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eMedicine Specialties > Neurology > Headache and Pain

Thoracic Outlet Syndrome

Manish K Singh, MD, Assistant Professor, Pain Management, Department of Neurology, Drexel College of Medicine, Hahnemann University hospital
Jashvant Patel, MD, Medical Director, Department of Pain Medicine and Comprehensive Rehabilitation, Medical College of Pennsylvania Hahnemann University

Updated: Nov 29, 2007

Introduction

Background

Thoracic outlet syndrome (TOS) is complex clinical entity characterized by various neurovascular signs and symptoms of the upper limb. It includes several different types of disorders, as follows:

  • Neurologic TOS
    • Classic (true) neurologic TOS
    • Common (disputed) neurologic TOS
  • Vascular TOS
    • Arterial TOS
    • Venous TOS
  • Combined neurovascular TOS

TOS can involve various components of the brachial plexus, the blood vessels, or both at different sites between the base of the neck and the axilla.

The arterial form is caused by compression of the subclavian artery, the venous form is caused by compression of the subclavian vein, and the neurologic form is caused by brachial plexus compression. Combined neurovascular TOS is usually traumatic.

Pathophysiology

Most authors suggest that nonspecific neurologic TOS results from injury to the brachial plexus, by either traction or compression, at some point within the cervicoaxillary canal.

True (classic) neurologic TOS, which is rare, is caused by congenital anomalies. Usually these anomalies include a taut fibrous band or rudimentary cervical rib.

Frequency

United States

The exact prevalence of TOS is difficult to assess. True neurogenic or vascular TOS is considered rare, but common (nonspecific/disputed) neurogenic TOS is more prevalent.

Sex

TOS is more common in women than in men. The sex ratio varies depending on the type of TOS.

  • The female-to-male ratio in neurologic-type TOS is approximately 3.5:1.
  • The venous type is more common in males than in females, and the arterial type has no sexual predilection.

Clinical

History

Because of complex etiology and absence of good diagnostic tests, patient history is important in TOS.

  • In common neurogenic TOS, pain is the most common and earliest complaint. Detailed history characterizing the patient's pain may lead to appropriate diagnostic and therapeutic plans.
    • The location of pain is an important part of the history.
      • Ask the patient to describe the pain location and type on a pain diagram (anterior/posterior and lateral view of human picture).
      • Pain, numbness, and/or tingling of the upper extremity are common presenting features of neurogenic TOS.
      • Sometimes the patient may report pain in the chest, neck, and/or face and even headache.1
    • Precipitating factors include repetitive or stressful activity, such as prolonged computer keyboard use or overhead work, which can provoke or intensify pain.
      • Most patients report a history of an automobile accident or work-related injury.
      • Alleviating factors may exist and may provide additional clues for possible etiologies.
    • Various terms can be used to describe quality of pain, but it is usually a dull aching type in neurogenic TOS.
    • Spreading or radiation of pain is also important in evaluation of neuropathic pain. If retrosternal pain (radiation from intercostobrachial nerve, a branch of T2 intercostal nerve) is noticed on the left side, it can be confused with pain of cardiac or pulmonary origin.2,3
    • Use some type of rating system to evaluate pain severity or intensity with a degree of objectivity and reproducibility. Different types of pain scales may be used. Numerical scales are more useful and reliable. The Visual Analog Scale (VAS) is a commonly used numerical scale.
  • Arterial TOS often is associated with aching, fatigue, weakness, and pallor due to brachial ischemia.
  • Cold temperature always worsens symptoms.

