Neurodegenerative decline following a mild traumatic brain injury: a case report

Abstract

Background

A growing body of research suggests that mild traumatic brain injury (mTBI) increases the chance of developing neurodegenerative disease in adults. Elderly patients are of great concern due to an increased risk of head injury due to falls.

Case report

The patient was a 71-year-old White, non-Hispanic female who fell from a ladder and suffered an initially undiagnosed mild traumatic brain injury (mTBI). Seventeen months after injury, she was evaluated by a concussion specialist who retrospectively diagnosed mTBI. Subsequent neuropsychological evaluation resulted in a diagnosis of probable Lewy body dementia. The patient experienced rapid neurological decline and died thirty-three months after the initial fall.

Conclusions

Mild traumatic brain injury (mTBI) and its persisting symptoms are frequently misdiagnosed, often leading to symptom-based overmedication and lack of appropriate targeted treatment. This highlights the need for advanced training for providers on mTBI and the potential for persisting symptoms associated with it. Providers also need to understand the risk of neurological decline following mTBI, especially in the elderly population. Clinicians should not rely exclusively on patient self-report for diagnosis and treatment of mTBI and should use a multidisciplinary approach. In addition, disparities in rural access to specialized care must be addressed to ensure equitable post-injury outcomes.

Introduction

In 2023, the American Congress of Rehabilitation Medicine (ACRM) Mild TBI Task Force established updated criteria for diagnosing mild traumatic brain injury (mTBI) [1]. Diagnosis is based on a plausible mechanism of injury, clinical signs, and the presence of acute symptoms supported by clinical evaluation or laboratory findings. Neuroimaging is not required but may support diagnosis when abnormalities are present. The ACRM also considers “concussion” interchangeable with mTBI [1].

Currently, there is a growing body of evidence that an mTBI increases the risk of developing a neurodegenerative disease in adults. Fann et al. used a cohort of 2,794,852 individuals and found that risk of dementia was higher in those with a history of TBI with a hazard ratio (HR) of 1.24 [2]. Similarly, Schneider et al. found an increased risk of dementia in adults (mean age of 54 years at baseline) with a hazard ratio of 1.44 [3]. They also found evidence of dose–response (1 head injury with 1.25 HR and 2 + head injuries with 2.14 HR) and stronger association with females versus males [3]. Mavroudis et al. found a moderate increase in dementia risk with mTBI (OR = 1.96) [4]. Meta-analyses by Snowden et al. and Perry et al. showed that a history of mTBI increased an individual’s risk of neurodegenerative disease, including dementia [5, 6]. In a 5-year multicenter study, Sercy et al. found that mTBI increased the risk of developing a neurodegenerative disease and found an increase in mortality from a neurodegenerative disease after an mTBI [7].

Elderly patients are of great concern due to an increased risk of head injury due to falls [8]. In 2014, Gardner et al. completed a retrospective cohort study of patients ≥ 55 years old with a diagnosis of TBI without baseline dementia [9]. They found that mild TBI impacted dementia risk more with increasing age [9]. Individuals age 55–64 had a HR of 1.11, while those aged 65–74 had a HR of 1.25 [9]. Ordoobadi et al. looked specifically at adults aged 66 years and older who had experienced a trauma and were seen in the emergency room or in-patient setting [10]. They found that 10.6% of older adults were diagnosed with Alzheimer disease and related dementias (ADRD) within the first year after they fell [10]. Related to these findings, Eman Abdulle and van der Naalt found that 44% of elderly people with concussions had an incomplete recovery after 6 months [11]. This period of persisting symptoms after a concussion includes a combination of long-term (> 3 months) somatic, cognitive, and psychosocial symptoms [12, 13].

This case is unique because of the delayed diagnosis of mTBI in an elderly patient, prolonged polypharmacy prior to neurological referral, and rapid progression to probable Lewy Body dementia within 33 months of injury. Few published case reports describe such a timeline in a rural healthcare setting. Therefore, the purpose of this case report is to present a case of mTBI and neurodegenerative decline, leading to death.

