“If you want others to be happy, practice compassion. If you want to be happy, practice compassion..”
– 14th Dalai Lama

Traumatic Brain Injury (TBI)

Traumatic brain injury (TBI) is a significant health concern affecting millions of individuals worldwide, with 5.3 million individuals living with TBI-related disabilities in the United States. TBI, described as a “silent epidemic,” can lead to a debilitating condition called Chronic Traumatic Encephalopathy (CTE), a neurodegenerative disease thought to be associated with a history of repetitive head impacts, such as those sustained through contact sports or military combat. Because CTE develops slowly with symptoms often not appearing until years after the precipitating head traumas, it is often unrecognized and undiagnosed.


see also:


Neurobiology of Pain

Central Sensitization


Gabapentin (Neurontin) & Pregabalin (Lyrica)

Honokiol & Magnolol (Magnolia species)

Palmitoylethanolamide (PEA)

Cannabidiol (CBD)

NRF2 Activators


Definitions and Terms Related to Pain

Key to Links:

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Traumatic Brain Injury (TBI)

In recent years attention has increasingly focused on the neurological consequences of sports-related traumatic brain injury, particularly concussion. Concussion occurs frequent  in contact sports with up to 3.8 million sports-related concussions occuring annually in the United States. One study found symptoms of post-concussion syndrome in 19-28 percent of high school athletes who had no documented history of previous concussions. While most sport-related head injury are minor and the majority recover within a few days or weeks, a small number of individuals develop long-lasting or progressive symptoms associated with a condition called Chronic Traumatic Encephalopathy (CTE).


Chronic Traumatic Encephalopathy (CTE)

Chronic traumatic encephalopathy (CTE) is a progressive degenerative disease caused by repetitive injuries to the brain from trauma, including concussions, occurring over a period of time. Repeated blows to the head may set off a slow series of events that may lead to brain problems. Since not everyone with a history of brain trauma gets CTE, other things like genetics may play a role. But head impacts are the only proven cause and biological changes can be seen even with a single traumatic brain injury. Doctors first identified CTE in the 1920s calling it “dementia pugilistica” in aging boxers, but the condition has been found in athletes who competed  only through high school or college. 


Risks  for CTE

The greatest risk  for CTE is in cases of repetitive concussion or mild traumatic brain injury in which at least 17% of individuals develop the condition. While the precise incidence of CTE after repetitive head injury is unknown,  it is likely much higher. It is unknown what severity or recurrence of head injury is necessary to trigger CTE. Even brain trauma without concussion can lead to CTE.  Although the long-term neurological and neuropathological findings associated with repetitive brain injury are best known in boxing and professional football players, other sports are associated with post-concussive syndromes include hockey, rugby, karate, horse riding, and parachuting. People who have played contact sports like football and ice hockey are at highest risk. Another groups of individuals prone to repetitive head trauma includes military veterans who also may be at risk for CTE, with many veterans returning from combat displaying symptoms of CTE.

Neurobehavioral changes associated with CTE

CTE results from cumulative damage to the brain and usually manifests symptoms years later. The symptoms of CTE are insidious. They may first manifest as deteriorations in attention, concentration, and memory, as well as disorientation and confusion, and may occasionally be accompanied by dizziness and headaches. Mood conditions may occur such as depression along with irritability, emotional instability, aggressiveness and paranoia. With progression, additional symptoms may develop including a lack of insight and poor judgment which may lead to substance abuse. In summary:

  1. Irritability
  2. Sleep disturbances
  3. Emotional instability
  4. Memory loss
  5. Confusion
  6. Impulsive or erratic behavior
  7. Bad judgment
  8. Poor impulse control
  9. Aggressiveness
  10. Depression
  11. Paranoia
  12. Substance abuse
  13. Dementia
  14. Headache


The Neurobiology of CTE


In normal physiological conditions, the blood-brain barrier (BBB) prevents entry of most drugs, chemicals, toxins and peripheral blood cells into the brain. Trauma to the brain and its associated stress induces a local inflammatory response causing disruption and dysfunction of the BBB increasing its permeability. This results in the infiltration of peripheral immune and inflammatory cells such as neutrophils, monocytes, mast cells, and T cells into the brain. These cells become “activated,” immediately releasing inflammatory proteins called cytokines and chemokines within hours post-injury. These mast cell-derived inflammatory mediators further increase blood brain barrier (BBB) permeability and activate localized brain resident immune cells such as microglia and astrocytes. When activated, microglia and astrocytes increase production of similar inflammatory cytokines. Further, all of these inflammatory mediators increase vascular permeability and increase escape and recruitment of immune and inflammatory cells at the site of injury.

