A Case of Acute Stuttering Resulting after a Sports-related Concussion : Current Sports Medicine Reports

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Case Report

A Case of Acute Stuttering Resulting after a Sports-related Concussion

Toldi, James DO1; Jones, Jared MD2

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Current Sports Medicine Reports 20(1):p 10-12, January 2021. | DOI: 10.1249/JSR.0000000000000795
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Acute onset of stuttering has not been frequently described as a manifestation of concussion. Our case describes a 15-year-old male high school football player that develops acute onset stuttering after a concussion sustained during a football game and eventually makes a full recovery after a multidisciplinary approach to treatment.

Case Report

A 15-year-old boy with no significant medical history presented 3 d after a helmet to helmet collision during a football game. There was no loss of consciousness (LOC), and he continued to play initially until a severe headache forced him out of the game. By the end of the game, he had developed new-onset stuttering, as well as more classic concussion symptoms, like fogginess, dizziness, and headache. Unfortunately, since this was an away game, he was not able to be evaluated by his athletic trainer, so he presented to the emergency room that evening. A head CT was negative for acute intracranial pathology. Examination was unremarkable other than the stuttering speech and mildly slowed cognition with noted slowed processing speed and difficulty with word finding. Coordination, gait, reflexes, and sensation were all normal, and cranial nerves were noted to be intact.

He presented to the clinic for follow-up the next day and continued to complain of stuttering, as well as frontal headache and other classic concussion symptoms. Detailed neurologic examination was unremarkable except for stuttering and trouble with word finding. Vestibular/ocular-motor screening was attempted but aborted prior to completion because of increased headache and dizziness. He scored a 17/22 on the Postconcussion Symptom Scale (PCSS) and 69/132 for severity, with increased score for dizziness, feeling mentally “foggy,” and difficulty concentrating. A magnetic resonance imaging (MRI) of his brain was normal. He was instructed to use Tylenol for pain control and to avoid nonsteroidal anti-inflammatory drugs (NSAIDs) because of potential risk of bleeding. He was prescribed relative brain and physical rest. Follow-up was arranged in the sports medicine clinic in 4 d.

At follow-up, he reported persistent, but mildly improved stuttering. His headache had improved some, but he continued to complain of photophobia and phonophobia. At this time, he also began to endorse depressed mood. His symptom score had increased from 17/22 to 21/22, and severity increased to 90/132, noting new symptoms of depressed mood and photophobia. Examination was notable for improvement in stuttering since the last encounter, but still present, otherwise unchanged from previous examination. He was discharged with instructions to follow-up in the sports medicine clinic in 1 wk and was referred for vestibular physical therapy, behavioral health for anxiety, and depressed mood, a neurosurgeon who also was a member of the concussion treatment team for thoroughness and a second opinion for the patient's family, and speech therapy for further evaluation and treatment of the stuttering.

At follow-up, he had noted significant improvement in all symptoms. He was able to speak without stuttering when calm, but stuttering returned when excited or anxious. He continued to endorse photophobia and phonophobia which still induced headaches. He was able to complete one full session of vestibular PT since his previous visit but required numerous breaks because of recurrent headache. PCSS remained at 21/22, but he stated that he felt more like himself and severity improved to 85/132. He was instructed to continue with vestibular PT, behavioral health, speech therapy, and to increase his physical activity in a subsymptom threshold manner.

Subsequent follow-up, 6 wk after injury, he noted complete resolution of his stuttering, and all symptoms except headache. He reported that the stuttering had resolved approximately 2 wk prior (approximately 1 month after initial injury). He was seen and evaluated by our concussion colleague in neurosurgery with recommendations to continue with our current treatment regimen. He also had completed one session of speech therapy and was given a prescription for home speech exercises. He also had a brief counseling session with our behavioral therapist and was given some techniques to help cope with anxiety and stress related to his injury. He was discharged with instructions to continue with prescribed therapies and to follow-up in the sports medicine clinic in 2 wk, but was lost to follow-up at this point.


Kutcher and Giza (1) describe concussion as a complex pathophysiologic response to biomechanical forces on the brain. They further describe concussion as a transient constellation of neurologic symptoms that reflect a functional rather than structural injury. They separate signs and symptoms of concussion into four main categories: cognitive/mental status, physical, affect, and sleep. Cognitive changes typically seen are slowed mentation, confusion, difficulty with attention, and many others. Physical symptoms commonly seen include headache, nausea/vomiting, photophobia/phonophobia, dizziness, slurred speech, blurry vision, and incoordination. Depression, anxiety, and emotional lability are common affective disturbances. Sleep disturbances are widely varied. Stuttering, however, is not a commonly described symptom of concussion.

