Back Clinic Functional Medicine Team. Functional medicine is an evolution in the practice of medicine that better addresses the healthcare needs of the 21st century. By shifting the traditional disease-centered focus of medical practice to a more patient-centered approach, functional medicine addresses the whole person, not just an isolated set of symptoms.
Practitioners spend time with their patients, listening to their histories and looking at the interactions among genetic, environmental, and lifestyle factors that can influence long-term health and complex, chronic disease. In this way, functional medicine supports the unique expression of health and vitality for each individual.
By changing the disease-centered focus of medical practice to this patient-centered approach, our physicians are able to support the healing process by viewing health and illness as part of a cycle in which all components of the human biological system interact dynamically with the environment. This process helps to seek and identify genetic, lifestyle, and environmental factors that may shift a person’s health from illness to well-being.
After a neurological exam, physical exam, patient history, x-rays and any previous screening tests, a doctor may order one or more of the following diagnostic tests to determine the root of a possible/suspected neurological disorder or injury. These diagnostics generally involve neuroradiology, which uses small amounts of radioactive material to study organ function and structure and ordiagnostic imaging, which use magnets and electrical charges to study organ function.
Neurological Studies
Neuroradiology
MRI
MRA
MRS
fMRI
CT scans
Myelograms
PET scans
Many others
Magnetic Resonance Imaging (MRI)
Shows organs or soft tissue well
No ionizing radiation
Variations on MRI
Magnetic resonance angiography (MRA)
Evaluate blood flow through arteries
Detect intracranial aneurysms and vascular malformations
Magnetic resonance spectroscopy (MRS)
Assess chemical abnormalities in HIV, stroke, head injury, coma, Alzheimer’s disease, tumors, and multiple sclerosis
Functional magnetic resonance imaging (fMRI)
Determine the specific location of the brain where activity occurs
Computed Tomography (CT or CAT Scan)
Uses a combination of X-rays and computer technology to produce horizontal, or axial, images
Shows bones especially well
Used when assessment of the brain needed quickly such as in suspected bleeds and fractures
Myelogram
Contrast dye combined with CT or Xray
Most useful in assessing spinal cord
Stenosis
Tumors
Nerve root injury
Positron Emission Tomography (PET Scan)
Radiotracer is used to evaluate the metabolism of tissue to detect biochemical changes earlier than other study types
Used to assess
Alzheimer’s disease
Parkinson’s disease
Huntington’s disease
Epilepsy
Cerebrovascular accident
Electrodiagnostic Studies
Electromyography (EMG)
Nerve Conduction Velocity (NCV) Studies
Evoked Potential Studies
Electromyography (EMG)
Detection of signals arising from the depolarization of skeletal muscle
May be measured via:
Skin surface electrodes
Not used for diagnostic purposes, more for rehab and biofeedback
Needles placed directly within the muscle
Common for clinical/diagnostic EMG
Diagnostic Needle EMG
Recorded depolarizations may be:
Spontaneous
Insertional activity
Result of voluntary muscle contraction
Muscles should be electrically silent at rest, except at the motor end-plate
Practitioner must avoid insertion in motor end-plate
At least 10 different points in the muscle are measured for proper interpretation
Procedure
Needle is inserted into the muscle
Insertional activity recorded
Electrical silence recorded
Voluntary muscle contraction recorded
Electrical silence recorded
Maximal contraction effort recorded
Samples Collected
Muscles
Innervated by the same nerve but different nerve roots
Innervated by the same nerve root but different nerves
Different locations along the course of the nerves
Helps to distinguish the level of the lesion
Motor Unit Potential (MUP)
Amplitude
Density of the muscle fibers attached to that one motor neuron
Proximity of the MUP
Recruitment pattern can also be assessed
Delayed recruitment can indicated loss of motor units within the muscle
Early recruitment is seen in myopathy, where the MUPs tend to be of low amplitude short duration
Polyphasic MUPS
Increased amplitude and duration can be the result of reinnervation after chronic denervation
Complete Potential Blocks
Demyelination of multiple segments in a row can result in a complete block of nerve conduction and therefore no resulting MUP reading, however generally changes in MUPs are only seen with damage to the axons, not the myelin
Damage to the central nervous system above the level of the motor neuron (such as by cervical spinal cord trauma or stroke) can result in complete paralysis little abnormality on needle EMG
Denervated Muscle Fibers
Detected as abnormal electrical signals
Increased insertional activity will be read in the first couple of weeks, as it becomes more mechanically irritable
As muscle fibers become more chemically sensitive they will begin to produce spontaneous depolarization activity
Fibrillation potentials
Fibrillation Potentials
DO NOT occur in normal muscle fibers
Fibrillations cannot be seen with the naked eye but are detectable on EMG
Often caused by nerve disease, but can be produced by severe muscle diseases if there is damage to the motor axons
Positive Sharp Waves
DO NOT occur in normally functioning fibers
Spontaneous depolarization due to increased resting membrane potential
Abnormal Findings
Findings of fibrillations and positive sharp waves are the most reliable indicator of damage to motor axons to the muscle after one week up to 12 months after the damage
Often termed �acute� in reports, despite possibly being visible months after onset
Will disappear if there is complete degeneration or denervation of nerve fibers
Nerve Conduction Velocity (NCV) Studies
Motor
Measures compound muscle action potentials (CMAP)
Sensory
Measures sensory nerve action potentials (SNAP)
Nerve Conduction Studies
Velocity (Speed)
Terminal latency
Amplitude
Tables of normal, adjusted for age, height and other factors are available for practitioners to make comparison
Terminal Latency
Time between stimulus and the appearance of a response
Useful in assessing demyelinative peripheral neuropathies
Sources
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
Day, Jo Ann. �Neuroradiology | Johns Hopkins Radiology.� Johns Hopkins Medicine Health Library, 13 Oct. 2016, www.hopkinsmedicine.org/radiology/specialties/ne uroradiology/index.html.
