Alm Per A
Department of Neuroscience, Uppsala University, Uppsala, Sweden.
Front Hum Neurosci. 2020 Nov 9;14:569519. doi: 10.3389/fnhum.2020.569519. eCollection 2020.
Stuttering is one of the most well-known speech disorders, but the underlying neurological mechanisms are debated. In addition to genetic factors, there are also major non-genetic contributions. It is here proposed that infection with group A beta-hemolytic streptococcus (GAS) was a major underlying cause of stuttering until the mid-1900s when penicillin was introduced in 1943. The main mechanism proposed is an autoimmune reaction from tonsillitis, targeting specific molecules, for example within the basal ganglia. It is here also proposed that GAS infections may have continued to cause stuttering to some extent, to the present date, though more rarely. If so, early diagnosis of such cases would be of importance. Childhood cases with sudden onset of stuttering after throat infection may be particularly important to assess for possible GAS infection. The support for this hypothesis primarily comes from three lines of argument. First, medical record data from the 1930s strongly indicates that there was one type of medical event in particular that preceded the onset of childhood stuttering with unexpected frequency: diseases related to GAS throat infections. In particular, this included tonsillitis and scarlet fever, but also rheumatic fever. Rheumatic fever is a childhood autoimmune sequela of GAS infection, which was a relatively widespread medical problem until the early 1960s. Second, available reports of changes of the childhood prevalence of stuttering indicate striking parallels between stuttering and the incidence of rheumatic fever, with: (1) decline from the early 1900s; (2) marked decline from the introduction of penicillin in the mid 1940s; and (3) reaching a more stable level in the 1960s. The correlations between the data for stuttering and rheumatic fever after the introduction of penicillin are very high, at about 0.95. Third, there are established biological mechanisms linking GAS tonsillitis to immunological effects on the brain. Also, a small number of more recent case reports have provided further support for the hypothesis linking stuttering to GAS infection. Overall, it is proposed that the available data provides strong evidence for the hypothesis that GAS infection was a major cause of stuttering until the mid-1900s, interacting with genetic predisposition.
口吃是最广为人知的言语障碍之一,但其潜在的神经机制仍存在争议。除了遗传因素外,非遗传因素也有重要影响。本文提出,直到20世纪中叶1943年青霉素问世之前,A组β溶血性链球菌(GAS)感染是口吃的一个主要潜在病因。所提出的主要机制是扁桃体炎引发的自身免疫反应,其靶向特定分子,例如基底神经节内的分子。本文还提出,GAS感染可能在一定程度上持续导致口吃,直至今日,不过这种情况更为罕见。如果是这样,此类病例的早期诊断将至关重要。对于咽喉感染后突然出现口吃的儿童病例,评估其是否可能感染GAS可能尤为重要。这一假说的支持主要来自三条论据。首先,20世纪30年代的病历数据有力表明,有一种医疗事件在儿童口吃发作之前出现的频率异常高:与GAS咽喉感染相关的疾病。特别是,这包括扁桃体炎和猩红热,还有风湿热。风湿热是GAS感染的一种儿童自身免疫后遗症,在20世纪60年代初之前是一个相对普遍的医学问题。其次,关于儿童口吃患病率变化的现有报告表明,口吃与风湿热的发病率之间存在惊人的相似之处,具体表现为:(1)从20世纪初开始下降;(2)从20世纪40年代中期青霉素问世后显著下降;(3)在20世纪60年代达到更稳定的水平。青霉素问世后口吃和风湿热的数据之间的相关性非常高,约为0.95。第三,已有将GAS扁桃体炎与对大脑的免疫影响联系起来的生物学机制。此外,最近的一些病例报告也为将口吃与GAS感染联系起来的假说提供了进一步支持。总体而言,本文提出现有数据为以下假说提供了有力证据:直到20世纪中叶,GAS感染是口吃的一个主要病因,并与遗传易感性相互作用。