Nerve Injection Injury Research Articles

Peripheral Nerve Injury After Deoxycholic Acid (ATX-101) Injection in an Experimental Rat Model.

Deoxycholic acid (ATX-101) is a drug administered by subcutaneous injection for local fat reduction. However, ATX-101 treatment has been reported to cause marginal mandibular nerve injury with noticeable functional deficits when targeting submental fat. As a cytolytic agent with some selectivity for adipocytes, ATX-101 may damage the lipid-rich myelin surrounding peripheral nerves. This study seeks to characterize the nerve injection injury from ATX-101 in an experimental rat model. Using a rat sciatic nerve injection model, intrafascicular and extrafascicular injections of deoxycholic acid (ATX-101) were compared to lidocaine (positive control) and saline (negative control). Nerves were harvested at a 2-week endpoint for histomorphometric analysis. Cross-sectional area of nerve injury was significantly increased by ATX-101 injection at 75±15% with intrafascicular ATX-101 (p<0.001), 41±21% with extrafascicular ATX-101 (p<0.01), and 38±20% with positive control lidocaine (p<0.01) compared to 7±13% with negative control saline. Demyelinating injury was a significant mechanism of injury in the affected nerve fibers compared to uninjured nerve fibers (p<0.04), but there was no difference in axon-to-myelin area ratio between the lidocaine and ATX-101 cohorts. After two weeks, Wallerian degeneration was evident with only small regenerating nerve fibers present in the ATX-101-injured groups compared to saline (2.54±0.26um vs 5.03±0.44um, p<0.001) in average width. Deoxycholic acid (ATX-101) is capable of extensive nerve injury in rats. The mechanism of action for ATX-101 does not preferentially target myelin more than other common neurotoxic agents. Appropriate knowledge of surgical anatomy and injection technique is necessary for any practitioners providing ATX-101 injections.

All aspects of sciatic nerve injection injury: an experiment with 78 rats.

In this study, we evaluate sciatic nerve injuries due to intramuscular injections, which is an important medicolegal problem frequently encountered in medical practice, with an extended experimental rat model of peripheral nerve injury. A total of 78 male Wistar albino rats were divided into five main groups, including a control group, a sham saline group, and groups that received benzathine penicillin G, diclofenac sodium, and dexamethasone, respectively. These pharmaceutical agents were applied to the sciatic nerves of all rats after exploration in the epineurial, endoneurial, and intrafascicular compartments, excluding the control group. Outcomes were evaluated for all rats and their sciatic nerves according to functional, electrophysiological, and histopathological results. Injuries were most evident in the groups that received penicillin G and diclofenac sodium, and this finding was statistically significant. It was also found that endoneurial and intrafascicular injections may cause more harm than epineurial injections. We have demonstrated that any medical injections applied to the epineurial, endoneurial, or intrafascicular compartments of the sciatic nerve may cause functional and electrophysiological loss with or without deterioration of the peripheral nerve architecture.

Effects of Dexamethasone on Bupivacaine-Induced Peripheral Nerve Injection Injury in the Rat Sciatic Model

Introduction The aim of this study was to investigate the effect of perineural dexamethasone against intraneural bupivacaine. Material and Methods Rats were divided into 9 groups with 6 animals in each group; Group 1 (Intraneural saline 600 µL–2ndday), Group 2 (Intraneural saline 600 µL–7th day), Group 3 (Intraneural saline 600 µL + perineural dexamethasone 0.5 mg/kg-2nd day), Group 4 (Intraneural saline 600 µL + perineural dexamethasone 0.5 mg/kg-7th day), Group 5 (Intraneural bupivacaine 10 mg/kg–2nd day), Group 6 (Intranueral bupivacaine 10 mg/kg–7th day), Group 7 (Intraneural bupivacaine 10 mg/kg + perineurald exam ethasone 0.5 mg/kg-2nd day), Group 8 (Intraneural bupivacaine 10 mg/kg + perineural dexamethasone 0.5 mg/kg-7th day), Group 9 (Control group). At the end of the application period, histopathological and immunohistochemical examinations were analyzed. Results and Conclusion It was observed that caspase 3 levels significantly increased in the 5th and 6th groups compared to the 1st and 2nd groups (p < 0.01). However, in the 7th and 8th groups, these levels were similar with 1st and 2nd groups. While a significant decrease in S 100 levels was detected in group 6 (p < 0.05), a significant increase occurred in Group 8 and reached the same levels as Group 2. According to histopathological evaluation, edema, vacuolization and myelin degeneration were significantly increased in groups 5 and 6 (p < 0.05). However, in the 8th group, the mentioned data showed a significant decrease and reached the same levels as group 2. As a result, perineural dexamethasone was found to have protective effects against intraneural bupivacaine induced sciatic nerve damage.

