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Biomedical subjects

F J Freeman

Publications and source records attributed to F J Freeman.

18 recordsLinked to original sources
PubMed1992

Brain blood flow related to acoustic laryngeal reaction time in adult developmental stutterers.

The 1980s witnessed renewed interest in the relation between developmental stuttering and central nervous system (CNS) abnormalities. We have reported differences between nonstutterers and developmental stutterers on electrophysiologic (QTE) and metabolic (rCBF) measures of brain function. A critical step in the interpretation of results of functional brain imaging studies is to determine the relation, if any, of identified CNS abnormalities to speech motor control in persons who stutter. In this study we addressed the interpretation of rCBF findings by asking whether we could identify patterns of impaired acoustic laryngeal reaction time (LRT) as a function of response complexity parallel to rCBF findings. Stutterer subgroups determined by clinical severity ratings were not differentiated by LRT values as a function of response complexity. Stutterers with relative blood flow asymmetry below the normal median value involving both left superior and middle temporal regions of interest (ROIs) showed significantly longer LRT for the complex response than did normal speakers and stutterers with above-normal median relative flow values to at least one of these temporal ROIs. Stutterer subgroups based on reduced cingulate flow alone were not differentiated by LRT values. Findings are consistent with Goldberg's (1985) model of CNS premotor processing. Findings also suggest that stutterer subgroups might be distinguished by the presence, loci, and relative magnitude of cortical and/or subcortical rCBF abnormality in regions that subserve a fluency-generating system.

Adult↗
PubMed1992

Multichannel electromyographic observations in spasmodic dysphonia patients and normal control subjects.

Spasmodic dysphonia is primarily a disorder of vocalization. Increasing evidence, however, suggests that individuals with this disorder comprise a heterogeneous population characterized by abnormal motor control throughout the vocal tract. Multichannel simultaneous electromyography was performed on 11 spasmodic dysphonia patients and 10 normal awake subjects to investigate both the distribution of neuromotor abnormality within the vocal tract (eg, intrinsic and extrinsic laryngeal muscles, tongue, and palate) and the contribution of activation of higher central nervous system centers to observed abnormality. Experimental tasks ranged from vegetative (quiet breathing) to simple linguistic (short sentences). Digitized electromyographic signals were analyzed to compute the amplitude envelope and extract a set of parameters that represent amplitude characteristics. Electrode insertions were cross-validated by quantitative analysis of patterns of activation across selected reference tasks and by traditional qualitative methods. Between-group differences were found for measures of normalized median and peak token amplitudes. These differences are both task- and measure-dependent. Results highlight the complex and interactive effects of muscle, task, and quantitative measures on between-group differences.

Adult↗
PubMed1991

Heterogeneity in spasmodic dysphonia. Neurologic and voice findings.

Spasmodic dysphonia is a disturbance of phonation with laryngeal spasms. We report voice and neurologic examination findings in 45 subjects. Neurologic abnormalities were found in 32 subjects (71.1%). Rapid alternating movement abnormalities, weakness, and tremor were common. Incoordination and spasticity were rare. Lower extremity findings were frequent. Abnormalities were bilateral. Spasmodic dysphonia severity was related to age. Type, severity, and duration of vocal symptoms were not different for subjects with or without neurologic abnormalities. Vocal tremor was more frequent in neurologically abnormal subjects. Involvement of a pallidothalamic-supplementary motor area system could account for neurologic findings, brain imaging findings, and clinical heterogeneity. The view emerging is that spasmodic dysphonia is a manifestation of disordered motor control involving systems of neurons rather than single anatomical sites.

Adult↗
PubMed1991

Regional cerebral blood flow in developmental stutterers.

Stuttering is a poorly understood communication disorder with a 1% global prevalence. Recently, there has been a resurgence of interest in a neurogenic origin for the disorder, although no research has established clear neurological differences between "developmental" (stuttering onset in childhood) stutterers and nonstutterers. We have used xenon 133 single-photon emission computed tomography to study regional cerebral blood flow (rCBF) in 20 stutterers. Analysis revealed global, absolute flow reductions. Relative flow asymmetries (left less than right) were identified in three hemispheric regions: anterior cingulate and superior and middle temporal gyri. Milder changes were found in the left inferior frontal gyrus. Stutterers had rCBF values below median for either anterior cingulate or middle temporal gyri. With one exception, severe stutterers had rCBF values below median for the anterior cingulate gyrus. All stutterers with rCBF values above median in the cingulate gyrus had rCBF values below median in the middle temporal gyrus, and severity of their disorder was either mild or moderate. Our findings suggest that stuttering is a neurogenic disorder involving recognized cortical regions of speech-motor control.

Adult↗
PubMed1991

Laryngeal reaction time profiles in spasmodic dysphonia: relationship to cortical electrophysiologic abnormality.

