Acknowledging the subsequent information below,�approximately more than 2 million people are injured in automobile accidents each year and among those incidents, the majority of the people involved are diagnosed with whiplash and/or neck injury by a healthcare professional. When the complex structure of the neck is subjected to trauma, tissue damage and other medical complications may occur. Vertebral artery dissection, or VAD, is characterized by a flap-like tear on the inner lining of the vertebral artery in charge of supplying blood to the brain. After the tear, blood can then enter the arterial wall and form a blood clot, thickening the artery wall and often impeding blood flow.
Through years of experience practicing chiropractic care,�VAD may often follow after trauma to the neck, such as that which occurs in an automobile accident, or whiplash injury. The symptoms of vertebral artery dissection include head and neck pain as well as intermittent or permanent stroke symptoms, such as difficulty speaking, impaired coordination and loss of vision. VAD, or vertebral artery dissection, is generally diagnosed with a contrast-enhanced CT or MRI scan.
Abstract
A 30-year-old woman presented to an emergency department with sudden onset of transient loss of left peripheral vision. Owing to a history of migraine headaches, she was released with a diagnosis of ocular migraine. Two days later, she sought chiropractic care for the chief symptom of severe neck pain. The chiropractor suspected the possibility of vertebral artery dissection (VAD). No manipulation was performed; instead, MR angiography (MRA) of the neck was obtained, which revealed an acute left VAD with early thrombus formation. The patient was placed on aspirin therapy. Repeat MRA of the neck 3?months later revealed resolution of the thrombus, without progression to stroke. This case illustrates the importance for all healthcare providers who see patients with neck pain and headache to be attentive to the symptomatic presentation of possible VAD in progress.
Background
Vertebral artery dissection (VAD) leading to stroke is an uncommon but potentially serious disorder. The incidence of stroke related to the vertebrobasilar system varies from 0.75 to 1.12/100?000 person-years. The pathological process in VAD typically involves dissection of the wall of the artery followed sometime later by thrombus formation, which may cause arterial occlusion or may lead to embolisation, causing occlusion of one or more of the distal branches off the vertebral artery, including the basilar artery, which can be catastrophic. VAD typically occurs in patients who have an inherent, transitory weakness in the arterial wall. In at least 80% of cases, the initial symptoms include neck pain with or without headache.
Many patients with VAD may in the early stages present to chiropractors seeking relief from neck pain and headache, without realising they are experiencing VAD. In many of these cases, the patient later develops a stroke. Until recently, it was assumed that the dissection (and subsequent stroke) was caused by cervical manipulative therapy (CMT). However, while early studies found an association between visits to a chiropractor and subsequent stroke related to VAD, recent data suggest that this relationship is not causal.
This case report is illustrative of the scenario in which a patient with an undiagnosed VAD in evolution consulted a chiropractor for neck pain and headache. After thorough history and examination, the chiropractor suspected VAD and did not perform CMT. Instead, the patient was referred for further evaluation, which detected a VAD in progress. Prompt diagnosis and anticoagulant treatment were thought to have averted progression to a stroke.
Case Presentation
A 30-year-old otherwise healthy woman consulted a chiropractor (DBF), reporting of right-sided neck pain in the suboccipital region. The patient reported that, 3?days previously, she had gone to the local hospital emergency department (ED) because of the sudden onset of loss of left peripheral vision. The visual symptoms interfered with her ability to see through her left eye; this was accompanied by �numbness� in her left eyelid. About 2?weeks prior to this ED visit, she had experienced an episode of acute left-sided neck pain with severe left-sided headache. She also related a history of migraine headache without prodrome. She was released from the ED with a tentative diagnosis of ocular migraine. She had never been previously diagnosed with ocular migraine, nor had she ever experienced any visual disturbances with her previous migraines.
Shortly after the left-sided ocular symptoms resolved, she suddenly developed right-sided neck pain without provocation, for which she sought chiropractic treatment. She also reported a transient episode of right-sided visual disturbance occurring that same day as well. This was described as sudden blurriness that was of short duration and resolved spontaneously earlier in the day of her presentation for chiropractic examination. When she presented for the initial chiropractic examination, she denied current visual disturbance. She said that she was not experiencing any numbness, paraesthesia or motor loss in the upper or lower extremities. She denied ataxia or difficulty with balance. Medical history was remarkable for childbirth 2� months prior to initial presentation. She stated that her migraine headaches were associated with her menstrual cycle. Family history was remarkable for a spontaneous ascending thoracic aortic aneurysm in her older sister, who was about 30?years of age when her aneurysm had occurred.
Investigations
Based on the history of sudden onset of severe upper cervical pain and headache with visual disturbance and ocular numbness, the DC was concerned about the possibility of early VAD. Urgent MR angiography (MRA) of the neck and head, along with MRI of the head, was ordered. No cervical spine examination or manipulation was performed because of the suspicion that the neck pain was related to VAD rather than to a �mechanical� cervical disorder.
MRA of the neck demonstrated that the left vertebral artery was small and irregular in calibre, extending from the C7 level cephalad to C2, consistent with dissection. There was a patent true lumen with a surrounding cuff of T1 hyper-intensity, consistent with dissection with subintimal thrombus within the false lumen (Figures 1 and ?2). MRI of the head with and without contrast, and MRA of the head without contrast, were both unremarkable. Specifically, there was no intracranial extension of dissection or evidence of infarction. MR perfusion of the brain revealed no focal perfusion abnormalities.
Figure 1: Axial proton density image demonstrates circumferential hyper-intensity surrounding the left cervical vertebral artery (representing the false lumen). Note decreased calibre of true lumen (black flow void) with respect to the right vertebral artery.
Figure 2: Axial image from three-dimensional time-of-flight MRA demonstrates T1 hypointense dissection flap separating the true lumen (lateral) from the false lumen (medial). MRA, MR angiography.
Differential Diagnosis
The ED released the patient with a tentative diagnosis of ocular migraine, due to her history of migraine headaches. However, the patient stated that the left-sided headache was atypical��like nothing I’ve ever experienced before.� Her previous migraines were associated with her menstrual cycle, but not with any vision changes. She had never been previously diagnosed with ocular migraine. MRA of the cervical region revealed that the patient actually had an acute dissection with thrombus formation in the left vertebral artery.
Treatment
Owing to the potential of impending stroke associated with an acute VAD with thrombus formation, the patient was admitted to the neurology stroke service for close neurological monitoring. During her admission, the patient did not experience any recurrence of neurological deficits and her headaches improved. She was discharged the following day with a diagnosis of left VAD and transient ischaemic attack. She was instructed to avoid vigorous exercise and trauma to the neck. Daily aspirin (325?mg) was prescribed, to be continued for 3�6?months after discharge.
Outcome and Follow-Up
After discharge from the stroke service, the patient had no recurrence of headache or visual disturbances, and her posterior neck pain symptoms resolved. Repeat imaging was performed 3?months after presentation, which demonstrated improved calibre of the cervical left vertebral artery with resolution of the thrombus within the false lumen (Figure 3). Imaging of the intracranial compartment remained normal, without evidence of interval infarction or perfusion asymmetry.
Figure 3: Maximum intensity projection (MIP) images from three-dimensional time-of-flight MRA (left image is at time of presentation and right image is at 3-month follow-up). The initial imaging demonstrates markedly diminutive calibre of the left vertebral artery
Discussion
The pathophysiological process of VAD is thought to start with degeneration of the tissues at the medial-adventitial border of the vertebral artery, leading to the development of microhaematomata within the wall of the artery and, eventually, arterial tear. This can lead to leakage of blood into the arterial wall, causing occlusion of the lumen with subsequent thrombus formation and embolisation, resulting in stroke related to one of the branches of the vertebral artery. This pathological process is similar to that of spontaneous carotid artery dissection, spontaneous thoracic aortic dissection and spontaneous coronary artery dissection. All these conditions tend to occur in younger adults and some have speculated that they may be part of a common inherited pathophysiological process. Notable in this case is the fact that the patient’s older sister had experienced a spontaneous thoracic aortic aneurysm (probably a dissection) at around the same age (30?years) as this patient was when she experienced her VAD.
While the dissection is often sudden, the luminal compromise and complications of VAD can develop gradually leading to variable symptoms and presentation, depending on the stage of the disease. The dissection itself, which develops some time before the onset of neural ischaemia, can cause stimulation of nociceptive receptors within the artery, producing pain that is most commonly felt in the upper cervical spine or head. Only after the pathophysiological process progresses to the point of complete arterial occlusion or thrombus formation with distal embolisation does the full manifestation of infarction occur. However, as illustrated in this case, neurological symptoms can develop early in the process, particularly in cases in which the true lumen demonstrates significant calibre decrease secondary to compression.
There are several interesting aspects to this case. First, it highlights the importance of spine clinicians being alert to the possibility that what may appear to be typical �mechanical� neck pain could be something potentially more sinister, such as VAD. The sudden onset of severe suboccipital pain, with or without headache, and accompanying brainstem related neurological symptoms, should alert the clinician to the possibility of VAD. As in the case reported here, patients with a history of migraine will typically describe the headache as different from their usual migraine. A careful neurological examination should be performed, looking for possible subtle neurological deficits, although the neurological examination will often be negative in the early stages of VAD.
Second, a triad of symptoms raised concern that the patient might be experiencing a VAD in progress. The symptom triad included: (1) spontaneous onset of severe upper cervical pain; (2) severe headache that was distinctly different from the patient’s usual migraine headaches; and (3) brainstem-related neurological symptoms (in the form of transient visual disturbance). Notably, careful neurological examination was negative. Nonetheless, the history was of sufficient concern to prompt immediate investigation.
When VAD is suspected but no frank signs of stroke are present, immediate vascular imaging is indicated. While the optimal imaging evaluation of VAD remains controversial, MRA or CTA are the diagnostic studies of choice given their excellent anatomic delineation and ability to evaluate for complications (including infarction and changes in brain perfusion). Some advocate the use of Doppler ultrasound; however, it has limited utility given the course of the vertebral artery in the neck and limited evaluation of the vertebral arteries cephalad to the origin. Additionally, ultrasound imaging is unlikely to allow visualisation of the dissection itself and thus can be negative in the absence of significant arterial occlusion.
Third, this case is interesting in light of the controversy about cervical manipulation as a potential �cause� of VAD. While case reports have presented patients who have experienced stroke related to VAD after cervical manipulation, and case�control studies have found a statistical association between visits to chiropractors and stroke related to VAD, further investigation has indicated that the association is not causal. Cassidy et al found that a patient who experiences stroke related to VAD is just as likely to have visited a primary care practitioner as to have visited a chiropractor prior to having the stroke. The authors suggested that the most likely explanation for the statistical association between visits to chiropractors and subsequent VAD is that a patient who experiences the initial symptoms of VAD (neck pain with or without headache) seeks medical attention for these symptoms (from a chiropractor, primary care practitioner, or another type of practitioner), then subsequently experiences the stroke, independent of any action taken by the practitioner.
It is important to note that, while there have been reported cases of carotid artery dissection after cervical manipulation, case�control studies have not found this association. The initial symptoms of carotid dissection (neurological symptoms, with neck and head pain less common than VAD), aortic dissection (sudden onset of severe, �tearing� pain) and coronary artery dissection (acute severe chest pain, ventricular fibrillation) are likely to cause the individual to immediately seek ED care, rather than seek chiropractic care. However, VAD has seemingly benign initial symptoms�neck pain and headache�which are symptoms that commonly cause patients to seek out chiropractic care. This may explain why only VAD is associated with visits to chiropractors, while these other types of dissections are not; patients with these other conditions, which have much more alarming symptoms, simply do not present to chiropractors.
This case is a good example of a patient with VAD in progress presenting to a chiropractor for the purpose of seeking relief from neck pain. Fortunately, the chiropractor was astute enough to ascertain that the patient’s symptoms were not suggestive of a �mechanical� cervical spine disorder, and appropriate diagnostic investigation was performed. However, if manipulation had been performed, the VAD that was already in progress from natural history may have been blamed on manipulation, after being detected on MRA imaging. Fortunately, in this case, the chiropractor was able to assist with early detection and treatment, and subsequently a stroke was likely averted.
Learning Points
A case is presented in which a patient saw a chiropractor, while seeking treatment for neck pain, and the history raised concern for possible vertebral artery dissection (VAD).
Rather than providing manipulative treatment, the chiropractor referred the patient for advanced imaging, which confirmed the diagnosis of VAD.
The case illustrates the importance of paying attention to subtle historical factors in patients with VAD.
It also serves as an example of a patient with a VAD in progress seeking the services of a chiropractor for the initial symptoms of the disorder.
In this case, early detection of the dissection occurred and the patient had a full recovery without any subsequent stroke.
Acknowledgments
The authors would like to acknowledge the assistance of Pierre Cote, DC, PhD, for his assistance with reviewing this manuscript.
Footnotes
Contributors: All the authors acknowledge that they have contributed the following to the submission of this manuscript: conception and design, drafting of the manuscript, critical revisions of the manuscript, literature review and references, and proof reading of the final manuscript.
Competing interests: None declared.
Patient consent: Obtained.
Provenance and peer review: Not commissioned; externally peer reviewed.
Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Cited by Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
2.�Boyle E, Cote P, Grier AR et al.�Examining vertebrobasilar artery stroke in two Canadian provinces.�Spine�2008;33(4 Suppl):S170�5.�doi:10.1097/BRS.0b013e31816454e0�[PubMed]
3.�Lee VH, Brown RD Jr, Mandrekar JN et al.�Incidence and outcome of cervical artery dissection: a population-based study.�Neurology�2006;67:1809�12.�doi:10.1212/01.wnl.0000244486.30455.71[PubMed]
4.�Schievink WI.�Spontaneous dissection of the cartoid and vertebral arteries.�N Engl J Med�2001;344:898�906.�doi:10.1056/NEJM200103223441206�[PubMed]
5.�Volker W, Dittrich R, Grewe S et al.�The outer arterial wall layers are primarily affected in spontaneous cervical artery dissection.�Neurology�2011;76:1463�71.�doi:10.1212/WNL.0b013e318217e71c�[PubMed]
6.�Gottesman RF, Sharma P, Robinson KA et al.�Clinical characteristics of symptomatic vertebral artery dissection: a systematic review.�Neurologist�2012;18:245�54.�doi:10.1097/NRL.0b013e31826754e1[PMC free article]�[PubMed]
7.�Cassidy JD, Boyle E, Cote P et al.�Risk of vertebrobasilar stroke and chiropractic care: results of a population-based case-control and case-crossover study.�Spine�2008;33(4�Suppl):S176�83.�doi:10.1097/BRS.0b013e3181644600�[PubMed]
8.�Rothwell DM, Bondy SJ, Williams JI.�Chiropractic manipulation and stroke: a population-based case-control study.�Stroke�2001;32:1054�60.�doi:10.1161/01.STR.32.5.1054�[PubMed]
9.�Smith WS, Johnston SC, Skalabrin EJ et al.�Spinal manipulative therapy is an independent risk factor for vertebral artery dissection.�Neurology�2003;60:1424�8.�doi:10.1212/01.WNL.0000063305.61050.E6[PubMed]
10.�Volker W, Besselmann M, Dittrich R et al.�Generalized arteriopathy in patients with cervical artery dissection.�Neurology�2005;64:1508�13.�doi:10.1212/01.WNL.0000159739.24607.98�[PubMed]
11.�Evangelista A, Mukherjee D, Mehta RH et al.�Acute intramural hematoma of the aorta: a mystery in evolution.�Circulation�2005;111:1063�70.�doi:10.1161/01.CIR.0000156444.26393.80�[PubMed]
12.�Tweet MS, Hayes SN, Pitta SR et al.�Clinical features, management, and prognosis of spontaneous coronary artery dissection.�Circulation�2012;126:579�88.�doi:10.1161/CIRCULATIONAHA.112.105718[PubMed]
13.�Choi S, Boyle E, Cote P et al.�A population-based case-series of Ontario patients who develop a vertebrobasilar artery stroke after seeing a chiropractor.�J Manipulative Physiol Ther�2011;34:15�22.�doi:10.1016/j.jmpt.2010.11.001�[PubMed]
14.�Naggara O, Louillet F, Touze E et al.�Added value of high-resolution MR imaging in the diagnosis of vertebral artery dissection.�AJNR Am J Neuroradiol�2010;31:1707�12.�doi:10.3174/ajnr.A2165�[PubMed]
16.�Nebelsieck J, Sengelhoff C, Nassenstein I et al.�Sensitivity of neurovascular ultrasound for the detection of spontaneous cervical artery dissection.�J Clin Neurosci�2009;16:79�82.�doi:10.1016/j.jocn.2008.04.005�[PubMed]
17.�Bendick PJ, Jackson VP.�Evaluation of the vertebral arteries with duplex sonography.�J Vasc Surg1986;3:523�30.�doi:10.1016/0741-5214(86)90120-5�[PubMed]
18.�Murphy DR.�Current understanding of the relationship between cervical manipulation and stroke: what does it mean for the chiropractic profession?�Chiropr Osteopat�2010;18:22�doi:10.1186/1746-1340-18-22[PMC free article]�[PubMed]
19.�Engelter ST, Grond-Ginsbach C, Metso TM et al.�Cervical artery dissection: trauma and other potential mechanical trigger events.�Neurology�2013;80:1950�7.�doi:10.1212/WNL.0b013e318293e2eb�[PubMed]
20.�Peters M, Bohl J, Th�mke F et al.�Dissection of the internal carotid artery after chiropractic manipulation of the neck.�Neurology�1995;45:2284�6.�doi:10.1212/WNL.45.12.2284�[PubMed]
21.�Nadgir RN, Loevner LA, Ahmed T et al.�Simultaneous bilateral internal carotid and vertebral artery dissection following chiropractic manipulation: case report and review of the literature.�Neuroradiology2003;45:311�14.�doi:10.1007/s00234-003-0944-x�[PubMed]
22.�Dittrich R, Rohsbach D, Heidbreder A et al.�Mild mechanical traumas are possible risk factors for cervical artery dissection.�Cerebrovasc Dis�2007;23:275�81.�doi:10.1159/000098327�[PubMed]
23.�Chung CL, Cote P, Stern P et al.�The association between cervical spine manipulation and carotid artery dissection: a systematic review of the literature.�J Manipulative Physiol Ther�2014; doi:10.1016/j.jmpt.2013.09.005�doi:10.1016/j.jmpt.2013.09.005�[PubMed]
24.�Thomas LC, Rivett DA, Attia JR et al.�Risk factors and clinical features of craniocervical arterial dissection.�Man Ther�2011;16:351�6.�doi:10.1016/j.math.2010.12.008�[PubMed]
25.�Klineberg E, Mazanec D, Orr D et al.�Masquerade: medical causes of back pain.�Cleve Clin J Med2007;74:905�13.�doi:10.3949/ccjm.74.12.905�[PubMed]
Holistic: Migraine headaches are typically debilitating, and require a comprehensive approach for successful treatment. It is helpful to consider migraine headache as a symptom of an underlying imbalance, rather than simply a diagnosis. A holistic approach is a satisfying way to think about and treat migraine headache. Physicians trained in this approach will consider a broad array of features that may contribute to the experience of migraine headache, including disturbances within the following key areas:
Nutrition
Digestion
Detoxification
Energy production
Endocrine function
Immune system function/inflammation
Structural function
Mind-body health
Migraine headache is an excellent example of biologic uniqueness; the underlying factors participating in each individual�s outcome may differ quite a bit from person to person. The journey of identifying and addressing these factors often results in an impressive improvement in frequency and intensity of the expression of migraine. Committed individuals will find the added benefit of better general health along the way.