Astrocytes undergo reactive changes in a setting of TBI, becoming hypertrophic with swelling and extension of processes in the first few days, followed by glial scar formation and with reactive gliosis persisting up to several months post-injury. Although scarring may be potentially protective against further injury, it can act to inhibit axonal regrowth and regeneration. Another feature of astrocyte reactivity in TBI is that of proliferation, manifested by an up-regulated expression of glial fibrillary acidic protein, close to the lesion site that appears to peak in the acute phase after TBI. As such, astrocytes, like microglia, can elicit both beneficial and detrimental effects. Moreover, as astrocytes make microglia more responsive to pro-inflammatory stimuli and neurotoxic reactive astrocytes are induced by activated microglia, such processes could work in concert after TBI.


Normal, optimal inflammatory responses and physiological levels of inflammatory mediators are beneficial and protect the body as they remove unwanted waste materials and repair damaged tissues. As such, the initial, acute inflammatory response is protective, and lipid mediators such as eicosanoids (prostaglandins and leukotrienes produced from the essential fatty acid arachidonic acid) play critical roles in the initial response, with interactions between prostaglandins, leukotrienes and pro-inflammatory cytokines amplifying inflammation.

See: Neuroinflammation

Normally, these altered and reactive immune cells diminish their activity within 10–14 days post-injury and the inflammatory response ceases. However, in some cases of TBI and other injuries, this neuroinflammation continues and becomes chronic. The resolution of neuroinflammation has previously been considered a passive process. Recent research, however, has identified mediators with the capacity to actively resolve inflammation, endogenous agents called resolvins, protectins & maresins, that are involved with the process of shutting down neuroinflammation. It is hoped that in the future the means of harnessing these agents tfor therapeutic purposes will become available. What is believed at this time, however, is that production of these agents may be promoted by low dose aspirin and omega-3 essential fatty acids while NSAIDs may inhibit their production.


Traumatic Brain Injury and the Gut Microbiome

The gut–brain axis is a communication network linking together the central nervous system and the gut (enteric) nervous system via bidirectional pathways. The gut microbiota has a central role and is significantly altered following injury, leading to a pro-inflammatory state within the central nervous system (CNS). Therapeutic strategies such as probiotics may offer neuroprotective benefits by targeting the dysregulated gut-microbiota-brain axis and restoring a healthier gut microbiota.

See: Leaky Gut and the Gut Microbiomecoming soon; articles below


How Brain Trauma Leads to CTE

The pathology of CTE is characterized by the buildup of abnormal proteins known as “tau” and amyloid β-peptide. Many of the symptoms associated with CTE and abnormal levels of tau and amyloid β-peptide are also found in neurodegenerative disorders and aging, which include cognitive factors such as impaired concentration, memory and language. Brain trauma resulting in neuroinflammatory processes such as free radical generation from oxidative stress, microglia upregulation, mitochondrial dysfunction, and calcium imbalance, result in hyperphosphorylated tau.The exact mechanism by which tau hyperphosphorylation leads to CTE from brain trauma remains yet to be definitively explained but it is believed that repetitive brain trauma leads to CTE through tau oligomerization following axonal deformation and microtubular destabilization. Over time, tau develops into filamentous neurofibrillary tangles (NFTs) which interfere with white matter tracts in the brain and cause signaling and communication abnormalities through denervation injury leading to neuronal loss and  symptomatic manifestations of brain dysfunction.


As CTE is associated with the excessive build-up of β-amyloid (Aβ) and hyperphosphorylated forms of the microtubule- associated protein, tau, it has been proposed that this is the underlying pathogenic basis for this disease. However, manifestation of CTE can be highly multifactorial with clear gene–environment interactions, and precipitating factors are highly variable. Genome-wide analysis has highlighted several risk genes, many of which alter clearance of misfolded proteins and modulate inflammation, while environment also influences expression via systemic inflammation (e.g., obesity), which may make targeting risk factors and the immune system important treatment strategies.


