terça-feira, 2 de junho de 2015

Principles of Manual Therapy -- Russian School

By Andrei Pikalov
Having been in the United States and worked with chiropractors for almost a year, I have found them very interested in the principles and practice of the Russian schools of manual therapy (MT). 
I hope to start a number of articles describing the achievements of Russian doctors in this field, to share this exciting information and to help further develop the chiropractic science through international contacts. With such cooperation, the health of our patients will improve.
Russian doctors who practice manipulative treatment (manipulative therapy -- MT) refer to their field as manual medicine (MM), and define it as "the system of manual diagnostic and treatment methods directed to the detection and treatment of disturbances of activity of the locomotor apparatus, which are manifested by functional joint blocks, hypermobility and regional postural imbalance."
The basic principle of MM is the use of exact nosology to determine indications/contraindications for MT and the treatment method of choice. Manual therapists (MT) use well known diagnostic methods such as clinical and paraclinical evaluations, x-ray, etc., but they put special emphasis on uncovering pathobiomechanical disturbances of the locomotor system and use special methods of manual examination to achieve this aim. Diagnosis could be based upon anamnesis, patient's complaints, static and motion palpations, or passive range of motion tests. MTs, along with chiropractors, accept the complexity of diagnostic and treatment procedures for joints using MT arises from the structure of these joints. MM accepts the following classification of joints:
1. number of joint surfaces: 
  • ordinary (simple)
  • compound (multiple)
  • complex
  • combined

2. form of joint surfaces: 
  • spherical
  • elliptical
  • block-shaped
  • condylar
  • cylindrical
  • saddle-shaped
  • flat

3. number of axes which determine the function of the joint: 
  • one
  • two
  • polyaxis1

Another basic principle of MM states that the development of a pathological process in the joint shouldn't be considered separately from the entire locomotor system (including vertebral column and muscular system); that MTs should extract from a clinical picture of certain diseases (such as spondylosis, degenerative joint disease, arthrosis, periarthrosis, etc.) the pathobiomechanical evidence of functional blockage, local hypermobility, myodystony, myodystrophia, regional postural imbalance of musculature, dysfunctions of posture and movement.2
According to the Russian School of MM, functional blockage is the basic evidence of locomotor system pathology. Functional blockage is a reversible restriction of joint motion connected with reflex changes of the joint ligaments and muscles, and limited by both extra- and intra-articular joint processes. The reasons for functional joint blockages are different, but they are first of all connected with overload or inadequate joint load; microtrauma; forced hypodynamia; somatosomatic and viscerosomatic reflexes; and dystrophic/degenerative joint diseases. The joint may also be in the state of hypermobility (reversible increase in motion volume which is connected with a lack of supportive [myofixational] structures).
Disturbed motion at the vertebral motion segments (VMS) can be either a restriction or an increase. Both are candidates for MT, but each demands a different treatment procedure.
Not all hypermobility equals functional disturbance. There are people who have stretched joint capsules and ligaments due to their constitution, and their motion is greater than the physiological average, yet they don't present any complaint. Similar increases in joint motion can be seen in artists, gymnasts, or acrobats who have increased their ranges of motion considerably through training.
Hormonal changes during pregnancy can also loosen the joint capsule and ligaments, and may lead to pathological hypermobility and other neuromuscular disorders.
General hypermobility is conducive to muscular dysfunctions and functional blockages and influences methods of treatment chosen for MT. The local pathological hypermobility could be caused by decompensation or general hypermobility, local overloads, traumas or degenerative changes. MTs believe that the human muscular system specifically reacts by adapting to external conditions, and especially through the development of bone, joint, and ligament pathology: tonus-and-force relationships between tonic and phasic muscles are changeable (tonic are shortened and phasic are lengthened). This process supports the formation of specific postural syndromes such as cervical hyperlordosis, oblique pelvis, hyperabduction, etc.
Thus, functional joint blockage, hypermobility, and muscular dysfunction (regional postural muscular imbalance) can be determined by specific MM diagnostic procedures.
MM follows a certain treatment protocol: relaxation (general and regional), mobilization, manipulation.
Relaxation (general and regional) provides the opportunity to perform manipulations directed to the elimination of functional blockages. The aim of relaxation is to loosen spasmotic muscles; this is accomplished through massage (point massage, segmental massage, classical massage, shiatsu, etc.). General relaxation is reached with the patient's adaptation to the treatment circumstances and good psychological contact between the patient and the doctor.
Mobilization is a hands-on treatment directed to the restitution of normal ranges of joint motion that have been reduced due to functional blockages or spasmotic, shortened muscles. Mobilization includes repetitive, rhythmic movements of certain body parts through the passive range.2 Mobilization is performed by traction which varies in level of force used: 1) minimal, which the pressure of joint surfaces became zero; 2) continuous, without disturbance of elastic structures; 3) and stretching of elastic structures up to physiological limits.3
Mobilization consists of repetitive movements that constantly increase in volume on the side of restricted motion. Mobilization by pressure is performed by the contact finger (spots bone or hypothenar) pressure to restore normal range of motion.
Mobilization is performed slowly during the expiration phase of breathing (5-10 respiratory cycles). Mobilization can be both specific (application) to one concreate joint in one direction) and nonspecific (influence several joints at the same time).
Manipulation influences the joint with a short, quick thrust directed to the immediate elimination of functional blockage. Manipulation is performed as a thrust or traction thrust, and it is specific. Conditions for the fulfillment of manipulation are the same as for mobilization, but the difference is in the low amplitude, single, and rapid movement. The MT will recommend to the patient to rest for two to three hours after the procedure and may recommend immobilization of the joint for one-two days.
References 
  1. Barvinchenko AA. Atlas of Manual Medicine. Moscow, Voenizdat, 1992.

  2. Kogan OG, Naidin VL. Medical Rehabilitation in Neurology and Neurosurgery. Moscow, Medicine, 1988.

  3. Schneider W, Dvorak J, Dvorak V, Tritschler T. Manuelle Medizin Therapie. Georg Thieme Verlag Stuttgart, New York, 1986.
    Acknowledgement
    The author wishes to thank Ms. Ashley Cleveland for her invaluable assistance with manuscript preparation.