Health: At its core, chiropractic is about allowing the body to naturally seek its natural balance, allowing all systems to work together. When it is unencumbered it can actually begin to heal itself. However, it can only attain proper function when it is at its proper structure.
When the structure becomes impaired through disease, stress, or injury, function becomes impaired. The degree of impairment often depends on a variety of factors including the nature of the root cause, the length of time it is left unchecked, and the patient�s support system.
Chiropractic is an exceptional part of a patient�s wellness team, addressing existing conditions as well as preventing many health issues. While most people relate the physical aspect of chiropractic to the practice, it is really a whole body approach to wellness. Chiropractic address body, mind, and spirit.
Health
Body
Chiropractic for physical health helps manage pain and heal injuries. Patients who receive regular chiropractic care enjoy a greater range of motion and improved mobility as well as decreased or even the elimination of pain in the body. Spinal misalignments can cause misalignments I other parts of the body which can cause a variety of symptoms from pain to impeded organ function.
When a part of the body is injured, such as the ankle, the body attempts to compensate. It may cause the pelvis to tilt or the spine to curve. The patient may experience pain in the hips, knees, and lower back.
Chiropractic addresses these issues, seeking out the root of the problem and then working to bring the body back into perfect balance. It is a viable and effective treatment for back pain, joint pain, sprains, carpal tunnel syndrome, headaches, and tendonitis. However, it can also be used to treat digestive disorders, asthma, and allergies.
Mind
Imbalances of the mind, such as depression and anxiety are not only destructive and debilitating on their own, they can also exacerbate pain and immobility in the body. These conditions often occur when there is an imbalance of some kind, usually within the brain.
When the body itself is out of alignment, it can inhibit the transmission of messages between the brain and vital nerves. Misalignment that blocks the central nervous system can cause imbalances in the brain, leading to conditions like depression.
Spinal misalignments and pain put a great deal of stress on the body which can affect the mental state. Physical stress that comes from injury or illness can bring about anxiety and panic disorders. When left unchecked, it can lead to mental health issues that can affect family, work, and social activities.
Chiropractic for mental health addresses several mental health issues by aligning the physical body and promoting whole body wellness through lifestyle changes, diet, exercise, and other therapies like massage. When the whole body is in alignment, mind, body and spirit are healthier.
Spirit
You don�t hear a lot about chiropractic for spiritual healing, but many practitioners are discovering the spiritual benefits of the treatment. Doctors have long known that a person�s thoughts contribute to their physical health. A person�s spirituality, their connection to whatever that means to them, plays a very significant part in their overall wellness both mentally and physically.
Chiropractic for spiritual healing may incorporate meditation, yoga, massage, and breathing exercises into treatment. When the physical body is out of balance, the spirit can become imbalanced as well. Bring the body into alignment, and the spirit will follow.
The nervous system is what controls the entire body; when there is interference, the energy cannot flow as it should, causing discomfort and disease mentally, physically, and spiritually. When the flow of energy is without interference, the body can begin to heal itself.
Injury Medical Clinic: Elderly & Geriatric Fitness
Biochemistry of Pain:�All pain syndromes have an inflammation profile. An inflammatory profile can vary from person to person and can also vary in one person at different times. The treatment of pain syndromes is to understand this inflammation profile. Pain syndromes are treated medically, surgically or both. The goal is to inhibit/suppress the production of inflammatory mediators. And a successful outcome is one that results in less inflammation and of course less pain.
Biochemistry Of Pain
Objectives:
Who are the key players
What are the biochemical mechanisms?
What are the consequences?