Effect of electroacupuncture on the expression of agrin and acetylcholine receptor subtypes in rats with tibialis anterior muscular atrophy induced by sciatic nerve injection injury.

ObjectiveTo investigate the effects of electroacupuncture (EA) on mRNA and protein expression of agrin, acetylcholine receptor (AChR)-ε and AChR-γ in a rat model of tibialis anterior muscle atrophy induced by sciatic nerve injection injury, and to examine the underlying mechanism of action.MethodsFifty-four adult Sprague-Dawley rats were divided into four groups: healthy control group (CON, n=6); sciatic nerve injury group (SNI, n=24), comprising rats euthanased at 1, 2, 4 and 6 weeks, respectively, after penicillin injection-induced SNI (n=6 each); CON+EA group (n=12), comprising healthy rats euthanased at 4 and 6 weeks (after 2 and 4 weeks, respectively, of EA at GB30 and ST36); and SNI+EA group, comprising rats euthanased at 4 and 6 weeks (after 2 and 4 weeks, respectively, of EA). The sciatic nerve functional index (SFI), tibialis anterior muscle weight, muscle fibre cross-sectional area (CSA), and changes in agrin, AChR-ε, and AChR-γ expression levels were analysed.ResultsCompared with the control group (CON), SNI rats showed decreased SFI. The weight of the tibialis anterior muscle and muscle fibre CSA decreased initially and recovered slightly over time. mRNA/protein expression of agrin and AChR-ε were downregulated and AChR-γ expression was detectable (vs zero expression in the CON/CON+EA groups). There were no significant differences in CON+EA versus CON groups. However, the SNI+EA group exhibited significant improvements compared with the untreated SNI group (p<0.05).ConclusionsEA may alleviate tibialis anterior muscle atrophy induced by sciatic nerve injection injury by upregulating agrin and AChR-ε and downregulating AChR-γ.

Surgical management and outcome of iatrogenic radial nerve injection injuries

ObjectiveIatrogenic injury to the radial nerve can occur following intramuscular or intravenous injections of the upper extremity. In this study, we review the injury mechanism, operative techniques, and outcomes of patients evaluated for radial nerve injection injuries. MethodsData from 33 patients evaluated by the senior authors (DGK and DHK) from 1970–2011 with radial nerve injection injuries were reviewed retrospectively. All patients had injury of the nerve during injection. All corrective operations involved the use of direct intraoperative nerve action potential (NAP) recordings and either neurolysis, neurectomy, or suture/graft repair. The Louisiana State University Health Science (LSUHS) grading system was used for clinical assessment. ResultsOf the 33 patients, 23 underwent surgical intervention for persistent neurological deficit and/or pain. Of the 24 patients evaluated for injuries at the arm level, 17 required surgical exploration and repair for persistent symptoms. Nine patients required external neurolysis because the lesions were in continuity and positive NAP recording was across the lesion. All of these patients achieved a Grade 4 or better in functional recovery. Eight patients with lesions in continuity but in which NAP could not be recorded underwent either end-to-end suture (7) or graft repair (1) following resection of a 3.0cm non-recordable segment. All patients achieved Grade 3 or 4 functional recovery. Six patients with forearm injuries involving the superficial sensory branch of radial nerve underwent either neurolysis (3) or neurectomy (3). ConclusionsSurgical exploration may be indicated when pain or disabling motor deficits persist. Early diagnosis and operative intervention can achieve favorable outcomes through exploration and radial nerve repair.

