Published peer-reviewed research shows that Cognitive FX treatment leads to meaningful symptom reduction in post-concussion symptoms for 77% of study participants. Cognitive FX is the only PCS clinic with third-party validated treatment outcomes.
READ FULL STUDY
If you completed your Lyme antibiotic course and still can't shake the fatigue, the brain fog, the pain that doesn't have a clear cause, you're not imagining it. The infection cleared, but something else didn't. Many patients spend years being told there's nothing wrong, or that their symptoms are psychological, when measurable brain dysfunction is actually driving what they feel.
This is known as post-treatment Lyme disease (PTLD), and it affects about 14% of patients even when Lyme is caught and treated early. Emerging evidence suggests that treating the persistent brain dysfunction driving these symptoms — rather than continuing to target the cleared infection — offers a promising path forward for the estimated 2 million Americans living with post-Lyme symptoms.
In this article, we cover:
Note: The Cognitive FX EPIC treatment protocol has been evaluated in an independent peer-reviewed cohort study of 64 patients with persistent post-concussion symptoms, which found meaningful symptom reduction in 77% of participants. The same treatment approach is applied to PTLD based on the shared mechanistic overlap between post-concussion syndrome and post-infectious brain dysfunction. Individual results vary. Book a free consultation to find out if you're a candidate.
Post-treatment Lyme disease occurs when patients experience persistent symptoms lasting six months or longer after completing standard antibiotic treatment for Lyme disease. The Infectious Diseases Society of America defines PTLD by three core symptoms: severe fatigue, widespread musculoskeletal pain, and cognitive difficulties — including memory problems, concentration issues, and the brain fog many patients describe.The statistics are consequential. In a prospective cohort study, 14% of ideally-treated Lyme patients developed PTLD, compared to just 4% in healthy controls. These were not late-diagnosed or inadequately treated patients — they received textbook care: early diagnosis, prompt antibiotic treatment, appropriate duration. Yet more than one in seven still developed chronic, debilitating symptoms.
The national impact is substantial. With approximately 476,000 Lyme disease cases diagnosed annually in the United States, this translates to roughly 48,000 to 95,000 new PTLD cases every year. Modeled estimates suggest around 2 million Americans may currently be living with persistent post-Lyme symptoms — a condition with no FDA-approved treatments and limited recognition in mainstream medicine.PTLD is distinct from "chronic Lyme disease"—a term the CDC explicitly discourages because it implies ongoing bacterial infection. In PTLD, antibiotics have successfully eliminated the bacteria, but symptoms persist due to the infection's lasting effects on immune function, inflammation, and brain structure.
While fatigue and pain dominate PTLD discussions, cognitive dysfunction (brain fog, memory issues, difficulty concentrating) may be the most disabling symptom and the one that receives least attention from traditional treatment approaches. Cognitive complaints are among the most common presentations in PTLD, with symptoms severe enough to significantly impact work, relationships, and quality of life.The cognitive symptoms of PTLD include memory impairment (particularly short-term memory), difficulty concentrating for extended periods, slowed information processing speed, word-finding difficulties, problems with executive function and planning, and the pervasive brain fog that patients often describe as thinking through cotton or wading through mud.
These aren't subtle changes. PTLD patients score significantly below population norms on standardized quality of life measures, with impairment comparable to multiple sclerosis and other serious chronic illnesses.
What makes these cognitive symptoms particularly frustrating is their invisibility. Physical exam findings are typically minimal. Routine laboratory tests come back normal. Patients look fine to outside observers, yet struggle to perform basic cognitive tasks that were once effortless. Many report that doctors dismiss their complaints as anxiety or depression, when in fact measurable brain dysfunction is driving their symptoms.
For years, PTLD patients were told their cognitive symptoms were 'all in their head' in the dismissive sense. Multimodal imaging research has demonstrated that PTLD symptoms are indeed in the head, in the literal and measurable sense — and increasingly in a treatable one.Multimodal neuroimaging in a cohort of 12 PTLD patients compared to 18 healthy controls documented distinctive white matter abnormalities in the frontal lobe during working memory tasks. Using functional magnetic resonance imaging (fMRI) alongside diffusion tensor imaging (DTI), the researchers found patterns that had not been previously documented in this patient group.
