Aprosodia

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Aprosodia is a neurological condition characterized by the inability of a person to properly convey or interpret emotional prosody. Prosody in language refers to the ranges of rhythm, pitch, stress, intonation, etc. These neurological deficits can be the result of damage of some form to the non-dominant hemisphere areas of language production. The prevalence of aprosodias in individuals is currently unknown, as testing for aprosodia secondary to other brain injury is only a recent occurrence.

Contents

Types

Productive

Receptive

Receptive aprosodia can result from impairment at one or more sensory and/or cognitive levels ranging from hearing (signal acquisition) to auditory processing (signal isolation) to emotional comprehension (signal interpretation). For example, the first two difficulties impair an individual's ability to observe and discern changes in stress and intonation, whereas the third impairs an individual's ability to assess the significance of those stress and intonation changes that he or she correctly observes and discerns; impairment of the third type correlates significantly with expressive aprosodia. [3]

Causes

Localized brain damage

One cause of aprosodia is trauma to one of several specific areas of the brain, resulting in the inability to properly process or convey emotional cues. This brain damage can occur in the form of ischemic damage from stroke. [4]

Alcohol use disorder

An inability to process or exhibit emotions in a proper manner has been shown to exist in people who consume excessive amounts of alcohol and those who were exposed to alcohol while fetuses (FAexp). Initially, when people with an alcohol use disorder are detoxified and FAexp individuals were tested for impairment in cognitive function, it was limited to testing the non-affective aspects of language, as those were the more easily recognized by a physician not trained in analyzing affective prosody. When tested using the aprosodia battery, it was found that those with alcohol use disorder who detoxified and FAexp individuals demonstrated significant impairment in their ability to detect affective prosody when used by others. The major factors which influence affective prosody in those impacted by alcohol use, from greatest to least impact, are: alcohol use by mother, age at onset of chronic abuse of alcohol, age at initial abuse, how chronic the abuse is, and the age when a person first becomes drunk. [5]

Aprosodia as a symptom

Aprosodia has also been shown to appear secondary to several diseases such as multiple sclerosis or post traumatic stress disorder. [6] It is likely that as time passes more diseases will be shown to exhibit aprosodia as a symptom. Aprosodia is a condition that was not often tested for in the presence of neurological deficits; however, as more becomes known about it, the aprosodia battery will likely be administered more frequently. For example, the first study testing for aprosodia in MS did not occur until 2009. [7]

Diagnosis

Emotional batteries

Emotional batteries consist of asking patients to read various sentences with specific emotional indicators. Their performance is subjectively analyzed by an expert to determine if they are aprosodic. The analysis is often performed by two experts independently, with one of the judges not being present during the interview in case the patient was still able to use facial cues. [8]

Assessment questionnaire

Another method implemented to test for aprosodia involves having questionnaires filled out by those close to the patient. The doctors and nurses taking care of a patient are also requested to fill out a questionnaire if aprosodia is suspected. This diagnosis method occurs more as an indicator that the aprosodia battery should be administered rather than being used as a singular diagnosis tool. Implementation of the questionnaire is expected to become more widespread as aprosodia is revealed to be a side-effect of more diseases. [8]

Aprosodia vs. dysprosody

Brain imaging studies related to speech functions have yielded insights into the subtle difference between aprosodia and dysprosody. The major differences in these result from functions which are characterized as belonging mainly to the left or right hemisphere. Several of the functions have been described as dominant and lateralized functions of the corresponding hemispheres, while some have been found to arise from communication between the two hemispheres. [1]

Treatment

The two main forms of treatment are cognition based and imitation based. Cognitive treatments attempt to rebuild the "emotional toolbox" of those with aprosodia. The basis for this treatment is the belief that there exists a defined set of emotional responses that can be chosen for a given scenario. Choosing the proper emotional response can very much be likened to choosing the proper word when describing an object, and this deficiency can be likened to Broca's Aphasia but for emotions. Imitative treatments attempt to help "kickstart" the motor systems involved in the production of both vocal and facial emotive gestures. The basis for this treatment is the belief that the pathways responsible for the motor elements of expressive prosody were damaged. It is hypothesized that the motor damage occurs at the level of planning as well as the level of execution. [9]

The methods of treatment are being evaluated and changed through several iterations to reach the most beneficial treatment for those with aprosodia. Although the biggest limitation on progress of aprosodia treatment is sample size, some significant data has been found to influence each subsequent phase of study. The Rosenbek lab at the University of Florida is currently in a new phase of treatment study based on combinations of the cognitive-linguistic and imitative therapies delivered in a randomized fashion in an effort to gain more insight into what most prominently affects aprosodia treatment. [8]

Research

Research into the perisylvan region of the right hemisphere has shown that there are similarly mapped analogues to the speech center in the left hemisphere. This is especially evident in those areas resembling Broca's area and Wernicke's area. [10]

