Introduction

Chronic Traumatic Encephalopathy (CTE) looms as a pressing concern for retired athletes from full-contact sports, such as rugby and American football [1]. While these sports are renowned for their intense physical demands and full-contact nature, in the context of rugby, the spotlight has primarily focused on the potential risks of recurrent Traumatic Brain Injuries (TBI) including its long-term consequence Post-Concussion Syndrome (PCS), with relatively less attention given to CTE. Both conditions share a critical commonality: the mechanism of action and the potential for long-term consequences. The primary distinction lies in CTE being a progressive neurodegenerative disease while PCS tends to be stable or to improve over time. A possible progression from PCS to CTE is being discussed [2].

A definitive diagnosis of CTE can only be obtained postmortem through autopsy [3]. To address the challenges in diagnosing CTE during an individual’s lifetime, the National Institute of Neurological Disorders and Stroke has developed clinical criteria for Traumatic Encephalopathy Syndrome (TES), a clinical disorder closely associated with CTE [4].

In this article, we present the case of a recently retired senior professional rugby player, formerly the captain of the UK national team, who exhibited symptoms suggesting CTE. This player underwent protocols of Hyperbaric Oxygen Therapy (HBOT), which have shown promise in treating PCS. Alongside the case presentation, we underscore the critical importance of raising awareness for the early diagnosis of TES and discuss the biological effects of the used HBOT protocol.

Case Presentation

A 36-year-old male, formerly the captain of the English rugby national team (with consent, hereafter referred to as ‘FC’), retired from professional rugby two years prior due to concerns about his cognitive health. Despite his retirement, FC’s cognitive challenges persisted to deteriorate and did not show any sign of improvement. Motivated by the potential benefits of Hyperbaric Oxygen Therapy (HBOT) for brain injuries, he sought medical evaluation at the AVIV hyperbaric clinic in Dubai.

Medical history: Over a twenty-year rugby career, FC sustained 20 documented concussions and numerous undocumented head injuries. Many of these went unreported due to their frequent occurrence. These repetitive traumas culminated in noticeable changes in FC’s cognitive function: memory lapses, heightened sound sensitivity, difficulty maintaining grip, stuttering, dizziness during rapid head movements, and mood changes. Even though he retired from professional sports, these symptoms intensified over time, leading him to seek potential therapeutic intervention.

Initial Evaluation: A thorough pre-HBOT evaluation encompassed:

• A detailed physical assessment.
• A computerized neurocognitive test (NeuroTraxTM & CANTAB®) administered by a neuropsychologist.
• Advanced brain imaging, including MRI with perfusion and DTI, and a SPECT scan.

Physical examination revealed bilateral hematoma auris [5] and a mild horizontal nystagmus to the right. Brain MRI exhibited hyperintensities in both frontal and the right parietal regions, categorized as Fazekas grade 1 (Figure 1). The SPECT scan showed areas with reduced uptake, signifying decreased/altered brain metabolism in the frontal and parietal regions of the brain. Neurocognitive assessments identified significant impairments in focused and sustained attention, alongside reduced information processing speed.

Figure 1: Brain MRI exhibited hyperintensities in both frontal and the right parietal regions.

Intervention: FC underwent 60 HBOT sessions, performed daily, 5 days per week. Each session, lasting 90 minutes, exposing him to 100% oxygen at two atmospheres (2ATA), interspersed with 5-minute air breaks every 20 minutes.

Post-HBOT Evaluation: Following the HBOT protocol, the initial assessments were repeated and compared to the baseline tests with the following findings:

• SPECT scan comparisons revealed evidence of enhanced uptake/activity in the previously affected brain regions and could determine improved uptake in areas related to facial recognition, written word meaning, attention, spatial memory, directionality, somatosensory integration, visuo-motor coordination, memory and control networks, language perception, processing and memory (Table 2).

Table 1: Perfusion MRI

• MRI-perfusion scan showed marked improvements in the post-treatment MRI perfusion as compared to the baseline, in brain regions related to spatial memory, directionality, smell, memory encoding and retrieval, visuo-motor coordination, hearing and language processing (Figure 2, Table 1).

Figure 2: MRI-perfusion scan showed marked improvements in the post-treatment MRI perfusion as compared to the baseline.

Table 2: (SPECT) The brain regions that had significant improvement post Hyperbaric Oxygen Therapy

• MRI-DTI revealed notable improvements in the post-treatment MRI-DTI compared to the baseline scan. The improvement in Fractional Anisotropy (FA), which assesses white matter integrity and directionality, in brain regions related to learning, memory, behavior, sensation, perception, visual processing, formation of new memories, decision making, cognitive processing of visual information, episodic memory, language and social emotional processing. The improvement in Mean Diffusivity (MD), which reflects white matter fiber density, in brain regions related to coordination of arms and legs, learning and formation of new memories, refinement of motor function, processing of visual information, episodic memory, language, social emotional processing, visual memory, face recognition, and sensory pathways.

Cognitive tests highlighted significant improvements, as compared to the baseline assessments, in the domains of verbal and nonverbal memory, executive function, cognitive flexibility, attention, information processing speed, and fine motor skills.

Clinical outcomes: Post-HBOT, the previous symptoms including sound sensitivity, stuttering, frequent dizziness, and involuntary release of objects were fully resolved. Notably, as reported by FC and those close to him, the mood disturbances had also ceased.

Discussion

Chronic Traumatic Encephalopathy (CTE) is a progressive neurodegenerative condition believed to be a consequence of repeated head trauma, encompassing both concussions and sub-concussive blows to the head [6]. Diagnosis of CTE, however, remains elusive during a person’s lifetime, leading to the use of the term Traumatic Encephalopathy Syndrome (TES) in clinical practice. The diagnostic criteria for TES, as established by the National Institute of Neurological Disorders and Stroke, encompass four key components: substantial exposure to repetitive head impacts (RHIs), core clinical features of cognitive impairment or neurobehavioral dysregulation, a progressive course, and the exclusion of other neurologic, psychiatric, or medical conditions [4]. CTE shares a common etiological pathway with Post-Concussion Syndrome (PCS) or Chronic Traumatic Brain Injury (CTBI) [7]; however, there are significant differences in causation and presentation. While CTE is believed to result from recurrent head injuries at varying velocities, PCS may originate from a single head injury or multiple incidents. Although both conditions exhibit similar symptoms, CTE progresses chronically over time, whereas CTBI is diagnosed when there is a chronification of TBI symptoms, characterized by persistent but relatively stable symptoms.

In the case presented, FC experienced repeated brain injuries at different velocities, with at least 20 documented concussions and likely many more unreported incidents. His physical evaluation revealed the hallmark of repeated head trauma in contact sports: Cauliflower ears. This condition arises when the external portion of the ear sustains impact, forming a blood clot or fluid collection under the perichondrium. As a result, the cartilage becomes separated from its nutrient-supplying perichondrium, leading to the formation of fibrous tissue in the overlying skin. This results in a permanently swollen and deformed outer ear, resembling cauliflower, hence the name [5].