Double crush syndrome was first described by Upton and McComas in 1973 to involve both a proximal and distal nerve lesion in the same limb [18]. The authors theorized that a proximal lesion in a nerve would make that nerve more vulnerable to distal lesions. Most literature on double crush syndrome describes the upper extremity; however the theory has been applied to the lower extremity as well [9, 19, 20]. Etiologies of proximal compression of the effected limb include radiculopathy, plexopathy, and proximal tibial nerve compression. Systemic disease such as diabetes or alcohol abuse may cause neurologic symptoms contributing to the double crush syndrome [9, 14].

Proximal tibial nerve compression, or “soleal sling syndrome ,” is compression of the tibial nerve beneath the fibrous sling between the tibia and fibula at the origin of the soleus muscle [21]. Patients present with numbness, tingling, hypersensitivity, dysesthesia, plantar foot pain, and weakness in the foot or toes. The area of compression occurs approximately 9 cm distal to the medial tibial plateau, making a medial calf approach to the compression site feasible [22]. In a retrospective review of 69 proximal tibial nerve decompressions, Williams et al. stated that all patients had severe pain on physical exam with gentle palpation of the calf 9 cm distal to the popliteal crease [21]. The authors point out that in patients with available electrodiagnostic studies, none of the tests suggested a tibial nerve compression at the level of the soleal sling, thus making it a clinical diagnosis only.

There may be a substantial conduction block between the stimulation sites at the knee and ankle in proximal tibial nerve compression that is not found in tarsal tunnel syndrome. Stimulation of the abductor hallucis muscle at the level of the knee would be markedly reduced in comparison to stimulation at the ankle, with the response of the gastrocnemius muscle at the knee normal, thus indicating a conduction block in the calf [23].

Patients with double crush syndrome who undergo tibial nerve decompression experience either partial relief of symptoms or no relief of symptoms. Following failed tarsal tunnel syndrome in patients with double crush syndrome, repeat tarsal tunnel decompression is not indicated. Treatment is focused on the second “crush”: radiculopathy, plexopathy, proximal tibial nerve compression, or systemic disease.

Incomplete initial tarsal tunnel decompression may result in partial improvement or no improvement of symptoms. If the initial procedure was performed by a different physician, review of the operative report as well as inspection of incision size can provide insight as to whether or not a complete release was performed. If initial release was not complete, a second complete tarsal tunnel decompression is indicated. Complete proximal and distal release must be performed including release of the medial and lateral plantar nerve tunnels as well as excision of the septa dividing the nerve tunnels. If relief is not provided following revision decompression, a peripheral nerve stimulator or referral to pain management center is considered.

Space-occupying lesions are often cause for tarsal tunnel syndrome and include soft tissue mass, low-lying muscle belly, talocalcaneal coalition, varicosities, nerve tumor, or post-traumatic osseous projections (Fig. 20.4) [24]. Pfeiffer and Cracchiolo suggest that a space-occupying lesion at the area of the tarsal tunnel producing symptoms is the best indication for operative treatment [8]. If the primary etiology causing nerve compression and pathology is not addressed at time of decompression, patient will complain of only partial improvement of symptoms or no improvement of symptoms. Decompression alone without excising the soft tissue mass, schwannoma, or talocalcaneal coalition, or without ligation of varicosities, will not provide complete relief of symptoms. Revision surgical intervention is warranted to address the etiology of the tarsal tunnel syndrome.

Preoperative imaging studies may provide the surgeon with assessment of soft tissue or bony abnormalities in the tarsal tunnel region for complete preoperative planning. MRI or ultrasound will evaluate the presence of soft tissue mass or nerve tumor in the tarsal tunnel region [25]. Talocalcaneal coalition is best evaluated on CT scan if suspected. We routinely send patients with suspected venous insufficiency and tarsal tunnel symptoms for venous studies. If reflux is present, patients are sent to a vascular surgeon for consult and possible closure of the great saphenous vein prior to surgical decompression of the tarsal tunnel.

Incorrect diagnosis is a common cause for failure of tarsal tunnel syndrome resulting in no improvement of symptoms following tibial nerve decompression. Differential diagnosis includes tibialis posterior tendonitis, plantar fasciitis, calcaneal stress fracture, hindfoot degenerative joint disease, inflammatory arthritis, plantar fibromatosis, gout, sinus tarsi syndrome, and peripheral vascular disease [14]. Repeat tarsal tunnel decompression is not indicated in these patients. Rather, treatment is focused on the correct etiology.

Intraneural damage occurs at the axonal level and may be caused by chronic compression, stretch, traction, crush injury, or systemic disease. As damage is intraneural, extraneural decompression will not alleviate symptoms. Treatment is aimed at addressing the cause of intraneural pathology . Blood sugar control in diabetic patients and treatment of alcohol abuse in patients with alcoholic neuropathy can halt the progression of intraneural damage [9]. Medications used for chronic pain syndromes may influence pain caused by intraneural damage. Through action on both central and peripheral nerve pathways, medications including nonsteroidal anti-inflammatories, steroids, tricyclic antidepressants, serotonin reuptake inhibitors, anti-epileptics, narcotics, calcium channel blockers, antiarrhythmics, sympatholytics, and N-methyl-d aspartate antagonists may provide symptomatic relief [20].

Clinical signs of intraneural damage include persistent sensory change, muscle wasting, and abnormal two-point discrimination , indicating actual loss of nerve fibers and Wallerian degeneration [14]. A Tinel sign may be used as an indication of nerve regeneration. Early and late nerve pathology demonstrate distinct muscular and sensory signs and symptoms. Loss of neural input to a muscle (late nerve pathology) secondary to Wallerian degeneration causes actual wasting of the muscle, while early nerve pathology due to compression causes only weakness of the muscle. Late nerve compression with intraneural damage increased the threshold of intensity required to elicit a sensory response, while early nerve pathology causes a hypersensitive response [14].

Easley and Schon reviewed 21 patients with failed tarsal tunnel surgery treated with revision neurolysis using a vein wrap [26]. The authors state that the majority of failures in their series occurred in nerves with intraneural compromise (seven failures out of 17 cases). We do not recommend revision neurolysis in patients with suspected intrinsic nerve pathology. Careful inspection of the tibial nerve during the initial decompression procedure is paramount in the success of the procedure. If scarring is present within the nerve as well as loss of vascular striations, this should be noted in the operative report and used to dictate future treatment if necessary. If treatment of the underlying pathology fails, patients are referred to pain management and/or considered for a peripheral nerve stimulator.