Osteopathic manipulative treatment in a patient with idiopathic dysautonomia: a case presentation

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Disorders of the gastrointestinal (GI) tract as a whole affect one in three people. Of those who seek further inves-tigation from a gastroenterologist, one in five will not reach an etiologic explanation of their symptoms.1Many of thesepatients fall into the category of “functional gastrointestinal disorders,” which includes such diagnoses as irritable bowelsyndrome and functional dyspepsia. These diagnoses are reached through extensive history given by the patient andrequire that “organic” etiologies be ruled out.2Because the functional GI disorders have no identified etiology, patientmanagement consists primarily of supportive therapies di-rected at the patient’s unpredictable symptoms. These pa-tients often have conditions similar to many chronic disease patients, such as anxiety and depression. Many times theyare frustrated and searching for support, so sufficient care requires tact, time, and patience.1,3A select subsets ofpatients can have additional unexplained symptoms spanning multiple organ systems, which has led some to believethat an autonomic etiology may be causing the viscera to function inappropriately.2,4,5Because of chronic autonomic stimulation of the viscera, there may be somatic segmental facilitation, resulting in a viscerosomatic reflex. This is exemplified by musculoskeletal complaints or somatic dys- function at the same spinal levels as the visceral innerva- tions. Osteopathic manipulative treatment can be used to interrupt the viscerosomatic reflex, resulting in improve- ment of both the visceral and musculoskeletal symptoms.

The following is a case of a patient who presents with a long history of unexplained GI, cardiovascular, and neuro- logic symptoms. Having had extensive investigations in neurology, cardiology, and gastroenterology, the patient was frustrated and looking for relief from his chronic symp- toms.

Case report

A 48-year-old Caucasian male administrator presented with a nine-year history of vague GI disturbance, transient gen- eralized fasciculations and paresthesias, and diffuse back pain. His GI symptoms included early satiety, sensation of bloating, abdominal cramping, nausea and vomiting, and increased flatus that occurred approximately 30 minutes after every meal and usually lasted for hours. The functional debilitation caused by the symptoms resulted in eating very little throughout the day. Over the previous decade, the patient had seen gastroenterologists at multiple institutions in which a battery of radiographic, endoscopic, and functional tests were performed, with no definitive diagnosis. Regarding the patient’s neurologic symptoms, neurology had been consulted to rule out known organic etiology of his fasciculations and paresthesias. Studies included numerous magnetic resonance imaging scans, computed tomography scans, and electromyograms, all of which resulted equivo- cally. At the time of presentation, the patient’s most severe back pain was sharp and located over his right sacroiliac joint, which he equated to a football injury 10 years prior; however, he stated that over the previous five years, his back pain had migrated between his cervical, thoracic, and lumbar regions in a waxing and waning manner for weeks at a time. His pain was aggravated by lifting, standing, or bending forward. Alleviators included heat, massage, mo- bility, physical therapy, and stretching. He did not relate any bladder or bowel incontinence, or saddle anesthesia.

The patient was an active, married individual who par- ticipated in both aerobic and strength training programs at least three to four times/week. He did not smoke tobacco or drink alcohol and there was no history of illicit drug use. He did, however, consume two cups of coffee every day, which he admitted was decreased from seven cups two years prior. His family was healthy, although he recalled that both his maternal and paternal grandmothers complained of GI dis- turbances similar to his. Past medical history included pre- mature birth, mild sleep apnea, and postural orthostatic tachycardia syndrome (POTS). According to the patient, the cardiologist who originally diagnosed him with POTS re- ferred to his condition as “dysautonomia,” of which POTS was only a component. The patient had two right inguinal surgeries for an undescended testis, which resulted in or- chiectomy.

The patient was taking three medications at the time of presentation. Ramelteon 8 mg at bedtime and temazepam 15 mg at bedtime were taken to aid sleep. Polyethylene glycol was used daily for constipation. Although he could not remember the names of the previous drugs he had taken for his condition, some information was gained on previous treatment. He had been on numerous antacids, both proton pump inhibitors (PPIs) and H2-antagonists, and pro-motility agents, which offered minimal relief. At one point, he re- membered being prescribed an anticholinesterase agent— although he could not recall the name—that also gave min- imal relief. In an attempt to identify a common food-based etiology to his GI disturbance, the patient had tried both gluten-free and lactose-free diets. Previous testing for celiac sprue had been negative; however, elimination of gluten protein from his diet had resulted in the most relief, al- though his symptoms were still functionally debilitating on a daily basis.

