Showing posts with label Neuropathy. Show all posts
Showing posts with label Neuropathy. Show all posts

Sunday, January 19, 2014

Suprascapular Neuropathy

Background

Suprascapular neuropathy is a less common cause of shoulder pain in athletes but is seen particularly in those who participate in overhead activities. Athletes who participate regularly in overhead sports are more susceptible to developing suprascapular neuropathy. Sports such as baseball, volleyball, and tennis demand skills that place substantial load on the athlete’s shoulder when the upper limb is in an overhead or abducted and externally rotated position (see image below).[1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20]

Clinically relevant anatomy of the subscapular nerClinically relevant anatomy of the subscapular nerve (SSN) and the structures it innervates. The SSN is vulnerable to entrapment at the superior scapular notch and the spinoglenoid notch, beneath the inferior transverse scapular ligament. The inset depicts the clinical appearance in an individual with predominantly right-sided atrophy of the infraspinatus muscle due to suprascapular neuropathy.

Epidemiologic studies have demonstrated that athletes who participate in these and other overhead sports are at higher risk for overuse injuries of the shoulder in particular, including rotator cuff tendinopathy and injuries to the glenoid labrum.[6, 21, 22, 23, 24, 25, 26] Suprascapular neuropathy has been reported to cause 1-2% of all shoulder pain[27] and is therefore often overlooked. However, the prevalence in higher risk athletic populations, such as volleyball players, has been reported to be as high as 33%.[27] Therefore, suprascapular neuropathy should be considered when evaluating shoulder pain in an overhead athlete.

NextEpidemiologyFrequencyUnited States

Although the true incidence is unknown, several authors believe that suprascapular neuropathy is underreported. Suprascapular neuropathy was thought to be a diagnosis of exclusion given the similar clinical presentation as glenohumeral joint and rotator cuff pathology. However, increasing awareness and improvement in diagnostic modalities has resulted in increasing diagnosis.[27, 28] The condition has been described in various athletes, including weight lifters and baseball players, although the prevalence of suprascapular neuropathy appears to be highest among volleyball players.[1, 4, 7, 9, 11, 12, 13, 15, 18, 19, 21, 29, 30, 31]

Studies have reported that 13-33% of elite volleyball athletes have signs of suprascapular neuropathy.[27, 7, 9, 11, 12, 13, 15, 18, 19, 31] This observation lends credence to the term “volleyball shoulder.”

In addition to overhead athletes, some other higher risk populations for suprascapular neuropathy include patients with massive rotator cuff tears resulting in fatty infiltration of the muscle. Patients with posterior labral tears resulting in paralabral cysts that can compress the nerve are also a higher risk population.[27]

PreviousNextFunctional Anatomy

The suprascapular nerve (SSN) is a mixed nerve that provides the motor innervation of the supraspinatus and infraspinatus muscles and the sensory and proprioceptive innervation of the posterior aspect of the glenohumeral joint, as well as the acromioclavicular joint, subacromial bursa, and scapula.[32, 33, 34, 35] This nerve carries afferents from approximately 70% of the shoulder joint. The nerve arises from the upper trunk of the brachial plexus and is composed predominantly of C5-C6 level fibers. Some authors suggest that the nerve may also receive contributions from the fourth cervical nerve root in as many as 25% of people. Although the suprascapular nerve is a mixed nerve, it typically carries no cutaneous afferent fibers. The SSN is thought to carry cutaneous afferent fibers in only 15-25% of the general population.

In its initial course, the SSN courses posterior and parallel to the inferior belly of the omohyoid muscle and anterior to the trapezius muscle in the posterior triangle of the neck. The nerve then passes dorsally through the suprascapular notch, where it is retained by the transverse scapular ligament, into the suprascapular fossa, where 2 motor branches to the supraspinatus muscle originate. Just proximal to the suprascapular notch, the SSN gives off the superior articular branch, which travels with its fellow nerve through the notch before proceeding laterally to innervate the acromioclavicular joint and its associated bursa and the coracoclavicular and coracohumeral ligaments (see below).

Clinically relevant anatomy of the subscapular nerClinically relevant anatomy of the subscapular nerve (SSN) and the structures it innervates. The SSN is vulnerable to entrapment at the superior scapular notch and the spinoglenoid notch, beneath the inferior transverse scapular ligament. The inset depicts the clinical appearance in an individual with predominantly right-sided atrophy of the infraspinatus muscle due to suprascapular neuropathy.