Nutritional Considerations: Holisitic
Food Allergy/Intolerance
Numerous well-designed studies have demonstrated that detection and removal of foods not tolerated will greatly reduce or eliminate migraine manifestations. True allergy may not be associated with migraine in most individuals, but food intolerance is more common. Migraine frequency and intensity have been demonstrated to respond well to elimination diets, in which commonly offending foods are removed for several weeks. Elimination diets are easy to perform (although they do require a high degree of commitment and education), and can help in identifying foods that are mismatched to an individual. The majority of patients who undergo an elimination diet learn that their diets were contributing to chronic symptoms, and they typically feel much better during the elimination phase. Common foods that act as migraine triggers include: chocolate, cow�s milk, wheat/gluten grains, eggs, nuts, and corn. In children specifically, common migraine triggers include cheese, chocolate, citrus fruits, hot dogs, monosodium glutamate, aspartame, fatty foods, ice cream, caffeine withdrawal, and alcoholic drinks, especially red wine and beer.
There are several methods which may be used to detect food allergies. Laboratory testing can be convenient, but is not always a reliable means of detecting food intolerance. (See Summary of Recommendations for information on how to implement the elimination diet).
Foods such as chocolate, cheese, beer, and red wine are believed to cause migraine through the effect of �vasoactive amines� such as tyramine and beta-phenylethylamine. These foods also contain histamine. Individuals who are sensitive to dietary histamine seem to have lower levels of diamine oxidase, the vitamin B6-dependent enzyme that metabolizes histamine in the small bowel. The use of vitamin B6 improves histamine tolerance in some individuals, presumably by enhancing the activity of this enzyme.
Other diet-related triggers associated with migraine headache include: glucose/insulin imbalances, excessive salt intake, and lactose intolerance. Aspartame, commonly used as a sweetener, may also trigger migraines. Each of these factors may be readily avoided by adopting more conscious eating habits, and by carefully reading labels.
Magnesium
An estimated 75% of people consuming the standard American diet (SAD) are not getting adequate magnesium, and it is felt to represent one of the most common micronutrient deficiencies, manifested by a diverse range of problems. Though many elements can contribute to magnesium depletion, stress is among them, and both acute and chronic stress are associated with increased episodes of migraine. Daily doses of magnesium should be first line considerations for migraine sufferers (caution if kidney function is impaired), and intravenous magnesium can be very helpful in an emergency room setting, but probably only works to terminate an acute migraine if the individual is truly magnesium deficient.
Essential Fatty Acids
It is important to remember that the brain is largely composed of fat. Although essential fatty acids have not received much research attention relative to migraine, there may be a significant role of fatty acids and their metabolites in the pathogenesis of migraine headache. Two small placebo-controlled studies demonstrated that omega-3 fatty acids significantly outperformed placebo in reducing headache frequency and intensity. High quality fish oil should always be used. A good frame of reference is that each capsule should contain at least 300 mg of EPA and 200 mg of DHA. A reasonable starting dose would be two to four capsules twice daily with meals.
Digestive Function: Holistic
Holistic practitioners are generally sensitive to the centrality of the gastrointestinal tract in producing overall health. Though we utilize a reductionistic approach to understanding human anatomy and physiology, we might consider that no system functions as an independent entity (GI, endocrine, cardiovascular, immune, etc.), and that a complex symphony of interrelated functions cuts across organ systems. For example, much of the immune system is found in the Peyer�s patches of the GI tract; in this light, we can see how food, chemicals, and unhealthy microbes might produce immune system activation from gastrointestinal exposure. We also recognize the importance of a balanced ecosystem of intestinal microbes; intestinal dysbiosis, or disordering of the gastrointestinal ecology, may readily produce symptoms, both within and distant from the GI tract. Some colonic bacteria act upon dietary tyrosine to produce tyramine, a recognized migraine trigger for some individuals. H. pylori infection is a probable independent environmental risk factor for migraine without aura, especially in patients not genetically or�hormonally susceptible. A high percentage of migraine patients experienced relief from migraines when H. Pylori infection was eradicated.
Detoxification: Holistic
Patients with migraine headache sometimes report that strong chemical odors such as tobacco smoke, gasoline, and perfumes may act as triggers. It is not uncommon for migraineurs to report that they are triggered by walking down the laundry soap aisle in the grocery store. Support for phase 1 and especially phase 2 detoxification may be beneficial for these individuals, as toxic overload or impaired enzymes of detoxification could theoretically be a significant mediator of headaches. Susceptibility to toxicity may be potentiated by a combination of excessive toxic exposures, genetic polymorphisms leading to inadequate detoxification enzyme production, or depletion of nutrient cofactors that drive phase two detoxification conjugation reactions Support for detoxification function is particularly important in modern life, given our exposure to unprecedented high levels of toxic chemicals. Some nutrients that supply support for detoxification function include: n-acetyl cysteine (NAC), alpha lipoic acid, silymarin (milk thistle), and many others.
Energy Production: Holistic
Riboflavin (Vitamin B2)
Energy production within the parts of the cell called mitochondria can be impaired in some migraine sufferers. Riboflavin is a key nutrient that is involved in energy production at this level. Riboflavin at 400 mg/day is an excellent therapeutic choice for migraine headache because it is well tolerated, inexpensive, and provides a protective effect from oxidative toxicity. Its use in children has been investigated, leading to similar conclusions,suggesting that, for pediatric and adolescent migraine prophylaxis, 200 mg per day was an adequate dose, but four months were necessary for optimal results.
Coenzyme Q10
CoenzymeQ10 (CoQ10) is also a critical component of energy function, and is an important antioxidant. Evidence supports the administration of CoQ10 in reducing the frequency of migraines by 61%. After three months of receiving 150 mg of CoQ10 at breakfast, the average number of headache days decreased from seven to three per month. Another study, using 100 mg of water soluble CoQ10 3x/day, revealed similar results. CoQ10 deficiency appears to be common in the pediatric and adolescent population, and can be an important therapeutic consideration in these age groups. Like riboflavin, CoQ10 is well tolerated (though expensive), with little risk of toxicity. It must be used with extreme caution in patients who also take warfarin, as CoQ10 may counteract the anticoagulation effects of warfarin. It is also noteworthy that many medications can interfere with CoQ10 activity, including statins, beta-blockers, and certain antidepressants and antipsychotics.
Endocrine (Hormone) Function
Female Hormones
It does not appear coincidental that migraine onset correlates with the onset of menstruation and that episodes are linked to menstruation in roughly 60% of female migraineurs. Although there is no universal agreement over the precise relationship between female hormones and migraine headache, it is apparent that the simultaneous fall of estrogen and progesterone levels before the period correlates with menstrual migraine. Estrogen gel used on the skin can reduce headaches when used premenstrually. Some researchers have found that continuous use of estrogen may be necessary to control menstrual migraines, which tend to be more severe, frequent, longer lasting, and debilitating than general migraines. Although published studies are lacking, many practitioners have used transdermal or other bioidentical forms of progesterone premenstrually with success. Of course, the risks of using hormones must be weighed against the benefits. Interestingly, administration of magnesium (360 mg/day) during second half of the menstrual cycle in 20 women with menstrually related migraines resulted in a significant decrease of headache days.
Melatonin
Melatonin, the next downstream metabolite of serotonin, is important in the pathogenesis of migraines. Decreased levels of plasma and urinary melatonin have been observed in migraine patients, and melatonin deficiency appears to increase risk for migraine. Melatonin has been used with some success, presumably via a restorative effect on circadian rhythms. A small study in children demonstrated significant improvement in their migraine or tension headache frequency with a 3 mg nightly dose of melatonin Melatonin appears to modulate inflammation, oxidation, and neurovascular regulation in the brain, and in one study, a dose of 3 mg/day was shown to be effective in reducing migraine headache frequency by at least 50% in 25 of 32 individuals. Ironically, some patients anecdotally report an increase of headaches (generally not migraine) when administered melatonin. The brains of migraineurs do not seem adaptable to extremes; a regular schedule of sleep and meals and avoidance of excessive stimulation are advisable to reduce excessive neural activation.
Immune Function/Inflammation: Holistic
Medications that produce an anti-inflammatory effect, such as aspirin and nonsteroidal agents, frequently produce an improvement in migraine symptoms during an acute attack. The herbs described below also play a role in reducing inflammation. Inflammation and oxidative stress can be identified in many conditions and disease states. It is important to acknowledge that the standard �modern� lifestyle is pro-inflammatory; our bodies are constantly reacting to one trigger after another (foods mismatched to our physiology, toxic burden, emotional stressors, excessive light and other stimulation) that activate our inflammatory cytokines (messengers of alarm). Providing broad-based support through lifestyle change and targeted nutrients may improve outcomes substantially, and this may be achieved foundationally by simplifying our�ingestions/exposures and supporting metabolic terrain. Herbal therapies are included in this section because of their relevant effects upon inflammation.
Feverfew (Tanacetum parthenium)
The precise mechanism of action of feverfew as a migraine preventive is unknown Though at least three studies found no benefit with feverfew, several controlled studies have revealed favorable results in improving headache frequency, severity, and vomiting when feverfew was compared to placebo. There are several caveats that should accompany the use of this herb:
Because of its anti-platelet effects, feverfew must be used with caution in patients on blood thinning products; avoid in patients on warfarin/Coumadin.
Feverfew does not have a role in managing acute migraine headache.
When withdrawing feverfew, do so with a slow taper, since rebound headache may occur.
Feverfew is not known to be safe during pregnancy and lactation.
Proceed with caution if an individual has an allergy to other members of the Asteraceae family (yarrow, chamomile, ragweed).
Most commonly reported adverse effects are oral ulceration (particularly for those chewing the leaves raw), and GI symptoms, reversible with discontinuation.
Feverfew is otherwise well tolerated. The typical dosage range is 25-100 mg 2x/day of encapsulated dried leaves with meals.
Butterbur (Petasites hybridus)
Butterbur is another effective herbal therapy for migraine headache. Butterbur is well tolerated, with no known interactions. Some individuals have reported diarrhea when using butterbur. In one study, its efficacy was demonstrated in children and adolescents between the ages of 6 and 17 years. Its safety is unknown during pregnancy and lactation. The plant�s pyrrolizidine alkaloids can toxic to the liver and carcinogenic, so only extracts that have specifically removed these compounds should be utilized. Many of the studies on Butterbur utilized the product Petadolex� because it is a standardized extract that has removed these alkaloids of concern. The usual dosage is 50 mg, standardized to 7.5 mg petasin and isopetasin, 2-3x/day with meals (although recent studies show that higher doses appear to be more effective1,2 ). Interestingly, butterbur�s diverse qualities make it useful for other conditions, including seasonal allergic rhinitis, and possibly painful menstrual cramps.
Ginger (Zingiber officinalis)
Ginger root is a commonly used botanical, known to suppress inflammation and platelet aggregation. Little clinical investigation has been performed relative to ginger use in migraine headache, but anecdotal reports and speculation based on its known properties make it a safe and appealing choice for migraine treatment. Some practitioners advise patients with acute migraine to sip a cup of warm ginger tea. Though evidence for this practice is lacking, it is a low-risk, pleasant, and relaxing intervention, and ginger is known to have anti-nausea effects. The most anti-inflammatory support is found in fresh preparations of ginger and in the oil.
Structural Considerations: Holistic
Practitioners of manual medicine seem to achieve success in reducing headache through various techniques such as spinal manipulation, massage, myofascial release, and craniosacral therapy Manual medicine practitioners frequently identify loss of mobility in the cervical and thoracic spine in migraineurs. While many forms of physical medicine seem helpful in shortening the duration and intensity of an episode of migraine, literature support is sparse with regard to manipulation as a modality to prevent recurrent migraine episodes. However, a randomized controlled trial of chiropractic spinal manipulation performed in 2000 revealed a significant improvement in migraine frequency, duration, disability, and medication use in 83 treatment group participants. Tension headache may also respond favorably to these techniques because of the structural component involved in muscular tension. The incidence of migraine in patients with TMJ dysfunction is similar to that in the general population, whereas the incidence of tension headache in patients with TMJ dysfunction is much higher than in the general population. Craniosacral therapy is a very gentle manipulative technique that may also be safely attempted with migraine.
Mind-Body Health: Holistic
There are few things more insulting than to be told by a medical professional to �Just reduce your stress.� Though the total load of stress experienced by an individual can be reduced through paring down unnecessary obligations, many everyday life stressors are unavoidable and cannot be simply eradicated. Thus, the answer to reducing stress for unavoidable contributors lies in two important areas: enhancing physical and mental resilience to stress, and modifying the emotional response to stress.
A multitude of programs to reduce the impact of stress on our physical and emotional well-being are rapidly becoming mainstream. For example, mindfulness meditation programs by Jon KabatZinn, PhD and many others are being offered to communities by hospitals around the country. This technique is simple to perform and has demonstrated positive outcomes in heart disease, chronic pain, psoriasis, hypertension, anxiety, and headaches. Breathwork and guided imagery techniques are likewise effective in producing a relaxation response and helping patients to feel more empowered about their health.
Biofeedback and relaxation training have been used with mixed success for migraine headache. Thermal biofeedback uses the temperature of the hands to help the individual learn that inducing the relaxation response will raise hand temperature and facilitate other positive physiologic changes in the body. Learning how to take more active control over the body may reduce headache frequency and severity. The effectiveness of biofeedback and relaxation training in reducing the frequency and severity of migraine headaches has been the subject of dozens of clinical studies, revealing that these techniques can be as effective as medication for headache prevention, without the adverse effects. Other relevant modalities to consider in this light include cognitive behavioral therapy, neurolinguistic programming, hypnosis, transcutaneous electrical nerve stimulation, and laser therapy.
Exercise should not be overlooked as a modality helpful in migraine headache. Thirty-six patients with migraine who exercised 3x/week for 30 minutes over six weeks experienced significant improvement in headache outcomes. Pre-exercise beta-endorphin levels in these individuals were inversely proportional to the degree of improvement in their post-exercise headache parameters. All patients should understand the critical importance of exercise on general health.
Acupuncture: Holistic
A discussion about a holistic integrative approach to migraine headache would be incomplete without acupuncture, which is an effective treatment modality for acute and recurrent migraine. A qualified/licensed practitioner of Traditional Chinese Medicine or a physician trained in medical acupuncture should be consulted.
Holistic: Summary Of Recommendations
Since initiators of migraine headache may be cumulative, identify and avoid them when possible. Consider the basic areas of dysfunction bulleted on the first page of this syllabus.
