TBI vs. Anxiety: A Clinician's Guide to the Overlap
RULE IN, RULE OUT — A DIFFERENTIAL DIAGNOSIS SERIES
Written by K. Hollis Brennan, LPC, CSP
Looking for a client-friendly version? A companion Easy-to-Read guide covering one piece of this picture (autonomic dysfunction after brain injury) is available to share with survivors and family members. Read it here.
A Diagnosis That Covers Too Much Ground
Renata* is 29, three years out from a car accident that left her with a diagnosis of generalized anxiety disorder and a plethora of changes in her life. In her medical chart, her symptoms line up: racing heart, trouble sleeping, irritability, difficulty concentrating, constant low-grade dread. Yet in my office, they don't line up nearly as cleanly. Her heart rate climbs from 76 to 130 within two minutes of standing, no matter her mood or state of mind. Scrolling her phone or riding in a car as a passenger brings on dizziness and nausea. A few times a month she gets a rising, unplaceable feeling in her stomach, a wave of deja vu, and then loses the next thirty seconds; she doesn't remember them as frightening; they're just absent. Renata's exhausted by mid-afternoon most days, snaps at her kids over noise she didn't used to notice, and has put on fifteen pounds despite no changes in her eating habits.
None of this is technically incompatible with anxiety. However, all of it is also compatible with at least five other things related to brain injury. "Anxiety" is often a label that a lot of different, distinguishable problems get filed under, because anxiety is what the resulting behavior and self-report look like from the outside, regardless of the physiological or psychological causes.
This, again, is the Invisibility Gap. Graduate counselor training teaches anxiety disorders as disorders of threat appraisal and avoidance. It does not teach that a single brain injury can independently disrupt the autonomic network, the vestibular and ocular-motor system, the seizure threshold, the pituitary axis, the frontolimbic circuits that regulate emotional reactivity, sleep architecture, and the cognitive bandwidth a person has for life. A disruption to any one of these systems can produce a presentation that many good clinicians will reasonably read as anxiety. So, how do we tell physiological changes caused by an injury apart from the physiological changes caused by psychological misappraisal when they result in the same reported symptoms? Let's dive in.
*Composite, de-identified for teaching purposes.
What You'll Learn
Clinicians who read this guide can expect to be able to:
Explain why anxiety after brain injury can represent at least seven distinct underlying mechanisms rather than a single disorder.
Apply a multi-domain screening framework spanning autonomic, vestibular/oculomotor, seizure, neuroendocrine, sleep, frontolimbic, and cognitive-load pathways.
Identify domain-specific red flags that should prompt a medical referral before, or alongside, a psychotherapy treatment plan.
Determine which specialist a given symptom pattern should be routed to and formulate an optimal referral that gives that specialist useful information and guidance for their process.
Describe modifications to first-line anxiety interventions when a co-occurring mechanism is suspected or confirmed.
Seven Pathways
Each of the following is a distinct, independently documented mechanism by which a brain injury can produce a presentation that looks like anxiety. They are not mutually exclusive, and a single client can have several active at once. This list is also not exhaustive or inclusive of all of the varieties of aftermath of a brain injury.
1. Autonomic dysfunction (dysautonomia)
Evidence consistently demonstrates that concussions are associated with measurable autonomic nervous system changes. The autonomic nervous system regulates involuntary and largely unconscious bodily functions. Changes after injury occur most reliably in heart rate and heart rate variability responses to a physiologic challenge such as standing or exertion (Pertab et al., 2018; Mercier et al., 2022). Differences can persist past six months even in people who otherwise report full symptom recovery (Hilz et al., 2017).
At the acute, severe end of injury, paroxysmal sympathetic hyperactivity can happen, with consensus diagnostic criteria established by Baguley et al., 2014. While in intensive care, a survivor might experience sudden episodes where the body’s “fight or flight” system misfires all at once. This causes the heart to race, blood pressure to spike, breathing to speed up, body temperature rises, and sweating to increase, often with the muscles stiffening or the body locking into an unusual position. These episodes come and go (they’re temporary, not constant) and are not commonly reported outside of the critical care environment. The outpatient presentation is usually the tail end of this acute dysregulation, orthostatic symptoms, exercise intolerance, and heart rate spikes.