Case report

Initial injury

The patient was a 71-year-old White, non-Hispanic female who fell approximately eight feet from a stepladder onto a cement floor on October 18, 2021. She was taken to the emergency room (ER) by a friend who found her in her bathroom cleaning the blood from her face. The patient reported that she did not remember how she had gotten into the house but knew that she had fallen from the stepladder. She presented to the ER with a scraped lower left leg, swelling above her left eye, and a cut to her lip at the midline, which needed suturing. The patient denied other injuries or pain at the ER and denied loss of consciousness. There was no neurological testing done during the exam. In a follow-up visit four days later, the patient had bruising on her head, she reported no brain fog, difficulty concentrating, vision changes, aversion to light, or fatigue. She stated that she could not remember the exact events of the fall. Again, a neurological exam was not done. The physician determined that the patient did not have any signs or symptoms of a concussion.

According to family members and available primary care documentation, the patient was independent in all activities of daily living prior to the fall, with no reported cognitive impairment, memory concerns, or functional limitations. She was socially active and had only required routine annual medical care.

Retrospective mTBI diagnostic criteria

While a concussion was not diagnosed at the time of the injury, a retrospective review of the clinical history meets the 2023 ACRM criteria for mTBI [1]. Criterion 1 was satisfied by a fall from approximately eight feet onto a cement floor, constituting a biomechanically plausible mechanism of injury. The patient’s reported inability to recall how she entered the house following the fall meets Criterion 2, post-traumatic amnesia. Criterion 3 was met by acute symptoms including confusion and memory deficit. Based on these elements, the concussion specialist determined the presentation was consistent with a prior mTBI and persistent post-concussive symptoms.

Anxiety, depression, insomnia, and polypharmacy

On December 6, 2021, seven weeks after her initial fall, the patient had an office visit with her primary care physician to discuss a marked increase in her anxiety and issues with sleep. She had been previously diagnosed with a history of mild depressive disorder and was taking 30 mg of citalopram daily. She was taking no other medications and had only seen her physician for her yearly physicals during the previous five years. On exam, the patient’s PHQ-9 score was 12, indicating moderate depression, and her GAD-7 score was 8, indicating mild anxiety. Her physician added 50 mg of trazodone each night for anxiety and to aid her sleep. Eleven days later, that dose of trazodone was increased to 75 mg. Seventeen days later, the dose increased to 100 mg each night due to continued insomnia and anxiety.

On March 8, 2022, just over 4.5 months since her initial fall, the patient received an upsetting text message and experienced an acute episode of altered mental status characterized by confusion and repetitive questioning. She was repeatedly asking if she hit her head and if she had hurt someone. A friend who was visiting at the time witnessed her rapidly deteriorating state and took her to the ER, where she was diagnosed with transient global amnesia. She was admitted overnight and released the next day, with her symptoms completely resolved at 24 h. This episode was diagnosed as transient global amnesia; however, documentation of key features needed to distinguish between alternative etiologies was limited. A formal differential diagnosis beyond transient global amnesia was not documented in the medical record or discussed with family. Additional diagnostic workup beyond neuroimaging was not documented. Neuroimaging (CT and MRI) revealed no acute intracranial abnormalities and was interpreted as consistent with age-related changes. However, the radiology report did not provide detailed characterization of cortical atrophy, vascular changes, or regional abnormalities.

Throughout the ensuing 12 months, the patient’s medications were adjusted 14 times, accompanied by multiple doctors' appointments and worsening symptoms of insomnia, anxiety, depression, and stomach pain. She began isolating herself and was unable to attend her usual social functions. Prior to her doctor’s appointments, she would struggle with intense anxiety for five to seven days leading up to the appointment. Her anxiety was triggered by the Likert scale depression questions asked by the nurse or CMA before her physician visits. She confided to family members that the questions were asked too quickly and that she did not understand how she was supposed to answer. A summary timeline of cognitive and functional decline is presented in Table 1.