Three novel activation regions appeared in white matter (typically only gray matter activates during cognitive tasks). PTLD patients showed hypoactivation in expected brain regions with compensatory activation in alternative areas—suggesting the brain was working harder through different pathways to achieve the same results. Response times were significantly slower, though accuracy was maintained. Most importantly, white matter integrity correlated directly with symptom severity: higher axial diffusivity was associated with fewer symptoms, potentially representing healing or compensation mechanisms.
Earlier PET imaging using a radiotracer that binds to a marker of activated microglia and reactive astrocytes found widespread neuroinflammation across eight brain regions in 12 PTLD patients compared to 19 healthy controls. This provided objective evidence that PTLD involves persistent neurological inflammation long after the bacterial infection resolves.These imaging studies validate patient experiences. The cognitive difficulties are neurological, not psychological. The brain fog reflects measurable dysfunction in specific brain regions. And because the dysfunction is localized and measurable, it may be targetable with the right therapeutic approach.
Current medical guidelines from the CDC and IDSA provide no specific treatment recommendations beyond symptomatic management. This gap leaves both patients and physicians frustrated, often leading to extended antibiotic regimens despite the evidence that this approach does not work.
The antibiotic controversy has been contested for decades. Two randomized placebo-controlled trials found that 90 days of intravenous ceftriaxone followed by oral doxycycline showed no benefit over placebo for PTLD symptoms.
A subsequent European trial found no benefit from 12 weeks of doxycycline or clarithromycin-hydroxychloroquine after initial ceftriaxone treatment, with a high rate of adverse events in the antibiotic groups. Systematic reviews of the randomized controlled trials of prolonged antibiotic therapy for PTLD have found no clinically meaningful benefit for quality of life, cognition, fatigue, or depression, alongside a substantial rate of adverse events. The adverse events aren't trivial.
Extended intravenous antibiotic therapy for PTLD carries documented risks including C. difficile infection, intravenous line complications, and antibiotic-resistant infections, some serious enough to require hospitalization. These risks must be weighed against the lack of demonstrated benefit.
Antibiotics don't work for PTLD because PTLD isn't caused by persistent viable bacteria in most cases. Xenodiagnosis studies, in which uninfected ticks are allowed to feed on PTLD patients, have not recovered live spirochetes, suggesting the persistent symptoms are not driven by ongoing viable infection.
The problem is what the infection left behind: bacterial cell wall fragments known as peptidoglycan can persist in the liver and joints long after Borrelia burgdorferi has been cleared by antibiotics. These structurally unique fragments, modified by tick-derived sugars, cannot be processed normally by human tissues. They act as persistent inflammatory triggers, driving ongoing immune activation without live bacteria present.
The problem isn't active infection—it's what the infection left behind
Understanding the mechanism explains why extended antibiotics provide no benefit and what actually drives persistent symptoms
Additional mechanisms include immune dysregulation with elevated pro-inflammatory chemokines such as CCL19, potential autoimmune responses in which the immune system attacks host tissues through molecular mimicry, and central sensitization in which the nervous system remains hyperactivated long after the initial insult. These mechanisms don't respond to antibiotics because they aren't caused by active infection.
The heterogeneity of PTLD also complicates treatment. Clinical characterization studies have documented meaningful variation in symptom presentation across patients, suggesting different underlying mechanisms may require different treatment approaches. A one-size-fits-all approach, whether antibiotics or any other single intervention, is unlikely to succeed for such a diverse condition.
If PTLD involves measurable brain dysfunction, as imaging research has shown, then targeted neurorehabilitation addressing those specific brain changes is a logical treatment approach. This represents a different framework: treating the neurological and cognitive sequelae that persist after the infection resolves, rather than continuing to target an infection that antibiotics have cleared.
Personalized, imaging-guided neurorehabilitation rests on three principles. First, brain imaging can identify specific dysfunction patterns in individual patients. The imaging studies described above show that PTLD involves localized, measurable abnormalities in brain structure and function, particularly in the frontal lobe white matter and across regions of neuroinflammation.These aren't diffuse, untargetable changes; they're specific regional dysfunctions that can be mapped and addressed.
Second, neuroplasticity—the brain's capacity to reorganize and form new neural connections—supports rehabilitation potential throughout life, even in chronic conditions. Research on traumatic brain injury, stroke, and other neurological conditions consistently demonstrates that targeted cognitive training induces measurable neuroplastic changes. Brain activation patterns can be modified, functional connectivity can be enhanced, and cognitive performance can improve through systematic, intensive training protocols.