Inflammation Review:
Key Players
Why Does My Shoulder Hurt? A Review Of The Neuroanatomical & Biochemical Basis Of Shoulder Pain
ABSTRACT
If a patient asks �why does my shoulder hurt?� the conversation will quickly turn to scientific theory and sometimes unsubstantiated conjecture. Frequently, the clinician becomes aware of the limits of the scientific basis of their explanation, demonstrating the incompleteness of our understanding of the nature of shoulder pain. This review takes a systematic approach to help answer fundamental questions relating to shoulder pain, with a view to providing insights into future research and novel methods for treating shoulder pain. We shall explore the roles of (1) the peripheral receptors, (2) peripheral pain processing or �nociception�, (3) the spinal cord, (4) the brain, (5) the location of receptors in the shoulder and (6) the neural anatomy of the shoulder. We also consider how these factors might contribute to the variability in the clinical presentation, the diagnosis and the treatment of shoulder pain. In this way we aim to provide an overview of the component parts of the peripheral pain detection system and central pain processing mechanisms in shoulder pain that interact to produce clinical pain.
INTRODUCTION: A VERY BRIEF HISTORY OF PAIN SCIENCE ESSENTIAL FOR CLINICIANS
The nature of pain, in general, has been a subject of much controversy over the past century. In the 17th century Descartes� theory1 proposed that the intensity of pain was directly related to the amount of associated tissue injury and that pain was processed in one distinct pathway. Many earlier theories relied upon this so-called �dualist� Descartian philosophy, seeing pain as the consequence of the stimulation of a �specific� peripheral pain receptor in the brain. In the 20th century a scientific battle between two opposing theories ensued, namely specificity theory and pattern theory. The Descartian �specificity theory� saw pain as a specific separate modality of sensory input with its own apparatus, while �pattern theory� felt that pain resulted from the intense stimulation of non-specific receptors.2 In 1965, Wall and Melzack�s 3 gate theory of pain provided evidence for a model in which pain perception was modulated by both sensory feedback and the central nervous system. Another huge advance in pain theory at around the same time saw the discovery of the specific mode of actions of the opioids.4 Subsequently, recent advances in neuroimaging and molecular medicine have vastly expanded our overall understanding of pain.
So how does this relate to shoulder pain?�Shoulder pain is a common clinical problem, and a robust understanding of the way in which pain is processed by the body is essential to best diagnose and treat a patient�s pain. Advances in our knowledge of pain processing promise to explain the mismatch between pathology and the perception of pain, they may also help us explain why certain patients fail to respond to certain treatments.
BASIC BUILDING BLOCKS OF PAIN
Peripheral sensory receptors: the mechanoreceptor and the �nociceptor�
There are numerous types of peripheral sensory receptors present in the human musculoskeletal system. 5 They may be classified based on their func�tion (as mechanoreceptors, thermoreceptors or nociceptors) or morphology (free nerve endings or different types of encapsulated receptors).5 The dif�ferent types of receptor can then be further subclas�sified based on the presence of certain chemical markers. There are significant overlaps between dif�ferent functional classes of receptor, for example
Peripheral Pain Processing: �Nociception�
Tissue injury involves a variety of inflammatory mediators being released by damaged cells including bradykinin, histamine, 5-hydroxytryptamine, ATP, nitric oxide and certain ions (K+ and H+). The activation of the arachidonic acid pathway leads to the production of prostaglandins, thromboxanes and leuko- trienes. Cytokines, including the interleukins and tumor necrosis factor ?, and neurotrophins, such as nerve growth factor (NGF), are also released and are intimately involved in the facilitation of inflammation.15 Other substances such as excitatory amino acids (glutamate) and opioids (endothelin-1) have also been implicated in the acute inflammatory response.16 17 Some of these agents may directly activate nociceptors, while others bring about the recruitment of other cells which then release further facilitatory agents.18 This local process resulting in the increased responsiveness of nociceptive neurons to their normal input and/or the recruitment of a response to normally subthreshold inputs is termed �peripheral sensitization�.�Figure 1 summarizes some of the key mechanisms involved.
NGF and the transient receptor potential cation channel subfamily V member 1 (TRPV1) receptor have a symbiotic relationship when it comes to inflammation and nociceptor sensitization. The cytokines produced in inflamed tissue result in an increase in NGF production.19 NGF stimulates the release of histamine and serotonin (5-HT3) by mast cells, and also sensitizes nociceptors, possibly altering the properties of A? fibers such that a greater proportion become nociceptive. The TRPV1 receptor is present in a subpopulation of primary afferent fibers and is activated by capsaicin, heat and protons. The TRPV1 receptor is synthesized in the cell body of the afferent fibre, and is transported to both the peripheral and central terminals, where it contributes to the sensitivity of nociceptive afferents. Inflammation results in NGF production peripherally which then binds to the tyrosine kinase receptor type 1 receptor on the nociceptor terminals, NGF is then transported to the cell body where it leads to an up regulation of TRPV1 transcription and consequently increased nociceptor sensitivity.19 20 NGF and other inflammatory mediators also sensitize TRPV1 through a diverse array of secondary messenger pathways. Many other receptors including cholinergic receptors, ?-aminobutyric acid (GABA) receptors and somatostatin receptors are also thought to be involved in peripheral nociceptor sensitivity.
