INTRODUCTION
It is well known that peroneal neuropathy is the most common mononeuropathy in the lower limb
1,
2 and it is vulnerable to damage around the fibular head because of the anatomical position between the peroneal nerve and fibula when it winds around the fibular head.
3,
4 However, the peroneal nerve can be injured anywhere along its course of the leg such as the calf, ankle or foot.
5
Clinically, peroneal neuropathy can be suspected when patients complain of foot drop or sensory change of dorsum of their foot, but the differential diagnosis is needed to rule out L4, 5 radiculopathies caused by the herniated nucleus pulposus of the lumbar spine, lumbosacral plexopathy or sciatic neuropathy in which a peroneal division is predominantly damaged.
6,
7 However, limitations always exists in differential diagnosis by means of only clinical symptoms and physical findings. It is very difficult when a patient complains of atypical symptoms. Therefore, an electrodiagnostic study is used to make the diagnosis.
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These electrodiagnostic findings are closely related with the degree of damage and prognosis, and those resulted by stimulating distal portion of the lesion are different according to the duration from the onset of the nerve damage.
8 According to electodiagnostic findings, types of peroneal neuropathy are reported as conduction block, axonal loss or mixed axonal loss/conduction block and the axonal loss type is the most common, reaching 60% of the entire peroneal neuropathies.
8
Generally, traumatic tibio-fubular fracture can be suspected as one of the common causes of peroneal neuropathy, but the mechanism of injury is not clearly identified
9 and further investigation is required. In this case, there is a strong likelihood that direct laceration and compression were the causes of peroneal neuropathy. However, we consider there can be indirect mechanisms because there have been patients that complained of foot drop after the sole diaphyseal fracture not located closely with the course of the peroneal nerve. If peroneal neuropathy after tibio-fibular fracture can be caused by indirect and direct mechanisms, further analysis will be needed. Therefore, we searched patients diagnosed as peroneal neuropathy by the electrodiagnostic studies and confirmed the existence of tibio-fibular fracture. We investigated fracture site, fracture type and electrodiagnostic findings by their medical records and radiologic findings retrospectively. They were classified into two groups according to the existence of the fracture around the fibular head,
10 known as the most vulnerable site of peroneal nerve,
9 to find out the injury mechanism of peroneal neuropathy after tibio-fibular fracture. A group without the fibular head fracture was further classified according to the site of the fracture and the degree of severity of the two groups was investigated.
DISCUSSION
There were only 9 patients out of the total 34 with fibular head fracture that were considered to have inflicted direct damage to the peroneal nerve in this study. On the other hand, there were 25 patients without fibular head fracture, which outnumbered the patients with fibular head fracture. The electrodiagnostic findings of 25 patients without fibular head fracture were investigated and there were 18 patients with peroneal neuropathy and 7 patients with deep peroneal neuropathy. Common peroneal nerve, as a lateral branch of sciatic nerve, is separated from a sciatic nerve at the distal third portion of a thigh, and descends posterior to the fibular head, winding around the neck of the fibula, running toward the anterior portion of the leg, then enters the anterior compartment penetrating through the superficial head of the peroneus longus muscle. The fiber of peroneus longus muscle at this part comprises the tendinous arch called fibular tunnel right above the common peroneal nerve, which is known as one of the causes of peroneal neuropathy.
3 After passing through the fibular tunnel, the common peroneal nerve divides in to the deep peroneal nerve and superficial peroneal nerve.
Considering the course of peroneal nerve and the anatomy around fibular head, all patients without fibular head fracture should have been diagnosed as deep peroneal neuropathy. However, 18 out of 25 patients were diagnosed as common peroneal neuropathy.
This study showed that among patients with peroneal neuropathy after traumatic tibio-fibular fracture, there were more patients without fibular head fracture that would have been thought to inflict direct damage on the peroneal nerve than patients with fibular head fracture, and there were more patients diagnosed as common peroneal neuropathy than patients diagnosed as deep peroneal neuropathy by electrodiagnosis. This study also showed that diaphyseal segment fracture was the most common type of tibio-fibular fracture among patients without fibular head fracture who complained of foot drop, and type A (simple type) was the most common type (14 cases) among the diaphyseal segment fracture.
These results implied that peroneal neuropathy after tibio-fibular fracture was caused more frequently by indirect injury such as traction injury, compression over the fibular head after surgery or immobilization, compartment syndrome or entrapment neuropathy than by direct injury such as direct compression or dissection. In other words, direct nerve injury was not the only reason that caused peroneal neuropathy.
