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Attention parameters were studied in 60 patients with stuttering by a corrective visual method. The stuttering patients showed a tendency to a slower completion of corrections and a greater standard deviation compared to healthy subjects. It was ascertained that the nature of attention in patients with stuttering was similar to the character of attention in patients with manic-depressive psychosis in a state of depression.
In studies of the acute effects of haloperidol on the severity of stuttering in 12 subjects not in treatment at the time of drug evaluation, a single 0.5 mg haloperidol injection was found to increase fluency in 9 to 12 subjects, as compared with saline placebo. The average improvement in those subjects who improved was 25% on reading and 40% on spontaneous speech. Side effects from this dose of haloperidol were minimal. The effects of apomorphine on speech were not statistically significant, but increased fluency was seen in a number of subjects on the reading test. The results of this study suggest that acute drug evaluation studies may be valuable in determining the effects of various psychotropic agents on the severity of stuttering. The increased fluency after haloperidol, an agent which is felt to turn off the dopaminergic system via postsynaptic blockade, and after low-dose apomorphine, which appears to inhibit the dopamine system via presynaptic effects is consistent with a role for central dopaminergic systems in the pathogenesis of stuttering. Further studies are needed to confirm this hypothesis.
Results obtained in a single encephalography examination of 79 stuttering and 143 healthy children, both 7 to 10 years old, were compared. While the difference in the frequency between the two groups with respect to focal findings without peak potentials and a focal and generalised tendency to attacks could not be substantiated, 29.1 per cent of all children in the group of stutterers showed a background activity that was too slow for their age. This finding is interpreted as an expression of delayed development which, because of a psychic compensation capacity not corresponding to the age of the test person, offers a favourable basic condition for the development of stuttering. The danger of a misinterpretation of electroencephalographic findings obtained from specific study groups without comparison with a normal population is pointed out.
When parents are concerned about the development of stuttering in their child they often consult their pediatrician or family physician. Theories on the development of stuttering are briefly examined in this article, and guidelines are provided to help the physician determine if the child's dysfluencies are within the normal range. Referral to a speech therapist should be considered when any of the following are noted: excessive repetition of the first syllable of words; tremor of the muscles of mouth or jaw, increase in pitch or loudness, or evidence of fear or emotion as the child struggles with a word; evidence that the child avoids certain words or situations; and excessive concern of parents, teachers or the dysfluent individual. Two approaches to therapy, traditional and behavioural, are described. The latter has resulted in significant gains in fluency among stutterers.
Stuttering (dysfluent speech) affects the social and emotional development of its victims. The family physician is often the first professional to encounter the stutterer and his family. The severity of stuttering is determined not only by the number of prolongations and hesitations, but also by the patient's fear of the dysfluent moment and, in turn, the creation of avoidance behaviors to hide the disability. The etiology remains unclear, but both biologic and psychologic factors are involved.
Data on a comparative clinico-physiological study of children with neurotical and pseudoneurotic stuttring are presented. Clinically 60 patients from 2.5 to 6 years were studied, among them the articulatory and respiratory component of expressive speech formation was studied in 30 cases. The data indicate the complication and deepening of the neurotical and pseudoneurotic symptomatology in the age group from 5 to 6 years. A correlation of clinical and physiological parameters showed that neurotical stuttering appears against the background of a normally formed speech stereotype. In treating neurotical stuttering more attention should be paid to medicamental tranquilizing therapy and a correct psychotherapeutical approach, along with logopedical lessons. In pseudo-neurotical stuttering there is a pathological onthogenesis of the speech functioning--an abnormal formation of the speech stereotype. In both cases durative logopedical correlational work and an active goal-directed medicamental treatment are required.
This study required six groups of judges, three experimental groups and three control groups (all n = 5), to categorize consecutive 5.0-sec speech intervals as Stuttered or Nonstuttered on four judgment occasions. Between the second and third occasions, each experimental group was trained to categorize correctly one of three sets of speech intervals: agreed intervals, which had been unanimously prejudged to be Stuttered or Nonstuttered; disagreed intervals, which had been prejudged to be Stuttered by approximately half of a large group of judges; or randomly selected intervals, including both agreed and disagreed intervals. Results replicated and extended an earlier finding of improved interjudge agreement for judges trained with highly agreed intervals (Ingham, Cordes, & Gow, 1993): Training with highly agreed intervals was shown to be more effective than equivalent exposure to those intervals without feedback, and training with highly agreed intervals was shown to be more effective than training with, or exposure to, poorly agreed or randomly selected intervals.
