mTBI vs. PTSD: A Clinician's Guide to the Overlap

RULE IN, RULE OUT — A DIFFERENTIAL DIAGNOSIS SERIES

By K. Hollis Brennan, LPC, CSP

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Why “Atypical” Presentations May Be Typical… For Brain Injury

You have a client who is not responding to your standard PTSD protocol. Exposure is producing destabilization rather than habituation. Therapy homework is often incomplete, and it doesn’t seem to be from avoidance, instead the client cannot hold the cognitive thread long enough to finish a thought record. EMDR stalls at desensitization, and the client reports that bilateral stimulation itself triggers headaches, dizziness, or worse, seizure activity. You are delivering competent clinical work, but something about this presentation does not fit your model.

This is one of the most common clinical scenarios I see: A client with an unidentified mild traumatic brain injury (mTBI) embedded in what appears to be a straightforward PTSD case. The problem is not your clinical skills, it is what I call the Invisibility Gap, the space between what graduate training covers about psychological trauma and the missing training for what physical trauma to the brain actually does to the neural substrate you are treating. Most mental health training programs devote minimal or no didactic time to acquired brain injury. The result is that mTBI, more commonly called a concussion, remains chronically under-recognized in therapy caseloads, and clients who need coordinated care receive single-diagnosis treatment addressing only half the clinical picture, leaving counselors in the dark on treatment options.

This article is the first installment in our Rule In, Rule Out series, designed to give clinicians a practical differential-diagnosis framework for the conditions most commonly confused with, or co-occurring alongside, acquired brain injury. We are not here to replace your clinical judgment, if you're reading this, we know you are working hard to support your clients. We are here to sharpen your tools for clients with brain injury-specific knowledge that changes treatment outcomes.

Clinicians who read this guide can expect to be able to:

1. Explain why standard symptom checklists (NSI, PCL-5) are insufficient for differentiating mTBI from PTSD.

2. Apply a structured five-step assessment framework using the OSU-TBI-ID, PCL-5/CAPS-5, PHQ-9, GAD-7, and collateral data to construct a weighted differential diagnosis.

3. Identify eight clinical red flags indicating that undiagnosed mTBI may be complicating a client's PTSD presentation.

4. Describe necessary modifications to EMDR, CPT, and PE protocols when brain injury is present, including assessment of seizure risk prior to bilateral stimulation.

5. Determine appropriate treatment sequencing when mTBI and PTSD are both active and competing for limited cognitive resources.

6. Formulate an effective referral to brain injury-specialized providers, including essential referral components and collaborative care coordination strategies.

The Diagnostic Problem: Overlapping Symptoms, Different Mechanisms

Symptom checklists are a clinically necessary starting point, but they are insufficient for differential diagnosis between mTBI and PTSD, because both conditions produce extraordinarily similar self-report profiles through fundamentally different neurological mechanisms.

Zhang et al. (2021) used magnetoencephalography (MEG) and machine-learning classification to examine diagnostic overlap in trauma-exposed populations. [1] The central finding should give every clinician working with trauma caseloads pause. The participants with PTSD who had no history of head injury scored just as highly on standard concussion symptom questionnaires as participants with confirmed mTBI. The surface symptoms were statistically indistinguishable.

What differs is the way the brain works when it is operating under these two different conditions. In people with mTBI, the brain's electrical signals (the rhythms it uses to take in what you see and hear, hold your attention, and coordinate your movements) were disrupted in the areas responsible for processing and organizing incoming information (thalamic relay, sensory-motor coordination, and information-integration networks). In people with PTSD, the disruption showed up in brain regions that store and react to frightening memories (amygdala-hippocampal and temporal-limbic circuits). Even though both groups reported nearly the same symptoms, a computer program, analyzing only their brain wave patterns, could correctly tell mTBI and PTSD apart roughly 80–90% of the time.