Additionally, in studying the brain regions associated with aprosodia, brain imaging tests were performed to determine if aprosodia is both a lateralized and dominant function of the right hemisphere areas of language production. Aprosodia can be considered a dominant function of the right hemisphere because strong correlation was found between deficits in affective prosody and distribution of lesions in the cortices of those with right brain damage. No correlation was found between the distribution of cortical lesions in patients with left brain damage and the types of aphasic deficits pronounced in those patients. Aprosodia can be considered a lateralized function of the right hemisphere because of the differences in the ability of a patient to respond to affective prosodic information in those with left brain damage when compared to those with right brain damage. Patients with affective-prosodic deficits in the left hemisphere (dysprosodic patients) showed improvement in understanding and repeating prosodic information when other conveyed linguistic information was simplified, i.e. requiring the patient to mainly determine prosodic information contained in an interaction. This improvement in processing affective prosodic information under reduced linguistic processing demands did not occur for patients with right brain damage. [1]

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">Expressive aphasia</span> Language disorder involving inability to produce language

Expressive aphasia is a type of aphasia characterized by partial loss of the ability to produce language, although comprehension generally remains intact. A person with expressive aphasia will exhibit effortful speech. Speech generally includes important content words but leaves out function words that have more grammatical significance than physical meaning, such as prepositions and articles. This is known as "telegraphic speech". The person's intended message may still be understood, but their sentence will not be grammatically correct. In very severe forms of expressive aphasia, a person may only speak using single word utterances. Typically, comprehension is mildly to moderately impaired in expressive aphasia due to difficulty understanding complex grammar.

<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 often suffer of anosognosia – they are 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.

Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical condition. Anosognosia results from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neuropsychiatric disorder. A deficit of self-awareness, the term was first coined by the neurologist Joseph Babinski in 1914, in order to describe the unawareness of hemiplegia.

<span class="mw-page-title-main">Conduction aphasia</span> Inability to repeat speech despite being able to perceive and produce it

In neurology, 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.

Expressive language disorder is one of the "specific developmental disorders of speech and language" recognized by the tenth edition of the International Classification of Diseases (ICD-10). As of the eleventh edition, it is considered to be covered by the various categories of developmental language disorder. Transition to the ICD-11 will take place at a different time in different countries.

<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.

In linguistics, prosody is the study of elements of speech that are not individual phonetic segments but which are properties of syllables and larger units of speech, including linguistic functions such as intonation, stress, and rhythm. Such elements are known as suprasegmentals.

Amusia is a musical disorder that appears mainly as a defect in processing pitch but also encompasses musical memory and recognition. Two main classifications of amusia exist: acquired amusia, which occurs as a result of brain damage, and congenital amusia, which results from a music-processing anomaly present since birth.

<span class="mw-page-title-main">Primary progressive aphasia</span> Gradual impairment of language processing capabilities

In neuropathy, primary progressive aphasia (PPA) is a type of neurological syndrome in which language capabilities slowly and progressively become impaired. As with other types of aphasia, the symptoms that accompany PPA depend on what parts of the brain's left hemisphere are significantly damaged. However, unlike most other aphasias, PPA results from continuous deterioration in brain tissue, which leads to early symptoms being far less detrimental than later symptoms.

<span class="mw-page-title-main">Lateralization of brain function</span> Specialization of some cognitive functions in one side of the brain

The lateralization of brain function is the tendency for some neural functions or cognitive processes to be specialized to one side of the brain or the other. The median longitudinal fissure separates the human brain into two distinct cerebral hemispheres, connected by the corpus callosum. Although the macrostructure of the two hemispheres appears to be almost identical, different composition of neuronal networks allows for specialized function that is different in each hemisphere.

Language disorders or language impairments are disorders that involve the processing of linguistic information. Problems that may be experienced can involve grammar, semantics (meaning), or other aspects of language. These problems may be receptive, expressive, or a combination of both. Examples include specific language impairment, better defined as developmental language disorder, or DLD, and aphasia, among others. Language disorders can affect both spoken and written language, and can also affect sign language; typically, all forms of language will be impaired.

<span class="mw-page-title-main">Frontal lobe disorder</span> Brain disorder

Frontal lobe disorder, also frontal lobe syndrome, is an impairment of the frontal lobe of the brain due to disease or frontal lobe injury. The frontal lobe plays a key role in executive functions such as motivation, planning, social behaviour, and speech production. Frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, neurodegenerative diseases, neurodevelopmental disorders, neurosurgery and cerebrovascular disease. Frontal lobe impairment can be detected by recognition of typical signs and symptoms, use of simple screening tests, and specialist neurological testing.

Dysprosody, which may manifest as pseudo-foreign accent syndrome, refers to a disorder in which one or more of the prosodic functions are either compromised or eliminated.

Apraxia of speech (AOS), also called verbal apraxia, is a speech sound disorder affecting an individual's ability to translate conscious speech plans into motor plans, which results in limited and difficult speech ability. By the definition of apraxia, AOS affects volitional movement pattern. However, AOS usually also affects automatic speech.

<span class="mw-page-title-main">Right hemisphere brain damage</span> Medical condition

Right hemisphere brain damage (RHD) is the result of injury to the right cerebral hemisphere. The right hemisphere of the brain coordinates tasks for functional communication, which include problem solving, memory, and reasoning. Deficits caused by right hemisphere brain damage vary depending on the location of the damage.