A client's report might sound like:
Orthostatic symptoms- “I get dizzy or lightheaded when I stand up too fast.” “I feel like I might black out if I get up quickly.” “I have to sit on the edge of the bed for a minute before I stand.” “My vision goes dark or spotty when I stand.”
Exercise intolerance- “Even a little bit of activity wipes me out for the rest of the day.” “I used to be able to walk/work out and now even light effort makes me feel awful.” “If I overdo it on a short walk, I crash for hours afterward.” It’s a disproportionate reaction to a small amount of exertion, not just normal tiredness.
Heart rate spikes- “My heart starts racing out of nowhere.” “My heart pounds really hard and fast, and I don’t know why.” “I’ll be sitting calmly and suddenly my pulse shoots up.” The key clinical clue is that it happens without a fear trigger or worried thought attached to it.
2. Vestibular and ocular-motor dysfunction
Dizziness is second only to headache in frequency after concussion, and the differential spans central, peripheral, and non-vestibular causes (see this post-concussive dizziness review). The Vestibular/Ocular Motor Screening tool (VOMS) often given by cognitive therapists and speech pathologists rates symptom provocation across smooth pursuits, saccades, convergence, the vestibulo-ocular reflex, and visual motion sensitivity, with a positive result commonly defined as any item scoring 2 or higher; a Level-A guideline recommends screening with it when vestibular or visual symptoms are endorsed, and specialist referral if symptoms persist beyond a month (Concussion Ontario guideline). We will talk about the additional specialists below.
A clinical review on panic and medical illness notes that comorbid vestibular abnormality and panic or anxiety disorder are highly prevalent together, which cuts both ways: a positive VOMS does not rule anxiety out, and an anxiety diagnosis does not rule a vestibular injury out (Chen & Simon) in fact we should be expecting overlap and co-morbidity.
Client reports to listen for include dizziness or nausea triggered by specific visual or motion situations (i.e. scrolling a phone, reading, screens, being a passenger in a car, busy visual environments like grocery stores or malls, quick head turns, or looking at moving objects). Clients may report trouble tracking text while reading, losing their place on the page, words seeming to “swim” or double. Headaches or fatigue that spike specifically after visual tasks, not generically through the day may be induced by the vestibular system. Feeling unsteady, off-balance, or like they need to hold onto something when standing or turning, as opposed to feeling lightheaded when standing up fast (that one’s more orthostatic) puts clients at risk of additional injuries. Discomfort in visually busy or brightly lit spaces, for example our offices which often include fluorescent lighting and patterned carpet.
Clarifying intake question to ask: “Does this happen more when you’re moving your eyes or head, or looking at something moving, or when you’re thinking about something stressful?”
Behavioral observation in session can help you connect the dots with your client. Watch whether they turn their whole body instead of just their head when you move or they look toward a sound. The whole-body substitution for a head turn is a classic compensation pattern. Watch for squinting, shielding their eyes, or closing one eye under normal room lighting. Watch whether maintaining eye contact or following your hand/gesture seems to provoke visible physical discomfort. If the room has a window, patterned surface, or fluorescent light and they mention queasiness or headache onset tied to it mid-session, accommodate and document any changes once the lighting is low, you stop talking with your hands, etc. More on accomodations below.
3. Post-traumatic seizures
A large study in Norway followed people who were hospitalized for a traumatic brain injury and tracked how many later developed epilepsy. Within 2 years, about 3 out of 100 people had developed epilepsy. For people with a severe brain injury specifically, that number rose to about 13 out of 100 by the 5-year mark. People with a severe brain injury were roughly 25 times more likely to develop epilepsy than people who hadn’t had a brain injury at all (Norwegian cohort study, 2024).
Temporal lobe seizures in particular can produce intense fear, a rising epigastric sensation, deja vu, and autonomic surges that are frequently mistaken for panic attacks, sometimes for years, before video-EEG monitoring or imaging identifies it. Routine scalp EEG misses a meaningful share of temporal lobe epilepsy, since the seizure focus often sits deep in the mesial temporal lobe, so a single normal EEG unfortunately does not close this differential.