A large number of inflammatory mediators have been specifically implicated in shoulder pain and rotator cuff disease.21�25 While some chemical mediators directly activate nociceptors, most lead to changes in the sensory neuron itself rather than directly activating it. These changes may be early post- translational or delayed transcription dependent. Examples of the former are changes in the TRPV1 receptor or in voltage- gated ion channels resulting from the phosphorylation of membrane-bound proteins. Examples of the latter include the NGF-induced increase in TRV1 channel production and the calcium-induced activation of intracellular transcription factors.
Molecular Mechanisms Of Nociception
The sensation of pain alerts us to real or impending injury and triggers appropriate protective responses. Unfortunately, pain often outlives its usefulness as a warning system and instead becomes chronic and debilitating. This transition to a chronic phase involves changes within the spinal cord and brain, but there is also remarkable modulation where pain messages are initiated � at the level of the primary sensory neuron. Efforts to determine how these neurons detect pain-producing stimuli of a thermal, mechanical or chemical nature have revealed new signaling mechanisms and brought us closer to understanding the molecular events that facilitate transitions from acute to persistent pain.
The Neurochemistry Of Nociceptors
Glutamate is the predominant excitatory neurotransmitter in all nociceptors. Histochemical studies of adult DRG, however, reveal two broad classes of unmyelinated C fiber.
Chemical Transducers To Make The Pain Worse
As described above, injury heightens our pain experience by increasing the sensitivity of nociceptors to both thermal and mechanical stimuli. This phenomenon results, in part, from the production and release of chemical mediators from the primary sensory terminal and from non-neural cells (for example, fibroblasts, mast cells, neutrophils and platelets) in the environment36 (Fig. 3). Some components of the inflammatory soup (for example, protons, ATP, serotonin or lipids) can alter neuronal excitability directly by inter- acting with ion channels on the nociceptor surface, whereas others (for example, bradykinin and NGF) bind to metabotropic receptors and mediate their effects through second-messenger signaling cascades11. Considerable progress has been made in understanding the biochemistry basis of such modulatory mechanisms.
Extracellular Protons & Tissue Acidosis
Local tissue acidosis is a hallmark physiological response to injury, and the degree of associated pain or discomfort is well correlated with the magnitude of acidification37. Application of acid (pH 5) to the skin produces sustained discharges in a third or more of polymodal nociceptors that innervate the receptive field 20.
Cellular & Molecular Mechanisms Of Pain
Abstract
The nervous system detects and interprets a wide range of thermal and mechanical stimuli as well as environmental and endogenous chemical irritants. When intense, these stimuli generate acute pain, and in the setting of persistent injury, both peripheral and central nervous system components of the pain transmission pathway exhibit tremendous plasticity, enhancing pain signals and producing hypersensitivity. When plasticity facilitates protective reflexes, it can be beneficial, but when the changes persist, a chronic pain condition may result. Genetic, electrophysiological, and pharmacological studies are elucidating the molecular mechanisms that underlie detection, coding, and modulation of noxious stimuli that generate pain.
Introduction: Acute Versus Persistent Pain
Figure 5. Spinal Cord (Central) Sensitization
Glutamate/NMDA receptor-mediated sensitization.�Following intense stimulation or persistent injury, activated C and A? nociceptors release a variety of neurotransmitters including dlutamate, substance P, calcitonin-gene related peptide (CGRP), and ATP, onto output neurons in lamina I of the superficial dorsal horn (red). As a consequence, normally silent NMDA glutamate receptors located in the postsynaptic neuron can now signal, increase intracellular calcium, and activate a host of calcium dependent signaling pathways and second messengers including mitogen-activated protein kinase (MAPK), protein kinase C (PKC), protein kinase A (PKA) and Src. This cascade of events will increase the excitability of the output neuron and facilitate the transmission of pain messages to the brain.
Disinhibition.�Under normal circumstances, inhibitory interneurons (blue) continuously release GABA and/or glycine (Gly) to decrease the excitability of lamina I output neurons and modulate pain transmission (inhibitory tone). However, in the setting of injury, this inhibition can be lost, resulting in hyperalgesia. Additionally, disinhibition can enable non-nociceptive myelinated A? primary afferents to engage the pain transmission circuitry such that normally innocuous stimuli are now perceived as painful. This occurs, in part, through the disinhibition of excitatory PKC? expressing interneurons in inner lamina II.
