Low Back PaIn
Low back pain can be one of the most debilitating conditions that a person can experience. Symptoms range from dull aches to piercing sensations, sometimes even running down the leg, that make it very hard to move or stand. The pain often starts suddenly without warning and can lasts for more than three months. If you have or currently have low back pain, you know that it can negatively affect the quality of your life. Loss of sleep, inability to concentrate at work, social and athletic activities come to a stop. Living with lower back pain is something no one should have to endure. The good news is that you don’t have to suffer any longer. You can decide right now to do something about it. To take your health back, to take your life back.
Now, I don’t want you to think this is an easy process, but I do want you to realize it will be worth it. The truth is, most likely you have had this problem long before you started feeling the pain. Most back issues are the result of years of damage and degeneration that have finally manifested into dysfunction, and if ignored, eventually disease. Back pain can be caused by a number of different factors, including (but by no means limited to):
Disc issues
Poor Posture/Joint misalignments
SCiatica
Sprains/Strains
Scoliosis
Lower Cross Syndrome
Kidney stones
With so many causes of low back pain, it would be illogical to provide the same treatment regardless of the cause, but that is exactly what most people do. Pain killers and anti-inflammatories are the standard of care for mild to moderate low back pain. These do nothing to address the cause of your pain, and more importantly, they do nothing to stop the ongoing damage and degeneration. A thorough and complete examination by a qualified doctor is essential in proper and effective identification and correction of the cause.
The medical term for spinal misalignment is Interspinal segmental joint dysfunction (ISJD) or Subluxation. This occurs when one or more spinal bones has shifted out of alignment, altering joint mechanics. Like a car that needs a wheel alignment, this causes uneven and unnatural pressure on the joint structures, most importantly, the spinal discs and the spinal nerves. The resulting effect is a dysfunction of the physiology of muscular and/or organ systems associated with that nerve root.Some (but not all) areas that can be effected by spinal misalignments of the lower back include:Large Intestine, Appendix, abdomen, Buttocks, Groin, Reproductive Organs, Bladder, Prostate, Sciatic Nerve, Colon, Thighs, Knees,legs, Feet
Research has shown that psychological and emotional factors may also be contributing factors. Proper physical, bio-chemical and mental/emotional factors should be assessed to determine the root cause of the dysfunction, as well as address any pathological symptoms that may have arisen.
Spinal manipulative therapy, otherwise know as a chiropractic adjustment, has proven to be superior to alternate options including: traditional medical management (muscle relaxants, pain meds, anti-inflammatories), physical therapy, pain management, exercise, acupuncture, bed rest and massage. The only dose-response efficacy study of SMT for LBP suggested that 12 visits over 6 weeks provided the most favorable outcomes.
Structural or functional instability may present in a very similar fashion to intersegmental joint restriction. Patients with lumbar instability will benefit from spinal stabilization rather than manipulation, although ISJD and global instability are not always mutually exclusive. Myofascial release techniques may be appropriate for lesions in the lumbar and pelvic muscles, as well as the hamstrings. Flexibility exercises and rehab focused on helping find and maintain a neutral spine posture. The addition of spinal stabilization exercises may help to reduce pain, disability, medication intake as well as future episodes of lower back pain.
A herniated disk refers to an injury with one of the cushions (disks) between the individual bones in your spine known as vertebrae. A spinal disk is like a jelly donut, a softer center within a tough exterior. Sometimes called a “slipped” or “ruptured disk”, a herniated disk occurs when the outside of the donut begins to get small tears. Over time, if not corrected, these tears will eventually perforate the entire disc causing some of the softer “jelly” to leak through a crack in the tougher exterior causing irritation to the nerves. Symptoms can arise from either inflammatory/chemical irritation or mechanical compression of the nerve root. Disc herniations are part of a disease process that starts with minor repetitive disc sprain, leading to herniation and ending in degeneration.
The most common cause is misalignment of the spinal bones (subluxation) causing uneven pressure on the disc, dehydration, chronic inflammation, sports, work related chronic micro-traumas such as sitting for long periods of time and muscle inhibition due to poor ergonomics, stress, inactivity or lack of motion in the spine or poor lifestyle habits.
Only the outside portion of the disc contains sensory nerve fibers, so disruption to the disc may be asymptomatic. Once symptoms occur, they may include either local pain or radiating from the low back into the gluteal area, leg and/or foot, numbness or tingling, weakness, muscle loss or compensation, organ dysfunction.
Although a disc may be herniated, it does necessarily result in pain. Pain only occurs when there is irritation to the sensory portion of the nerve. The severity and location of the herniation will determine degree of pain and dysfunction, and whether surgery is needed. Most disc herniations can be managed successfully without the need for surgery through realignment of spinal structures, spinal decompression, balancing muscles and supporting the healing process with specific exercises and nutrition.
Sciatica refers to pain radiating from the sciatic nerve. The sciatic nerve begins at the 4th lumbar vertebrae to the base of the spine known as the sacrum. The nerve travels through the hips and buttocks and down the leg. The classic symptom of radiating pain down one leg is the hallmark of Sciatica.
Sciatica is caused due to irritation or pressure on the Sciatic nerve, typically from either a misalignment of the spinal bones or pelvis, a herniated disc at L5-S1 level or dysfunction in one of the muscles along its path, typically the piriformis muscle.
Symptoms may include pain along nerve path, mild ache, a sharp shooting or burning sensation, numbness, tingling, muscle weakness in affected leg or foot. It can be aggravated by sitting for long periods of time, especially on a wallet.
When inflamed, the sciatic nerve can cause pain deep to the buttock, hamstring, knee, lower leg, or foot. The root cause is found in the lower back and deep gluteal area. The nerve can be irritated by a bulging disc, bone spurs, subluxations or problems with the muscles and/or fascia along the nerve path. Correction includes spinal manipulation, muscle reactivation, nerve mobilization and muscle flexibility exercises, myofascial soft tissue release and spinal decompression in the event of disc involvement.
Although scoliosis is described as an abnormal lateral curvature of the spine, it is generally recognized as more than a simple lateral deviation, but rather one that includes vertebral rotation and an alteration of the normal curvature of kyphosis/lordosis. A genetic component is suspected since scoliosis tends to run in families and is more common in children born to older mothers.
Scoliosis can be classified as “congenital” (i.e. present at birth), “secondary” to another disorder (i.e. spinal muscular atrophy) or “idiopathic”, which constitutes 85% of all cases of scoliosis.
Scoliosis may be subclassified based upon age of onset:
0-5 years of age Congenital scoliosis
6-12 years of age Early onset scoliosis
13-18 years of age Adolescent idiopathic scoliosis
Scoliosis may develop at any time between birth and adulthood but is most common during times of rapid skeletal growth. (6-24 months, 5-8 years, and 11-14 years)
The majority of patients with mild to moderate scoliosis are asymptomatic, with only 23% of patients have back pain at the time of presentation. Although scoliosis is most commonly asymptomatic in children, the presence of the disease more than triples one’s risk for developing spine pain as an adult. Thoracic curves above 50 degrees may impair respiratory function, and curves reaching 90 degrees often lead to cardiorespiratory failure.
Plain film radiographs are the criterion standard for assessing scoliosis and radiographic monitoring of adolescent idiopathic scoliosis should be performed yearly, while early onset scoliosis and juvenile scoliosis should be monitored at six month intervals. Repeat radiographs have been shown to increase scoliosis patients’ risk for developing various cancers including: leukemia, GI, lung, and breast. The increased risk of breast cancer may be reduced from 110% to less than 4% if films are taken from a posterior to anterior position as opposed to anterior to posterior.
The primary treatment goal for scoliosis is to stop curve progression. Additional objectives are to improve postural aesthetics, and manage any associated spinal pain or respiratory dysfunction. Curve correction is possible through conservative care including, spinal manipulation, and neurological and musculoskeletal exercises.
Proper exercise can prevent a progression of the curve and may decrease need for bracing. The “Scientific Exercises Approach to Scoliosis” (SEAS) is a proven and tested exercise regimen for the treatment of scoliosis.
Brace treatments are typically reserved for curves between 30 and 40 degrees in patients who are still growing with a chance for progression.
Braces are successful at preventing surgery in approximately three out of four patients. Bracing compliance is critical, but the number of hours a day the brace should be worn varies in the literature from 12-23.
A major consideration in determination of surgical appropriateness is the assessment of skeletal maturity to determine the likelihood of progression. Less than 0.3% of all scoliosis cases require surgical correction. Consideration for surgical intervention is generally reserved for curves that exceed 40 degrees.
Lower Crossed Syndrome is an adaptive pattern of postural dysfunction characterized by alternating tightness and weakness of muscles located in the core & pelvis. Tight muscles (hypertonicity) typically are the erectors, rectus femoris, iliopsoas, hamstrings, piriformis and TFL combined with a concurrent weakness in the gluteal and abdominal muscles, particularly the transverse abdominous. Lower cross syndrome is a consequence of excessive sitting and adaptive neuromuscular patterning. The condition alters normal biomechanics of the body and frequently contributes to back, hips and pelvis pain. Longstanding biomechanical dysfunction is thought to result in premature degenerative change as well as changes in neurological motor control.
The postural deficits associated with lower crossed syndrome are known contributors to many lower extremity problems, including hip pain, iliotibial band syndrome, patellofemoral pain syndrome, and plantar fasciitis. Poor posture can negatively affect proprioception, balance, gait, and functional performance, and has even been associated with increased mortality rates in older adults.
Joint dysfunction may arise secondary to muscular imbalance often creating a predictable pattern of joint dysfunction involving the L4/5, L5/S1, sacroiliac and hip joints.
Management of lower crossed syndrome should first attempt to eliminate abnormal proprioceptive input through joint mobilization and myofascial release. Rehab then progresses sequentially through stretching, strengthening, and finally, facilitation of normal movement patterns.
This law necessitates that hypertonic muscles be lengthened before embarking on the process of strength training. Stretching and myofascial release should be directed at the thoracolumbar extensors, iliopsoas, rectus femoris, quadratus lumborum, TFL, hamstrings and piriformis. Additionally, release of myofascial adhesions may be necessary in the gluteal muscles.
Strengthening exercises should focus on the abdominal and gluteal muscles. Functional rehabilitation must include proprioception and exercises to “groove new movement patterns.
Head and Neck Pain
It is widely accepted that the majority of headaches are caused by imbalances in one or more of the following:
- neurological
- circulatory
- muscular
- chemical
Headaches are symptoms created by your nervous system to indicate that there is tissue damage occurring quicker than your body can repair it. Headaches are not Deficiencies of aspirin, Tylenol, pain killers or any other medication. In fact, research shows that these products may be a major cause of headaches.
Neurological: The primary cause of nerve irritation in the body is spinal imbalance called Subluxation. The nerve that is primarily responsible for the muscular, circulatory, and neurological causes of headaches is the trigeminal nerve. The trigeminal nerve is made of cells that originate in the brain stem and travel down as low as the 2nd cervical level of the spinal cord. The trigeminal nerve is the largest nerve in the head and upper neck. Its branches affect: muscles of the head, neck, and jaw.
- skin of the head, neck, and scalp
- blood vessels to the head, neck, and brain, sinus mucosa
- brain and nervous system covering called meninges
- jaw, inner and middle ear
- glands in the head and neck, etc
The upper two vertebrae in the spine are where the brain stem and the trigeminal nerve lives. The primary cause of interference to these sensitive nerves are subluxation of the 1st and 2nd cervical vertebrae.
Circulatory: Blood flow is responsible for providing water, oxygen, and nutrients to the cells’ tissues directly involved with headache suffering. Spinal distortions cause nervous imbalance, decreased blood flow, and increased tissue breakdown which leads to irritation of delicate muscle and nervous system tissue.