Manipulative Vascular Accidents in Proper Perspective, Part I

By Brad McKechnie, DC, DACAN
To properly engage in a discussion of the risks associated with cervical manipulation, risks associated with other medical procedures and drug regimens must also be investigated. The following is a review of literature pertaining to morbidity and mortality related to medical procedures and drug regimens.
Stremple et al.,1 studied postoperative morbidity and mortality rates in the Veterans' Administration hospital system for a variety of diagnoses between 1987 and 1988. The list compiled by the authors contained only those surgical procedures for which there was a legitimate presumption that the patient's death was related to the procedure performed. 
  • There were 428 small intestine surgeries performed during the year-long study period; 90 patients died from the surgical procedure or from postsurgical complications. The risk of dying from small intestine surgery was 21.03 percent (1 in 4.76).

  • There were 4,493 colon surgeries performed during the same period; 330 patients died (1 in 14).

  • The VA system performed 2,056 appendectomies between 1987 and 1988; 28 patients died from the surgery, a mortality rate of 1.36 percent (1 in 74).

  • The VA system performed 7,112 cholecystectomies; 139 deaths resulting from the procedures. These results placed the mortality rate for cholecystectomy in the VA system at 1.95 percent (1 in 51).

  • Steiner studied the operative mortality rate for cholecystectomy in Maryland and found that there was a 1 in 200 risk of mortality associated with this procedure.7

Brennan et al.,2 reviewed 30,121 randomly selected, acute care, nonpsychiatric hospital records from 51 New York State hospitals in 1984. They found that adverse events occurred in 3.7 percent of all hospitalizations with 27.6 percent of adverse events due to negligence. Additionally, 70.5 percent of the adverse events gave rise to disability lasting less than six months, 2.6 caused permanently disabling injuries, and 13.6 led to death. The authors concluded that "there is substantial amount of injury to patients from medical management and many injuries are the result of substandard care." The 3.7 percent adverse event occurrence rate indicates that there were 1,114 adverse events taking place in the hospitals studied during the year-long research period. As discussed above, 13.6 percent of the adverse events resulted in death, which equates to 151 deaths in the study period. This places the death rate associated with the 51 randomly selected facilities in New York at 0.5 percent or 1 in 200!
Iatrogenic Esophageal Perforation
In a series of 21 patients with iatrogenic perforations of the esophagus there was an overall mortality rate of 28.6 percent. Perforations of the esophagus were the result of hiatal surgical procedures, following diagnostic endoscopy, endoscopic dilation for achalasia, and foreign bodies.3
Idiopathic Scoliosis Surgery
Sponseller et al,4 studied the outcome of surgical treatment for idiopathic scoliosis in 46 adults over 25 years of age. They found that 18 adults (40 percent) had a minor complication from the surgery and 20 percent had a major complication such as pulmonary embolus, psuedoarthrosis, deep infection, or major re-operation. There was one death due to pulmonary embolus out of the 46 patients studied.
Pulmonary Embolism
Hospitalized patients are at increased risk for developing deep venous thrombosis and subsequent pulmonary embolism. According to King21, these problems have been found to be the most common preventable causes of morbidity and mortality in hospitalized patients. Data from autopsy studies indicate that pulmonary embolism is responsible for 50,000 to 100,000 deaths in hospitalized patients each year.
Iatrogenic Illness
Bedell et al., studied the incidence of iatrogenic cardiac arrests among patients hospitalized in 1981 at a university teaching hospital. During this one year study, there were 203 cardiac arrests in which resuscitation was attempted; 28 of the 203 cardiac arrests resulting in iatrogenic complications. Iatrogenic complications were considered to be errors in the use of medications, complications of procedures, or suboptimal response by physicians to emergent clinical symptoms and signs. Seventeen of the 28 iatrogenic cardiac arrest patients died.5
Steel et al., found that 36 percent (1 in 2.78) of 815 consecutive patients on a general medical service of a university-based hospital experienced an iatrogenic illness. In two percent of the series (16 patients), the iatrogenic illness produced death.16
Stambouly and Pollack13 evaluated 541 consecutive admissions to a pediatric intensive care unit and found that 4.6 percent (25 admissions) were due to iatrogenic illnesses. Drug-induced conditions accounted for 32 percent of the iatrogenic illness admissions. Complications of medical-surgical acts were responsible for 68 percent of the admissions. The mortality rate in this study for death from iatrogenic events was 1 in 27. A breakdown of the iatrogenic medical-surgical admissions revealed that four patients developed postoperative complications after tonsillectomies and adenoidectomies; one child with congenital heart disease was admitted to the pediatric intensive care unit following inadvertent laceration of the internal carotid artery during internal jugular venous cannulation prior to surgery; one neonate required closure of a deep laceration which occurred during Cesarean section delivery; and two patients developed cardiac arrests following cardiac catheterization with one patient dying as a result of the procedure.13
Trunet et al.,12 prospectively studied all patients admitted to a multidisciplinary intensive care unit to determine how many of the admissions were iatrogenic. Of the 325 patients admitted during the year, 12.6 percent (41 patients) were hospitalized because of iatrogenic disease. The breakdown of the nature of the iatrogenic errors revealed that 23 admissions were due to drug administrations, nine were due to adverse drug reactions, and 14 were due to therapeutic errors. In addition, iatrogenic disease was fatal in the case of eight patients (20 percent).
Coronary Arteriography
A multihospital survey of the complications of coronary arteriography revealed an overall mortality rate of 0.45 percent (1 in 222). The mortality rate in hospitals that performed less than 100 examinations per year was eight times higher than for those institutions performing more than 400 examinations per year.11
Lumbar Surgical Risks
The Veterans Administration hospital system1 performed 3,868 laminectomies between 1987 and 1988. Nineteen patients died from these procedures, placing the mortality rate for laminectomies performed within the VA system at 0.49 percent (1 in 204). Additionally, there were 1,643 spinal fusions performed in the VA system during the same year. Twenty-five patients died as the result of the spinal fusion procedures performed. The mortality rate associated with this procedure in the VA system was 1.95 percent (1 in 51). In one study by Oppel, there were nine intra-operative deaths and eight postoperative deaths as the result of 3,038 lumbar spine operations conducted by 15 teams of surgeons in Austria and Germany, leading to a total mortality rate of 0.5 percent (1 in 200). In another study of 2,504 lumbar spine operations for sciatica there was a mortality rate of 1.2 percent (1 in 83) documented.9
Stolkes et al.,10 prospectively studied 412 primary and 69 re-operations for herniated lumbar discs, and compiled a list of intra-operative and postoperative complications. In their study, one patient died from postoperative complications, placing the mortality rate in their series at 1 in 481. Deyo8 examined the rates of postoperative complications and mortality, as recorded in a hospital discharge registry for the state of Washington (1986-1988), for patients who had an operation on the lumbar spine. Patients with malignant lesions, fractures, or infection were excluded from the study. During the study period there were 18,122 hospitalizations for procedures relating to the lumbar spine with 84 percent involving a herniated disc or stenosis. The overall mortality rate for the study period was 0.07 percent (1 in 1,430).