The Endocannabinoid System

It has been suggested that the endocannabinoid system (ECS) may be hypofunctional, and/or dysfunctional in neurodegenerative diseases such as CTE and Alzheimer’s disease. While CBD does not act directly at the CB1 receptor, it may act indirectly by enhancing ECS tone. CBD exerts actions on the serotonin receptors and the serotonergic system, including the 5-HT1A receptor. The serotonergic system is implicated in neurodegeneration across various regions of the brain that have been associated with cognitive decline.


Peroxisome proliferator-activated receptor gamma (PPARγ) is a receptor found in the nucleus of cells that is involved in the regulation of inflammation. CBD can bind to and activate PPARγ, and PPARγ activation is  anti-inflammatory and it improves mitochondrial function and resistance to oxidative stress. Palmitoylethanolamide (PEA) is an endogenous fatty acid amide displaying  antiinflammatory, neuroprotective and analgesic actions and is thought to be “cannabomimetic,” in that it has actions on the ECS. Moreover, research suggests that PEA has a neuroprotective effect by reducing inflammation and tissue injury associated with spinal cord trauma via PPAR signaling.


Neuronal loss and gliosis  are pronounced in the hippocampus, the amygdala, the mammillary bodies, medial thalamus, substantia nigra, locus ceruleus and nucleus accumbens, all areas of the brain associated with chronic pain and addiction. If the disease is advanced, neuronal loss is also found in the insular cortex and to a lesser degree in the frontal and temporal cortex.


Diagnosing CTE

Presently there are no available blood tests or biomarkers for the diagnosis of CTE. In the past, the diagnosis of CTE required post-mortem brain evaluation. Recent advances in neuroimaging offer the promise of detecting subtle changes in axonal integrity in acute TBI and CTE. Standard T1- or T2-weighted structural MR imagining is helpful for quantitating pathology in acute TBI, but diffusion tensor MRI (DTI) is a more sensitive method to assess axonal integrity. In chronic moderate to severe TBI, abnormalities on DTI have been reported in the absence of observable lesions on standard structural MRI. More severe white matter abnormalities on DTI have been associated with greater cognitive deficits by neuropsychological testing.


The neurofibrillary degeneration of CTE is distinguished from other tauopathies by preferential involvement of the superficial cortical layers, irregular, patchy distribution in the frontal and temporal cortices, propensity for sulcal depths, prominent perivascular, periventricular and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes.


Headache in TBI

The mechanism of headache in TBI is unknown. The immediate mechanism may be the tearing of trigeminal nerve fibers that innervate the meninges, the outer tissues layers that surround the brain and spinal cord. Small fiber (calcitonin gene related peptide (CGRP) positive) meningeal nerves penetrate and may become attached to the calvarial bones of the skull. With traumatic impact producing movement of the meningeal surface, these nerves becomes stretched or torn.


A new class of medications that target the calcitonin gene-related peptide (CGRP) and recently FDA approved for treatment of migraine headaches may offer benefit for TBI-related headaches. 

Treatment of CTE

Currently there is no specific treatment known for CTE. The focus of current treatments for CTE is on preventing head injury in the first place and reducing secondary brain trauma. Other prevention strategies include getting plenty of rest and limiting physical activity. It also recommends surrounding yourself with a calm and supportive environment.


Since chronic neuroinflammation contributes to the development and presumed maintenance of CTE, there are at least theoretical approaches to reducing chronic neuroinflammation. The suggestions below have reasonable evidence for possible effectiveness and excellent evidence for safety.


Palmitoylethanolamide (PEA)

Palmitoylethanolamide (PEA) is a safe and effective agent for reducing nerve pain and has been shown to have anti-inflammatory actions allowing for the reduction of peripheral and central sensitization as mediated via both neuronal and nonneuronal cells, including microglia and peripheral and central mast cells. PEA has multiple mechanisms of action and neuroprotective effects including a role in maintaining cellular homeostasis in the face of neuroinflammation. PEA downmodulates mast cell activation and has neuroprotective effects against amyloid β-peptide-induced learning and memory impairment in mice. A commonly recommended dose for managing nerve pain with PEA is 600 mg twice a day.