Muscular: Muscle spasm or tension is a sign that there is nervous system imbalance caused by Postural Imbalance, Spinal Distortion (Subluxation), Chemical Imbalance, Past history of trauma and Emotional Stress, Muscles that are directly related to the production and maintenance of tension headaches:
- Sub-occipital
- Parietal
- Splenius
- Muscles of the eyes
- Muscle of the scalp
- Muscles of the neck
Chemical: Lotions, shampoo’s, tooth paste, and deodorants, Prescription and non-prescription drugs, House hold cleaning supplies, Diet (MSG, Nitrites, Serotonin levels), Dehydration, Alcohol, Caffeine, Emotional stress
To end headaches the primary objectives should be:
- To detect and correct areas of imbalance in the spinal and nervous systems
- A complete chiropractic wellness care plan to restore normal function
- Specific changes in diet, hydration, and exercise
- Discontinued use of chemical irritants; OTCs and prescription drugs
- Restore the natural healing potential of the body
If you live with migraine headaches, you know how debilitating they can be. In fact, according to the World Health Organization, migraines are one of the 10 most disabling conditions in the world. Migraines are a neurological condition often caused by issues associated with nerves and blood vessels in the head and neck that causes a unique set of symptoms including:
- Severe throbbing pain, often on just one side of your head
- Sensitivity to light, sound, and smell, often before a migraine occurs, this is called an “aura”
- Tingling or pain in your face or jaw
- Numbness and tingling in your hands
- Nausea
- Pain that lasting up to 3 days
strong>Vascular risk factors include hypertension, hypercholesteralemia, impaired insulin sensitivity, coronary artery disease, and a history of stroke. Migraines tend to become “chronic” following overuse of NSAIDs such as acetaminophen, naproxen, aspirin, opiates, barbiturates, and triptans. One study demonstrated that NSAIDs were beneficial when used less than 10 days a month but induced migraine progression to a chronic state when used at a higher frequency.
The presence of migraine increases one’s risk of cardiovascular disease (stroke and myocardial infarction) by approximately 25%. Those experiencing migraine with aura have an almost twofold increased risk of cardiovascular disease.
Common migraine triggers include:
- Certain foods, including caffeine, alcohol (especially beer or red wine with tannins),, dairy, MSG, soy sauce, citrus foods, papayas, avocados, red plums, overripe bananas, dried fruits with sulfites (figs, raisins, etc), sour cream, buttermilk, nuts, peanut butter, sourdough bread, aged meats and cheeses, processed meats, and anything fermented, pickled or marinated.
- Lack of sleep or an irregular sleep schedule< /span>
- Dehydration
- Smoking
- Strong odors, like perfumes
- bright or flickering lights, fluorescent lighting
- Hormonal fluctuations, especially during the menstrual cycle
- Changes in weather, especially increases in barometric pressure
- Medical factors, including stress, sleep apnea, certain medications, including estrogen, oral contraceptives, vasodilators nitroglycerine, histamines, reserpine, hydralazine, and ranitidine
Chiropractic care has been shown to help treat migraine headaches with techniques like spinal manipulation, diet modification, and rehab exercises including spinal muscle stabilization and stretching. This type of treatment can also help prevent migraine headaches when properly administered. One study showed that some people who seek chiropractic treatment saw a 90% drop in the number of migraine attacks, and the same study showed that 49% of participants experienced significant pain reduction. Soft tissue manipulation and massage therapy have demonstrated success in the treatment of migraine headache, including trigger point therapy in the SCM, upper trapezius, and/or suboccipital.
The patient’s self-management should focus on trigger avoidance and stress management. A headache diary is essential to help identify and eliminate triggers. Patients with medication triggers, including oral contraceptives and hormones should consult with their medical provider about changing or discontinuing those drugs. Exercising for 40 minutes, three times per week has shown similar benefit to a proven prophylactic medication. Overweight patients are more susceptible to migraine and should be given dietary advice. Migraineurs with aura should be counseled on the increased risk of stroke associated with smoking and oral contraceptive use. Limited data supports the use of Feverfew (125mg/ day), riboflavin (400mg/ day), and Magnesium (400-600mg/ day) for the prevention of migraine in non-pregnant patients.
Sprain/Strain injuries are the most common injuries in the neck. A strain is an injury to the active support structures of the neck muscles, while a sprain is an injury to the passive structures, the ligaments.
Sprain/strain injuries may result from a single traumatic event or from chronic repetitive mechanical overloading. With chronic overuse injury or postural distortions, a repetitive stress is applied over an extended period of time which leads to muscle fatigue, inflammation and micro-tearing. This can be caused by prolonged static postures in poor workstations, overhead activity, poor bra support, sedentary lifestyles, repetitive movements, pregnancy and obesity.
Acute injuries occur with whiplash from motor vehicle accidents, sporting accidents, activities of daily living like pushing, pulling, moving heavy objects, falls.
In both cases, weakness of the cervical musculature, particularly the deep neck flexors, may be a predisposing factor to injury. Symptoms from sprain/strain type injuries may begin abruptly in acute condtions but more commonly develop gradually in the hours or days following an injury. Complaints often include constant dull neck pain that intensifies or becomes sharp with movement. Rest may relieve acute symptoms but often leads to inactivity-stiffness. The pain is generally limited to the cervical spine, trapezius or between the shoulder. Suboccipital headaches are common, particularly when the upper cervical spine is involved. Altered proprioceptive input may result in varying degrees of vertigo. Additional symptoms may be generated from muscular spasm or adhesions to the fascia.
Restoration of normal mobility and joint function should be the goal. Gentle range of motion exercises and isometric strengthening should be implemented to tolerance in the acute phase of healing. Myofascial release and stretching exercises may be needed for the scalene, trapezius, levator, pectoral, SCM and other paracervical muscles. Nerve mobilization techniques may be necessary to restore normal neurodynamics. Spinal manipulation is a valuable tool for the restoration of normal joint mechanics in sprain/strain injuries. However, care must be taken in order to avoid further damage to hypermobile joints. Restrictions in the upper thoracic spine are common in cervical pain patients as well and need to be addressed.
Ergonomic and postural training may include a discussion of workstation ergonomics, sleep posture and modification of activities of daily living to promote healing and prevent recurrence of symptoms.
Degenerative disc disease (DDD) is a chronic disease that takes many years to develop due to improper alignment (subluxation) and biomechanics of the spine. Symptoms associated with DDD can be broken down into two categories; Discogenic pain and Nerve root interference.
With discogenic pain, only the outer third of the disc has a nerves supply, which means that pain is not felt until the disease process has been progressing for a substantial period of time. Additionally, chemically mediated inflammation causes an increase in nociception (pain) activity.
The primary goal of spinal discs are to aid in proper movment of the spine, not to support the weight of the body. As the spinal bones begin to subluxate, the neck loses it protective arc, and the weight of the head shifts from the back of the spine, onto the discs. Over time, if the discs placed under excessive force, they will break down and lose their height. This causes a compressive irritation to the nerve root exiting the spine and can have negative health consequences to any structure that nerve innervates. Neurologic radiculopathy, sensory, motor or visceral deficits associated with the specific level of nerve root compression. The nerves of the cervical spine supply the following:
Blood supply to the head pituitary gland, brain, middle ear, sympathetic nervous system (fight or flight response), eyes, optic nerve, auditory nerves, sinuses, tonsils, tongue, sensation to the head and face, neck muscles, vocal cords, thyroid gland, shoulders, arms and hands, diaphragm.
Treatment consists of reliving inflammation, reducing compressive forces and restoring normal mechanics. Cervical traction, myofascial release and joint manipulation procedures should be directed at sites of chronic cervical involvement with the goal to restore proper joint biomechanics and aid in disc hydration. Home exercises, postural advice and the use of a cervical support pillow can help accelerate the healing process. Care should be taken to avoid prolonged cervical extension, rotation or lateral flexion. In addition, appropriate ergonomic modifications should be made at home and at work.
Vertigo or Dizzyness may arise from one or multiple anatomical structures including the brain stem, cerebellum, the vestibular (inner ear), visual, and/or spinal proprioceptive systems. The most common cause of vertigo is BPPV, which is responsible for between 17 and 42% of all cases. Vestibular Habituation Training and the use of Brandt-Daroff exercises resolve symptoms in 98% of BPPV cases within two weeks.
The cervical spine is the most essential contributor toward equilibrium. The upper cervical (C0-3) facet joints are highly innervated, supplying up to 50% of all cervical proprioceptive input. The cervical spine muscles are extensively supplied with muscle spindles providing additional contributions. Abnormal stimulation from joint dysfunction or muscle hyperactivity provides conflicting input with visual and vestibular systems confusing the brain into a temporary state of dizziness. Cervical spine proprioception may be affected by conditions that alter mechanoreceptive input including: degeneration, inflammation, joint dysfunction, disc lesion, muscle hypertonicity or trauma. A sensation of Cervicogenic symptoms are generally provoked by movement and eased by maintaining a stable position. Continuous symptoms or the sensation of spinning suggest a more central origin.
Diagnosis of cervicogenic vertigo include loss of cervical range of motion, upper cervical tenderness, and upper cervical segmental joint restriction. Deep palpation of the suboccipital region may reproduce vertigo. Hypertonicity in the suboccipital, paracervical, trapezius, SCM, and pectoral muscles are also common. Deep neck flexor weakness has been identified as a primary component of cervicogenic headache and may very well be a contributor to cervicogenic vertigo. Dysfunction between cervical proprioception and hypertonicity in the SCM and upper trapezius may contribute to cervicogenic vertigo.
Since cervicogenic vertigo, by definition, results from upper cervical dysfunction, spinal manipulation is a cornerstone of treatment. Because cervicogenic vertigo is multi-factoral in origin, successful management requires a multi-faceted approach. Therapy must address associated soft tissue components. Myofascial release and/or stretching may be needed in the suboccipital, SCM, upper trapezius, levator, and pectoral muscles. Postural correction may be necessary for upper crossed syndrome, and breathing exercises are appropriate for those with dysfunctional respiration.
Other hypothetical models for cervicogenic vertigo include vascular compression and vasomotor changes secondary to irritation of the cervical sympathetic chain.
The temporomandibular joint (TMJ) is made of the temporal bone of the skull and the mandible (the jaw bone). They fit together to form a hinge-like joint.
Dentist have long known the temporomandibular joint dysfunction can cause functional problems throughout the body. Symptoms far removed from the joint itself like headaches, back pain, and pain across the shoulders can be caused by a dysfunctional TMJ. Correction TMJ problems brings great relief to many people who have “tried everything but nothing worked”.
When the temporomandibular joint and its associated structures are functioning abnormally, neurologic confusion can result. This particular area of the body receives a very high percentage of nerve communication from the brain. Confusion within this system can overflow into other systems of the body, causing health problems literally throughout the body by way of improper nerve function.
Examination includes determining the balance of the temporomandibular joint activity and the muscles that move the jaw through its range of motion. When an imbalance of TMJ function is found, it can often be corrected by balancing the jaw’s muscular activity with Applied Kinesiology techniques. It is sometimes necessary to have the bite (occlusion) balanced by a dentist to maintain muscle and temporomandibular joint balance.
To feel for TMJ dysfunction, take your index fingers and place them in front of your ears. While your fingers are in this position, open and close your jaw. Can you feel any clicking or grinding? Does the jaw seem to open evenly? Or can you feel a slight side to side shift as you open your jaw? You can also observe yourself in the mirror. Does your jaw open smooth or does it sway side to side as it opens? These can be subtle clues the body is not functioning properly. Finally, you should be able to place three knuckles of the non-dominant hand in your mouth. If this is difficult or impossible to do, its possible a TMJ dysfunction has caused a loss in range of motion to your jaw. This can cause headaches, neck pain and over time, degeneration to the joint.
Upper Crossed Syndrome, also known as forward head posture, describes a predictable pattern of common muscle imbalance involving the neck and upper torso. This occurs when postural muscles (including the upper trapezius, levator, SCM, and pec major) are predisposed to tightness while “phasic” muscles (including the rhomboid, serratus anterior, scalenes, and middle & lower trapezius) respond to dysfunction by becoming weaker. The process typically begins when a muscle or muscle group is overused in a certain direction and becomes shorter and tighter (adaptive shortening). The antagonist muscles opposing this action are subject to prolonged stretch and tend to become longer and weaker (stretch weakness). Upper crossed syndrome is a direct result of “flexor-dominated” postures (i.e. forward use of the arms and head). This process begins in the classroom as a child and progresses with age throughout the working years. Most occupations, from computer operator to manual labor, are “flexor-dominated”. Workstation users are particularly predisposed from prolonged static flexor dominated postures. It is crucial that you arrange your workstation to facilitate a proper posture as best as possible. Minimize sitting for long periods of time and take frequent work breaks to take short walks around the office to reset your posture.
Upper crossed syndrom often presents with neck pain, interscapular pain, and headaches. The condition is thought to contribute to many upper body diagnoses, including cervical and thoracic intersegmental joint dysfunction, sprain/strain, discogenic pain, degeneration, vertigo, rotator cuff syndrome, thoracic outlet syndrome, costovertebral dysfunction, and TMD.
Upper crossed syndrome creates a predictable pattern of joint dysfunction involving the atlanto-occipital joint, C4-5, C7-T1, T4-5, and the glenohumeral joint. Management of upper crossed syndrome should first attempt to eliminate abnormal proprioceptive input through joint mobilization and myofascial release. Rehab then progresses sequentially through stretching, strengthening, and finally, facilitation of normal movement patterns.