Microglial activation.�Peripheral nerve injury promotes release of ATP and the chemokine fractalkine that will stimulate microglial cells. In particular, activation of purinergic, CX3CR1, and Toll-like receptors on microglia (purple) results in the release of brain-derived neurotrophic factor (BDNF), which through activation of TrkB receptors expressed by lamina I output neurons, promotes increased excitability and enhanced pain in response to both noxious and innocuous stimulation (that is, hyperalgesia and allodynia). Activated microglia also release a host of cytokines, such as tumor necrosis factor ? (TNF?), interleukin-1? and 6 (IL-1?, IL-6), and other factors that contribute to central sensitization.
The Chemical Milieu Of Inflammation
Peripheral sensitization more commonly results from inflammation-associated changes in the chemical environment of the nerve fiber (McMahon et al., 2008). Thus, tissue damage is often accompanied by the accumulation of endogenous factors released from activated nociceptors or non-neural cells that reside within or infiltrate into the injured area (including mast cells, basophils, platelets, macrophages, neutrophils, endothelial cells, keratinocytes, and fibroblasts). Collectively. these factors, referred to as the �inflammatory soup�, represent a wide array of signaling molecules, including neurotransmitters, peptides (substance P, CGRP, bradykinin), eicosinoids and related lipids (prostaglandins, thromboxanes, leukotrienes, endocannabinoids), neurotrophins, cytokines, and chemokines, as well as extracellular proteases and protons. Remarkably, nociceptors express one or more cell surface receptors capable of recognizing and responding to each of these pro-inflammatory or pro-algesic agents (Figure 4). Such interactions enhance excitability of the nerve fiber, thereby heightening its sensitivity to temperature or touch.
Unquestionably the most common approach to reducing inflammatory pain involves inhibiting the synthesis or accumulation of components of the inflammatory soup. This is best exemplified by non-steroidal anti-inflammatory drugs, such as aspirin or ibuprofen, which reduce inflammatory pain and hyperalgesia by inhibiting cyclooxygenases (Cox-1 and Cox-2) involved in prostaglandin synthesis. A second approach is to block the actions of inflammatory agents at the nociceptor. Here, we highlight examples that provide new insight into cellular mechanisms of peripheral sensitization, or which form the basis of new therapeutic strategies for treating inflammatory pain.
NGF is perhaps best known for its role as a neurotrophic factor required for survival and development of sensory neurons during embryogenesis, but in the adult, NGF is also produced in the setting of tissue injury and constitutes an important component of the inflammatory soup (Ritner et al., 2009). Among its many cellular targets, NGF acts directly on peptidergic C fiber nociceptors, which express the high affinity NGF receptor tyrosine kinase, TrkA, as well as the low affinity neurotrophin receptor, p75 (Chao, 2003; Snider and McMahon, 1998). NGF produces profound hypersensitivity to heat and mechanical stimuli through two temporally distinct mechanisms. At first, a NGF-TrkA interaction activates downstream signaling pathways, including phospholipase C (PLC), mitogen-activated protein kinase (MAPK), and phosphoinositide 3-kinase (PI3K). This results in functional potentiation of target proteins at the peripheral nociceptor terminal, most notably TRPV1, leading to a rapid change in cellular and behavioral heat sensitivity (Chuang et al., 2001).
Irrespective of their pro-nociceptive mechanisms, interfering with neurotrophin or cytokine signaling has become a major strategy for controlling inflammatory disease or resulting pain. The main approach involves blocking NGF or TNF-? action with a neutralizing antibody. In the case of TNF-?, this has been remarkably effective in the treatment of numerous autoimmune diseases, including rheumatoid arthritis, leading to dramatic reduction in both tissue destruction and accompanying hyperalgesia (Atzeni et al., 2005). Because the main actions of NGF on the adult nociceptor occur in the setting of inflammation, the advantage of this approach is that hyperalgesia will decrease without affecting normal pain perception. Indeed, anti-NGF antibodies are currently in clinical trials for treatment of inflammatory pain syndromes (Hefti et al., 2006).
Glutamate/NMDA Receptor-Mediated Sensitization
Acute pain is signaled by the release of glutamate from the central terminals of nociceptors, generating excitatory post-synaptic currents (EPSCs) in second order dorsal horn neurons. This occurs primarily through activation of postsynaptic AMPA and kainate subtypes of ionotropic glutamate receptors. Summation of sub-threshold EPSCs in the postsynaptic neuron will eventually result in action potential firing and transmission of the pain message to higher order neurons.
