Shoulder Nerve Compression Syndromes

Shoulder Nerve Compression Syndromes

Normal Anatomy



Un nervio es una estructura parecida a una cuerda que está formada por múltiples axones que salen de la medula espinal. Un axón es una extensión de una celular nerviosa y múltiples células nerviosas forman el cerebro y la medula espinal que envía la señal de las funciones de todas las acciones del cuerpo humano. Los nervios tienen 3 funciones principales en el sistema musculoesquelético. 1- Proveen de retroalimentación sensitiva del medio ambiente a través de sensores específicos que se comunican con el cerebro para ser interpretada la información y posteriormente se envía una señal al axón del nervio. Los tipos de funciones sensitivas interpretadas por el cerebro incluyen sensación de tacto, vibración, posición de las articulaciones, calor y frio. 2- el nervio se inserta en el musculo para inervarlo y que realice funciones motores precisas. 3- Para avisar y prevenir que el cuerpo sea dañado por factores ambientales por vía de fibras de dolor, que al estimularse avisan a la persona de un peligro inminente tanto del medio ambiente como de dolor interno como una apendicitis o una piedra en el riñón.


The brachial plexus is a network of nerves that form from the nerves that exit the neck (cervical root C5-T1), then intermingle to forming the brachial plexus which ends in specific nerves thatcontrol the entire upper limb including the shoulder, elbow, wrist and hand. The five major nerves arising from the brachial plexus are the musculocutaneous nerve, Axillary nerve, Median nerve, Ulnar nerve and Radial nerve. Other nerves that arise from the brachial plexus are the suprascapular nerve, long thoracic nerve, thoracodorsal nerve and dorsal scapular nerve which supply shoulder muscles. As the nerves travel between muscle layers, they can become compressed through a phenomenon called the edge effect whereby a nerve enters into a muscle that has a dense fascial cover and the change in pressure from the muscle to the dense fascial edge can create compression if repetitive gliding on the fascial edge with repetitive activities causes swelling of the nerve. Injury that is secondary to direct trauma or indirect through pulling injuries that stretch a nerve can also cause nerve symptoms of numbness, tingling and pain. These symptoms are the hallmark of nerve pain, which continue their stimulation with or without the use of our limbs. Rest pain then, with symptoms of numbness, tingling or weakness alerts an examiner that a nerve compression is most likely the cause of the problem.


Pathology

Nerve compression syndromes are normally found in adults of all ages and it is rare to find nerve compression syndromes in patients younger than 20 years of age. Nerve compression syndromeshave several causes including injury, repetitive use with poor body posture, medical conditions like diabetes, thyroid disorder or kidney failure to name a few. With aging, the body experiences decreasing tissue flexibility as the water content of cells decrease, collagen type of tissue changes to the less flexible type and the elastin part of muscle and ligaments decrease further decreasing muscle flexibility. As the nerves travel through muscle tissue layers and we place our limbs in poor ergonomic positions during work or leisure activities, nerve compressions are at risk of occurring. Examples of poor body position causing a nerve compression syndrome is when a job requires answering the phone all day long, having the employee hold the phone with the elbow bent for hours, the employee will begin to develop compression of the ulnar nerve which causes elbow and forearm pain associated with ring and small finger numbness. If this is not corrected by having the employee use a headset that eliminates the need to hold the phone in their hand, progression of symptoms requiring surgery may occur.


Nerve compression in the neck and shoulder typically present with pain in the neck and shoulderoften causing referred pain down the arm or to the shoulder blade. Other symptoms can include numbness, tingling, a cool limb sensation, muscle weakness, atrophy, discoloration of the arm and hand, and functional limitations that include dropping objects, inability to button shirts, comb your hair or brush your teeth. Nerve pain has a constant presenceoccurring without the use of the limb but is often aggravated with use. The quality of the pain can vary froma dull ache to severe intolerable sharp stabbing pain. The temporal appearance is also variable and at times unpredictable presenting without rhyme or reason.Examples of nerve compression syndromes about the shoulder area include suprascapular nerve compression, Quadrangular space syndrome, Parsonage Turner syndrome, Thoracic Outlet Syndrome, and Complex Regional Pain Syndrome.
Suprascapular nerve Compression typically occurs in two locations. When the suprascapular nerve exits the brachial plexus, it passes through the suprascapular notch that has as its roof, the transverse scapularligament. This space that the suprascapular nerve travels through can become excessively tight causing a dull constant ache in the shoulder that is deep in quality and occurs at rest aggravated with use of the arm. The use of an EMG/NCS can be helpful in making the diagnosis as well as the use of diagnostic injections given in the office to confirm the diagnosis. Below is a picture of the suprascapular nerve compressed at the level of the suprascapular notch and Spinoglenoid notch.