This study combines measures of linguistic and vocal performance and long-latency auditory electrophysiology to investigate task-dependent variability in spasmodic dysphonia (SD). Linguistic performance was evaluated using several measures of relatively complex linguistic ability (i.e., discourse analysis). Vocal performance was evaluated by measuring acoustic laryngeal reaction time (LRT) for tasks that differ in complexity. Normal structure of the cortex and subcortex was confirmed by magnetic resonance imaging. Cortical function was measured using multichannel quantitative auditory evoked potentials (AEPs). As a group, SD subjects who demonstrated subtle linguistic deficits also demonstrated prolonged LRT for the complex task and repeated and persistent auditory electrophysiologic abnormalities over the anterior quadrant of the left hemisphere. As a group, linguistically normal SD subjects demonstrated no significant increase in LRT for the complex task and no recurrent electrophysiologic abnormalities over the left anterior cortex relative to normal controls. Results support a neurogenic origin of SD and suggest that some aspects of inter- and intrasubject variability may be related to differences in loci and magnitude of cortical abnormalities.

Adult↗
PubMed1991

Laryngeal electromyographic activity in adductor and abductor spasmodic dysphonia.

Vocal symptoms in spasmodic dysphonia (SD) range from strain-strangle phonation and glottal-stop phonatory breaks of adductor SD to breathy phonation and aspirate phonatory breaks of abductor SD. Many SD subjects show both symptom types. Heterogeneity in vocal symptoms contributes to controversy surrounding the etiology(s) of SD. Acoustic/perceptual analyses of vocal symptoms are inconclusive in resolving this controversy. This investigation moves the search for distinguishing features of adductor and abductor SD to the level of neuromuscular control and analysis of intrinsic laryngeal muscle (adductor and abductor) activity. Subjects rated perceptually as primarily adductor or abductor SD sustained production of vegetative gestures and isolated speech sounds (/i/ and /s/). Qualitative and quantitative analyses of electromyographic signals recorded from thyroarytenoid (TA) failed to differentiate SD subjects by symptom type. Analysis of TA and posterior cricoarytenoid (PCA) activity in one abductor SD revealed high levels in both muscles during production of the voiced vowel. Data suggest that a possible explanation for symptom heterogeneity in SD is the relation between disrupted neuromotor input to laryngeal muscles and reflexive or conscious compensations constrained by laryngeal biomechanics.

Adult↗
PubMed1990

Evidence for cortical dysfunction in spasmodic dysphonia: regional cerebral blood flow and quantitative electrophysiology.

Cortical function was evaluated in 26 subjects with spasmodic dysphonia. Quantitative topographic electrophysiologic mapping (QTE) was employed to provide quantitative analyses of EEG spectra and auditory and visual long-latency evoked potentials. Single-photon emission computed tomography (SPECT) of the cerebral transit of Xenon-133 was used to evaluate regional cerebral blood flow. Left hemispheric abnormalities in cortical function were found by both techniques in 10 subjects and by at least one technique in 18 subjects. Right hemispheric abnormalities were observed by both techniques in 8 subjects and by at least one technique in 18 subjects. Most patients with cortical dysfunction in one hemisphere had cortical dysfunction in the other, while only 4 subjects had unilateral lesions as found by one of the two techniques. Eight subjects were normal by all measurements. Underlying structural abnormalities were detected by magnetic resonance imaging in 5/24 subjects. However, functional abnormalities (SPECT or QTE) were not observed at sites of structural abnormalities. SPECT and QTE were significantly related in identification of left hemispheric dysfunction (p = .037) with a trend in the right hemisphere (p = .070), and a significant congruence of SPECT and QTE findings occurred in the left anterior cortical quadrant (p = .011). These findings indicate that dysfunction of cortical perfusion and/or cortical electrophysiology is associated with spasmodic dysphonia in the majority of subjects studied.

Adult↗
PubMed1987

Permeability studies on liposomes formed from polymerizable diacetylenic phospholipids and their potential applications as drug delivery systems.

We have investigated the permeability and entrapment characteristics of liposomes formed from a group of polymerizable phospholipids, containing diacetylenic groups in one or both of their acyl chains. Permeability was assessed by the release of an entrapped dye, 6-carboxyfluorescein. Diacetylenic phosphatidylcholine (PC) liposomes were found to exhibit a wide range of permeability properties, depending on: the nature of the diacetylenic lipid, i.e. mixed-chain (mc) or identical-chain (id), the extent of polymerisation, vesicle size, and cholesterol content. Ultraviolet-initiated polymerisation affected a significant decrease in the permeability of C25idPC liposomes. The increase in permeability of liposomes formed from four other diacetylenic lipids (C25mcPC, C23idPC, C23mcPC and C20idPC) after polymerisation was attributed to disturbances in the packing of lipid molecules, and/or the limited ability of small unilamellar vesicles to accommodate long polymers. The C20idPC lipid is atypical, forming irregular monomeric and polymeric vesicles. The permeability of C25idPC liposomes was also assessed by the release of [3H]inulin. C25idPC liposomes exhibited low permeabilities to [3H]inulin in their monomeric and polymeric states. Incubation of C25idPC liposomes in human plasma caused a substantial increase in the permeability of monomeric vesicles to both carboxyfluorescein and [3H]inulin. The permeability of polymerised C25idPC liposomes, however, was unaffected in the presence of plasma, with vesicles retaining most of their entrapped [3H]inulin after 50 h. These findings demonstrate that polymeric C25idPC liposomes exhibit high resistance to the destructive actions of plasma components, such as high-density lipoproteins (HDLs). Polymeric C25idPC liposomes may have an application in drug delivery systems.

