As modern warfare has developed, the load carried by soldiers has increased progressively since the 18th century.8 The average load currently carried on the march by various infantry units weighs from 40-60 kg.8 A substantial portion of this weight compresses the shoulder and neck region. The brachial plexus, containing the nerve supply to the arm, can be injured by this weight.2,3,15 The injury results from shoulder compression that then may compress or stretch the plexus. However, the mechanism of the lesion is unclear. Compression neuropathy of the brachial plexus is particularly common in soldiers, but may occur in association with other activities such as scouting14 or mountaineering.7
Features of compression neuropathy of the shoulder region (backpack palsy) have been reported in basic combat trainees.2,3,15 The severity of axonal loss induced by compression predicts the prognosis. Two-thirds of the patients recover substantially within 2 months, however persistent or permanent sequelae occur in 28%2 to 33%.3
Heavy backpacks used without waist support increase the risk of compression neuropathy, particularly when the carrier is working with his or her hands in difficult terrain.3 The use of pack frames with waistbelts reduces the occurrence of compression neuropathy in basic trainees from 1.17/1000 without the pack frame to 0.157/1000 with a pack frame.2 Poorly developed shoulder musculature14 and previous anomaly or injuries in the shoulder or vertebral region3 may predispose patients to compression neuropathy. Potentially confounding effects include the individual's weight, height, and physical fitness as risk factors of compression neuropathy. Further, brachial plexopathy is one of the presentations of hereditary neuropathy with liability to pressure palsies (HNPP),11 but its relative contribution to the developing compression neuropathies in the shoulder region is not clear.2,3,15
To evaluate the risk for these lesions, we ascertained the incidence of compression plexopathy of the shoulder region in a Finnish cohort of 152,095 military conscripts. In addition, we identified the common presenting symptoms and signs, and examined electromyography (EMG) and nerve conduction study (NCS) findings. We asked which factors, including HNPP, predispose to this condition. We hypothesized that a low body mass index (BMI) and low level of performance in fitness tests are predisposing factors to the plexus lesion.
MATERIALS AND METHODS
We retrospectively identified consecutive military conscripts (N = 55; one female) with symptoms of compression neuropathy after load carriage on the shoulders. We identified patients by a computer search of the medical records of our hospital for 1998 to 2004 using ICD-10 diagnosis codes for brachial plexus compression and lesions of long thoracic, suprascapular, axillary, musculocutaneous, median, radial, and ulnar nerves. We also reviewed reports of all EMG recordings from the same period to confirm all patients with compression neuropathy were included. The patients had been referred to the hospital by general practitioners employed in garrisons. The mean age of the patients was 20 years (range, 18-22 years). The mean duration of the conscript service before the diagnosis was 3 months (range, 1-11 months), but 22 patients (40%) had neural compression during the first month of their tour of duty. The right hand was affected in 26 and the left hand in 31 patients, including two patients with a bilateral lesion.
We calculated the total time the conscripts were at risk in the service. Training and background information of the patients were obtained from a data register and compared with all conscripts in the service area of the hospital. The details of service associated with symptom onset were extracted from patient reports. A physical examination was performed on each patient. In 36 patients, a physiotherapist evaluated muscle strength and constructed an individual rehabilitation plan. Followup information from outpatient visits was available for 32 patients (58%). The mean followup duration was 3 months (range, 1-7 months).
A consulting clinical neurophysiologist examined 54 patients with a Cadwell 2400A (Cadwell, Kennewick WA) EMG system. In one patient, amelioration of the symptoms during a prolonged followup in primary care made EMG recording unnecessary. Concentric needle electrodes were used to record EMG from muscles innervated by at least three different motor nerves originating from the C5-T1 roots, including the median, ulnar, radial, suprascapular, axillary, musculocutaneous, long thoracic, and dorsal scapular nerves. On average, seven muscles were recorded per patient. We evaluated the scope, severity, and age of the damage. Plate electrodes were used for motor and sensory NCS from the long thoracic nerve, median, axillary, ulnar, me- dial, and lateral antebrachial cutaneous nerves. On average, five nerves were recorded per patient. We analyzed motor and sensory distal latencies, conduction velocity, and response amplitudes. Skin temperature was considered and the patients' hands were warmed if necessary. The lesion was classified as plexopathy when two or more motor nerves were affected. As brachial plexus compression lesions commonly do not affect all of its elements, the entire plexus was not tested exhaustively in patients who had clinical symptoms of mononeuropathy. Control EMG and NCS recordings were available in 14 patients.