Physical

  • Hyperabduction and depression of the shoulder may provoke symptoms in patients with TOS.
  • Various stress tests or provocative maneuvers are used by the clinician to evaluate TOS. The sensitivity and specificity of these maneuvers have been reported to be low.
    • Roos maneuver: When in the surrender posture, the patient reports paresthesia and numbness in extremities within 1 minute. This maneuver usually provokes symptoms in lateral cord distribution.
    • Wright maneuver: This maneuver requires the patient to hold the arms next to the ears. Paresthesias usually are noted down the medial scapular border and into lower trunk distribution.
    • Elevated-arm stress test: In this test, the patient keeps arms abducted with flexed elbows for 3 minutes while flexing and extending the fingers. Results are considered positive if the patient cannot do this for 3 minutes.
    • Hyperabduction test: The radial pulse is diminished after elevating the involved arm above the head.
    • Adson maneuvers: While the patient is in a sitting position, ask the patient to inspire deeply, hold his breath, and extend his neck. Then, turn the patient's head passively as far as possible toward one side and then the other. When the head is turned toward the unaffected side, or sometimes the affected side, obliteration of the radial pulse with a drop in blood pressure in the arm is considered a positive result. While turning the head in either direction, the pulse may disappear on both sides, but, on the affected side, a longer lag occurs in its return. During this maneuver, a bruit may develop that is best heard in the supraclavicular space.4
    • Military maneuver (ie, costoclavicular bracing): This maneuver provokes symptoms when the patient elevates the chin and pulls the shoulder joint behind in an extreme "attention" position.5
  • In common neurogenic TOS, physical examination usually does not reveal appreciable sensory loss or motor atrophy in the limb.
    • Upper trunk involvement results in deltoid, upper arm, and medial scapular border pain.
    • Lower trunk involvement can cause dull ache in the medial forearm and paresthesias in the fourth and fifth fingers.
    • Tenderness to palpation over the brachial plexus and paresthesia on percussion may be observed (Tinel sign). Most patients demonstrate hypersensitivity to mechanical compression over the supraclavicular and infraclavicular fossae.
    • The Spurling sign (ie, pain during direct compression of the foraminal exit areas of cervical nerve roots) may help in making the diagnosis of cervical radiculopathy.
    • Vasomotor involvement caused by TOS must be differentiated from coexistent or other causes of vasomotor instability (eg, complex regional pain syndrome [reflex sympathetic dystrophy or causalgia]).
  • In classic neurologic TOS, wasting (especially intrinsic hand muscle atrophy) is a characteristic feature. Signs of decreased pain and temperature sensation may be present in the C8 through T1 distribution.
  • In arterial TOS, usual findings include cool and pale extremity. This finding depends on the extent of compression and injury to the subclavian artery.
  • In venous TOS, the affected limb may be swollen and tender. It may exhibit cyanosis (dusky coloration), venous distension, and ischemic changes in the upper extremity. Strenuous physical activities of extremity can evoke these symptoms and signs. Venous thrombosis can develop at the site of compression.

Causes

  • Most authors suggest that nonspecific neurologic TOS results from injury to the brachial plexus, by either traction or compression, at some point within the cervicoaxillary canal.
  • True (classic) neurologic TOS is caused by congenital anomalies and usually includes a taut fibrous band or rudimentary cervical rib. Other anatomic anomalies include elongated transverse process of C7.
  • Trauma or repetitive activities may produce TOS (eg, motor vehicle accident hyperextension injury, effort vein thrombosis).
  • Certain postures of the body may exacerbate or provoke the symptoms of TOS (eg, hyperabduction with external rotation of arm, depression of shoulder).

Differential Diagnoses

Ankylosing Spondylitis
Syringomyelia
Cervical Spondylosis: Diagnosis and Management
Torticollis
Median Neuropathy
Traumatic Peripheral Nerve Lesions
Metastatic Disease to the Spine and Related Structures
Ulnar Neuropathy
Radial Mononeuropathy
Reflex Sympathetic Dystrophy

Other Problems to Be Considered

Brachial plexus traction injury
Raynaud disease
Chronic arterial insufficiency
Peripheral nerve entrapment
Peripheral neuropathy
Chronic phlebothrombosis
Somatization disorder
Malingering
Spinal cord disease

Workup

Laboratory Studies

  • A thorough history and physical examination are the most important components in establishing the diagnosis of TOS. Use of radiographic and laboratory tests may improve the diagnostic yield. Various screening tests may be appropriate to exclude other causes of upper extremity pain and paresthesia.

Imaging Studies

  • Radiographs may exhibit bony anomalies.
    • Chest x-ray may demonstrate cervical or first rib, Pancoast tumor clavicle, or other skeletal deformity.
    • Cervical spine radiograph may be helpful in showing a cervical rib, an elongated transverse process, or scoliosis.
  • Color flow duplex scanning can identify interruption of blood flow to the affected extremity.
  • Arteriogram can identify blockage of the artery from thrombi or emboli. It also can detect aneurysms that may be compressing the plexus.
  • Venography (subclavian vein) is confirmatory and remains the criterion standard. This study can demonstrate the site of obstruction or the presence of thrombus.
  • CT scan or MRI is useful to exclude cord lesions and radiculopathy and may exhibit plexus distortion.