The clinical translation: mTBI disrupts the brain's capacity to integrate and coordinate incoming information, like sensory gating, processing speed, and working memory. PTSD disrupts the brain's capacity to regulate threat processing, for example intrusive memories, hyperarousal, avoidance.

Both drain cognitive and emotional resources. Both disrupt sleep. Both emerge from types of traumatic events. But they require fundamentally different treatment strategies, and when co-occurring, they interact in ways that can render standard protocols for either condition less effective, sometimes even contraindicated.

When a client presents with a PTSD-consistent trauma history but shows atypical treatment response (i.e. slow cognitive processing that impedes exposure homework, sensory overload in session, word-finding difficulty during narrative processing, or paradoxical worsening with interventions that should produce improvement) the differential rule out model should include mTBI. These symptoms may be unrecognized brain injury features confounding your trauma work.

A Five-Step Assessment Framework for the mTBI-PTSD Differential

Differential diagnosis between mTBI and PTSD is a weight-of-evidence process, not a single-measure determination. The following framework structures the clinical reasoning.

Step 1: Anchor the Injury History with the OSU-TBI-ID

The OSU-TBI-ID (Ohio State University Traumatic Brain Injury Identification Method) is the gold-standard structured interview for documenting mechanism, severity, and timing of TBIs across the lifespan. This is a systematic interview that captures concussions your client may not spontaneously report from their lifetime. A single “mild” concussion tells one clinical story; three concussions over fifteen years, particularly with incomplete recovery between events, tells a very different one.

Clinical Note: Many clients do not conceptualize prior head injuries as “brain injuries.” If you need a one question screener, try: “Have you ever hit your head or neck and felt strange after or had trouble remembering what happened?” If yes, ask about falls, sports impacts, motor vehicle accidents, blast exposure, domestic violence, and childhood injuries specifically or use the OSU-TBI-ID screener.

Step 2: Differentiate Symptom Clusters with the PCL-5 and NSI

If you suspect TBI, as part of your care plan, regularly administer the PCL-5 (PTSD Checklist for DSM-5) and the Neurobehavioral Symptom Inventory (NSI) concurrently. While total scores overlap significantly between mTBI and PTSD populations, item-level analysis provides more diagnostic traction. NSI items target vestibular symptoms (dizziness, balance problems), sensory sensitivity (light, noise), and headache cluster more heavily toward mTBI. PCL-5 items targeting re-experiencing (Criterion B), avoidance (Criterion C), and hyperarousal (Criterion E) cluster more toward PTSD.

When both instruments are elevated, dual diagnosis should be considered.

For structured diagnostic interview, the CAPS-5 (Clinician-Administered PTSD Scale) can clarify whether reported concentration difficulty reflects trauma-related dissociation or mTBI-related cognitive inefficiency (brain fog), a distinction the PCL-5 self-report alone cannot make.

Step 3: Screen Comorbid Mood Disruption

The PHQ-9 and GAD-7 capture depression and anxiety severity, both of which frequently accompany mTBI and PTSD independently and can further blur the diagnostic picture. Elevated mood symptoms may be primary, secondary to either condition, or independently comorbid. Tracking scores across time helps clarify directionality and treatment response, but only when interpreted against the expected neurological recovery trajectory, which is our next step.

Step 4: Map the Symptom Course

Timeline is one of the most reliable differentiators and the most underutilized in clinical practice. mTBI symptoms typically emerge immediately following the injury event and follow a gradual improvement trajectory, with cognitive and somatic complaints predominating early. Though, some TBI symptoms worsen over the acute phase due to continued diffuse axonal injury.

PTSD symptoms may emerge days to months after the traumatic event, can follow a waxing-and-waning course. However, psychological and physiological symptoms related to trauma cues are sudden and related to the trauma experienced.

mTBI symptoms related to the environment often build with exposure time, and are related to cognitive and sensory processing for example, sensitivity to light, sound, headaches, confusion, disorientation, and memory difficulties. When both conditions co-occur, the symptom timeline often reveals a distinctive layered pattern that clinicians can learn to recognize retrospectively, even when it was not identified in real time.