All Finnish men become liable for 6-month, 9-month, or 12- month military service at the age of 18 years. Military service is voluntary for women, and approximately 500 women undergo training in the Finnish Defense Forces every year. The dates of entry and transfer or discharge of every conscript in the Finnish Defense forces are registered. These dates formed the basis for calculating the total time at risk, which was 102,516 person- years during 1998 to 2004 within the service area of our hospital. This was calculated by registering the dates of entry and transfer or discharge of every conscript in the service area of the hospital.
The Finnish Defense Forces updates a conscript training register that contains training and background information on all Finnish conscripts within the service area of our hospital (n = 152,095 from 1998-2004). We obtained the background variables such as service data and physical fitness from the conscript training register of the Finnish Defense Forces to describe the conscripts. The data included the age, gender, height, weight, and aerobic fitness as measured using a running test with 12-minute duration. We also obtained measures of muscle strength (distance of horizontal jump, number of sit-ups, push-ups, pull-ups, and back-lifts) to calculate a physical fitness score. The aerobic and physical fitness information was measured during the first weeks of service. Six patients with confirmed HNPP or polyneuropathy, one patient with a tumor, and one patient with previous plexus compression were excluded from the analysis because these conditions are known risk factors of brachial plexus palsy.
A 10-digit social security number is assigned to every person living in Finland. After approval by the appropriate authorities and the ethical committee, it may be used in scientific research. This personal identification number was used for linking conscripts' background data in the conscript training register with the neurologic medical records of our hospital.
Incidences were calculated by dividing the number of conscripts with new neural compression in the shoulder region by the total time at risk. Incidence was expressed per 100,000 conscripts per year and calculated with 95% confidence intervals (CI). We used Student's t tests to determine differences in the continuous, normally distributed data (length, weight, the result of 12-minute running test, and physical fitness score) between the persons with neural compression and the control subjects. A p value ≤ 0.05 was considered significant. We used SPSS 12.0.1 for Windows software (version 12.0; SPSS Inc, Chicago, IL) for statistical analysis.
The incidence of the neural compression after load carriage on the shoulders was 53.7 (95% confidence interval [CI], 39.5-67.8) per 100,000 conscripts per year.
The typical symptoms included gradually progressing paresthesias, numbness, and weakness of the upper extremity during a march carrying a heavy backpack. A full syndrome occasionally was preceded by a transient weakness of the upper limb. Motor weakness was the dominant feature and most affected the shoulder girdle and elbow flexors which caused difficulty in arm movements (eg, doing push-ups). The lesion was generally painless at the onset. However, pain was associated with muscular activity involving the affected shoulder after development of clear weakness or atrophy, particularly in patients with long thoracic nerve lesions. Sensory disturbances were rare in clinical examination despite the frequent occurrence of paresthesias at the lesion onset. When present, they occurred usually in the lateral shoulder and arm region and radial aspect of forearm, thumb, and index finger.5
Electromyography and NCS recordings of the 47 patients without predisposing factors to compression injury revealed lesions in one motor nerve in 22 patients. One patient had mononeuropathy in both arms. The long thoracic nerve was affected in 15 patients, suprascapular nerve in four, and axillary nerve in three, and the musculocutaneous and accessory nerves were affected in one of the patients with mononeuropathy. However, the clinical picture and physiotherapeutic evaluation suggested a more extensive neural lesion in nine of these 23 patients.
Electromyography and NCS suggested a unilateral lesion of the brachial plexus was present in 19 patients and bilateral lesions of the brachial plexus were present in two patients. The axillary nerve was most affected in 10 patients, the long thoracic nerve in four patients, the musculocutaneous nerve in five patients, the suprascapular nerve in three patients, and the radial nerve in one patient. The EMG findings were normal in two patients and inconclusive in one. The clinical picture corresponded to a plexus lesion in these two patients.
The type of load carried did not distinguish patients with mononeuropathy from those with a more extensive lesion. The lesion occurred when carrying a backpack with a frame in 14 patients; in five the long thoracic nerve was most affected. Twenty-five patients carried a backpack without a frame; in seven the long thoracic nerve was most affected. Variable items such as containers, bazookas, or tent equipment carried on the shoulders produced the symptoms in the rest of the patients. A detailed history of the damage mechanism was lacking in two patients. Because the data were analyzed retrospectively, we cannot provide complete information on the weights and duration of the load carriage. However, weights exceeding 30 kg carried for several hours often were reported in descriptions of the conditions producing the symptoms.