Other Tests

  • Electromyography/nerve conduction study may be useful to exclude coexistent abnormalities such as peripheral nerve entrapment or cervical radiculopathy.
  • Sensory evoked potentials are of limited value in making the diagnosis of neurogenic-type TOS and have no established value in vascular-type TOS.

Treatment

Medical Care

Most patients with TOS require only symptomatic treatment and appropriate consultation. Arterial, venous, and neurologic features may coexist; treatment should be directed toward the dominant component.

  • Common neurologic-type TOS requires conservative management that commonly includes pharmacologic therapy and gentle physiotherapy.
    • Patients with common neurologic-type TOS may respond to physical therapy, which increases the range of motion of the neck and shoulders, strengthens the rhomboid and trapezius muscles, and induces a more erect posture.
    • Aggressive physiotherapy, particularly traction, should be avoided, because it may worsen brachial plexus symptoms.
    • For true neurologic TOS, sectioning of the congenital band is an appropriate option.
  • Vascular (arterial and venous) TOS is less common and often requires surgical treatment.
    • Patients with vascular-type TOS need immediate heparinization and vascular surgery consultation.
    • Anticoagulant therapy (ie, warfarin) may be needed for a minimum of 3 months in vascular-type TOS to prevent recurrent or ongoing thromboembolic occlusion.
  • Analgesic drug therapy for TOS can be divided into the following categories:
    • Nonopioid analgesics (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], acetaminophen): NSAIDs commonly are used in patients with mild to moderately severe pain. They inhibit inflammatory reactions and pain by decreasing prostaglandin synthesis. Acetaminophen is a safe choice for treatment of pain during pregnancy and breastfeeding.
    • Opioid analgesics: Opioids are used commonly as an analgesic for many pain syndromes. Opioid therapy can be a safe and effective option in patients with intractable nonmalignant pain and no history of drug abuse.6 Quang-Cantagrel et al report that failure of one opioid cannot predict the patient's response to another opioid.7 High doses of tramadol may provide effective and safe relief in neuropathic pain.
    • Antidepressants: Antidepressant medications play a major role in treatment of neuropathic pain.
      • Tricyclic antidepressants - Amitriptyline (Elavil), nortriptyline (Pamelor)
      • Selective serotonin reuptake inhibitor (SSRI) antidepressants - Paroxetine (Paxil), fluoxetine (Prozac), sertraline (Zoloft)
      • Other antidepressants - Nefazodone (Serzone), venlafaxine (Effexor)
    • Anticonvulsants
      • Sodium channel antagonists have been used in the management of neuropathic pain for several years. These medications are started slowly and administered as needed. Monitor the patient carefully.
      • Several anticonvulsant drugs (eg, clonazepam, topiramate, gabapentin, lamotrigine, tiagabine, zonisamide) have been tried in treatment of TOS.
      • In studies by Nicholson and Rowbothan, gabapentin has been reported to be effective in the management of chronic neuropathic pain syndromes.
      • Controlled studies for the effect of lamotrigine are not yet available, but Jain noted that the drug has demonstrated effect in neuropathic pain.
    • Other adjunct analgesics: Muscle relaxants (eg, metaxalone [Skelaxin], cyclobenzaprine [Flexeril], benzodiazepines, tizanidine) may be helpful to decrease spasm and provide pain relief.

Surgical Care

Careful evaluation and selection of the patient is very important.

  • Surgical management of TOS commonly includes supraclavicular and transaxillary approaches for anatomic decompression.8
  • For classic neurologic TOS, sectioning of the congenital band with a supraclavicular approach is the appropriate option. If necessary, the tip of the rudimentary cervical rib can be removed.
  • Spinal cord stimulation may be considered carefully for management of severe chronic pain that has been refractory to other conservative modalities.9
  • Cherington et al reported on 5 patients who suffered serious injuries after surgery for TOS. These patients had few or no clinical abnormalities on examination prior to the surgery.
  • Other studies, including one of 8 patients who sustained brachial plexus injuries resulting in clinical and electrophysiologic deficits after TOS surgery, have been reported.10

Consultations

Consultation may be needed depending on the type of TOS and pathology, as follows:

  • Neurology
  • Orthopedic surgery
  • Vascular surgery
  • Physical medicine and rehabilitation

Activity

Aggressive physiotherapy, particularly traction, should be avoided, because it may worsen brachial plexus symptoms.

Medication

Drug therapy for TOS can be divided into the following categories:

Nonsteroidal anti-inflammatory agents (NSAIDs)

These agents inhibit inflammatory reactions and pain by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis. NSAIDs may provide pain relief in the patient with TOS.


