Shear wave elastography of tibial nerve in patients with diabetic peripheral neuropathy-A cross-sectional study.

OBJECTIVE: To explore the role of shear wave elastography of the tibial nerve as a potential ultrasonographic method for the diagnosis of tibial neuropathy in patients with type 2 diabetes. MATERIALS AND METHODS: This cross-sectional study included 50 subjects each in case (patients with diabetic tibial neuropathy diagnosed on the basis of clinical features and nerve conduction study) and control groups (non-diabetic non-neuropathic healthy volunteers). The exclusion criteria included the presence of type 1 diabetes, a known history of neuropathy from other causes except for type 2 diabetes, or a history of leg or ankle fracture. Cross-sectional area and shear wave velocity values of the tibial nerve were measured in both groups. Demographic details and body mass index were obtained in both groups and additionally, the duration of type 2 diabetes and HbA1c values in the case group were also noted. Wilcoxon Mann-Whitney U test was used to compare these variables in study groups. ROC curve analysis provided additional findings. RESULTS: Tibial nerve stiffness was significantly higher in the case group (p-value < 0.001). The study groups did not significantly differ in the Cross-sectional area of the tibial nerve (p-value 0.57). The case group exhibited a higher frequency of loss of the fascicular pattern of the tibial nerve (40% vs 18%, p-value 0.027). Duration of diabetes mellitus and HbA1c values did not significantly affect Shear wave velocity values in the case group. At the cut-off value of Shear wave velocity of 3.13 m/s, sensitivity and specificity to diagnose diabetic peripheral neuropathy were 94% and 88% respectively. CONCLUSION: Increased nerve stiffness is seen in patients with diabetic peripheral neuropathy. Shear wave elastography might prove as a novel noninvasive technology for screening/early diagnosis of diabetic peripheral neuropathy.

Combining reverse end-to-side neurorrhaphy with rapamycin treatment on chronically denervated muscle in rats.

This preliminary research determines whether a combination of reverse end-to-side neurorrhaphy and rapamycin treatment achieves a better functional outcome than a single application after prolonged peripheral nerve injury. We found that the tibial nerve function of the reverse end-to-side + rapamycin group recovered better, with a higher tibial function index value, higher amplitude recovery rate, and shorter latency delay rate (P < 0.05). The reverse end-to-side + rapamycin group better protected the gastrocnemius muscle with more forceful contractility, tetanic tension, and a higher myofibril cross-sectional area (P < 0.05). Combining reverse end-to-side neurorrhaphy with rapamycin treatment is a practical approach to promoting the recovery of chronically denervated muscle atrophy after peripheral nerve injury.

Motor demyelinating tibial neuropathy in COVID-19.

Ten patients suffering from residual symptoms after the resolution of COVID-19, which manifested as fatigue in the lower limbs, have been submitted to nerve conduction studies. Motor demyelinating neuropathy features mainly of the tibial nerves but also the peroneal, median, and ulnar nerves were objectified. These findings might be considered as new neurological characteristics of SARS-CoV-2 infection.

The injection site in the tarsal tunnel to minimize neurovascular injury for heel pain: an anatomical study.

INTRODUCTION: The aim of this study was to investigate the location and distribution patterns of neurovascular structures and determine the effective injection point in the tarsal tunnel for heel pain. METHODS: Fifteen adult non-embalmed cadavers with a mean age of 71.5 years were studied. The most inferior point of the medial malleolus of the tibia (MM) and the tuberosity of the calcaneus (TC) were identified before dissection. A line connecting the MM and TC was used as a reference line. The reference point was expressed in absolute distance along the reference line using the MM as the starting point. For measurements using MRI, the depth from the skin was measured to inferior at an interval of 1 cm from the MM. RESULTS: The posterior tibial artery, lateral plantar nerve, and medial plantar nerve were located from 29.0 to 37.3% of the reference line from the MM. The distribution frequencies of the medial calcaneal nerve on the reference line from the MM were 0%, 8.60%, 37.15%, 37.15%, and 17.10%, respectively. The mean depth of the neurovascular structures was 0.3 cm. DISCUSSION: This study recommended an effective injection site from 45.0 to 80.0% of the reference line.