We retrospectively evaluated three fluent asthmatic children who developed speech dysfluency following administration of theophylline. The dysfluency ceased in all three, following discontinuation of the medication. The medication was re-instituted in two patients, prompting return of dysfluency. It is unknown whether the patients had characteristics of "acquired stuttering" or "developmental stuttering." We urge appropriate testing should this complication again occur. This might then provide pharmacologic information regarding stuttering.
Self-repairing of speech errors demonstrates that speakers possess a monitoring device with which they verify the correctness of the speech flow. There is substantial evidence that this speech monitor not only comprises an auditory component (i.e., hearing one's own speech), but also an internal part: inspection of the speech program prior to its motoric execution. Errors thus may be detected before they are actually articulated. In the covert repair hypothesis of disfluency, this internal error detection possibility has been extended with an internal correction counterpart. Basically, the covert repair hypothesis contends that disfluencies reflect the interfering side-effects of covert, prearticulatory repairing of speech programming errors on the ongoing speech. Internally detecting and correcting an error obstructs the concurrent articulation in such manner that a disfluent speech event will result. Further, it is shown how, by combining a small number of typical overt self-repair features such as interrupting after error detection, retracing in an utterance, and marking the correction with editing terms, one can parsimoniously account for the specific forms disfluencies are known to take. This reasoning is argued to apply to both normal and stuttered disfluency. With respect to the crucial question concerning what makes stuttering speakers so greatly disfluent, it is hypothesized that their abilities to generate error-free speech programs are disordered. Hence, abundant stuttering derives from the need to repeatedly repair one's speech programs before their speech motor execution.
A 30-year-old woman developed a sudden onset of stuttering in the early stage of Japanese B encephalitis. Cranial CT scan, EEG and electrodiagnostic studies revealed no definite focal abnormality. Her stuttering persisted for 1 week and subsided spontaneously. Stuttering can be a rare early manifestation in Japanese B encephalitis.
Speech techniques can always become automatic with exercises provided the only purpose is the initiation and formation of particular habitual speech-motor patterns such as the coordination of respiration and phonation. However, if the speech-technical measures alienate the stutterer's spontaneous speech, exercises designed to automate speech flow seem bound to fail, since the stutterer cannot fully identify himself with a manner of speech which is not the expression of himself. The anxiety inherent in some speech situations should be allayed by the speaker's accustomization to the adverse stimuli they produce. However, in the final analysis, the irrationality of speech situations defies a systematic approach. Thus, it is the relaxation method connected with the process of graded desensitization of the stutterer which is therapeutically effective and not his adaptation to particular speech situations.
Stuttering priapism is intermittent, prolonged, painful, pathologic erections with intervening periods of detumescence. An adolescent had stuttering priapism associated with withdrawal from sustained-release methylphenidate. To our knowledge, this is the first such report of stuttering priapism associated with stimulant drugs for treatment of attention deficit hyperactivity disorder.
Keratin intermediate filaments are important cytoskeletal structural proteins involved in maintaining cell shape and function. Mutations in the epidermal keratin genes, keratin 5 or keratin 14 lead to the disruption of keratin filament assembly, resulting in an autosomal dominant inherited blistering skin disease, epidermolysis bullosa simplex (EBS). We investigated a large EBS kindred who exhibited a markedly heterogeneous clinical presentation and detected two distinct keratin 5 mutations in the proband, the most severely affected. One missense mutation (E170K) in the highly conserved helix initiation peptide sequence of the 1A rod domain was found in all the affected family members. In contrast, the other missense mutation (E418K) was found only in the proband. The E418K mutation was located in the stutter region, an interruption in the heptad repeat regularity, whose function as yet remains unclear. We hypothesized that this mutated stutter allele was clinically silent when combined with the wild type allele but aggravates the clinical severity of EBS caused by the E170K mutation on the other allele. To confirm this in vitro, we transfected mutant keratin 5 cDNA into cultured cells. Although only 12.7% of the cells transfected with the E170K mutation alone showed disrupted keratin filament aggregations, significantly more cells (30.0%) cotransfected with both E170K and E418K mutations demonstrated keratin aggregation (p < 0.05). These transfection assay results corresponded to the heterogeneous clinical findings of the EBS patient in this kindred. We have identified the first case of both compound heterozygous dominant (E170K) and recessive (E418K) mutations in any keratin gene and confirmed the significant involvement of the stutter region in the assembly and organization of the keratin intermediate filament network in vitro.