Possible mechanisms for indirect injury of peroneal nerve are as follows. First, the limited motion toward the longitudinal direction of common peroneal nerve can be a cause of indirect injury. Berry and Richardson
3 reported that fibular tunnel limited the motion toward the longitudinal direction of common and deep peroneal nerves 0.5 cm at most and due to this, severe ankle inversion or posterior dislocation of hip joint could cause the traction force over common peroneal nerve toward the longitudinal direction.
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18
Second, the fact that the traction injury can occur over the entire length of nerve as well as the maximal point of the traction supports the common peroneal neuropathy that occurs after the traction that inflict maximal damage on deep peroneal nerve, distal portion of common peroneal nerve. Haftek
19 reported the result that nerve fibers and endoneurial tubes were damaged at the point even except the maximal point of the damage.
Third, peroneal nerve can be damaged by the swelling or hemorrhage inside the nerve at the fibular tunnel. Nobel
20 reported 2 cases of peroneal neuropathy caused by hematoma inside the peroneal nerve sheath after diaphyseal fracture of tibia and suggested the mechanism the torsional forces that occurred during the trauma transmitted the traction force along the nerve and dissected the nutritional vessels of the nerve, consequently inflicting the nerve damage. Stoff and Greene
18 suggested the hypotheses acute onset peroneal neuropathy after ankle inversion was caused by the traction force that inflicted directly on fibular head and delayed onset peroneal neuropathy after ankle inversion was caused by the hematoma within the peroneal nerve. The subjects had tibio-fibular fracture without ankle inversion in this study. However, an external force strong enough to cause the fracture could outweigh the traction force that occurred at ankle inversion. Therefore, the above two mechanisms can be applied to our subjects. Also, Whitesides and Heckman
21 reported neuropathy caused by the compartment syndrome occurred in 10% of patients with closed fracture of tibia.
Fourth, compression caused by immobilization such as splint or cast and leg edema as a cause of peroneal neuropathy during treatment process can be a cause of indirect injury. Baima and Krivickas
22 reported that injury of ligament or bone could cause peroneal neuropathy, but peroneal neuropathy occurred more frequently during treatment process than during traumatic event and mentioned these. There was a general notion that nerve injury after fracture would be caused by direct trauma, but as mentioned above, there are many cases that have reported consistently about peroneal neuropathy that occurred during the treatment or healing process of fracture. In addition, there are many cases that have been reported about other peripheral neuropathies that occurred during the healing or treatment process of fracture.
23,
24
Meanwhile, the fact that common peroneal neuropathy was covered only by the skin and fascia at the head and neck portion of the fibula support the hypothesis that peroneal nerve can be easily damaged by the direct contusion or laceration. In other words, peroneal nerve can be damaged by the direct injury mechanism. Nine cases in our study had fibular head fracture, and the direct damage caused by contusion or compression could be suspected as the mechanism of peroneal nerve injury.
In this study, there was no statistical significance in the correlation between the existence of fibular head fracture and the severity or the electrodiagnostic findings. Neither was there any statistical significant relationship between the site of fracture and the severity or the electrodiagnostic findings in the group without fibular head fracture. Therefore we expect there would be no difference in prognosis according to the existence of fibular head fracture or the site of fracture. Also, considering the fact that there were only 2 patients with complete lesion out of the total set of 34 patients, close observation for occurrence of peroneal neuropathy during healing and treatment process will be needed and if peroneal neuropathy occurs, intensive rehabilitation and follow up of patients will be needed because there is a possibility for recovery.
In our study, there were 9 patients that could be considered as cases for direct nerve injury, even though there were more patients that could be considered as patients with the indirect nerve injury, peroneal neuropathy by the direct nerve injury must not be underestimated.
There are some limitations in our study. The number of subjects was relatively small. Electrodiagnostic studies were not performed by one person, because this study was performed retrospectively, we could not consider the error of inter-reliability. In addition, we could not fully estimate the relationship between the electrodiagnostic study and clinical symptoms because of poor description of medical records and it was not easy for us to check correct duration from the onset in some cases. Imaging studies such as ultrasonography were not performed in the group that was considered as the indirect nerve injury to find out structural damage of the nerve. However, it was meaningful to verify that there was no statistical significance in the correlation between the severity and incidence of peroneal neuropathy or the site of fracture. It would be beneficial in further research for mechanism of peroneal neuropathy, to perform combined imaging studies such as ultrasonography or MRI for confirmation of the structural damage and study the relation between those findings with the electrodiagnostic findings.