Table 1.

tsdgxcg

Date	Time since injury	Key events	Cognitive status	Functional status
10/2021	0 months	Fall ~ 8 ft from ladder; facial laceration; no neuro exam	Amnesia for event; denied LOC; no formal testing	Independent
10/2021	0.1 months	Follow-up visit; bruising; denied symptoms	Memory gap about fall; no reported deficits	Independent
12/2021	1.5 months	PCP visit for anxiety/insomnia	PHQ-9 = 12, GAD-7 = 8; no cognitive testing	Independent but anxious
03/8/2022	4.5 months	ER for acute confusion; diagnosed TGA	Acute confusion; repetitive questioning	Temporary functional decline
03/2022	5 months	MRI/CT reported normal aging	No documented deficits	Independent
2022 (ongoing)	6–14 months	14 medication changes	Increasing anxiety; difficulty with questionnaires	Social withdrawal
03/2023	17 months	Concussion specialist visit	Impaired learning, attention, focus	Avoidant behavior
04/2023	18 months	Trazodone taper	Temporary clarity	Improved engagement
06–07/2023	20–21 months	Hallucinations emerge	Visual hallucinations; paranoia	Safety concerns
07/2023	21 months	Multiple ER visits	Delusions, confusion	Unable to live alone
08/2023	22 months	Memory care admission	Sequencing deficits	Needs help dressing, bathing
08/2023	22 months	Neuropsych evaluation	Probable Lewy Body dementia	Assisted living
01/2024	27 months	Behavioral escalation	Disorientation; wandering	Unsafe; memory care
06/2024	32 months	Recurrent falls	Severe dementia	Bedbound
07/2024	33 months	Death	End-stage dementia	Total dependence

Concussion specialist and gerontologist

In March of 2023, the patient was seen in a concussion clinic and after a full evaluation, the physician determined that the patient had pervasive anxiety, fear avoidant behavior, and perseverative thinking that had been limiting for her. She was particularly sensitive to social and environmental sensitivity, especially in large groups. The physician noted that the patient reported some cognitive impairment, issues with learning new things, troubles with focusing and maintaining attention and understanding. The physician noted in his documentation that the patient and family did not report any symptoms that would suggest progressive dementia. The physician’s note stated:

“History and exam are consistent with a history of presumed initial concussion and postconcussive syndrome. However, we discussed this specifically as it pertains to likely phenotype of postconcussion syndrome in her case dysautonomia. Dysautonomia in the sense of increased sympathetic tone, fight or flight type tone manifesting as fear avoidant behavior, environmental hypersensitivity, intolerance etc. Anxious and perseverative behaviors then serve as self-fulfilling prophecy which further encourages of somatic symptoms. We discussed this pathophysiology in detail, answering all questions and concerns and provided reassurance. We spent a lot of time discussing practical ways of slowly increasing activities and small safe ways to encourage improved confidence, avoid social isolation etc. I think that with time and progressive desensitization type approach she will slowly improve.”

The patient began attending concussion rehabilitation in April of 2023, and her trazodone was decreased due to extreme confusion witnessed during an overnight stay with family. Lorazepam, 0.25 mg, 2x/day was added to help decrease anxiety. The concussion specialist recommended scheduling an appointment with a neuropsychologist to complete a full evaluation. The neuropsychologist was not able to put the patient on her schedule until August—a 4-month wait. The patient continued concussion rehabilitation, but it was not decreasing the patient’s symptoms, so the concussion specialist recommended seeing a gerontologist for an exam and medication review. The patient saw the gerontologist on April 18, 2023, where he stated that he did not believe the patient had any underlying neurologic problems and wanted to see how her mental status would do since the adjustments had been made to her medication regime. He recommended decreasing the trazodone to 25 mg a night after 2 weeks on 50 mg, then attempting to eliminate the use of trazodone.

Rapid neurodegenerative decline

Over a three-week period following the dose reduction of trazodone from 100 to 50 mg nightly, family members reported observable improvements in orientation, clearer speech, and decreased acute confusion. However, this improvement was temporary and followed by persistent, well-formed visual hallucinations involving unfamiliar individuals inside her home, as well as misperceptions of faces in inanimate objects. Hallucinations increased in frequency over the next two months and were accompanied by worsening anxiety and difficulty distinguishing perceptual disturbances from reality.

In mid-July, the patient was taken to the ER due to extreme paranoia and hallucinations. A urinary tract infection was diagnosed and treated. She was kept overnight for observation and treatment, then released. One week later, she was once again having extreme paranoia that her partner was going to hurt her, so her family took her to the ER, where she was kept for 2 nights and transferred to an in-patient adult psychiatric unit for medication adjustments.