The viral polymerase of influenza virus, a negative-strand RNA virus, is believed to polyadenylate the mRNAs by stuttering at a stretch of five to seven uridine residues which are located close to the 5' ends of the viral RNA templates. However, a mechanism of polyadenylation based on a template-independent synthesis of the poly(A) tail has not been excluded. In this report, we present new evidence showing the inherent ability of the viral polymerase to stutter at the poly(U) stretch of a viral RNA template during RNA replication. Variants which possess 1- to 13-nucleotide-long insertions at the poly(U) stretch have been identified. These results support a stuttering mechanism for the polyadenylation of influenza virus mRNAs.
The present study attempted to determine how a rhythmic beat affects ongoing behavior. A regular stimulus beat was presented to normal subjects who had been instructed to push a bar from side to side. Other subjects had been instructed to emit a vocal response. The individual vocal and motor responses became synchronized with the individual beats of the rhythm. The time between stimulus beats determined the modal interresponse time. These results indicate a synchronization effect: ongoing behavior tends to become synchronized with an ongoing stimulus rhythm. An attempt was made to apply these findings to the problem of stuttering, which can be considered as a disturbance of the natural rhythm of speech. Stutterers were instructed to synchronize their speech with a simple regular beat presented to them tactually by a portable apparatus. The result was a reduction of 90% or more of the stuttering for each subject during the period of synchronization. This effect endured for extended periods of spontaneous speech as well as for reading aloud and was found to be attributable to the rhythmic nature of the stimulus and not to other factors.
A stuttering therapy program in which adult stutterers were hospitalized and treated in small groups (n = 4) under token economy conditions is described. The Token System reinforced reductions and penalized increases in stuttering during conversation. The therapy program was divided into three stages. Initially, subjects were treated by the token system, which was then integrated with a delayed auditory feedback schedule designed to instate and shape a prolonged speech pattern into normal fluent speech. Finally, subjects passed through a speech situation hierarchy while under token control conditions. Experiments conducted in the first two stages of treatment are described. The first-stage experiments examined the design of the token system; the second-stage experiment assessed the effect of a contingent punishment schedule integrated with the delayed auditory feedback procedure in order to shape rate of speaking as well as fluency.
Stuttering and aphasia emerged as salient clinical features in an adult with multifocal brain damage and paroxysmal EEG activity. Anticonvulsant treatment was associated with reversal of the stuttering and with marked improvement in language abilities.
Polymorphisms of three different dopaminergic genes, dopamine D2 receptor (DRD2), dopamine beta-hydroxylase (D beta H), and dopamine transporter (DAT1), were examined in Tourette syndrome (TS) probands, their relatives, and controls. Each gene individually showed a significant correlation with various behavioral variables in these subjects. The additive and substractive effects of the three genes were examined by genotyping all three genes in the same set of subjects. For 9 of 20 TS associated comorbid behaviors there was a significant linear association between the degree of loading for markers of three genes and the mean behavior scores. The behavior variables showing the significant associations were, in order attention deficit hyperactivity disorder (ADHD), stuttering oppositional defiant, tics, conduct, obsessive-compulsive, mania, alcohol abuse and general anxiety-behaviors that constitute the most overt clinical aspects of TS. For 16 of the 20 behavior scores there was a linear progressive decrease in the mean score with progressively lesser loading for the three gene markers. These results suggest that TS, ADHD, stuttering oppositional defiant and conduct disorder, and other behaviors associated with TS, are polygenic, due in part to these three dopaminergic genes, and that the genetics of other polygenic psychiatric disorders may be deciphered using this technique.