Clinical spectrum of neuropathy after primary total knee arthroplasty: A series of 54 cases.

INTRODUCTION: Neuropathy after total knee arthroplasty (TKA) can cause significant morbidity but is inconsistently reported. METHODS: We reviewed the clinical, electrodiagnostic and perioperative features of all patients who underwent primary TKA at our institution and developed a new neuropathy within 8 weeks postoperatively. RESULTS: Fifty-four cases were identified (incidence 0.37% [95% confidence interval, 0.28-0.49]) affecting the following nerve(s): peroneal (37), sciatic (11), ulnar (2), tibial (2), sural (1), and lumbosacral plexus (1). In all cases with follow-up data, motor recovery typically occurred within 1 year and was complete or near-complete. CONCLUSIONS: Post-TKA neuropathy is uncommon, typically does not require intervention and usually resolves within 1 year. Post-TKA neuropathy most often affects the nerves surgically at risk. Anesthesia type does not correlate with post-TKA neuropathy. An inflammatory etiology for post-TKA neuropathy is rare but should be considered in specific cases. Muscle Nerve 59:679-682, 2019.

CT can stratify patients as low risk for tibial neuropathy following a talus fracture.

OBJECTIVE: Determine the incidence of tibial neuropathy following talus fractures and CT's ability to stratify patients at risk for developing post-traumatic neuropathy. MATERIALS AND METHODS: In this IRB-approved retrospective analysis, 71 talus fractures and 8 contralateral control ankle CTs were reviewed by one observer blinded to clinical information. CT evidence suggestive of tibial neurovascular bundle injury included nerve displacement, perineural fat effacement/edema, and bone touching nerve. The association between these CT findings and clinically evident tibial neuropathy was analyzed. A semi-quantitative likelihood score was assigned based on the degree of the CT findings around the nerve. Interobserver agreement was calculated between 2 other readers. RESULTS: Twenty-five percent of patients in this cohort had clinical evidence of tibial neuropathy. There was a high specificity (0.87-0.93) and negative predictive value (0.83-0.87), a moderate accuracy (0.80-0.82), but a lower sensitivity (0.33-0.56) associated with the CT findings. Among the CT findings, nerve displacement (p < 0.0001) and bone touching nerve (p = 0.01) were associated with tibial neuropathy. A likelihood score of 2-5 was associated (p = 0.007-0.015) with tibial neuropathy. The presence of tibial neuropathy and nerve recovery were not associated with hospital length of stay, while CT findings were. There was substantial agreement between the three readers: likelihood scores 2+ (k = 0.78) and 3+ (k = 0.72). CONCLUSIONS: Tibial neuropathy occurs following talus fractures, and CT findings may help surgeons narrow down the number of patients requiring close neurological follow-up.

CD4+ αß T cell infiltration into the leptomeninges of lumbar dorsal roots contributes to the transition from acute to chronic mechanical allodynia after adult rat tibial nerve injuries.

