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17 Articles in Volume 19, Issue #7
Analgesics of the Future: Inside the Potential of 3 Drug Delivery Systems
Balancing Pain Care - and Opioids - in the Aging Adult
Book Review: A Useful Guide for New Pain Practitioners
Correspondence: Opioid Tapering & Discontinuation
Effective Interventions for Post-Stroke Shoulder Subluxation and Pain
Family: Their Role and Impact on Pain Management
Introducing the "Phoenix Sign:" Improved Vascular Perfusion of the Dorsalis Pedis Artery after a Subanesthetic Dose of Lidocaine
Medication Management of Chronic Pain in Patients with Comorbid Cardiovascular Disease
Multisite Pain May Be Associated with Fractures in the Elderly
Reconciling the New HHS Opioid Tapering Guideline with CDC and State Policies
Research Insights: Impaired Motor Imagery in Chronic Pain Conditions
Tapentadol: A Real-World Look at Misuse, Abuse, and Diversion
Temporomandibular Disorders in Performance Artists (Part 2)
Thoracic Outlet Syndrome Presenting as an Acute Stroke Mimic
Untangling Chronic Pain and Hyperarousal with Heart Rate Variability: A Case Report
What topicals exist for post-herpetic neuralgia pain?
When to Keep Your License: Older Physicians and Boundary Issues

Thoracic Outlet Syndrome Presenting as an Acute Stroke Mimic

Often misdiagnosed, the authors highlight how osteopathic assessment and manipulation may help to uncover the syndrome’s musculoskeletal etiologies.
Pages 37-39

Thoracic outlet syndrome (TOS) is a broad term used to encompass a multitude of clinically distinct syndromes that originate from compression of one or more neurovascular structures traversing through the thoracic outlet.1 The syndrome is subcategorized by neurovascular structure affected (arterial, venous, or neurologic), or by anatomical structure that causes compression of the neurovascular structures running through the scalene triangle.2

Neurogenic TOS accounts for 95% of all TOS presentations.3 There is a complexity in diagnosing TOS due to its many presentations. For instance, neurogenic TOS may mimic stroke symptoms (mononeuropathy) resulting in an unnecessary in-patient admission and extensive stroke workup. Medical teams must undertake a careful history and physical examination to catch what a previous team may have missed or to elicit additional history that a patient may have omitted.

In this retrospective case, the authors report on a patient with neurogenic TOS that was mistaken for an acute stroke, including clinical presentation, diagnostic steps, and treatment. The case highlights the value of osteopathic examination in helping to reveal musculoskeletal (MSK) etiologies of complex or confounding patient presentations.

iStockPhotoThoracic outlet syndrome is often under- or misdiagnosed.

Common Symptoms of Neurogenic TOS

The types of thoracic outlet syndrome may be defined by the four most common sites of anatomical compression:

  • within the scalenes (scalenus anticus syndrome)
  • between clavicle and first rib (costoclavicular syndrome)
  • under the pectoralis minor (pectoralis minor syndrome)
  • and under a congenital band or “cervical rib” (bony extension of the C7 transverse process).1

Most TOS cases are diagnosed between the ages of 20 and 50 and the prevalence of neurogenic-TOS is three to four times greater in women.4 A vast majority (95%) of patients with TOS are diagnosed with neurogenic-TOS and 15% of these patients also present with symptoms of arterial compression.3 Neurogenic TOS more commonly develops following trauma to the neck girdle area or from repetitive and stressful work-related activities.4

Symptoms of neurogenic-TOS vary widely depending on the site of impingement and parts of the brachial plexus involved. Upper plexus (C5-C7) symptoms may manifest as headache; face, jaw, or occipital pain; vertigo; blurred vision; or paresthesia of the first three digits. Lower plexus (C8-T1) symptoms may manifest as dull pain in the neck, shoulder, axilla, or medial aspect of the upper extremity; ulnar neuropathy (muscle atrophy in the hand or paresthesia in the fourth and fifth digits); or paresthesia of the medial forearm (T1 dermatome).5 Symptoms may not follow a dermatomal or myotomal distribution pattern unless there is cervical root nerve compression.6 While provocative tests such as Adson’s and Wright’s may be performed on physical examination, these tests have high false-positive rates and are not well-demonstrated in their reliability and validity.7 Moreover, mononeuropathies may present in neurogenic-TOC, causing focal sensory or motor deficits that may be easily mistaken for symptoms of a more serious condition such as stroke.8

Case Patient


The patient is a 57-year-old African American female with a history of adult polycystic kidney disease (PKD) and hypertension who presented to the emergency department (ED) with a complaint of left shoulder and arm pain; tingling; decreased range of motion (ROM); left palmar numbness and tingling; and midline lumbar back pain for three days. The patient reported numbness and swelling of bilateral hands that had resolved prior to presentation. The patient also complained of floating spots in her visual field when turning her head that had started two days before arriving to the ED. She denied recent fever/chills, chest pain, shortness of breath, trauma or infection, significant weight loss, history of malignancy, blurry/loss of vision, saddle anesthesia, and incontinence. She also denied discoloration or cold sensations to her left hand and digits. The patient reported a smoking history of 19 pack-years, denying alcohol or recreational drug use. She was admitted to the authors’ in-patient unit for cerebrovascular accident (CVA) workup following preliminary testing.