Upper Extremity
Shoulder Impingement
The shoulder joint consist of 3 bones; the shoulder blade (scapula), the upper arm (humerus) and the collarbone (clavicle). The humerus is held in contact with the scapula by 4 muscles known as rotator cuff muscles and by a cartilaginous ring around the scapula, called the glenoid labrum. The labrum adds surface area to the scapula and can often be the site of tearing, causing frozen shoulder or instability.
Shoulder Impingement is caused when the tendon of one of the rotator cuff muscles (supraspinatus) becomes painfully entrapped between part of the scapula known as the acromion and the the humerus during elevation and/or internal rotation of the arm.
Repetitive irritation of this tendon can lead to a cascade of shoulder dysfunction including supraspinatus tendon disruption, subacromial bursitis, biceps tendonitis, degeneration of associated joints and eventually, rotator cuff rupture..
What causes shoulder impingement?
Shoulder impingement results from repetitive injury and its development is partially related to repeated overhead activities involved in sports, including swimming, baseball, volleyball, weightlifting, or tennis. These and other activities can lead to muscular imbalances, most commonly in the rotator muscles, creating the risk for shoulder impingement. The rotator cuff is a dynamic stabilizer of the glenohumeral (shoulder) joint and works to depress the humeral head during arm elevation. Rotator cuff imbalances can result in the loss of normal humeral head depression as a result. Other factors such as poor posture, leading to tight chest muscles and weakened back and shoulder complex, injuries such as falls, anatomical abnormalities, thickening of a cushion in the shoulder known as the bursa can all be contributing factors to shoulder impingement syndrome.
Initial symptoms may be limited range of motion, pain when sleeping on the side of affected shoulder or during overhead activity and while reaching behind the back to fasten a bra or close a zipper. As the condition progresses, the patient may develop a constant ache that is present at rest and with simple movements in addition to muscle weakness and sensory changes.
Successful management of impingement syndrome should initially focus on restoring range of motion while avoiding aggravating movements i.e. elevation and internal rotation. Patients should avoid overhead presses, lateral raises, and push-ups. Selective rest may be necessary for some patients. Shoulder mobilization has been shown to decrease pain and improve range of motion in patients. Manual manipulation is needed to address restrictions in the cervical, upper thoracic and shoulder areas. There is evidence to suggest that cervicothoracic and thoracic spine manipulation may help decrease shoulder pain while improving mobility and function. Soft tissue manipulation or myofascial release of associated hypertonic muscles with specific emphasis on the pec, biceps, subscapularis, infraspinatus, teres minor and levator. Kinesio-Tape, applied across the supraspinatus, deltoid and teres minor, may promote scapular movement and strength with faster recovery times and lower disability. Ultrasound, anti-inflammatory modalities, and ice may be useful in the earliest stages. However, most passive therapy modalities provide little benefit for chronic patients.
Home rehabilitation exercises consisting of stretching should address tightness in the posterior capsule and internal rotators with specific emphasis on the: pec, biceps, subscapularis, infraspinatus, teres minor, levator and a cross body stretch. Strengthening may begin incrementally as the patient’s pain-free range of motion allows. Strengthening should begin with isometric exercises and progress as tolerated. Eccentric strengthening of the rotator cuff combined with eccentric/concentric exercises for the scapular stabilizers may produce improved outcomes. Specific strengthening should include: scapular retractions, shoulder flexion, isolated supraspinatus, horizontal abduction, extension, external rotation and reverse shrugs
Frozen Shoulder (Adhesive Capsulitis)
Frozen shoulder, also known as Adhesive capsulitis, is a painful limitation of active and passive motion in the shoulder joint (glenohumeral and scapular joints). Adhesive capsulitis can appear without warning and have no obvious cause.
Typically, adhesive capsulitis starts with achiness in the shoulder that becomes sharp at end range. A gradual progressive loss of shoulder range of motion over the next several weeks to months with development of new nerve growth contributing to a heightened pain response. Finally, as the shoulder capsule undergoes progressive fibrosis, pain and significant loss of range of motion for the next several months to a year occurs. This period of prolonged immobilization may lead to long-term detrimental consequences, including atrophy, degeneration, and permanent motion restrictions.
Adhesive capsulitis is most common in the 40-65-year old population with women being affected more frequently. Medical issues such as Type 1 & 2 diabetes and thyroid disease may increase one’s risk for developing adhesive capsulitis.
Symptoms include progressive pain, most focal to the insertion of the deltoid, with sharp intensification at end range motion. Night pain and sleep disturbances are common. Functional range of motion limit reaching overhead, behind the back, or to the side. A thorough evaluation must identify the presence of biomechanical deficits, including upper crossed syndrome and scapular movement dysfunction. Normal scapular movement is responsible for up to 1/3 of total arm elevation, thus scapular dysfunction may have a significant impact on range of motion in adhesive capsulitis patients. Cervical spine intersegmental dysfunction is also recognized as a contributor and should be assessed for restrictions and as a source for potential referred pain.
Treatments
Manual techniques should include active and passive stretching of the shoulder capsule with end range mobilization. Several studies suggest that joint mobilization can produce a significant improvement in shoulder abduction. Scapular mobilization should be a component of treatment. Exercises to correct postural deficits, including lower crossed syndrome and improve scapular mobility and function as well as cervical and thoracic spinal manipulation has been shown to be helpful in the treatment of shoulder pain and dysfunction.
Carpal tunnel syndrome (CTS) is a compression of the median nerve within the carpal tunnel at the anterior portion of the wrist, resulting in sensory and/or motor deficits in the lateral portion of the palm, as well as the lateral 3 ½ fingers. Prolonged wrist flexion or extension and repetitive wrist movements are the primary cause.
Risk factors include diabetes, hypothyroidism, rheumatoid arthritis, alcoholism, increased Body Mass Index (BMI), renal disease and short stature. Additionally, prior trauma resulting in fracture, dislocation or osteoarthritis may narrow the canal and fluid retention during pregnancy can be causative factors as well.
CTS is sometimes part of a “double crush syndrome” wherein the median nerve is sensitized to compression within the carpal tunnel as a result of more proximal irritation. Common double crush sites for CTS include cervical spine and disc degeneration, , muscles in the cervical region, pronator syndrome, ligament of Struthers, lacertus fibrosis, pronator teres muscle and the arch of the flexor digitorum. If left untreated, CTS may result in permanent neurologic damage.
Conservative treatments may include myofascial release to the forearm, wrist, and hand, kinesiotape, manipulation of cervical spine or bones in the shoulder, elbow and/or wrist, home stretching directed at hypertonic muscles in the neck, chest, pronator and wrist flexors. Additional home exercises should include chin retraction, carpal tunnel mobilization and median nerve floss. Studies suggest that taking 100-200mg of Vitamin B6 (pyridoxamine) daily may help relieve carpal tunnel symptoms. One study demonstrated that 68% of patients taking 100mg of vitamin B6, twice per day, experienced symptom alleviation (vs 14% of the control group).
Lower Extremity
Plantar Fasciitis is an inflammatory condition causing pain on the underside of the foot near the heel. The pain is commonly intense in the morning and reduces to a dull achy pain as the day progresses. This is commonly caused by abnormal gait, excessive supination or pronation, leg-length inequality, obesity, bad shoes, running on irregular surfaces, standing for long periods, or a shortened calf muscle.
Active Release Technique is extremely effective in treating this condition and restoring the normal function of the foot. In addition, chiropractic adjustments help to restore the proper biomechanics of the foot and leg. Rehab and orthotics are also recommended in treating this condition. Plantar fascia mobilization may be performed at home by rolling a golf ball or frozen water bottle beneath the plantar fascia.
Stretching exercises are appropriate for the gastroc, soleus, hamstring, and plantar fascia.
Ankle joint mobilization and manipulation can help restore normal motion, particularly dorsiflexion.
Patients who hyperpronate and those with fallen arches will benefit from arch supports or orthotics.
Strengthening exercises are appropriate for the gastroc, soleus, posterior tibialis, and intrinsic muscles of the foot. (82) Examples include marble and towel gripping exercises. Strengthening exercises for the posterior tibialis should be implemented to help arch support. Strengthening of the flexor digitorum brevis is an important component of treatment and may be accomplished by performing toe flexion with an exercise band. (36) Eccentric heel raises with the great toe positioned in passive dorsiflexion (i.e. great toe propped up with a towel) have shown benefit for plantar fasciitis patients.
The Achilles tendon is the largest and strongest tendon in the human body, but is simultaneously a vulnerable link in the locomotion chain. (1) The tendons’ structural prowess is relentlessly confronted by functional demands, that can be up to 12 ½ times body weight while running. (2)
The Achilles tendon may be acutely strained or ruptured as the result of an excessive stretch or eccentric force. Consistent with other types of acute strains, Achilles tendon injuries may occur when the musculotendonous unit transitions from eccentric deceleration to concentric propulsion. This happens during the “mid-stance” phase of gait. (3) Strains occur when collagen fibers are stretched by more than 4%. Ruptures occur when stretch exceeds 8%. (4,5)
Unlike acute injuries that cause inflammation, tendinopathy is characterized by repeated overloading, microtearing, failed healing, and subsequent tendon degeneration. (3,4,6,7). The process begins with collagen fiber disruption and ends in a disorganized healing process that fails to regenerate a “normal” tendon. Failed healing is blamed on a hyperplastic, but ineffective, microvascular system. (8,9)
An appreciation of gait mechanics is germane to understanding Achilles tendon injuries. During normal gait, the foot approaches the ground with 3-4 degrees of supination, allowing ground contact to occur on the lateral portion of the calcaneus. As a shock-absorbing mechanism, the foot initially relaxes into subtalar pronation. At mid-stance, the foot converts into a rigid lever and begins to supinate in anticipation of propulsion. Tibial external rotation accompanies ankle supination. Inefficient conversion from shock absorber to rigid lever results in hyperpronation which stresses the medial calcaneotendinous attachment of the Achilles tendon. (10)
Injuries to the Achilles tendon may be classified as “insertional” or “non-insertional.” Insertional tendinopathy, as its name implies, describes damage to tendon fibers at their insertion on the posterior calcaneus. This process may result in calcification and bony exostosis producing a prominent enlargement of the posterior calcaneus, also called a “Haglund deformity” or “pump bump.” Non-insertional Achilles tendinitis most commonly involves the vulnerable “watershed area”, 2-6 cm proximal to the calcaneal insertion. (11) This region of the tendon has a smaller cross-sectional area, is relatively hypovacular, and is subject to a repetitive “wringing” motion during supination/ pronation. This susceptible mid section is the most common site for degeneration and rupture. (12,13)
Achilles tendon injuries affect between 250,000 and 1 million people per year in the United States. (14,15) Most are middle-aged males in their third or fourth decade of life. (14,16) Interestingly, Achilles tendon injuries occur more frequently on the left side. (16) Patients who have suffered prior Achilles tendon rupture are at significantly higher risk for contralateral tendon rupture. (17)
Two-thirds of all Achilles tendon injuries involve athletes. (18) Runners are up to 10 times more likely to suffer Achilles tendon injuries compared to age-matched controls. (18) The Achilles is the most common site of tendinopathy in runners. (77) Athletes are at greater risk during speed training or sprinting. (19) Runners who assume a midfoot or forefoot strike pattern may be at even greater risk of injury. (20) Not surprisingly, a higher risk has been identified in other sports that involve running or jumping. The estimated incidence of Achilles tendinopathy is: running sports, 53%; soccer, 11%; dance, 9%; gymnastics, 5%; racquet sports, 2%; football, 1%. (14,21)
Extrinsic risk factors for Achilles injury include improper warm up, overtraining, running on hard surfaces, excessive stair or hill climbing, improper arch support/ footwear, poor conditioning and abruptly returning to activity after a period of inactivity. (19,22-26) Wearing high-heeled shoes may lead to shortening of the gastroc/soleus, predisposing women to Achilles tendinopathy. (27) Intrinsic factors include hyperpronation, pes planus, cavus foot, gastroc/soleus inflexibility or weakness, limited ankle dorsiflexion, and limited subtalar motion. (14,22-26) Systemic risk factors include diabetes, hypertension, inflammatory arthropathy, gout, obesity, and the use of corticosteroids or quinolones (broad spectrum antibiotics). (28,81,84)
Patients may present with symptoms from an acute strain or a more gradual onset repetitive irritation. Complaints include pain or tenderness in the tendon or heel that intensifies with activity, especially walking or running. Patients may report difficulty when attempting to stand on their toes or walking steps- particularly down stairs. Morning pain and stiffness are common. Patients may report warmth and swelling that increases throughout the day, related to activity. Symptoms may be tracked using the VISA-A questionnaire. (29)
Palpating the point of maximum tenderness can help localize the site of injury to either the “water shed area,” or the calcaneal insertion. Mid tendon pain suggests non-insertional tendinitis, whereas posterior calcaneal pain suggests insertional tendinitis. Fusiform swelling and tendinous or bony enlargement are common in cases of chronic tendinopathy. Those with insertional tendinopathy may demonstrate evidence of bony enlargement or spurring on the posterior calcaneus.