Step 5: Build the Evidence Map

Structured questions to map symptom course include:

1. What symptoms appeared within the first 72 hours?

2. Which symptoms developed or worsened later?

3. Are there symptoms that were initially improving but have plateaued or worsened?

4. Does the symptom profile shift based on context (e.g., worse in cognitively demanding environments vs. worse when exposed to trauma reminders)?

Conceptualize the differential as a weighted evidence model. No single data source determines the diagnosis. Converging evidence from injury history (OSU-TBI-ID), symptom profiles (PCL-5, NSI, PHQ-9, GAD-7), temporal course, collateral reports, and (when available) neuropsychological testing or physiological data (qEEG, MEG) produces a clinically useful picture. Where evidence converges on both conditions, dual diagnosis is the most accurate formulation and we will tell you how to make your trauma treatment protocols more effective for this client population.

The mTBI Recovery Timeline: A Critical Care Window

Most clinicians treating PTSD are not familiar with the expected course of mTBI recovery. Here is a simplified overview:

mTBI phase	Predominant Symptoms	Co-Occurring PTSD
Acute phase (0–72 hours)	Most pronounced cognitive disruption. Confusion, disorientation, headache, nausea, and light/noise sensitivity are expected. Mood screening during this window captures acute injury effects, not stable psychiatric symptoms. A general sense of being neurologically “offline.”	The brain injury symptoms are so loud that trauma responses, if present, are effectively masked. The client may not yet be experiencing intrusive re-experiencing or hypervigilance because the injured brain does not yet have the processing bandwidth to generate a full PTSD response.
Early recovery (1–4 weeks)	The period of most rapid improvement. Sleep disruption, cognitive fog, irritability, and emotional lability are common but should show a measurable downward trend.	PHQ-9 and GAD-7 elevations during this period may reflect the neurological injury itself rather than an independent mood disorder.
Subacute phase (1–3 months)	The majority of uncomplicated mTBI cases resolve or substantially improve within this window. Symptoms that plateau or worsen during this phase, particularly mood and anxiety symptoms, warrant closer evaluation for comorbid PTSD, pre-injury psychiatric history, or injury complications. This is the window where dual diagnosis most commonly becomes clinically apparent.	When co-occurring, the cognitive fog starts to lift, the headaches become less constant, and sensory tolerance gradually improves. Yet, instead of the client feeling progressively better, new symptoms appear or intensify: Nightmares, startle responses, avoidance patterns, and emotional reactivity shift from the blunted, fatigued quality of acute brain injury to the anxious, hypervigilant quality of active trauma processing. The brain has recovered enough capacity to begin processing the threat, and that processing is dysregulated.
Persistent symptoms (3–12 months)	Approximately 15–30% of mTBI patients develop persistent post-concussion symptoms beyond three months.	When depression and anxiety scores remain elevated at this stage, they are unlikely to resolve with neurological recovery alone and should be treated as independent clinical targets, while continuing to account for the cognitive constraints brain injury imposes on treatment.
Extended recovery and stabilization (12–24 months)	Neuroplastic adaptation continues during this period, though the rate of spontaneous improvement slows significantly. This is the critical care window for integrated treatment. After 24 months, residual symptoms are more likely to represent the client's new neurological baseline.	The brain has stabilized enough to tolerate trauma-focused intervention, and functional gains from targeted rehabilitation and therapy are still achievable.

A Case Example

Let's bring this into the real world. Consider a client who was in a serious car accident eight months ago. In the emergency room, she was evaluated for a concussion and she reported a loss of consciousness, post-traumatic amnesia of approximately 20 minutes, and acute headache and confusion. She was diagnosed with mTBI and referred for concussion management. Over the first two months, her headaches improved, her cognitive fog began to clear, and the concussion clinic noted steady progress. At three months, she was discharged from concussion management with the note “post-concussive symptoms resolving.”