Manipulative Therapy of Cervical Spine and Cerebral Blood Flow

Study Proposal

By Andrei Pikalov
The neck conveys vital structures from and to the head and trunk. It enables the head to be placed in a position to receive from the environment all information other than that provided by touch. 
The function of the cervical vertebrae is very important in supporting the head and its weight (approximately 7 kg.). The cervical spine is completely encircled by intricate layers of muscles that perform the complex function of controlled movement and stabilization of the cervical spine. The neck carries elements of the autonomous nervous system which take part in the activity of internal organs.11
The cervical spine, as a highly loaded part of a human's vertebrae, is subject to different disorders, and most of them are connected with the patient's age. At the same time, morphological, structural, and dystrophic alterations of the cervical spine may promote different disturbances of the vertebral arterial circulation and sympathetic innervation.1
Spano (1982) suggests that any morphological and structural alteration of the cervical spine may lead to stenosis or substenosis of the vertebral arterial circulation and hence to brain stem anoxia.1 These problems arise from a common malady of mankind -- cervical spondylosis (which is a general term indicating restrictive changes in the vertebral bodies about the interspace, usually associated with chronic discopathy).
The physiologic degenerative aging process, as elsewhere, occurs in the cartilaginous and ligamentous structures of the cervical spine. The process is especially accentuated by the repeated stress and strains imposed by this very mobile structure.11 Cervical disc degeneration (cervical spondylosis) may occur and may remain asymptomatic. It may give rise to local pain or it may give rise to both local and referred pain from posterior joint strains, resulting from spinal instability. It may lead to the production of a neurocentral osteophyte, causing root irritation or impairment of root conduction. Certain symptoms may arise from irritation of the sympathetic plexus around the vertebral artery, and on occasion, symptoms may be related to obstruction of a vertebrae itself by neurocentral osteophyte.9 As it is known from anatomy and physiological features of the cervical sympathetic trunk, the larynx, heart, lungs, and bronchi are likely to be affected in the event of stimulation or irritation of the preganglionic fibers of the sympathetic nervous system following static or dynamic alterations of the cervical spine.1 Consequently, we have to consider two main complications of cervical spondylosis: the influence on cervical blood flow and the influence on the sympathetic nervous system.
The brain receives blood supply from a.carotis and a.vertebralis systems. Each vertebral artery arises in the supraclavicular space from the subclavian artery and ascends in a bony canal in the cervical vertebrae to enter the skull through the foramen magnum. There, each gives off into the posterior cerebellar artery and the anterior and posterior spinal arteries. At the ponomedullary junction, the two vertebral arteries join to form the basilar artery. The vertebrobasilar system normally nourishes the cervical cord, brain stem, cerebellum, thalamus, auditory, and vestibular functions of the inner ear, and usually the medial temporal and occipital lobes of the cerebral hemisphere.2
Since the vertebral arteries have a long extracranial course and pass through the transverse process of C6 to C2 vertebrae before entering the cranial cavity, one might expect them to be subject to trauma, spondylotic compression, and a variety of vascular diseases.4 Although, the two vertebral arteries contribute between 10 and 15 percent of the cerebral blood flow, they supply blood to over 90 percent of the cervical spinal cord, nerve roots, and their supporting tissues. Generally, the brain has very rich collateral blood supply through a.carotis, and a.basilaris, so attempting to think of improvement of cervical blood flow in a.vertebrae is improbable, but it is not excluded.
Cerebral vessels are different from those in the periphery. The sympathetic fibers appear to have little functional significance except perhaps to regulate blood pressure effects in the larger vessels around the circle of Willis. The control of cerebral blood flow depends mainly on autoregulation, an intrinsic mechanism regulating vessel diameter in order to keep cerebral blood flow constant in spite of a variety of anatomical and metabolic variations.3 Ischemia inhibits the process of cerebral autoregulation, and the presence of collaterals cannot compensate. When autoregulation fails, cerebral blood flow has a linear relationship to blood pressure. Elderly patients tend to lose some of this autoregulatory compensation (especially with cervical spondylosis development) and so are normally prone to the effects of hypotension and hypertension.3
The blood vessels of the head receive their preganglionic sympathetic innervation from T1 to T2, but C8, T3, and even T4 may also contribute. The axons pass out into the sympathetic chain and ascend to synapse in the stellate and the superior cervical sympathetic ganglia. The postganglionic fibers distribute from the superior cervical sympathetic ganglion with the external and internal carotid arteries to the head. The intracranial postganglionics follow along the internal carotid artery to the circle of Willis and along branches of the external carotid, and distribute to the adventicia and the smooth muscle if intracranial vessels including arterioles of the pia mater, but not to the blood vessels in the brain substance. Postganglionic fibers also distribute to the middle menigeal artery. Postganglionic fibers from the stellate ganglion ascend along the vertebral arteries and basilar artery. These sympathetic fibers to the intracranial blood vessels are vasoconstrictors.5 Thus, anatomical data shows close connection between cervical structures and cervical blood vessels, and certain influence of cervical sympathetic network on cerebral blood flow is doubtless.
Next, we will consider sympathetic structures of the neck. The superior, middle, and inferior cervical ganglia send gray rami to all eight cervical spinal nerves. The superior cervical ganglion sends to the first four cervical nerves, the smaller middle cervical ganglion supplies the next two, and the large inferior cervical ganglion projects a gray ramus to the seventh and eight cervical nerves.6
In the cervical spine, the gray rami from sympathetic cervical ganglion join the ventral primary divisions well outside the intervertebral foramina. The three sympathetic ganglia are usually in the connective tissue between the longus colli and longus capitis and the carotid sheath. The multiple branches of the cervical sympathetic chain include those ascending along the internal and external carotid arteries and those to the pharinx, cardiac plexus, and other areas, as well as those to the spinal nerves. The sympathetic chain, therefore, is not technically part of the spinal column but a related structure.9
Before dividing into anterior and posterior primary divisions each spinal nerve gives off a small recurrent or meningeal branch, which is joined by a filament from the communicating cord between the anterior division of the nerve and the sympathetic, and then runs upwards through the intervertebral foramen to the spinal canal, where it is distributed to the vertebrae and ligaments, the blood vessels of the canal, and to the dura mater. To the intraspinal nerves formed in this manner by the union of the recurrent or menigeal branches of the spinal nerves with the sympathetic filaments from the rami communicantes, Toldt gives the name of n.sinuvertebrales.7,10 It winds around the pedicle on each side and splits into ascending and descending branches to supply the structures noted with various sensory modalities of position, pain, temperature, and so forth.9 Cervical manipulations (CM) influence not only subluxations of cervical vertebrae but affect all structures of the neck: ligaments, muscles, vessels, and especially nerves. The response of the sympathetic system for cervical manipulations (sympathetic stimulation) was clearly shown in a number of studies.12-16 It is possible to conclude through these data that CMs have complex influence on cerebral blood flow which should be attentively investigated.
Experimental Proposal: Design and Method
Total time involved is one year.
Phase I. Analytical investigation. Detailed literature research is performed and possible mechanisms of influence of spinal manipulative therapy (SMT) on cervical blood flow are proposed.
Phase II. Practical study. Patients between the ages of 30 to 65 with symptoms of cervical spondylosis will be examined by superficial rheoencephalography or Doppler equipment. All signs and characteristics of cerebral blood flow will be noted. After routine chiropractic examination patients take a prescribed course of chiropractic treatment with emphasis on cervical spine, 5-15 procedures. After treatment, repeated examination should be done under the same conditions.
Phase III. Analysis of results. Statistical processing of data. Preparation of final report and article to a refereed journal.
References 
  1. Spano D, Darling P: Cardiovascular changes in degenerative cervicopathy. Chiropractic treatment. In: Mazzarelli JP, ed. Chiropractic Interprofessional Research. Torino: Edisoni Minerva Medica, p.77-88, 1982.