Additionally, PEA has been studied in combination with luteolin, a naturally occuring flavinoid found in fruit peels. Luteolin has been shown to have neuroprotective properties, likely related to its NRF2 activator effects. An ultramicronized formulation of PEA and luteolin, co-ultraPEALut, has evidence to support benefit in TBI. A commercial product, Merica, is now available that contains PEA and luteolin.


See: Palmitoylethanolamide (PEA) for more information.

Cannabinoids: Cannabidiol (CBD) & THC

Pre-clinical studies have assessed the therapeutic potential of cannabinoids found in marijuana (cannabis) and manipulations of the endocannabinoid system to reduce TBI pathology. Specifically, manipulations of endocannabinoid degradative enzymes, CB1 and CB2 receptors have shown promise in modulating cellular and molecular hallmarks of TBI pathology such as cell death, excitotoxicity, neuroinflammation, cerebrovascular breakdown, and cell structure and remodeling. TBI-induced behavioral deficits, such as learning and memory, neurological motor impairments, post-traumatic convulsions or seizures, and anxiety also respond to manipulations of the endocannabinoid system.


Cannabidiol (CBD)

Cannabinoids have been found to have beneficial effects on the neurodegeneration, demyelination, and autoimmune processes occurring in the pathology of multiple sclerosis, a condition with overlapping mechanisms to CTE. In mouse studies CBD (5mg/kg) diminished inflammation, demyelination, axonal damage and inflammatory cytokine expression and reduces neurobehavioral deficits and histological damage in the mouse model of multiple sclerosis.



Citicoline is an organic compound manufactured by the body and present in every cell of the human body. It is  identified as cytidine 5’-diphosphocholine, cytidine diphosphate choline, or CDP-choline. CDP-choline is an essential precursor for the synthesis of cell membranes and the neurotransmitter acetylcholine in the central nervous system.


Citicoline is approved for use in TBI in 59 countries. Numerous studies have been conducted on the effects of citicoline in patients with cognitive impairments resulting from head injury, stroke, and other causes. Evidence suggests that citicoline supports cognitive health and neurological recovery. Specifically, citicoline has been used as a supportive therapy after traumatic brain injury (TBI) for more than 3 decades. A 2017 study concluded that while citicoline does not significantly affect global outcomes after acute TBI it may offer benefit in improving the neurocognitive state of chronic TBI patients. A second 2017 study concluded from 12 clinical trials that citicoline significantly improves functional outcomes after TBI.

See: Citicoline


NRF2 Activators

The neuroinflammatory process has been shown to be related to oxidative stress and increased production of free radicals including superoxide. It has been suggested that reduction of this neuro-inflammation may be achieved by enhancing mitochondrial activity with use of NRF2 activators such as resveratrol and curcumin to stimulate sirtuins and facilitate production of natural antioxidants including superoxide dismutase.

For more information, please see Mitochondrial Dysfunction, Antioxidants and NRF2 Activators


Very limited research has recently shown NAD+ intravenous therapy as a promising treatment for several different neurological conditions, including CTE. Studies have shown increasing NAD+ levels can promote neurogenesis, or the growth of new brain cells, even after trauma.

See: NAD Therapy – Springfield Wellness Center – Springfield LA


Glial Cell Inhibitors

Medications or supplements that inhibit glial activation might theoretically reduce the evolution of CTE. Various inhibitors of glial activation that are being evaluated for clinical use in the managment of chronic pain include minocycline, a tetracycline-class antibiotic, low dose naltrexone, palmitoylethanolamide (PEA) and Acetyl-L-carnitine. There is some evidence as well that gabapentin may inhibit glial cell activation as another mechanism of action responsible for its effectiveness in treating nerve pain. Furthermore, there may be a role for antioxidants and NRF2 activators as well in the management of chronic nerve pain related to glial cell activation.


Anti-Inflammatory Diet

Given the role of chronic inflammation in CTE, it is not a large step to consider the possibility that systemic inflammation as influenced by diet may play a contributory role in the process. Certainly no studies are likely available that explore this question but clearly a healthy diet cannot hurt. The same is to be said for exercise of course.

See: Anti-Inflammatory Diet


Treating the Neuropathic Process

Due to the potential role of stress, anxiety and sleep deprivation in the evolution of CTE, behavioral approaches are also emphasized. Foremost along these lines are mindful exercises including meditation, deep relaxation techniques, yoga, tai chi, music therapy and hypnosis. Cognitive Behavior Training (CBT).