While at the psychiatric unit, the attending physician informed family members that the patient could not live alone at home and suggested an assisted living or memory care facility to continue medication adjustments and have a safe place through those adjustments. She was transferred to a memory care unit on August 8, 2023, when her treatments at the psychiatric unit were completed. In the memory care unit, it was discovered that the patient was struggling with activities of daily living, particularly with sequencing tasks. She was unable to shower by herself and struggled to get dressed on her own because of the sequencing issues.

On August 11, 2023, the patient saw a neuropsychiatrist for a full evaluation. During the interview portion of the appointment, the neuropsychiatrist said that she did not believe based on the interview, that the patient had dementia, but warned that more testing needed to be completed. After a full mental assessment, the patient was diagnosed with “probable Lewy Body dementia,” and it was recommended that she stay in assisted living until she needed the increased care of a memory care unit. The patient was then “graduated” out of memory care and into an assisted living community.

The diagnosis of “probable Lewy body dementia” was based on established clinical criteria, which require progressive cognitive decline accompanied by core clinical features [14]. In this case, core clinical features supporting the diagnosis included well-formed visual hallucinations and fluctuating cognition. While parkinsonian motor features and REM sleep behavior disorder are also characteristic of Lewy body dementia, documentation of these features was limited in this case [14].

Neuroimaging completed earlier in the disease course showed no structural abnormalities beyond changes due to aging. Formal neuropsychological testing demonstrated impairments in attention, executive functioning, and spatial processing, patterns commonly associated with Lewy body dementia. Because there was no autopsy completed, the classification remains “probable” rather than definitive.

Over the next 5 months, the patient resided in assisted living and her symptoms progressed rapidly. She was found wandering at night by staff and was sleeping a lot during the day. Anger and aggressive behaviors increased, and at times she was very resistant to taking medications. She wandered into other residents’ rooms and became more confused about where her room was located. At one point, the patient was found attempting to brush her teeth with a razor used for shaving. She was not injured, but this action necessitated a need for her to move to a memory care unit.

The patient had a difficult transition to the memory care unit, struggling with depression and anxiety. Hospice services were utilized to help quickly adjust medications as her symptoms changed. She was hallucinating most of the time, mainly seeing dogs and children. At times, she would bend over and pet a dog that she was hallucinating. She worried that “the children” were not being taken care of, and that she was being forced to babysit. Her confusion was increasing. Over the six months she was in the memory care unit, she quickly moved through the final stages of Lewy body dementia. In the third week of June 2024, the patient experienced multiple falls despite the efforts of memory care and hospice staff to ensure her safety. The patient became bedridden on June 22, 2024. She was unable to get out of bed, eat, or drink. On July 1, 2024, two years and nine months after the initial mTBI, the patient died due to complications of Lewy Body dementia.

Discussion

Although it is not possible to determine whether earlier recognition of mTBI would have altered the neurodegenerative decline, the patient’s early post-injury symptoms were managed primarily as psychiatric conditions without neurologic evaluation. This case illustrates the diagnostic complexity that arises when post-traumatic symptoms overlap with anxiety, depression, and sleep disturbance in older adults. The broader literature supports an association between TBI and later-life dementia risk, but individual cases still need to be interpreted carefully.

This case underscores the importance of early objective cognitive and neurologic assessment following head injury, particularly in older adults. Reliance on symptom self-report alone may be insufficient, as patients may underreport or fail to recognize deficits. Early use of standardized cognitive screening tools and timely referral for neuropsychological evaluation may improve diagnostic accuracy and guide appropriate management.

Several additional factors may have contributed to the patient’s rapid clinical decline. The patient had a pre-existing history of depression, and advancing age is an independent risk factor for neurodegenerative disease. There is also a possibility that prodromal Lewy body dementia was present prior to the fall and that the injury or subsequent stressors unmasked an underlying neurodegenerative process. Medication effects, particularly the use of trazodone and later benzodiazepines, may have contributed to cognitive fluctuations and confusion. Additionally, concurrent medical conditions, including urinary tract infection and episodes consistent with delirium, may have further exacerbated cognitive and functional decline.

The patient’s clinical course was also complicated by polypharmacy. The use of trazodone and later benzodiazepines may have contributed to sedation, impaired cognition, and increased fall risk. In older adults, particularly those with emerging neurodegenerative disease, these medications are known to worsen confusion and functional decline. The frequent medication adjustments over a short period may have masked the underlying neurologic condition and delayed accurate diagnosis. These factors highlight the multifactorial nature of this patient’s clinical course and should be considered within the broader healthcare environment in which care was delivered. Access to that care is especially important in rural settings.