Features favoring a seizure over panic disorder or a panic attack specifier include impaired consciousness, an attack roughly under two minutes, and automatisms (an involuntary, stereotyped, and repetitive motor or verbal behavior performed without conscious awareness or volitional control and often with no memory of doing so afterwards), while preserved consciousness and attacks lasting five minutes or longer favor diagnoses like panic disorder or a panic attack specifier (Cholette-Tétrault et al., 2026).
4. Neuroendocrine dysfunction (post-traumatic hypopituitarism)
When researchers combine results across multiple studies, roughly 27 to 32 out of every 100 people with a brain injury end up with some degree of pituitary gland dysfunction. That number varies quite a bit from study to study, mostly because researchers don’t all test for hypopituitarism the same way or at the same point in someone’s recovery (Bensalah et al., 2020).
The hypopituitarism symptom list overlaps heavily with an anxiety presentation: fatigue, weight change, cognitive slowing, and mood and sleep disturbance with a few differential symptoms including cold intolerance, decreased libido, and menstrual irregularity. Consensus guidance recommends screening at three to six months post-injury for anyone hospitalized over 48 hours or with ongoing symptoms, but a Veterans Affairs study found screening rates in primary care are exceedingly low in practice (Minneapolis VA study).
Questions to ask during intake if your client endorses a head injury (which by now we hope is a standard intake question you ask all of your clients!):
Fatigue- “Is this a tiredness that enough rest fixes, or a heaviness/exhaustion that’s there no matter how much you sleep?” Anxiety-driven fatigue usually responds at least partially to rest or distraction; endocrine fatigue often doesn’t, regardless of sleep.
Temperature- “Do you find yourself cold when people around you are comfortable, for example do you need a sweater indoors, or have cold hands and feet a lot?” This one has almost no anxiety equivalent, which makes it a useful differentiator on its own.
Weight- “Has your weight changed in a way that doesn’t match your eating or activity levels, meaning you have gained or lost without really changing anything?” Anxiety can affect appetite and weight, but usually tracks with reported eating/activity changes; endocrine weight shifts do not.
Libido/menstrual- “Have you noticed a change in sex drive, or [for menstruating clients] any change in your cycle, is it irregular, lighter, or stopped?” This is rarely volunteered and rarely asked; it’s one of the more specific flags on the list.
Cognitive slowing- “Does your thinking feel slow or foggy? Does this happen when you are stressed or in general?” Worth distinguishing a client's report of “I can’t focus because my mind is racing” (anxiety) from “my mind feels like it’s moving through mud” (more consistent with endocrine or diffuse injury effects).
A timing question that speaks to onset- “When did these symptoms start relative to the injury, and have they been steady, getting worse, or coming and going with stress?” Anxiety symptoms tend to fluctuate with stressors; hypopituitarism-pattern symptoms tend to be more constant and slowly progressive.
It is worth knowing that benzodiazepines, opioids, and anti-epileptic medications can themselves mimic pituitary dysfunction, which complicates the picture further once a client is already on psychiatric medication.
5. Frontolimbic circuit disruption
The medial prefrontal cortex normally inhibits amygdala reactivity; when the white matter connecting them (particularly the uncinate fasciculus) is damaged, that inhibition weakens. A study of adolescents with moderate-to-severe TBI found altered frontal-amygdala connectivity predicted affective dysregulation, this means that changes in how two brain regions communicate with each other were linked to kids having a harder time managing their emotions. The authors noted that limbic pathways are especially vulnerable to the contusional and torsional forces of brain trauma, the limbic system (amygdala, hippocampus, hypothalamus) handles emotion, memory, reward, and basic drives across the whole lifespan (Bickart et al., 2023).
Clinically, this often looks less like worry and more like disproportionate irritability, a shortened fuse, or affective swings a family describes as a personality change driven by reduced top-down control rather than threat appraisal.