The incidence of food intolerance is high in patients with migraine headache; consider a comprehensive elimination diet for four to six weeks, during which time the following foods are eliminated: dairy products, gluten-containing grains, eggs, peanuts, coffee/black tea, soft drinks, alcohol, chocolate, corn, soy, citrus fruits, shellfish, and all processed foods. Careful reintroduction of one food at a time, no more often than every 48 hours, may help identify a food culprit. Meticulous recording of foods reintroduced is necessary. Most patients feel improved vitality during the elimination phase. Foods that clearly produce migraine (or other) symptoms should be avoided or used on a rotation schedule of not more than once every four days. If multiple foods introduced back into the diet seem to produce migraine headache, consider the possibility of altered intestinal permeability (leaky gut syndrome).
Consider the following supplements (Consult a qualified practitioner for advice):
Magnesium glycinate: 200-800 mg/day in divided doses (decrease to tolerance if diarrhea occurs)
Vitamin B6 (pyridoxine): 50-75 mg/day, balanced with B complex o 5-HTP: 100-300 mg 2x/day, with or without food, if clinically appropriate
Vitamin B2 (riboflavin): 400 mg/day, balanced with B complex
Coenzyme Q10: 150 mg/day
Consider hormonal therapies
Trial of melatonin: 0.3-3 mg at bedtime
Trial of progesterone or estradiol, carefully individualized, under medical supervision.
Botanical medicines
Feverfew: 25-100 mg 2x/day with meals
Butterbur: 50 mg 2-3x/day with meals
Ginger root
Fresh ginger, approximately 10 gm/day (6 mm slice)
Dried ginger, 500 mg 4x/day
Extract standardized to contain 20% gingerol and shogaol; 100-200 mg 3x/day for prevention, and 200 mg every 2 hours (up to 6 x/day) for acute migraine
Manual medicine may be helpful for some individuals.
Acupuncture
Mind-body support
Thermal biofeedback
Read The Relaxation Response by Herbert Benson, MD
Mindfulness meditation programs
Centering prayer
Breathwork
Guided imagery
Yoga, tai chi, qi gong, etc.
Many other modalities to consider!
Conclusion: Holistic Medicine
Patients will often request a more natural and self directed approach to health care. The recommendations above are typically very safe to implement, and are often welcomed by migraine sufferers. A practitioner with an integrative holistic focus will investigate an extensive array of predisposing factors to determine the underlying features most likely involved in a given individual�s condition. In this way, we treat the individual, rather than his or her diagnosis, and we will generate a favorable impact upon his/her overall health in the process.
Chiropractic Care & Headaches
�American Board of Integrative Holistic Medicine. All rights reserved.
Consider the following, sciatica is a medical term used to describe a collective group of symptoms resulting from the irritation or compression of the sciatic nerve, generally due to an injury or aggravated condition. Sciatica is commonly characterized by radiating pain along the sciatic nerve, which runs down one or both legs from the lower back. The following case vignette discusses Mr. Winston’s medical condition, a 50-year-old bus driver who reported experiencing chronic, lower back and leg pain associated with sciatica during a 4-week time period. Ramya Ramaswami, M.B., B.S., M.P.H., Zoher Ghogawala, M.D., and James N. Weinstein, D.O., provide a comprehensive analysis of the various treatment options available to treat sciatica, including undergoing lumbar disk surgery and receiving nonsurgical therapy.
On a personal note, as a practicing doctor of chiropractic, choosing the correct treatment care for any type of injury or condition can be a personal and difficult decision. If the circumstances are favorable, the patient may determine what is the best form of treatment for their type of medical issue. While nonsurgical therapies, such as chiropractic care, can often be utilized to improve symptoms of sciatica, more severe cases of sciatica may require surgical interventions to treat the source of the issue. In most cases, nonsurgical therapies should be considered first, before turning to surgical therapies for sciatica.
Case Vignette
A Man with Sciatica Who is Considering Lumbar Disk Surgery
Ramya Ramaswami, M.B., B.S., M.P.H.
Mr. Winston, a 50-year-old bus driver, presented to your office with a 4-week history of pain in his left leg and lower back. He described a combination of severe sharp and dull pain that originated in his left buttock and radiated to the dorsolateral aspect of his left thigh, as well as vague aching over the lower lumbar spine. On examination, passive raising of his left leg off the table to 45 degrees caused severe pain that simulated his main symptom, and the pain was so severe that you could not lift his leg further. There was no leg or foot weakness. His body-mass index (the weight in kilograms divided by the square of the height in meters) was 35, and he had mild chronic obstructive pulmonary disease as a result of smoking one pack of cigarettes every day for 22 years. Mr. Winston had taken a leave of absence from his work because of his symptoms. You prescribed 150 mg of pregabalin per day, which was gradually increased to 600 mg daily because the symptoms had not abated.
Now, 10 weeks after the initial onset of his symptoms, he returns for an evaluation. The medication has provided minimal alleviation of his sciatic pain. He has to return to work and is concerned about his ability to complete his duties at his job. He undergoes magnetic resonance imaging, which shows a herniated disk on the left side at the L4�L5 root. You discuss options for the next steps in managing his sciatica. He is uncertain about invasive procedures such as lumbar disk surgery but feels limited by his symptoms of pain.
Treatment Options
Which of the following would you recommend for Mr. Winston?
Undergo lumbar disk surgery.
Receive nonsurgical therapy.
To aid in your decision making, each of these approaches is defended in a short essay by an expert in the field. Given your knowledge of the patient and the points made by the experts, which option would you choose?
Option 1: Undergo Lumbar Disk Surgery Option 2: Receive Nonsurgical Therapy
1. Undergo Lumbar Disk Surgery
Zoher Ghogawala, M.D.
Mr. Winston�s case represents a common scenario in the management of symptomatic lumbar disk herniation. In this particular case, the patient�s symptoms and the physical examination are consistent with nerve-root compression and inflammation directly from an L4�L5 herniated disk on his left side. The patient does not have weakness but has ongoing pain and has been unable to work for the past 10 weeks despite receiving pregabalin. Two questions emerge: first, does lumbar disk surgery (microdiskectomy) provide outcomes that are superior to those with continued nonoperative therapy in patients with more than 6 weeks of symptoms; and second, does lumbar microdiskectomy improve the likelihood of return to work in patients with these symptoms?
The highest quality data on the topic come from the Spine Patient Outcomes Research Trial (SPORT). The results of the randomized, controlled trial are difficult to interpret because adherence to the assigned treatment strategy was suboptimal. Only half the patients who were randomly assigned to the surgery group actually underwent surgery within 3 months after enrollment, and 30% of the patients assigned to nonoperative treatment chose to cross over to the surgical group. In this study, the patients who underwent surgery had greater improvements in validated patient-reported outcomes. The treatment effect of microdiskectomy was superior to that of nonoperative treatment at 3 months, 1 year, and 2 years. Moreover, in an as-treated analysis, the outcomes among patients who underwent surgery were superior to those among patients who received nonoperative therapy. Overall, the results of SPORT support the use of microdiskectomy in this case.
Results of clinical trials are based on a comparison of treatment options in study populations and may or may not apply to individual patients. SPORT did not specify what type of nonoperative therapy was to be used. Physical therapy was used in 73% of the patients, epidural injections in 50%, and medical therapies (e.g., nonsteroidal antiinflammatory drugs) in more than 50%. In the case of Mr. Winston, pregabalin has been tried, but physical therapy and epidural glucocorticoid injections have not been attempted. Despite widespread use of physical therapy for the treatment of lumbar disk herniation, the evidence supporting its effectiveness is inconclusive, according to published guidelines of the North American Spine Society. On the other hand, there is evidence that transforaminal epidural glucocorticoid injection provides short-term relief (30 days) in patients with nerve-root symptoms directly related to a herniated disk. Overall, there is evidence, from SPORT and from a randomized trial from the Netherlands published in the Journal, that early surgery between 6 and 12 weeks after the onset of symptoms provides greater alleviation of leg pain and better overall pain relief than prolonged conservative therapy.
The ability to return to work has not been formally studied in comparisons of operative with nonoperative treatments for lumbar disk herniation. Registry data from the NeuroPoint-SD study showed that more than 80% of the patients who were working before disk herniation returned to work after surgery. The ability to return to work may be dependent on the type of vocation, since patients who are manual laborers may need more time to recover to reduce the risk of reherniation.
It is well recognized that many patients who have a symptomatic lumbar disk herniation will have improvement spontaneously over several months. Surgery can alleviate symptoms more quickly by immediately removing the offending disk herniation from the affected nerve root. The risk�benefit equation will vary among individual patients. In the case of Mr. Winston, obesity and mild pulmonary disease might increase the risk of complications from surgery, although in SPORT, 95% of surgical patients did not have any operative or postoperative complication. For Mr. Winston, a patient with pain that has persisted for more than 6 weeks, microdiskectomy is a rational option that is supported by high-quality evidence.
2. Receive Nonsurgical Therapy
James N. Weinstein, D.O.
This case involves a common presentation of low back pain radiating to the buttock and posterolateral thigh that might represent either referred mechanical pain or radiculopathy. Classic radiculopathy resulting from compression of a lower lumbar nerve root (L4, L5, or S1) results in pain that radiates distal to the knee and is often accompanied by weakness or numbness in the respective myotome or dermatome. In this case, the pain is proximal to the knee and is not associated with weakness or numbness. In SPORT, surgery resulted in faster recovery and a greater degree of improvement than nonoperative treatment in patients with pain that radiated distal to the knee and was accompanied by neurologic signs or symptoms. However, since Mr. Winston would not have met the inclusion criteria for SPORT, the results of diskectomy in this case would be somewhat unpredictable. He does not have radiculopathy that radiates below the knee, and he does not have weakness or numbness; nonoperative treatment should be exhausted before any consideration of a surgical procedure that in most cases has not been shown to be effective in patients with this type of presentation. In this issue of the Journal, Mathieson and colleagues report the results of a randomized, controlled trial that showed that pregabalin did not significantly alleviate pain related to sciatica. Mr. Winston has been treated only with pregabalin; therefore, other conservative options should be explored.
Saal and Saal reported that more than 80% of patients with radiculopathy associated with a lumbar disk herniation had improvement in a matter of months with exercise-based physical therapy. In the nonoperative SPORT cohort, patients had significant improvement from baseline, and approximately 60% of those with classic radiculopathy who initially received nonoperative treatment avoided surgery. Mr. Winston has had minimal treatment and has had symptoms for only 10 weeks. He should undergo a course of exercise-based physical therapy and a trial of a nonsteroidal antiinflammatory medication and may consider a lumbar epidural glucocorticoid injection. Although there is little evidence of the effectiveness of these nonoperative options alone, the combination of these treatments and the benign natural history of the patient�s condition could result in alleviation or resolution of symptoms. If these interventions � and time � do not resolve his symptoms, surgery could be considered as a final option, but it may not have long-term effectiveness and could in and of itself cause the possibility of more harm than good. Mr. Winston has risk factors, such as obesity and a history of smoking, that have been shown to contribute to poor surgical outcomes of certain spinal procedures.
Mr. Winston has symptoms of back pain that interfere with his quality of life. He would need to understand, through shared decision making, that a nonsurgical approach is likely to be more effective than surgery over time.
Information referenced from the National Center for Biotechnology Information (NCBI) and the New England Journal of Medicine (NEJM). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Cited by Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
1. Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical vs nonoperative treatment for lumbar disk herniation: the Spine Patient Outcomes Research Trial (SPORT): a randomized trial. JAMA2006;296:2441–2450
2. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical vs nonoperative treatment for lumbar disk herniation: the Spine Patient Outcomes Research Trial (SPORT) observational cohort. JAMA2006;296:2451–2459
3. Kreiner DS, Hwang SW, Easa JE, et al. An evidence-based clinical guideline for the diagnosis and treatment of lumbar disc herniation with radiculopathy. Spine J2014;14:180–191
4. Ghahreman A, Ferch R, Bogduk N. The efficacy of transforaminal injection of steroids for the treatment of lumbar radicular pain. Pain Med2010;11:1149–1168
6. Ghogawala Z, Shaffrey CI, Asher AL, et al. The efficacy of lumbar discectomy and single-level fusion for spondylolisthesis: results from the NeuroPoint-SD registry: clinical article. J Neurosurg Spine2013;19:555–563
8. Lurie JD, Tosteson TD, Tosteson AN, et al. Surgical versus nonoperative treatment for lumbar disc herniation: eight-year results for the spine patient outcomes research trial. Spine (Phila Pa 1976)2014;39:3–16
11. Pinto RZ, Maher CG, Ferreira ML, et al. Drugs for relief of pain in patients with sciatica: systematic review and meta-analysis. BMJ2012;344:e497–e497
12. Pearson A, Lurie J, Tosteson T, et al. Who should have surgery for an intervertebral disc herniation? Comparative effectiveness evidence from the Spine Patient Outcomes Research Trial. Spine2012;37:140–149
These assessment and treatment recommendations represent a synthesis of information derived from personal clinical experience and from the numerous sources which are cited, or are based on the work of researchers, clinicians and therapists who are named (Basmajian 1974, Cailliet 1962, Dvorak & Dvorak 1984, Fryette 1954, Greenman 1989, 1996, Janda 1983, Lewit 1992, 1999, Mennell 1964, Rolf 1977, Williams 1965).
Clinical Application of Neuromuscular Techniques: Upper Trapezius
Lewit (1999) simplifies the need to assess for shortness by stating, �The upper trapezius should be treated if tender and taut.� Since this is an almost universal state in modern life, it seems that everyone requires MET application to this muscle. Lewit also notes that a characteristic mounding of the muscle can often be observed when it is very short, producing the effect of �Gothic shoulders�, similar to the architectural supports of a Gothic church tower (see Fig. 2.13).
Assessment for Shortness of Upper Trapezius (13) (Fig. 4.30)
Figure 4.30 Assessment of the relative shortness of the right side upper trapezius. One side is compared with the other (for both the range of unforced motion and the nature of the end-feel of motion) to ascertain the side most in need of MET attention.
Test for upper trapezius for shortness (a) See scapulohumeral rhythm test (Ch. 5) which helps identify excessive activity or inappropriate tone in levator scapula and upper trapezius, which, because they are postural muscles, indicates shortness (Fig 5.13A, B). Greenman (1996) describes a functional �firing sequence� assessment which identifies general imbalance and dysfunction involving the upper and lower fixators of the shoulder (Fig. 4.31).
Figure 4.31 Palpation assessment for upper and lower fixators of the shoulder, including upper trapezius (Greenman 1996).
The patient is seated and the practitioner stands behind. The practitioner rests his right hand over the right shoulder area to assess firing sequence of muscles. The other hand can be placed either on the mid-thoracic region, mainly on the side being assessed, or spanning the lower back to palpate quadratus firing. The assessment should be performed at least twice so that various hand positions are used for different muscles (as in Fig. 4.31).
Greenman bases his description on Janda (1983), who notes the �correct� sequence for shoulder abduction, when seated, as involving: supraspinatus, deltoid, infraspinatus, middle and lower trapezius and finally contralateral quadratus. In dysfunctional states the most common substitutions are said to involve: shoulder elevation by levator scapulae and upper trapezius, as well as early firing by quadratus lumborum, ipsilateral and contralateral.
Inappropriate activity of the upper fixators results in shortness, and of the lower fixators in weakness and possible lengthening (see Ch. 2 for discussion of postural/phasic, etc. muscle characteristics).
Test for upper trapezius for shortness (b) The patient is seated and the practitioner stands behind with one hand resting on the shoulder of the side to be tested and stabilising it. The other hand is placed on the ipsilateral side of the head and the head/neck is taken into contralateral sidebending without force while the shoulder is stabilised (see Fig. 4.30).
The same procedure is performed on the other side with the opposite shoulder stabilised. A comparison is made as to which sidebending manoeuvre produced the greater range and whether the neck can easily reach 45� of side-flexion in each direction, which it should. If neither side can achieve this degree of sidebend, then both trapezius muscles may be short. The relative shortness of one, compared with the other, is evaluated.
Test for upper trapezius for shortness (c) The patient is seated and the practitioner stands behind with a hand resting over the muscle on the side to be assessed. The patient is asked to extend the arm at the shoulder joint, bringing the flexed arm/elbow backwards. If the upper trapezius is stressed on that side it will inappropriately activate during this movement. Since it is a postural muscle, shortness in it can then be assumed (see discussion of postural muscle characteristics in Ch. 3).
Test of upper trapezius for shortness (d) The patient is supine with the neck fully (but not forcefully) sidebent contralaterally (away from the side being assessed). The practitioner is standing at the head of the table and uses a cupped hand contact on the ipsilateral shoulder (i.e. on the side being tested) to assess the ease with which it can be depressed (moved caudally) (Fig. 4.32).
Figure 4.32 MET treatment of right side upper trapezius muscle. A Posterior fibres, B middle fibres, C anterior fibres. Note that stretching in this (or any of the alternative positions which access the middle and posterior fibres) is achieved following the isometric contraction by means of an easing of the shoulder away from the stabilised head, with no force being applied to the neck and head itself.