Four patients (7%) were diagnosed with hereditary neuropathy and liability to pressure palsies (HNPP). Electro- myography and NCS detected generalized neuropathy with focal conduction abnormalities at common entrapment sites, suggesting HNPP13 in five patients. In three patients the diagnosis was confirmed by genetic testing after revealing gene deletion for peripheral myelin protein 22. One patient had a brother with confirmed HNPP, making another cause of neuropathy unlikely. In one patient, a test for the gene for peripheral myelin protein 22 revealed no deletion or duplication. One patient had a mild polyneuropathy of unknown etiology. In one patient, additional examination revealed a tumor infiltrating the accessory and glossopharyngeal nerves on the affected side. One patient had a previous brachial plexus paresis in the affected hand 3 years before the present symptoms. These patients were excluded from additional analyses.
The conscripts' anthropometric measurements and indicators of physical performance were not associated with the compression neuropathy (Table 1).
Recovery of the upper extremity function was complete in 13 of 32 patients during followup. Seventeen patients showed some recovery. One patient with a lesion in the suprascapular nerve showed no recovery at the 2-month followup. Electromyography and NCS control recordings were not available for this patient. One patient with a mild polyneuropathy had worsened symptoms by the 1-month followup. Four patients recovered from the time from symptom onset to their only outpatient visit.
Knowing factors associated with the occurrence of compression neuropathy should allow better design of preventive methods and safety guidelines. Our approach for this problem was aimed at full use of all available information to understand these factors. Our data suggest the incidence of compression neuropathy in the shoulder region of Finnish conscripts is low. The incidence is clearly lower than in previous military personnel estimates,2 possibly because of differences in methods of training and equipment. We are unaware of reports of the rate of brachial plexus compression in a more general population.
We note several limitations. Detection bias might occur but is likely low because of the health-care structure serving army conscripts in Finland. During their military service, all conscripts are obliged to use the military health- care services. Even when receiving first aid in the civilian sector, they are transferred to a military health-care service for continuing treatment and service fitness evaluation. However, it is possible some patients with rapidly recovering symptoms of plexus compression were not sent to our hospital. The patients were transferred to the civilian sector after the end of the conscription period, resulting in variable and relatively short followup times. The review was retrospective, so there was some missing data on potentially confounding factors (eg, weights and duration of loading). However, this would not influence the data on incidence. The lesions are relatively uncommon, so it would be difficult to have an adequately powered study examining the major potentially confounding factors. Again, this would not influence data on the incidence.
We think the reported patients had a lesion caused by load carriage because distinguishing compression neuropathy from other diseases affecting brachial plexus is relatively straightforward. For example, recall information of the damage mechanism separates compression neuropathy from the stinger/burner syndrome, a short-lasting burning pain and paresthesia occurring in subjects playing contact sports after lateral flexion of the neck or fixed brachial plexus compression between the shoulder pad and superior scapula.10 The thoracic outlet syndrome produces symptoms from the lower plexus region, and is characterized by pain and paresthesias in the ulnar region of the arm. Sporadic4 or hereditary1 neuralgic amyotrophies (plexus neuritis) or multifocal motor neuropathy may create a clinical picture resembling brachial plexus paresis at disease onset.6 However, pain in the affected limb usually is associated with these conditions. Brachial plexus compression neuropathy is generally painless15 as was the case in our patients.
The symptoms and signs of compression neuropathy agreed with those described previously.2,3,15 Load and length of marches have been recognized as risk factors of neural compression injury in the shoulder region.2 Often, the affected conscripts reported carrying weights exceeding 30 kg for several hours in association with the onset of symptoms, as previously reported.7
The number of patients with shoulder compression neuropathy reported in previous studies has varied between four14 and 19,7 and a case report format is common.3,15 Electromyography and NCS findings customarily are reported only from some patients.2,3 The effects of weight, height, and physical and aerobic fitness, or contribution of polyneuropathy to the development of shoulder compression neuropathy have not been discussed.
Lesions in the suprascapular nerve branching from the medial upper trunk, and in axillary and musculocutaneous nerves branching from the plexus distally after cord formation under the clavicle, suggest direct compression of the nerve trunks often contributes to the injury. However, the long thoracic nerve separates from the nerve roots before the brachial plexus formation shortly after the roots exit the intervertebral foramina,6 and it can be compressed at this region only very close to the neck. The long thoracic nerve passes deep under the clavicle over the first and second ribs,5 and may be compressed in this region in association with forces generating severe brachial plexus injury. However, 84% of the long thoracic nerve lesions in our patients were not associated with a more extensive injury in EMG and NCS. Long thoracic nerve injury in the upper costal region also can result from traction between its fixation points at the medial scalene muscle and superior portion of the serratus anterior muscle (Fig 1) when the ipsilateral arm is outstretched and in the overhead position, as in playing tennis.12 It is possible load carriage pulls shoulders backward in some patients and causes a traction injury of the long thoracic nerve. The use of a backpack with a frame and waistbelt seems to increase the relative occurrence of the isolated long thoracic nerve lesions.2 The proportion of long thoracic nerve lesions also was larger in our patients who had carried a backpack with a frame, although isolated long thoracic nerve lesions were not more frequent. Recovery from a long thoracic nerve lesion may take as much as 2 years, and probability of complete resolution of scapular winging is low.9 Prevention of these lesions by improving the design of backpacks, including adjustment of the shoulder straps, and possible use of horizontal sternum straps across both shoulder straps to prevent posterior traction of the shoulders should be considered.