Effect of Electroacupuncture on the Expression of Glycyl‐tRNA Synthetase and Ultrastructure Changes in Atrophied Rat Peroneus Longus Muscle Induced by Sciatic Nerve Injection Injury

Glycyl-tRNA synthetase (GlyRS) is one of the key enzymes involved in protein synthesis. Its mutations have been reported to cause Charcot-Marie-Tooth disease which demonstrates muscular atrophy in distal extremities, particularly manifested in peroneus muscles. In this situation, the dysfunctions of mitochondria and sarcoplasmic reticulum (SR) affect energy supply and excitation-contraction coupling of muscle fibers, therefore resulting in muscular atrophy. Although the treatment of muscular atrophy is a global urgent problem, it can be improved by electroacupuncture (EA) treatment. To investigate the mechanism underlying EA treatment improving muscular atrophy, we focused on the perspective of protein synthesis by establishing a penicillin injection-induced sciatic nerve injury model. In our model, injured rats without treatment showed decreased sciatic functional index (SFI), decreased peroneus longus muscle weight and muscle fiber cross-sectional area, aggregated mitochondria with vacuoles appearing, swollen SR, and downregulated mRNA and protein expression levels of GlyRS and myosin heavy chain IIb (MHC-IIb). The injured rats with EA treatment showed significant recovery. These results indicated that EA stimulation can alleviate peroneus longus muscular atrophy induced by iatrogenic sciatic nerve injury through promoting the recovery of GlyRS and muscle ultrastructure and increasing muscle protein synthesis.

Sciatic nerve injection injury in children: Management and outcome

Background: Sciatic nerve injury is a common complication following IM gluteal injection in children. A controversy still exists regarding management and outcome.Objective: To find the outcome of conservative and surgical treatment and compare it with other studies.Patients and Methods: This is a retrospective study of 24 children( less than 15 years old) with sciatic nerve injection injury at the gluteal region. The child age, gender, type of injection drug, time of injury with complete neurological examination and EMG study were recorded. Conservative treatment including physiotherapy and surgical treatment including surgical exploration and neurolysis at the buttock region were done with follow-up 6 months to one year.Results: Patient’s age ranged from 6 months to 15 years; there were 18 male and 6 female. The most common IM drugs are analgesic in 40% and antibiotic in 18%. Neurological complaint was 22 foot drop (33.3%) and pain in 2 patient (8.7%). Surgery was done in 16 cases (66.6%) and 8 patients (33.3%) were treated conservatively . Outcome of surgery was good in (62.5%) and poor in (37.5).Conclusions: we recommend surgery 2-3 months after conservative treatment including physiotherapy, analgesia, and EMG follow up, if no neurological recovery occurred. The outcome of surgery was good in the child with sciatic nerve injection injury