  2. Rowland LP, ed. Merritt's Textbook of Neurology. Philadelphia, London: Lea & Febiger. p.181, 1989. (964 pages)

  3. Pryse-Phillips WE, Murray TJ: Essential Neurology. New York: Medical Examination Publishing Company, 1992. (726 pages)

  4. Adams RD, Victor M: Principles of Neurology. New York, 1989. (1,286 pages)

  5. Crosby EC, et al.: Correlative Anatomy of the Nervous System. New York: The Macmillan Company, 1962. (731 pages)

  6. Stratton DB: Neurophysiology. New York: McGraw-Hill Book Company, 1980. (387 pages)

  7. Toldt C: Atlas of Human Anatomy. New York: The MacMillican Co., 1942.

  8. Jeffreys E: Disorders of the Cervical Spine. London: Butterworths, 1980. (147 pages)

  9. Sherk HH, et al., ed. The Cervical Spine. Philadelphia: JB Lippincott Co., 1989. (881 pages)

  10. Jackson B: The Cervical Syndrome. Springfield: Charles C. Thomas, 1976. (335 pages)

  11. Turek SL: Orthopaedics. Philadelphia: JB Lippincott Co., 1984. (1,756 pages)

  12. Wood KW: Resolution of spasmodic dysphonia via chiropractic manipulative management. JMPT. 1991;14(6):376-8.

  13. Yates RG, et al.: Effects of chiropractic treatment on blood pressure and anxiety: a randomized, controlled trial. JMPT. 1988;11(6):484+.

  14. Wiles MR, et al.: Chiropractic and visceral disease: a brief survey. J Can Chiro Assoc. 1982;26(2):65-68.

  15. Briggs L, Boone WR: Effects of a chiropractic adjustment on changes in pupillary diameter: a model for evaluating somatovisceral response. JMPT. 1988;11:181-189.

  16. Sato A: The reflex effects of spinal somatic nerve stimulation on visceral function. JMPT. 1992;15(1):57-61.

How Dangerous Is Manipulation?

By Ronald L. Rupert
Current, reliable information is the most valuable commodity a chiropractor can possess. It is applied to patient treatment and education, all consulting endeavors, medicolegal issues, rebutting insurance claim denials, research, and virtually all other professional issues. 
For this reason, as we discussed in the February 25, 1994 issue of Dynamic Chiropractic, sophisticated computerized indexes like Medline, Biosis, Exerpta Medica and CHIROLARS (the chiropractic index), have been created. The physician, with the use of any computer and modem, can have instant access to the professional literature and transfer this information, like a fax, across a standard telephone line.
Once you have become a subscriber to one or more of these important resources it takes some time to become accustomed to search strategies and to optimize your use of these databases. One of the more important aspects of online literature searching is using the proper language or terms to ask for the information you want. On the surface this might appear simple, but in reality it can be quite complicated. For the purpose of this column, we can only superficially deal with search language. In subsequent articles, we will be able to explain this process thoroughly.
The most basic unit of search language is what the National Library of Medicine calls a Medical Subject Heading (MeSH). These MeSH terms define the vocabulary by which all information is indexed. Most health care databases (Exerpta Medica, Medline, Toxline, Nursing and Allied Health, etc.) use these headings. The chiropractic librarians' organization, CLIBCON; Canadian Memorial's Index, CRAC, and CHIROLARS use over 90 percent MeSH terms. The remaining 10 percent is a supplemental thesaurus of terms important to chiropractic.
Having a standardized language for indexing (and retrieving information) is important because authors use so many different words to express the same or similar concepts. Let's look at a few of the terms authors use for literature related to therapy for low back pain. (* = proper MeSH term)