Stuttering may be caused by neurogenic factors, psychogenic factors, or a combination of the two, and delineating causative factors is often difficult. Acute onset stuttering has been linked to psychological factors since the early 1900s when Bleumel described “hysterical” stuttering (2). A 1997 article from Mayo Clinic looked at psychogenic stuttering in patients with and without neurologic disease and found no significant distinguishing features to differentiate stuttering attributable to neurogenic factors from purely psychogenic factors (3).

Some studies have attempted to establish a link between traumatic brain injury (TBI) and acute onset stuttering, but most were unable to discern psychogenic from neurogenic causes (2–5). Acute onset stuttering following concussion has not been frequently described. However, a 2017 study describes the ease of finding unofficial reports, mainly forum posts, made by individuals, lending to the idea that postconcussive stuttering may be more common than reported (6). The article suggests that most report onset of stuttering within 24 h, with about half of those reporting onset within 1 h of injury (6).

Yeoh et al. (7) claim to be the first to describe acute stuttering following a head injury in the case of a 12-year old boy who developed stuttering after a skateboarding injury with brief LOC. They also noted other cerebellar dysfunctions, including truncal ataxia with a positive Rhomberg and an intention tremor. Brain imaging was normal in this case and the boy had complete resolution of symptoms by the next morning. Fumeya and Hideshima (8) described multiple cases of cerebellar concussion that resulted in speech disturbances. One of their cases reported dysarthric speech that resolved within 48 h, but MRI demonstrated a high intensity signal within the right superior cerebellar peduncle. Another of their cases described explosive and slurred speech that resolved within 1 month, and MRI findings of an abnormal signal intensity in the right cerebellar hemisphere. This patient also was noted to have a skull fracture with a 5-min LOC at the time of injury. Strasberg et al. (9) reported expressive aphasia described as stuttering after an assault associated with LOC and a 14.8-mm subdural hematoma with associated midline shift noted on CT. Stuttering was the only abnormal physical examination finding in this case, and at 4-month follow-up, the patient continued to endorse mild stuttering.

Ludlow and Loucks (10) describe speech as a dynamic motor function that incorporates many areas of the brain, including the cerebellum. They continue to explain that neural timing is different in persons who stutter when compared with those with normal speech. They then describe multiple cases of imaging that confirmed brain lesions of various forms associated with acquired stuttering, concluding that there is no particular area of the brain where a lesion is more likely to produce stuttering. However, a high percentage of lesions that produce stuttering are not located within the primary speech and language regions.

A 2018 article on acquired stuttering in war veterans found that the risk for developing acquired stuttering was much greater in those with concomitant TBI and posttraumatic stress disorder than either alone (4). Thus, suggesting that the combination of both psychological and physical injuries may contribute significantly to development of acquired stuttering (4). In a systematic review on acquired stuttering comparing neurogenic to psychogenic stuttering they concluded that secondary to the overlap in symptoms, it was unreliable to make the diagnosis based solely on speech pattern characteristics (5). Instead, they suggest that a rapid, favorable response to psychologic treatment, often with resolution after only one to two treatment sessions, may more accurately differentiate psychogenic from neurogenic stuttering (5).


Stuttering is often multifactorial without clear etiologies. Many cases of reported acute-onset stuttering cannot be fully differentiated from psychological or physical etiology, and likely are a combination of both. Our patient has some similarities to all of the above described cases. However, his MRI was negative for any lesions within the brain. His stuttering was persistent with gradual improvement over approximately 1 month, which is in contrast to many described cases that report abrupt resolution within 24 h to 48 h. Our patient also did not exhibit any ataxia or other problems with coordination that appear to coincide with cerebellar injuries that have been described with imaging suggestive of actual neurological injury. As with most described cases, we feel that there was a significant psychological component involved (and was likely more prominent in our patient than the other cases) and differentiating between the psychogenic and neurogenic contributing causes is extremely difficult if not impossible. However, given the rarity of reported stuttering after concussion or minor TBI, further investigation and utilization of ancillary services is warranted. We feel that our multidisciplinary approach to treatment, enlisting the help of speech therapy, vestibular PT, and behavioral health, may be crucial to facilitating full recovery as promptly as possible. The prompt return to baseline functioning further limits the missed school and athletic time which is imperative for our student athletes.

The authors declare no conflict of interest and do not have any financial disclosures.


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