Dopamine Function in Developmental Stuttering
|ClinicalTrials.gov Identifier: NCT00024960|
Recruitment Status : Completed
First Posted : October 10, 2001
Last Update Posted : July 2, 2017
|First Submitted Date||October 9, 2001|
|First Posted Date||October 10, 2001|
|Last Update Posted Date||July 2, 2017|
|Study Start Date||October 3, 2001|
|Primary Completion Date||Not Provided|
|Current Primary Outcome Measures||Not Provided|
|Original Primary Outcome Measures||Not Provided|
|Change History||Complete list of historical versions of study NCT00024960 on ClinicalTrials.gov Archive Site|
|Current Secondary Outcome Measures||Not Provided|
|Original Secondary Outcome Measures||Not Provided|
|Current Other Pre-specified Outcome Measures||Not Provided|
|Original Other Pre-specified Outcome Measures||Not Provided|
|Brief Title||Dopamine Function in Developmental Stuttering|
|Official Title||Assessment of Pre- and Post-Synaptic Dopamine Function in Developmental Stuttering Using 11C-Raclopride and Positron Emission Tomography|
This study will use positron emission tomography (PET) to examine the role of the chemical messenger dopamine in stuttering. It will measure and compare the number of dopamine receptors and the amount of dopamine released in the brains of stutterers with that of normal volunteers. The results may provide information about how drugs that block dopamine's effect might work to enable fluent speech.
Healthy normal volunteers and people with developmental stuttering between the ages of 18 and 55 may be eligible for this study. Candidates will be screened with a medical history and possibly a physical examination and laboratory tests.
Participants will have a hearing test and cognitive function tests to measure speech, language, memory and visual skills. In addition, they will undergo the following procedures:
Participants may be asked to return for up to two scanning sessions within a year. For these scans, only 1 injection of radioactive water will be given.
|Detailed Description||Clinical responses to dopamine (DA) antagonists from patients with developmental stuttering suggest that the pathophysiology of this disorder may involve an abnormality of central DA systems. This hypothesis has never been tested using methods that measure both pre- and postsynaptic dopaminergic mechanisms within the CNS. A new PET technique permits evaluation of these mechanisms in human subjects. 11C raclopride, a relatively selective D2 receptor antagonist, is used to estimate postsynaptic DA receptor binding potential following establishment of equilibrium conditions. A low dose bolus of amphetamine is then used to release DA from the presynaptic neuron and displace the ligand from postsynaptic binding sites, in order to estimate the size of the releasable presynaptic DA pool. We propose to use this technique in individuals with developmental stuttering and control subjects to test the hypothesis that stuttering is due to dopaminergic hyperactivity within the CNS. The cause of this hyperactivity is hypothesized to be due to an increase in either the postsynaptic binding potential or the size of the releasable presynaptic dopamine vesicular pool (in which case postsynaptic receptors may be down regulated). Our studies should help conjoin and modify this pathophysiological model. If low dose amphetamine can be used to demonstrate a difference between people who stutter and controls, a second study will be conducted to see if stuttering behavior per se has a measurable effect on DA release that differs from the effect of similar speech tasks in control subjects. Lastly, in a third study, DA releasability will be measured in those recovered from stuttering and those not affected by stuttering but are part of families who have many members that stutter. The culmination of these studies is to attempt isolation of a DA marker that can be used as a phenotyping tool in genetic studies of stuttering.|
|Study Design||Not Provided|
|Target Follow-Up Duration||Not Provided|
|Sampling Method||Not Provided|
|Study Population||Not Provided|
|Study Groups/Cohorts||Not Provided|
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
|Study Completion Date||October 29, 2010|
|Primary Completion Date||Not Provided|
Subjects must be between the ages of 18 and 55.
Subjects must be in good general health except for the primary neurological diagnosis of stuttering.
Subjects may not have evidence of hypertension or cardiovascular disease, cerebrovascular disease or hyperthyroidism.
EKG and thyroid function tests must be within normal limits.
Subjects must have no history of traumatic head injury including any head trauma that resulted in loss of consciousness or history of substance abuse, including alcohol (excluding caffeine).
Subjects will be screened for history of psychiatric illness, such as depression, anxiety or obsessive-compulsive disorders according to DSM-IV; subjects with such diagnoses will be excluded.
Subjects will be screened for a past medical history or family history of speech-language disorders; subjects with a personal or significant family history of speech-language disorders unrelated to the diagnoses of stuttering or aphasia will be excluded. Also those subjects with immediate family members having a significant history of heart attack or stroke will be excluded.
Women who are pregnant or currently breast-feeding will be excluded from this study.
Subjects with pacemakers, aneurysm clips, cochlear implants, shrapnel fragments or have a significant history of exposure to small metallic objects, which might have become lodged in the tissues of the head, or neck will be excluded due to the MRI.
The following criteria must be met to identify an individual who stutters:
Affected individual regards him or herself as having a stuttering disorder, reporting instances during speech where they know exactly what they wish to say, but can not be due to production impairment; these instances may be accompanied by a feeling of tension somewhere within the vocal tract. Individuals may have sought treatment for their stuttering.
Speech-language pathologist confirms diagnosis of stuttering disorder in affected individuals, documenting presence of silent or sound prolongations, syllable repetitions, word/phrase repetitions, interjections and pauses at non-linguistic loci in their speech. Affected individuals will be at least 5% dysfluent in at least 2 of the speaking tasks used to assess fluency.
Recovered stutterers must have a history of stuttering documented by the speech pathologist responsible for evaluation or treatment of this individual during childhood. A history of stuttering may alternatively be documented by a parent and at least one other family member or friend. Recovered individuals must report that they no longer monitor their speech on a routine basis or use speech therapy techniques while speaking.
Speech-language pathologist must judge that recovered individuals are currently free of overt stuttering (less than 1 stuttering behavior/100 words).
Onset of stuttering in both affected individuals and recovered stutterers must have occurred in childhood (between 3 and 10 years-of-age), unrelated to psychological or neurological trauma.
|Ages||18 Years to 55 Years (Adult)|
|Accepts Healthy Volunteers||No|
|Contacts||Contact information is only displayed when the study is recruiting subjects|
|Listed Location Countries||United States|
|Removed Location Countries|
|Other Study ID Numbers||020008
|Has Data Monitoring Committee||Not Provided|
|U.S. FDA-regulated Product||Not Provided|
|IPD Sharing Statement||Not Provided|
|Responsible Party||Not Provided|
|Study Sponsor||National Institute on Deafness and Other Communication Disorders (NIDCD)|
|PRS Account||National Institutes of Health Clinical Center (CC)|
|Verification Date||October 29, 2010|