backachetherapy*
lumbalgiacare
low back pain*management
lumbagotherapeutic intervention
back pain*treatment
By using the MeSH headings "low back pain" and "therapy," you can make a single search that will retrieve all of the articles related to the therapy of low back pain, regardless of the terms used by the author, because indexers convert all other terms to the proper MeSH term.
Most headings are very simple. Most anatomical structures are just as you might suspect; e.g., cervical vertebrae (not cervical spine), head, knee, intervertebral disc and hand. With subscriptions to online systems, a list of these headings are either provided free of charge or for a reasonable fee (as in the National Library of Medicine's MeSH heading book).
In view of the American Heart Association's recent claim that the danger of cervical manipulation was "small but significant" (Dynamic Chiropractic, March 11, 1994), let's look at articles related to the dangers of manipulation. This is a somewhat complex online query. Normally a single heading would be used to find information, however MeSH has a number of inconsistencies. If we are searching for articles about the adverse effects of adjustments or spinal manipulation, NLM uses the term "manipulation, orthopedic" if it involves manipulation by an osteopath, physical therapist or medical physician. The term can be coupled with the subheading "adverse effects." However, for chiropractic adjustment there is no MeSH term, and the NLM will usually call such chiropractic adjustments or manipulative procedures "chiropractic-methods." So, to find all articles related to the adverse effects of manipulation, one would look for "adverse effects" and "manipulation, orthopedic" or "chiropractic-methods." (Note that we use "adverse effects" and not complications." This is because NLM uses "adverse effects" in relation to treatment and "complications" in relation to diseases.) Fortunately, most searches are much more straightforward. When using this search strategy in CHIROLARS, we find approximately 2,500 articles dealing with manipulation, orthopedic and approximately 200 articles related to the adverse effects of manipulation, orthopedic.
One of the most interesting articles located was: Dvorak, T; Baumgartner, H; Burn, L; et al. Consensus and recommendations as to the side-effects and complications of manual therapy of the cervical spine. Journal of Manual Medicine 1991; 6: 117-8.
This article was a consensus process conducted by some of the leading medical advocates of spinal manipulation in Europe. They naturally began with a review of the literature, which cited previous morbidity studies where neurologic complications occurred once in every 400,000 high velocity manipulations of the cervical spine. The authors discuss contraindications of cervical manual procedures. They note: "Side effects and complications, especially the frequency, could be reduced by: proper diagnosis, helping to identify the absolute and relative contraindications for manual treatment; [and] recognition of index of suspicion." Other studies placed the risk of serious adverse effects from cervical adjustments at one in a million or less. Clearly spinal manipulation is relatively safe when compared to alternative drug and surgical interventions.

Orthotic Therapy: The Postural Imperative

By William M. Austin, DC, CCSP, CCRD
Prescribing therapeutic orthotic support as an adjunct to chiropractic care aids in the prompt resolution of numerous clinical conditions and improves a patient's ability to maintain improved body mechanics and function. 
Orthotics enhance the stability and balance of the pedal foundation, enhancing the integrity of overall musculoskeletal alignment and interrelationships.1
Because the feet are the foundation of the body, their influence must be considered even in cases involving other body structures. If a patient's condition is affected by gravitational forces, structural imbalance, or joint disturbances, orthotics are helpful in speeding recovery and preventing reoccurrence of problem conditions. In cases of specific trauma that produce an area of weakness, healing can be accelerated when strong support is provided by a balanced foundation.2
Treating the Whole Patient
Recognition of integrated relationships in the musculoskeletal system is a fundamental concept of chiropractic, and central to its effectiveness. The ability to see the body as an interrelated unit, instead of treating isolated symptoms, generates results that build patient satisfaction and professional success.
In the same way, understanding the relationship between a balanced pedal foundation and total postural health improves the effectiveness of individual case management. Forces of gravity work through the interrelated linkages of the feet, knees, and legs into the spine and pelvis. These forces also impact on a patient's ability to respond to and maintain adjustments.3The body functions as a closed kinetic chain, where movement at one joint influences movement at other joints.4
Foot dysfunction occurs in an estimated 80 percent of people over the age of 40. Often, patients are unaware of their problem because symptoms refer to structures away from the pedal function. Many pelvic and spinal distortions can be traced to altered foot biomechanics.5 It is the doctor's responsibility to check for evidence of underlying deficiencies that influence a patient's particular complaint, and prescribe appropriate correction.
Tracing the Kinetic Chain
Excessive pronation of the subtalar joint is the most common foot disorder that contributes to chronic postural problems.6 A natural inroll of the foot must occur during gait so that body weight shifts forward, knees can flex, and natural shock absorbers protect upper body structures from heel strike forces. When the degree and duration of pronation exceed established norms, consequences extend throughout the closed kinetic chain. For example:
At the knee: Flattening of the longitudinal arch stretches the retinaculum on the medial side. The patella is pulled laterally in the femoral grove during flexion, setting the stage for chondromalacia patellae.7
In the pelvis: Lack of pedal support prolongs inward rotation of the lower extremity, causing inward hip rotation related to myofascial back pain.7
At the spine: Excessive pronation effectively creates a functional short leg, leading to pelvic unleveling. Shear strain on the articular facet joints, compensatory scoliosis, and intra-articular capsule changes are possible consequences.7
Orthotic Correction
Flexible orthotics serve to control motion within the foot, including the angle and timing of pronation.8 IT is important to facilitate but not restrict movement, to avoid a compensatory hypermobility elsewhere in the kinetic chain. Resilient flexible orthotics allow movement to occur, but check the degree of inroll as if a wedge were placed at the point of weakness.
Several studies verify the effectiveness of orthotic support in stabilizing the pedal foundation for better postural health. In one, pronation measurements were taken on both an injured and a normal foot. When an orthotic was worn on the injured foot, the degree of pronation was almost equal.2
Another study8 involving the used of flexible orthotics focused on three key postural measurements: 
  1. Femoral head height. Healthy posture shows little or no difference in head height. Variance reflects functional or structural problems in the feet, knees, pelvis, or spine.

  2. Sacrovertebral angle. The accepted optimum angle is 110 degrees. Pelvic tilt or lumbar lordosis will cause a change in angle measurement.

  3. Lumbosacral disc angle. The standard measurement is between five and nine degrees. Outside these limits, weightbearing stress can effect the facet articulation and disc.