But at four months, she began having nightmares about the accident. By five months, she was avoiding driving entirely and had stopped going to the grocery store because the fluorescent lighting and ambient noise triggered panic and extreme fatigue. At six months, her primary care provider diagnosed PTSD and referred her for therapy. Her new therapist initiated gentle, trauma-informed exposure therapy, but the client could not sustain imaginal exposure for more than 10 minutes before losing her train of thought. She became visibly fatigued and reported a return of headaches. The therapist interpreted this as avoidance and confidently increased the exposure demands. The client's progress deteriorated.

What the therapist did not recognize was the layered timeline: the mTBI had improved enough to unmask the PTSD, but the concussion had not fully resolved. Persistent cognitive fatigue, residual sensory sensitivity, and reduced processing speed were still present, operating below the threshold of clinical detection because the most dramatic mTBI symptoms had cleared. However, residual symptoms affected the client's capacity to engage in an attention-intensive trauma protocol.

The Remote Injury: When Brain Injury History Is Measured in Decades, Not Months

Not every client with an unidentified mTBI walks into your office in the acute or subacute window. Many present a decade or more after injury, often reporting a long and frustrating treatment history. These are the clients who have cycled through multiple providers, received multiple diagnoses (depression, generalized anxiety, ADHD, treatment-resistant PTSD), and some have internalized the belief that they are simply not trying hard enough or that therapy does not work for them.

The OSU-TBI-ID remains essential here, because it reframes the clinical picture. A remote mTBI (particularly when compounded by multiple sub-concussive events, incomplete recovery, or a pre-injury history of neurodevelopmental vulnerability) may have established a permanent shift in the client's cognitive baseline. Processing speed, working memory capacity, executive function, and sensory-gating efficiency may be operating at a lower threshold than the client's apparent intelligence (and history or known self) suggests. A client may present with a pre-injury sense of self, and a post-injury sense of self, with a deep reluctance or limited ability to acknowledge one another, never mind integrate.

Session length, homework complexity, the speed at which you introduce new concepts, the sensory environment of your office, and the attentional demands of your chosen protocol all need to be calibrated appropriately. Screening for remote brain injury also changes the narrative for the client: Many survivors describe profound relief when they learn that the cognitive difficulties they have been attributing to personal failure, aging, or “just anxiety” have a neurological basis that was never identified or communicated to them. That reframing is itself a therapeutic event, and it often marks the point where treatment begins to gain traction after years of stalling.

Treatment Implications for Specific Modalities

EMDR: Seizure Risk and Bilateral Stimulation Alternatives

⚠ Clinical Safety Note: EMDR Seizure Risk Brain injury survivors (particularly those with cortical contusions, temporal lobe involvement, or a history of post-traumatic seizures) are at elevated risk for seizure activity. Rapid bilateral eye movements can, in susceptible individuals, lower the seizure threshold. Before initiating EMDR with a client who has a known or suspected brain injury, assess seizure history and risk factors. For clients with elevated seizure risk, tactile bilateral stimulation (alternating taps) or auditory bilateral stimulation (alternating tones) may be used as alternatives to saccadic eye movements. Consult with the client's neurologist when seizure history is present. [4]

Beyond seizure risk, EMDR with brain-injured clients often requires reduced set lengths, more frequent breaks, simplified cognitive interweaves, providing pre-written options for negative and positive cognitions, and modified session duration. A standard 60-minute EMDR session may need to become 45 minutes of active processing with built-in pacing breaks. Clinical experience indicates that pushing through cognitive fatigue during desensitization produces session-level abreaction without consolidation, and the client leaves activated, fatigued, and not processed.

TF-CPT and PE: Cognitive Load Considerations

Trauma-Focused Cognitive Processing Therapy (TF-CPT) relies on the client's ability to identify, articulate, and restructure maladaptive cognitions. This process demands intact working memory, sustained attention, and abstract reasoning. When mTBI has compromised these capacities, CPT worksheets may be cognitively inaccessible without adaptations. Modifications include simplified worksheets, verbal rather than written processing, shorter sessions, and extended timelines for the protocol.