The patient lived in rural Iowa and her access to specialized providers (neuropsychologists, concussion specialists, gerontologists) was extremely limited. Rural healthcare systems are overburdened, and it is often difficult to provide referrals to appropriate specialists due to wait times and distance. The patient’s concussion diagnosis took seventeen months, and an additional four months was needed for an appointment with a neuropsychologist. For her to receive appropriate and targeted interventions, she needed a multidisciplinary team to evaluate the case. Once she saw a concussion specialist, the multidisciplinary healthcare team was put into place and her care was targeted to her neurological decline. This case highlights the rural healthcare disparities that exist due to proximity to specialists and a lack of a multidisciplinary approach to care. When there is a healthcare team working together on a complex case, critical evaluation and appropriate care can decrease the risk of inappropriate polypharmacy and improve long-term outcomes after mTBI.

These challenges highlight opportunities for system-level improvements in the evaluation and management of mTBI, particularly in rural settings. Potential interventions include the use of telehealth consultations (e.g., tele-neuropsychology or e-consults with concussion specialists), implementation of standardized mTBI screening protocols in emergency and primary care settings, and pharmacist-led medication reviews to identify and reduce inappropriate polypharmacy. These approaches have the potential to improve early recognition and reduce delays in appropriate care.

Other healthcare providers could have been involved in the patient’s diagnosis and treatment. For example, the treating pharmacist could have evaluated the increased change in medications over those seventeen months and discussed the concern of polypharmacy in a patient who had taken very few medications over her previous five years. A dietitian could have been utilized to ensure appropriate nutrients were being consumed for recovery. In mTBIs, a neurometabolic cascade brings excess potassium, calcium, and sodium into the cells of the brain, causing an increased need for adenosine triphosphate due to the neuron working harder to maintain equilibrium [15]. Additionally, mTBIs cause a decrease in cerebral blood flow, which leads to an energy crisis [16]. The use of nutrition and supplements to treat concussions is still an emerging field of research. Appropriate nutritional adjustments after diagnosis of mTBIs may help with brain recovery (15).

Epidemiologic studies demonstrate an association between TBI and increased dementia risk at the population level; however, they do not establish causation at the individual level. This case does not show that mTBI directly caused Lewy body dementia. Instead, it highlights a possible connection between the head injury and the later development of neurodegenerative disease in a vulnerable older adult. What makes this case unique is the delayed recognition of mTBI, the early presentation of psychiatric symptoms, and the rapid progression to Lewy body dementia within a rural healthcare setting. The timeline provides helpful clinical context, but it does not establish a clear cause-and-effect relationship. It does, however, suggest that the injury may have contributed to or unmasked an underlying neurodegenerative process.

Limitations

This case report is limited by its retrospective nature, lack of baseline cognitive testing prior to injury, absence of neuropathological confirmation, and reliance on family-reported symptom timelines. Because this is a single case, causal relationships cannot be inferred.

Additionally, retrospective application of mTBI diagnostic criteria introduces potential recall bias. Neuropsychological testing results were summarized from clinical documentation rather than raw testing data. Without neuropathologic confirmation, definitive diagnosis of Lewy body dementia cannot be established.

Conclusion

Although the outcome may not have been preventable for this patient (due to the lack of a cure for this neurodegenerative decline and resulting Lewy Body dementia), earlier comprehensive neurologic evaluation may have facilitated earlier supportive interventions and caregiver planning.

Author contributions

Melanie Mason researched, wrote, and edited the manuscript. James Geiselman and Shawn Spooner researched and edited the manuscript.

Funding

The authors did not receive funding to conduct this case report.

Data availability

All data generated or analyzed during this study are included in this published article.

Declarations

Ethics approval and consent to participate

Informed consent for publication was obtained from the patient’s family. All identifying information has been anonymized.

Disclosure statement

While the primary author is a family member, clinical data were independently reviewed and verified by co-authors who were not involved personally.

Consent for publication

Written informed consent was obtained from the patient’s next of kin for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

Not applicable.