The suprascapular nerve can also be compressed in an area called the spinoglenoid notch from the presence of a ganglion cyst (fluid filled sack) that forms most commonly from fluid leaking from the shoulder joint caused by a SLAP lesion which is a tear in the labrum which seals the glenoid rim. Above is a picture of the spinoglenoid ganglion cyst causing compression of the suprascapular nerve. The result of compressing the suprascapular nerve at the suprascapular notch is the atrophy or withering away of the muscle of the supraspinatus and infraspinatus. The compression of the spinoglenoid notch causes atrophy of the infraspinatus. The consequence of this compression is weakness of the rotator cuff muscles that raise the arm and rotate the arm to the outside.


Like Suprascapular nerve compression, Quadrangular space syndrome (QSS) is compression of the axillary nerve that arises, from the brachial plexus. This nerve is accompanied by the posterior humeral circumflex artery (PHCA) at the level of the shoulder and as this neurovascular bundle passes through the space called the quadrangular space, named so because of the square shape it forms being framed by three muscles and the medial side of the humeral bone, it can become compressed. The inferior border of the quadrangular space is the teres major muscle, the superior border is formed by the teres minor, the long head of the triceps forms the medial border and the medial side of the humeral neck forms the lateral border. This condition is rare and often presents with shoulder pain elicited by repetitive overhead activities which can occur in overhead athletes when muscle hypertrophy, congenital bands or scarring after an injury can be the underlying cause. Other rarer causes include benign cysts or arterial aneurysms in the area. Patients present with pain in the shoulder of a deep quality that is induced by placing the arm in certain positions overhead. A nerve conduction study can be of assistance butoftentimes can be negative. A MR angiogram focusing on the area is helpful and treatment is symptomatic initially.


Parsonage Turner Syndromealso called brachial neuritis is a rare syndrome of unknown cause which has been linked to a viral origin that affects the brachial plexus. It has also been reported in persons receiving an immunization injection to the side of the shoulder that presents with symptoms. The history is classic and helpful in making the diagnosis. Patients with this condition present with an insidious onset of intense shoulder pain that progresses over a 2-3 day period and slowly dissipates after 2 weeks but is then followed by weakness in the shoulder and upper limb muscles that in some instances progresses to atrophy and paralysis. The majority of patients have complete resolution of their symptoms over time but it can take up to 2 years to resolve. The diagnosis is one of exclusion requiring the ruling out other causes but noting the history of pain followed by weakness is often helpful. Treatment is symptomatic focusing on maintaining limb mobility and electrical stimulation to maintain joint flexibility and muscle mass.



Thoracic Outlet Syndrome: Accessory Muscle Thoracic Outlet Syndrome: Accessory Rib



Thoracic Outlet Syndrome (TOS) also known as Thoracic Outlet Compression (TOC) is a nerve compression syndrome of the thoracic outlet or where the brachial plexus exits the neck area to travel down the arm as individual nerves. Patients with thoracic outlet Syndrome present with a history of either a minor or major injury, a history of repetitive overhead activity or a history of administrative duties working in front of a computer for a prolonged periods of time causing the muscles of the neck and shoulder to become tense creating a dynamic functional brachial plexus compression. Thoracic outlet compression is classified into four types, two are vascular types forming 2% of the total (Types 1 and 2) and two are nerve types forming 98% (Type 3 and 4) :

    1. Subclavian artery compression
    2. Internal Jugular vein compression
    3.Neurogenic Thoracic Outlet
    4. Disputed neurogenic thoracic outlet comprise the four types.

The true neurogenic type occurs in less than 1% of patients and patients often have all the features of a nerve compression including pain, muscle atrophy, weakness and lack of sensation to the arm and hand. The nerve conduction study is often positive and confirms the diagnosis. The disputed neurogenic thoracic outlet compression is the most common type and comprises 97% of the entire group. Patients present with pain of the entire upper limb, neck, shoulder, elbow, forearm, wrist and hand. Symptoms of numbness with measurable decreased in the sensation as measured by the two point discrimination test is often found with associated muscle weakness. Rarely is there true muscle atrophy. The patient describes a cool sensation of the limb that may also have mild discoloration. Pain occurs with and without use of the limb but is aggravated with use. Night awakening is common. The nerve conduction study is typically negative in this condition but the history and physical exam findings are classic.
A diagnostic injection can be given in the office with lidocaine at the inter-scalene level to confirm the diagnosis. If more than 50% of the pain is alleviated with the injection, and the rest of the clinical picture is present, without another diagnosis to explain the symptoms after a thorough workup, then a presumptive diagnosis of disputed neurogenic thoracic outlet compression is made. A cervical plain x-ray, cervical MRI and EMG/NCS is useful during the workup to make sure a cervical cause vs a peripheral nerve compression is not simulating the symptoms of thoracic outlet compression.