Third, precision medicine approaches outperform standardized treatments for complex neurological conditions. Research on fMRI-guided transcranial magnetic stimulation for depression shows that personalized targeting based on individual brain imaging produces superior outcomes compared to standardized anatomical targeting. The principle applies broadly: when dealing with heterogeneous conditions affecting brain function differently across individuals, personalized treatment plans based on each patient's specific dysfunction patterns will outperform generic protocols.
Breakthrough Johns Hopkins research using fMRI and DTI demonstrates measurable, localized brain dysfunction in post-treatment Lyme disease patients
Cognitive FX applies fMRI-guided personalized neurorehabilitation to persistent post-concussion syndrome. Based on the substantial overlap in symptoms and brain dysfunction patterns between post-concussion syndrome and post-treatment Lyme disease, the same approach is applied to PTLD patients whose primary disability is cognitive dysfunction.
The treatment process begins with brain mapping. Patients undergo functional NeuroCognitive Imaging (fNCI), a specialized fMRI protocol that measures brain activity across multiple cognitive tasks. This is a dynamic functional assessment showing how different brain regions activate during memory tasks, attention challenges, and executive function demands. The imaging reveals regions of neurovascular uncoupling — where blood flow and neural activity fall out of sync, indicating dysfunction in the coupling mechanisms necessary for normal brain function.
The fNCI results are compared against a normative database from healthy controls and analyzed using sophisticated statistical algorithms to identify each patient's unique pattern of dysfunction. Some patients may show frontal lobe white matter abnormalities similar to the Johns Hopkins PTLD cohort. Others may demonstrate different regional dysfunctions. The key is that treatment is customized based on the individual's specific brain imaging findings, not applied generically.
The Enhanced Performance in Cognition (EPIC) treatment protocol targets identified dysfunctions through intensive, multidisciplinary therapy. The approach follows a Prepare-Activate-Rest cycle designed to promote neurovascular coupling restoration. The Prepare phase uses aerobic exercise and neuromuscular training to enhance cerebral blood flow and prime the brain for cognitive work. The Activate phase employs targeted cognitive therapies, neuromuscular exercises, sensory-motor integration, and occupational therapy—all calibrated to challenge the specific brain regions and functions identified as dysfunctional on imaging. The Rest phase provides adequate recovery time, essential for neuroplastic consolidation.
Treatment is intensive and accelerated—typically one week of full-day therapy—rather than extended over months. This format leverages principles of intensive neurorehabilitation that show superior outcomes to traditional once-weekly therapy models for many neurological conditions.
Post-treatment imaging provides objective measurement of improvements, showing changes in brain activation patterns and neurovascular coupling. This isn't relying solely on subjective symptom reporting; it's documenting measurable changes in brain function.
Peer-reviewed research on the Cognitive FX approach documents meaningful outcomes across multiple measures. An independent observational study by Dutch researchers followed 64 patients undergoing the Cognitive FX EPIC treatment protocol, measuring symptom burden and functioning before treatment, immediately after, and at six-month follow-up. Meaningful reduction in symptom burden was observed in 77% of participants, with improvements in anxiety, depression, fatigue, sleep, vestibular-ocular functioning, neurocognitive functioning, and participation. The study authors note that the observational, non-randomized design does not provide direct evidence of treatment effectiveness. Individual results vary.
This is rare third-party validation in the neurorehabilitation field, most of which relies on internal outcome data. It also matters that these outcomes are from patients with persistent post-concussion syndrome— a condition that shares mechanistic overlap with PTLD but is not the same. Direct outcome data specifically for PTLD patients treated with this approach are limited.
The rationale for applying the protocol to PTLD is based on the substantial imaging and clinical overlap: both conditions involve cognitive dysfunction, both show measurable brain dysfunction on advanced imaging, both fail to respond to traditional medical treatments, and both appear to involve neurovascular coupling dysfunction. The imaging researchers themselves noted that their findings may apply to post-acute COVID and other post-infectious syndromes with similar symptom profiles.