For more information, see: Cognitive Behavior Training (CBT)




  1. NAD Therapy – San Diego CA
  2. NAD Therapy – Springfield Wellness Center – Springfield LA



Traumatic  Brain Injury – Understanding Chronic Traumatic Encephalopathy

  1. White matter integrity and cognition in chronic traumatic brain injury: a diffusion tensor imaging study. – PubMed – NCBI – 2007
  2. Chronic Traumatic Encephalopathy in Athletes – Progressive Tauopathy following Repetitive Head Injury – 2010
  3. Chronic Traumatic Encephalopathy in Professional American Football Players – Where Are We Now? – 2018
  4. The Biological Basis of Chronic Traumatic Encephalopathy following Blast Injury – A Literature Review – 2017
  5. Current Understanding of Chronic Traumatic Encephalopathy – 2014
  6. Role of Tau Acetylation in Alzheimer’s Disease and Chronic Traumatic Encephalopathy – The Way Forward for Successful Treatment – 2017
  7. Does neuroinflammation drive the relationship between tau hyperphosphorylation and dementia development following traumatic brain injury? – PubMed – NCBI
  8. Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer’s Disease Pathogenesis – 2017
  9. The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease – 2018
  10. Does neuroinflammation drive the relationship between tau hyperphosphorylation and dementia development following traumatic brain injury? – PubMed – NCBI
  11. Neurological diseases and pain – 2012
  12. From blast to bench – a translational mini-review of post-traumatic headache – 2017


Traumatic Brain Injury – Gut, Brain and Microbiome Axis

  1. The Brain-Gut-Microbiome Axis – 2018
  2. Gut-Brain Psychology – Rethinking Psychology From the Microbiota–Gut–Brain Axis – 2018
  3. Microbiome—The Missing Link in the Gut-Brain Axis – Focus on Its Role in Gastrointestinal and Mental Health – 2018
  4. Gut-microbiota-brain axis and effect on neuropsychiatric disorders with suspected immune dysregulation. – 2015
  5. Microbiome, probiotics and neurodegenerative diseases: deciphering the gut brain axis. – PubMed – NCBI – 2017
  6. Gut microbiome in health and disease – linking the microbiome- gut-brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases – 2016
  7. A Review of Traumatic Brain Injury and the Gut Microbiome – Insights into Novel Mechanisms of Secondary Brain Injury and Promising Targets for Neuroprotection – 2018
  8. The bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease. – PubMed – NCBI
  9. Microbiome-microglia connections via the gut-brain axis. – PubMed – NCBI


Traumatic Brain Injury – Epigenetics

  1. TBI-induced nociceptive sensitization is regulated by histone acetylation – 2017


Traumatic Brain Injury – Pharmacogenetics

  1. The pharmacogenomics of severe traumatic brain injury


CTE Treatment

  1. Salsalate treatment following traumatic brain injury reduces inflammation and promotes a neuroprotective and neurogenic transcriptional response with concomitant functional recovery – 2017
  2. Nanoparticle-based therapeutics for brain injury – 2018


CTE – Marijuana (Cannabis) and Cannabinoids

  1. Endocannabinoids and traumatic brain injury – 2011
  2. Endocannabinoids – A Promising Impact for Traumatic Brain Injury. – 2017
  3. Natural cannabinoids improve dopamine neurotransmission and tau and amyloid pathology in a mouse model of tauopathy. – PubMed – NCBI
  4. Preventive Effects of Resveratrol on Endocannabinoid System and Synaptic Protein Modifications in Rat Cerebral Cortex Challenged by Bilateral Common Carotid Artery Occlusion and Reperfusion – 2018
  5. Cannabidiol Reduces Aβ-Induced Neuroinflammation and Promotes Hippocampal Neurogenesis through PPARγ Involvement – 2011
  6. Critical role of mast cells and peroxisome proliferator-activated receptor gamma (PPARγ) in the induction of myeloid-derived suppressor cells by marijuana cannabidiol in vivo – 2015
  7. Endocannabinoid Degradation Inhibition Improves Neurobehavioral Function, Blood–Brain Barrier Integrity, and Neuroinflammation following Mild Traumatic Brain Injury – 2015
  8. Palmitoylethanolamide Reduces Neuropsychiatric Behaviors by Restoring Cortical Electrophysiological Activity in a Mouse Model of Mild Traumatic Brain Injury – 2017
  9. Cannabidiol for neurodegenerative disorders – important new clinical applications for this phytocannabinoid? – 2013
  10. Modulation of Astrocyte Activity by Cannabidiol, a Nonpsychoactive Cannabinoid – 2017
  11. Unique treatment potential of cannabidiol for the prevention of relapse to drug use – preclinical proof of principle – 2018
  12. Cannabis Therapeutics and the Future of Neurology – 2018