Other studies indicate that changes in the projection neuron, itself, contribute to the dis- inhibitory process. For example, peripheral nerve injury profoundly down-regulates the K+- Cl- co-transporter KCC2, which is essential for maintaining normal K+ and Cl- gradients across the plasma membrane (Coull et al., 2003). Downregulating KCC2, which is expressed in lamina I projection neurons, results in a shift in the Cl- gradient, such that activation of GABA-A receptors depolarize, rather than hyperpolarize the lamina I projection neurons. This would, in turn, enhance excitability and increase pain transmission. Indeed, pharmacological blockade or siRNA-mediated downregulation of KCC2 in the rat induces mechanical allodynia.
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Why does my shoulder hurt? A review of the neuroanatomical and biochemical basis of shoulder pain
Benjamin John Floyd Dean, Stephen Edward Gwilym, Andrew Jonathan Carr
Cellular and Molecular Mechanisms of Pain
Allan I. Basbaum1, Diana M. Bautista2, Gre?gory Scherrer1, and David Julius3
1Department of Anatomy, University of California, San Francisco 94158
2Department of Molecular and Cell Biology, University of California, Berkeley CA 94720 3Department of Physiology, University of California, San Francisco 94158
Molecular mechanisms of nociception
David Julius* & Allan I. Basbaum�
*Department of Cellular and Molecular Pharmacology, and �Departments of Anatomy and Physiology and W. M. Keck Foundation Center for Integrative Neuroscience, University of California San Francisco, San Francisco, California 94143, USA (e-mail: julius@socrates.ucsf.edu)
Concussions are traumatic brain injuries that affect brain function. Effects from these injuries are often temporary but can include headaches, problems with concentration, memory, balance and coordination. Concussions are usually caused by a blow to the head or violent shaking of the head and upper body. Some concussions cause loss of consciousness, but most do not. And it is possible to have a concussion and not realize it. Concussions are common in contact sports, such as football. However, most people gain a full recovery after a concussion.
Can also happen due to excessive shaking of the head or acceleration/deceleration
Mild injuries (mTBI/concussions) are the most common type of brain injury
Glasgow Coma Scale
Common Causes Of Concussion
Motor vehicle collisions
Falls
Sports injuries
Assault
Accidental or intentional discharge of weapons
Impact with objects
Prevention
Prevention of concussive injuries can be paramount
Encourage Patients To Wear Helmets
Competitive sports, especially boxing, hokey, football and baseball
Horseback riding
Riding bicycles, motorcycles, ATVs, etc.
High elevation activates such as rock climbing, zip lining
Skiing, snowboarding
Encourage Patients To Wear Seatbelts
Discuss the importance of wearing seatbelts at all times in vehicles with all of your patients
Also encourage use of appropriate booster or car seats for children to ensure adequate fit and function of seat belts.
Driving Safely
Patients should never drive while under the influence of drugs, including certain medications or alcohol
Never text and drive
Make Spaces Safer For Children
Install baby gates and window latches in the home
May in areas with shock-absorbing material, such as hardwood mulch or sand
Supervise children carefully, especially when they�re near water
Prevent Falls
Clearing tripping hazards such as loose rugs, uneven flooring or walkway clutter
Using nonslip mats in the bathtub and on shower floors, and installing grab bars next to the toilet, tub and shower
Ensure appropriate footwear
Installing handrails on both sides of stairways
Improving lighting throughout the home
Balance training exercises
Balance Training
Single leg balance
Bosu ball training
Core strengthening
Brain balancing exercises
Concussion Verbiage
Concussion vs. mTBI (mild traumatic brain injury)
mTBI is the term being used more commonly in medical settings, but concussion is a more largely recognized term in the community by sports coaches, etc.
The two terms describe the same basic thing, mTBI is a better term to use in your charting
Evaluating Concussion
Remember that there does not always have to be loss of consciousness for there to be a concussion
Post-Concussion Syndrome can occur without LOC as well
Symptoms of concussion may not be immediate and could take days to develop
Monitor for 48 post head injury watching for red flags
Blurred eyesight or other vision problems, such as dilated or uneven pupils
Confusion
Dizziness
Ringing in the ears
Nausea or vomiting
Slurred speech
Delayed response to questions
Memory loss
Fatigue
Trouble concentrating
Continued or persistent memory loss
Irritability and other personality changes
Sensitivity to light and noise
Sleep problems
Mood swings, stress, anxiety or depression
Disorders of taste and smell
Mental/Behavioral Changes
Verbal outbursts
Physical outbursts
Poor judgment
Impulsive behavior
Negativity
Intolerance
Apathy
Egocentricity
Rigidity and inflexibility
Risky behavior
Lack of empathy
Lack of motivation or initiative
Depression or anxiety
Symptoms In Children
Concussions can present differently in children
Excessive crying
Loss of appetite
Loss of interest in favorite toys or activities
Sleep issues
Vomiting
Irritability
Unsteadiness while standing
Amnesia
Memory loss and failure to form new memories
Retrograde Amnesia
Inability to remember things that happened before the injury
Due to failure in recall
Anterograde Amnesia
Inability to remember things that happened after the injury
Due to failure to formulate new memories
Even short memory losses can be predictive of outcome
Amnesia may be up to 4-10 times more predictive of symptoms and cognitive deficits following concussion than is LOC (less than 1 minute)
Return To Play Progression
Baseline: No Symptoms
As the baseline step of the Return to Play Progression, the athlete needs to have completed physical and cognitive rest and not be experiencing concussion symptoms for a minimum of 48 hours. Keep in mind, the younger the athlete, the more conservative the treatment.