The emergence of long COVID has brought new attention and research funding to post-infectious syndromes, and PTLD patients stand to benefit.The symptom overlap is substantial: debilitating fatigue that doesn't improve with rest, cognitive dysfunction described as brain fog, exercise intolerance, autonomic dysfunction, and pain that persists long after the acute infection resolves.
Neuroimaging studies in long COVID patients show findings strikingly similar to PTLD. Multiple studies using fMRI have identified lower functional connectivity in multiple brain regions, altered brain activation patterns during cognitive tasks with shift to compensatory brain regions, hypo-connectivity that correlates inversely with cognitive function and directly with fatigue, and measurable abnormalities in frontal lobe and brainstem regions linked to fatigue, cognitive problems, and other symptoms.
Long COVID brain imaging research has documented similar patterns to PTLD, and clinical recommendations increasingly point to neurorehabilitation as a treatment option for post-infectious cognitive symptoms. This reflects growing recognition that post-infectious brain dysfunction requires brain-focused treatment approaches.
The mechanistic parallels extend beyond symptoms to underlying pathophysiology. Northwestern's 2025 peptidoglycan persistence findings in PTLD mirror proposed mechanisms for long COVID, where viral debris and immune dysregulation persist despite viral clearance. Both conditions involve neuroinflammation, both show measurable brain changes on imaging, and both demonstrate limited response to traditional medical treatments.
This convergence suggests that effective treatments for PTLD cognitive dysfunction may also benefit long COVID patients—and vice versa. The field is moving toward recognizing post-infectious brain dysfunction as a distinct therapeutic target, regardless of the triggering pathogen.
Not every PTLD patient needs advanced neurorehabilitation—but certain presentations strongly suggest brain-focused treatment would be beneficial. Consider fMRI-guided neurorehabilitation if you experience:
Persistent cognitive symptoms (memory problems, brain fog, concentration difficulties) that significantly impact daily function despite completing appropriate Lyme disease treatment. Failed response to standard PTLD management approaches including symptomatic treatments and extended antibiotic courses. Cognitive dysfunction that's worse than your pain or fatigue, or cognitive symptoms that prevent return to work or school. Symptoms lasting six months or longer with no significant improvement. Normal or near-normal results on routine neurological exams and standard brain imaging (MRI, CT), yet persistent debilitating symptoms.
The ideal candidate is someone whose primary disabling symptom is cognitive dysfunction rather than primarily pain or fatigue, though many PTLD patients experience all three. Brain-focused rehabilitation specifically targets the neurological aspects of PTLD—the measurable brain dysfunction shown on functional imaging. It's complementary to other supportive treatments (physical therapy for pain, sleep optimization, nutritional support) rather than mutually exclusive.
Timing matters. While neuroplasticity allows for improvement even years after symptom onset, earlier intervention may prevent maladaptive compensation patterns from becoming entrenched. The Johns Hopkins study found that duration of illness correlated with certain brain changes, suggesting the brain continues adapting (for better or worse) over time.
"Is this just another unproven treatment promising false hope?" The distinction lies in independently reported outcomes and objective measurement. Unlike PTLD approaches promoted based on testimonials alone, the Cognitive FX method has been analyzed by external researchers and published in a peer-reviewed journal. Outcomes are measured through repeat brain imaging, not just symptom surveys. The approach targets the measurable brain dysfunction documented in peer-reviewed imaging studies, rather than the persistent-infection theory that antibiotic trials have not supported.
"How is this different from regular cognitive rehabilitation?" Standard cognitive rehabilitation uses generic protocols applied similarly to all patients. fMRI-guided treatment customizes therapy based on each patient's unique brain dysfunction pattern revealed through imaging. Regular rehab may last months with once or twice weekly sessions. Intensive neurorehabilitation uses accelerated daily protocols shown to produce faster, more robust neuroplastic changes. Traditional approaches often lack objective measures of brain function change. This approach uses pre- and post-treatment imaging to document improvements in brain activation patterns and neurovascular coupling.
"What about the cost and time commitment?" Treatment typically requires one week of intensive daily therapy, making it more time-efficient than months of traditional rehabilitation. While costs are significant, the approach may be more cost-effective than years of ineffective symptomatic treatments, repeated doctor visits, and lost work productivity. Some patients' insurance covers functional neuroimaging and rehabilitation services, though coverage varies. The intensive format requires travel to the clinic, but one-week commitment may be more feasible than ongoing local weekly appointments spanning months.