BACKGROUND: Antigen-specific and MHCII-restricted CD4+ αß T cells have been shown or suggested to play an important role in the transition from acute to chronic mechanical allodynia after peripheral nerve injuries. However, it is still largely unknown where these T cells infiltrate along the somatosensory pathways transmitting mechanical allodynia to initiate the development of chronic mechanical allodynia after nerve injuries. Therefore, the purpose of this study was to ascertain the definite neuroimmune interface for these T cells to initiate the development of chronic mechanical allodynia after peripheral nerve injuries. METHODS: First, we utilized both chromogenic and fluorescent immunohistochemistry (IHC) to map αß T cells along the somatosensory pathways for the transmission of mechanical allodynia after modified spared nerve injuries (mSNIs), i.e., tibial nerve injuries, in adult male Sprague-Dawley rats. We further characterized the molecular identity of these αß T cells selectively infiltrating into the leptomeninges of L4 dorsal roots (DRs). Second, we identified the specific origins in lumbar lymph nodes (LLNs) for CD4+ αß T cells selectively present in the leptomeninges of L4 DRs by two experiments: (1) chromogenic IHC in these lymph nodes for CD4+ αß T cell responses after mSNIs and (2) fluorescent IHC for temporal dynamics of CD4+ αß T cell infiltration into the L4 DR leptomeninges after mSNIs in prior lymphadenectomized or sham-operated animals to LLNs. Finally, following mSNIs, we evaluated the effects of region-specific targeting of these T cells through prior lymphadenectomy to LLNs and chronic intrathecal application of the suppressive anti-αßTCR antibodies on the development of mechanical allodynia by von Frey hair test and spinal glial or neuronal activation by fluorescent IHC. RESULTS: Our results showed that during the sub-acute phase after mSNIs, αß T cells selectively infiltrate into the leptomeninges of the lumbar DRs along the somatosensory pathways responsible for transmitting mechanical allodynia. Almost all these αß T cells are CD4 positive. Moreover, the temporal dynamics of CD4+ αß T cell infiltration into the lumbar DR leptomeninges are specifically determined by LLNs after mSNIs. Prior lymphadenectomy to LLNs specifically reduces the development of mSNI-induced chronic mechanical allodynia. More importantly, intrathecal application of the suppressive anti-αßTCR antibodies reduces the development of mSNI-induced chronic mechanical allodynia. In addition, prior lymphadenectomy to LLNs attenuates mSNI-induced spinal activation of glial cells and PKCγ+ excitatory interneurons. CONCLUSIONS: The noteworthy results here provide the first evidence that CD4+ αß T cells selectively infiltrate into the DR leptomeninges of the somatosensory pathways transmitting mechanical allodynia and contribute to the transition from acute to chronic mechanical allodynia after peripheral nerve injuries.

A3 adenosine receptor agonist attenuates neuropathic pain by suppressing activation of microglia and convergence of nociceptive inputs in the spinal dorsal horn.

Peripheral nerve injuries cause glial activation and neuronal hyperactivity in the spinal dorsal horn. These changes have been considered to be involved in the underlying mechanisms for the development and maintenance of neuropathic pain. Using double immunofluorescence labeling, we previously demonstrated that spinal microglial activation induced by nerve injury enhanced convergence of nociceptive inputs in the spinal dorsal horn from uninjured afferents. The adenosine A3 receptor (A3AR) agonists have been shown to have antinociceptive activities in several experimental neuropathic pain models. However, the mechanisms underlying these antinociceptive actions of the A3AR agonist are still not fully explored. In this study, the effects of the A3AR agonist (i.e., IB-MECA) on microglial activation, enhancement of convergent nociceptive inputs, and nocifensive behaviors were examined after tibial nerve injury. Injury to the tibial nerve initially caused hyposensitivity to touch stimulus at 3 days, and then resulted in tactile allodynia at 14-day post-injury. The daily systemic administration of IB-MECA (0.1 mg/kg/day) for 8 days in a row starting on the day of nerve injury or 7 days after nerve injury prevented the development of behaviorally assessed hypersensitivities, and spinal microglial activation induced by nerve injury. These treatments also suppressed anomalous convergence of nociceptive primary inputs in the spinal dorsal horn. The present findings indicate that the A3AR agonist attenuates neuropathic pain states by suppressing enhanced microglial activation, and anomalous convergence of nociceptive inputs in the spinal dorsal horn from uninjured afferents after injury to the peripheral nerve.

A Case of Posterior Tibial Nerve Injury After Arthroscopic Calcaneoplasty.

We report the first case of distal posterior tibial nerve injury after arthroscopic calcaneoplasty. A 59-year-old male had undergone right arthroscopic calcaneoplasty to treat retrocalcaneal bursitis secondary to a Haglund's deformity. The patient complained of numbness in his right foot immediately after the procedure. Two years later and after numerous assessments and investigations, a lateral plantar nerve and medial calcaneal nerve lesion was diagnosed. In the operating room, the presence of an iatrogenic lesion to the distal right lateral plantar nerve (neuroma incontinuity involving 20% of the nerve) and the medial calcaneal nerve (complete avulsion) was confirmed. The tarsal tunnel was decompressed, and both the medial and the lateral plantar nerve were neurolyzed under magnification. To the best of our knowledge, our case report is the first to describe iatrogenic posterior tibial nerve injury after arthroscopic calcaneoplasty. It is significant because this complication can hopefully be avoided in the future with careful planning and creation of arthroscopic ports and treated appropriately with early referral to a nerve specialist if the patient's symptoms do not improve within 3 months.