Cerebellar cognitive affective syndrome (CCAS), also called Schmahmann's syndrome is a condition that follows from lesions (damage) to the cerebellum of the brain. It refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum. Impairments of executive function include problems with planning, set-shifting, abstract reasoning, verbal fluency, and working memory, and there is often perseveration, distractibility and inattention. Language problems include dysprosodia, agrammatism and mild anomia. Deficits in spatial cognition produce visual–spatial disorganization and impaired visual–spatial memory. Personality changes manifest as blunting of affect or disinhibited and inappropriate behavior. These cognitive impairments result in an overall lowering of intellectual function. CCAS challenges the traditional view of the cerebellum being responsible solely for regulation of motor functions. It is now thought that the cerebellum is responsible for monitoring both motor and nonmotor functions. The nonmotor deficits described in CCAS are believed to be caused by dysfunction in cerebellar connections to the cerebral cortex and limbic system.

Emotional prosody or affective prosody is the various paralinguistic aspects of language use that convey emotion. It includes an individual's tone of voice in speech that is conveyed through changes in pitch, loudness, timbre, speech rate, and pauses. It can be isolated from semantic information, and interacts with verbal content.

Alcohol-related brain damage alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe, limbic system, and cerebellum, with widespread cerebral atrophy, or brain shrinkage caused by neuron degeneration. This damage can be seen on neuroimaging scans.

References

  1. 1 2 3 Ross, Elliott D.; Monnot, Marilee (2008). "Neurology of affective prosody and its functional–anatomic organization in right hemisphere". Brain and Language. 104 (1). Elsevier BV: 51–74. doi:10.1016/j.bandl.2007.04.007. ISSN   0093-934X. PMID   17537499.
  2. ↑ Williamson, John B.; Harrison, David W.; Shenal, Brian V.; Rhodes, Robert; Demaree, Heath A. (2003). "Quantitative EEG Diagnostic Confirmation of Expressive Aprosodia". Applied Neuropsychology. 10 (3). Informa UK Limited: 176–181. doi:10.1207/s15324826an1003_07. ISSN   0908-4282. PMID   12890643.
  3. ↑ Raithel, V. (2005). The Perception of Intonation Contours and Focus by Aphasic and Healthy Individuals. Language in performance. Narr. pp. 28–29. ISBN   978-3-8233-6167-1 . Retrieved 2024-07-22.
  4. ↑ Heilman, Kenneth M.; Leon, Susan A.; Rosenbek, John C. (2004). "Affective aprosodia from a medial frontal stroke☆". Brain and Language. 89 (3). Elsevier BV: 411–416. doi:10.1016/j.bandl.2004.01.006. ISSN   0093-934X. PMID   15120533.
  5. ↑ Monnot, M.; Nixon, S.; Lovallo, W.; Ross, E. (2001). "Altered emotional perception in alcoholics: deficits in affective prosody comprehension". Alcoholism: Clinical and Experimental Research. 25 (3): 362–369. doi:10.1111/j.1530-0277.2001.tb02222.x. ISSN   0145-6008. PMID   11290846.
  6. ↑ Freeman, Thomas W.; Hart, John; Kimbrell, Tim; Ross, Elliott D. (2009). "Comprehension of Affective Prosody in Veterans With Chronic Posttraumatic Stress Disorder". The Journal of Neuropsychiatry and Clinical Neurosciences. 21 (1). American Psychiatric Association Publishing: 52–58. doi:10.1176/jnp.2009.21.1.52. ISSN   0895-0172. PMID   19359452.
  7. ↑ Beatty, William W; Orbelo, Diana M; Sorocco, Kristen H; Ross, Elliott D (2003). "Comprehension of affective prosody in multiple sclerosis". Multiple Sclerosis Journal. 9 (2). SAGE Publications: 148–153. doi:10.1191/1352458503ms897oa. ISSN   1352-4585. PMID   12708810.
  8. 1 2 3 Rosenbek, J. C. (2009, October 6). Chair - Department of Communicative Disorders, University of Florida. [Telephone interview]
  9. ↑ Rosenbek, John C.; Rodriguez, Amy D.; Hieber, Bethany; Leon, Susan A.; Crucian, Gregory P.; Ketterson, Timothy U.; Ciampitti, Maribel; Singletary, Floris; Heilman, Kenneth M.; Gonzalez Rothi, Leslie J. (2006). "Effects of two treatments for aprosodia secondary to acquired brain injury". The Journal of Rehabilitation Research and Development. 43 (3). Journal of Rehabilitation Research & Development: 379–390. doi:10.1682/jrrd.2005.01.0029. ISSN   0748-7711. PMID   17041823.
  10. ↑ Bookheimer, Susan (2002). "Functional MRI of Language: New Approaches to Understanding the Cortical Organization of Semantic Processing". Annual Review of Neuroscience. 25 (1). Annual Reviews: 151–188. doi:10.1146/annurev.neuro.25.112701.142946. ISSN   0147-006X. PMID   12052907.
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