"Will this cure my PTLD?" fMRI-guided neurorehabilitation doesn't cure PTLD in the sense of eliminating all underlying pathophysiology. PTLD is likely multifactorial, involving persistent inflammation, immune dysregulation, and potentially ongoing low-grade tissue processes. What imaging-guided treatment addresses specifically is the neurological and cognitive dysfunction component: the measurable brain changes driving cognitive symptoms. For patients whose primary disability is cognitive dysfunction, this treatment component may produce meaningful functional improvement. For patients with predominantly pain or fatigue without significant cognitive involvement, brain-focused rehabilitation may be less relevant.
The realistic goal is meaningful functional improvement: return to work, restoration of cognitive abilities, and reduction in debilitating symptoms — not necessarily complete elimination of all symptoms. The available data on the Cognitive FX treatment approach in patients with persistent post-concussion symptoms show meaningful symptom reduction in the majority of treated patients. Direct outcome data specifically for PTLD are not yet available; the approach is applied to PTLD based on the mechanistic overlap between post-concussion syndrome and post-infectious brain dysfunction. Individual results vary.
PTLD research is experiencing unprecedented momentum, driven partly by long COVID parallels bringing research attention and funding. The NIH announced a $16 million five-year initiative in 2023 funding five major PTLD research projects focused on immunologic biomarkers, peptidoglycan persistence mechanisms, autoantibody development, and predictive models for who develops PTLD.
Emerging treatment approaches under investigation include drugs targeting specific inflammatory pathways (FGFR inhibitors showed promise in 2024 Tulane study), monoclonal antibodies to clear persistent peptidoglycan debris, immunomodulatory approaches addressing dysregulated immune responses, and stem cell therapies with anti-inflammatory and regenerative properties. These represent exciting possibilities, but all remain investigational without clinical availability yet.
The paradigm shift already underway involves recognizing PTLD as primarily a post-infectious neuroinflammatory and neurodegenerative condition rather than persistent infection. This reframes treatment from eradicating bacteria (antibiotics) to addressing lasting neurological impacts (neurorehabilitation, anti-inflammatory therapies, cognitive treatments). It shifts focus from one-size-fits-all protocols to personalized medicine based on individual pathophysiology and brain dysfunction patterns.
Brain imaging is becoming integral to this future. As functional neuroimaging technology becomes more accessible and imaging biomarkers become validated, expect wider adoption of imaging-guided treatment selection and monitoring. Imagine a future where PTLD patients routinely receive baseline brain imaging to characterize their specific dysfunction, treatment selection based on imaging findings rather than trial-and-error, and objective outcome tracking through serial imaging to adjust protocols.
Two new treatment trials for PTLD in 2022—a milestone for a condition long considered untreatable. These trials focus on understanding biological drivers and developing targeted interventions. As our understanding of PTLD mechanisms improves, treatments will become increasingly sophisticated and effective.
For PTLD patients struggling with persistent cognitive symptoms, several concrete steps can help:
Document your cognitive difficulties systematically. Track specific deficits (memory, attention, processing speed), their severity, and functional impact. Bring documentation to medical appointments to ensure cognitive symptoms receive appropriate attention alongside pain and fatigue.
Seek evaluation at specialized centers familiar with post-infectious neurological dysfunction. Johns Hopkins Lyme Disease Research Center offers clinical evaluation, though availability may be limited. Neurorehabilitation centers with functional neuroimaging capabilities can assess whether imaging-guided treatment is appropriate. For patients considering Cognitive FX specifically, consultation can determine if your presentation fits their treatment model.
Consider clinical trial participation. Johns Hopkins and other institutions conduct PTLD treatment studies. Participation provides access to cutting-edge interventions while contributing to research advancing the field. Visit ClinicalTrials.gov and search "post-treatment Lyme disease" for current opportunities.
Optimize foundational health factors. While not addressing underlying PTLD mechanisms, good sleep hygiene, appropriate nutrition, stress management, and gentle graduated exercise support overall brain health and may enhance response to targeted treatments.
Connect with support communities. Organizations like Global Lyme Alliance, Bay Area Lyme Foundation, and Johns Hopkins Lyme Disease Research Center offer patient resources, research updates, and community connections. Living with chronic symptoms is isolating; community support matters.
