Fidan T, Ceyhan S, Fidan V. Streptococcal Serology in Children With Stuttering. Ear, Nose & Throat Journal. 2024;104(8):513-515. April 19, 2024. doi:10.1177/01455613241244946
Stuttering and Post-Streptococcal Neuroimmune Conditions: An Emerging and Underrecognized Connection
Stuttering is traditionally seen as a speech disorder caused by a mix of genetics, brain development, and speech planning. Recent research, though, suggests that for some children, stuttering can start or get worse after the immune system is activated by an infection, especially by group A beta-hemolytic Streptococcus (GABHS).
This pattern is particularly relevant to clinicians and families familiar with PANS and PANDAS, in which sudden-onset or worsening neuropsychiatric symptoms follow infection-triggered immune dysregulation. While stuttering is not part of the current PANS/PANDAS diagnostic criteria, accumulating evidence suggests it may represent another immune-mediated, basal ganglia–related symptom in certain children.
This pattern is particularly relevant to clinicians and families familiar with PANS and PANDAS, in which sudden-onset or worsening neuropsychiatric symptoms follow infection-triggered immune dysregulation. While stuttering is not part of the current PANS/PANDAS diagnostic criteria, accumulating evidence suggests it may represent another immune-mediated, basal ganglia–related symptom in certain children.
What the Study Found
A case–control study examined children with developmental stuttering, comparing 26 children who stutter with 25 age- and sex-matched controls. Investigators measured three markers of prior streptococcal immune activation:
- Antistreptolysin O (ASO)
- Anti–DNase B
- Antistreptokinase
Key findings:
- Children who stutter had much higher levels of all three antistreptococcal antibodies than the control group (p < 0.0001 for all).
- 77–81% of children who stutter had elevated ASO or anti-DNase B titers, compared with 12–16% of controls.
- The results suggest increased immune reactivity to streptococcal infection in the stuttering group.
The authors interpret these findings as consistent with a post-infectious autoimmune mechanism, similar to what is seen in PANDAS and other conditions that follow streptococcal infection.
Why This Matters for PANS and PANDAS
PANS and PANDAS are known for sudden or newly worsening neuropsychiatric symptoms, often linked to the basal ganglia, after the immune system is activated. Stuttering shares several features with this pattern:
- Childhood onset
- Waxing and waning course
- Male predominance
- Exacerbation with stress or illness
- Overlap with tic disorders and Tourette syndrome
- Sensitivity to dopaminergic modulation
Importantly, the basal ganglia are central to:
- Motor initiation and inhibition
- Speech timing and fluency
- Habit and motor pattern regulation
In PANDAS, immune problems that affect basal ganglia signaling, often through cross-reactive antibodies, are believed to cause symptoms like tics, OCD, and motor issues. The same brain circuits are involved in both developmental and acquired stuttering, which suggests there may be shared risk pathways.
A Neuroimmune Hypothesis for Stuttering in a Subset of Children
The study supports, but does not prove, a model in which:
- Streptococcal infection triggers an abnormal immune response
- Antibodies or inflammatory mediators cross-react with basal ganglia structures
- Speech motor planning and fluency are disrupted
- Symptoms may wax and wane, particularly with immune triggers
This does not suggest that most stuttering is autoimmune in origin. Rather, it raises the possibility that a small but clinically meaningful subgroup of children, particularly those with sudden onset, regression, or co-occurring neuropsychiatric symptoms, may warrant broader medical consideration.
Clinical Implications
The authors do not argue for routine infectious or immune testing in all children who stutter.
However, their findings support consideration of immune evaluation when stuttering:
- Begins abruptly or follows an infection
- Co-occurs with tics, OCD, emotional lability, regression, or anxiety
- Shows a relapsing–remitting pattern
- Worsens during illness or inflammatory states
In such cases, clinicians may consider:
- A careful infection history
- Selective streptococcal testing when clinically indicated
- Monitoring symptom patterns over time rather than relying on single time-point labs
It is important to note that this study does not provide treatment recommendations. Immune-modulating therapies should only be considered in the right clinical settings.
Where This Fits in the Broader PANS/PANDAS Landscape
This research adds to the growing evidence that immune problems triggered by infection can cause a wide range of neuropsychiatric symptoms, not just those listed in current diagnostic criteria.
In the past, symptoms like eating restriction, urinary problems, and cognitive regression were not widely recognized in PANS. Speech dysfluency may be another symptom to study, especially in children with obvious immune triggers.
Further research is needed to:
In the past, symptoms like eating restriction, urinary problems, and cognitive regression were not widely recognized in PANS. Speech dysfluency may be another symptom to study, especially in children with obvious immune triggers.
Further research is needed to:
- Replicate findings in larger cohorts
- Clarify mechanisms
- Identify which children may fall into this immune-mediated subgroup
Key Takeaway
Stuttering is not currently considered a core symptom of PANS or PANDAS. However, emerging evidence suggests that in some children, stuttering may be linked to immune activation after a strep infection, affecting the basal ganglia and overlapping with tic disorders and other neuroimmune conditions.
Recognizing this possibility does not change the definition of stuttering. However, it broadens the discussion, encourages careful clinical observation, and highlights the need not to dismiss sudden, regressive, or infection-related symptoms as only developmental or psychiatric.
Gabriella True
