated with lesions to the left posterior superior temporal lobe, but no such unilateral case has yet been documented without damage to the white matter tract connecting superior temporal lobes bilaterally or bilateral damage to the superior temporal lobe. In cases where unilateral damage to the left superior temporal lobe has been documented, patients exhibited problems processing both speech and non-speech sounds (in other words, not typical of auditory verbal agnosia). [19] These facts, in combination with the existence of cases of damage to these white matter tracts without detectable cortical damage, in combination with cases of pure word deafness resulting enlargement of the third ventricle alone suggest that the disorder results from damage to the left-right superior temporal circuit rather than the superior temporal area on one hemisphere or the other.

Many of the bilateral cases share one essential feature: after the first (unilateral) lesion, speech perception was typically intact after an initial period of disturbance. Only after the second lesion (in the other hemisphere) were permanent speech perception problems the consistent outcome. The fact that most of these patients only manifested auditory verbal agnosia subsequent to the second lesion supports the hypothesis that both sides of the superior temporal gyrus are necessary. [2]

Auditory verbal agnosia is rarely diagnosed in its pure form. Auditory verbal agnosia can present as the result of acute damage or chronic, progressive degeneration over time. Cases have been documented that result from severe acute head trauma resulting in bilateral temporal lobe damage. [4] In contrast, auditory verbal agnosia has also been documented to present progressively over several years. In one such case, the patient exhibited progressive word deafness over a 9-year period but did not exhibit any other cognitive of mental deterioration. This patient was found, using MRIs, to have cortical atrophy in the left superior temporal lobe region. [11]

Treatments

Sign language therapy

Sign language therapy has been identified as one of the top five most common treatments for auditory verbal agnosia. This type of therapy is most useful because, unlike other treatment methods, it does not rely on fixing the damaged areas of the brain. This is particularly important with AVA cases because it has been so hard to identify the causes of the agnosia in the first place, much less treat those areas directly. Sign language therapy, then, allows the person to cope and work around the disability, much in the same way it helps deaf people. In the beginning of therapy, most will work on identifying key objects and establishing an initial core vocabulary of signs. After this, the patient graduates to expand the vocabulary to intangible items or items that are not in view or present. Later, the patient learns single signs and then sentences consisting of two or more signs. In different cases, the sentences are first written down and then the patient is asked to sign them and speak them simultaneously. [21] Because different AVA patients vary in the level of speech or comprehension they have, sign language therapy learning order and techniques are very specific to the individual's needs.

Tumor removal

In incidents where tumors and their pressure effects are the cause of pure word deafness, removal of the tumor has been shown to allow for the return of most auditory verbal comprehension. [22]

Treatments used for Landau-Kleffner syndrome

Intravenous immunoglobulin therapy

Treating auditory verbal agnosia with intravenous immunoglobulin (IVIG) is controversial because of its inconsistency as a treatment method. Although IVIG is normally used to treat immune diseases, some individuals with auditory verbal agnosia have responded positively to the use of IVIG. [23] Additionally, patients are more likely to relapse when treated with IVIG than other pharmacological treatments. IVIG is, thus, a controversial treatment as its efficacy in treating auditory verbal agnosia is dependent upon each individual and varies from case to case.

Diazepam therapy

In a study conducted by Masaaki Nagafuchi et al. (1993), a 7-year-old girl began taking a dose of 2 mg diazepam orally every day. She demonstrated major improvements in behavior and comprehension of speech while under diazepam therapy. Within a month, conversation problems were eliminated. After a year of therapy, her repetition ability was almost normal. After two years, her ability to discriminate monosyllabic words was within the normal range. Her audiological recognition had remained normal from the time of onset (i.e., she could recognize familiar noises such as a baby crying or a telephone ringing). [24]

See also

Related Research Articles

<span class="mw-page-title-main">Aphasia</span> Inability to comprehend or formulate language

In aphasia, a person may be unable to comprehend or unable to formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, epilepsy, autoimmune neurological diseases, brain infections, or neurodegenerative diseases.

<span class="mw-page-title-main">Language center</span> Speech processing areas of the brain

In neuroscience and psychology, the term language center refers collectively to the areas of the brain which serve a particular function for speech processing and production. Language is a core system that gives humans the capacity to solve difficult problems and provides them with a unique type of social interaction. Language allows individuals to attribute symbols to specific concepts, and utilize them through sentences and phrases that follow proper grammatical rules. Finally, speech is the mechanism by which language is orally expressed.