6. Sleep disruption
A meta-analysis found roughly half of people with TBI experience some sleep disturbance, with 25–29% meeting criteria for a sleep disorder. They also noted greater insomnia symptoms in those with comorbid anxiety or depression (Mathias & Alvaro, 2012). A later meta-analysis put post-TBI insomnia at 29%, roughly double the general adult rate. The relationship runs bidirectionally in that poor sleep intensifies anxiety symptoms, and an undiagnosed brain injury can disrupt sleep architecture directly, independent of any psychiatric process. This means that differentiating between anxiety caused sleep disturbance and brain injury caused sleep disturbance that create or exacerbates anxiety is likely impossible in many cases, and not clinically valuable. A few other things to consider on intake:
Daytime sleepiness, not just nighttime insomnia- “Are you falling asleep during the day, even when you don’t want to?” Anxiety classically produces trouble falling or staying asleep, not excessive daytime sleepiness. Real hypersomnia alongside insomnia leans toward an organic sleep-architecture problem from the injury itself, and is worth reviewing diagnostic criteria for sleep-wake disorders and a sleep medicine referral rather than anxiety-focused sleep hygiene work alone.
Snoring and witnessed apneas- Sleep apnea is common, can be caused or worsened by brain injury, produces fragmented non-restorative sleep that may look exactly like anxiety-driven exhaustion and irritability, and needs a sleep study, not therapy.
When not sleeping, what are they doing- “Are you lying there with your mind racing about something specific, or do you just wake up and can’t get back to sleep for no clear reason?” Content-driven wakefulness points toward anxiety; wakefulness with no mental content, or waking up repeatedly through the night without being able to say why, points more toward a disrupted sleep-wake cycle.
Timing relative to the injury- Again, ask about onset. Sleep disruption that started right after the injury and has stayed fairly constant, independent of how anxious the person feels that week, is more consistent with direct injury to sleep-regulating structures than with an anxiety-driven pattern that should track with symptom severity.
7. Cognitive overload and fatigue
The Neurobehavioral Symptom Inventory, a standard post-concussion measure, groups affective/psychological, somatic, and cognitive items into one total score, which means cognitive fatigue and anxiety-type items are frequently summed together in a way that obscures which is actually driving distress. A 2025 review of post-concussion syndrome (PCS) notes PCS frequently shares subjective cognitive complaints, fatigue, anxiety, and heightened somatic vigilance with functional neurological presentations (Mavroudis et al., 2025).
In practice, a client whose cognitive bandwidth is exhausted by midday can present as anxious simply because they no longer have the reserve to tolerate normal demands, this may lead to their mind going blank, worries about forgetting and how they present to others, and irritability or frustration with themselves and the demands of their day, but this is a problem of resource depletion, not constant threat appraisal cycles. Pay attention to what your client worries about and when they worry about it. Track these symptoms when you see them for full hour sessions late in the afternoon compared to morning sessions or shorter sessions, you may see a pattern emerge related to cognitive fatigue.
A Multi-Domain Screening Framework
No single instrument separates these seven pathways from each other or from a primary anxiety disorder. The goal of this framework is to help you document evidence for DSM-5 diagnoses as appropriate and to generate the right referral for ICD-10 matters.
Screen for brain injury history at intake, every time, regardless of presenting complaint. Ask about loss of consciousness, a head strike, blast exposure, intimate partner violence, sports injuries, fights, and motor vehicle accidents, however remote.
Administer the GAD-7 as a severity index, then have a direct conversation about DSM-5 criteria: What specifically does your client worry about, and do avoidant behavior and thinking patterns relate to worry content or physical/situational triggers? Both?
PTs, OTs, and Medical providers can run an orthostatic vital sign screen (seated heart rate and blood pressure after five quiet minutes, then standing at one, three, and ideally ten minutes) if there's any report of a racing heart, lightheadedness, or heat/exertion sensitivity. Therapists, social workers, counselors, speech pathologists, an non-medical providers can ask: “Does your heart race or do you feel lightheaded specifically when you stand up, exercise, or get hot? How soon after standing does it start, and how long does it last?” Many clients have a smartwatch or fitness tracker that logs heart rate continuously. Ask them to check it next time they feel the sensation and report back what it showed, or to screenshot a spike if one occurs. Record data reported (ideally 3-4 times over the course of a week or two) for your referral.