Prolonged Exposure (PE) depends on within-session habituation during imaginal exposure. If the client's cognitive stamina cannot sustain the 20–45 minutes of continuous imaginal exposure that PE typically requires, habituation does not occur and sensitization may result. [5] Clinicians working with co-occurring mTBI should consider graduated exposure durations and monitor cognitive fatigue indicators (for example: increased word-finding difficulty, processing speed drop-off, irritability spike) as session-termination signals distinct from emotional distress.

Sequencing: Stabilize the Brain, Then Process the Trauma

When both conditions are active, focus on stabilizing the brain injury first to create the neurological foundation for effective trauma processing. This means establishing adequate sleep architecture, building cognitive stamina through graduated activity, reducing sensory overload, managing headaches and vestibular symptoms, and critically setting realistic expectations with the client about treatment pacing.

The treatment sequence is not arbitrary. A client who cannot sustain 30 minutes of focused cognitive engagement is not yet a candidate for intensive trauma reprocessing. Attempting trauma-focused work prematurely is one of the most common causes of what appears to be “treatment-resistant PTSD” in brain-injured populations.

The distinction between treatment-resistant PTSD and unrecognized brain injury confounding treatment is one of the most consequential differential questions in trauma therapy.

Integrative approaches like neurofeedback for neural hyperarousal regulation, mindfulness-based interventions adapted for cognitive fatigue, and carefully graded exposure can bridge the stabilization and trauma-processing phases, particularly for clients with high comorbidity burden. [6]

Clinical Red Flags: When to Suspect Undiagnosed mTBI in Your PTSD Caseload

The following patterns should prompt clinicians to expand the differential diagnosis to include mTBI, even when the initial presentation appears consistent with PTSD alone.

• Treatment response anomaly: Trauma-focused therapy is technically well-delivered but the client is not improving at expected rates, or is deteriorating/regressing. Standard protocol adherence is not producing standard outcomes.

• Symptom disproportionality: The client reports, or you witness, cognitive symptoms (processing speed, word-finding, memory changes) disproportionate to the severity of their PTSD presentation. Cognitive complaints exceed what the trauma diagnosis alone would predict.

• Sensory/cognitive indicators: Sensory overload (light sensitivity, noise sensitivity, difficulty in visually busy environments) persists outside of trauma-related triggering contexts. The sensory reactivity is generalized, not cue-specific.

• Unexplained somatic symptoms: Headaches, dizziness, or balance complaints are present and don't align with expected thoughts related to anxiety. These symptoms persist even when anxiety is well-managed.

• Temporal pattern in session: The client's cognitive performance visibly degrades across the session, not at the start (which suggests avoidance) but progressively (which suggests fatigue). Word-finding difficulties, processing speed drops, and irritability increase as the session continues.

• Intelligence-performance discrepancy: There is a noticeable gap between the client's apparent intelligence (and emotional intelligence) and their functional cognitive performance. They demonstrate insight and verbal ability early in sessions but cannot sustain it.

• Mechanism of injury clue: The traumatic event involved any mechanism consistent with TBI: Acceleration/deceleration, direct impact, blast, fall, being choked, or assault to the head. If the traumatic event could have injured the brain, it may have.

• History indicators: The client has a history of multiple concussions, contact sports, military service, or domestic violence, even if they do not identify these as “brain injuries.” Cumulative exposure matters, and self-report often underestimates injury history. In fact, most people do not know that a concussion is a brain injury.