Range of motion testing will likely reveal deficits in passive dorsiflexion with pain on resisted plantarflexion. In some patients, single leg heel raises will elicit pain, while in others, repetitive hopping may be needed to elicit complaints. The Silfverskiold test can help differentiate Achilles vs. gastroc tightness in patients with limited dorsiflexion. Clinicians may perform the “calf squeeze test” (Thompson test) to exclude tendon rupture in those who have difficulty ambulating. The test has excellent validity and is performed by squeezing the calf of a prone patient and observing for passive plantar flexion of the foot. (30) Clinicians should perform motion palpation of the subtalar joint to assess mobility and identify restrictions.
Plantaris tendon pathology is associated with chronic mid-portion Achilles tendinopathy. (87-89) The plantaris tendon typically resides deep and adjacent to the Achilles medial border. Repetitive irritation of either tendon may lead to inflammation, scar tissue formation, and adhesion. This restricts gliding and leads to painful tethering when load is applied. (90) In some cases, the plantaris tendon has been known to thicken or even invaginate into the Achilles tendon, thereby thwarting traditional conservative management of Achilles tendinopathy. Tenderness on the medial mid-tendon is suggestive of plantaris involvement, while ultrasound or MRI may be necessary for a definitive diagnosis.
Clinicians must assess for contributory functional deficits throughout the kinetic chain.
Runners with non-insertional tendinopathy demonstrate an increased incidence of foot hyperpronation (subtalar eversion). (76) Foot hyperpronation manifests as: loss of the medial longitudinal arch, forefoot abduction (i.e. “too many toes sign”), calcaneal eversion, and navicular drop. Assess for weakness in the posterior tibialis by observing for calcaneal eversion during heel raises. Gastroc/soleus flexibility may be assessed by measuring and comparing passive ankle dorsiflexion. Clinicians should assess knee flexor/hamstring strength, as weakness in this muscle is a known risk factor for Achilles tendon pain. (31) Weakness or delayed activation of the hip abductors (gluteus medius) should be identified and corrected. Functional orthopedic testing for hip abductor weakness would include the Trendelenberg sign, overhead squat test, and single leg squat test. Weakness or delayed activation of the gluteus medius is associated with ankle dysfunction. (32)
Hallux limitus (limitation in passive dorsiflexion of the first metarsophalangeal joint) disrupts normal foot functional stability and has been associated with Achilles tendon pain. (33) Functional hallux limitus assessment is performed on a long-sitting patient. The clinician places their thumb under the patient’s first metatarsal head and forces the patient’s foot into maximum dorsiflexion and pronation to simulate a ground reaction force. The clinician then pinches the patient’s great toe with their opposite hand and passively moves the toe into dorsiflexion. Dorsiflexion of the great toe should be fluid and produce concurrent plantar flexion of the patient’s metatarsal head into the clinician’s thumb. A sense of “jamming” or “locking” upon dorsiflexion or a lack of concurrent first metatarsal plantar flexion suggests hallux limitis. Assessment of the patient’s shoe insole may help to identify hallux limitus by revealing a lack of wear under the first metatarsal head with disproportionate wear under the second through fifth metatarsal heads and pad of the great toe. (34)
Radiographs are often unnecessary for the diagnosis of Achilles tendinopathy. (35) The Ottowa Ankle Rules define the appropriateness for imaging patients with ankle or midfoot pain, following trauma. (36-38,74,75) No clearly defined rules exist for imaging non traumatic heel pain. Clinicians may consider radiographs in cases of significant trauma with altered gait or when necessary to rule out other pathology, including calcaneal epiphysitis/ avulsion. Radiographs of Achilles tendonopathy may demonstrate tendon calcifications and spurs/ enthesophytes on the posterior calcaneus. Ultrasound may be an efficient cost-effective means of evaluating the Achilles tendon. (39) Ultrasound or MRI may help identify and define tendon pathology.
The differential diagnosis for Achilles tendinopathy includes fracture, avulsion, neoplasm, infection, ankle sprain, retrocalcaneal bursitis, posterior ankle impingement, Os-trigonum syndrome, tenosynovitis, tendon dislocation, gastroc musculotendinous strain (tennis leg), sural neuroma, systemic inflammatory disease, and calcaneal apophysitis (Sever’s disease). In children and adolescents, the epiphyseal growth plate is 2 to 5 times weaker than in adults. This group is more likely to suffer epiphyseal injuries in the form of calcaneal apophysitis (Sever’s disease) from stressors that would likely cause Achilles tendinopathy in adults. (40)
Nonoperative treatment is the mainstay for Achilles tendinopathy. (81) “Traditional” treatment plans based solely on rest, therapy modalities, orthotics, and NSAIDs have failed to demonstrate benefit for Achilles tendinopathy patients. (41) Passive modalities including ice, ultrasound, electrical stimulation, and low-level laser also lack support. (42) The current standard of care for Achilles tendinopathy includes a combination of rest, eccentric rehabilitation, and correction of mechanical faults. Studies have demonstrated excellent results in up to 85% of patients undergoing appropriate conservative care. (43) Initially, patients may need to limit or stop activities that cause pain. Significant strains may require the use of crutches or a boot. Runners may need to switch to swimming, cycling, or other activities that limit stress to the Achilles tendon. Patients should avoid shoes with an excessively rigid heel tab to reduce irritation.
Eccentric exercise programs are effective for treating Achilles tendinopathy. (41,44-54) Eccentric training is more effective than concentric training for reducing pain and improving function. (52,55) In fact, research suggests that eccentric strength training programs are more than twice as effective as concentric programs for the treatment of Achilles tendinopathy. (52) A proven program by Alfredson (45) incorporates single leg eccentric heel drops off the edge of a step. Heel drops should be performed with the knee both straight and bent, three sets of 15 repetitions, twice per day for 12 weeks. Heel drops should occur slowly on a 4-10 second count. (56) The patient should use the non-injured leg to return to the “heel up” start position, thereby avoiding concentric contractions. Moderate pain during this exercise is acceptable but if pain is excessive, the patient should assist downward motion with the non-injured leg.
Soft tissue manipulation, stretching, and myofascial release techniques are necessary to promote flexibility of the calf muscles. Stretching of the calf muscles should be performed with the knee straight to address the gastroc and with the knee bent to lengthen the soleus. Clinicians should consider the use of IASTM to release adhesions within the Achilles tendon. As an additional benefit, IASTM may accelerate healing, possibly via controlled microtrauma. (57,78-80) Manipulation may be necessary to eliminate restrictions in the kinetic chain, particularly within the ankle. (58) Clinicians may consider the use of a 7-15 mm heel lift (bilaterally) to minimize dorsiflexion stress. Arch supports or orthotics may be necessary to correct hyperpronation. (76) Patients with hallux limitus may benefit from wearing shoe inserts with a “cut out” beneath the first metatarsal head. (59)
The treatments described thus far are directed at a “contractile dysfunction” model. If the patient’s complaints are not resolving as intended, it is important to consider the Mechanical Diagnosis Therapy (MDT) concept of “derangement”. Many cases of “derangement” tendinopathy have responded to end-range plantar flexion, although a recent review of the literature provides no clinical trials of this concept. End range plantar flexion is performed on a regular basis, 10 repetitions every 2-3 hours. A clinical indicator that the patient may respond well to repetitive end-range movements is worsening of their symptoms after dorsiflexion exercises.
Athletes should introduce new activities slowly and avoid increasing activity, particularly running, by more than 10% per week. Runners should begin on smooth, shock-absorbent surfaces and start out at a lower intensity and distance- first increasing distance, then pace. Athletes should avoid training on hard or unlevel surfaces, including hills. Return-to-play criteria for Achilles tendon strains or ruptures include the “Triple 5”:
1. Ankle dorsiflexion is within 5 degrees of the uninjured side,
2. Calf circumference (measured 10 cm distal to the tibial tuberosity) is within 5 mm of the uninjured side, and
3. The patient is able to perform 5 sets of 25 single leg heel raises. (60)
Patients who fail a trial of conservative care should be referred, but proven alternatives are scarce. Medical co-management is of limited benefit. NSAIDs may relieve symptoms but have little long-term effect on outcome. (61,62) Cortisone injections are unproven for the treatment of Achilles tendinopathy and carry a possible increased risk of tendon rupture. (63,64) Extracorporeal shock-wave therapy (ESWT) or platelet-rich plasma (PRP) injections are controversial alternatives. (65-68) ESWT (originally developed as lithotripsy) is thought to break up calcific deposits and stimulate fibroblast activity to encourage healing. ESWT may be appropriate for recalcitrant cases (81,82). PRP treatments consist of injecting platelet-rich plasma into a tendon to create a concentrated trigger of growth factors and chemoattractants for macrophages and fibroblasts, which gradually repair the damaged collagen. (69) Some clinicians suggest benefit from PRP injections, but others refute its usefulness for Achilles tendinopathy, (81,83) including at least one randomized clinical trial. (70)
Surgical management is often considered for Achilles tendon ruptures, although several studies, including at least one randomized clinical trial, suggests at least equivalent results between surgical and conservative management. (59,71,72,85)
Medial tibial stress syndrome (MTSS), aka Medial Tibial Traction Periostitis, describes exercise-induced pain along the posteromedial border of the tibia. The condition is commonly referred to as “Shin splints” and is a familiar malady in athletes and soldiers where it affects up to 1/3 of those populations. (1-4) MTSS is responsible for approximately 15% of all running injuries. (1)
The condition affects the vulnerable insertion points of the tibial fascia and deep ankle flexors along the medial tibial crest. MTSS is believed to result from repetitive eccentric contraction of the deep flexors during running, jumping, or impact loading. (5) Repetitive traction on the medial tibial crest, results in myofascial strain, periosteal inflammation, and bony stress reaction. (6-13) Early etiological theories focused on myofascial strain, but current evidence suggests that a bony stress reaction is the most likely cause of MTSS. (14-20)
Newer research suggests that traction periostitis may be an inflammatory precursor to tibial stress fracture. (21) The stress of exercise can weaken bone. Healthy bone responds to this stress by remodeling itself more densely. Stress reactions occur when the normal adaptive remodeling response is unable to keep pace with the loads of excessive training, i.e. high demands with inadequate recovery times. (22,23) Prolonged insult may lead to tibial stress fracture, and many authors now believe that MTSS and stress fracture represent two different points along a continuum of bony stress reaction. (24,25)
The leading mechanism of injury is repetitive eccentric contraction from running or jumping on hard surfaces. (26-28) Excessive or improper training is the leading factor for the development of MTSS. (2,3,29-33) Common training errors include the terrible too’s (too much, too fast, too long.) (31-34) Athletes who run more than 20 miles per week are at increased risk of developing MTSS. (35) Inexperienced runners or those with poor technique are at greater risk. (4) Running with a narrow or “crossover” gait increases tibial stress. (87)
Foot hyperpronation is a significant risk factor for the development of MTSS, as a collapsing foot puts additional stress on the suspect tissues. (4,10,12,14,28,36) Interestingly, the use of orthotics is associated with the development of MTSS, although orthotic use should not be viewed as an independent risk factor since those using orthotics are likely to hyperpronate. (4) Females are affected more frequently and have a 1.5-3.5 increased likelihood of progressing to stress fracture. (4,37) Additional risk factors include a prior history of MTSS and increased BMI. (4)
The clinical presentation of MTSS includes vague, diffuse pain over the middle to distal posteromedial tibia. Athletes often present following an increase in activity intensity or duration. Symptoms are often worse with exertion – particularly at the beginning of a work-out. (38) Initially, symptoms may subside during training, but as the condition progresses, symptoms may linger throughout activity or even at rest. (38) Pain that persists more than five minutes post-activity carries a higher suspicion of stress fracture. (49) Clinicians should be alert for symptoms of numbness or paresthesia, which could suggest exercise-induced compartment syndrome.