Subjects in the study wore spinal pelvic stabilizers for four months, but received no chiropractic adjustments and made no other lifestyle changes. At the end of the period, measured improvements occurred in all three areas.
Members of a runners' club demonstrated that orthotics provide a high level of symptom relief.2Almost 350 people who had been using orthotics for an average of two years completed identical questionnaires about specific musculoskeletal symptoms. Complete resolution or great improvement in their symptoms was reported by 75 percent of respondents.
Among their complaints were pain in the knees, feet, ankles, shins, and hips. The top three conditions in those diagnosed by health care professionals were excessive pronation, plantar fascitis, and Achilles tendinitis.
A study focusing on patients with leg length inequality involved 1,157 subjects with discrepancies of less than 10 millimeters. Over a 15-year period, they demonstrated a 75 percent reduction in low back pain, sciatic pain, and hip pain when shoe insert were worn. Pain would often occur the same day that inserts were not used, and go away when used resumed.9
Identifying Pedal Imbalance Every chiropractic patient is a potential candidate for orthotic therapy. With a trained eye, many doctors can determine the likelihood of pedal imbalance as the patient walks into the examining room. Clues include: 
  • Foot flare: toeing out while walking indicates excessive inroll in one or both feet.

  • Medial patellar rotation: impact of pronation on the knee as described above manifests in abnormal rotation of the patella.

  • Bowed Achilles tendon: inroll of the foot stresses soft tissues, creating a distinctive curve of the Achilles tendon.

These factors serve as general indicators of foot imbalance. During the routine patient exam, be alert to more specific symptoms, including: 
  1. The presence of shin splints, patellofemoral disorders, Achilles tendinitis, plantar fascitis, or stress fractures.2

  2. Local signs such as corns, calluses, bunions, neuralgia, or altered circulation.8

  3. Leg length inequality, especially in the presence of low back pain, unilateral hip arthrosis, or lower extremity stress.1

  4. General complaints of leg cramps, knee or hip pain, spinal distortion, cervical tension, mid-thoracic or low back pain, sciatica, or fatigue.8

  5. Arch collapse:

Summary
The integrity of the body's pedal foundation has a direct impact on total musculoskeletal health. The closed kinetic relationship between the feet and upper body structures can affect the effectiveness and longevity of chiropractic care and correction.
Flexible orthotic support normalizes foot structure and motion to provide a more stable base for the musculoskeletal complex. Even though the feet may not hurt, symptoms referred elsewhere in the body manifest as chronic pain or lack of permanence in chiropractic adjustments.
Clinical studies and field research verify the value of orthotics in relieving pain and improving structural integrity. Flexible orthotics control pedal motion without restricting function and creating compensatory hypermobility in other structures.
References 
  1. Gross ML, Davlin LB, Evanski PL: Effectiveness of orthotic shoe inserts in the long-distance runner. Am J Sports Med 1991; 19(4): 409-412.

  2. Rubin CT: Skeletal strain and functional significance of bone architecture. Calcif Tissue Int1984; 36(Sppl 1): 511-518.

  3. Hyland JK: 15 seconds to a grateful patient. Chiro Prod 1993; 8(1) 47.

  4. Steindler A: Kinesiology of the Human Body under Normal and Pathological Conditions, Ed. 3. Springfield, Charles C. Thomas, 1970.

  5. Schafer RC: Clinical Biomechanics: Musculoskeletal Actions and Reactions. Baltimore, Williams & Wilkins, 1983.

  6. Root ML: Clinical Biomechanics II: Normal and Abnormal Function of the Foot. Los Angeles, Clinical Biomechanics Corp., 1977.

  7. Greenawalt MH: Spinal Pelvic Stabilization, 4th Ed., Roanoke, Foot Levelers, Inc., 1990.

  8. Christensen KD: Orthotics: Do They Really Help A Chiropractic Patient? Roanoke, Foot Levelers, Inc., 1990.

  9. Friberg O: Clinical symptoms and biomechanics of lumbar spine and hip joint in leg length inequality. Spine 1983; 6(6): 643-650.

Parkinson Disease


Diagnosis

The diagnosis of Parkinson disease is clinical, and relies on the presence of the cardinal features of bradykinesia, rigidity, tremor, and postural instability, coupled with gradual symptom progression and a sustained response to therapy with levodopa.4 However, some of these features are shared by other neurologic conditions. Conditions commonly misdiagnosed as Parkinson disease include nonparkinsonian tremors such as essential tremor, and diseases with parkinsonian features such as vascular parkinsonism, progressive supranuclear palsy, and drug-induced parkinsonism.5,6 Table 1describes common disorders to consider in the differential diagnosis.1,4,79
Features that increase the likelihood of Parkinson disease include those associated with bradykinesia, such as micrographia, a shuffling walk, and difficulties performing motor tasks such as turning in bed, rising from a chair, or opening jars.10 Features that make Parkinson disease less likely include falls in the early stages of the disease, poor response to levodopa, symmetry at onset, rapid progression, lack of tremor, and dysautonomia.9
The diagnosis of Parkinson disease is difficult and diagnostic error is common, particularly in the early stages.5,6 A physician who rarely diagnoses Parkinson disease should consider referring a patient suspected of having it to a physician who has more experience with the disease to confirm the diagnosis.4,11 No clinical decision rules are of proven usefulness in diagnosing early disease,4although the Parkinson's UK Brain Bank criteria improve diagnostic accuracy in patients with advanced disease.11 Given the inherent uncertainty of diagnosis in early disease and the increasing diagnostic accuracy with disease progression, physicians caring for patients with Parkinson disease should periodically reevaluate the diagnosis.4

Features that increase the likelihood of Parkinson disease include those associated with bradykinesia, such as micrographia, a shuffling walk, and difficulties performing motor tasks such as turning in bed, rising from a chair, or opening jars.10 Features that make Parkinson disease less likely include falls in the early stages of the disease, poor response to levodopa, symmetry at onset, rapid progression, lack of tremor, and dysautonomia.9
The diagnosis of Parkinson disease is difficult and diagnostic error is common, particularly in the early stages.5,6 A physician who rarely diagnoses Parkinson disease should consider referring a patient suspected of having it to a physician who has more experience with the disease to confirm the diagnosis.4,11 No clinical decision rules are of proven usefulness in diagnosing early disease,4although the Parkinson's UK Brain Bank criteria improve diagnostic accuracy in patients with advanced disease.11 Given the inherent uncertainty of diagnosis in early disease and the increasing diagnostic accuracy with disease progression, physicians caring for patients with Parkinson disease should periodically reevaluate the diagnosis.4


Table 1.