** Any one of these flags warrants further inquiry. Three or more in combination strongly suggest that mTBI should be formally assessed.**

Complex PTSD and Traumatic Brain Injury: Compounded Disruption

When a client presents with a history of prolonged, repeated trauma (i.e. childhood abuse, domestic violence, combat deployments, trafficking) the clinical picture often meets criteria for Complex PTSD (cPTSD), characterized by the core PTSD triad plus disturbances in self-organization: Chronic affect dysregulation, negative self-concept, and relational disruption. What is less commonly recognized is how frequently these same populations have co-occurring brain injuries, again often unassessed.

Domestic violence is the leading cause of TBI in women, and the majority of these injuries go undocumented and untreated. [7] Combat veterans sustain blast-related mTBI at rates that far exceed the general population and outpace clinical identification protocols. [8] Children in abusive homes are subjected to shaking, hitting, and falls during critical neurodevelopmental periods. The result is that the very populations most likely to develop cPTSD are the most likely to carry undiagnosed brain injuries as well.

The affect dysregulation of cPTSD looks identical to the emotional lability of frontal lobe injury. The negative self-concept of cPTSD is reinforced by the cognitive inefficiency of brain injury; a client who cannot organize their thoughts, loses words mid-sentence, and cannot complete tasks that used to be effortless develops a self-narrative of brokenness that mirrors the shame-driven story of complex trauma. Relational disruption, the third hallmark of cPTSD, is compounded when brain injury reduces the social cognition, pragmatic language, and impulse regulation capacities that relationships depend on. Treating cPTSD without screening for brain injury in these populations risks building a therapeutic framework on an incomplete foundation, leading the clinician to address the psychological wound while the neurological wound continues to undermine every intervention you deploy.

The clinical imperative is straightforward. Any client whose history includes repeated interpersonal violence, combat exposure, or childhood physical abuse should receive structured brain injury screening as part of the standard trauma assessment, regardless of how long ago the trauma or head injury occurred.

Scope of Practice and Referral Pathways

Identifying the mTBI-PTSD overlap does not require you to become a brain injury specialist; it requires you to recognize when your client's presentation exceeds the scope of single-diagnosis treatment and to know where to refer.

The most effective model for co-occurring mTBI-PTSD is collaborative care: The referring clinician continues the therapeutic alliance and trauma work (with modifications), while specialized brain injury providers address neurorehabilitation, neuropsychological assessment, vestibular therapy, and brain injury-specific medical consultation.

Consider referring your client to specialists across the following disciplines as clinically indicated:

• Neuropsychologist for formal cognitive skills assessment to inform rehabilitation and therapy work.

• Rehabilitation psychologist for adjustment-to-disability counseling and cognitive rehabilitation usually in the acute phase.

• Neurologist for medical diagnosis, imaging interpretation, and seizure risk evaluation. Note many "mild" TBIs are not visible in brain scans.

• Psychiatrist or neuropsychiatrist for medication management calibrated to the brain-injured client's altered pharmacological sensitivity.

• Speech-language pathologist specializing in cognitive and communication rehabilitation skills.

• Physical therapist with vestibular rehabilitation expertise for dizziness, balance, and visual motion sensitivity.

• Occupational therapist for functional cognitive strategies and return-to-activity planning.

• Neuro-optometrist for visual processing and oculomotor assessment when balance or dizziness is an issue.

• Vocational rehabilitation counselor when vocational impact is present.

• For clients managing multiple concurrent referrals, a care coordinator or case manager through insurance or advocacy organizations can reduce the organizational burden that brain-injured clients are least equipped to carry on their own. Find support at your local state Brain Injury Alliance.

  
  

What to Include in a Referral

A referral that communicates the clinical question clearly gives the receiving clinician substantially more diagnostic traction. Request your client sign a Release of Information if they are comfortable doing so to make care coordination ethical and effective.

Include in your referral: Injury mechanism and timeline, current symptom profile with specific cognitive complaints, treatment history and response patterns, current medications, and the clinical question you want the specialist to answer. A referral that says “rule out mTBI given history of car accident in 2023, current report of memory difficulties, and headaches” provides far more useful direction than one that says “evaluate for neurocognitive concerns.” This direction will not eliminate other potential diagnoses like dementia; rather it gives the clinician a clear path to start on.

