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The authors present a retrospective study of 52 patients with main trunk tibial neuropathy. They found trauma and ischemia to be the most frequent causes, followed by tumors. These etiologic groups are underrepresented in the literature. Electrodiagnostic examination was helpful for localizing the lesion as well as for excluding S1 radiculopathies, with which tibial neuropathies can be confused clinically.
Early in life, Walker Hound pups from several litters, later determined to have peroneal and tibial neuropathy, had been given supplements of either evaporated milk and corn syrup mixed with well water or powdered bitch milk formula mixed with well water. Other pups not given supplements were not affected. Pelvic limb monoparesis, areflexia, analgesia, and muscular atrophy developed by 2 weeks of age. Abnormalities detected by light and electron microscopy included scattered swollen axons containing increased organelles and whorled neurofilaments. The clear association between clinical signs of disease and dietary supplementation of pups among healthy dogs in a kennel, as well as lack of an obvious pattern of inheritance, suggested an environmentally acquired toxin, specifically the well water. Attempts to reproduce neuropathy in a litter of Beagle pups 2 years after initial evaluation of the disease syndrome were unsuccessful. Atomic absorption studies performed on the well water to detect heavy metals did not reveal toxic concentrations. Toxins that may have been responsible for the neuropathy in these pups were not identified.
An uncommon cause of bilateral tibial and peroneal compression neuropathy is reported. After taking alcohol and drugs, a young heroin-addicted man lay unconscious overnight in supine position, with both legs crossing the wooden board at the end of the bed, the posterior aspect of the flexed knees pressing against its edge. The following day, he had weakness of foot flexion and extension and a sensory loss consistent with a bilateral tibial and peroneal neuropathy. Symptoms resolved rapidly in the left side; in the right side, a conduction block was still demonstrable 3 weeks later.
Baker's cysts are rare cause of peripheral nerve entrapment and only a few cases of tibial nerve entrapment resulting from the popliteal cyst in the calf muscle have been reported in the literature. We present a case of rheumatoid arthritis complicated by a Baker's cyst with a tibial nerve entrapment. It is important to diagnose a Baker's cyst early and to differentiate it from thrombophlebitis, a popliteal aneurysm, tumor or muscle tear to effect optimal therapy and to obviate a potential neuropathy. Prompt recognition of these cases may save the patients unnecessary procedures and delay in treatment.
OBJECTIVES: To increase awareness of entrapment neuropathy caused by rupture of Baker's cyst. METHODS: A patient with psoriatic arthritis, ruptured Baker's cyst, and entrapment neuropathy is reported and the literature on this complication is reviewed. RESULTS: Nerve entrapment caused by rupture of Baker's cyst is rare. Neurological examination and demonstration of Baker's cyst by Color Doppler Duplex Ultrasound (CDDU) help in making the diagnosis. Nerve Conduction Study (NCS) may confirm the diagnosis of posterior tibial nerve entrapment. CONCLUSIONS: Peripheral nerve entrapment should be considered in patients with Baker's cysts and loss of sensation along the plantar aspect of the foot or other neurological symptoms or findings.
Entrapment neuropathies of the tibial nerve are relatively rare. They are often misdiagnosed largely because of the clinician's low index of suspicion. The clinical features, diagnostic studies, and treatment of these disorders are reviewed in detail in this article. Almost all of these disorders can now be confirmed through nerve conduction and other image studies.
This evidence-based review was performed to evaluate the utility of nerve conduction studies (NCSs) and needle electromyography (EMG) in the diagnosis of tibial neuropathy at the ankle (tarsal tunnel syndrome, TTS). A total of 317 articles on TTS were identified that were published in English from 1965 through April 2002, from the National Library of Medicine MEDLINE database. All articles were reviewed on the basis of six selection criteria. The results of this search revealed that four articles met five or more criteria. All four articles examined the use of electrodiagnostic (EDX) techniques for the evaluation of patients with clinically suspected TTS, and were included in this practice parameter. Each of these four studies was considered to meet Class III level of evidence. NCSs were abnormal in some patients with suspected TTS. Sensory NCSs were more likely to be abnormal than motor NCSs but the actual sensitivity and specificity could not be determined. The sensitivity of needle EMG abnormalities could not be determined. NCSs may be useful for confirming the diagnosis of tibial neuropathy at the ankle, recommendation Level C. Well-designed studies are needed to evaluate more definitively EDX techniques in TTS.
While peroneal and tibial neuropathies have been described as a complication of total knee arthroplasty (TKA), a computerized literature search failed to reveal any previously reported cases of associated sacral plexopathy or sciatic neuropathy. This case report describes the diagnosis and management of a patient found to have evidence of a right sacral plexopathy and a left sciatic neuropathy, following bilateral TKA. This case suggests that these may be rare complications of TKA.
Entrapment neuropathies of the tibial nerve by Baker's cysts occur infrequently. We present a patient with entrapment neuropathy of the tibial nerve by a Baker's cyst which is preoperatively evaluated by nerve conduction study and magnetic resonance imaging. We present this case with a review of the literatures.
Tibial mononeuropathies most commonly occur at the popliteal fossa or tarsal tunnel. We present an unusual case of nontraumatic tibial neuropathy of uncertain etiology occurring in the mid lower leg. External neurolysis resulted in an excellent recovery.