Radioguided Occult Lesion Localization in Deep Schwannomas of the Peripheral Nerves: Results of a Preliminary Case Series.

BACKGROUND: The detection of small deep schwannomas of the peripheral nerves has been increasing since the the use of precise neuroimaging techniques has become more widespread; however, although nonpalpable lesions can be well defined by images, it is often difficult to identify them during the surgical procedure. The authors report seven cases of nonpalpable small deep schwannomas surgically treated after their identification using the radioguided occult lesion localization (ROLL) technique. METHODS: Seven men, whose ages ranged from 34 to 70 years (mean 52 years), presented with symptomatic nonpalpable peripheral nerve lesions; two cases involved the sciatic nerve, two the femoral nerve, two the radial nerve, and one the tibial nerve. Before the operation, all the patients were studied by ultrasonography and magnetic resonance imaging (MRI); 1 h before the surgery 3-5 MBq of 99mTc labeled with human albumin macroaggregates was injected into the lesion. A gamma detection probe permitted the preoperative and intraoperative detection of the nonpalpable schwannomas. CONCLUSIONS: The ROLL technique provides good support for identifying small lesions of the peripheral nerves both preoperatively and intraoperatively. This technique permits the use of minimally invasive approaches performed with local anesthesia, with good cosmetic results and acceptance by the patients.

Squatting-induced bilateral peroneal nerve palsy in a sewer pipe worker.

Compression neuropathy of the common peroneal nerve (CPN) at the fibula head is a common condition, but it has not attracted attention in working environments. Here, we report a 38-year-old sewer pipe worker who presented with bilateral CPN palsy following 6h working with a squatting posture in a narrow sewer pipe. During the work, he could not stretch his legs sufficiently because of the confined space. His symptoms deteriorated with repetition of the same work for 1 week. Motor nerve conduction study showed conduction block at the fibula head of bilateral CPNs, compatible with compression neuropathy at this lesion. Three months after cessation of work requiring the causative posture, his symptoms and neurophysiological abnormalities had resolved completely. Almost all seven of his co-workers presented transiently with similar and milder symptoms, although one showed CPN palsy for 6 months. Prolonged squatting posture in a confined space causes acute compression neuropathy at the fibula head in the CPN. More attention should be paid to 'confined space worker's compression neuropathy'.

A Complication of Posterior Malleolar Fracture Fixation.

We present a case of tibial nerve impingement by an anteroposterior screw inserted for stabilization of a posterior malleolar fracture. This specific complication has not previously been described in published studies, although numerous reports have described various forms of peripheral nerve entrapment. We discuss the merits of fixation of these fractures using a posterolateral approach.

Combined common peroneal and tibial nerve injury after knee dislocation: one injury or two? An MRI-clinical correlation.