There should be an easy �springing� sensation as the practitioner pushes the shoulder towards the feet, with a soft end-feel to the movement. If depression of the shoulder is difficult or if there is a harsh, sudden end-point, upper trapezius shortness is confirmed.
This same assessment (always with full lateral flexion) should be performed with the head fully rotated away from the side being treated, half turned away from the side being treated, and slightly turned towards the side being treated, in order to respectively assess the relative shortness and functional efficiency of posterior, middle and anterior subdivisions of the upper portion of trapezius.
MET Treatment of Chronically Shortened Upper Trapezius
MET treatment of upper trapezius, method (a) (Fig. 4.32) In order to treat all the fibres of upper trapezius, MET needs to be applied sequentially. The upper trapezius is subdivided here into anterior, middle and posterior fibres. The neck should be placed into different positions of rotation, coupled with the sidebending as described in the assessment description above, for precise treatment of the various fibres.
The patient lies supine, arm on the side to be treated lying alongside the trunk, head/neck sidebent away from the side being treated to just short of the restriction barrier, while the practitioner stabilises the shoulder with one hand and cups the ear/mastoid area of the same side of the head with the other:
With the neck fully sidebent and fully rotated contralaterally, the posterior fibres of upper trapezius are involved in the contraction (see below). This will facilitate subsequent stretching of this aspect of the muscle.
With the neck fully sidebent and half rotated, the middle fibres are involved in the contraction.
With the neck fully sidebent and slightly rotated towards the side being treated the anterior fibres of upper trapezius are being treated.
The various contractions and subsequent stretches can be performed with practitioner�s arms crossed, hands stabilising the mastoid area and shoulder.
The patient introduces a light resisted effort (20% of available strength) to take the stabilised shoulder towards the ear (a shrug movement) and the ear towards the shoulder. The double movement (or effort towards movement) is important in order to introduce a contraction of the muscle from both ends simultaneously. The degree of effort should be mild and no pain should be felt. The contraction is sustained for 10 seconds (or so) and, upon complete relaxation of effort, the practitioner gently eases the head/neck into an increased degree of sidebending and rotation, where it is stabilised, as the shoulder is stretched caudally.
When stretching is introduced the patient can usefully assist in this phase of the treatment by initiating, on instruction, the stretch of the muscle (�as you breathe out please slide your hand towards your feet�). This reduces the chances of a stretch reflex being initiated. Once the muscle is being stretched, the patient relaxes and the stretch is held for 10�30 seconds.
CAUTION: No stretch should be introduced from the cranial end of the muscle as this could stress the neck. The head is stabilised at its side-flexion and rotation barrier.
Disagreement
There is some disagreement as to the head/neck rotation position as described in the treatment method above, which calls (for posterior and middle fibres) for sidebending and rotation away from the affected side.
Liebenson (1996), suggests that the patient �lies supine with the head supported in anteflexion and laterally flexed away and rotated towards the side of involvement�.
Lewit (1985b) suggests: �The patient is supine � the therapist fixes the shoulder from above with one hand, sidebending the head and neck with the other hand so as to take up the slack. He then asks the patient to look towards the side away from which the head is bent, resisting the patient�s automatic tendency to move towards the side of the lesion.� (This method is described below.)
The author has used the methods described above with good effect and urges readers to try these approaches as well as those of Liebenson and Lewit, and to evaluate results for themselves.
MET treatment of acutely shortened upper trapezius, method (b) Lewit suggests the use of eye movements to facilitate initiation of PIR before stretching, an ideal method for acute problems in this region.
The patient is supine, while the practitioner fixes the shoulder and the sidebent (away from the treated side) head and neck at the restriction barrier and asks the patient to look, with the eyes only (i.e. not to turn the head), towards the side away from which the neck is bent.
This eye movement is maintained, as is a held breath, while the practitioner resists the slight isometric contraction that these two factors (eye movement and breath) will have created.
On exhalation and complete relaxation, the head/neck is taken to a new barrier and the process repeated. If the shoulder is brought into the equation, this is firmly held as it attempts to lightly push into a shrug. After this 10 second contraction the muscle will have released somewhat and slack can again be taken out as the head is repositioned before a repetition of the procedure commences.
Dr. Alex Jimenez offers an additional assessment and treatment of the hip flexors as a part of a referenced clinical application of neuromuscular techniques by Leon Chaitow and Judith Walker DeLany. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
1.�Ballou SK, Keefer L. Multicultural considerations in the diagnosis and management of irritable bowel syndrome: a selective summary.�Eur J Gastroenterol Hepatol.�2013;25:1127�1133.�[PubMed]
2.�Gonzales Gamarra RG, Ruiz S�nchez JG, Le�n Jim�nez F, Cubas Benavides F, D�az V�lez C. [Prevalence of irritable bowel syndrome in the adult population of the city of Chiclayo in 2011]�Rev Gastroenterol Peru.�2012;32:381�386.�[PubMed]
3.�Gwee KA, Lu CL, Ghoshal UC. Epidemiology of irritable bowel syndrome in Asia: something old, something new, something borrowed.�J Gastroenterol Hepatol.�2009;24:1601�1607.�[PubMed]
4.�Krogsgaard LR, Engsbro AL, Bytzer P. The epidemiology of irritable bowel syndrome in Denmark. A population-based survey in adults ? 50 years of age.�Scand J Gastroenterol.�2013;48:523�529.�[PubMed]
5.�Ibrahim NK, Battarjee WF, Almehmadi SA. Prevalence and predictors of irritable bowel syndrome among medical students and interns in King Abdulaziz University, Jeddah.�Libyan J Med.�2013;8:21287.[PMC free article]�[PubMed]
6.�Lee YY, Waid A, Tan HJ, Chua AS, Whitehead WE. Rome III survey of irritable bowel syndrome among ethnic Malays.�World J Gastroenterol.�2012;18:6475�6480; discussion p. 6479.�[PMC free article][PubMed]
7.�Ghoshal UC, Abraham P, Bhatt C, Choudhuri G, Bhatia SJ, Shenoy KT, Banka NH, Bose K, Bohidar NP, Chakravartty K, et al. Epidemiological and clinical profile of irritable bowel syndrome in India: report of the Indian Society of Gastroenterology Task Force.�Indian J Gastroenterol.�2008;27:22�28.�[PubMed]
8.�Bures J, Cyrany J, Kohoutova D, F�rstl M, Rejchrt S, Kvetina J, Vorisek V, Kopacova M. Small intestinal bacterial overgrowth syndrome.�World J Gastroenterol.�2010;16:2978�2990.�[PMC free article][PubMed]
9.�Dibaise JK, Young RJ, Vanderhoof JA. Enteric microbial flora, bacterial overgrowth, and short-bowel syndrome.�Clin Gastroenterol Hepatol.�2006;4:11�20.�[PubMed]
10.�Bouhnik Y, Alain S, Attar A, Flouri� B, Raskine L, Sanson-Le Pors MJ, Rambaud JC. Bacterial populations contaminating the upper gut in patients with small intestinal bacterial overgrowth syndrome.�Am J Gastroenterol.�1999;94:1327�1331.�[PubMed]
11.�Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review.�Gastroenterol Hepatol (N Y)�2007;3:112�122.�[PMC free article]�[PubMed]
12.�Posserud I, Stotzer PO, Bj�rnsson ES, Abrahamsson H, Simr�n M. Small intestinal bacterial overgrowth in patients with irritable bowel syndrome.�Gut.�2007;56:802�808.�[PMC free article]�[PubMed]
13.�Ghoshal U, Ghoshal UC, Ranjan P, Naik SR, Ayyagari A. Spectrum and antibiotic sensitivity of bacteria contaminating the upper gut in patients with malabsorption syndrome from the tropics.�BMC Gastroenterol.�2003;3:9.�[PMC free article]�[PubMed]
14.�Carrara M, Desideri S, Azzurro M, Bulighin GM, Di Piramo D, Lomonaco L, Adamo S. Small intestine bacterial overgrowth in patients with irritable bowel syndrome.�Eur Rev Med Pharmacol Sci.�2008;12:197�202.�[PubMed]
15.�Ghoshal UC, Ghoshal U, Das K, Misra A. Utility of hydrogen breath tests in diagnosis of small intestinal bacterial overgrowth in malabsorption syndrome and its relationship with oro-cecal transit time.�Indian J Gastroenterol.�2006;25:6�10.�[PubMed]
16.�Ghoshal UC, Kumar S, Mehrotra M, Lakshmi C, Misra A. Frequency of small intestinal bacterial overgrowth in patients with irritable bowel syndrome and chronic non-specific diarrhea.�J Neurogastroenterol Motil.�2010;16:40�46.�[PMC free article]�[PubMed]
17.�Pimentel M, Chow EJ, Lin HC. Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome.�Am J Gastroenterol.�2000;95:3503�3506.�[PubMed]
18.�Sachdeva S, Rawat AK, Reddy RS, Puri AS. Small intestinal bacterial overgrowth (SIBO) in irritable bowel syndrome: frequency and predictors.�J Gastroenterol Hepatol.�2011;26 Suppl 3:135�138.�[PubMed]
19.�Park H. The role of small intestinal bacterial overgrowth in the pathophysiology of irritable bowel syndrome.�J Neurogastroenterol Motil.�2010;16:3�4.�[PMC free article]�[PubMed]
20.�Ghoshal UC, Shukla R, Ghoshal U, Gwee KA, Ng SC, Quigley EM. The gut microbiota and irritable bowel syndrome: friend or foe?�Int J Inflam.�2012;2012:151085.�[PMC free article]�[PubMed]
21.�Brown AC. Ulcerative colitis, Crohn�s disease and irritable bowel syndrome patients need fecal transplant research and treatment.�J Crohns Colitis.�2014;8:179.�[PubMed]
22.�Sampath K, Levy LC, Gardner TB. Fecal transplantation: beyond the aesthetic.�Gastroenterology.�2013;145:1151�1153.�[PubMed]
23.�Grace E, Shaw C, Whelan K, Andreyev HJ. Review article: small intestinal bacterial overgrowth–prevalence, clinical features, current and developing diagnostic tests, and treatment.�Aliment Pharmacol Ther.�2013;38:674�688.�[PubMed]
24.�Yakoob J, Abbas Z, Khan R, Hamid S, Awan S, Jafri W. Small intestinal bacterial overgrowth and lactose intolerance contribute to irritable bowel syndrome symptomatology in Pakistan.�Saudi J Gastroenterol.�2011;17:371�375.�[PMC free article]�[PubMed]
25.�Gwee KA, Bak YT, Ghoshal UC, Gonlachanvit S, Lee OY, Fock KM, Chua AS, Lu CL, Goh KL, Kositchaiwat C, et al. Asian consensus on irritable bowel syndrome.�J Gastroenterol Hepatol.�2010;25:1189�1205.�[PubMed]
26.�Lacy BE, Gabbard SL, Crowell MD. Pathophysiology, evaluation, and treatment of bloating: hope, hype, or hot air?�Gastroenterol Hepatol (N Y)�2011;7:729�739.�[PMC free article]�[PubMed]
27.�Harder H, Serra J, Azpiroz F, Passos MC, Aguad� S, Malagelada JR. Intestinal gas distribution determines abdominal symptoms.�Gut.�2003;52:1708�1713.�[PMC free article]�[PubMed]
28.�Kumar S, Misra A, Ghoshal UC. Patients with irritable bowel syndrome exhale more hydrogen than healthy subjects in fasting state.�J Neurogastroenterol Motil.�2010;16:299�305.�[PMC free article][PubMed]
29.�Hungin AP, Mulligan C, Pot B, Whorwell P, Agr�us L, Fracasso P, Lionis C, Mendive J, Philippart de Foy JM, Rubin G, Winchester C, de Wit N. Systematic review: probiotics in the management of lower gastrointestinal symptoms in clinical practice — an evidence-based international guide.�Aliment Pharmacol Ther.�2013;38:864�886.�[PMC free article]�[PubMed]
30.�Attar A, Flouri� B, Rambaud JC, Franchisseur C, Ruszniewski P, Bouhnik Y. Antibiotic efficacy in small intestinal bacterial overgrowth-related chronic diarrhea: a crossover, randomized trial.�Gastroenterology.�1999;117:794�797.�[PubMed]
31.�Marcelino RT, Fagundes-Neto U. [Hydrogen test (H2) in the air expired for the diagnosis of small bowel bacterial overgrowth]�Arq Gastroenterol.�1995;32:191�198.�[PubMed]
32.�Santavirta J. Lactulose hydrogen and [14C]xylose breath tests in patients with ileoanal anastomosis.�Int J Colorectal Dis.�1991;6:208�211.�[PubMed]
33.�Ghoshal UC. How to interpret hydrogen breath tests.�J Neurogastroenterol Motil.�2011;17:312�317.[PMC free article]�[PubMed]
34.�Yang CY, Chang CS, Chen GH. Small-intestinal bacterial overgrowth in patients with liver cirrhosis, diagnosed with glucose H2 or CH4 breath tests.�Scand J Gastroenterol.�1998;33:867�871.�[PubMed]
35.�Ghoshal UC, Ghoshal U, Ayyagari A, Ranjan P, Krishnani N, Misra A, Aggarwal R, Naik S, Naik SR. Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time.�J Gastroenterol Hepatol.�2003;18:540�547.�[PubMed]
36.�Lu CL, Chen CY, Chang FY, Lee SD. Characteristics of small bowel motility in patients with irritable bowel syndrome and normal humans: an Oriental study.�Clin Sci (Lond)�1998;95:165�169.�[PubMed]
37.�Sciarretta G, Furno A, Mazzoni M, Garagnani B, Malaguti P. Lactulose hydrogen breath test in orocecal transit assessment. Critical evaluation by means of scintigraphic method.�Dig Dis Sci.�1994;39:1505�1510.�[PubMed]
38.�Rao SS, Camilleri M, Hasler WL, Maurer AH, Parkman HP, Saad R, Scott MS, Simren M, Soffer E, Szarka L. Evaluation of gastrointestinal transit in clinical practice: position paper of the American and European Neurogastroenterology and Motility Societies.�Neurogastroenterol Motil.�2011;23:8�23.[PubMed]
39.�Yu D, Cheeseman F, Vanner S. Combined oro-caecal scintigraphy and lactulose hydrogen breath testing demonstrate that breath testing detects oro-caecal transit, not small intestinal bacterial overgrowth in patients with IBS.�Gut.�2011;60:334�340.�[PubMed]
40.�Rana SV, Sharma S, Sinha SK, Kaur H, Sikander A, Singh K. Incidence of predominant methanogenic flora in irritable bowel syndrome patients and apparently healthy controls from North India.�Dig Dis Sci.�2009;54:132�135.�[PubMed]
41.�Dridi B, Henry M, El Kh�chine A, Raoult D, Drancourt M. High prevalence of Methanobrevibacter smithii and Methanosphaera stadtmanae detected in the human gut using an improved DNA detection protocol.�PLoS One.�2009;4:e7063.�[PMC free article]�[PubMed]
42.�Chatterjee S, Park S, Low K, Kong Y, Pimentel M. The degree of breath methane production in IBS correlates with the severity of constipation.�Am J Gastroenterol.�2007;102:837�841.�[PubMed]
43.�Lunia MK, Sharma BC, Sachdeva S. Small intestinal bacterial overgrowth and delayed orocecal transit time in patients with cirrhosis and low-grade hepatic encephalopathy.�Hepatol Int.�2013;7:268�273.[PubMed]
44.�Resmini E, Parodi A, Savarino V, Greco A, Rebora A, Minuto F, Ferone D. Evidence of prolonged orocecal transit time and small intestinal bacterial overgrowth in acromegalic patients.�J Clin Endocrinol Metab.�2007;92:2119�2124.�[PubMed]
45.�Hamilton I, Worsley BW, Cobden I, Cooke EM, Shoesmith JG, Axon AT. Simultaneous culture of saliva and jejunal aspirate in the investigation of small bowel bacterial overgrowth.�Gut.�1982;23:847�853.[PMC free article]�[PubMed]
46.�Corazza GR, Sorge M, Strocchi A, Benati G, Di Sario A, Treggiari EA, Brusco G, Gasbarrini G. Non-absorbable antibiotics and small bowel bacterial overgrowth.�Ital J Gastroenterol.�1992;24:4�9.�[PubMed]
47.�Kuwahara T, Ogura Y, Oshima K, Kurokawa K, Ooka T, Hirakawa H, Itoh T, Nakayama-Imaohji H, Ichimura M, Itoh K, et al. The lifestyle of the segmented filamentous bacterium: a non-culturable gut-associated immunostimulating microbe inferred by whole-genome sequencing.�DNA Res.�2011;18:291�303.�[PMC free article]�[PubMed]
49.�Fromm H, Sarva RP, Ravitch MM, McJunkin B, Farivar S, Amin P. Effects of jejunoileal bypass on the enterohepatic circulation of bile acids, bacterial flora in the upper small intestine, and absorption of vitamin B12.�Metabolism.�1983;32:1133�1141.�[PubMed]
50.�Yoshida T, McCormick WC, Swell L, Vlahcevic ZR. Bile acid metabolism in cirrhosis. IV. Characterization of the abnormality in deoxycholic acid metabolism.�Gastroenterology.�1975;68:335�341.[PubMed]
51.�Bj�rneklett A, Fausa O, Midtvedt T. Bacterial overgrowth in jejunal and ileal disease.�Scand J Gastroenterol.�1983;18:289�298.�[PubMed]