Alkynes↗
PubMed1987

Spasmodic dysphonia subsequent to head trauma.

Spasmodic dysphonia (SD) is a low-incidence voice disorder of unknown origin. A subgroup of seven patients with SD from our larger pool of 70 report vocal symptoms subsequent to head injury. This article is a case report of the neurodiagnostic findings, including computed tomography, magnetic resonance imaging, auditory brain-stem response, brain electrical activity mapping, and single photon emission computed tomography for three such patients. For each patient, two or more tests revealed positive neurologic findings. Each test, except computed tomography, demonstrated abnormalities in one or more patients. Two principles of clinical management are derived: (1) information regarding head trauma sustained before SD symptom onset is significant; (2) the absence of neuropathology on a single measure of central nervous system function should not be considered conclusive evidence that no neurologic lesions exist.

Adult↗
PubMed1987

Episodic reactive dysphonia: a case study.

This case study exemplifies successful diagnosis through stroboscopic fiberoptic examination, illustrates the critical importance of a careful case history, and demonstrates potential hazards of supposedly benign environmental substances for hypersensitive individuals.

Adult↗
PubMed1987

Spasmodic dysphonia.

Few speech disorders have been more controversial as to etiology and treatment as spasmodic dysphonia. This article reviews the historical background and origins of spasmodic dysphonia theories and the legacy of their implications on the current treatment of afflicted patients. The evolution and impact of "organic theories" is discussed and a personal perspective on the central nervous system investigations performed by the authors is briefly elucidated and their practical experience in managing spasmodic dysphonia patients is offered for the reader's consideration.

Female↗
PubMed1985

Interruptions as a variable in stuttering and disfluency.

Parental verbal behavior is often cited as a major precipitating and maintaining factor in the onset and development of stuttering. Parents are frequently counseled to avoid interrupting their stuttering child. The purpose of the present study was to determine (a) whether mothers of preschool stutterers interrupt children's speech more frequently than mothers of nonstutterers, (b) whether stutterers interrupt the speech of mothers more frequently than nonstutterers, and (c) whether there is relationship between interruptive behavior and the occurrence of children's disfluencies. Twenty-four preschool boys (12 stutterers and 12 nonstutterers) and their mothers participated in the study. Ten-min, conversational speech samples of mothers interacting with their own children, unfamiliar stutterers, and unfamiliar nonstutterers were analyzed. Results indicated that mothers of nonstutterers interrupted the disfluent speech of stutterers significantly more often than did mothers of stutterers. Most importantly, all mothers interrupted children's disfluent speech significantly more than they interrupted children's fluent speech. Further, all children demonstrated a tendency to be disfluent when they interrupted a mother.

Child, Preschool↗
PubMed1985

Mother and child speech rates as a variable in stuttering and disfluency.

Three questions were addressed in this study: (a) Do mothers of stuttering children talk faster than mothers of nonstuttering children, (b) do stuttering children talk faster than nonstuttering children, and (c) is there a relationship between child's rate of speech and mother's rate of speech in dyadic conversation? Twelve nonstuttering preschool boys and their mothers were matched with 12 stutterers and their mothers. Ten min of free-play interaction between alternated mother-child dyads were video recorded. Speech rates, defined as syllables per second in fluent utterances, were calculated. Results demonstrated that mothers of stutterers talked significantly faster to all children. Stutterers spoke slower than nonstutterers, and severe stutterers spoke slower than moderate stutterers. A correlational analysis revealed that the more the child stuttered, the slower he talked during fluent speech. Further, the slower the child talked during fluent speech, the faster the mother interacting with him talked. The results reveal an interactive and complex relationship between mother and child speech rates. The interpretation of results relating to child speech rates was complicated by post hoc analyses revealing a significant relationship between speech rates and utterance length.

Child, Preschool↗
PubMed1978

Laryngeal muscle activity during stuttering.

Laryngeal muscle activity during fluent and stuttered utterances was investigated via electromyography. Analysis revealed that stuttering was accompanied by high levels of laryngeal muscle activity and disruption of normal reciprocity between abductor and adductor muscle groups. Results are interpreted as demonstrating the existence of a laryngeal component in stuttering and showing a strong correlation between abnormal laryngeal muscle activity and moments of stuttering.

Action Potentials↗