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.

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.

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.

A rare case of an acute soleus arcade syndrome complicated by a ganglion cyst: diagnosis by dynamic ultrasound.

The soleus arcade syndrome is a rare compression neuropathy of the tibial nerve that often remains undiagnosed due to low clinical awareness and difficult diagnosis. We present the case of a female patient admitted with acute worsening of a pre-existing sensory tibial neuropathy and acute tibial nerve palsy after knee joint injection. After a knee magnetic resonance imaging remained non-diagnostic, dynamic ultrasonography was performed. Constriction by the soleus arcade and proximal swelling of the tibial nerve could be demonstrated during plantarflexion of the ankle by means of a dynamic examination in the standing patient. The patient underwent surgery and recovered fully. This proposed diagnostic approach can be used to identify soleus arcade syndrome by ultrasound.

Ultrasound Imaging for Posterior Knee Pain: Tibial Nerve Schwannoma Not Popliteus Muscle Strain.

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Modified Lambrinudi Arthrodesis for the Acute Treatment of Neurogenic Clubfoot: A Case Report.

Neurogenic contracture often results in spastic, nonreducible equinovarus deformity. Rigid contracture leads to pain, instability, and bracing difficulties. This case report details the utilization of the modified Lambrinudi triple arthrodesis intended to create a plantigrade, functional limb that is amenable to an extremity brace in a case of an acquired neurologic clubfoot. LEVELS OF EVIDENCE: Therapeutic, Level IV: Case Report.

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'.

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.

Estudos de condução nervosa no nervo tibial através do tunel do tarso em pacientes de hanseníase / Nerve conduction studies of the tibial nerveacross the tarsal tunnel in leprosy patients

Os autores avaliaram todos os exames de condução nervosa do nervo tibial dos pacientes com suspeita de neuropatia da hanseníase, aguda ou subaguda, atendidos no Ambulatório de Hansenologia do Instituto Lauro de Souza Lima (ILSL) no período de dois anos. Foram incluídos 75 pacientes, 52 masculinos e 23 femininos, com média de idade de 44,5 anos (21 a 73 anos), totalizando 150 nervos. Procurou-se caracterizar o comprometimento neurofisiológico individualizando-se os ramos plantar medial (PM) e plantar lateral (PL), observou-se que o mais envolvido foio PL com 57,4%, seguido do PM com 42,6%. O tipo de lesão nervosa mais frequente foi a de predomínio axonal, com 66%, seguida pela mielínica, com 28,7%.O envolvimento mais freqüente e desproporcional dor amo PL, além de evidenciar o caráter compressivo do comprometimento do tibial no túnel do tarso, remete a uma mononeuropatia múltipla compressiva nos membros inferiores. A alta prevalência do comprometimento do nervo tibial foi considerada uma marcada doença, da mesma forma que a neuropatia ulnar.

The authors assessed all tibial nerve conduction studies (NCS) of the patients under suspicious of acute or subacute leprosy neuropathy, who have been attended the Leprosy Ambulatory Clinic of the ILSL during a period of two years. Seventy-five patients have been included as follows: 52 male and 23 female, between 21 and 73 years old, with the mean age of 44.5 totaling 150 nerves The medial plantar (MP) and lateral plantar ( (LP) branches were studied separately. The most involved was the LP with 57.4%, followed bythe MP with 42.6%. The most frequent injury among the abnormal nerves was the axonal lesion with 66%, followed by the myelin lesion with 28.7%. The most frequent and disproportional involvement of thePL branch not only demonstrates the compressivecharacter of the tibial nerve injury in the tarsaltunnel but also indicates a multiple entrapment mononeuropathy in the lower limbs. The high prevalence of the tibial nerve injury was considered a hallmark of the disease, as well as the ulnar neuropathy.

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.

Endogenous analgesic action of the pontospinal noradrenergic system spatially restricts and temporally delays the progression of neuropathic pain following tibial nerve injury.