52.�Vanner S. The small intestinal bacterial overgrowth. Irritable bowel syndrome hypothesis: implications for treatment.�Gut.�2008;57:1315�1321.�[PubMed]
53.�Kinross JM, von Roon AC, Holmes E, Darzi A, Nicholson JK. The human gut microbiome: implications for future health care.�Curr Gastroenterol Rep.�2008;10:396�403.�[PubMed]
54.�Clauw DJ. Fibromyalgia: an overview.�Am J Med.�2009;122:S3�S13.�[PubMed]
55.�Pimentel M, Wallace D, Hallegua D, Chow E, Kong Y, Park S, Lin HC. A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing.�Ann Rheum Dis.�2004;63:450�452.�[PMC free article]�[PubMed]
56.�Simr�n M, Stotzer PO. Use and abuse of hydrogen breath tests.�Gut.�2006;55:297�303.[PMC free article]�[PubMed]
57.�Gasbarrini A, Lauritano EC, Gabrielli M, Scarpellini E, Lupascu A, Ojetti V, Gasbarrini G. Small intestinal bacterial overgrowth: diagnosis and treatment.�Dig Dis.�2007;25:237�240.�[PubMed]
58.�Ghoshal UC, Srivastava D, Verma A, Misra A. Slow transit constipation associated with excess methane production and its improvement following rifaximin therapy: a case report.�J Neurogastroenterol Motil.�2011;17:185�188.�[PMC free article]�[PubMed]
59.�Bala L, Ghoshal UC, Ghoshal U, Tripathi P, Misra A, Gowda GA, Khetrapal CL. Malabsorption syndrome with and without small intestinal bacterial overgrowth: a study on upper-gut aspirate using 1H NMR spectroscopy.�Magn Reson Med.�2006;56:738�744.�[PubMed]
60.�Haboubi NY, Lee GS, Montgomery RD. Duodenal mucosal morphometry of elderly patients with small intestinal bacterial overgrowth: response to antibiotic treatment.�Age Ageing.�1991;20:29�32.�[PubMed]
61.�Shindo K, Machida M, Koide K, Fukumura M, Yamazaki R. Deconjugation ability of bacteria isolated from the jejunal fluid of patients with progressive systemic sclerosis and its gastric pH.�Hepatogastroenterology.�1998;45:1643�1650.�[PubMed]
62.�Wanitschke R, Ammon HV. Effects of dihydroxy bile acids and hydroxy fatty acids on the absorption of oleic acid in the human jejunum.�J Clin Invest.�1978;61:178�186.�[PMC free article]�[PubMed]
63.�Shanab AA, Scully P, Crosbie O, Buckley M, O�Mahony L, Shanahan F, Gazareen S, Murphy E, Quigley EM. Small intestinal bacterial overgrowth in nonalcoholic steatohepatitis: association with toll-like receptor 4 expression and plasma levels of interleukin 8.�Dig Dis Sci.�2011;56:1524�1534.�[PubMed]
64.�Ghoshal UC, Park H, Gwee KA. Bugs and irritable bowel syndrome: The good, the bad and the ugly.�J Gastroenterol Hepatol.�2010;25:244�251.�[PubMed]
65.�Barbara G, Stanghellini V, Brandi G, Cremon C, Di Nardo G, De Giorgio R, Corinaldesi R. Interactions between commensal bacteria and gut sensorimotor function in health and disease.�Am J Gastroenterol.�2005;100:2560�2568.�[PubMed]
66.�Cherbut C, Aub� AC, Blotti�re HM, Galmiche JP. Effects of short-chain fatty acids on gastrointestinal motility.�Scand J Gastroenterol Suppl.�1997;222:58�61.�[PubMed]
67.�Ramakrishna BS, Roediger WE. Bacterial short chain fatty acids: their role in gastrointestinal disease.�Dig Dis.�1990;8:337�345.�[PubMed]
68.�Dumoulin V, Moro F, Barcelo A, Dakka T, Cuber JC. Peptide YY, glucagon-like peptide-1, and neurotensin responses to luminal factors in the isolated vascularly perfused rat ileum.�Endocrinology.�1998;139:3780�3786.�[PubMed]
69.�Balsari A, Ceccarelli A, Dubini F, Fesce E, Poli G. The fecal microbial population in the irritable bowel syndrome.�Microbiologica.�1982;5:185�194.�[PubMed]
70.�Nobaek S, Johansson ML, Molin G, Ahrn� S, Jeppsson B. Alteration of intestinal microflora is associated with reduction in abdominal bloating and pain in patients with irritable bowel syndrome.�Am J Gastroenterol.�2000;95:1231�1238.�[PubMed]
71.�Cummings JH, Macfarlane GT. The control and consequences of bacterial fermentation in the human colon.�J Appl Bacteriol.�1991;70:443�459.�[PubMed]
72.�Camilleri M. Probiotics and irritable bowel syndrome: rationale, mechanisms, and efficacy.�J Clin Gastroenterol.�2008;42 Suppl 3 Pt 1:S123�S125.�[PubMed]
73.�Spiller R. Probiotics: an ideal anti-inflammatory treatment for IBS?�Gastroenterology.�2005;128:783�785.�[PubMed]
74.�Ford AC, Spiegel BM, Talley NJ, Moayyedi P. Small intestinal bacterial overgrowth in irritable bowel syndrome: systematic review and meta-analysis.�Clin Gastroenterol Hepatol.�2009;7:1279�1286.�[PubMed]
75.�Cuoco L, Salvagnini M. Small intestine bacterial overgrowth in irritable bowel syndrome: a retrospective study with rifaximin.�Minerva Gastroenterol Dietol.�2006;52:89�95.�[PubMed]
76.�Di Stefano M, Corazza GR. Treatment of small intestine bacterial overgrowth and related symptoms by rifaximin.�Chemotherapy.�2005;51 Suppl 1:103�109.�[PubMed]
77.�Pimentel M, Lembo A, Chey WD, Zakko S, Ringel Y, Yu J, Mareya SM, Shaw AL, Bortey E, Forbes WP. Rifaximin therapy for patients with irritable bowel syndrome without constipation.�N Engl J Med.�2011;364:22�32.�[PubMed]
78.�Hwang L, Low K, Khoshini R, Melmed G, Sahakian A, Makhani M, Pokkunuri V, Pimentel M. Evaluating breath methane as a diagnostic test for constipation-predominant IBS.�Dig Dis Sci.�2010;55:398�403.�[PubMed]
79.�Low K, Hwang L, Hua J, Zhu A, Morales W, Pimentel M. A combination of rifaximin and neomycin is most effective in treating irritable bowel syndrome patients with methane on lactulose breath test.�J Clin Gastroenterol.�2010;44:547�550.�[PubMed]
80.�Bengmark S. Colonic food: pre- and probiotics.�Am J Gastroenterol.�2000;95:S5�S7.�[PubMed]
81.�Quigley EM, Quera R. Small intestinal bacterial overgrowth: roles of antibiotics, prebiotics, and probiotics.�Gastroenterology.�2006;130:S78�S90.�[PubMed]
82.�Xiao SD, Zhang DZ, Lu H, Jiang SH, Liu HY, Wang GS, Xu GM, Zhang ZB, Lin GJ, Wang GL. Multicenter, randomized, controlled trial of heat-killed Lactobacillus acidophilus LB in patients with chronic diarrhea.�Adv Ther.�2003;20:253�260.�[PubMed]
83.�O’Mahony L, McCarthy J, Kelly P, Hurley G, Luo F, Chen K, O�Sullivan GC, Kiely B, Collins JK, Shanahan F, et al. Lactobacillus and bifidobacterium in irritable bowel syndrome: symptom responses and relationship to cytokine profiles.�Gastroenterology.�2005;128:541�551.�[PubMed]
84.�Tsuchiya J, Barreto R, Okura R, Kawakita S, Fesce E, Marotta F. Single-blind follow-up study on the effectiveness of a symbiotic preparation in irritable bowel syndrome.�Chin J Dig Dis.�2004;5:169�174.[PubMed]
85.�Kim YG, Moon JT, Lee KM, Chon NR, Park H. [The effects of probiotics on symptoms of irritable bowel syndrome]�Korean J Gastroenterol.�2006;47:413�419.�[PubMed]
86.�Park JS, Yu JH, Lim HC, Kim JH, Yoon YH, Park HJ, Lee SI. [Usefulness of lactulose breath test for the prediction of small intestinal bacterial overgrowth in irritable bowel syndrome]�Korean J Gastroenterol.�2010;56:242�248.�[PubMed]
87.�Mann NS, Limoges-Gonzales M. The prevalence of small intestinal bacterial vergrowth in irritable bowel syndrome.�Hepatogastroenterology.�2009;56:718�721.�[PubMed]
88.�Scarpellini E, Giorgio V, Gabrielli M, Lauritano EC, Pantanella A, Fundar� C, Gasbarrini A. Prevalence of small intestinal bacterial overgrowth in children with irritable bowel syndrome: a case-control study.�J Pediatr.�2009;155:416�420.�[PubMed]
89.�Nucera G, Gabrielli M, Lupascu A, Lauritano EC, Santoliquido A, Cremonini F, Cammarota G, Tondi P, Pola P, Gasbarrini G, et al. Abnormal breath tests to lactose, fructose and sorbitol in irritable bowel syndrome may be explained by small intestinal bacterial overgrowth.�Aliment Pharmacol Ther.�2005;21:1391�1395.�[PubMed]
90.�Reddymasu SC, Sostarich S, McCallum RW. Small intestinal bacterial overgrowth in irritable bowel syndrome: are there any predictors?�BMC Gastroenterol.�2010;10:23.�[PMC free article]�[PubMed]
91.�Lombardo L, Foti M, Ruggia O, Chiecchio A. Increased incidence of small intestinal bacterial overgrowth during proton pump inhibitor therapy.�Clin Gastroenterol Hepatol.�2010;8:504�508.�[PubMed]
92.�Parodi A, Dulbecco P, Savarino E, Giannini EG, Bodini G, Corbo M, Isola L, De Conca S, Marabotto E, Savarino V. Positive glucose breath testing is more prevalent in patients with IBS-like symptoms compared with controls of similar age and gender distribution.�J Clin Gastroenterol.�2009;43:962�966.[PubMed]
93.�Rana SV, Sinha SK, Sikander A, Bhasin DK, Singh K. Study of small intestinal bacterial overgrowth in North Indian patients with irritable bowel syndrome: a case control study.�Trop Gastroenterol.�2008;29:23�25.�[PubMed]
94.�Majewski M, McCallum RW. Results of small intestinal bacterial overgrowth testing in irritable bowel syndrome patients: clinical profiles and effects of antibiotic trial.�Adv Med Sci.�2007;52:139�142.[PubMed]
95.�Lupascu A, Gabrielli M, Lauritano EC, Scarpellini E, Santoliquido A, Cammarota G, Flore R, Tondi P, Pola P, Gasbarrini G, et al. Hydrogen glucose breath test to detect small intestinal bacterial overgrowth: a prevalence case-control study in irritable bowel syndrome.�Aliment Pharmacol Ther.�2005;22:1157�1160.[PubMed]
Irritable bowel syndrome, or IBS, is a prevalent condition characterized by abdominal pain or discomfort, bloating, connected to altered stool form (such as diarrhea and constipation) as well as passage. Approximately 4 percent to 30 percent of individuals world-wide suffer from IBS. Small intestinal bacterial overgrowth, or SIBO, which was clinically demonstrated in patients with structural abnormalities in the gut, such as ileo-transverse anastomosis, stricture, fistula, slow motility and reduced gut defense, may also be characterized by abdominal pain or discomfort, bloating, flatulence and loose motion. It’s been recognized that SIBO may occur in the absence of structural abnormalities. These patients may be incorrectly diagnosed with IBS, or irritable bowel syndrome.
How common is SIBO diagnosed in IBS?
Small intestinal bacterial overgrowth has been described as the excessive presence of bacteria, forming 105 units per milliliter on culture of their intestine aspirate. As this is an invasive test, lots of noninvasive techniques like lactulose and glucose hydrogen breath tests (LHBT and GHBT) are broadly used to diagnose SIBO. This issue has been recognized among people with IBS. In a variety of research studies, frequency of SIBO among patients presenting IBS varied from 4 percent to 78 percent, according to Table ?1, more so among patients with diarrhea-predominant IBS. Not only quantitative increase (SIBO) but qualitative change from the gut bacteria (dysbiosis) was reported among patients with IBS. Research studies utilizing antibiotics and probiotics have caused disagreement to care for this disease with lately transplantation which led to a paradigm shift. Nonetheless, it’s essential to understand the wide-variability in frequency of SIBO among people with IBS. A wide-variability in frequency may indicate it is vital to evaluate the evidence carefully to determine whether the association between IBS and SIBO is under-projected in previous research studies.
The research studies are examined by people on discordance with the connection between IBS and SIBO as well as their strength and weakness, such as evidence on exploitation of gut flora on indications of IBS and other issues.
Assessment of Studies on SIBO in IBS
Table ?1 summarizes the outcomes among patients with IBS from research studies on individuals with SIBO. As can be noted in the table, the frequency of people with IBS and SIBO varied from 4 percent to 78 percent and from 1 percent and 40 percent among controls. Frequency of individuals with SIBO and IBS was greater than among controls. It might be concluded that SIBO is correlated with IBS. It’s essential to assess the explanations in various research studies.
Critical Evaluation of Studies on SIBO in IBS
Can IBS phenotype determine frequency of SIBO?
IBS is a state that’s heterogeneous. The sub-types may be diarrhea or constipation-predominant or may be alternating. Patients with diarrhea-predominant IBS have organic cause including SIBO compared to other types of IBS. In a study on 129 patients with non-diarrheal IBS, 73 with long-term diarrhea, for example diarrhea-predominant IBS, and 51 healthy controls, frequency of SIBO with GHBT was 11 (8.5 percent), 16 (22 percent) and 1 (2%), respectively. Similar findings are reported in various studies. Diarrheal IBS needs to be evaluated in comparison to other sorts of IBS for SIBO. Research studies that contained percentage of individuals are extremely likely to reveal frequency of SIBO.
Bloating is a symptom commonly reported among patients with IBS. Frequency of bloating has been reported to vary from Asia by 26 percent to 83 percent in research studies on IBS. The pathogenesis of bloating may be correlated with increased quantity of gas in the gut, its abnormal source and improved gut sense in response to distension of the gut. Patients with SIBO may have increased amount of gas inside the gut, so it’s plausible to believe IBS patients with bloating that is noticeable are expected to have SIBO. There is limited data with this specific circumstance. Evidence also demonstrated that both fasting along with post-substrate (e.g., sugar, lactulose) breath hydrogen is considerably higher compared to individuals with IBS compared to controls. Probiotics and antibiotics, which are demonstrated to reduce gas, are demonstrated to ease bloating. It has been noted that treatment can revert hydrogen breath tests back to normal. Patients with IBS, flatulence and bloating should be evaluated for SIBO. More data is involved with this issue.
Can techniques used to diagnose SIBO determine its frequency?
Several techniques are used to diagnose SIBO; including GHBT LHBT,14C breath test, and culture of aspirate. The principle of hydrogen breath tests is summarized in Figure 1. Dietary carbohydrates produce hydrogen in the gut. In patients with SIBO, the bacteria in the small bowel ferment these carbohydrates, producing hydrogen, which gets absorbed and is exhaled in the breath.
Figure 1
Hydrogen breath test involves giving patients a load of carbohydrate (generally in the sort of glucose and lactulose) and measuring expired hydrogen concentrations in a period of time. Identification of SIBO using hydrogen breath test depends upon the bodily principle of patients with SIBO, glucose may be fermented by bacteria in the intestine resulting in production of hydrogen gas that is consumed and exhaled in expired air (Figure ?1, A1). By contrast, lactulose, which may function as a non-absorbable disaccharide, will produce an early summit due to fermentation in the small intestine (normally within 90-min) or two summit (as a consequence of small intestine fermentation and minute from colon), if SIBO is present (Figure ?1, B2 and B3). There are limits in hydrogen breath test for identification of SIBO. There may be similarities in patients with problems and SIBO employing rapid transit making differentiation difficult. An ancient summit can be positive in people with gut transit time. By way of instance, in a study from India, median oro-cecal transit interval was 65 minutes (variety 40-110 moments) in healthy subjects. In another study from Taiwan, mean transit interval was 85 min. It’s been substantiated in Western individuals recently by simultaneously using LHBT and radio-nuclide method to gauge gut transport. Double summit standards for evaluation of SIBO using LHBT is quite insensitive. Sensitivity of GHBT to diagnose SIBO is 44 percent contemplating the culture of gut aspirate as a regular standard. As a result, it’s estimated that the researchers who used a historic summit standards in LHBT could discover a greater frequency of SIBO among people with IBS along with controls. In contrast, those who would use either GHBT or double summit benchmark in LHBT might locate a minimum frequency of SIBO alike in patients with IBS and controls. It is well worth noting from Table ?1 that the frequency of SIBO among people with IBS and controls on LHBT (early summit standards) varied from 34.5 percent to 78 percent and 7 percent to 40 percent, respectively; in contrast with the frequency GHBT varied from 8.5 percent to 46 percent and 2 percent to 18percent.
