A clinical, evidence-based model to inform clients and their parents about the nature of stuttering is indispensable for the field. In this paper, we propose the Erasmus Clinical Model of Stuttering 2.0 for children who stutter and their parents, and adult clients. It provides an up-to-date, clinical model summary of current insights into the genetic, neurological, motoric, linguistic, sensory, temperamental, psychological and social factors (be it causal, eliciting, or maintaining) related to stuttering. First a review is presented of current insights in these factors, and of six scientific theories or models that have inspired the development of our current clinical model. Following this, we will propose the model, which has proven to be useful in clinical practice. The proposed Erasmus Clinical Model of Stuttering visualizes the onset and course of stuttering, and includes scales for stuttering severity and impact, to be completed by the (parent of) the person who stutters. The pathway of the model towards stuttering onset is based on predisposing and mediating factors. In most children with an onset of stuttering, stuttering is transient, but if stuttering continues, its severity and impact vary widely. The model includes the circle of Engel (1977), which visualizes unique interactions of relevant biological, psychological, and social factors that determine the speaker’s experience of stuttering severity and its impact. Discussing these factors and their interaction with an individual client can feed into therapeutic targets. The model is supplemented by a lifeline casus.

Dit artikel is de inleiding op het direct hierna volgende (Oonk e.a. 2022) waar een nieuw praktijkmodel over het ontstaan en ontwikkeling van stotteren wordt voorgesteld. In de dagelijkse praktijk van vooral Nederlandstalige logopedisten (-stottertherapeuten) is tot nu toe veel gebruik gemaakt van het klinische werkmodel van Bertens (1994; 2017). Dit model gaat uit van een primaire neuromusculaire timingsstoornis, welke zich niet alleen uit in het spreken, maar ook in algemene zin aanwezig is. Dit model echter, is aan revisie toe. Volgens de recente literatuur is de algemene aard van die timingstoornis niet bewezen, en zijn er veel vroegere (meer primaire) factoren aantoonbaar van belang bij het ontstaan van stotteren, met name in de genetica en in de neurologie. In dit artikel wordt deze literatuur kort samengevat, alsmede worden enkele recente modellen omschreven. Met name regulatie en terugkoppeling krijgen in recente modellen meer aandacht. Er is geen volledigheid nagestreefd, maar dit artikel is meer een tutoriale opmaat voor het hierna te presenteren model.

In dit artikel wordt een nieuw model gepresenteerd dat kan dienen als praktijkmodel voor de spreekkamer. Doel is om de ontwikkeling van stotteren en de bijbehorende processen duidelijk te maken aan personen die stotteren en ouders van kinderen die stotteren. Als aanloop voor dit nieuwe model geeft een voorbeeldcasus een visuele illustratie van de ontwikkeling van stotteren in de vormvan een levenslijn. Deze levenslijn toont hoe ontwikkelingsfactoren samen met min of meer toevallige omstandigheden van invloed kunnen zijn op de ontwikkeling van stotteren. Het praktijkmodel geeft structurering van het ontstaan en de ontwikkeling van stotteren en de factoren die hierbij een rol spelen, gebaseerd op de nieuwste onderzoeksresultaten. Na het ontstaan van beginnend stotteren worden twee sporen getoond: herstel van stotteren en verdere ontwikkeling. Diverse aspecten die van invloed zijn op het verloop van het stotteren worden weergegeven. De uitkomst van die ontwikkeling op het gebied van last van het stotteren en ernst van het stotteren kan verschillend zijn, zowel tussen personen die stotteren als binnen één persoon die stottert. Zowel de levenslijn als het praktijkmodel kunnen helpen om achtergrondinformatiete structureren en inzicht te geven in het fenomeen stotteren en het gesprek te openen over de therapiedoelen en de gewenste uitkomsten van therapie. Dit artikel is een eerste presentatie. De modellen kunnen op basis van ervaringen en ruggespraak met de gebruikers worden bijgesteld en aangepast.

Background: Stuttering is a well-known condition that affects mainly children. Often, they recover as they get older. However, a drug-induced form of stuttering may occur at any age. The aim of the present study was to detect drugs that have been associated with stuttering and discuss the mechanisms involved. Method: A descriptive study based on reports submitted to the global pharmacovigilance database VigiBase of the WHO was conducted. Results: A total of 3,385 reports of dysphemia were retrieved from VigiBase. These reports were contributed by 51 countries. Antiepileptics, antidepressants, immunosuppressants, antipsychotics, and centrally acting sympathomimetics were among the most frequently implicated drugs. Conclusion: A wide variety of drugs has been linked to the occurrence or recurrence of stuttering. Several mechanisms, such as increased dopamine levels, reduction of GABA, anticholinergic properties of drugs, or changes in serotonin levels, have been associated with the development of drug-induced stuttering. Paradoxically, agents known to reduce stuttering in some people may induce it in others.

Developmental Stuttering (DS) is a speech disorder which is characterized by repetitions, prolongations, or pauses that disrupt the normal flow of speech. It occurs in approximately 58% of the pre-school children and recovers spontaneously in 70-80% of the cases, resulting in a prevalence of about 1% in adolescence. However, unrecovered people who stutter (PWS) can experience lifelong negative consequences, like participation restrictions, irritation and embarrassment. It is known that DS has a clear genetic basis, that PWS have increased dopamine activity, and that the severity of stuttering can be reduced by dopamine blockers. Here we describe functional and structural grey and white matter abnormalities that are present in PWS. It appears that the precentral gyrus (primary motor cortex), inferior frontal gyrus (IFG), superior temporal gyrus (STG), middle temporal gyrus (MTG), supplementary motor area (SMA), middle frontal gyrus (MFG), rolandic operculum (RO) and corpus callosum (CC) are important key players in DS. Although not all data support each other in all details, here we attempt to give a shared overview of current research and its directions, both in adults and children with DS. It has become clear that some brain differences already exist during childhood rather than resulting from compensatory attempts, and can therefore be used as markers for the development and monitoring of DS. Increased knowledge about DS could potentially open new ways for treatment of PWS, and may prevent the symptoms of persistent DS. This could results in less anxiety, shame, and irritation during social interaction, and would make the life of millions of stutterers a lot easier and more pleasant.

Developmental Stuttering (DS) is a speech disorder which is characterized by repetitions, prolongations, or pauses that disrupt the normal flow of speech. It occurs in approximately 5-8% of the pre-school children and recovers spontaneously in 70-80% of the cases, resulting in a prevalence of about 1% in adolescence. However, unrecovered people who stutter (PWS) can experience lifelong negative consequences, like participation restrictions, irritation and embarrassment. It is known that DS has a clear genetic basis, that PWS have increased dopamine activity, and that the severity of stuttering can be reduced by dopamine blockers. Here we describe functional and structural grey and white matter abnormalities that are present in PWS. It appears that the precentral gyrus (primary motor cortex), inferior frontal gyrus (IFG), superior temporal gyrus (STG), middle temporal gyrus (MTG), supplementary motor area (SMA), middle frontal gyrus (MFG), rolandic operculum (RO) and corpus callosum (CC) are important key players in DS. Although not all data support each other in all details, here we attempt to give a shared overview of current research and its directions, both in adults and children with DS. It has become clear that some brain differences already exist during childhood rather than resulting from compensatory attempts, and can therefore be used as markers for the development and monitoring of DS. Increased knowledge about DS could potentially open new ways for treatment of PWS, and may prevent the symptoms of persistent DS. This could results in less anxiety, shame, and irritation during social interaction, and would make the life of millions of stutterers a lot easier and more pleasant.