Post-treatment Lyme disease leaves hundreds of thousands of patients in a difficult position: cleared of infection but far from well, validated by recent research but not served by current treatments. The recognition that PTLD involves measurable, localized brain dysfunction explains why cognitive symptoms persist and points toward treatment approaches that address what the infection left behind.
The clinical question shifts from 'why won't this infection go away' to 'how do we restore brain function after the infection's impact.' For patients whose primary disability is cognitive dysfunction — the brain fog, memory problems, and concentration difficulties that prevent work and normal life — imaging-guided neurorehabilitation offers a treatment approach grounded in objective brain measurement, supported by peer-reviewed research, and offering evidence-based expectations of meaningful improvement for many. Individual results vary.
Objective brain imaging validates your experience. No more being dismissed or told it's psychological. We show you exactly what's wrong with your brain function and track measurable improvements.
One intensive week, not months of ineffective treatments. Our EPIC protocol delivers concentrated, daily therapy proven more effective than traditional once-weekly approaches. You invest one week, not endless months.
Treatment backed by published research. Unlike most neurorehabilitation clinics relying solely on testimonials, our approach has peer-reviewed published outcomes and independent academic validation.
You may benefit from our approach if:
✓ Cognitive dysfunction (brain fog, memory problems, concentration difficulties) is significantly impacting your daily life
✓ You completed appropriate Lyme treatment but symptoms persist 6+ months
✓ Extended antibiotics and other treatments have failed
✓ Cognitive symptoms prevent you from working, studying, or living normally
✓ You want objective evidence of what's wrong—and proof that treatment is working
The fMRI-guided neurorehabilitation approach may be a fit for you if:
A free consultation with the Cognitive FX team can determine whether your specific presentation fits the treatment model, walk through the fNCI imaging process, explain what to expect from the one-week intensive EPIC protocol, and set realistic expectations for your case.
If persistent post-Lyme cognitive symptoms are keeping you from work, relationships, or daily life, fMRI-guided neurorehabilitation may help. Take our brief assessment to see if you're a candidate, schedule a free consultation, or call us at 385-446-4161 to speak with our team. Individual results vary.
Alina Fong, Ph.D. is a clinical neuropsychologist and the Clinical Director and Co-Founder of Cognitive FX. She earned her Ph.D. in Clinical Neuropsychology with an emphasis in Neuroimaging from Brigham Young University, where she received the American Psychological Association Division 40 Graduate Student Research Award for her neuroimaging research. Dr. Fong has over 17 years of clinical experience treating traumatic brain injury, beginning with her work at the VA Salt Lake City Healthcare System and Utah Valley Regional Medical Center, where she directed the neurotrauma rehabilitation and sports concussion clinics. She developed the EPIC Treatment protocol and has personally overseen treatment for nearly 8,000 brain injury patients, including professional athletes from the NFL, NHL, and Olympics. She serves as Vice President of the Brain Injury Alliance of Utah, sits on the board of the United States Brain Injury Alliance, and advises PINK Concussions. Dr. Fong has authored peer-reviewed research on functional MRI and concussion treatment and has presented at over 60 medical conferences, including the Federal Interagency Conference on TBI and the American Medical Society for Sports Medicine.
Tinnitus—a buzzing, hissing, or ringing in the ears—is a common and frustrating symptom after a mild traumatic brain injury (mTBI). While it often resolves within days, for some patients it lingers...
Headaches are the most common symptom after a traumatic brain injury. The vast majority of people with TBI headaches experience symptom improvement within weeks; however, for some patients, headaches...
“I feel like there’s a tight band around my head.” “My head feels like it’s blowing up like a balloon.” “I have a constant pressure headache.” “I feel like my head is being pulled apart between the...
Most patients with COVID-19 recover within a few days or weeks after a brief acute infection. However,about 10%experience long-term symptoms such as brain fog, fatigue, headaches, shortness of...
Very few clinics offer specialized treatment forpost concussion syndrome (PCS). Cognitive FX specializes exclusively in treating the root causes of lingering post-concussion symptoms (as well as...
For Immediate Release – April 3, 2017, Provo, UT
Published peer-reviewed research shows that Cognitive FX treatment leads to meaningful symptom reduction in post-concussion symptoms for 77% of study participants. Cognitive FX is the only PCS clinic with third-party validated treatment outcomes.
READ FULL STUDY