For medical practitioners: Ask about dizziness, visual strain with screens or motion, and balance problems; if present, run a brief VOMS-style provocation screen or refer for one, and pair it with a functional measure like the Dizziness Handicap Inventory.
For non-medical providers: Ask about dizziness, visual strain with screens or motion, and balance problems, and consider administering the Dizziness Handicap Inventory directly; note behavioral signs in session such as whole-body substitution for head turns or light sensitivity. If present, refer for a VOMS-style provocation screen with a vestibular therapist.
Ask directly about brief, stereotyped episodes: a rising stomach sensation, deja vu, a smell or taste that isn't there, loss of time, or reports from others of staring spells or automatisms. Any of these warrants a referral for outpatient or ambulatory EEG, and please remember a single normal scalp EEG does not rule a seizure disorder out.
Screen for sleep disruption with a brief validated tool like the Sleep Disorders Questionnaire and ask specifically about snoring, witnessed apneas, and sleep timing, since several sleep disorders mimic or worsen anxiety independently.
Ask about fatigue, weight change, temperature intolerance, and libido or menstrual changes; if present alongside a qualifying injury (hospitalization over 48 hours, or ongoing symptoms), flag for endocrine screening at the three-to-six-month mark if that hasn't already happened.
Ask client, family, or a collateral source whether the client's temperament has changed, are they more irritable, have a shorter fuse, less emotional control than before the injury? Include collateral report when possible since the client themselves may not recognize this shift as different from "just being anxious."
You may notice this is a lot of screeners, questionnaires, and a longer form of intake. You're right. This may take several sessions to get through, but the results could change the client's outcomes with your work together, and perhaps even change their recovery trajectory. Weigh the combined picture. A positive screen in any domain warrants a referral to the matching specialist before, or alongside, finalizing a purely psychiatric treatment plan; a picture with no positive domain screens, content-driven worry, and a clear cognitive appraisal pattern supports proceeding with standard anxiety care, with periodic re-screening built in especially for folks in the acute/subacute phases of recovery from TBI.
Course Over Time
Acute (0–4 weeks) | Paroxysmal sympathetic hyperactivity can appear after moderate-to-severe injury; early post-traumatic seizures are most likely in this window and raise risk of later epilepsy; dizziness and fatigue are common and easily read as fear in a legitimately (and understandably) frightened, newly injured patient. |
Subacute (1–3 months) | Orthostatic and vestibular symptoms tend to emerge with return to activity; sleep disruption is near its peak; this is often exactly when a new psychiatric referral for an "adjustment disorder" often lands in your inbox (or fax machine for us dinosaurs out here), well before the three-to-six-month endocrine screening window has opened for medical providers, assuming the client has long-term follow-up care, which is rare. |
Chronic/persistent (3 months–2 years) | This is the window consensus guidelines target for hypopituitarism screening; autonomic and cognitive differences can remain measurable even in clients who report feeling otherwise recovered; by now many clients already carry an established anxiety or panic diagnosis and sometimes months or years of content-focused therapy. |
Remote (2+ years, including decades post injury) | Epilepsy risk from a moderate-to-severe injury continues to accrue for years, not just in the acute window; injury history is often forgotten or never disclosed; symptoms across any of the seven pathways can be stable, fluctuating, or re-triggered by an unrelated illness, pregnancy, or a second head injury. |
Case Example: Four Years of Panic Attacks
Marcus* was 34 when he was referred for "treatment-resistant panic disorder." For four years he'd had episodes several times a month in which he experienced a sudden rising feeling in his chest and stomach, a strange and specific smell no one else could smell, a few seconds of deja vu, and then a memory gap. He'd come back to himself mid-sentence or mid-task with no memory of the previous thirty to sixty seconds. He'd been through two courses of CBT for panic and a trial of an SSRI, with no real change in frequency, intensity, duration, or symptom presentation.