Fifteen percent of people might have methanogenic flora in the gut. Methanobrevibacter smithii, Methanobrevibacter stadmanae and perhaps several of those coliform bacteria are methanogens. In these areas, only hydrogen breath tests may not diagnose SIBO, estimation of methane may also be demanded (Figure ?1). Table ?1 shows that 8.5 percent to 26 percent of IBS sufferers and 0 percent to 25 percent of controls exhaled methane inside their breath. Whether methane was not expected in them, SIBO could not have been diagnosed. Methane was not estimated, which could have resulted in underestimation of frequency of SIBO as outlined in a proportion of the research study. Methane production in excess is connected to constipation. Consequently, methane estimation in breath, which is inaccessible in several commercially available hydrogen breath test machines, is particularly vital in patients employing constipation-predominant IBS. Some could have slow transit through the small intestine making prolonged testing as a lot of hours required and many people may not want to undergo such testing. However, a period of testing for them may overlook SIBO’s identification.
The jejunal aspirate culture has traditionally been used as the gold standard to diagnose SIBO, according to Figure ?2. On the other hand, the limitations of this test include invasiveness in addition to the challenges posed by attempting to civilization all strains and species. In fact, usage of air during endoscopy might lead to a false negative impact as anaerobes do not rise when these are exposed to oxygen. Furthermore, a massive percentage of germs are not cultured. By contrast, single lumen catheter passed through the nose or through the biopsy channel of endoscope, may lead to contamination with oro-pharyngeal flora supplying false positive result. Therefore, we left a double-lumen catheter to prevent these oro-pharyngeal contamination (Figure ?2). Studies on SIBO one of patients with IBS using qualitative civilization of small bowel aspirate are scanty (Table ?1). A study by Posserud et al reported that a frequency of SIBO of 4 percent among people with IBS. Taking the result of study using GHBT, the sensitivity of 44 percent to diagnose the intestine aspirate appears to have the incidence of SIBO . More studies are essential on this issue.
Figure 2
Figure 3
13C and�14C based tests have also been developed based on the bacterial metabolism of D-xylose (Figure ?3). Of acids containing13C and�14C may be used to diagnose SIBO. The glycocholic acid breath test contains the managing of the bile acid14C glycocholic acid, as well as the discovery of14CO2, which may be increased in SIBO (Figure 3), according to the clinical and experimental data from the various research studies on SIBO associated with IBS. While evidence may appear conclusive, further research studies may be required to properly determine the results.
Information referenced from the National Center for Biotechnology Information (NCBI) and the National University of Health Sciences. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
1.�Ballou SK, Keefer L. Multicultural considerations in the diagnosis and management of irritable bowel syndrome: a selective summary.�Eur J Gastroenterol Hepatol.�2013;25:1127�1133.�[PubMed]
2.�Gonzales Gamarra RG, Ruiz S�nchez JG, Le�n Jim�nez F, Cubas Benavides F, D�az V�lez C. [Prevalence of irritable bowel syndrome in the adult population of the city of Chiclayo in 2011]�Rev Gastroenterol Peru.�2012;32:381�386.�[PubMed]
3.�Gwee KA, Lu CL, Ghoshal UC. Epidemiology of irritable bowel syndrome in Asia: something old, something new, something borrowed.�J Gastroenterol Hepatol.�2009;24:1601�1607.�[PubMed]
4.�Krogsgaard LR, Engsbro AL, Bytzer P. The epidemiology of irritable bowel syndrome in Denmark. A population-based survey in adults ? 50 years of age.�Scand J Gastroenterol.�2013;48:523�529.�[PubMed]
5.�Ibrahim NK, Battarjee WF, Almehmadi SA. Prevalence and predictors of irritable bowel syndrome among medical students and interns in King Abdulaziz University, Jeddah.�Libyan J Med.�2013;8:21287.[PMC free article]�[PubMed]
6.�Lee YY, Waid A, Tan HJ, Chua AS, Whitehead WE. Rome III survey of irritable bowel syndrome among ethnic Malays.�World J Gastroenterol.�2012;18:6475�6480; discussion p. 6479.�[PMC free article][PubMed]
7.�Ghoshal UC, Abraham P, Bhatt C, Choudhuri G, Bhatia SJ, Shenoy KT, Banka NH, Bose K, Bohidar NP, Chakravartty K, et al. Epidemiological and clinical profile of irritable bowel syndrome in India: report of the Indian Society of Gastroenterology Task Force.�Indian J Gastroenterol.�2008;27:22�28.�[PubMed]
8.�Bures J, Cyrany J, Kohoutova D, F�rstl M, Rejchrt S, Kvetina J, Vorisek V, Kopacova M. Small intestinal bacterial overgrowth syndrome.�World J Gastroenterol.�2010;16:2978�2990.�[PMC free article][PubMed]
9.�Dibaise JK, Young RJ, Vanderhoof JA. Enteric microbial flora, bacterial overgrowth, and short-bowel syndrome.�Clin Gastroenterol Hepatol.�2006;4:11�20.�[PubMed]
10.�Bouhnik Y, Alain S, Attar A, Flouri� B, Raskine L, Sanson-Le Pors MJ, Rambaud JC. Bacterial populations contaminating the upper gut in patients with small intestinal bacterial overgrowth syndrome.�Am J Gastroenterol.�1999;94:1327�1331.�[PubMed]
11.�Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review.�Gastroenterol Hepatol (N Y)�2007;3:112�122.�[PMC free article]�[PubMed]
12.�Posserud I, Stotzer PO, Bj�rnsson ES, Abrahamsson H, Simr�n M. Small intestinal bacterial overgrowth in patients with irritable bowel syndrome.�Gut.�2007;56:802�808.�[PMC free article]�[PubMed]
13.�Ghoshal U, Ghoshal UC, Ranjan P, Naik SR, Ayyagari A. Spectrum and antibiotic sensitivity of bacteria contaminating the upper gut in patients with malabsorption syndrome from the tropics.�BMC Gastroenterol.�2003;3:9.�[PMC free article]�[PubMed]
14.�Carrara M, Desideri S, Azzurro M, Bulighin GM, Di Piramo D, Lomonaco L, Adamo S. Small intestine bacterial overgrowth in patients with irritable bowel syndrome.�Eur Rev Med Pharmacol Sci.�2008;12:197�202.�[PubMed]
15.�Ghoshal UC, Ghoshal U, Das K, Misra A. Utility of hydrogen breath tests in diagnosis of small intestinal bacterial overgrowth in malabsorption syndrome and its relationship with oro-cecal transit time.�Indian J Gastroenterol.�2006;25:6�10.�[PubMed]
16.�Ghoshal UC, Kumar S, Mehrotra M, Lakshmi C, Misra A. Frequency of small intestinal bacterial overgrowth in patients with irritable bowel syndrome and chronic non-specific diarrhea.�J Neurogastroenterol Motil.�2010;16:40�46.�[PMC free article]�[PubMed]
17.�Pimentel M, Chow EJ, Lin HC. Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome.�Am J Gastroenterol.�2000;95:3503�3506.�[PubMed]
18.�Sachdeva S, Rawat AK, Reddy RS, Puri AS. Small intestinal bacterial overgrowth (SIBO) in irritable bowel syndrome: frequency and predictors.�J Gastroenterol Hepatol.�2011;26 Suppl 3:135�138.�[PubMed]
19.�Park H. The role of small intestinal bacterial overgrowth in the pathophysiology of irritable bowel syndrome.�J Neurogastroenterol Motil.�2010;16:3�4.�[PMC free article]�[PubMed]
20.�Ghoshal UC, Shukla R, Ghoshal U, Gwee KA, Ng SC, Quigley EM. The gut microbiota and irritable bowel syndrome: friend or foe?�Int J Inflam.�2012;2012:151085.�[PMC free article]�[PubMed]
21.�Brown AC. Ulcerative colitis, Crohn�s disease and irritable bowel syndrome patients need fecal transplant research and treatment.�J Crohns Colitis.�2014;8:179.�[PubMed]
22.�Sampath K, Levy LC, Gardner TB. Fecal transplantation: beyond the aesthetic.�Gastroenterology.�2013;145:1151�1153.�[PubMed]
23.�Grace E, Shaw C, Whelan K, Andreyev HJ. Review article: small intestinal bacterial overgrowth–prevalence, clinical features, current and developing diagnostic tests, and treatment.�Aliment Pharmacol Ther.�2013;38:674�688.�[PubMed]
24.�Yakoob J, Abbas Z, Khan R, Hamid S, Awan S, Jafri W. Small intestinal bacterial overgrowth and lactose intolerance contribute to irritable bowel syndrome symptomatology in Pakistan.�Saudi J Gastroenterol.�2011;17:371�375.�[PMC free article]�[PubMed]
25.�Gwee KA, Bak YT, Ghoshal UC, Gonlachanvit S, Lee OY, Fock KM, Chua AS, Lu CL, Goh KL, Kositchaiwat C, et al. Asian consensus on irritable bowel syndrome.�J Gastroenterol Hepatol.�2010;25:1189�1205.�[PubMed]
26.�Lacy BE, Gabbard SL, Crowell MD. Pathophysiology, evaluation, and treatment of bloating: hope, hype, or hot air?�Gastroenterol Hepatol (N Y)�2011;7:729�739.�[PMC free article]�[PubMed]
27.�Harder H, Serra J, Azpiroz F, Passos MC, Aguad� S, Malagelada JR. Intestinal gas distribution determines abdominal symptoms.�Gut.�2003;52:1708�1713.�[PMC free article]�[PubMed]
28.�Kumar S, Misra A, Ghoshal UC. Patients with irritable bowel syndrome exhale more hydrogen than healthy subjects in fasting state.�J Neurogastroenterol Motil.�2010;16:299�305.�[PMC free article][PubMed]
29.�Hungin AP, Mulligan C, Pot B, Whorwell P, Agr�us L, Fracasso P, Lionis C, Mendive J, Philippart de Foy JM, Rubin G, Winchester C, de Wit N. Systematic review: probiotics in the management of lower gastrointestinal symptoms in clinical practice — an evidence-based international guide.�Aliment Pharmacol Ther.�2013;38:864�886.�[PMC free article]�[PubMed]
30.�Attar A, Flouri� B, Rambaud JC, Franchisseur C, Ruszniewski P, Bouhnik Y. Antibiotic efficacy in small intestinal bacterial overgrowth-related chronic diarrhea: a crossover, randomized trial.�Gastroenterology.�1999;117:794�797.�[PubMed]
31.�Marcelino RT, Fagundes-Neto U. [Hydrogen test (H2) in the air expired for the diagnosis of small bowel bacterial overgrowth]�Arq Gastroenterol.�1995;32:191�198.�[PubMed]
32.�Santavirta J. Lactulose hydrogen and [14C]xylose breath tests in patients with ileoanal anastomosis.�Int J Colorectal Dis.�1991;6:208�211.�[PubMed]
33.�Ghoshal UC. How to interpret hydrogen breath tests.�J Neurogastroenterol Motil.�2011;17:312�317.[PMC free article]�[PubMed]
34.�Yang CY, Chang CS, Chen GH. Small-intestinal bacterial overgrowth in patients with liver cirrhosis, diagnosed with glucose H2 or CH4 breath tests.�Scand J Gastroenterol.�1998;33:867�871.�[PubMed]
35.�Ghoshal UC, Ghoshal U, Ayyagari A, Ranjan P, Krishnani N, Misra A, Aggarwal R, Naik S, Naik SR. Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time.�J Gastroenterol Hepatol.�2003;18:540�547.�[PubMed]
36.�Lu CL, Chen CY, Chang FY, Lee SD. Characteristics of small bowel motility in patients with irritable bowel syndrome and normal humans: an Oriental study.�Clin Sci (Lond)�1998;95:165�169.�[PubMed]
37.�Sciarretta G, Furno A, Mazzoni M, Garagnani B, Malaguti P. Lactulose hydrogen breath test in orocecal transit assessment. Critical evaluation by means of scintigraphic method.�Dig Dis Sci.�1994;39:1505�1510.�[PubMed]
38.�Rao SS, Camilleri M, Hasler WL, Maurer AH, Parkman HP, Saad R, Scott MS, Simren M, Soffer E, Szarka L. Evaluation of gastrointestinal transit in clinical practice: position paper of the American and European Neurogastroenterology and Motility Societies.�Neurogastroenterol Motil.�2011;23:8�23.[PubMed]
39.�Yu D, Cheeseman F, Vanner S. Combined oro-caecal scintigraphy and lactulose hydrogen breath testing demonstrate that breath testing detects oro-caecal transit, not small intestinal bacterial overgrowth in patients with IBS.�Gut.�2011;60:334�340.�[PubMed]
40.�Rana SV, Sharma S, Sinha SK, Kaur H, Sikander A, Singh K. Incidence of predominant methanogenic flora in irritable bowel syndrome patients and apparently healthy controls from North India.�Dig Dis Sci.�2009;54:132�135.�[PubMed]
41.�Dridi B, Henry M, El Kh�chine A, Raoult D, Drancourt M. High prevalence of Methanobrevibacter smithii and Methanosphaera stadtmanae detected in the human gut using an improved DNA detection protocol.�PLoS One.�2009;4:e7063.�[PMC free article]�[PubMed]
42.�Chatterjee S, Park S, Low K, Kong Y, Pimentel M. The degree of breath methane production in IBS correlates with the severity of constipation.�Am J Gastroenterol.�2007;102:837�841.�[PubMed]
43.�Lunia MK, Sharma BC, Sachdeva S. Small intestinal bacterial overgrowth and delayed orocecal transit time in patients with cirrhosis and low-grade hepatic encephalopathy.�Hepatol Int.�2013;7:268�273.[PubMed]
44.�Resmini E, Parodi A, Savarino V, Greco A, Rebora A, Minuto F, Ferone D. Evidence of prolonged orocecal transit time and small intestinal bacterial overgrowth in acromegalic patients.�J Clin Endocrinol Metab.�2007;92:2119�2124.�[PubMed]
45.�Hamilton I, Worsley BW, Cobden I, Cooke EM, Shoesmith JG, Axon AT. Simultaneous culture of saliva and jejunal aspirate in the investigation of small bowel bacterial overgrowth.�Gut.�1982;23:847�853.[PMC free article]�[PubMed]
46.�Corazza GR, Sorge M, Strocchi A, Benati G, Di Sario A, Treggiari EA, Brusco G, Gasbarrini G. Non-absorbable antibiotics and small bowel bacterial overgrowth.�Ital J Gastroenterol.�1992;24:4�9.�[PubMed]
47.�Kuwahara T, Ogura Y, Oshima K, Kurokawa K, Ooka T, Hirakawa H, Itoh T, Nakayama-Imaohji H, Ichimura M, Itoh K, et al. The lifestyle of the segmented filamentous bacterium: a non-culturable gut-associated immunostimulating microbe inferred by whole-genome sequencing.�DNA Res.�2011;18:291�303.�[PMC free article]�[PubMed]
49.�Fromm H, Sarva RP, Ravitch MM, McJunkin B, Farivar S, Amin P. Effects of jejunoileal bypass on the enterohepatic circulation of bile acids, bacterial flora in the upper small intestine, and absorption of vitamin B12.�Metabolism.�1983;32:1133�1141.�[PubMed]
50.�Yoshida T, McCormick WC, Swell L, Vlahcevic ZR. Bile acid metabolism in cirrhosis. IV. Characterization of the abnormality in deoxycholic acid metabolism.�Gastroenterology.�1975;68:335�341.[PubMed]
51.�Bj�rneklett A, Fausa O, Midtvedt T. Bacterial overgrowth in jejunal and ileal disease.�Scand J Gastroenterol.�1983;18:289�298.�[PubMed]
52.�Vanner S. The small intestinal bacterial overgrowth. Irritable bowel syndrome hypothesis: implications for treatment.�Gut.�2008;57:1315�1321.�[PubMed]
53.�Kinross JM, von Roon AC, Holmes E, Darzi A, Nicholson JK. The human gut microbiome: implications for future health care.�Curr Gastroenterol Rep.�2008;10:396�403.�[PubMed]
54.�Clauw DJ. Fibromyalgia: an overview.�Am J Med.�2009;122:S3�S13.�[PubMed]
55.�Pimentel M, Wallace D, Hallegua D, Chow E, Kong Y, Park S, Lin HC. A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing.�Ann Rheum Dis.�2004;63:450�452.�[PMC free article]�[PubMed]
56.�Simr�n M, Stotzer PO. Use and abuse of hydrogen breath tests.�Gut.�2006;55:297�303.[PMC free article]�[PubMed]
57.�Gasbarrini A, Lauritano EC, Gabrielli M, Scarpellini E, Lupascu A, Ojetti V, Gasbarrini G. Small intestinal bacterial overgrowth: diagnosis and treatment.�Dig Dis.�2007;25:237�240.�[PubMed]
58.�Ghoshal UC, Srivastava D, Verma A, Misra A. Slow transit constipation associated with excess methane production and its improvement following rifaximin therapy: a case report.�J Neurogastroenterol Motil.�2011;17:185�188.�[PMC free article]�[PubMed]
59.�Bala L, Ghoshal UC, Ghoshal U, Tripathi P, Misra A, Gowda GA, Khetrapal CL. Malabsorption syndrome with and without small intestinal bacterial overgrowth: a study on upper-gut aspirate using 1H NMR spectroscopy.�Magn Reson Med.�2006;56:738�744.�[PubMed]
60.�Haboubi NY, Lee GS, Montgomery RD. Duodenal mucosal morphometry of elderly patients with small intestinal bacterial overgrowth: response to antibiotic treatment.�Age Ageing.�1991;20:29�32.�[PubMed]
61.�Shindo K, Machida M, Koide K, Fukumura M, Yamazaki R. Deconjugation ability of bacteria isolated from the jejunal fluid of patients with progressive systemic sclerosis and its gastric pH.�Hepatogastroenterology.�1998;45:1643�1650.�[PubMed]