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Ultrasonography is a new imaging method for visualizing peripheral nerves. In vasculitic neuropathy, pain or axonopathy often can prevent the lesion from being localized during electrophysiological examinations, but the ability of ultrasonography to evaluate it morphologically is unknown. Our aim was to determine whether ultrasonography could be used to detect abnormalities in tibial vasculitic neuropathy at the medial ankle. We evaluated 11 tibial nerves in 8 patients with tibial vasculitic neuropathy, and 35 tibial nerves in 35 control subjects. In the controls, the tibial nerve was successfully visualized as a hyperechoic nodule with multiple round hypoechoic areas transversely; in the patients, the tibial nerve appeared enlarged and hypoechoic. The affected nerve area was significantly larger (13.5 +/- 3.7 mm(2)) than in controls (7.2 +/- 1.5 mm(2)). Our results suggest that ultrasonography is a useful neuroimaging method for evaluation of tibial vasculitic neuropathy, especially when nerve conduction study findings are inconclusive.
Results are reported of surgery to the posterior tibial nerve affected by leprosy in 50 patients. A total of 90 neurolyses were performed using a similar technique. Study of the effect of surgery on the course of plantar sensitivity showed that 3 groups of nerves can be distinguished. Nerves in group 1 (21 totally paralyzed nerves) responded poorly to surgery (38% useful results) while on the contrary nerves in group 3 (non-paralyzed nerves) represented the ideal indication, surgery being truly prophylactic. In group 2 nerves a useful result was obtained in 82%. Indications for use of this surgical procedure are discussed, and more particularly the parameters affecting the quality of the results: severity of lesion, immunologic type of disease.
Bilateral tibial nerves of 18 albino rats were mechanically compressed between knee and ankle. Beginning on the fifth day after compression, ultrasound thermotherapy of 0.5 or 1.0watt/cm2 was applied over the area of nerve compression in one limb for one minute three times per week. The other side (control) was not treated. Motor distal latency (DL), motor nerve conduction velocity (NCV) of the segment with nerve compression, and amplitude of the evoked compound muscle action potential (ACMAP) were measured before and immediately after nerve compression and two or three times per week after compression. The recovery rates of NCV and ACMAP of the tibial nerve treated with ultrasound of 0.5watt/cm2 were significantly faster than those of the control nerve. There was no significant change in the recovery rate of DL. However, if ultrasound of 1.0watt/cm2 was applied, the recovery rate of ACMAP of the treated nerve was slower than that of the control nerve. There were no significant changes in the recovery rates of DL and NCV. Low doses of ultrasound thermotherapy may facilitate recovery of compression neuropathy, but higher doses may induce an adverse effect.
A series of 58 operations on 36 patients were performed for decompression of the posterior tibial nerve for the treatment of diabetic neuropathy. Preoperative symptoms included lack of sensation, pain, or both. Eleven of the 36 patients had neurotrophic ulcers, which were treated simultaneously. The operation was found to be effective for relief of pain in 24 of the 28 patients with that complaint (86 percent). Restoration of sensation was less consistent with improvement noted in 18 of the 36 patients (50 percent). The follow-up period ranged from 12 to 84 months (mean, 32 months) and five patients had some degree of recurrent symptoms. No patient has developed a new ulcer after nerve decompression. Wound complications were minimal (12 percent), even though ulcers were treated simultaneously. No patient required surgical treatment for the decompression incision, although one did require hospital admission for treatment of a wound infection. In general, the procedure seemed to be a worthwhile treatment, which should be considered ill selected diabetics with symptomatic neuropathy.
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Delayed neuropathy induced by organophosphorus esters has been reported to be more selective for large diameter myelinated fibers, especially in distal portions of long nerves. This concept was re-evaluated in chickens by quantitatively comparing the effects of the organophosphates tri-ortho-tolyl (TOTP) and phenyl saligenin phosphate (PSP) on two separate nerves, the branch of the tibial nerve that supplies the gastrocnemius muscle, and the small cervical nerve that innervates the biventer cervicis muscle. Histograms illustrating the distribution of myelinated fibers within each nerve showed that the biventer nerve is composed of a population of fibers smaller than those within the tibial nerve branch. However, the number of myelinated fibers measured per mm2 of endoneurium was reduced in both nerves 10 and 15 days after organophosphate administration, providing indirect evidence that fiber diameter is not critical in determining susceptibility to organophosphorus-induced delayed neuropathy (OPIDN). More direct evidence was provided by fiber diameter histograms of both biventer nerves and tibial nerve branches taken from hens that received PSP. In comparison to control values, there was a decrease in all fiber sizes in both nerves, indicating that factors other than axonal size are important in determining nerve fiber susceptibility to OPIDN.
Serial measurements of nerve conduction velocities and amplitudes were performed in 27 patients with congenital lactic acidemia over 1 year of sodium dichloroacetate (DCA) administration. Patients were treated with oral thiamine (100 mg) and DCA (initial dose of 50 mg/kg) daily. Nerve conduction velocity and response amplitude were measured in the median, radial, tibial, and sural nerves at 0, 3, 6, and 12 months, and plasma DCA pharmacokinetics were measured at 3 and 12 months. Baseline electrophysiologic parameters in this population were generally below normal but as a group were within 2 standard deviations of normal means. Although symptoms of neuropathy were reported by only three patients or their families, nerve conduction declined in 12 patients with normal baseline studies, and worsening of nerve conduction occurred in the two who had abnormalities at baseline. Peripheral neuropathy appears to be a common side effect during chronic DCA treatment, even with coadministration of oral thiamine. Nerve conduction should be monitored during DCA treatment.