OBJECT Knee dislocations are often accompanied by stretch injuries to the common peroneal nerve (CPN). A small subset of these injuries also affect the tibial nerve. The mechanism of this combined pattern could be a single longitudinal stretch injury of the CPN extending to the sciatic bifurcation (and tibial division) or separate injuries of both the CPN and tibial nerve, either at the level of the tibiofemoral joint or distally at the soleal sling and fibular neck. The authors reviewed cases involving patients with knee dislocations with CPN and tibial nerve injuries to determine the localization of the combined injury and correlation between degree of MRI appearance and clinical severity of nerve injury. METHODS Three groups of cases were reviewed. Group 1 consisted of knee dislocations with clinical evidence of nerve injury (n = 28, including 19 cases of complete CPN injury); Group 2 consisted of knee dislocations without clinical evidence of nerve injury (n = 19); and Group 3 consisted of cases of minor knee trauma but without knee dislocation (n = 14). All patients had an MRI study of the knee performed within 3 months of injury. MRI appearance of tibial and common peroneal nerve injury was scored by 2 independent radiologists in 3 zones (Zone I, sciatic bifurcation; Zone II, knee joint; and Zone III, soleal sling and fibular neck) on a severity scale of 1-4. Injury signal was scored as diffuse or focal for each nerve in each of the 3 zones. A clinical score was also calculated based on Medical Research Council scores for strength in the tibial and peroneal nerve distributions, combined with electrophysiological data, when available, and correlated with the MRI injury score. RESULTS Nearly all of the nerve segments visualized in Groups 1 and 2 demonstrated some degree of injury on MRI (95%), compared with 12% of nerve segments in Group 3. MRI nerve injury scores were significantly more severe in Group 1 relative to Group 2 (2.06 vs 1.24, p < 0.001) and Group 2 relative to Group 3 (1.24 vs 0.13, p < 0.001). In both groups of patients with knee dislocations (Groups 1 and 2), the MRI nerve injury score was significantly higher for CPN than tibial nerve (2.72 vs 1.40 for Group 1, p < 0.001; 1.39 vs 1.09 for Group 2, p < 0.05). The clinical injury score had a significantly strong correlation with the MRI injury score for the CPN (r = 0.75, p < 0.001), but not for the tibial nerve (r = 0.07, p = 0.83). CONCLUSIONS MRI is highly sensitive in detecting subclinical nerve injury. In knee dislocation, clinical tibial nerve injury is always associated with simultaneous CPN injury, but tibial nerve function is never worse than peroneal nerve function. The point of maximum injury can occur in any of 3 zones.

Metabolic brain activity suggestive of persistent pain in a rat model of neuropathic pain.

Persistent pain is a central characteristic of neuropathic pain conditions in humans. Knowing whether rodent models of neuropathic pain produce persistent pain is therefore crucial to their translational applicability. We investigated the spared nerve injury (SNI) model of neuropathic pain and the formalin pain model in rats using positron emission tomography (PET) with the metabolic tracer [18F]fluorodeoxyglucose (FDG) to determine if there is ongoing brain activity suggestive of persistent pain. For the formalin model, under brief anesthesia we injected one hindpaw with 5% formalin and the FDG tracer into a tail vein. We then allowed the animals to awaken and observed pain behavior for 30min during the FDG uptake period. The rat was then anesthetized and placed in the scanner for static image acquisition, which took place between minutes 45 and 75 post-tracer injection. A single reference rat brain magnetic resonance image (MRI) was used to align the PET images with the Paxinos and Watson rat brain atlas. Increased glucose metabolism was observed in the somatosensory region associated with the injection site (S1 hindlimb contralateral), S1 jaw/upper lip and cingulate cortex. Decreases were observed in the prelimbic cortex and hippocampus. Second, SNI rats were scanned 3weeks post-surgery using the same scanning paradigm, and region-of-interest analyses revealed increased metabolic activity in the contralateral S1 hindlimb. Finally, a second cohort of SNI rats was scanned while anesthetized during the tracer uptake period, and the S1 hindlimb increase was not observed. Increased brain activity in the somatosensory cortex of SNI rats resembled the activity produced with the injection of formalin, suggesting that the SNI model may produce persistent pain. The lack of increased activity in S1 hindlimb with general anesthetic demonstrates that this effect can be blocked, as well as highlights the importance of investigating brain activity in awake and behaving rodents.

Effect of adenosine A1 receptor agonist on the enhanced excitability of spinal dorsal horn neurons after peripheral nerve injury.