Naproxen sodium (Anaprox, Naprelan, Naprosyn)

For relief of mild to moderately severe pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis.

Dosing

Adult

275 mg PO tid or 550 mg PO bid

Pediatric

Not established

Interactions

Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; may increase phenytoin levels

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug


Ibuprofen (Motrin, Advil)

NSAIDs used commonly for patients with mild to moderately severe pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Dosing

Adult

400-800 mg PO q8h; not to exceed 3200 mg/d

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Interactions

Probenecid may increase toxicity; may decrease effects of loop diuretics; may increase serum lithium levels; may prolong PT in patients taking anticoagulants

Contraindications

Documented hypersensitivity; active peptic ulcer disease; renal or hepatic impairment; concomitant or recent use of anticoagulants; hemorrhagic conditions

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, or decreased renal or hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.


Acetaminophen (Tylenol, Feverall, Tempra, Aspirin Free Anacin)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Dosing

Adult

650-1000 mg PO initially; may be repeated if necessary at same dose after 6h

Pediatric

<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d (3-6 y: not to exceed 720 mg/d; 6-12 y: not to exceed 2.6 g/d)
>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h

Interactions

Rifampin can reduce analgesic effects; barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Contraindications

Documented hypersensitivity; known G-6-PD deficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in persons with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate serious illness; contained in many OTC products, and combined use with these products may result in cumulative doses exceeding recommended maximum dose


Oxycodone (OxyContin)

Long-acting form of opioid currently used commonly for severe pain. Start with small dose and increase gradually.

Dosing

Adult

10-160 mg PO q12h

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Phenothiazines may antagonize analgesic effects; MAOIs, general anesthesia, CNS depressants, and tricyclic antidepressants may increase toxicity

Contraindications

Documented hypersensitivity; presence of intracranial lesion associated with impaired intracranial pressure (hydromorphone); concurrent or recent use of MAOIs; poor respiratory function (eg, COPD, cor pulmonale, emphysema, status asthmaticus, kyphoscoliosis)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in COPD, emphysema, renal insufficiency, impaired respiratory and cardiac function, and severe renal disease


Morphine sulfate (MS Contin, Duramorph, Astramorph)

Effective analgesic with good safety profile and ease of reversibility with naloxone. Various IV doses used; commonly titrated until desired effect obtained.
Oral morphine sulfate includes Avinza, Kadian, and MS Contin. These medications are available in multiple different strengths (15-120 mg).

Dosing

Adult

Starting dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg IV/IM/SC; reassess hemodynamic effects of dose

Pediatric

Infants and children: 0.1-0.2 mg/kg IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; may initiate at 0.05 mg/kg/dose

Interactions

Phenothiazines may antagonize analgesic effects; TCAs, MAOIs, and other CNS depressants may potentiate adverse effects

Contraindications

Documented hypersensitivity; hypotension; potentially compromised airway in which establishing airway control rapidly would be difficult

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate


Fentanyl transdermal patch (Duragesic)

Potent narcotic analgesic with much shorter half-life than morphine sulfate. Excellent choice for pain management and sedation with short duration (30-60 min); easy to titrate. Easily and quickly reversed by naloxone. When using transdermal dosage form, most patients' pain controlled with 72-h dosing intervals; however, some patients may require dosing intervals of 48 h.

Dosing

Adult

12 mcg/h TD; replace q48-72h
25 mcg/h (10 cm2) TD; replace q48-72h
50 mcg/h (20 cm2) TD; replace q48-72h
75 mcg/h (75 cm2) TD; replace q48-72h
100 mcg/h (100 cm2) TD; replace q48-72h

Pediatric

Not established

Interactions

Phenothiazines may antagonize analgesic effects; TCAs may potentiate adverse effects

Contraindications

Documented hypersensitivity; hypotension; potentially compromised airway

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with hypotension, respiratory depression, constipation, nausea, emesis, or urinary retention; idiosyncratic reaction, known as chest wall rigidity syndrome, may require neuromuscular blockade to increase ventilation

Antidepressants

This complex group of drugs has central and peripheral anticholinergic effects, as well as sedative effects. They have central effects on pain transmission. They increase synaptic concentration of serotonin and/or norepinephrine in CNS by inhibiting their reuptake by the presynaptic neuronal membrane.