Hereditary neuropathy with liability to pressure palsies is an autosomal dominant disorder characterized by recurrent mononeuropathies or plexopathies, and by occurrence of focal myelin thickenings at nerve biopsy. It is associated with a chromosomal deletion encompassing the peripheral myelin protein 22 gene. Acute painless brachial plexopathy has been considered strongly suggestive of HNPP in the general population because of the 100% occurrence of HNPP in patients with compression neuropathy of the brachial plexus.11 Although we did not systematically analyze the genetic markers of HNPP, NCS and EMG findings suggest such a high association is unlikely. Symptoms were induced by lighter loads in patients with HNPP. This should be considered when brachial plexus paresis appears after carrying a relatively light load.
The conscripts with plexopathy were as tall as and had similar weight to their peers. Contrary to our expectations, good physical fitness did not decrease the risk of the neural compression of the shoulder region. The patients tended to perform better in the aerobic fitness test and have a higher physical fitness score than the control subjects, although the study was underpowered to make this judgment (Table 1). Some patients with strong musculature and good fitness reported an exceptional amount of carried equipment because of competitive demands of the field service exercise associated with the occurrence of the compression neuropathy. It is possible conscripts in good physical condition carry heavier loads during some exercises than the less-fit conscripts. Excessive loads and activities should be detected and prevented by the supervising personnel.
Brachial plexus compression related to load carriage occasionally occurs in healthy young persons and has typical symptoms and signs. The vulnerability to this condition is not easily predicted from body structure in general or from the level of physical fitness. Although the number of patients in our series was large, it still may have been too small to detect risk factors. Because of compression rarity (47 of 152,095 conscripts), adequately powering a study like this is difficult in factors not standing out clearly between the two groups. Rather than selecting people for load carriage on the basis of these types of factors, awareness of the condition and its symptoms should be increased and design of the backpacks should be changed to prevent these lesions.
We thank H. M. Larni for drawing the figure and for comments on the manuscript.
1. Airaksinen E, Iivanainen M, Karli P, Sainio K, Haltia M. Hereditary recurrent brachial plexus neuropathy with dysmorphic features. Acta Neurol Scand
2. Bessen R, Belcher V, Franklin R. Rucksack paralysis with and without rucksack frames. Mil Med
3. Daube J. Rucksack paralysis. JAMA
4. Dillin L, Hoaglund FT, Scheck M. Brachial neuritis. J Bone Joint Surg Am
5. Ebraheim N, Lu J, Porshinsky B, Heck B, Yeasting R. Vulnerability of long thoracic nerve: an anatomic study. J Shoulder Elbow Surg
6. Ferrante M. Brachial plexopathies: classification, causes and consequences. Muscle Nerve
7. Hirasawa Y, Sakakida K. Sports and peripheral nerve injury. Am J Sports Med
8. Knapik J, Reynolds K, Harman E. Soldier load carriage: historical, physiological, biomechanical and medical aspects. Mil Med
. 2004; 169:45-56.
9. Lorei M, Hershman E. Peripheral nerve injuries in athletes. Sports Med
10. Markey K, di Benedetto M, Curl W. Upper trunk brachial plexopathy: the stinger syndrome. Am J Sports Med
11. Pareyson D, Solari A, Taroni F, Borri S, Fallica E, Scaioli V, Ciano C, Sghirlanzoni A. Detection of hereditary neuropathy with liability to pressure palsies among patients with acute painless mononeuropathy or plexopathy. Muscle Nerve
12. Shultz J, Leonard J. Long thoracic neuropathy from athletic activity. Arch Phys Med Rehabil
13. Uncini A, Di Gugliemo G, Di Muzio A, Gambi D, Sabatelli M, Mignona T, Tonali P, Marzella R, Finelli P, Archidiacono N, Rocchi M. Differential electrophysiological features of neuropathies associated with 17p11.2 deletion and duplication. Muscle Nerve
14. White H. Pack palsy: a neurological complication of scouting. Pediatrics
15. Wilson W. Brachial plexus palsy in basic trainees. Mil Med
. 1987; 152:519-522.