62.�Wanitschke R, Ammon HV. Effects of dihydroxy bile acids and hydroxy fatty acids on the absorption of oleic acid in the human jejunum.�J Clin Invest.�1978;61:178�186.�[PMC free article]�[PubMed]
63.�Shanab AA, Scully P, Crosbie O, Buckley M, O�Mahony L, Shanahan F, Gazareen S, Murphy E, Quigley EM. Small intestinal bacterial overgrowth in nonalcoholic steatohepatitis: association with toll-like receptor 4 expression and plasma levels of interleukin 8.�Dig Dis Sci.�2011;56:1524�1534.�[PubMed]
64.�Ghoshal UC, Park H, Gwee KA. Bugs and irritable bowel syndrome: The good, the bad and the ugly.�J Gastroenterol Hepatol.�2010;25:244�251.�[PubMed]
65.�Barbara G, Stanghellini V, Brandi G, Cremon C, Di Nardo G, De Giorgio R, Corinaldesi R. Interactions between commensal bacteria and gut sensorimotor function in health and disease.�Am J Gastroenterol.�2005;100:2560�2568.�[PubMed]
66.�Cherbut C, Aub� AC, Blotti�re HM, Galmiche JP. Effects of short-chain fatty acids on gastrointestinal motility.�Scand J Gastroenterol Suppl.�1997;222:58�61.�[PubMed]
67.�Ramakrishna BS, Roediger WE. Bacterial short chain fatty acids: their role in gastrointestinal disease.�Dig Dis.�1990;8:337�345.�[PubMed]
68.�Dumoulin V, Moro F, Barcelo A, Dakka T, Cuber JC. Peptide YY, glucagon-like peptide-1, and neurotensin responses to luminal factors in the isolated vascularly perfused rat ileum.�Endocrinology.�1998;139:3780�3786.�[PubMed]
69.�Balsari A, Ceccarelli A, Dubini F, Fesce E, Poli G. The fecal microbial population in the irritable bowel syndrome.�Microbiologica.�1982;5:185�194.�[PubMed]
70.�Nobaek S, Johansson ML, Molin G, Ahrn� S, Jeppsson B. Alteration of intestinal microflora is associated with reduction in abdominal bloating and pain in patients with irritable bowel syndrome.�Am J Gastroenterol.�2000;95:1231�1238.�[PubMed]
71.�Cummings JH, Macfarlane GT. The control and consequences of bacterial fermentation in the human colon.�J Appl Bacteriol.�1991;70:443�459.�[PubMed]
72.�Camilleri M. Probiotics and irritable bowel syndrome: rationale, mechanisms, and efficacy.�J Clin Gastroenterol.�2008;42 Suppl 3 Pt 1:S123�S125.�[PubMed]
73.�Spiller R. Probiotics: an ideal anti-inflammatory treatment for IBS?�Gastroenterology.�2005;128:783�785.�[PubMed]
74.�Ford AC, Spiegel BM, Talley NJ, Moayyedi P. Small intestinal bacterial overgrowth in irritable bowel syndrome: systematic review and meta-analysis.�Clin Gastroenterol Hepatol.�2009;7:1279�1286.�[PubMed]
75.�Cuoco L, Salvagnini M. Small intestine bacterial overgrowth in irritable bowel syndrome: a retrospective study with rifaximin.�Minerva Gastroenterol Dietol.�2006;52:89�95.�[PubMed]
76.�Di Stefano M, Corazza GR. Treatment of small intestine bacterial overgrowth and related symptoms by rifaximin.�Chemotherapy.�2005;51 Suppl 1:103�109.�[PubMed]
77.�Pimentel M, Lembo A, Chey WD, Zakko S, Ringel Y, Yu J, Mareya SM, Shaw AL, Bortey E, Forbes WP. Rifaximin therapy for patients with irritable bowel syndrome without constipation.�N Engl J Med.�2011;364:22�32.�[PubMed]
78.�Hwang L, Low K, Khoshini R, Melmed G, Sahakian A, Makhani M, Pokkunuri V, Pimentel M. Evaluating breath methane as a diagnostic test for constipation-predominant IBS.�Dig Dis Sci.�2010;55:398�403.�[PubMed]
79.�Low K, Hwang L, Hua J, Zhu A, Morales W, Pimentel M. A combination of rifaximin and neomycin is most effective in treating irritable bowel syndrome patients with methane on lactulose breath test.�J Clin Gastroenterol.�2010;44:547�550.�[PubMed]
80.�Bengmark S. Colonic food: pre- and probiotics.�Am J Gastroenterol.�2000;95:S5�S7.�[PubMed]
81.�Quigley EM, Quera R. Small intestinal bacterial overgrowth: roles of antibiotics, prebiotics, and probiotics.�Gastroenterology.�2006;130:S78�S90.�[PubMed]
82.�Xiao SD, Zhang DZ, Lu H, Jiang SH, Liu HY, Wang GS, Xu GM, Zhang ZB, Lin GJ, Wang GL. Multicenter, randomized, controlled trial of heat-killed Lactobacillus acidophilus LB in patients with chronic diarrhea.�Adv Ther.�2003;20:253�260.�[PubMed]
83.�O’Mahony L, McCarthy J, Kelly P, Hurley G, Luo F, Chen K, O�Sullivan GC, Kiely B, Collins JK, Shanahan F, et al. Lactobacillus and bifidobacterium in irritable bowel syndrome: symptom responses and relationship to cytokine profiles.�Gastroenterology.�2005;128:541�551.�[PubMed]
84.�Tsuchiya J, Barreto R, Okura R, Kawakita S, Fesce E, Marotta F. Single-blind follow-up study on the effectiveness of a symbiotic preparation in irritable bowel syndrome.�Chin J Dig Dis.�2004;5:169�174.[PubMed]
85.�Kim YG, Moon JT, Lee KM, Chon NR, Park H. [The effects of probiotics on symptoms of irritable bowel syndrome]�Korean J Gastroenterol.�2006;47:413�419.�[PubMed]
86.�Park JS, Yu JH, Lim HC, Kim JH, Yoon YH, Park HJ, Lee SI. [Usefulness of lactulose breath test for the prediction of small intestinal bacterial overgrowth in irritable bowel syndrome]�Korean J Gastroenterol.�2010;56:242�248.�[PubMed]
87.�Mann NS, Limoges-Gonzales M. The prevalence of small intestinal bacterial vergrowth in irritable bowel syndrome.�Hepatogastroenterology.�2009;56:718�721.�[PubMed]
88.�Scarpellini E, Giorgio V, Gabrielli M, Lauritano EC, Pantanella A, Fundar� C, Gasbarrini A. Prevalence of small intestinal bacterial overgrowth in children with irritable bowel syndrome: a case-control study.�J Pediatr.�2009;155:416�420.�[PubMed]
89.�Nucera G, Gabrielli M, Lupascu A, Lauritano EC, Santoliquido A, Cremonini F, Cammarota G, Tondi P, Pola P, Gasbarrini G, et al. Abnormal breath tests to lactose, fructose and sorbitol in irritable bowel syndrome may be explained by small intestinal bacterial overgrowth.�Aliment Pharmacol Ther.�2005;21:1391�1395.�[PubMed]
90.�Reddymasu SC, Sostarich S, McCallum RW. Small intestinal bacterial overgrowth in irritable bowel syndrome: are there any predictors?�BMC Gastroenterol.�2010;10:23.�[PMC free article]�[PubMed]
91.�Lombardo L, Foti M, Ruggia O, Chiecchio A. Increased incidence of small intestinal bacterial overgrowth during proton pump inhibitor therapy.�Clin Gastroenterol Hepatol.�2010;8:504�508.�[PubMed]
92.�Parodi A, Dulbecco P, Savarino E, Giannini EG, Bodini G, Corbo M, Isola L, De Conca S, Marabotto E, Savarino V. Positive glucose breath testing is more prevalent in patients with IBS-like symptoms compared with controls of similar age and gender distribution.�J Clin Gastroenterol.�2009;43:962�966.[PubMed]
93.�Rana SV, Sinha SK, Sikander A, Bhasin DK, Singh K. Study of small intestinal bacterial overgrowth in North Indian patients with irritable bowel syndrome: a case control study.�Trop Gastroenterol.�2008;29:23�25.�[PubMed]
94.�Majewski M, McCallum RW. Results of small intestinal bacterial overgrowth testing in irritable bowel syndrome patients: clinical profiles and effects of antibiotic trial.�Adv Med Sci.�2007;52:139�142.[PubMed]
95.�Lupascu A, Gabrielli M, Lauritano EC, Scarpellini E, Santoliquido A, Cammarota G, Flore R, Tondi P, Pola P, Gasbarrini G, et al. Hydrogen glucose breath test to detect small intestinal bacterial overgrowth: a prevalence case-control study in irritable bowel syndrome.�Aliment Pharmacol Ther.�2005;22:1157�1160.[PubMed]
These assessment and treatment recommendations represent a synthesis of information derived from personal clinical experience and from the numerous sources which are cited, or are based on the work of researchers, clinicians and therapists who are named (Basmajian 1974, Cailliet 1962, Dvorak & Dvorak 1984, Fryette 1954, Greenman 1989, 1996, Janda 1983, Lewit 1992, 1999, Mennell 1964, Rolf 1977, Williams 1965).
Clinical Application of Neuromuscular Techniques: Pectoralis Major and Latissimus Dorsi
Assessment of Shortened Pectoralis Major and Latissimus Dorsi
Latissimus and pectoral test (a) Observation is as accurate as most palpation for evidence of pectoralis major shortening. The patient will have a rounded shoulder posture � especially if the clavicular aspect is involved.
Or
The patient lies supine with upper arms on the table, hands resting palm down on the lower abdomen. The practitioner observes from the head and notes whether either shoulder is held in an anterior position in relation to the thoracic cage. If one or both shoulders are forward of the thorax, pectoralis muscles are short (Fig. 4.24).
Figure 4.24 Observation assessment in which pectoral shortness on the right is suggested by the inability of the shoulder to rest on the table.
Latissimus and pectoral test (b) The patient lies supine with the head several feet from the top edge of the table, and is asked to rest the arms, extended above the head, on the treatment surface, palms upwards (Fig. 4.25).
Figure 4.25 Assessment of shortness in pectoralis major and latissimus dorsi. Visual assessment is used: if the arm on the tested side is unable to rest along its full length, shortness of pectoralis major is probable; if there is obvious deviation of the elbow laterally, probable latissimus shortening is indicated.
If these muscles are normal, the arms should be able to easily reach the horizontal when directly above the shoulders, and also to be in contact with the surface for almost all of the length of the upper arms, with no arching of the back or twisting of the thorax.
If either arm cannot reach the vertical above the shoulder, but is held laterally, elbow pulled outwards, then latissimus dorsi is probably short on that side. If an arm cannot rest with the dorsum of the upper arm in contact with the table surface without effort, then pectoral fibres are almost certainly short.
Pectoralis major test. Assessment of shortness in pectoralis major (Fig. 4.26) Assessment of the subclavicular portion of pectoralis major involves abduction of the arm to 90� (Lewit 1985b). In this position the tendon of pectoralis major at the sternum should not be found to be unduly tense, even with maximum abduction of the arm, unless the muscle is short.
Figure 4.26 Palpation assessment for shortness of subclavicular portion of pectoralis major.
For assessment of sternal attachment the arm is brought into elevation and abduction as the muscle, as well as the tendon on the greater tubercle of the humerus, is palpated. If the sternal fibres have shortened, tautness will be visible and tenderness of the tissues under palpation will be reported.
Pectoralis Major Test: Assessment for Strength of Pectoralis Major
Patient is supine with arm in abduction at the shoulder joint and medially rotated (palm is facing down) with the elbow extended. The practitioner stands at the head and secures the opposite shoulder with one hand to prevent any trunk torsion and contacts the dorsum of the distal humerus, on the tested side, with the other.
The patient attempts to lift the arm and to adduct it across the chest, against resistance, as strength is assessed in the sternal fibres.
Different arm positions can be used to assess clavicular and costal fibres: for example with an angle of abduction/elevation of 135� costal and abdominal fibres will be involved; with abduction/elevation of 45� the clavicular fibres will be assessed. The practitioner should palpate to ensure that the �correct� fibres contract when assessments are being made.
If this postural muscle tests as weak it may be useful to use Norris�s (1999) approach of strengthening it by means of a slowly applied isotonic eccentric (isolytic) contraction, before proceeding to an MET stretching procedure.
MET Treatment of Short Pectoralis Major
Pectoralis major MET method (a) (Fig. 4.27A, B) The patient lies supine with the arm abducted in a direction which produces the most marked evidence of pectoral shortness (assessed by palpation and visual evidence of the particular fibres involved as described in tests above). The more elevated the arm (i.e. the closer to the head), the more focus there will be on costal and abdominal fibres. With a lesser degree of abduction (to around 45�), the focus is more on the clavicular fibres. Between these two extremes lies the position which influences the sternal fibres most directly.
Figure 4.27A MET treatment of pectoral muscle � abdominal attachment. Note that the fibres being treated are those which lie in line with the long axis of the humerus.
Figure 4.27B An alternative hold for application of MET to pectoral muscle � sternal attachment. Note that the patient needs to be close to the edge of the table in order to allow the arm to be taken towards the floor once the slack has been removed, during the stretching phase after the isometric contraction.
The patient lies as close to the side of the table as possible so that the abducted arm can be brought below the horizontal level in order to apply gravitational pull and passive stretch to the fibres, as appropriate. The practitioner stands on the side to be treated and grasps the humerus.
A useful arm hold, which depends upon the relative size of the patient and the practitioner, involves the practitioner grasping the anterior aspect of the patient�s flexed upper arm just above the elbow, while the patient cups the practitioner�s elbow and holds this contact throughout the procedure (see Fig. 4.27B).
The patient�s hand is placed on the contact (attachments of shortened fibres) area on the thorax so that the hand acts as a �cushion�. This is both more physically comfortable and also prevents physical contact with emotionally sensitive areas such as breast tissue. The practitioner�s thenar or hyperthenar eminence is placed over the patient�s �cushion� hand in order to stabilise the area during the contraction and stretch, preventing movement of it.
Commencing with the patient�s arm in a position which takes the affected fibres to just short of their restriction barrier (for a chronic problem), the patient introduces a light contraction (20% of strength) involving adduction against resistance from the practitioner, for 7�10 seconds.
As a rule the long axis of the patient�s upper arm should be in a straight line with the fibres being treated. If a trigger point has previously been identified in pectoralis, the practitioner should ensure � by means of palpation if necessary, or by observation � that the fibres housing the triggers are involved in the contraction.
As the patient exhales following complete relaxation of the area, a stretch through the new barrier is activated by the patient and maintained by the practitioner. Stretch is achieved via the positioning and leverage of the arm as the contact hand on the thorax acts as a stabilising point only.
The stretch needs to be one in which the arm is first pulled away (distracted) from the thorax, with the patient�s assistance (�ease your arm away from your shoulder�), before the stretch is introduced which involves the humerus being taken below the horizontal (�ease your arm towards the floor�).
During the stretching phase it is important for the entire thorax to be stabilised. No rolling or twisting of the thorax in the direction of the stretch should be permitted. The stretching procedure should be thought of as having two phases: first the slack being removed by distracting the arm away from the contact/stabilising hand on the thorax; second, movement of the arm towards the floor, initiated by the practitioner bending his knees.
Stretching (after an isometric contraction) should be repeated two or three times in each position. All attachments should be treated, which calls for the use of different arm positions, as discussed above, each with different stabilising (�cushion�) contacts as the various fibre directions and attachments are isolated.