Cadaveric studies reveal that the suprascapular notch may be either U -shaped or V -shaped, and some physicians believe that this anatomic variation may be related to an individual’s predisposition to SSN entrapment at this level. After supplying the supraspinatus, the nerve subsequently travels inferolaterally to wrap around the spine of the scapula at the spinoglenoid notch.

In roughly 15-80% of cadavers studied, the spinoglenoid (inferior transverse scapular) ligament traverses this notch, creating a tunnel through which the nerve travels. Interestingly, the spinoglenoid ligament is reportedly more common in males than in females; this observation may provide an anatomic basis for any possible sex-related predominance in the prevalence of volleyball shoulder. The inferior articular branch, which contains afferents from the posterior glenohumeral joint capsule, joins the suprascapular nerve at the level of the spine of the scapula. After exiting the fibro-osseous tunnel at the spinoglenoid notch the nerve turns inferomedially before arborizing into 3 or 4 terminal branches that supply the infraspinatus muscle.

PreviousNextSport-Specific Biomechanics

Suprascapular nerve entrapment or injury can occur at the suprascapular notch or the spinoglenoid notch. The resulting clinical presentation depends on the location of the suprascapular neuropathy. Selective involvement of the suprascapular nerve at the spinoglenoid notch level results in the isolated atrophy and weakness of the infraspinatus muscle that has been described as an infraspinatus syndrome. The available literature suggests that the most common site of entrapment among volleyball athletes is the spinoglenoid notch.[12, 36]

Several mechanisms have been proposed for suprascapular neuropathy. These mechanisms include repeat traction and microtrauma, direct compression of the nerve by surrounding normal anatomy or compression by pathologic space occupying lesions, and ischemia of the nerve from repetitive trauma. However, general agreement is that the suprascapular nerve may be vulnerable to injury due to compressive forces or repetitive distraction.

One mechanism is a traction injury that overhead athletes can be susceptible to, given the great amount of motion at the shoulder. The importance of the scapula in the throwing motion and other overhead sport-specific skills is now well appreciated. As the scapula protracts and retracts with functional use of the upper limb, some traction of the suprascapular nerve can be expected to occur at one or both notches through which it traverses. This concept forms the basis of the “sling effect," which proposes that, in certain functional positions of the upper limb, the suprascapular nerve is exposed to damaging sheer stress in the suprascapular notch. Similar reasoning leads to the prediction that the nerve is vulnerable to traction injury as it bends around the spine of the scapula at the spinoglenoid notch.

Some authors have proposed that individuals in whom the suprascapular nerve angles sharply around the spinoglenoid notch may be particularly prone to this mechanism of injury. The so-called "SICK scapula" (defined by Burkhart et al as scapular protraction, inferior border prominence, coracoid tightness, and scapular dyskinesis) that occurs in adaptive response to chronic shoulder overuse and functional instability may also theoretically contribute to the increased tension on the suprascapular nerve via the sling effect.[6]

Demirhan et al reported that the spinoglenoid ligament, when present, inserts into the posterior glenohumeral capsule.[37] They also observed that the ligament becomes taut when the ipsilateral upper limb is adducted across the body or internally rotated; this motion results in traction of the suprascapular nerve at the spinoglenoid notch. Other possible mechanisms in which the suprascapular nerve may be compromised include Sandow and Ilic’s proposal that the suprascapular nerve nerve is vulnerable to direct compression by the medial border of the spinatus tendons at the spinoglenoid notch when the upper limb is abducted and externally rotated.[18] This mechanism would appear to be a further manifestation of posterior (or internal) impingement.

Ferretti, who has written extensively about volleyball shoulder, hypothesized that the mechanism of selective injury to the terminal portion of the suprascapular nerve in volleyball players is traction on the nerve due to repetitive, sudden, eccentric activation of the infraspinatus during the deceleration phase of the floater serve.[12, 15]

Another mechanism of injured is due direct compression on the nerve by a space-occupying lesion. Several studies have reported that the suprascapular nerve may be compressed in the vicinity of the spinoglenoid notch by ganglion cysts arising from the glenohumeral joint.[24, 36, 38, 39, 40] These ganglion cysts, like Baker cysts that occur in the popliteal fossa after meniscal degeneration or injury, are likely to be the consequence of an injury to the posterior glenoid labrum with resultant leakage of synovial fluid.[41]

Finally, some investigators have also proposed that suprascapular neuropathy can result from ischemia caused by migration of posttraumatic microemboli from the suprascapular artery (which generally follows a course parallel to the companion nerve) to the vasa nervorum.