Neuronal hyperactivity has been implicated in abnormal pain sensation following peripheral nerve injuries. Previous studies have indicated that the activation of adenosine A1 receptors (A1R) in the central and peripheral nervous systems produces an antinociceptive effect. However, the mechanisms involved in the peripheral effect are still not fully understood. The effects of the local application of the selective A1R agonist, 2-chloro-N(6)-cyclopentyladenosine (CCPA) on neuronal hyperactivity were examined in this study using a neuropathic pain model induced by a tibial nerve injury. We utilized Fos protein-like immunoreactivity induced by noxious heat stimulation to examine changes in the number of Fos protein like immunoreactive (Fos-LI) neuron profiles in the spinal dorsal horn, and behavioral analysis for mechanical and thermal sensitivities. The nerve injury induced an exaggerated Fos response to noxious heat stimulation. The number of Fos-LI neuron profiles was significantly decreased and their distribution was restricted to the central terminal field of the spared peroneal nerve 3 days after the injury. The number of Fos-LI neuron profiles returned to control levels and a large number of these profiles were observed in the central terminal field of the injured tibial nerve 14 days after the injury. These enhanced Fos responses were attenuated by the local application of CCPA. The nerve injury also resulted in mechanical allodynia and thermal hyperalgesia. The local application of CCPA inhibited thermal hyperalgesia, but was less effective against mechanical allodynia. These results indicated that activation of peripheral A1R plays a role in the regulation of nerve injury-induced hyperalgesia.

Lower extremity nerve entrapments in athletes.

Nerve entrapments are a potential cause of lower extremity pain in athletes. Signs and symptoms suggestive of nerve entrapment include anesthesia, dysesthesias, paresthesias, or weakness in the distribution of a peripheral nerve. The physical examination may reveal an abnormal neurologic examination finding in the distribution of a peripheral nerve, positive nerve provocative testing, and positive Tinel sign over the area of entrapment. Electrodiagnostic studies, radiographs, magnetic resonance imaging studies, and sonographic evaluation may assist with the diagnosis of these disorders. Initial treatment usually involves conservative measures, but surgical intervention may be required if conservative treatment fails. This article discusses the diagnosis and treatment of common lower extremity nerve entrapments in athletes. A high index of suspicion for nerve entrapments enables the clinician to identify these conditions in a timely manner and institute an appropriate management program, thus improving patient outcomes.

Sciatic and tibial neuropathies.

The sciatic nerve is the body's largest peripheral nerve. Along with their two terminal divisions (tibial and fibular), their anatomic location makes them particularly vulnerable to trauma and iatrogenic injuries. A thorough understanding of the functional anatomy is required to adequately localize lesions in this lengthy neural pathway. Proximal disorders of the nerve can be challenging to precisely localize among a range of possibilities including lumbosacral pathology, radiculopathy, or piriformis syndrome. A correct diagnosis is based upon a thorough history and physical examination, which will then appropriately direct adjunctive investigations such as imaging and electrodiagnostic testing. Disorders of the sciatic nerve and its terminal branches are disabling for patients, and expert assessment by rehabilitation professionals is important in limiting their impact. Applying techniques established in the upper extremity, surgical reconstruction of lower extremity nerve dysfunction is rapidly improving and evolving. These new techniques, such as nerve transfers, require electrodiagnostic assessment of both the injured nerve(s) as well as healthy, potential donor nerves as part of a complete neurophysiological examination.

Inhibition of transmitter release and attenuation of anti-retroviral-associated and tibial nerve injury-related painful peripheral neuropathy by novel synthetic Ca2+ channel peptides.