Characteristics of Conditions Commonly Misdiagnosed as Parkinson Disease

CONDITIONCLINICAL FEATURES
Essential tremor
Symmetric postural tremor; worsens with movement; affects distal extremities, head, and voice; family history common; improves with alcohol, beta blockers7
Vascular parkinsonism
Clinical features similar to Parkinson disease; may have focal neurologic findings; stepwise progression with poor response to carbidopa/levodopa; presence of basal ganglia and/or thalamic infarcts on computed tomography or magnetic resonance imaging4,8
Drug-induced parkinsonism
Clinical features similar to Parkinson disease; drug history and drug withdrawal evaluation can confirm diagnosis; antiemetics and psychotropic drugs most common causative agents1
Dementia with Lewy bodies
Onset of motor symptoms accompanied by dementia and visual hallucinations; patients have marked fluctuations in attention and cognition; poor response to carbidopa/levodopa8
Atypical parkinsonism (includes progressive supranuclear palsy and multisystem atrophy)
Clinical features similar to Parkinson disease, but with other signs early in the disease process: prominent gait and speech impairment, prominent postural instability, and axial rigidity greater than extremity rigidity; absence of resting tremor and prominent autonomic dysfunction; poor response to carbidopa/levodopa1,9




ROLE OF IMAGING IN DIAGNOSIS


Imaging plays a limited role in diagnosis and should not be used routinely.4,11 Imaging may help when the clinical presentation makes it difficult to differentiate Parkinson disease from another disorder with similar characteristics. For example, limited-quality studies indicate that magnetic resonance imaging may help differentiate the disease from progressive supranuclear palsy.4 Better data support using single-photon emission computed tomography to distinguish the disease from essential tremor.4,11 Table 2 summarizes current recommendations for imaging in the diagnosis of Parkinson disease.4,9,11

Prognosis

Patients with Parkinson disease experience progressive decline in motor and cognitive function and increased mortality. Risk factors for more rapid decline in motor function include older age at diagnosis, and prominent bradykinesia and rigidity at diagnosis. Prominent tremor at diagnosis may predict a slower rate of disease progression.9 The incidence of dementia increases with patient age and duration of Parkinson disease, with 60 percent of patients who have the disease developing dementia within 12 years of diagnosis.12 In the Physicians' Health Study, which enrolled 22,071 male physicians between 40 and 83 years of age, the adjusted relative risk of mortality for the 560 men who developed the disease during 23 years of follow-up was 2.3.13 The relative risk of mortality was 1.8 in a longitudinal Dutch cohort of 6,969 men and women.14 In a community-based cohort in Norway, men with Parkinson disease at age 70 had a median life expectancy of eight years, and women with Parkinson disease at age 70 had a median life expectancy of 11 years.12

Treatment of Motor Symptoms


EARLY MEDICAL THERAPY

The American Academy of Neurology recommends initiating treatment once patients develop functional disability.15 Levodopa, nonergot dopamine agonists, and monoamine oxidase-B inhibitors can be used for initial therapy 4,11,15 (Table 3). Levodopa is administered with carbidopa, which inhibits the peripheral metabolism of levodopa, thereby allowing therapeutic concentrations of levodopa to enter the brain without disabling adverse effects. The combination of carbidopa and levodopa (Sinemet) is the most effective agent available for the treatment of motor symptoms. However, its early use is associated with earlier development of dyskinesias (abnormal involuntary movements). Dopamine agonists such as pramipexole (Mirapex) and ropinirole (Requip) directly stimulate dopamine receptors. They are less effective than levodopa in treating motor symptoms of Parkinson disease, but have a lower incidence of dyskinesias. Compared with carbidopa/levodopa, dopamine agonists cause more sleepiness, edema, nausea, and hallucinations, and have higher dropout rates in clinical trials.16
Ergot-derived dopamine agonists such as cabergoline, bromocriptine (Parlodel), lisuride, and pergolide should not be used as first-line treatments because of the risk of serosal fibrosis and cardiac valvulopathies. (note: Lisuride and pergolide are not available in the United States.) If ergot-derived dopamine agonists are used, baseline and annual echocardiography, chest radiography, and testing of erythrocyte sedimentation rate and renal function should be performed.4,11 Monoamine oxidase-B inhibitors are less effective than either carbidopa/levodopa or dopamine agonists in treating motor symptoms of Parkinson disease, cause less dyskinesia than carbidopa/levodopa, and generate fewer adverse effects than dopamine agonists.4,11,15,17 Administering carbidopa/levodopa in combination with a dopamine agonist in early disease does not delay the development of dyskinesias.18
The choice of initial therapy should be guided by the patient's preferences after a discussion of the risks and benefits of each class of medications, taking into account the degree of the patient's functional disability. Although up to 40 percent of patients who have Parkinson disease use an alternative therapy,19 no good evidence shows that any herbal medication or supplement is effective for treatment of the disease, and there is no convincing evidence that any such treatment is neuroprotective.20 In particular, vitamin E should not be used for neuroprotection because there is good evidence indicating that it does not slow disease progression.4,20

LATE MEDICAL THERAPY

As Parkinson disease progresses, initial therapy becomes less effective and additional motor complications develop, including dyskinesias and motor fluctuations. The patient's “on time,” when medication is effectively controlling the disease's symptoms, becomes shorter, and “off time” occurs when disease symptoms recur gradually or abruptly. These complications impair function and quality of life.21
Several medications are used as adjunctive therapy with levodopa to help reduce motor fluctuations. Dopamine agonists decrease off time in patients and improve function. The nonergot dopamine agonists pramipexole and ropinirole are preferred to the ergot agonists, for reasons previously noted.4,11,21 Apomorphine (Apokyn) is a nonergot dopamine agonist injected subcutaneously that decreases off time. It has significant adverse effects, and treatment should be started in an experienced center.4,11 Monoamine oxidase-B inhibitors also decrease off time in patients. CatecholO-methyltransferase inhibitors decrease levodopa metabolism, allowing for more levodopa to enter the brain. They also modestly decrease off time.4,11,21,22 The catechol O-methyltransferase inhibitor tolcapone (Tasmar) is associated with fatal hepatotoxicity and should be avoided.4,11 These treatments all increase dyskinesias and other adverse effects, including hallucinations, nausea, vomiting, constipation, hypotension, insomnia, and somnolence.4,11,21,23 A Cochrane review that indirectly compared these drugs concluded that dopamine agonists were most effective at reducing off time.23 Only amantadine has been shown to reduce dyskinesias. This effect is modest and may last less than eight months.4,11,21