Pontospinal noradrenergic neurons form part of an endogenous analgesic system that suppresses acute pain, but there is conflicting evidence about its role in neuropathic pain. We investigated the chronology of descending noradrenergic control during the development of a neuropathic pain phenotype in rats following tibial nerve transection (TNT). A lumbar intrathecal cannula was implanted at the time of nerve injury allowing administration of selective α-adrenoceptor (α-AR) antagonists to sequentially assay their effects upon the expression of allodynia and hyperalgesia. Following TNT animals progressively developed mechanical and cold allodynia (by day 10) and subsequently heat hypersensitivity (day 17). Blockade of α2-AR with intrathecal yohimbine (30 µg) revealed earlier ipsilateral sensitization of all modalities while prazosin (30 µg, α1-AR) was without effect. Established allodynia (by day 21) was partly reversed by the re-uptake inhibitor reboxetine (5 µg, i.t.) but yohimbine no longer had any sensitising effect. This loss of effect coincided with a reduction in the descending noradrenergic innervation of the ipsilateral lumbar dorsal horn. Yohimbine reversibly unmasked contralateral hindlimb allodynia and hyperalgesia of all modalities and increased dorsal horn c-fos expression to an innocuous brush stimulus. Contralateral thermal hyperalgesia was also reversibly uncovered by yohimbine administration in a contact heat ramp paradigm in anaesthetised TNT rats. Following TNT there is an engagement of inhibitory α2-AR-mediated noradrenergic tone which completely masks contralateral and transiently suppresses the development of ipsilateral sensitization. This endogenous analgesic system plays a key role in shaping the spatial and temporal expression of the neuropathic pain phenotype after nerve injury.

MRI findings in patients with tibial nerve compression near the knee.

The soleus sling has been recently identified as a site of compression of the tibial nerve resulting in tibial neuropathy. Diagnosis of soleal sling syndrome is difficult, and has been based mainly on clinical examination. Advances in MR imaging with high-resolution 3-Tesla scanners have made direct visualization of nerve pathology possible. With the use of high-resolution imaging and fat-suppression protocols, tibial nerve compression at the soleal fascial arch can be demonstrated in a subset of patients presenting with idiopathic tibial neuropathy. The purpose of this paper is to confirm the ability of MR imaging to demonstrate pathologic changes in the tibial nerve in patients presenting with soleal sling syndrome. Additionally, patients presenting with tibial neuropathy and ganglion cysts, both extra- and intraneural, were examined to determine if the site of compression corresponded to the region of the soleus sling. Nine patients were included in the study, two with idiopathic soleus sling syndrome, four with extraneural, and three with intraneural ganglion cysts. In the patients presenting with idiopathic soleus sling syndrome, MR imaging demonstrated a thickened soleus sling with T2 hyperintensity of the tibial nerve at the level of the sling and denervation changes in muscles of the posterior compartment of the leg. In patients with extraneural ganglion cysts, MR imaging demonstrated a "sandwich"-like compression of the tibial nerve between the cyst and the soleus sling with corresponding tibial nerve T2 hyperintensity and denervation change in posterior compartment muscles. No compression of the tibial nerve at the soleus sling was found in the intraneural ganglion population. We conclude that MR imaging is effective in demonstrating pathologic changes in the tibial nerve at the soleus sling. Based on the MRI findings, we also believe that the soleus sling is a component of the compression when patients present with extraneural ganglion cysts and tibial neuropathy near the knee; in these patients, we recommend release of the soleus sling as part of the definitive management.

Peroneal and tibial intraneural ganglion cysts in children.

BACKGROUND/AIMS: Intraneural ganglion cyst is a rare and underrecognized clinical entity in the pediatric population, which may cause pain as well as motor and sensory neurological deficits. This study presents 4 pediatric patients harboring ganglion cysts involving the peroneal and tibial nerves. METHODS: Data encompassing pre- and postoperative analyses of 4 pediatric patients with intraneural ganglion cyst was evaluated. RESULTS: Out of these 4 patients, 3 had an intraneural ganglion cyst involving the peroneal nerve, and 1 patient had his tibial nerve involved. Two patients were operated for recurrent ganglion cysts with severe postoperative neurological deficits, after preceding operations in other institutions. The other 2 patients had no history of previous surgery, and they had their initial surgical treatment in our institute for primarily diagnosed ganglion cysts. With a mean follow-up of 24 months, all patients experienced pain relief. Significant improvement of motor deficits was achieved in 3 patients. No recurrences were encountered during the 24-month follow-up. CONCLUSION: Intraneural ganglion cysts in children can be treated with excellent outcome in experienced and dedicated centers, which specialize in peripheral nerve microsurgery.