Step 1: Light Aerobic Activity
The Goal: Only to increase an athlete�s heart rate.
The Time: 5 to 10 minutes.
The Activities: Exercise bike, walking, or light jogging.
Absolutely no weight lifting, jumping or hard running.
Step 2: Moderate activity
The Goal: Limited body and head movement.
The Time: Reduced from typical routine.
The Activities: Moderate jogging, brief running, moderate-intensity stationary biking, and moderate-intensity weightlifting
Step 3: Heavy, non-contact activity
The Goal: More intense but non-contact
The Time: Close to typical routine
The Activities: Running, high-intensity stationary biking, the player�s regular weightlifting routine, and non- contact sport-specific drills. This stage may add some cognitive component to practice in addition to the aerobic and movement components introduced in Steps 1 and 2.
Step 4: Practice & full contact
The Goal: Reintegrate in full contact practice.
Step 5: Competition
The Goal: Return to competition.
Microglial Priming
After head trauma microglial cells are primed and can become over active
To combat this, you must mediate the inflammation cascade
Prevent repeated head trauma
Due to priming of the foam cells, response to follow-up trauma may be far more severe and damaging
What Is Post-Concussion Syndrome (PCS)?
Symptoms following head trauma or mild traumatic brain injury, that can last weeks, months or years after injury
Symptoms persist longer than expected after initial concussion
More common in women and persons of advanced age who suffer head trauma
Severity of PCS often does not correlate to severity of head injury
PCS Symptoms
Headaches
Dizziness
Fatigue
Irritability
Anxiety
Insomnia
Loss of concentration and memory
Ringing in the ears
Blurry vision
Noise and light sensitivity
Rarely, decreases in taste and smell
Concussion Associated Risk Factors
Early symptoms of headache after injury
Mental changes such as amnesia or fogginess
Fatigue
Prior history of headaches
Evaluation Of PCS
PCS is a diagnosis of exclusion
If patient presents with symptoms after head injury, and other possible causes have been ruled out => PCS
Use appropriate testing and imaging studies to rule out other causes of symptoms
Headaches In PCS
Often �tension� type headache
Treat as you would for tension headache
Reduce stress
Improve stress coping skills
MSK treatment of the cervical and thoracic regions
Constitutional hydrotherapy
Adrenal supportive/adaptogenic herbs
Can be migraine, especially in people who had pre-existing migraine conditions prior to injury
Reduce inflammatory load
Consider management with supplements and or medications
Reduce light and sound exposure if there is sensitivity
Dizziness In PCS
After head trauma, always assess for BPPV, as this is the most common type of vertigo after trauma
Dix-Hallpike maneuver to diagnose
Epley�s maneuver for treatment
Light & Sound Sensitivity
Hypersensitivity to light and sound is common in PCS and typically exacerbates other symptoms such as headache and anxiety
Management of excess mesencephalon stimulation is crucial in such cases
Sunglasses
Other light blocking glasses
Earplugs
Cotton in ears
Treatment Of PCS
Manage each symptom individually as you otherwise would
Manage CNS inflammation
Curcumin
Boswelia
Fish oil/Omega-3s � (***after r/o bleed)
Cognitive behavioral therapy
Mindfulness & relaxation training
Acupuncture
Brain balancing physical therapy exercises
Refer for psychological evaluation/treatment
Refer to mTBI specialist
mTBI Specialists
mTBI is difficult to treat and is an entire specialty both in the allopathic and complementary medicine
Primary objective is to recognize and refer for appropriate care
Pursue training in mTBI or plan to refer to TBI specialists
Sources
�A Head for the Future.� DVBIC, 4 Apr. 2017, dvbic.dcoe.mil/aheadforthefuture.
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
�Heads Up to Health Care Providers.� Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 16 Feb. 2015, www.cdc.gov/headsup/providers/.
�Post-Concussion Syndrome.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 28 July 2017, www.mayoclinic.org/diseases-conditions/post- concussion-syndrome/symptoms-causes/syc-20353352.