Clinical evaluation demonstrates diffuse tenderness over the posteromedial tibial border. Prolonged stress may generate a periosteal reaction detectable as a “rough” or “bumpy” feel upon palpation. (39)Tenderness from MTSS should involve at least 5 cm of the tibial border. (39) More focal tenderness, the presence of anterior tibial tenderness, or any significant swelling suggests stress fracture. Applying a vibrating tuning fork over the tibia may help detect stress fracture (75% sensitivity). (40) Single leg hopping is painful in about half of MTSS cases (and 70-100% of stress fractures) (41-43) The Talar Bump Test may help differentiate tibial stress fracture from MTSS.
Tenderness over the flexor digitorum longus and tibialis posterior is a clinical hallmark of the condition, although whether this is a primary cause or secondary effect remains uncertain. (44,45) Clinicians should assess for the presence of hypertonicity in the gastroc or soleus, as this finding is commonly associated with MTSS. (46,47)
The presence of foot hyperpronation may be assessed through the navicular drop test (performed by marking the navicular and measuring the amount of drop from non weight bearing to weight bearing.) (48) Clinicians should assess for other potential risk factors, including inflexibility or imbalance of the hamstring and quadriceps, genu varus or valgus, tibial torsion, femoral anteversion, and leg length discrepancies. (14) Hip abductor weakness is a common culprit of many lower chain overuse injuries and may be assessed through the “hip abductor weakness cluster”. (86) Excessive external rotation of the hip is another known contributor. (4,50)
Assessment of gait or running patterns can identify biomechanical errors. (51,52) Clinicians should assess joint mobility throughout the lower extremity. Neurovascular assessment is typically unremarkable. (38) The presence of sensory or motor loss suggests an alternate diagnosis, including exertional compartment syndrome, peripheral neuropathy, or radiculopathy.
Imaging of early and uncomplicated MTSS is often unnecessary. (53) Imaging is appropriate in the presence of: red flags, focal tenderness, pain at rest, or when the patient fails to improve with a reasonable trial of conservative care. (53) Radiographs taken within the first 2-3weeks are not likely to show any change; however, patients with longstanding MTSS may demonstrate periosteal reaction indicating callus formation and stress fracture. (55)
Clinicians should be vigilant for the possibility of stress fracture. Plain films frequently do not demonstrate the signs of tibial stress fracture (periosteal elevation/callus formation or cortical lucency ). (42,56,57) Unresponsive patients or those with a higher likelihood of stress fracture (runners) may benefit from advanced imaging, including MRI or bone scan. (58) MRI is highly sensitive (74-100%) and is best able to grade the progression of stress reaction from periosteal edema (Grade 1), to progressive bone marrow edema (Grade 2-3), to cortical stress fracture (Grade 4). (59-61)
In addition to stress fracture, the differential diagnosis of MTSS includes: exertional compartment syndrome, peripheral vascular disease, muscle strain, occult fracture, infection, neoplasm, DVT, peripheral neuropathy, popliteal artery entrapment syndrome, lumbosacral radiculopathy, and vascular claudication. (62-64)
The successful management of MTSS requires the removal of risk factors, and rest. Clinicians must identify the combination of training errors and biomechanical risk factors that led to the development of the patient’s condition. (65) No intervention has proven more successful than rest for the management of MTSS. (4) Unfortunately, patients often are affected by MTSS during a time when they are training for a sport or upcoming event. Continuance of the offending activity will often lead to undue chronicity, frustration for patient and clinician, and decreased performance capabilities. Athletes may need to decrease frequency, intensity, and duration of impact activities, including running and jumping. Athletes may need to consider non-weight bearing cross-training like stationary cycling or pool running. Initially, anti-inflammatory modalities, including ultrasound or e-stim may provide relief. (67) Ice or home ice massage may provide an anti-inflammatory or palliative benefit.
Resolution of MTSS requires correction of any associated kinetic chain dysfunction. (68-70) Stretching exercises and myofascial release are appropriate for the gastroc, soleus, hip external rotators, tibialis posterior, and tibialis anterior muscles. (71) Strengthening exercises may be appropriate for the tibialis posterior and hip abductors. Manipulation may be employed to resolve joint restrictions in the spine, sacroiliac joint, pelvis, and lower extremity. (69,70,74)
Arch supports or custom orthotics may be appropriate for patients with fallen arches (75), although at least one contradictory systematic review suggests that orthotics may be causative and are not useful for prevention. (76) The use of compressive taping, bracing, or stockings is thought to enhance bone remodeling and is used by some providers although supporting evidence is inconclusive. (77-79) Additional possibilities for the management of MTSS include dry needling, autologus blood injection, platlet rich plasma (PRP) injections, prolotherapy, and acupuncture. (74,80) Extracorporeal shock wave therapy (ECST) may speed recovery times. (81)
Return to activity should start slowly with a graded running program, beginning with a 1/4 mile run and progressing by 1/4 mile each time the athlete has no pain for two consecutive workouts. (82) Athletes should initially avoid running on hard or uneven surfaces and begin at a lower intensity and distance, increasing by no more than 10-15% per week. Runners should first increase distance, then pace, and avoid hard or unlevel surfaces, including hills. Runners with a narrow gait may benefit from incorporating a wider step width. (87) Clinicians should assess shoes for excessive wear and match the patient to the most appropriate show. (i.e. stability, neutral, cushioning) Running shoes lose half of their shock absorption capacity after 300-500 miles and should be replaced within that range. (83-85)
Surgical intervention, including posterior fasciotomy, is rarely indicated. (74)
Posterior tibial tendon dysfunction (PTTD) is the most common cause of adult-acquired flat foot. (1) Symptoms begin with pain and may progress to degeneration and deformity if left untreated. (1,3) Early recognition and management can lead to significantly improved outcomes. (1)
The deep compartment of the leg consists of three muscles: the posterior tibialis (PT), flexor digitorum longus (FDL), and flexor hallucis longus (FHL). The posterior tibialis is the deepest and largest muscle of the trio – typically comprising almost 60% of the cross sectional area of the entire deep compartment. (4-7) The posterior tibialis originates on the interosseous membrane and the posterior surfaces of the tibia and fibula. (4) The muscle’s tendon begins several centimeters above the ankle then courses through the deep posterior compartment of the leg behind the medial malleolus before turning toward its main attachment on the navicular tuberosity. (4) Ancillary attachments include the second and third cuneiform, cuboid, bases of the second, third, & fourth metatarsals, and sustentaculum tali of the calcaneous. (4,8-10)
Actions of the posterior tibialis muscle include inversion and plantar flexion of the foot. Because of its size and moment arm, the posterior tibialis is the primary elevator and dynamic stabilizer of the medial longitudinal arch of the foot. (5,11-15) During the normal gait cycle, the posterior tibialis lifts the medial longitudinal arch, thereby interlocking the tarsals (calcaneous, cuboid, talus, and navicular) into a rigid lever for propulsion. (12,17) The role of the posterior tibialis is most significant during push off. (18,19)
Early literature suggested that up to 50% of PTTD cases arose from trauma. (20,21) More recent literature suggests that the majority of cases begin from repeated micro trauma. (22) Repetitive stressors initiate a cascade of dysfunction that begins with “normal” inflammation but regresses to “failed healing”, fibrosis, and tendon degeneration. Degeneration affects the gliding resistance of the tendon and progressively diminishes the tendon’s ability to support the foot. (22) As the tendon becomes less effective, the longitudinal arch of the foot is allowed to collapse; thereby, increasing strain on the posterior tibialis. (22,25,26) The most common site for injury is a zone of relative hypovasulcarity directly posterior to the medial malleolus. (22,27,28)
The continuum of PTTD progresses through the following stages: (29)
I Tenosynovitis without deformity
IIA Flat foot deformity
IIB Flat foot deformity with excessive forefoot abduction
III Rigid forefoot abduction and hindfoot valgus
IV Deltoid ligament compromise
Like most cumulative trauma disorders, the etiology of posterior tibial tendon dysfunction is multi factoral. Problems typically arise when repetitive strain exceeds the tendon’s threshold for injury. Extrinsic factors that contribute to the development of posterior tibial tendinopathy include training errors- particularly those related to intensity, duration, and/or training on excessively hard surfaces. (30) In addition to the obvious contribution from hyperpronation, other intrinsic factors that increase the likelihood of developing PTTD include a history of obesity, diabetes, hypertension, seronegative arthropathy, steroid injection, surgery, or trauma. (1,31-33) A recent prescription of fluoroquinolones may increase the risk of tendon rupture. (35)
The stereotypical PTTD patient is an obese, middle-aged female. (1) Some researchers estimate that PTTD may be present in up to 10% of this population. (37) PTTD is typically unilateral- bilateral disease is rare. (1) Common presenting complaints of an irritated (but intact) posterior tibial tendon include insidious onset unilateral pain and swelling along the course of the tendon – most notably behind the medial malleolus. (38-41) Symptoms often begin following an increase in training intensity or duration. (42) Symptoms may be exacerbated by weight bearing activity, particularly, standing tiptoe and walking stairs or on uneven surfaces. (39,43) Loss of arch height and other associated biomechanical deformities may become evident as the condition progresses however, tendon degeneration begins long before physical deformity. (44) Patients who have altered gait may demonstrate abnormal shoe wear. (39) As the condition nears end-stage, patients may describe the feeling that they are walking on the inside of their ankle, and pain may transfer to the lateral ankle due to incursion of the distal fibula and calcaneous. (46)
Clinical evaluation will typically demonstrate tenderness and swelling posterior and inferior to the medial malleolus. (38,43,47-49) A significantly fallen arch with minimal pain and swelling over the posterior tibial tendon could indicate rupture. (50) Patients with PTTD demonstrate hind foot eversion proportionate to the degree of posterior tibialis weakness (48) Isometric strength testing may reproduce pain or weakness during resisted inversion (supination), and/or plantar flexion (43,49,50) Motion assessment may demonstrate a rigid hindfoot valgus deformity in later stages. (47) Clinicians should assess for pain and/or weakness of toe flexion to help differentiate tendinopathies involving the adjacent flexor digitorum longus and flexor hallucis longus.
Clinical evaluation should seek to classify the stage of the disease – collapse of the medial longitudinal arch corresponds to Stage IIA, while excessive forefoot abduction, (“too many toes” sign) signifies progression to Stage IIB. Hindfoot valgus that has progressed from flexible to rigid signifies Stage III. Tenderness below the lateral malleolus from bony incursion is a sign of Stage IV disease.
The single limb heel rise is a sensitive test to detect PTTD. (47,48) The test is performed by allowing the single leg standing patient to balance with one hand on the wall while attempting to rise on the toes of the affected foot for 8-10 repetitions. The inability to complete this test correlates to the degree of PTTD. (1,47)
PTTD is primarily a clinical diagnosis. (53) In general, plain films have little diagnostic value for soft tissue lesions. (53) Nonetheless, radiographs may be needed to exclude other possibilities from the differential diagnosis. Plain films would include weight bearing, AP and lateral views of the foot and ankle. (55) Collapse of the medial longitudinal arch is a classic radiographic finding associated with PTTD. As the disease progresses, films may demonstrate valgus mal-alignment of the talus and sub talar degeneration. (55-57) MRI may better demonstrate soft tissue lesions as well as the sub-tendinous bone marrow edema that often accompanies the condition. (55,57) Diagnostic ultrasound is a useful, low cost alternative for the diagnosis of PTTD. (55,58) Studies have shown that diagnostic ultrasound is only slightly less sensitive than MRI for defining PTTD. (59)
The differential diagnosis for PTTD includes flexor hallucis longus or flexor digitorum longus tendinopathy, posterior impingement, stress fracture, deltoid ligament injury, osteoarthritis, Lisfranc injury, and tarsal tunnel syndrome. (60,61)
Early identification of PTTD is essential to limit progression of the disease. (1) Conditions that advance may ultimately require surgery for the resultant instability, impingement, degeneration, and deformity. (1,3,79) Optimal management is partially dependent upon the stage of the disease. (1) Patients with acute tendon irritation (Stage I) may benefit from anti-inflamatory modalities and NSAIDs. (62-65) NSAIDS may not be a good choice for more chronic “tendinopathies” (66)
Arch supports and orthotics are mainstays of management, but have shown varying degrees of success. (67,68) The intended purpose of orthotics is to correct “flexible” deformities, i.e. maintain the medial arch and correct hind foot position, thus decreasing stress on the posterior tibial tendon. (69,70) Orthotics may help patients in the early stages of PTTD, but may be less beneficial once the foot has lost stability or has developed a rigid deformity. (69) Studies have shown that for unstable feet, orthotics do not consistently improve alignment or gliding resistance of the posterior tibialis. (69,73)
Active rehab should be directed at strengthening the posterior tibialis tendon as well as the peroneals, anterior tibialis, and gastroc/soleus. (84) Specific exercises would include resisted plantar flexion, heel rises, toe walking, inversion and adduction. (84) Strengthening the posterior tibialis via eccentric exercise leads to more rapid improvements in symptoms and function. (80) Stretching of the gastroc/ soleus is appropriate. (84) Exercises should be performed while wearing shoes and arch supports or orthotics. (62,74,75) Soft tissue manipulation and myofascial release should address the posterior tibialis and associated musculature. IASTM may be appropriate to stimulate healing of degenerated tendons.