The review of systems showed few findings beyond the history of his present illness. At times the patient felt weak and had myalgias. These generally go hand-in-hand with the fatigue and lethargy associated with his sleep apnea. A five-system physical examination was within normal limits. Pertinent findings on neurological examination included no sensory loss, weakness, or abnormal reflexes. All cranial nerves were intact and deep tendon reflexes were equal bilaterally.

The second office visit showed the patient pleased with treatment for his low back pain, given vast improvement. However, he relayed that the pain was now focused in his midthoracic area as well as at the base of the occiput. He had not seen noticeable improvement of his GI symptoms at that time. Key lesions included: C3 SrRr; T3-4 SrRl; T10-12 SrRl; bilateral sacrotuberous ligament restriction; bilateral SI joint restriction; left innominate anterior. Treat- ment of these somatic dysfunctions was achieved through soft tissue, myofascial release, muscle energy, and ligamen- tous articular strain techniques.

At the following office visit, the patient stated that he was doing well. His GI symptoms, although not absent, were the least problematic they had been in a number of years. However, he noted that his low thoracic back pain and neck pain, although better for a number of days, seemed to have returned. He located his thoracic pain at T10-L1 and described it as a tight band that wrapped around his flanks. Key lesions included: OA SrRl; C2-5 RlSl; C6 RrSr; T9 SlRr; T10 FBSrRr; T11-L3 SlRr; left SI restriction; superior mesenteric ganglion (SMG) and inferior mesenteric gan- glion (IMG) tenderness and restriction. Treatment of these somatic dysfunctions was achieved through muscle energy, articulatory, ligamentous articular strain, and integrated neuromuscular release techniques. Articulatory techniquesdirectly engage the restrictive barrier by repetitively forcingthe implicated tissues through their range of motion until thebarrier is reduced.6It was notable that while performingmyofascial release on the patient’s exquisitely tender SMGand IMG, pain began to radiate back through the band oftightness previously described by the patient, resulting insignificant bilateral paravertebral spasm at that level. Oncethe myofascial structures were restored to resting function,the pain and spasm in the low thoracic spine abated.On the fourth office visit, the patient relayed that both hisback pain and visceral symptoms were vastly improvedinitially. Unfortunately, as time progressed, his visceralsymptoms and neck pain began to return. Key lesions in-cluded: OA SrRl; C3-6 RlSl; T9-12 SlRr. Treatment ofthese somatic dysfunctions was achieved through muscleenergy, myofascial release, ligamentous articular strain, andfacilitated positional release techniques. Facilitated posi-tional release techniques are indirect. The region of somaticdysfunction is placed in a neutral position of flexion orextension and the tissues are positioned at the point of ease.An activating force is then applied to shorten the restrictedtissues and facilitate further release.6It was notable that alldysfunctional findings were palpably decreased from initialdysfunction treated in the clinic. Cervical somatic dysfunc-tion showed the most significant TART changes, whicheven still were decreased from initial findings.

‌Over the course of his visits at the clinic, this patient experienced vast improvement of both his visceral and mus- culoskeletal symptoms. Although he experienced improve- ment, because of the intermittent nature of his condition, he must follow up for symptomatic management.

Discussion

Like many patients at presentation, the initial assessment of the patient presented here reflects a lifetime of injuries and compensation, making decisions in treatment order and progression uncertain. Because corrections in specific dys- functional segments will result in functional compensation, the physician may find unpredictable changes exposed at subsequent visits, much as one peals away the layers of an onion. Such went the treatment of our patient. The initial assessment showed the primary dysfunction to be low back pain from previous trauma, but once resolved, subsequent visits revealed classic patterns relating his visceral and so- matic manifestations to abnormal autonomic function.

Much like dermatomes of the skin, all viscera has pre- dictable segmental innervation from the autonomic nervous system. With the chronic GI disturbance, one could predict to find facilitation anywhere from T5-L2, representing sym- pathetic innervation, or at the occipito-atlantal junction and upper cervical vertebrae, representing parasympathetic in-

Conclusion

‌Among the population of those diagnosed with a functional GI disorder, there lies a subpopulation of patients with idiopathic dysautonomia. In addition to their GI complaints, numerous findings consistent with autonomic dysregulation span multiple organ systems. Although the etiology of most functional GI disorders is unknown, it is possible that in a subpopulation of patients it is the result of primary dysau- tonomia. By treating somatic dysfunction that results from chronic segmental facilitation, autonomic balance may be restored, thereby offering relief from visceral complaints. Like many patients with functional GI disorders, their symptoms often require lifestyle changes that are frustrat- ing. Often times they have bounced from physician to phy- sician and specialty to specialty searching for effective treatment for their unexplainable condition. Because of this difficulty, any consistently successful means to improve their symptomatic disease will be received with great ap- preciation.

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