Other options include duloxetine hydrochloride (Cymbalta), venlafaxine (Effexor), and bupropion (Wellbutrin).


Nortriptyline (Pamelor)

Has demonstrated effectiveness in treatment of chronic and neuropathic pain.

Dosing

Adult

25-100 mg PO hs; not to exceed 200 mg/d

Pediatric

Children: 0.1 mg/kg PO hs initially; increase, as tolerated, up to 0.5-2 mg/d hs
Adolescents: 25-50 mg/d PO; increase gradually to 100 mg/d

Interactions

Cimetidine may increase levels; may increase PT in patients whose PT is stabilized with warfarin

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency, MAOIs within 14 d

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in cardiac conduction disturbances, history of hyperthyroidism, or renal or hepatic impairment; because of pronounced effects in cardiovascular system, best to avoid in elderly


Amitriptyline (Elavil)

Analgesic for certain chronic and neuropathic pain.

Dosing

Adult

25-100 mg PO hs; not to exceed 150 mg/d

Pediatric

Not established

Interactions

Phenobarbital may decrease effects; CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Contraindications

Documented hypersensitivity; MAOIs within 14 d; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in cardiac conduction disturbances, history of hyperthyroidism, or renal or hepatic impairment; avoid using in elderly patients

Selective serotonin reuptake inhibitors

These agents may be considered as alternative to TCAs.


Fluoxetine (Prozac)

Antidepressant with potent specific 5-HT uptake inhibition with fewer anticholinergic and cardiovascular adverse effects than TCAs.

Dosing

Adult

10 mg PO on waking initially; can be increased every 2 wk, not to exceed 60 mg/d

Pediatric

Not established

Interactions

Increases toxicity of diazepam and trazodone by decreasing clearance; increases toxicity of MAOIs and highly protein-bound drugs; other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan) may cause serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death); discontinue other serotonergic agents at least 2 wk prior to SSRIs

Contraindications

Documented hypersensitivity; pregnancy and lactation; severe renal or hepatic disease; MAOIs within last 2 wk

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Anxiety, insomnia or drowsiness, tremor, anorexia, anorgasmia, and other sexual dysfunctions have been reported; nausea, flulike symptoms, and agitation also are noted (resolve within 1-2 wk); caution in hepatic impairment and history of seizures; discontinue MAOIs inhibitors at least 14 d before initiating fluoxetine therapy


Sertraline (Zoloft)

Antidepressant with potent specific 5-HT uptake inhibition with fewer anticholinergic and cardiovascular adverse effects than TCAs.

Dosing

Adult

50 mg/d PO initially, increased at weekly intervals after several wk; not to exceed 200 mg/d

Pediatric

Not established

Interactions

Increases toxicity of diazepam and trazodone by decreasing clearance; increases toxicity of MAOIs and highly protein-bound drugs; other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan) may cause serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death); discontinue other serotonergic agents at least 2 wk prior to SSRIs

Contraindications

Documented hypersensitivity; pregnancy and lactation; severe renal or hepatic disease; MAOIs within last 2 wk

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Anxiety, insomnia or drowsiness, tremor, anorexia, anorgasmia, and other sexual dysfunctions have been reported; nausea, flulike symptoms, and agitation also are noted (resolve within 1-2 wk); caution in hepatic impairment and history of seizures; discontinue MAOIs inhibitors at least 14 d before initiating fluoxetine therapy


Paroxetine (Paxil)

Antidepressant with potent specific 5-HT uptake inhibition with fewer anticholinergic and cardiovascular adverse effects than TCAs.

Dosing

Adult

Start at 10 mg/d PO and titrate upward; not to exceed 50 mg/d

Pediatric

Not established

Interactions

Increases toxicity of diazepam and trazodone by decreasing clearance; increases toxicity of MAOIs and highly protein-bound drugs; other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan) may cause serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death); discontinue other serotonergic agents at least 2 wk prior to SSRIs

Contraindications

Documented hypersensitivity; pregnancy and lactation; severe renal or hepatic disease; MAOIs within last 2 wk

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Anxiety, insomnia or drowsiness, tremor, anorexia, anorgasmia, and other sexual dysfunctions have been reported; nausea, flulike symptoms, and agitation also are noted (resolve within 1-2 wk); caution in hepatic impairment and history of seizures; discontinue MAOIs at least 14 d before initiating paroxetine therapy

Benzodiazepines

By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters. They may act in the spinal cord to induce muscle relaxation.