Conservative care (including stretching, strengthening, modalities, NSAIDS and support ranging from orthotics to a rigid boot) has shown success rates ranging from 67-90%. (81-84) PTTD patients who do not respond to four weeks of conservative care may benefit from a walking cast or cam boot to immobilize the foot. (62,76) Those who have failed four months of conservative care and those with advanced disease (i.e. beyond Stage II, with non-correctable deformity and joint degeneration) may benefit from orthopedic or podiatric referral. (62,77,78)
Children's Health
Attention deficit/Hyperactivity disorder (ADD/ADHD) is defined as a child who is inattentive, impulsive, and hyperactive. Debate in the scientific community exists as to whether ADD/ADHD is due to environmental or genetic factors. Currently there are no diagnostic tests that can conclusively prove the existence of ADD/ADHD. Diagnosis is instead determined by a set number of characteristics.
Once a diagnosis is made based on a set of subjective characteristics, current medical approach to care for a child with ADD/ADHD is drug intervention. Many parents are understandably concerned about potential long-term adverse effects due to an ever-increasing reliance on psychotropic drugs. Harmful side effects can include addiction, nervousness, agitation, anxiety, irritability, depression, insomnia, headaches, growth impairment, weight loss and stomach pains.
Here is where a functional model of care differs. Allopathic medicine looks at the problem as a dysfunction in the genetics. Logically, the approach is to sublimate the shortcomings of the physiology with a drug intervention. Keep in mind, as stated earlier, there is currently no test that can conclusively prove an ADD/ADHD diagnosis. With functional medicine, we always start with the premise that health and vitality are our birth-right. Any shift from optimal is due to our physiological adaptation to a toxic environment, either internal or external. So let’s look at some of the possible factors that can cause a child to express ADD/ADHD symptoms.
Solving the Puzzle
Like most health challenges, the dysfunction is often multi-factorial and far to many factors to cover them all here, but let’s look at some of the more common factors.
First, we have to consider lifestyle. With technology becoming more and more intertwined in our lives, the amount of time kids spend in front of a screen (TV, cell phone, tablet) has risen dramatically. There are two major problems with this.
First, Studies have shown that watching television, tablet, etc. induces brainwave activity to switch from Beta waves, associated with active logical thought, to Alpha waves, associated with relaxed meditative states of suggestibility.
While Alpha waves achieved through meditation are beneficial (they promote relaxation and insight), too much time spent in the low Alpha wave state can cause unfocussed daydreaming and inability to concentrate. In order for the brain’s neural networks to develop normally a child needs specific stimuli from the outside environment that are not found on tablet and TV screens, causing brain development becomes stunted.
Secondly, Today’s tablets and smartphones give children almost constant access to perform a multitude of functions simultaneously. We are training our children’s brain to become accustomed to the fast pace, high stimulation that they don’t get in the real world. Think about your own lives. How often do you feel the need to check your cellphone while waiting in line or on the MRT? Technology is wonderful but it is training our brains to need content stimulated at a fast pace.
Our first recommendation is to limit the time your child spends in front of a screen. The American Academy of Pediatrics recommends that children spend no more than one to two hours a day interacting with screen-based media, such as TV and video games. And the recommendation for children under the age of two is no TV at all. Throughout life, but especially during the developmental years, you need to think of sensory stimulation as food for the brain. If you constantly feed it junk, junk is what you will get. That brings us up to our second factor to consider. Food.
Today’s diet is vastly different than the one our grandparents and even our parents grew up on. We are consuming more sugar in a month than they did in an entire year. To make matters worse, natural sugar cane has been replaced with inexpensive but toxic high fructose corn syrup (HFCS). We are eating meats infused with anti-biotics and estrogen. Preservatives and food coloring are in nearly every packaged food we buy. With the current trend of decreased quality of our food supply, it is not more important than ever to view food as more than just fuel. Food is the building blocks of our structure and function.
Hippocrates, the father of modern medicine stated “All disease begins in the gut”, and that certainly holds true with ADD/ADHD. Most Drugs for depression, generalized anxiety and social phobias alter a hormone called serotonin. They are either known as either SSRI or MAOI. Did you know that the majority of Serotonin (the “feel good hormone”) is made in the gut, not the brain? Serotonin is related to impulse control and aggression and has some cognitive functions, including memory and learning. A recent study conducted at Duke University, suggest that low serotonin levels may be partially responsible for causing attention deficit hyperactivity disorder (ADHD). Although the effect of low serotonin levels in people with ADHD is still not fully understood, research does suggest that there is a direct relationship between serotonin levels and ADHD.
The body makes serotonin by converting the amino acid Tryptophan. This conversion requires B3,B6, folate and iron. serotonin deficit can be brought on by inadequate levels of these B vitamins or iron. Supplementing with a quality B complex, ensuring adequate iron can save your child from a life-long dependency on psychotropic drugs like Ritalin. Brewer’s yeast can provide a natural source of the B’s provided your child does not have a candida infection. Brewer’s yeast is not recommended for any type of fungal infection. In addition it is not recommended to exceed 250mg of B-6 a day and excessive iron can be toxic. Consult a qualified health professional to ensure safety.
Now that we have addressed the hormonal issue, its time to clean up the overall diet. Food additives, such as dyes and/or preservatives, have been implicated in ADD/ADHD. A diet regimen of natural foods, with an emphasis on fresh and unprocessed has been shown to reduce the expression of ADD/ADHD. There are many reports of a beneficial effect from a whole-foods diet, and in particular, a gluten- dairy- and sugar-free diet can induce behavioral improvements. I am always amazed at how we as a society have abandoned the natural law of nature for philosophy of “better living through chemistry”. The truth is that no magic pill will save us, no matter what scientists and doctors tell us. If we want a better expression of health, we need to respect the natural laws of nature. Only through a symbiotic relationship including eating foods as they are found in nature. You will be amazed at how something as basic as changing diet can make a world of difference for your son or daughter.
If you would like more information about proper diet and how to implement it to your busy lifestyle, give our office a call. Eating healthy does not have to be difficult.
We have saved the most important piece for last. The function and development of your childs brain and nervous systm. Researchers found that when they tested ADD/ADHD children against controls, most often they exibit a right brain functional weakness.
The right hemisphere of the brain is responsible for calming thoughts and movement. Children with right brain lag have problems with impulse control, sitting still, decreased ability to pay attention, distractibility, hyperactivity, impulsivity, compulsive behaviors, spatial awareness, especially personal space. They can have difficulty perceiving their effect on people around them, difficulty with “comprehension”, poor timing skills. and poor posture. Problems understanding body language, facial expression and ‘social learning’ or non-verbal communication is commonplace with ADD/ADHD.
These are just some of the more common traits of a right brain developmental lag. The good news is that our brains shows an incredible capacity for neuroplasticity, the ability to develop new information pathways. If the brain is stimulated in a specific way, new neuro-pathways develop and the developmental lag can be corrected. Typically parents and teachers notice improved social behavior, better focus, improved attention span, significant decrease and often cessation of overt impulsivity, improved posture, better self-esteem, more confidence, and better grades. It is often life changing for the child, the parents, and the family as a whole. The care we provide for these children is life changing. It could make the difference between your child expressing his/her full potential or not. Healthy academic, social, and emotional development is crucial for life and it is my goal to help these children maximize their potential. If you would your child to realize his/her full potential, call our office now for a free consultation.
The incidence of autism and autism-like syndromes has been rising ever since its diagnostic creation in the 1940s. Often we are given the explanation that this is due to improvement in diagnostic criteria. While that certainly explains some of the statistical variance, it by no means excludes the fact that its prevalence is on the rise.
The partial explanation for the jump in statistics can be explained by the inclusion in the 1990s. Autism began to be recognized as occurring in a broad spectrum of severity. In 1994, Asperger syndrome was included in the DSM-IV. As of 2006, prevalence estimates for autism spectrum disorders (ASDs) stand one in 166. Autism Spectrum Disorder is actually only one of several developmental disorders that fall under the category of Pervasive Development Disorders (PDD) which is generally thought to include Asperger’s syndrome, Rett’s, Child Distinctive Disorder, PDD-NOS, and Autism Spectrum Disorder (ASD), and while these inclusions into PDD broadened the criteria, they in no way can explain the 10-fold increase since the 1980s.
The problem with the current model of care for children with PDD
The allopathic community offers very little answers when it comes to children on the spectrum of PDD. The current treatment model typically consists of medication and therapy focused on behavioral modification. The fundamental problem here is that PDD is a neuro-developmental dysfunction and therefore needs a neurological approach to treatment.
Our belief, based on the latest research, is that PDD is a result of abnormalities in connections among distributed neural systems. We think that the lack of synchronization between various areas of central nervous system leads to a lack of optimized communication. This lack of optimized activity leads to an under connectivity between brain regions and this result in a functional disconnection syndrome.
Neuroplasticity
Neuroplasticity refers to the brains unique ability to rewire itself and form new connections when exposed to specific and repeated sensory stimuli.
Research has shown that engaging the brain’s plasticity to drive beneficial changes requires exact stimuli delivered in the appropriate sequence with precise timing. The training must be intensive, repetitive, and progressively challenging. Individuals must be strongly engaged in the training, paying close attention.
Treatment must identify and focus on weakness in brain function.
The Behavioral approach has always been to focus on the child’s strengths’ and ignore their weaknesses. That may seem to make sense behaviorally, but neurologically it will only insure the disability gets worse. Examining the patient for specific patterns of muscle weakness and sensory loss can help localize primary dysfunction in brain function. Once this is accomplished, a neuro-specific rehabilitation is implemented to induce neuroplasticity of the dysfunctional regions in the brain.
Additionally, there is a strong correlation between PDD and gastrointestinal problems. Reestablishing proper gut function is a critical part in rehabilitation of the neurological functioning of your child (Please see IBS for detailed explanation)
Sensory based therapies include:
Visual integrated therapy
Light therapy.
Auditory integrated therapy
Breathing exercises
Oxygen therapy
Aerobic exercise.
Nutritional, herbal and homeopathy therapy
Creative visualization
Neuro/biofeedback
Somatosensory stimulation
Interactive metronome
Pervasive Development Disorders (PDD)
any developmental disability, is based upon the Diagnostic and Statistical Manual of Mental Disorders 3 Fourth Edition (DSM3IV),
The diagnosis of autism indicates that qualitative impairments in communication, social skills, and range of interests and activities exist. As no medical tests can be performed to indicate the presence of autism or any other PDD, the diagnosis is based upon the presence or absence of specific behaviors.
Asperger s Disorder
The essential features of Asperger’s Disorder are severe and sustained impairment in social interaction and the development of restricted, repetitive patterns of behavior, interest, and activity.
In contrast to Autistic Disorder, there are no clinically significant delays in language. In addition there are no clinically significant delays in cognitive development or in the development of age-appropriate self-help skills, adaptive behavior, and curiosity about the environment in childhood.
Rett’s Disorder
The essential feature of Rett’s Disorder is the development of multiple specific deficits following a period of normal functioning after birth. There is a loss of previously acquired purposeful hand skills before subsequent development of characteristic hand movement resembling hand wringing or hand washing. Interest in the social environment diminishes in the first few years after the onset of the disorder. There is also significant impairment in expressive and receptive language development with severe psychomotor retardation.
Childhood Disintegrative Disorder
The central feature of Childhood Disintegrative Disorder is a marked regression in multiple areas of functioning following a period of at least two years of apparently normal development. After the first two years of life, the child has a clinically significant loss of previously acquired skills in at least two of the following areas: expressive or receptive language; social skills or adaptive behavior; bowel or bladder control; or play or motor skills. Individuals with this disorder exhibit the social and communicative deficits and behavioral features generally observed in Autistic Disorder, as there is qualitative impairment in social interaction, communication, and restrictive, repetitive and stereotyped patterns of behavior, interests, and activities.
