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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.
Prosody refers to the variations in melody, intonation, pauses, stresses, intensity, vocal quality, and accents of speech. As a result, prosody has a wide array of functions, including expression on linguistic, attitudinal, pragmatic, affective and personal levels of speech. People diagnosed with dysprosody most commonly experience difficulties in pitch or timing control. People diagnosed with the condition can comprehend language and vocalize what they intend to say, however, they are not able to control the way in which the words come out of their mouths. Since dysprosody is the rarest neurological speech disorder discovered , not much is conclusively known or understood about the disorder. The most obvious expression of dysprosody is when a person starts speaking in an accent which is not their own. Speaking in a foreign accent is only one type of dysprosody, as the condition can also manifest itself in other ways, such as changes in pitch, volume, and rhythm of speech. It is still very unclear as to how damage to the brain causes the disruption of prosodic function. The only form of effective treatment developed for dysprosody is speech therapy.
There are several different types of dysprosody which have been classified. The most common types of dysprosody are associated with dysarthria and developmental coordination disorder, which affect motor processing in speech. Among the most studied types are:
There can also be some emotional and mental side effects to dysprosody. Each individual has a distinct voice characterized by all the prosodic elements. Once a person loses control of the timing, pitch, melody, etc. of his speech, he can also feel a sense of loss of personal identity, which can sometimes lead to depression.
In another reported case in 2004, a patient presented with dysprosody under interesting circumstances. The patient underwent surgery to correct a Reinke's edema, which originates in the vocal folds of the larynx. After the surgery, however, she began speaking in a foreign German accent. Neurological examinations were carried out on the patient through magnetic resonance imaging, but the results were completely normal. The only conclusion the doctors could make was that the surgery somehow changed the patient's vocal identification causing the new voice pattern. It was possible that the patient had a lack of oxygen to the brain during the surgery, which would have gone undetected by the resonance imaging, causing dysprosody. Although most causes of dysprosody are due to neurological damage, this case study shows that there can be other causes which are not necessarily neurologically based.
There are also more involved diagnostic evaluations for which contain both productive and comprehensive parts. In the productive part, the patient is asked to say sentences with certain instructions. In the comprehension section, the patient is asked to listen to sentences being said and then answer questions about how they were stated. In order to determine linguistic dysprosody, a patient is asked to read sentences that can either be a statement or a question using both declarative and interrogative intonations. How the patient uses prosodic contours to distinguish between asking a question and saying a statement is recorded. During the comprehension section of the evaluation, a clinician reads simple sentences with either a declarative or interrogative intonation and the patient is asked to identify whether the sentence is a question or a statement. Evaluation of these two parts can determine if the patient has linguistic dysprosody. Emotional dysprosody can be diagnosed by having a patient state a neutral sentence with different emotions, such as happy, sad, and angry. Patients with dysprosody will not be able to convey the emotions very well or differentiate their speech between the different emotions significantly. During the comprehension part, a clinician will say a sentence with specific emotional intonations and the patient must indicate the correct emotion. These techniques ultimately allow for the diagnosis of dysprosody and the degree of its severity in the patient.
Scientists have attributed major control of the Time aspects of prosody, including rhythm and timing, to the left hemisphere of the brain. On the other hand, pitch perception, such as singing and linguistics related to emotion, are believed to be organized in the right hemisphere. This belief led to the development of the "Functional Lateralization" hypothesis, stating that dysprosody can be caused by lesions in either the right or left hemispheres. It further states that the left is responsible for acoustic and temporal aspects of prosody, while the right is responsible for pitch and emotion. This hypothesis, however, has also been a cause for concern as studies have shown that people with left hemispheric damage exhibit prosodic deficiencies associated with the right hemisphere as defined by the functional lateralization hypothesis and vice versa. It has also been found that damage to the medulla, cerebellum, and basal ganglia may cause dysprosody. These conclusions have led scientists to believe that prosodic organization in the brain is extremely complex and cannot be attributed to hemispheric divisions alone. Although not well understood yet, studies to identify prosodic organization in the brain continue, primarily through the examination of damaged brain areas in patients with dysprosody and their resulting vocal deficiencies. In addition, dysprosody has been associated with several other conditions, including Parkinson's condition, Huntington's condition, gelastic epilepsy (gelastic seizure), and behavioral disorders such as apathy, akinesia and aboulia. Understanding these disorders and the areas of the brain affected in each case is key in conducting further studies of dysprosody. Scientists are continuing to study these patients in the hope of creating more concrete connections between areas of brain damage and prosodic abnormalities, which will hopefully someday lead to a full understanding of prosodic organization in the brain.