For neuropsychological assessment, specify that you are requesting TBI-specific evaluation and that you need the assessment to inform trauma therapy planning. This helps the neuropsychologist select appropriate measures and frame their recommendations in clinically actionable terms.

Always attach an ROI if you have one.

Now You Can Change Your Treatment

The Invisibility Gap means that clients are being seen by clinicians who have the skills to treat trauma but not the training to recognize when brain injury is altering the treatment landscape underneath them. That gap is not a failure of individual clinicians; it is a failure of the systems that trained them to include injuries to the very organ we treat.

You need three things to serve these clients well:

1. The knowledge to suspect brain injury, which, if you've read this far, you now have.

2. The tools to screen for it, they're linked in this article.

3. The referral pathways to ensure your client receives coordinated care. Connect with your local Brain Injury Association, a local Rehabilitation Psychologist, a local Neuropsychologist, and a local Psychiatrist to work with.

   
   

Thank you for taking the time to learn about brain injury!

K. Hollis Brennan, LPC, CSP is a Licensed Professional Counselor and Board Certified Specialist in Psychometry specializing in brain injury, trauma, and neuropsychological evaluation. She is a published co-author on TBI research in Criminal Justice and Behavior and Rehabilitation Psychology, a Disability Advocacy Committee member in APA's Rehabilitation Psychology Division 22, and a former researcher in the University of Denver Traumatic Brain Injury Lab. She founded Brain Injury Therapy to provide trauma-informed, neurodiversity and disability affirming care for survivors of brain injury and their families.

References

1. Zhang, J., Safar, K., Emami, Z., Ibrahim, G. M., Bhatt, M., Freedman, S., & Bhatt, P. (2021). Local and large-scale neural dynamics distinguish mTBI and PTSD: A magnetoencephalography and machine-learning study. Translational Psychiatry, 11(1), Article 172. https://doi.org/10.1038/s41398-021-01467-8

2. Manley, G. T. et al. (2025). A new characterisation of acute traumatic brain injury: The NIH-NINDS TBI Classification and Nomenclature Initiative. The Lancet Neurology, 24(6), 512–523. https://doi.org/10.1016/S1474-4422(25)00154-100154-1)

3. Iverson, G. L. (2005). Outcome from mild traumatic brain injury. Current Opinion in Psychiatry, 18(3), 301–317. https://doi.org/10.1097/01.yco.0000165601.29047.ae

4. Annegers, J. F., Hauser, W. A., Coan, S. P., & Rocca, W. A. (1998). A population-based study of seizures after traumatic brain injuries. New England Journal of Medicine, 338(1), 20–24. https://doi.org/10.1056/NEJM199801013380104

5. Foa, E. B., Hembree, E. A., & Rothbaum, B. O. (2007). Prolonged exposure therapy for PTSD: Emotional processing of traumatic experiences — Therapist guide. Oxford University Press.

6. van der Kolk, B. A., Hodgdon, H., Gapen, M., Musicaro, R., Suvak, M. K., Hamlin, E., & Spinazzola, J. (2016). A randomized controlled study of neurofeedback for chronic PTSD. PLOS ONE, 11(12), e0166752. https://doi.org/10.1371/journal.pone.0166752

7. Valera, E. M., & Berenbaum, H. (2003). Brain injury in battered women. Journal of Consulting and Clinical Psychology, 71(4), 797–804. https://doi.org/10.1037/0022-006X.71.4.797

8. Terrio, H., Brenner, L. A., Ivins, B. J., Cho, J. M., Helmick, K., Schwab, K., Scally, K., Bretthauer, R., & Warden, D. (2009). Traumatic brain injury screening: Preliminary findings in a US Army brigade combat team. Journal of Head Trauma Rehabilitation, 24(1), 14–23. https://doi.org/10.1097/HTR.0b013e31819581d8