A clinician newly working through this framework asked the question that hadn't been asked in four years of treatment: Had Marcus ever hit his head? He had, in a motorcycle accident six years prior, with a brief loss of consciousness he'd never mentioned because it "didn't seem related." The episode description included impaired awareness, a consistent olfactory aura, resolving under a minute, no memory of the event itself, no fear reported during the episodes (he found out from his wife that he looked frightened) which didn't fit panic disorder's usual shape. He was referred for an ambulatory EEG with a local hospital.
The EEG captured two events consistent with temporal lobe seizures. Neurology started an anti-seizure medication; his episodes dropped by more than half within two months, and the ones that remained no longer included the memory gap, which had been the most functionally disruptive part. He stayed in therapy, now targeting the real anxiety he'd developed about when the next episode would hit, a legitimate, separate problem layered on top of a seizure disorder that four years of panic-focused treatment had never touched.
*Composite, de-identified for teaching purposes.
Invisible Injuries & Invisible Gaps in Care
Clients rarely volunteer an old head injury unless asked specifically, and "did you ever hit your head" gets a different answer than "have you ever lost consciousness, been diagnosed with a concussion, or been in an accident involving your head?"
Why should non-medical providers screen for injuries that seem medical in nature? As a therapist, I can say, here more than almost anywhere else in behavioral health, screening matters because several of the above seven pathways, post-traumatic epilepsy risk in particular, don't resolve on a fixed timeline the way an acute injury narrative implies. We may be the ones to catch something life-saving, or at least game-changing.
I think of our role as similar to massage therapists who might be the ones to identify a cancerous-looking mole on their client's back. Screen for injury history at intake regardless of how long ago an event may have happened, and regardless of whether the client thinks it's relevant. Many don't, and some have never been asked in a way specific enough to surface the fact that yes, in fact, they have had a brain injury and it might be contributing to their current mental and physical wellbeing.
Treatment Implications by Modality
Cognitive Behavioral Therapy for Anxiety
Standard CBT targets cognitive content and avoidance. When any of the seven brain injury-related pathways above is active, content-focused CBT alone leaves the physiological driver unrecognized, and a client's concern about their unexplained symptoms is often rational risk-monitoring rather than a distortion that needs reframing. The more durable move is psychoeducation naming the actual mechanism once it's identified, creating an accommodating office environment, shortening sessions, creating a scaffolded plan for therapy homework that honors pacing needs, and care coordination with the client's medical team when possible.
Relaxation Training and Interoceptive Techniques (Somatic work)
⚠ Clinical Safety Note: standard relaxation training, particularly progressive muscle relaxation and slow, paced breathing, can further lower blood pressure and worsen symptoms in clients with orthostatic intolerance, please screen for it first.
Separately, hyperventilation-style breathing techniques, sometimes used deliberately in panic treatment, are also used diagnostically in EEG labs specifically because they can provoke seizure activity in susceptible patients; if a seizure disorder is suspected or unconfirmed, get neurology input before using deliberate hyperventilation or breath-holding techniques in session.
Eye Movement and Desensitization Reprocessing (EMDR)
⚠ Clinical Safety Note: standard EMDR relies on bilateral stimulation, most commonly eye movements, to facilitate processing. The evidence for a seizure risk specifically is thin (mostly a single case report describing seizure activity during EMDR sessions in a patient with comorbid epilepsy, plus informal clinical guidance rather than a controlled trial; Schneider et al., 2005) however there is a lack of research into this specifically for obvious harm induction reasons. In practice: screen for seizure history or any of the red flags above before using eye-movement-based bilateral stimulation, and when a seizure disorder is suspected or confirmed, use tactile or auditory bilateral stimulation (tapping, alternating tones) instead of eye movements, and get neurology's input first. This is a case where the lower-risk alternative is easy and costs little.
ACT
ACT is being actively studied for mTBI with encouraging early results (a feasibility trial found ACT outperformed CBT on functional disability and post-concussion symptoms; Faulkner et al., 2025), but we have an augmentation that should be included.