Parkinson's disease is a chronic neurodegenerative disorder that involves the loss of dopaminergic neurons in the brain. While common symptoms of Parkinson's disease are tremors, rigidity, bradykinesia, and postural instability, dysprosody is also a common problem. A common characteristic feature of dysprosody in Parkinson's is monopitch, or an inability to vary pitch when speaking.
Several studies have been performed investigating the link between Parkinson's and dysprosody. They have concluded that patients with Parkinson's disease tend to struggle with specific areas of prosody; they are less able to produce the loudness, pitch, and rhythm patterns required for expressing certain emotions, such as anger. In general, the voice modulations needed to express strong emotions are particularly difficult for patients with Parkinson's disease. Abnormal pauses in speech are also a characteristic of Parkinsonian dysprosody, including both pauses in general speech and intra-word pauses. A decrease in speech rate can also be observed in Parkinson's patients.
Studies have also shown a progression of dysprosody over time in patients with Parkinson's disease. Abnormalities in speech rate, pauses, and variation range in speech become worse as the condition progresses. The degradation of prosody in Parkinson's disease over time is independent of motor control issues, and is thus separate from those aspects of the condition. Studies have shown that treatment for Parkinson's disease can help with the dysprosody symptoms, however there is usually an improvement in pitch control only and not in the volume and emotional aspects of the condition. These treatments include medications such as L-DOPA as well as electrophysiological treatments.
Over time, there have also been cases of people with dysprosody gaining their native accent back with no course of treatment. Since the part of the brain responsible for dysprosody has not definitely been discovered, nor has the mechanism for the brain processes which cause dysprosody been found, there has not been much treatment for the condition by means of medication.
The next documented report of dysprosody occurred in 1919 by Arnold Pick, a German neurologist. He noticed a 29-year-old Czechoslovak had started speaking in a Polish accent following a stroke. Pick's patient also had right hemiparesis, a lesser version of hemiplegia, and aphasia after the stroke. Pick noticed that not only was the accent altered, but the timing of the speech was slower, and the patient spoke with uncharacteristic grammatical mistakes. Pick later wanted to follow up on his research but was not able to, since the patient had died with no autopsy performed.
The most well documented account of dysprosody was in 1943 by G. H. Monrad-Krohn. A woman, Astrid L., in Norway was hit with a shell fragment during an air raid in 1941 through her left frontal bone, leaving her brain exposed. She was unconscious for four days and when she regained consciousness at the hospital, she was hemiplegic on her right side, was having seizures, and was aphasic. Initially she could only speak in monosyllables, yes and no, but then started to form sentences. When first starting to speak again, she also spoke with uncharacteristic grammatical errors, but over time they became much less pronounced and eventually she gained back full fluency of speech. However, she sounded as though she was speaking her native Norwegian with a German accent. It was two years later that she was admitted to the Neurological University Clinic in Oslo, Norway and seen by Dr. Monrad-Krohn. Krohn examined the patient and noted that there was no noticeable difference in her fluency, motor functions, sensory functions, or coordination. Upon examination of her skull, he found a large scar on the left fronto-temporo-parietal region. This was not as helpful as Krohn would have liked. Since the scar was so extensive, it was impossible for Krohn to pinpoint the exact region of the brain which was causing this altered speech. Krohn then ran tests on Astrid to assess her language comprehension. He found that in addition to her altered speech patterns, she had trouble finding the Norwegian words for trivial objects, such as light switch and match box. She also had to repeat the examiner's questions aloud before answering, had to say words out loud to herself before writing them down, and had difficulty comprehending written instructions. Krohn could not understand how she had acquired a foreign accent; it could not be attributed to any known disorder or condition. For those with this type of dysprosody, sometimes the accents they speak are from countries to which the person has never been. This is very puzzling for neuroscientists, since dialects and accents are considered to be an acquired behavior of learning pitches, intonations and stress patterns.
There have been another 21 cases documented up until 1978. Thirteen of those cases were documented at the Mayo Clinic, while the others were documented at clinics and hospitals elsewhere.
There have been more recent occurrences of people who have developed accents after brain injuries, specifically strokes. In 1999, Judi Roberts had a stroke which paralyzed the right side of her body, leaving her unable to speak. Over time, her speech began to improve, eventually recovering full fluency, but she developed a British accent despite having lived in the US for her whole life. In 2006, another report was documented of Linda Walker, a native of England, who developed a foreign accent after having a stroke.
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