CTE – Citicoline

  1. Citicoline – The Unique Benefits 2018
  2. Is aura around citicoline fading? A systemic review – 2017
  3. Citicoline for traumatic brain injury – a systematic review & meta-analysis – 2017
  4. Nanoparticle-based therapeutics for brain injury – 2018
  5. Citicoline in severe traumatic brain injury: indications for improved outcome : A retrospective matched pair analysis from 14 Austrian trauma centers. – PubMed – NCBI – 2018
  6. Effect of citicoline on functional and cognitive status among patients with traumatic brain injury: Citicoline Brain Injury Treatment Trial (COBRIT). – PubMed – NCBI – 2012

CTE – Palmitoylethanolamide (PEA)

  1. Palmitoylethanolamide Reduces Neuropsychiatric Behaviors by Restoring Cortical Electrophysiological Activity in a Mouse Model of Mild Traumatic Brain Injury – 2017
  2. Palmitoylethanolamide is a new possible pharmacological treatment for the inflammation associated with trauma. – PubMed – NCBI
  3. Molecular evidence for the involvement of PPAR-δ and PPAR-γ in anti-inflammatory and neuroprotective activities of palmitoylethanolamide after spin… – PubMed – NCBI – 2013
  4. The Nuclear Receptor Peroxisome Proliferator-Activated Receptor-α Mediates the Anti-Inflammatory Actions of Palmitoylethanolamide – 2005Palmitoylethanolamide is a new possible pharmacological treatment for the inflammation associated with trauma. – PubMed – NCBI – 2013

CTE – Palmitoylethanolamide (PEA) & Luteolin

  1. Co-Ultramicronized Palmitoylethanolamide:Luteolin Promotes Neuronal Regeneration after Spinal Cord Injury – 2016
  2. A new co-ultramicronized composite including palmitoylethanolamide and luteolin to prevent neuroinflammation in spinal cord injury – 2013
  3. Anti-Inflammatory and Neuroprotective Effects of Co-UltraPEALut in a Mouse Model of Vascular Dementia – 2017
  4. PEA and luteolin synergistically reduce mast cell-mediated toxicity and elicit neuroprotection in cell-based models of brain ischemia. – PubMed – NCBI – 2016
  5. Neuroprotective Effects of Co-UltraPEALut on Secondary Inflammatory Process and Autophagy Involved in Traumatic Brain Injury. – PubMed – NCBI – 2016

CTE –  Diet

  1. Food-Derived Natural Compounds for Pain Relief in Neuropathic Pain – 2016
  2. Cannabimimetic phytochemicals in the diet – an evolutionary link to food selection and metabolic stress adaptation? – 2016

Emphasis on Education


Accurate Clinic promotes patient education as the foundation of it’s medical care. In Dr. Ehlenberger’s integrative approach to patient care, including conventional and complementary and alternative medical (CAM) treatments, he may encourage or provide advice about the use of supplements. However, the specifics of choice of supplement, dosing and duration of treatment should be individualized through discussion with Dr. Ehlenberger. The following information and reference articles are presented to provide the reader with some of the latest research to facilitate evidence-based, informed decisions regarding the use of conventional as well as CAM treatments.


For medical-legal reasons, access to these links is limited to patients enrolled in an Accurate Clinic medical program.


Should you wish more information regarding any of the subjects listed – or not listed –  here, please contact Dr. Ehlenberger. He has literally thousands of published articles to share on hundreds of topics associated with pain management, weight loss, nutrition, addiction recovery and emergency medicine. It would take years for you to read them, as it did him.


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