Clonazepam (Klonopin)

Suppresses muscle contractions by facilitating inhibitory GABA neurotransmission and other inhibitory transmitters.

Dosing

Adult

0.5-1 mg PO tid, for short course

Pediatric

Not established

Interactions

Phenytoin and barbiturates may reduce effects; CNS depressants increase toxicity

Contraindications

Documented hypersensitivity; severe liver disease; acute narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in chronic respiratory disease or impaired renal function; withdrawal symptoms can result from abrupt discontinuation of the medication

Anticonvulsants

Use of certain antiepileptic drugs, such as the GABA analogue gabapentin (Neurontin), has proven helpful in some patients with neuropathic pain. Other anticonvulsants (eg, clonazepam, topiramate, lamotrigine, zonisamide, tiagabine) also have been tried in chronic pain.

Pregabalin (Lyrica) can be effective, tolerable, and easy to titrate compared to gabapentin.


Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, exact mechanism of action unknown. Structurally related to GABA but does not interact with GABA receptors.

Dosing

Adult

100 mg PO hs to 1200 mg PO tid

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Interactions

Antacids may reduce bioavailability significantly (administer at least 2 h following antacids); may increase norethindrone levels significantly

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt withdrawal of this medication may precipitate seizures; caution in severe renal disease

Follow-up

Further Inpatient Care

  • Hospitalization usually is not required for patients with TOS, but this decision depends on the invasiveness of the treatment choice for pain control and the severity of the patient's condition. Sometimes, a short hospitalization is necessary for individuals who require a continuous nerve block. Patients with TOS may have associated conditions that may be amenable to surgery and require further inpatient care.

Further Outpatient Care

  • Patients with TOS generally are treated on an outpatient basis and require a variety of health care professionals to manage their condition optimally. Please refer to the Treatment section for a discussion of proper rehabilitation methods and other treatment options.

Prognosis

  • Neurogenic TOC usually requires chronic pain management.
  • Vascular-type TOC may have better outcome with appropriate management.
  • Patients with profound intrinsic muscle atrophy do not regain their function. Appropriate surgery may arrest the progressive deterioration.

Patient Education

  • Instruct the patient on the following:
    • Good posture
    • Job modification
    • Exercise programs

Miscellaneous

Medicolegal Pitfalls

  • Recognizing secondary causes (especially space-occupying lesions) of brachial plexus compression is important.
    • Pancoast tumors can invade the thoracic outlet and compress the plexus.
    • Enlargement of the supraclavicular or axillary lymph nodes (due to metastasis or inflammation) can compress the brachial plexus.
    • Malunited clavicular fractures may result in callus overgrowth and compression of the brachial plexus.

References

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  2. Schwartzman RJ. Brachial plexus traction injuries. Hand Clin. Aug 1991;7(3):547-56. [Medline].

  3. Urschel HC Jr, Razzuk MA, Hyland JW, et al. Thoraic outlet syndrome masquerading as coronary artery disease (pseudoangina). Ann Thorac Surg. Sep 1973;16(3):239-48. [Medline].

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Keywords

TOS, thoracic outlet syndrome, brachial plexus, neurologic TOS, vascular TOS, compression of the subclavian artery, compression of the subclavian vein, brachial plexus compression, congenital anomaly, arterial TOS, venous TOS, combined neurovascular TOS

Contributor Information and Disclosures

Author

Manish K Singh, MD, Assistant Professor, Pain Management, Department of Neurology, Drexel College of Medicine, Hahnemann University hospital
Manish K Singh, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American Association of Physicians of Indian Origin, American Headache Society, American Medical Association, and American Society of Regional Anesthesia and Pain Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Jashvant Patel, MD, Medical Director, Department of Pain Medicine and Comprehensive Rehabilitation, Medical College of Pennsylvania Hahnemann University
Jashvant Patel, MD is a member of the following medical societies: Alberta Medical Association, American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Society of Regional Anesthesia and Pain Medicine, and Medical Society of the State of New York
Disclosure: Nothing to disclose.

Medical Editor

Jorge E Mendizabal, MD, Consulting Staff, Corpus Christi Neurology
Jorge E Mendizabal, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, National Stroke Association, and Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

James H Halsey, MD, Professor, Department of Neurology, University of Alabama Medical Center
James H Halsey, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neuroimaging, Medical Association of the State of Alabama, New York Academy of Sciences, Pan American Medical Association, Sigma Xi, Society for Neuroscience, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

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