SURGERY

Most patients will develop disabling symptoms despite optimal medical therapy, and are candidates for deep brain stimulation, which targets either the subthalamic nucleus or the globus pallidus interna.24 Factors that predict a good response to surgery for advanced Parkinson disease include good response to levodopa, few comorbidities, absence of cognitive impairment, and absence of (or well-controlled) depression.24 Risks of surgery include intracranial hemorrhage; stroke; infection; lead migration, misplacement, or fracture; and death.24
A recent randomized multicenter trial compared best medical therapy to deep brain stimulation over six months. Patients receiving deep brain stimulation had significant gains in on time, and improvements in motor function and quality of life. However, adverse effects were more frequent in the surgical group; these included surgical site infection, falls, and depression.25 Deep brain stimulation does not slow disease progression, and patients eventually develop treatment-resistant symptoms such as gait freezing.2426


PHYSICAL, OCCUPATIONAL, AND SPEECH THERAPY

Physical therapy improves balance, muscle strength, and walking speed in patients with Parkinson disease.11,20 No evidence shows that one type of physical therapy is better than another.11 Although there is less evidence that occupational therapy is beneficial,11,20 it may help patients maintain family, social, and work roles and improve safety and motor function, and should be offered to those having difficulty performing tasks of daily living.11 Many patients who have the disease develop dysarthria, with low speech volume, decreased pitch, and pronunciation difficulties. Speech therapy, particularly therapy aimed at improving the volume of speech, is effective.11,20

Management of Nonmotor Symptoms

Even early in the course of Parkinson disease, nonmotor symptoms such as fatigue are common. Later in the course, nonmotor symptoms significantly lower patients' quality of life. Recognizing and treating these symptoms improve the quality of life for patients who have Parkinson disease, as well as for their caregivers.

FATIGUE AND SLEEP DISTURBANCE

Fatigue is present in one-third of patients with Parkinson disease at diagnosis, and is associated with severity of illness. It is less common in patients treated with carbidopa/levodopa.27 Methylphenidate (Ritalin) may improve fatigue in patients with the disease.28 Excessive daytime sleepiness occurs in more than one-half of patients who have Parkinson disease, and is caused by both the disease itself and the adverse effects of medications, such as dopamine agonists.29 Physicians should educate patients about good sleep hygiene.11 Melatonin is not effective for improving sleep.4 Three small randomized trials show that modafinil (Provigil) improves subjective measures of sleepiness without changing objective measures of sleep.28 It should not be used to prevent sleep attacks that may interfere with potentially hazardous activities.4 Physicians should advise patients with sleep attacks to refrain from hazardous activities, such as driving or operating machinery.11
In one study, rapid eye movement sleep behavior disorder was found in 46 percent of patients with Parkinson disease.30 This disorder is characterized by dramatic and potentially violent behaviors that occur during sleep, such as yelling, kicking, or jumping, and diagnosis is confirmed by video polysomnography in a sleep laboratory.31 Limited data suggest that rapid eye movement sleep behavior disorder may respond to low-dose clonazepam (Klonopin).31 Other movement disorders affecting sleep, such as restless legs syndrome and periodic limb movement disorder, occur in almost 20 percent of patients with Parkinson disease. One small study showed that taking carbidopa/levodopa at bedtime decreased the number of movements in patients with restless legs syndrome.28

DISORDERS OF AUTONOMIC FUNCTION

Autonomic dysfunction, evidenced by orthostatic hypotension, erectile dysfunction, urinary incontinence, and constipation, is present in most patients late in the disease. No treatments have demonstrated effectiveness in treating either orthostatic hypotension or urinary incontinence in Parkinson disease.4,28 Sildenafil (Viagra) may improve erectile dysfunction in patients with the disease,28 and one randomized trial showed that polyethylene glycol (Miralax) improved stool frequency and consistency.28 Drooling can be treated with either onabotulinumtoxinA (Botox)28 or glycopyrrolate.32

PSYCHIATRIC DISORDERS

Depression and psychosis occur in up to 50 percent of patients who have Parkinson disease.33 Mild depression can be difficult to diagnose, because some of the motor symptoms of Parkinson disease and depression overlap.4 Physicians should have a high index of suspicion for depression, and consider screening with the Beck Depression Inventory.34 Amitriptyline, desipramine (Norpramin), and nortriptyline (Pamelor) improve depression in patients with Parkinson disease.4,34,35 However, tricyclic antidepressants can cause anticholinergic adverse effects and should not be used in patients with cognitive impairment. When choosing an antidepressant, physicians should take into consideration comorbid conditions and the potential for drug interactions.4,11,34
Psychosis, manifested by visual or auditory hallucinations and delusions, is treated most effectively with clozapine (Clozaril). It requires weekly monitoring because of the risk of agranulocytosis.4,11,34 If regular monitoring is not possible, quetiapine (Seroquel) is modestly effective.4,11,34 Olanzapine (Zyprexa) worsens motor symptoms and is not effective for psychosis in patients with Parkinson disease.4,11,34 Typical antipsychotics (e.g., haloperidol) should be avoided because they will worsen motor symptoms.4

DEMENTIA

Dementia becomes more prevalent as Parkinson disease progresses. In two studies of patients with Parkinson disease, 44 percent of whom met the Diagnostic and Statistical Manual of Mental Disorders, 4th ed., criteria for dementia, the Mini-Mental State Examination had a sensitivity of 98 percent and a specificity of 77 percent, and the longer Cambridge Cognitive Examination had a sensitivity of 95 percent and a specificity of 98 percent.34 Clinicians should evaluate patients for other causes of dementia, and consider discontinuing anticholinergic or dopaminergic medications that may contribute to cognitive impairment.4,11 In controlled trials, rivastigmine (Exelon) therapy has led to small but clinically significant improvements in cognitive, clinical, and activities of daily living scales, but has caused increased tremor and vomiting.4,11,34 Donepezil (Aricept) also improves cognitive function. Although dropout rates in placebo-controlled trials with donepezil are lower than those with rivastigmine, no studies have directly compared the two agents. Either drug may be used for the treatment of dementia in patients with Parkinson disease.4,11,34
Data Sources: Ovid searches of Medline were completed using the terms Parkinson's disease, diagnosis, prognosis, and controlled clinical trial. Ovid searches of the Cochrane Database of Systematic Reviews were completed using the term Parkinson's disease. Searches of Dynamed, Essential Evidence Plus, and the National Guideline Clearinghouse were completed using the search term Parkinson's disease. Search date: January 2011.