Pectoralis major MET method (b) (Fig. 4.28) The patient is prone with face in a face hole or cradle. Her right arm is abducted to 90� and the elbow flexed to 90� palm towards the floor, with the upper arm supported by the table. The practitioner stands at waist level, facing cephalad, and places his non-table-side hand palm to palm with the patient�s so that the patient�s forearm is in contact with the ventral surface of the practitioner�s forearm. The practitioner�s table-side hand rests on the patient�s right scapula area, ensuring that no trunk rotation occurs.
Figure 4.28 MET for pectoralis major in prone position.
The practitioner eases the patient�s arm into extension at the shoulder until he senses the first sign of resistance from pectoralis. It is important when extending the arm in this way to ensure that no trunk rotation occurs and that the anterior surface of the shoulder remains in contact with the table throughout.
The patient is asked, using no more than 20% of strength, to bring her arm towards the floor and across her chest, with the elbow taking the lead in this attempted movement, which is completely resisted by the practitioner. The practitioner ensures that the patient�s arm remains parallel with the floor throughout the isometric contraction.
Following release of the contraction effort, and on an exhalation, the arm is taken into greater extension, with the patient�s assistance, and held at stretch for not less than 20 seconds.
This procedure is repeated two or three times, slackening the muscle slightly from its end-range before each subsequent contraction to reduce discomfort and for ease of application of the contraction.
Variations in pectoralis fibre involvement can be achieved by altering the angle of abduction � with a more superior angle (around 140�) the lower sternal and costal fibres, and with a lesser angle (around 45�) the clavicular fibres will be committed.
Pectoralis major MET method (c) Bilateral MET stretching of pectoralis major (sternocostal aspects) involves having the patient supine, knees and hips flexed, in order to provide stability to the spinal regions, preventing lumbar lordosis. A shallow but firm cushion should be placed between the scapulae, allowing a better excursion of the shoulders during this stretch. The chin should be tucked in and, if more comfortable, a small cushion placed under the neck. Ideally a strap/belt should be used to fix the thorax to the table, but this is not essential.
The practitioner stands at the head of the table and grasps the patient�s elbows or forearms, which are flexed, laterally rotated and held in a position to induce the most taut aspects of the muscles to become prominent.
Starting from such a barrier or short of it (acute/chronic), the patient is asked to contract the muscles by bringing the arms upwards and towards the table for 10 seconds or so during a held breath.
Following the contraction and complete relaxation, the arms are taken to a new or through the restriction barrier, as appropriate, during an exhalation. Repeat as necessary several times more.
Pectoralis major MET method (d) By adopting the same positions � but with the arms of the patient more laterally placed so that they are laterally rotated and in 90� abduction from the shoulder (upper arms are straight out sideways from the shoulder) and there is 90� flexion at the elbows, with the practitioner contacting the area just proximal to the flexed elbows � a more direct stretch of the clavicular insertions of the muscle can be achieved, using all the same contraction and stretch elements as in (b) above.
Latissimus Dorsi Test for Shortness
To screen latissimus dorsi (12), the standing patient is asked to bend forwards and allow the arms to hang freely from the shoulders as she holds a half-bend position, trunk parallel with the floor.
If the arms are hanging other than perpendicular to the floor there is probably some muscular restriction involved, and if this involves latissimus the arms will be held closer to the legs than perpendicular (if they hang markedly forward of such a position then trapezius shortening is probable, see below).
To screen latissimus in this position, one side at a time, the practitioner stands in front of the patient (who remains in this half-bend position) and, stabilising the scapula area with one hand, grasps the arm at elbow level and gently draws the tested side (straight) arm forwards. It should, without undue effort or excessive bind in the tissues being held, allow itself to be taken to a position where the elbow is higher than the level of the back of the head. If this is not possible, then latissimus is short.
MET Treatment of Short Latissimus Dorsi
Short latissimus dorsi MET method (a) The patient lies supine with the feet crossed (the side to be treated crossed under the non-treated side leg at the ankle). The patient is arranged in a light sidebend away from the side to be treated so that the pelvis is towards that side, and the feet and head away from that side. The heels are placed just off the edge of the table, so anchoring the lower extremities.
The patient places her arm on the side to be treated behind her neck, as the practitioner, standing on the side opposite that to be treated, slides his cephalad hand under the patient�s shoulders to grasp the treated side axilla. The patient grasps the practitioner�s cephalad arm at the elbow, making this contact more secure. The patients treated side elbow should point superiorly. The practitioner�s caudad hand is placed on the anterior superior iliac spine on the side being treated.
The patient is instructed to very lightly take the pointed elbow towards the sacrum and also to lightly try to bend backwards and towards the treated side. This should produce a light isometric contraction in latissimus dorsi on the side to be treated. After 7 seconds they are asked to relax completely as the practitioner transfers his body weight from the cephalad leg to the caudad leg, to sidebend the patient. Simultaneously the practitioner stands more erect and leans in a caudad direction.
This effectively lifts the patient�s thorax from the table surface and introduces a stretch into latissimus (especially if the patient has maintained a grasp on the practitioner�s elbow and the practitioner has a firm hold on the patient�s axilla).
This stretch is held for 15�30 seconds allowing a lengthening of shortened musculature in the region. (Note: starting position is as for Fig. 4.22.) Repeat as necessary.
Short latissimus dorsi MET method (b) The patient is side-lying, affected side up. The arm is taken into abduction to the point of resistance, so that it is possible to visualise, or palpate, the insertion of the shortened fibres on the lateral chest wall.
The condition is treated in either the acute or chronic mode of MET, at or short of the barrier, as appropriate.
As shown in Figure 4.29, the practitioner stands near the head of the patient, slightly behind, and holds the upper arm in the chosen position while applying the other hand to stabilise the posterior thorax area, or the pelvic crest, from where the stretch will be made.
Figure 4.29 Treatment of latissimus dorsi. A variety of different positions are required for the stabilising hand (on the chest wall as well as on the crest of the pelvis) to allow for precise application of stretches of fibres with different attachments, following the sequence of isometric contractions.
A build-up of tension should be palpated under the stabilising hand as the patient introduces an isometric contraction by attempting to bring the arm towards the ceiling, backwards and down (towards their own lower spine) against firm resistance, using only a modest amount of effort (20%) and holding the breath if appropriate (see notes on breathing, Box 4.2).
After 7�10 seconds, both the effort and breath are released and the patient relaxes completely, at which time the practitioner introduces stretch to or through the barrier (acute/chronic), bringing the humerus into greater adduction while applying a stretching/stabilising contact on the trunk (with separate contractions and stretches for each contact) anywhere between the lateral chest wall and the crest of the pelvis.
A downward movement of the humerus, towards the floor, assists the stretch following a separation of the practitioner�s two contact hands to remove all slack. As in the stretch of pectoralis major, there should be two phases � a distraction, taking out the slack, and a movement towards the floor of the practitioner, by flexing the knees � to induce a safe stretch. Repeat as necessary.
Ultimately, it should be possible to achieve complete elevation of the arm without stress or obvious shortness in latissimus fibres so that the upper arm can rest alongside the ear of the supine patient.
Dr. Alex Jimenez offers an additional assessment and treatment of the hip flexors as a part of a referenced clinical application of neuromuscular techniques by Leon Chaitow and Judith Walker DeLany. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
These assessment and treatment recommendations represent a synthesis of information derived from personal clinical experience and from the numerous sources which are cited, or are based on the work of researchers, clinicians and therapists who are named (Basmajian 1974, Cailliet 1962, Dvorak & Dvorak 1984, Fryette 1954, Greenman 1989, 1996, Janda 1983, Lewit 1992, 1999, Mennell 1964, Rolf 1977, Williams 1965).
Clinical Application of Neuromuscular Techniques: Quadratus Lumborum
Assessment of Shortness in Quadratus Lumborum (Figure 4.21)
Figure 4.21 Palpation assessment for quadratus lumborum overactivity. The muscle is palpated, as is gluteus medius, during abduction of the leg. The correct firing sequence should be gluteus, followed at around 25� elevation by quadratus. If there is an immediate �grabbing� action by quadratus it indicates overactivity, and therefore stress, so shortness can be assumed (see details of similar functional assessments in Ch. 5).
Review Lewit�s functional palpation test described under the heading assessment and treatment of tensor fascia lata.
When the leg of the side-lying patient is abducted, and the practitioner�s palpating hand senses that quadratus becomes involved in this process before the leg has reached at least 25� of elevation, then it is clear that quadratus is overactive. If it has been overactive for any length of time then it is almost certainly hypertonic and short, and a need for MET can be assumed.
Quadratus lumborum test (a) (See also Fig. 5.11A, B.) The patient is side-lying and is asked to take the upper arm over the head to grasp the top edge of the table, �opening out� the lumbar area. The practitioner stands facing the back of the patient, and has easy access for palpation of quadratus lumborum�s lateral border � a major trigger point site (Travell & Simons 1992) � with the cephalad hand.
Activity of quadratus is tested (palpated for) with the cephalad hand as the leg is abducted, while also palpating gluteus medius with the caudad hand. If the muscles act simultaneously, or if quadratus fires first, then it is stressed, probably short, and will benefit from stretching.
Quadratus lumborum test (b) The patient stands, back towards crouching practitioner. Any leg length disparity (based on pelvic crest height) is equalised by using a book or pad under the short leg side heel. With the patient�s feet shoulder-width apart, a pure sidebending is requested, so that the patient runs a hand down the lateral thigh/calf. (Normal level of sidebending excursion allows the fingertips to reach to just below the knee.) (See Fig. 3.2A, B, C.)
The side to which the fingertips travel furthest is assessed. If sidebending to one side is limited then quadratus on the opposite side is probably short. Combined evidence from palpation (test a) and this sidebending test indicate whether or not it is necessary to treat quadratus.
Box 4.8 Notes on Quadratus Lumborum
Norris (2000) describes the divided roles in which quadratus is involved: The quadratus lumborum has been shown to be significant as a stabiliser in lumbar spine movements (McGill et al 1996) while tightening has also been described (Janda 1983). It seems likely that the muscle may act functionally differently in its medial and lateral portions, with the medial portion being more active as a stabiliser of the lumbar spine, and the lateral more active as a mobiliser [see stabiliser/mobiliser discussion Ch. 2]. Such subdivision is seen in a number of other muscles for example the gluteus medius where the posterior fibres are more posturally involved (Jull 1994) the internal oblique where the posterior fibres attaching to the lateral raphe are considered stabilisers (Bergmark 1989) the external oblique where the lateral fibres work during flexion in parallel with the rectus abdominis (Kendall et al 1993).
Janda (1983) observes that, when the patient is sidebending (as in method (b)) �when the lumbar spine appears straight, with compensatory motion occurring only from the thoracolumbar region upwards, tightness of quadratus lumborum may be suspected�. This �whole lumbar spine� involvement differs from a segmental restriction which would probably involve only a part of the lumbar spine.
Quadratus fibres merge with the diaphragm (as do those of psoas), which makes involvement in respiratory dysfunction a possibility since it plays a role in exhalation, both via this merging and by its attachment to the 12th rib.
Shortness of quadratus, or the presence of trigger points, can result in pain in the lower ribs and along the iliac crest if the lateral fibres are affected. Shortness of the medial fibres, or the presence of trigger points, can produce pain in the sacroiliac joint and the buttock.
Bilateral contraction produces extension and unilateral contraction produces extension and sidebending to the same side.
The important transition region, the lumbodorsal junction (LDJ), is the only one in the spine in which two mobile structures meet, and dysfunction results in alteration of the quality of motion between these structures (upper and lower trunk/dorsal and lumbar spines). In dysfunction there is often a degree of spasm or tightness in the muscles which stabilise the region, notably: psoas and erector spinae of the thoracolumbar region, as well as quadratus lumborum and rectus abdominis.
Symptomatic differential diagnosis of muscle involvement at the LDJ is possible as follows: psoas involvement usually triggers abdominal pain if severe and produces flexion of the hip and the typical antalgesic posture of lumbago; erector spinae involvement produces low back pain at its caudad end of attachment and interscapular pain at its thoracic attachment (as far up as the mid-thoracic level); quadratus lumborum involvement causes lumbar pain and pain at the attachment of the iliac crest and lower ribs; and rectus abdominis contraction may mimic abdominal pain and result in pain at the attachments at the pubic symphysis and the xiphoid process, as well as forwardbending of the trunk and restricted ability to extend the spine.
There is seldom pain at the site of the lesion in LDJ dysfunction. Lewit (1992) points out that even if a number of these muscles are implicated, it is seldom necessary, using PIR methods, to treat them all since, as the muscles most involved (discovered by tests for shortness, overactivity, sensitivity and direct palpation) are stretched and normalised, so will others begin automatically to normalise.
MET for Shortness in Quadratus Lumborum (�banana�)
Quadratus lumborum MET method (a) (Fig. 4.22) The patient lies supine with the feet crossed (the side to be treated crossed under the non-treated side leg) at the ankle. The patient is arranged in a light sidebend, away from the side to be treated, so that the pelvis is towards that side, and the feet and head away from that side (�banana shaped�). As this sidebend is being achieved the affected quadratus can be palpated for bind so that the barrier is correctly identified.
Figure 4.22 MET treatment of quadratus lumborum utilising �banana� position.
The patient�s heels are placed just off the side of the table, anchoring the lower extremities and pelvis. The patient places the arm of the side to be treated behind her neck as the practitioner, standing on the side opposite that to be treated, slides his cephalad hand under the patient�s shoulders to grasp the treated side axilla. The patient grasps the practitioner�s cephalad arm at the elbow, with the treated side hand, making the contact more secure.
The patient�s treated side elbow should, at this stage, be pointing superiorly. The practitioner�s caudad hand is placed firmly but carefully on the anterior superior iliac spine, on the side to be treated. The patient is instructed to very lightly sidebend towards the treated side. This should produce an isometric contraction in quadratus lumborum on the side to be treated.
After 7 seconds the patient is asked to relax completely, and then to sidebend towards the nontreated side, as the practitioner simultaneously transfers his bodyweight from the cephalad leg to the caudad leg and leans backwards slightly, in order to sidebend the patient. This effectively stretches quadratus lumborum. The stretch is held for 15�20 seconds, allowing a lengthening of shortened musculature in the region. Repeat as necessary.
Quadratus lumborum MET method (b) (Fig 4.23) The practitioner stands behind the side-lying patient, at waist level. The patient has the uppermost arm extended over the head to firmly grasp the top end of the table and, on an inhalation, abducts the uppermost leg until the practitioner palpates strong quadratus activity (elevation of around 30� usually).
Figure 4.23 MET treatment of quadratus lumborum. Note that it is important after the isometric contraction (sustained raised/abducted leg) that the muscle be eased into stretch, avoiding any defensive or protective resistance which sudden movement might produce. For this reason, body weight rather than arm strength should be used to apply traction.
The patient holds the leg (and, if appropriate, the breath, see Box 4.2) isometrically in this manner, allowing gravity to provide resistance. After the 10-second (or so) contraction, the patient allows the leg to hang slightly behind him over the back of the table. The practitioner straddles this and, cradling the pelvis with both hands (fingers interlocked over crest of pelvis), leans back to take out all slack and to �ease the pelvis away from the lower ribs� during an exhalation.
The stretch should be held for between 10 and 30 seconds. (The method will only be successful if the patient is grasping the top edge of the table, so providing a fixed point from which the practitioner can induce stretch.)
Contraction followed by stretch is repeated once or twice more with raised leg in front of, and once or twice with raised leg behind the trunk in order to activate different fibres. The direction of stretch should be varied so that it is always in the same direction as the long axis of the abducted leg. This calls for the practitioner changing from the back to the front of the table for the best results. When the leg hangs to the back of the trunk the long fibres of the muscle are mainly affected; and when the leg hangs forward of the body the diagonal fibres are mainly involved.
Quadratus lumborum MET method (c) Gravity-induced postisometric relaxation of quadratus lumborum � self-treatment (See Fig. 3.2A�C and captions) The patient stands, legs apart, bending sideways. The patient inhales and slightly raises the trunk (a few centimetres) at the same time as looking (with the eyes only) away from the side to which side-flexion is taking place. On exhalation, the sidebend is allowed to slowly go further to its elastic limit, while the patient looks towards the floor, in the direction of the side-flexion. (Care is needed that very little, if any, forward or backward bending is taking place at this time.) This sequence is repeated a number of times.
Eye positions influence the tendency to flex and sidebend (eyes look down) and extend (eyes look up) (Lewit 1999). Gravity-induced stretches of this sort require holding the stretch position for at least as long as the contraction, and ideally longer. More repetitions may be needed with a large muscle such as quadratus, and home stretches should be advised several times daily. Quadratus lumborum MET method (d) The side-lying treatment of latissimus dorsi described below also provides an effective quadratus stretch when the stabilising hand rests on the pelvic crest (see Fig. 4.29).
Dr. Alex Jimenez offers an additional assessment and treatment of the hip flexors as a part of a referenced clinical application of neuromuscular techniques by Leon Chaitow and Judith Walker DeLany. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
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