⚠ Clinical Safety Note: “accepting” a symptom and committing to values-driven action is not the same as ignoring a physiological limit, and the two can get conflated in practice. For example, a client coached to stop fighting their fatigue and “just do the hike because family time is a core value” is a different outcome than a client learning to tolerate discomfort around a symptom that has no physical ceiling. Before using ACT’s acceptance/committed-action framework with exertion, heat, or position-triggered symptoms specifically, pair it with the same symptom-threshold pacing used in graded exercise rehab (set a known ceiling, dose activity below it, build up gradually) rather than open-ended acceptance of “however bad it gets.” Acceptance work is appropriate for the distress response to a symptom; it is not a substitute for knowing whether the symptom itself signals a physiological limit.
Vestibular and Exercise-Based Rehabilitation
Default to referral for vestibular rehabilitation therapy when VOMS or symptom history points that direction, rather than treating dizziness as a panic symptom to be exposure-treated. For general post-concussion exercise intolerance, a randomized trial in adolescents after sport-related concussion found individually dosed aerobic exercise, set just below each person's symptom threshold, led to faster recovery than a stretching program (Emery & Smirl, 2021) this suggests a referral for dosed activity with an occupational or physical therapist rather than prescribing rest may improve outcomes for certain clients.
Pharmacologic and Specialist Coordination
This is coordination, not prescribing, but it changes documentation. If seizures are suspected or confirmed, benzodiazepines used as a standalone anxiety treatment can mask breakthrough seizure activity without addressing it, and anti-seizure medication, not an anxiolytic, is the first-line treatment once confirmed. If endocrine dysfunction is suspected, please remember that benzodiazepines, opioids, and anti-epileptics can themselves mimic pituitary symptoms, muddying any screening done after they're started. If orthostatic symptoms are present, flag SNRIs as a class that can worsen them (based on case reports currently; Chikkaramanjegowda & de Leon, 2013; Attard et al., 2023), and note low-dose propranolol has randomized trial support for reducing standing tachycardia specifically, separate from its use for anxiety.
Sleep Intervention
Treat sleep disruption as a parallel target rather than a downstream symptom of anxiety that will resolve once the root problem is treated. Cognitive behavioral therapy for insomnia, the standard non-pharmacological approach in the general population, is specifically being studied for mild TBI populations (Dietch & Furst, 2020, Trials and pilots from Brooks and Furst) and referral for a sleep evaluation is reasonable any time snoring, witnessed apneas, or a clearly disrupted sleep-wake schedule is present alongside anxiety-type symptoms.
Clinical Red Flags: When to Expand the Differential
A history of head injury, blast exposure, or loss of consciousness exists anywhere in the client's history, however remote or minimized.
Physical symptoms (racing heart, lightheadedness, flushing) track with position change or exertion more than with worry content.
Dizziness, visual strain, or imbalance is present, especially if worsened by screens, scrolling, or being a passenger in a car.
Brief, stereotyped episodes occur (a rising stomach or chest sensation, deja vu, an out-of-place smell or taste, lost time, or staring spells) regardless of whether the client reports fear during them.
Anyone who knows the client well describes a personality change: more irritable, a shorter fuse, less emotional control than before a known or suspected injury.
Fatigue, weight change, temperature intolerance, or libido or menstrual changes accompany the anxiety-type symptoms.
Sleep is significantly disrupted independent of worry content, or snoring/witnessed apneas are present.
First-line CBT or SSRI treatment for anxiety produces partial or no improvement in physical symptom burden after eight to twelve sessions or an adequate medication trial.
A prior clean neuroimaging result or normal EEG has been used to rule out any brain-related explanation, despite ongoing symptoms.
The client cannot identify specific worry content when asked directly, despite an elevated anxiety screening score.
Episodes are witnessed by others as involving impaired awareness, automatisms (repetitive unintentional movements), or confusion afterward.
Symptom onset, even loosely, follows a head injury, motor vehicle accident, fall, or assault, regardless of how long ago.
Three or more of these in combination strongly suggest an expanded, multi-domain differential before finalizing, or continuing, an anxiety-only treatment plan.