PDD-NOS
The essential features of PDD-NOS are severe and pervasive impairment in the development of reciprocal social interaction or verbal and nonverbal communication skills. The criteria for Autistic Disorder are not met because of late age onset.
Autism Spectrum Disorder
The central features of Autistic Disorder are the presence of markedly abnormal or impaired development in social interaction and communication, and a markedly restricted repertoire of activity and interest. The manifestations of this disorder vary greatly depending on the developmental level and chronological age of the individual.
Women's Health Issues
Thyroid dysfunction are one of the most common and often mishandled problems concerning women’s health. Yes, men can have thyroid problems too but it is far less common. Because the thyroid does so much for proper physiological function, the symptoms of hypothyroid can be very diverse. Below is a list of the more common symptoms you might encounter if your thyroid is not functioning optimally:
- Fatigue, especially in the morning
- Weight gain despite adhering to a low-calorie diet
- Morning headaches that wear off as the day progresses
- Depression
- Constipation
- Hypersensitivity to cold weather
- Poor circulation and numbness in hands and feet
- Muscle cramps while at rest
- Outer third of eyebrow thins
- Slow wound healing
- Excessive amount of sleep required to function properly
- Chronic digestive problems, such as lack of stomach acid (hypochlorhydria)
- Itchy, dry skin
- Increased susceptibility to colds and other viral or bacterial infections and difficulty recovering from them
- Cold often
- High cholesterol
When assessing thyroid function, most allopathic doctors only run two tests; TSH and T4. In reality, that is an extremely inadequate investigation to diagnose a thyroid condition.A thorough examination of the thyroid needs to consider the following: irregular immune function, poor blood sugar control, gut infections, adrenal problems, hormonal imbalances, brain function, gluten sensitivity/intolerance. Any one of those conditions can cause an abnormal TSH and/or T4.
So what should your doctor be checking?
I’m glad you asked. A thorough blood panel for thyroid function would include; fasting blood glucose, TSH, TT4, FTI, FT4, Resin T3 Uptake, FT3, rT3, and TGB. Additionally, if Hashimoto’s disease is suspected (autoimmune disease that attacks the thyroid), a TPO Ab, and possibly a TGB Ab and TSH Ab should be done. Keep in mind that false positives are not uncommon with Ab tests. They will only show positive if you are currently having a autoimmune reaction.
The second thing to consider, when you get your lab results back, do not pay any attention to the lab ranges. They are worthless. Labs ranges are based on pathology, not functionality. Functional rages asses before disease sets in. Secondly, most blood test pathological ranges are simply the average of all the people who have had blood work analyzed by that lab in the last year. Most of whom we can assume are in some degree of poor health. We can also assume that many of them are taking medications which may skew results. Below is a guide to functional ranges for your lab work.
Functional ranges for blood tests:
- Functional fasting blood glucose is 85-100 mg/dL
- Functional TSH 1.8-3.0 uIU/mL
- Functional range Total Thyroxine (T4) (TT4) 6-12 ug/d
- Functional range Free thyroxine index (FTI): 1.2-4.9 mg/dl
- Functional range Free thyroxine (FT4): – 1.0-1.5 ng/dL
- Functional range Resin T3 Uptake: 28-38 md/dl
- Functional range Free thriiodothyroxine (FT3): 300-450 pg/mL
- Functional range Reverse T3 (rT3): 90-350 pg/ml
- Functional range Thyroid-binding globulin (TGB): 18-27 ug/dl
Traditionally, once a thyroid diagnosis is made, the patient will be put on a synthetic thyroid replacement hormone. Here we see a classic example of the major flaw in the allopathic philosophy. Patients typically get the same treatment regardless of the cause of the dysfunction. Would it surprise you to know that there are actually six different classifications of thyroid dysfunction? Only one of which can be effectively managed with hormone replacement therapy. The six classifications are as follows:
- Primary Hypothyroidism
- Hypothyroidism secondary to pituitary hypofunction
- Thyroid under-conversion
- Thyroid over-convesion and decreased TBG
- Thyroid binding globulin elevation
- Thyroid resistance
If you or someone you love either has or is suspected of having a thyroid dysfunction, you owe it to yourself to have a thorough examination and customized treatment plan. Call our office today and get the treatment you deserve.
Definitions of Thyroid Blood Panal
TSH (Thyrotropin)
- released by pituitary gland. Most common and sensitive marker of thyroid function. TSH increases when T4 drops and decreases when it rises.
Total Thyroxine (TT4):
- TT4 test measures both bound and unbound T4. Does not give an idea of how active T4 is, unless other markers are included, such as T3 uptake. T3 uptake indicates how much thyroid hormone is entering the cells. Total T4 can be altered by many drugs.
Free Thyroxine index (FTI)
- Measured by multiplying TT4 levels by the T3 uptake and determines how much active T4 is available. If TT4 is depressed, then T3 uptake is high; if the TT4 is high, then resin uptake is low. Even when drugs impact thyroid binding, the free thyroxine index should be within normal range if thyroid is functioning properly.
Free Thyroxine (FT4)
- measures amount of free, or active T4 in the blood. Factors that affect TT4 will not impact FT4. Free T4 is high with hyperthyroidism and low with hypothyroidism. Even a high TSH with normal T4 is enough to identify hypothyroidism. High T4 can be caused by taking heparin, acute illness, hereditary thyroid resistance. Low FT4 can be chronic or severe illness other than thyroid disease.
Resin T3 uptake
- measures the number of sites for active or unbound T3 to bind with proteins. The more binding sites open on the proteins, the lower the resin uptake result will be. Anything that reduces the binding sites, such as elevated testosterone or testosterone replacement therapy, can cause a low T4, because it leaves very few binding sites for thyroid hormone. Anything that raises the binding sites, such as estrogen or birth control pills, would cause a pattern of high total T4 and low T3 uptake.
Free Triiodothyroxine (FT3)
- measures free T3 hormone, and is best marker for measuring active thyroid hormones available to thyroid receptor sites.
Reverse T3 (rT3)
- measures the amount of reverse T3 that is produced. rT3 typically takes place in cases of extreme stress, such as major trauma, surgery, or severe chronic stress. It appears the increased production of T3 is due to an inability to clear rT3, as well as from elevated levels of cortisol.
Thyroid-Binding Globulin (TGB)
- measures the amount of proteins in the blood that transport thyroid hormones to the cells. Elevated testosterone can lower TBG levels, while elevated estrogen can raise TBG, both of which produce hypothyroid symptoms.
menstrual problems
30% to 50% of all women suffer pain, discomfort or dysregulation with menstruation. Symptoms can include:
Menstrual cramps Dysmenorrhea
Amenorrhea Heavy flow
Inability to get or stay pregnant
Loss of libido
Headaches Irritability
Mood swings Depression
Weight gain
The most common cause of menstrual dysregulation is unbalanced estrogen-progesterone levels. Current medical intervention would be to simply supplement with the deficient hormone in hope that this will restore function, without ever investigation the underlying cause of the dysfunction. Putting aside the obvious concerns of long term synthetic hormone use, by not addressing and correcting the underlying cause, you are setting yourself up for problems later in life.
Thyroid, cortisol, estrogen dominance, liver function and blood sugar all play critical roles in proper sex-hormone production. For example, many cosmetics on the market today contain dangerous endocrine disruptors called phthalates (pronounced THA-lates) can interfere with hormones in the body. To learn more about your exposure to phthalates or other toxicity in your cosmetics, visit the non-profit watchdog group the Environmental Group www.ewg.org Here you can research the toxicity of everyday products as well as the potential harm it may be doing to you and your family.
The number of contributing factors to hormone dysregulation are far to great to list them all here. For example, the inability to keep blood sugar stable will weakens and inflames the digestive tract as well as the immune barriers of the gut, lungs and brain. This drives the adrenal glands into exhaustion and sets the stage for hormonal imbalances (premenstrual syndrome, polycystic ovary syndrome, or a miserable transition into menopause). The take-away message is, before you decide to go on HRT or think menstrual problems are simply the cost of being a woman, give us a call. You don’t have to suffer any longer.
Osteoporosis
One out of every two women and one in eight men over the age of 50 will have an osteoporosis related fracture in their lifetime. After age 65 90% of all fractures have be shown to be caused by osteoporosis.
Osteoporosis is a condition that exists when the loss of bone over time has caused a dramatic weakening of the skeleton. Many people don’t realize that bone is living tissue made of Calcium and is constantly changing. They perform tasks that are critical to the functioning of the rest of the body, such as the manufacture of blood and the storage of nutrients, and the bones themselves are constantly being taken apart and rebuilt in a process called remodeling. Remodeling is when old bone is broken down and replaced with new bone. It is kind of a preventive- maintenance program that is vital for the day-to- day strength of our skeletons. The entire bone remodeling process is under the control of the central nervous system.
There are several factors that contribute to osteoporosis: abnormal biomechanical or structural stress, chemical stress such as insulin resistance due to high carbohydrate diet, mental/emotional stress and neurological stress. For example, your bones serve as the largest storage of alkalizing mineral (Calcium) in the body. When insufficient levels of these minerals exist in the bloodstream, for example to buffer an over acidic environment due to diet and stress, the body takes action by withdrawing calcium from the bones to buffer the blood.
Other common causes include eating dairy, deficiency in essential fatty acids (Omega-3) Magnesium or Vitamin D, high cortisol level due to stress, improper biomechanical movement patters, lack of weight bearing exercise, and insulin resistance causing the liver to produce less insulin like growth factor IgF, responsible for new bone growth. Osteoporosis is primarily a hormone or pH issue, not a calcium deficiency issue.
Prenatal
Scientists now know that maternal stress during pregnancy can have negative effects on the development of her child. During stress, hormones are released into the blood. These stress hormones have the ability to pass through the placenta causing the fetus to sense a mother’s stress. Statistics show that mothers of children with autism reported significantly higher stressors during their pregnancies. Four independent studies found associations between a mother’s stress level around the time of pregnancy and the development of social and emotional problems during childhood.
One study that followed children born to 2,900 women showed that maternal stress during pregnancy significantly correlated with the development of autism or ADHD by age 2.
Another study involving more than 3,000 mothers who completed anxiety and depression questionnaires at approximately 26 weeks of pregnancy were predictive of premature birth and low birth weight, which are risk factors for autism and other health conditions.
When we think of stress, most of us think of mental/emotional stress. While mental/emotional stress should not be ignored, it is important to consider other forms of stress as well. These may include postural and other biomechanical stressors, maternal nutritional and toxicity status (pre-natal vitamins should begin 2 months prior to conception), exposure to drugs, maternal overall health, and maternal psychosocial stress.
The importance of the prenatal environment to brain development cannot be stressed enough. A proper evaluation and correction of as many stressors as possible will not only improve the chances of robust development of the fetus, but improve outcomes during delivery.
As a quick side note, once your baby has come in to this world, it is important that you not clamp and cut the umbilical cord before it has stopped pulsing. The common practice of clamping the cord before the placenta has finished delivering life giving blood, immune and stem cells to your baby is simply for convenience purposes. Studies have shown that a delay in clamping the cord can add as much as 32% increase in blood volume to the baby, increased hemoglobin and iron stores.
As a new mother, your child is depending on you to be the guardian of his/her health. Giving your child every opportunity to thrive in life begins before the child is even born. Natural healthcare just makes sense in being a part of the plan.
Postpartum depression
Becoming a new mother should be one of the happiest times for a woman, yet approximately 15% of women will suffer from some form of postpartum depression. Like most health conditions, the contributing factor is rarely due to one cause, Adrenal fatigue is a strong suspect in the condition.
When an expectant mother is suffering from adrenal exhaustion, during her third trimester, she will begin to depend on her baby for adrenal hormones. Once the baby is born, the hormones that she depended on have been suddenly taken away. This causes a “withdrawal” like symptom in the mother and often leaves the new-born baby with run down adrenal. Supporting adrenal function while rebuilding the gland as well as removing chronic stress will often times be a miracle for these mothers. At the same time, it is critical to assess and address the baby’s adrenals as well.
For more information on adrenal fatigue, please click here.
Menopause
Many women are fortunate enough to go through menopause with few problems. Other are not so fortunate. The symptoms of perimenopause and menopause can exaggerate PMS problems, along with irregular menstrual cycles, more irritability, anxiety, depression, bloating, food cravings, and breast tenderness. Menopausal symptoms are caused by erratic estrogen dominance as the body’s supply of progesterone declines and by hormonal output alternately stopping and starting. Symptoms include memory loss, irritability, depression, water retention, and weight gain. Vaginal walls become drier and thinner and sexual interest may decline or increase. This is accompanied by increased susceptibility to yeast and bacterial infections, fibrocystic breasts, breast cancer, fibroids, or endometrial cancer. Sugar, alcohol, smoking, coffee and tea consumption can worsen symptoms. Becoming well informed about helpful lifestyle changes, a natural whole foods diet, nutritional supplements, and regular exercise can help maintain female health.