Peroneal and tibial intraneural ganglion cysts in the knee region: a technical note.

BACKGROUND: Recent research has resulted in an improved understanding of the pathogenesis and treatment of intraneural ganglia, particularly with respect to the most common form, the peroneal nerve at the fibular neck region. OBJECTIVE: To outline the mechanism for the development and propagation of intraneural ganglia located in the knee region, along with their treatment, as well as highlight how shared principles can be exploited for successful treatment of the more commonly occurring peroneal intraneural ganglia. METHODS: A surgical approach has been developed for peroneal intraneural cysts based on the pathogenesis. The treatment of the less common tibial intraneural cysts is designed along the same principles. RESULTS: A strategy consisting of (1) disarticulation (resection) of the superior tibiofibular joint (ie, the source), (2) disconnection of the articular branch connection (ie, the conduit), and (3) decompression (rather than resection) of the cyst has improved outcomes and eliminated intraneural recurrences in peroneal intraneural cysts. These same principles and techniques can be applied to the rarer tibial intraneural ganglia derived from the same joint. The mechanism of development and propagation for intraneural cysts in the knee region as well as a surgical technique and its rational are described and illustrated. CONCLUSION: Understanding the joint-related basis of intraneural cysts leads to simple targeted surgery that addresses the joint, its articular branch, and the cyst. The success of the shared surgical strategy for both peroneal and tibial intraneural ganglia confirms the principles of the unifying articular theory.

Effects of distal nerve injuries on dorsal-horn neurons and glia: relationships between lesion size and mechanical hyperalgesia.

Penetrating limb injuries are common and usually heal without long-lasting effects, even when nerves are cut. However, rare nerve-injury patients develop prolonged and disabling chronic pain (neuralgia). When pain severity is disproportionate to severity of the inciting injury, physicians and insurers may suspect exaggeration and limit care or benefits, although the nature of the relationship between lesion-size and the development and persistence of neuralgia remains largely unknown. We compared cellular changes in the spinal dorsal-horn (the initial CNS pain-processing area) after partial or total tibial-nerve axotomies in male Sprague-Dawley rats to determine if these changes are proportional to the numbers of peripheral axons cut. Unoperated rats provided controls. Plantar hind-paw responses to touch, pin, and cold were quantitated bilaterally to identify hyperalgesic rats. We also compared data from nerve-injured rats with or without hyperalgesic responses to mechanical hind-paw stimulation to evaluate concordance between pain behaviors and dorsal-horn cellular changes. Hyperalgesia was no less prevalent or severe after partial than after total axotomy. L(5) spinal-cord sections from rats killed 7 days postoperatively were labeled for markers of primary afferents (substance P calcitonin gene-related peptide isolectin B4, gamma aminobutyric acid, and glial fibrillary acidic protein), then labeled cells were stereologically quantitated in somatotopically defined dorsal-horn regions. Total axotomy reduced markers of primary afferents more than partial axotomy. In contrast, GABA-immunoreactive profiles were similarly reduced after both lesions, and in rats with sensory loss versus hyperalgesia. Numbers of GFAP-immunoreactive astrocytes increased independently of lesion size and pain status. Small nerve injuries can thus have magnified and disproportionate effects on dorsal-horn neurons and glia, perhaps providing a biological correlate for the disproportionate pain of post-traumatic neuralgias (including complex regional pain syndrome-I) that follow seemingly minor nerve injuries. However, the presence of similar dorsal-horn changes in rats without pain behaviors suggests that not all transcellular responses to axotomy are pain-specific.

Hereditary neuropathy with liability to pressure palsy combined with schwannomas of the median and medial plantar nerves.

A 42-year-old woman was surgically treated for carpal tunnel syndrome, revealing schwannoma of the median nerve. A year later, she developed a tarsal tunnel syndrome. At time of this diagnosis, hereditary neuropathy with liability to pressure palsies (HNPP) was diagnosed genetically and a schwannoma of the medial plantar nerve was treated surgically. The occurrence of HNPP and schwannomas in the same patient might be purely coincidental, but it is tempting to speculate that they share a common genetic basis.