Complex Regional Pain Syndrome (CRPS)
Complex Regional Pain Syndrome was previously known as RSD or Reflex sympathetic dystrophy. With improved understanding of this condition, RSD, now called CRPS is divided into three types:

    Type I CRPS is the classic RSD previously known as RSD presenting with a minor limb
    injury that causes the severe pain, limb swelling, discoloration, loss of motion, atrophy
    and poor function. It is believed to have a central neurogenic cause and it is theorized
    that a genetic predisposition may exist.
    primary offense having a central neurologic cause.
    Type II CRPS is also called causalgia and has a distinct nerve pathway compression is
    usually the cause.
    Type III CRPS is a grab bag of unexplained pain syndromes that includes fibromyalgia.
    Causes of CRPS can occur as a consequence of minor and often insignificant trauma or
    major violent trauma.

Symptoms in CRPS resultfrom nerve dysfunction affecting the musculoskeletal system and blood vessels feeding the affected area. Symptoms include severe constant pain, burning sensation, numbness, tingling, severe hypersensitivity to the touch called allodynia and an exaggerated response to a minor stimulus called hyperpathia. The limb may be swollen, have a cool sensation, and vary in appearance and color from a shiny glossy look to a mottled or a bluish discoloration due to the sympathetic fibers that come from nerves and innervate the local blood vessels. Joint stiffness, muscle atrophy, and changes in nail, loss of skin folds and hair growth are also seen.To make a diagnosis of CRPS, the history and physical exam is the most important and a geographic palpation that is superficial and then deep helps map the epicenter of the pain to determine if there is a specific nerve involved as occurs in type II CRPS.
Many tests are recommended to assist in making the diagnosis including bone scans, plain x-rays, MRI scans and stellate ganglion blocks. In our experience, astellate ganglion block is useful if performed correctly, to rule out CRPS. A bone scan is done by placing a special dye in your vein which circulates around the body and accumulates in areas of inflammation. It is positive in many conditions and so has very little usefulness in making a diagnosis of CRPS. Plain films show osteopenia or decreased bone density but again, the simple lack of use of a body part will show this and so again, adds very little to making an accurate diagnosis. A nerve conduction study (EMG/NCS) might be helpful if it is a type II CRPS with a specific nerve compression can be demonstrated.

From a treatment perspective, it is very important to distinguish the different types of CRPS since the causalgia typeII CRPS has a higher response rate and if a nerve compression syndrome is identified as the cause, surgical decompression will resolve the symptoms. On the other hand type I CRPS which occurs in the majority of patients is a nonsurgical condition with the exception of an implantable nerve stimulator used to control pain when other conservative options are exhausted.

The foundation of treating this condition is through a joint effort involving the physician, therapist and a pain consultant. Therapy has the best track record and is the foundation of treatment. Patient education which makes the case of using the limb in spite of the pain suffered is critical in obtaining treatment success. Use of nerve suppression pain medications like Neurontin, Lyrica and Elavil is also used. Stellate ganglion blocks given by the pain specialist with the concomitant use of a continuous nerve catheter will help initially in allowing the patient to participate in therapy and also to confirm the diagnosis. Several courses of stellate ganglion blocks are required however, for progress to be achieved.


Treatment: Nerve Compression Syndromes



All nerve compression syndromes are first treated by differentiating the severity of the compression. If the compression is severe, the likelihood of nonoperative measures to achieve a positive result is unlikely. Nonoperative measures however, are done in nerve compression syndromes that are mild to moderate under the following circumstances: The nerve compression has, a relatively short duration (less than six months), does not show signs of muscle wasting or lack of sensation, the pain symptoms are tolerable, the EMG/NCS does not show a severe compression, and the patient is willing to receive injections, correct poor ergonomic positions, use a brace when indicated and understands that a trial of six months of nonoperative treatment may fail, requiring surgery. If those conditions are met, a conservative trial is the way to go. The surgical treatment of nerve compression about the shoulder has the same principles as treating carpal tunnel syndrome in the wrist and that is to release the offending structures making the space where the nerve is travelling through, too tight.

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