<span class="mw-page-title-main">Receptive aphasia</span> Language disorder involving inability to understand language

Wernicke's aphasia, also known as receptive aphasia, sensory aphasia, fluent aphasia, or posterior aphasia, is a type of aphasia in which individuals have difficulty understanding written and spoken language. Patients with Wernicke's aphasia demonstrate fluent speech, which is characterized by typical speech rate, intact syntactic abilities and effortless speech output. Writing often reflects speech in that it tends to lack content or meaning. In most cases, motor deficits do not occur in individuals with Wernicke's aphasia. Therefore, they may produce a large amount of speech without much meaning. Individuals with Wernicke's aphasia are typically unaware of their errors in speech and do not realize their speech may lack meaning. They typically remain unaware of even their most profound language deficits.

<span class="mw-page-title-main">Broca's area</span> Speech production region in the dominant hemisphere of the hominid brain

Broca's area, or the Broca area, is a region in the frontal lobe of the dominant hemisphere, usually the left, of the brain with functions linked to speech production.

<span class="mw-page-title-main">Agnosia</span> Medical condition

Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information.

<span class="mw-page-title-main">Temporal lobe</span> One of the four lobes of the mammalian brain

The temporal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The temporal lobe is located beneath the lateral fissure on both cerebral hemispheres of the mammalian brain.

<span class="mw-page-title-main">Wernicke's area</span> Speech comprehension region in the dominant hemisphere of the hominid brain

Wernicke's area, also called Wernicke's speech area, is one of the two parts of the cerebral cortex that are linked to speech, the other being Broca's area. It is involved in the comprehension of written and spoken language, in contrast to Broca's area, which is primarily involved in the production of language. It is traditionally thought to reside in Brodmann area 22, which is located in the superior temporal gyrus in the dominant cerebral hemisphere, which is the left hemisphere in about 95% of right-handed individuals and 70% of left-handed individuals.

<span class="mw-page-title-main">Conduction aphasia</span> Medical condition

Conduction aphasia, also called associative aphasia, is an uncommon form of difficulty in speaking (aphasia). It is caused by damage to the parietal lobe of the brain. An acquired language disorder, it is characterised by intact auditory comprehension, coherent speech production, but poor speech repetition. Affected people are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as the person shows significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce. People have frequent errors during spontaneous speech, such as substituting or transposing sounds. They are also aware of their errors and will show significant difficulty correcting them.

<span class="mw-page-title-main">Global aphasia</span> Medical condition

Global aphasia is a severe form of nonfluent aphasia, caused by damage to the left side of the brain, that affects receptive and expressive language skills as well as auditory and visual comprehension. Acquired impairments of communicative abilities are present across all language modalities, impacting language production, comprehension, and repetition. Patients with global aphasia may be able to verbalize a few short utterances and use non-word neologisms, but their overall production ability is limited. Their ability to repeat words, utterances, or phrases is also affected. Due to the preservation of the right hemisphere, an individual with global aphasia may still be able to express themselves through facial expressions, gestures, and intonation. This type of aphasia often results from a large lesion of the left perisylvian cortex. The lesion is caused by an occlusion of the left middle cerebral artery and is associated with damage to Broca's area, Wernicke's area, and insular regions which are associated with aspects of language.

Transcortical sensory aphasia (TSA) is a kind of aphasia that involves damage to specific areas of the temporal lobe of the brain, resulting in symptoms such as poor auditory comprehension, relatively intact repetition, and fluent speech with semantic paraphasias present. TSA is a fluent aphasia similar to Wernicke's aphasia, with the exception of a strong ability to repeat words and phrases. The person may repeat questions rather than answer them ("echolalia").

<span class="mw-page-title-main">Language processing in the brain</span> How humans use words to communicate

In psycholinguistics, language processing refers to the way humans use words to communicate ideas and feelings, and how such communications are processed and understood. Language processing is considered to be a uniquely human ability that is not produced with the same grammatical understanding or systematicity in even human's closest primate relatives.

<span class="mw-page-title-main">Brodmann area 22</span>

Brodmann area 22 is a Brodmann's area that is cytoarchitecturally located in the posterior superior temporal gyrus of the brain. In the left cerebral hemisphere, it is one portion of Wernicke's area. The left hemisphere BA22 helps with generation and understanding of individual words. On the right side of the brain, BA22 helps to discriminate pitch and sound intensity, both of which are necessary to perceive melody and prosody. Wernicke's area is active in processing language and consists of the left Brodmann area 22 and Brodmann area 40, the supramarginal gyrus.