Pain Anxiety Depression�Everyone has experienced pain, however, there are those with depression, anxiety, or both. Combine this with pain and it can become pretty intense and difficult to treat. People that are suffering from depression, anxiety or both tend to experience severe and long term pain more so than other people.
The way anxiety, depression, and pain overlap each other is seen in chronic and in some disabling pain syndromes, i.e. low back pain, headaches, nerve pain and fibromyalgia. Psychiatric disorders contribute to the pain intensity and also increase the risk of disability.
Depression:�A (major depressive disorder or clinical depression) is a common but serious mood disorder. It causes severe symptoms that affect how an individual feels, thinks, and how the handle daily activities, i.e. sleeping, eating and working. To be diagnosed with depression, the symptoms must be present for at least two weeks.
Persistent sad, anxious, or �empty� mood.
Feelings of hopelessness, pessimistic.
Irritability.
Feelings of guilt, worthlessness, or helplessness.
Loss of interest or pleasure in activities.
Decreased energy or fatigue.
Moving or talking slowly.
Feeling restless & having trouble sitting still.
Difficulty concentrating, remembering, or making decisions.
Thoughts of death or suicide & or suicide attempts.
Aches or pains, headaches, cramps, or digestive problems without a clear physical cause and/or that do not ease with treatment.
Not everyone who is depressed experiences every symptom. Some experience only a few symptoms while others may experience several. Several persistent symptoms in addition to low mood are�required�for a diagnosis of major depression. The severity and frequency of symptoms along with the duration will vary depending on the individual and their particular illness. Symptoms can also vary depending on the stage of the illness.
PAIN ANXIETY DEPRESSION
Objectives:
What is the relationship?
What is the neurophysiology behind it?
What are the central consequences?
Brain Changes In Pain
Figure 1 Brain pathways, regions and networks involved in acute and chronic pain
Davis, K. D. et al. (2017) Brain imaging tests for chronic pain: medical, legal and ethical issues and recommendations Nat. Rev. Neurol. doi:10.1038/nrneurol.2017.122
PAIN, ANXIETY AND DEPRESSION
Conclusion:
Pain, especially chronic is associated with depression and anxiety
The physiological mechanisms leading to anxiety and depression can be multifactorial in nature
Pain causes changes in brain structure and function
This change in structure and function can alter the ability for the brain to modulate pain as well as control mood.
Autoimmunity:�One of the most common things is to leave the doctor�s office with a diagnosis of an autoimmune disease and no nutritional or lifestyle changing insight. Autoimmune diseases are related to inflammation. Keeping� the inflammation down is the goal with autoimmune attacks. The foods you eat make a huge difference in the frequency and severity of flare-ups. Steady dietary changes can help you reach your optimal self.
Is Autoimmune Disease A Result Of The Collective Perturbations Of The Exposome & Its Impact On The Immunometabolic System?
The western diet is associated with inflammation, and inflammation is central to autoimmunity and autoimmune diseases. Keeping the inflammation down can help in lengthening time between attacks. What to eat and what not to eat are the common questions. In order to quiet� inflammation triggers, educate ourselves and live a normal life is the focus.
My 2006 Seminar Series
�Understanding the Origins of Autoimmune Disease�
Autoimmunity:
The Central Question I Asked In This series,
Are We Allergic to Ourselves?
� Autoantibodies
� Are they really �autoantibodies�?
� Self or Non?self?
I would like to re?explore this question using what we have learned in 2018.
Presence of Anti?Chromatin, DNA and RNA Antibodies
What Biological Processes May Make Self Into Non?Self?
Post?translationalmodificationofProtein � Glycation of protein � Protein Oxidation � Amino Acid Conjugation of Protein (Citrullinated Protein/AntiCCP and RA)
ProteinSynthesisErrors
DNA and RNA Changes � Radiation Induced Crosslinking of DNA � Oxidation of DNA � Copy Errors not corrected by DNA repair process � Epigenetic Changes (the methylome)
Where Do Anti?Cyclic Citrullinated Peptides (AntiCCPs) Come From?
Activation of the immune system resulting in increased iNOS production of nitric oxide
Arginine residues in proteins can be converted in situ into citrulline with the release of nitric oxide by iNOS
The citrulline produced in the protein is now �foreign� and can be recognized by the immune system as such
Antibodies can then be produced against this �foreign protein�
Disease Modifying Anti?Rheumatic Drugs (DMARDs)
The Facts on Methotrexate For Rheumatoid Arthritis Treatment
Methotrexate is the most commonly prescribed drug to treat rheumatoid arthritis, yet it only helps about half of those who try it. Find out how it works and how to lessen its side effects.
Folate Inhibition To Block Immune Cell Proliferation
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