PreviousProceed to Clinical Presentation , Suprascapular Neuropathy

Wednesday, December 25, 2013

Bicycle Seat Neuropathy

Background

Bicycle seat neuropathy is one of the more common injuries reported by cyclists.[1, 2, 3, 4, 5] The injuries and symptoms are due to the cyclist supporting his or her body weight on a narrow seat, and they are believed to be related to either vascular or neurologic injury to the pudendal nerve.[2, 5, 6, 7, 8, 9, 10]

For excellent patient education resources, visit eMedicineHealth's Men's Health Center and First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles, Impotence/Erectile Dysfunction, Erectile Dysfunction FAQs, and Bicycle Safety.

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A wide frequency range has been reported for bicycle seat neuropathy, but it is believed to be underreported. The medical literature contains several case reports of reversible neuropathy[5, 9] and several retrospective studies surveying participants in long-distance cycling races and tours.[8, 11, 12]

Andersen and Bovim surveyed 260 cyclists participating in a long-distance bike tour that was 335.54 miles (540 km) in length.[8] Of responding males, 35 (22%) reported symptoms of either numbness or pain in the pudendal area. Thirty-three (21%) males reported penile numbness, with 10 (6%) male cyclists reporting symptoms that lasted longer than 1 week. In addition, 21 males (13%) reported symptoms of impotence, 11 of whom experienced symptoms for longer than 1 week, and 3 of whom reported impotence lasting longer than 1 month.[8]

Kuland and Brubaker reported that during the 1976 Bikecentennial tour, there was a 7% incidence of pudendal and/or penile numbness, but this study only surveyed 89 of 1200 participating cyclists.[11]

Weiss studied symptoms of cyclists participating in a 500-mile (804.97 km) bicycle tour.[12] Of the participating cyclists, 45% reported at least mild and transient perineal numbness; 10% reported the symptoms as severe, and 2% of the cyclists had to temporarily stop riding. Perineal numbness has also been documented in women cyclists. LaSalle et al surveyed 282 female members of a Dallas cycling club.[13] In this group, 34% of the women reported perineal numbness.

Potter et al assessed the differences between men and women with regard to bicycle saddle pressure distribution during seated cycling.[14] The authors noted that there were significant differences between the sexes in saddle loading, and these differences were especially relevant with regard to the position of the bicycle handlebar positions. In particular, the drops hand position shifted the rider's weight, such that more weight was supported on the anterior pelvic structures.[14]

PreviousNextSport-Specific Biomechanics

The cause of bicycle seat neuropathy has been attributed to several different ischemic events. Amarenco et al and Oberpenning et al hypothesized that compression of the pudendal nerve as it passes through the Alcock canal causes the condition.[9, 15] The Alcock canal is enclosed laterally by the ischial bone and medially by the fascial layer of the obturator internus muscle. The pudendal nerve exits the canal ventrally, below the symphysis pubis, and innervates the genital and perineal regions.

Oberpenning et al postulated that long-distance cycling results in the indirect transmission of pressure onto the perineal nerve within the Alcock canal.[9] Weiss and Bond separately proposed that bicycle seat neuropathy is due to temporary and transient ischemic injury to the dorsal branch of the pudendal nerve secondary to compression of the nerve between the bicycle seat and the symphysis pubis.[12, 16] Weiss also theorized that the genital branch of the genital-femoral nerve could be involved in cases in which scrotal paresthesia is reported.[12]

Bicycle seat design (eg, shape) may be the major extrinsic factor for the development of bicycle seat neuropathy.[1, 4, 6, 17, 18, 19, 20, 21] Results of computer modeling reported by Spears et al showed that wider bicycle seats that support the ischial tuberosities decrease pressure on the perineal area.[19] Other studies have also demonstrated the effect bicycle seat design has on penile blood flow[20] and penile oxygen pressure.[21]

PreviousProceed to Clinical Presentation , Bicycle Seat Neuropathy