N-type Ca(2+) channels (CaV2.2) are a nidus for neurotransmitter release and nociceptive transmission. However, the use of CaV2.2 blockers in pain therapeutics is limited by side effects resulting from inhibition of the physiological functions of CaV2.2 within the CNS. We identified an anti-nociceptive peptide (Brittain, J. M., Duarte, D. B., Wilson, S. M., Zhu, W., Ballard, C., Johnson, P. L., Liu, N., Xiong, W., Ripsch, M. S., Wang, Y., Fehrenbacher, J. C., Fitz, S. D., Khanna, M., Park, C. K., Schmutzler, B. S., Cheon, B. M., Due, M. R., Brustovetsky, T., Ashpole, N. M., Hudmon, A., Meroueh, S. O., Hingtgen, C. M., Brustovetsky, N., Ji, R. R., Hurley, J. H., Jin, X., Shekhar, A., Xu, X. M., Oxford, G. S., Vasko, M. R., White, F. A., and Khanna, R. (2011) Suppression of inflammatory and neuropathic pain by uncoupling CRMP2 from the presynaptic Ca(2+) channel complex. Nat. Med. 17, 822-829) derived from the axonal collapsin response mediator protein 2 (CRMP2), a protein known to bind and enhance CaV2.2 activity. Using a peptide tiling array, we identified novel peptides within the first intracellular loop (CaV2.2(388-402), "L1") and the distal C terminus (CaV1.2(2014-2028) "Ct-dis") that bound CRMP2. Microscale thermophoresis demonstrated micromolar and nanomolar binding affinities between recombinant CRMP2 and synthetic L1 and Ct-dis peptides, respectively. Co-immunoprecipitation experiments showed that CRMP2 association with CaV2.2 was inhibited by L1 and Ct-dis peptides. L1 and Ct-dis, rendered cell-penetrant by fusion with the protein transduction domain of the human immunodeficiency virus TAT protein, were tested in in vitro and in vivo experiments. Depolarization-induced calcium influx in dorsal root ganglion (DRG) neurons was inhibited by both peptides. Ct-dis, but not L1, peptide inhibited depolarization-stimulated release of the neuropeptide transmitter calcitonin gene-related peptide in mouse DRG neurons. Similar results were obtained in DRGs from mice with a heterozygous mutation of Nf1 linked to neurofibromatosis type 1. Ct-dis peptide, administered intraperitoneally, exhibited antinociception in a zalcitabine (2'-3'-dideoxycytidine) model of AIDS therapy-induced and tibial nerve injury-related peripheral neuropathy. This study suggests that CaV peptides, by perturbing interactions with the neuromodulator CRMP2, contribute to suppression of neuronal hypersensitivity and nociception.

Sustained effectiveness of percutaneous tibial nerve stimulation for overactive bladder syndrome: 2-year follow-up of positive responders.

INTRODUCTION AND HYPOTHESIS: The aim of the study was to describe effectiveness and safety of percutaneous tibial nerve stimulation (PTNS) at 2 years in women with overactive bladder (OAB) syndrome unresponsive to pharmacotherapy. METHODS: Of 30 women who had initial positive response to PTNS, 23 continued to receive maintenance treatment and were reassessed at 2 years using bladder symptom diaries and the Incontinence Impact Questionnaire (IIQ-7). They were also questioned on acceptability and any adverse effects of long-term peripheral neuromodulative treatment. RESULTS: Data from 23 women were available and 7 had been lost to follow-up. With maintenance treatment, the median nocturnal frequency at 2 years had decreased by 57 % (3.5 to 1.5 times/night), while the median IIQ-7 had reduced from 30.4 to 21.5 (both p<0.01) compared to pre-treatment baseline. Median nocturnal frequency and IIQ-7 scores at 2 years were comparable to those documented after initial response to treatment at 6 weeks, suggesting that maintenance therapy continued to suppress OAB symptoms. Daytime frequency and daily urgency incontinence episodes at 2 years were statistically similar to those documented at 6 weeks and remained lower than pre-treatment baseline (6.5 vs 11.8 and 2.0 vs 3.5, respectively, p<0.05). The women received a median of 8.42 treatments per year and the median length between treatments was 64.3 days. Apart from hypaesthesia in the toe of one responder lasting for 4 months, there were no reported side effects. CONCLUSIONS: Women receiving PTNS for intractable OAB syndrome reported significant symptom relief at 2 years. This remains a safe mode of second-line treatment with excellent durability.

An unusual case of aneurysmal tibial nerve compression detected in ED.

We present an unusual case of tibial nerve compression caused by a true tibial posterior artery aneurysm. A 61-year-old man was admitted to the emergency department due to suspected muscle rupture. He had experienced a sudden, intense right calf pain and swelling that had begun during walking. He had a 6-month-long history of symptoms suggestive to the tibial nerve dysfunction and a month-long history of neurologic finding consistent with the right tibial nerve paresis. An examination of the legs revealed a painful mass in the posterior-medial compartment of the right calf. Emergency ultrasound scanning of the right lower leg vascularization showed an expansive saccular aneurysm of the proximal segment posterior tibial artery with mural thrombus and splitting of the aneurysmal wall. An angiography confirmed the diagnosis. Under spinal anesthesia, we performed aneurysmectomy and decompressed the tibial nerve. The histologic examination was compatible with a true aneurysm of the right posterior tibial artery.