Typically, the ovaries make about 85% of a woman’s sex hormones and the adrenal glands make up the other 15%. During menopause, the adrenal glands take over secondary hormone production. In the event that a woman is suffering from adrenal exhaustion due to chronic stress, her adrenal glands cannot take up the extra work, causing the typical symptoms that are associated with menopause. In these women, restoring proper adrenal function as well as removing the chronic stress becomes critical to alleviating her symptoms. The fact is that in a properly functioning body, menopause should be asymptomatic.
Digenstive Issues
If you suffer from heartburn or acid reflux, a solution may be easier than you think.
The biggest misconception of heartburn sufferers is that they are producing too much stomach acid (HCl) and need to counteract this betrayal of the body with some “purple pill” or one of its cousins. The idea of continuously taking a pill for symptom relief and thinking you have solved the problem is like hanging up on the bill collector and expecting your finances to be ok. Sooner or later the bill always comes due.
Lets first consider the reality of HCl production. It peaks in our mid 20s and slowly declines thereafter. This decline is accelerated if we have spent decades consuming a typical Western diet of processed, refined and hard to digest foods. The body does its best to breakdown these products but will eventually burn out, much like your car will burn out if you keep the RPMs in the red. The reduced production in stomach acids compounded by years of poor eating habits cause a deficiency in the nutrients necessary for adequate digestion. With low stomach acid you will always suffer from indigestion like burning, gas, bloating, diarrhea and constipation because your stomach cannot breakdown foods.
One of the easiest ways to address heartburn is by first making sure that your body has the nutrients necessary to make stomach acids. Stomach acids play a vital role in your body’s physiology. The primary role of hydrochloric acid is not digestion, but to kill any parasites and such that you may have ingested with your food. In addition, stomach acid stimulates pancreas function. If you are taking an antacid, you are inadvertently suppressing your body’s natural process. All this sets up an environment for infection, allergies, weight gain, colitis and a host of other illnesses that always accompany a strategy of fighting the body’s innate intelligence for control.
Celery strengthens hydrochloric acid in the gut and provides mineral salts to the CNS. On an empty stomach, drink a 16-ounce glass of freshly pressed celery juice for 3 weeks. You need to drink it straight while you still have an empty stomach. Drink the juice immediately, before it can oxidize, which reduces its effectiveness. This works because celery contains unique sodium compositions, and these mineral salts are bonded with many bioactive trace minerals and nutrients. Over time, the mineral salts, minerals, and nutrients have the ability to completely restore your stomach’s hydrochloric acid production.
While you are restoring your ability to make stomach acids, pay attention to your food combinations. What most people do not realize is that starches and proteins breakdown at different rates, so while your carbohydrates have been fully digested, they sit in your stomach waiting for the protein to breakdown. This causes the carbohydrates to begin to ferment in your stomach producing gasses which irritate the stomach lining causing heartburn, reflux and gastric ulcers to name a few. If you are thinking your problem is too much stomach acids, the logical thing to do is reach for your Mylanta, Tums or Rolaids for relief, never realizing the problem is actually not enough digestive enzymes including hydrochloric acid (stomach acid). This endless suppression of the body’s natural process eventually takes a significant toll on your health.
Divide up your food groups. Start by splitting up starches and proteins. Stop eating meat, chicken, fish, eggs or beans with potatoes, rice, breads or pasta. Vegetables can be eaten with either choice of food, and not only make an excellent accompaniment, but are also full of vitamins and minerals. Another thing to consider is the fact that all raw foods naturally contain enzymes necessary for digestion. These enzymes are essentially destroyed at 118 degrees Fahrenheit, so if you are suffering from any form of indigestion raw is better. Consider a colorful salad to get more of these highly valuable digestive enzymes into your diet. In addition, you will feel better, lose weight and get better control over your blood sugar.
A word of caution to the reader, there are many more things to consider when dealing with digestive issues; peptic ulcers, ileocecal valve, hiatal hernia, to name just a few. The main point you should take away from this article is the philosophy of addressing the cause, not the symptom.
Peptic ulcers can easily be mistaken for heartburn. An easy way to distinguish if you have peptic ulcers is to by drinking apple cider vinegar on an empty stomach. If it causes irritation, it is suggestive of a compromised integrity of the stomach lining.
Hiatal hernia and ileocecal valve are also issues that can be easily fixed by a doctor trained in these techniques. Please download my hiatal hernia quick fix If you suspect a hiatal hernia is causing your symptoms. If it is not severe enough, fixing it without medical help, is possible. If you get relief from this technique but it is only temporary or your relief is only partial, seek professional help. Hippocrates, the father of modern medicine said “All disease begins in the gut”. Your gut makes up 80% of your total immune function and is the gateway to health. Without a properly functioning gut, immune function will be compromised leaving you susceptible to wide variety of health problems.
Allergies and toxic Sensitivities
Just 50 years ago, one person in thirty suffered from allergies. Today that number skyrocketed to one in three. Widespread air pollution, global warming causing longer pollen seasons, tobacco smoke, toxic chemicals, dust, processed food such as trans fats, GMOs, refined carbohydrates and sugar, and an out-of-balance internal ecology of microbes—are all contributing to the rise of allergies.
Research shows that allergies are often the cause of seemingly unrelated symptoms and can produce a wide range of common symptoms that are not ordinarily thought of as allergic; weight gain, chronic fatigue syndrome, depression, anxiety, depression muscle aches, joint pain, fibromyalgia, headaches, brain fog, attention deficit disorder, insomnia, stomachaches, bloating, constipation, diarrhea or irritable bowel syndrome.
Conventional medicine look at allergies as symptoms that get treated with drugs. If you suffer from allergies, you are probably familiar with the antihistamines, steroids, bronchodilators, and immune suppressants that are most often used to control symptoms. Unfortunate there is no such thing as a safe drug, these drugs come with side effects that range from fatigue, leaky gut, depression, impairment of immunity, and more. Instead of suppressing symptoms with drugs, the holistic approach seeks to discover the root causes of your allergies and strengthen the body, thereby restoring its natural function, not just suppressing symptoms. It is your body’s ability to deal with the allergen that is the key. It is not the allergen that is at fault, it is an inappropriate reaction of the immune system that involves the whole body.
Allergies, toxins and body pollution needs to be considered together. Food, airborne pollutants, and contact substances can easily overwhelm our bodies defenses. Breakdown in any one of the body’s elimination systems; skin, lungs, intestinal or urinary tract can trigger an allergic response from the nervous system. Restoring balance requires identifying and eliminating the irritant as well as rebuilding our body’s defense system. A diagnosis of an allergen based solely on a skin scratch test, which is the one most widely accepted by the traditional allergists, can be misleading because skin scratch test only evaluates for IgE mediated allergies. Only 25-30% of allergies are IgE mediated. There are multiple mechanisms of allergic reaction and the available tests measure only one mechanism. They do not consider IgA, IgG or cell mediated immune responses which may occurring up to 48 hours or more after exposure to the triggering allergen. All testing methods appear to have their limitations. Any test should be viewed simply as a piece of a complex puzzle; it is from a combination patient’s history, physical signs, symptoms and various test results – that the diagnosis is made.
The applied kinesiology approach to allergy and hypersensitivity is to identify items to which the patient is allergic or sensitive by how the nervous system reacts, as observed by its control of muscles evaluated by manual muscle testing. Kinesiology is the art and science of movement of the human body. Kinesiology is used to compare the strength and weakness of any muscle of the body in the presence and absence of any substance. A measured weakness in the presence of a substance is due to the effect of an allergy to the item the person is touching. This simple method can be used to detect your allergens.
While every patient is unique, and every case different, there are some common strategies to employ with allergies. We begin with considering the three factors we mentioned earlier; Food, airborne pollutants, and contact substances. Using kinesiological testing, we can narrow this field down considerably.
The most common airborne pollutants are mold and dust. Dust and mold is an excellent first step in detoxifying your personal space and protecting yourself from these major allergens. Dust mites are responsible for most of our allergies to dust. In other words, dust allergy is primarily an allergic reaction to the waste products and bodies of dust mites. What’s more, mites contain toxic enzymes that directly damage your respiratory lining, allowing increased penetration of airborne irritants and allergens. To catch the mites most effectively, use a vacuum with “a HEPA filter. A regular vacuum could simply blow the dust mites around the room. Get mite proof covers for your mattress, pillows, and comforter. At least once a week, launder all of your bedding in hot water to kill the dust mites. Keep the relative humidity in your home and workplace low and adding plants for filtering the air can go along way to keeping the air in your home allergen free.
An article in the journal Allergy, Asthma & Immunology Research. More than 100,000 new chemicals have been introduced into the environment in the past few decades. These chemicals commonly interfere with female and male hormones. Endocrine (hormone) disrupting chemicals are found in common everyday household products such as detergents and dryer sheets, all purpose cleaners, plastic bottles, metal food can liners, cosmetics, and more. To learn more about your toxic exposure to some of the products you are using, visit the Environmental Working Group (EWG) website. EWG is a non-profit organization, dedicated to informing the public about the dangers of hidden toxins in the products we use every day. They have a database of over 70,000 products that have been evaluated for endocrine disruptors, carcinogens (cancer causing) and overall toxic load. Their website is https://www.ewg.org/
Instead of reaching for a bottle of toxic chemicals to clean your kitchen, you can easily and cheaply make your own by using water and a few non toxic substances found in the kitchen. A few of the more common ones are baking soda, borax or vinegar. A few tablespoons mixed with water will provide an effective non-toxic solution for your cleaning needs.
Next, get into the habit of simply remove shoes when entering the home. According to a research study from the University of Arizona, shoes are commonly contaminated with large amounts of bacteria, including coliforms and Escherichia coli, indicating contact with fecal matter. Spreading these substances around the home is simply adding to the toxic burden your nervous system must combat.
And now to address the third and most complex of the three, the foods we eat. A nutrient-dense, whole-foods diet, rich in a variety of vegetables and fruits, has been shown to prevent or reverse allergy by improving immune function and antioxidant status. Unfortunately its not as simple as taking a handful of vitamins or increasing your intake of fruits and veggies.
In 1969, Dr. George Goodheart developed an approach to dealing with allergies in applied kinesiology by improving hydrochloric acid and calcium balance in the body. The value of calcium therapy for allergies was discredited because laboratory blood tests reveled no abnormal levels for calcium. Goodheard hypothesized that this was probably because the body’s compensatory mechanism takes over by leaching calcium from bones.
The first step in handling food based allergies is to address adequate stomach acids. A deficiency in stomach acids will not allow proper breakdown of food particles, leaving the intestines vulnerable to an immune response. In addition, stomach acids are responsible for stimulating the pancreas to release protein digesting enzymes. Thus, the loss of stomach acids further short circuits the digestive process. Finally, in addition to being a key component of food digestion, stomach acids have a vital role in killing pathogens that have been ingested. So the loss of stomach acids opens the door to infection and leaky gut.
The number one reason for a deficiency of hydrochloric acid is adrenaline. To address stomach acid loss without a careful evaluation as to the cause would just be like bailing water out of a boat with a hole in it. It will provide some relief but that relief is short-lived.
A quick and easy test to see if you are possibly not producing enough stomach acids is the “Baking Soda Test”: First thing in the morning on an empty stomach, add 1 tablespoon of baking soda in water and drink. Burping in under 3 minutes suggests you have enough HCl. If after 5 minutes, it may suggest you have decreased HCl levels.
Restoring HCl has been described in other sections of this website, As a quick review, barley grass juice extract powder, Papayas and celery will all strengthen the production of HCl.
Finally, allergy occurs when the part of your immune system that controls unwanted immune responses fails to function properly. It is actually an immune deficiency state that results in excessive inflammation. Many patients have received dramatic relief from allergies by spinal adjustments designed to improve neurologic function. These, along with other structural corrections done in applied kinesiology, are the basic and first approaches to treatment for allergic and hypersensitive reactions.
We have only scratched the surface of the complex topic concerning allergy elimination. If you or someone you love are suffering from allergies, there is hope. You don’t need to suffer any longer. Start by reducing your toxic load, addressing dietary issues and restoring gut function. If this does not provide relief, find a qualified functional medicine doctor that is trained in restoring proper function of the body, and get your life back.