When Several Pathways Overlap
These seven pathways are not mutually exclusive, and in practice they frequently stack. For example, a client can have orthostatic intolerance, vestibular symptoms, and disrupted sleep simultaneously, each contributing its own share to an overall picture that is even more likely to tick all the boxes on the GAD-7 for an anxiety diagnosis. On top of that, anxiety about unpredictable, unexplained symptoms is itself a rational secondary response that can, over time, come to meet criteria for an anxiety disorder. This gives us a true cognitive-behavioral target layered on top of one or more physiological ones, as it was for Marcus once his seizures were controlled. No single instrument sorts all of this cleanly. Clinical judgment, serial measurement, and coordination across several specialists at once, not in sequence, is the realistic standard of care.
Scope of Practice and Referral Pathways
This framework exists to generate well-supported referrals, not to replace the medical workup that confirms or rules out any of these seven mechanisms. Brain Injury Therapy functions as a referral resource for this differential, not as a service positioned to replace neurology, cardiology, endocrinology, or vestibular rehabilitation. Depending on which domain screens positive, appropriate targets include physiatry or PM&R with brain injury experience, neurology (general or epileptology, if seizure is suspected), cardiology with autonomic experience, vestibular-trained physical therapy, endocrinology, and sleep medicine. A local Brain Injury Association is often the fastest way to find who in a given region actually does this work.
What to Include in a Referral
Injury mechanism and approximate date(s), include if client reports loss of consciousness and how long. For clients with multiple in a short period of time (sports, IPV, military) report the whole time period, document worst immediate symtpoms experienced, and any standout injuries during that time.
(For example: Client reports experiencing domestic violence from April 2001 to June 2008, she noted several times her head was hit against a wall, she was hit in the head with a bottle, and was choked. She noted worst event included loss of consciousness for approximately 10 minutes with substantial changes in cognition and energy after that have never resolved.)
Which domain(s) screened positive and what specifically prompted the referral (orthostatic numbers, VOMS results, episode description, endocrine-pattern symptoms, sleep findings, or reported personality change).
For suspected seizure activity: episode duration, any aura, witnessed automatisms, post-episode confusion or memory gaps, and triggers if known.
Treatment history to date, including response or non-response to standard anxiety interventions and at what dose or duration.
The specific clinical question being asked. (For example, "please evaluate for a seizure disorder contributing to this client's panic-like episodes,") rather than a general request for evaluation.
Download the free template for your use here.
Now You Know Which Question to Ask
The Invisibility Gap here isn't a failure of clinical skill. It's that anxiety disorders are a wide enough label to catch at least seven distinct problems a brain injury can cause, and graduate training prepares clinicians to treat the mind, not the brain. We are not given the tools to ask which mechanism is actually underneath symptoms of anxiety in a client whose brain has been injured. Anxiety is also a common diagnosis after experiencing a brain injury for a plethora of legitimate reasons.
If you're reading this, you're already helping close the gap. Treating a stalled or atypical anxiety presentation as a question rather than a resistant client is the path forward. You now have seven physiological changes to screen for, a multi-domain framework for doing it, a set of red flags that tell you when to expand the differential, and a referral template built for better referrals to specialists. Those specialists and how to find them are linked throughout this article.
The next step is practical. Find out whether your region has a Brain Injury Association, and which neurology, cardiology, vestibular, endocrine, and sleep specialists nearby actually have brain injury experience, before your next client with a stalled anxiety presentation and an old head injury walks through the door. Statistically in a case load of 20 clients, at least 4 of them have a history of a brain injury. We guarentee you already have some folks in your office who could benefit from this screening, modality augmentation, and referral framework.
Disclaimer: This article is intended for licensed clinicians and is provided for educational purposes. It does not replace clinical judgment, supervision, or consultation with qualified medical or neuropsychological providers. Brain injury presentation varies significantly between individuals. If a client is experiencing a mental health crisis, direct them to the 988 Suicide & Crisis Lifeline or the nearest emergency room.
References
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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 justice-oriented care for survivors of brain injury and their families, including the clients whose anxiety turns out to have several different, equally real, sources.
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