Transcortical motor aphasia (TMoA), also known as commissural dysphasia or white matter dysphasia, results from damage in the anterior superior frontal lobe of the language-dominant hemisphere. This damage is typically due to cerebrovascular accident (CVA). TMoA is generally characterized by reduced speech output, which is a result of dysfunction of the affected region of the brain. The left hemisphere is usually responsible for performing language functions, although left-handed individuals have been shown to perform language functions using either their left or right hemisphere depending on the individual. The anterior frontal lobes of the language-dominant hemisphere are essential for initiating and maintaining speech. Because of this, individuals with TMoA often present with difficulty in speech maintenance and initiation.

<span class="mw-page-title-main">Foix–Chavany–Marie syndrome</span> Medical condition

Foix–Chavany–Marie syndrome (FCMS), also known as bilateral opercular syndrome, is a neuropathological disorder characterized by paralysis of the facial, tongue, pharynx, and masticatory muscles of the mouth that aid in chewing. The disorder is primarily caused by thrombotic and embolic strokes, which cause a deficiency of oxygen in the brain. As a result, bilateral lesions may form in the junctions between the frontal lobe and temporal lobe, the parietal lobe and cortical lobe, or the subcortical region of the brain. FCMS may also arise from defects existing at birth that may be inherited or nonhereditary. Symptoms of FCMS can be present in a person of any age and it is diagnosed using automatic-voluntary dissociation assessment, psycholinguistic testing, neuropsychological testing, and brain scanning. Treatment for FCMS depends on the onset, as well as on the severity of symptoms, and it involves a multidisciplinary approach.

<span class="mw-page-title-main">Cortical deafness</span> Medical condition

Cortical deafness is a rare form of sensorineural hearing loss caused by damage to the primary auditory cortex. Cortical deafness is an auditory disorder where the patient is unable to hear sounds but has no apparent damage to the structures of the ear. It has been argued to be as the combination of auditory verbal agnosia and auditory agnosia. Patients with cortical deafness cannot hear any sounds, that is, they are not aware of sounds including non-speech, voices, and speech sounds. Although patients appear and feel completely deaf, they can still exhibit some reflex responses such as turning their head towards a loud sound.

Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but rather a neurological inability of the brain to process sound meaning. While auditory agnosia impairs the understanding of sounds, other abilities such as reading, writing, and speaking are not hindered. It is caused by bilateral damage to the anterior superior temporal gyrus, which is part of the auditory pathway responsible for sound recognition, the auditory "what" pathway.

<span class="mw-page-title-main">Superior temporal sulcus</span> Part of the brains temporal lobe

In the human brain, the superior temporal sulcus (STS) is the sulcus separating the superior temporal gyrus from the middle temporal gyrus in the temporal lobe of the brain. A sulcus is a deep groove that curves into the largest part of the brain, the cerebrum, and a gyrus is a ridge that curves outward of the cerebrum.

Neuroscientists have learned much about the role of the brain in numerous cognitive mechanisms by understanding corresponding disorders. Similarly, neuroscientists have come to learn much about music cognition by studying music-specific disorders. Even though music is most often viewed from a "historical perspective rather than a biological one" music has significantly gained the attention of neuroscientists all around the world. For many centuries music has been strongly associated with art and culture. The reason for this increased interest in music is because it "provides a tool to study numerous aspects of neuroscience, from motor skill learning to emotion".

Phonagnosia is a type of agnosia, or loss of knowledge, that involves a disturbance in the recognition of familiar voices and the impairment of voice discrimination abilities in which the affected individual does not suffer from comprehension deficits. Phonagnosia is an auditory agnosia, an acquired auditory processing disorder resulting from brain damage, other auditory agnosias include cortical deafness and auditory verbal agnosia also known as pure word deafness.

<span class="mw-page-title-main">Sign language in the brain</span>

Sign language refers to any natural language which uses visual gestures produced by the hands and body language to express meaning. The brain's left side is the dominant side utilized for producing and understanding sign language, just as it is for speech. In 1861, Paul Broca studied patients with the ability to understand spoken languages but the inability to produce them. The damaged area was named Broca's area, and located in the left hemisphere’s inferior frontal gyrus. Soon after, in 1874, Carl Wernicke studied patients with the reverse deficits: patients could produce spoken language, but could not comprehend it. The damaged area was named Wernicke's area, and is located in the left hemisphere’s posterior superior temporal gyrus.

References

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