On exam, the patient was found to have limited active and passive ROM to her left shoulder at 45 degrees. She also displayed reduced strength of 4/5 to left upper extremity and left-hand grip strength, delayed motor functioning to left hand digits, and an inability to discriminate sharp and dull stimuli on the left palm.

Her mentation was intact and all other neurological findings on exam were within normal limits. Allen’s test was negative, and all other physical exam findings were benign. Neurology and physical medicine and rehabilitation (PM&R) were consulted. The PM&R team conducted an osteopathic structural exam which revealed hypertonic cervical paraspinal musculature, an inhalation dysfunction to the first left rib, and a group curve at L1-L4 RRSL. The patient experienced shooting pain and paresthesias radiating from the left shoulder down to the left forearm on shoulder abduction. Phalen’s test, Tinel’s sign, Adson’s test, and Wright’s test were negative.

A CT brain scan without contrast showed no acute intracranial processes or hemorrhage. CT angiogram of the brain was unremarkable, with no aneurysms or stenosis detected. Left shoulder and lumbosacral spine x-rays did not reveal any fractures or dislocation. However, while the neurology team recommended MRI of the brain and full stroke workup, the primary and PM&R team felt the etiology of the patient’s symptoms was due to neurogenic TOS.


Based on assessment, a decision was made to treat the patient’s TOS with osteopathic manipulation treatment (OMT). The patient was administered muscle energy to the inhalation dysfunction at the left first rib and myofascial release to the cervical paraspinal musculature. The patient tolerated the treatment well with no side effects. The patient reported alleviation of ROM restriction after treatment, but still endorsed mildly decreased sensation to her left palm. Upon reassessment, the patient demonstrated pain-free active left shoulder ROM to 120 degrees and passive to 135 degrees of abduction, a significant improvement from the original presentation of 45 degrees.

The patient reported a resolution of paresthesias to her left arm and forearm and a significant reduction in the sensory deficit to her left palm, as she displayed the ability to discern sharp and dull stimuli despite some remaining mild numbness. She reported resolution to the floating spots in her visual field that she had reported on presentation when rotating her head. She was discharged from the hospital with a scheduled primary care outpatient appointment; follow-up data is not yet available.


It is not uncommon for a patient to be admitted to the hospital for a “stroke mimic.” One comprehensive review cited that 74% of patients presenting with stroke symptoms were diagnosed with stroke,9 leaving 26% of these patients to have stroke mimic symptoms. There have been 33 patients with stroke or transient ischemic attacks associated with TOS reported in the medical literature, however, 26 of these reported cases were associated with a cervical rib and were thus associated with vascular TOC.10

In this case report, the patient demonstrated symptoms of neurogenic TOC likely secondary to compression of the lower brachial plexus branch (C8-T1) by the left first rib and scalene muscles. This assessment was supported by a physical exam which displayed bilateral anterior scalene muscle hypertonicity and an elevated left first rib (an inhalation dysfunction).

The neurovascular bundle sheath runs superior to the first rib and inferior to the clavicle, thus the authors expected that the elevation of the first rib could cause compression of the lower brachial plexus and lead to symptoms consistent with the patient’s presentation. Subsequent treatment to this area led to resolution of presenting symptoms by alleviating anatomical compression of structures contained within the left scalene triangle. Myofascial release of the scalene muscles promoted a reduction of the compression to the bundle sheath. Muscle energy to the first rib allowed further decompression of the space inferior to the clavicle by enhancing rib motion inferiorly (direction of exhalation).


The case presented gives an example of a somewhat odd presentation of thoracic outlet syndrome presenting as a stroke mimic. Most prior literature has only reported TOS in association with an acute stroke and not stroke-like symptoms. This case demonstrated the importance of a thorough MSK and osteopathic examination to investigate peripheral neuropathic symptoms. A detailed history should be obtained with emphasis placed on the location of weakness (discerning weakness due to pain versus true weakness), and acuity of such complaints in order to better characterize an etiology.

Uncovering an MSK etiology to a neurological symptomatology saved this patient from additional workup for a neurologic cause of her symptoms in the form of an extended in-patient stay and/or unnecessary and costly outpatient testing. Additionally, this retrospective case demonstrated how noninvasive, manipulative techniques could be used to treat mild forms of TOS and improve symptoms. These relatively simple techniques are generally well-tolerated and may be applied to the outpatient primary care setting. Moreover, OMT may be provided during multiple visits as a post-hospital course, offering a feasible and low-cost treatment regimen option.

Last updated on: December 6, 2019
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