اصابات العصب النسوي في الاطفال بسبب زرق الابر بالعضله: المعالجه و النتائج

خلفية الموضوع: اصابات العصب النسوي في الاطفال بسبب زرق الابر بالعضله العجزيه من المضاعفات الشائعه وخاصة في الاطفال، لازال هناك عدم اتفاق حول معالجة هذه الاصابات ونتائج العلاج. الغاية من الدراسة: هو تسليط الضوء على نتائج العلاج التحفضي و الجراحي ومقارنتها بالدراسات الاخرى. طرق معالجة الموضوع: المعلومات احصيت بصوره رجعيه من 24طفل تحت 15 سنه من العمر مصاب بضرر العصب النسوي بسبب زرق الابر بالعضله في المنطقه العجزيه، الفئه العمريه والجنس ونوع الدواء الذي تم زرقه و وقت الاصابه مع فحص عصبي شامل وتخطيط الاعصاب تم دراسته في كل مريض، العلاج التحفضي يشمل العلاج الطبيعي و علاج الالام و المقويات مع مساند للقدم والساق، العلاج الجراحي يشمل استكشاف العصب النسوي في منطقة الاليه مع تحرير العصب من الالتصاقات, المتابعه الطبيه كانت من 6شهور الى سنه واحده بعد الاصابه. النتائج: كانت الفئه العمريه تتراوح بين 6شهور الى 15سنه وكان هناك 18 طفل ذكر و 6 طفل انثى، اكثر الدواء المسبب للاصابه هو مسكنات الالام وخافض الحراره في 40% و المضادات الحيويه في 18%, كان هناك سقوط القدم في 22 حاله 83.3% مع وجود الم في 2 حاله 8.7%، التداخل الجراحي تم في 16 طفل 66.66%و العلاج التحفضي تم اجراءه في 8 طفل 33.3%, النتائج كانت جيده في 62.5% من الذين تم اجراء التداخل الجراحي لهم وكانت سيء في 37.5%. الاستنتاج: ننصح باجراء التداخل الجراحي بعد 2-3 شهر بعد الاصابه و العلاج التحفضي ومتابعه فحص تخطيط الاعصاب مع عدم وجود اي علامات التحسن الاعراض في القدم والساق، نتائج العمليه الجراحيه كانت جيده في معظم الاطفال المصابين بضرر العصب النسوي بسبب زرق الادويه بالعضله في المنطقة العجزيه.

The utility of three-dimensional optical projection tomography in nerve injection injury imaging.

The examination of nerve microarchitecture has hitherto been limited solely to two-dimensional imaging techniques. The objective of this study was to evaluate the ability of optical projection tomography to discern the nerve microarchitecture and injection injury in three dimensions. Five piglets were studied, whose median and lingual nerves were unilaterally injected post mortem with preset volumes of local anaesthetic, excised and subsequently made transparent with benzyl alcohol benzyl benzoate. Images were captured in three dimensions. The same contralateral nerves were used as controls. Using optical projection tomography, we observed differences between the internal organisation of the median and the lingual nerves, which potentially explain the variations in their susceptibility to injury. This was demonstrated in three dimensions as a disruption to the fascicles in the lingual nerve, and their displacement in the median nerve. This new technology offers potential for studying nerve microarchitecture topography and its tolerance to injection injury.

Early cyclosporin A treatment retards axonal degeneration in an experimental peripheral nerve injection injury model

Injury to peripheral nerves during injections of therapeutic agents such as penicillin G potassium is common in developing countries. It has been shown that cyclosporin A, a powerful immunosuppressive agent, can retard Wallerian degeneration after peripheral nerve crush injury. However, few studies are reported on the effects of cyclosporin A on peripheral nerve drug injection injury. This study aimed to assess the time-dependent efficacy of cyclosporine-A as an immunosuppressant therapy in an experimental rat nerve injection injury model established by penicillin G potassium injection. The rats were randomly divided into three groups based on the length of time after nerve injury induced by cyclosporine-A administration (30 minutes, 8 or 24 hours). The compound muscle action potentials were recorded pre-injury, early post-injury (within 1 hour) and 4 weeks after injury and compared statistically. Tissue samples were taken from each animal for histological analysis. Compared to the control group, a significant improvement of the compound muscle action potential amplitude value was observed only when cyclosporine-A was administered within 30 minutes of the injection injury (P < 0.05); at 8 or 24 hours after cyclosporine-A administration, compound muscle action potential amplitude was not changed compared with the control group. Thus, early immunosuppressant drug therapy may be a good alternative neuroprotective therapy option in experimental nerve injection injury induced by penicillin G potassium injection.

Pathophysiology and Etiology of Nerve Injury Following Peripheral Nerve Blockade

This review synthesizes anatomical, anesthetic, surgical, and patient factors that may contribute to neurologic complications associated with peripheral nerve blockade. Peripheral nerves have anatomical features unique to a given location...

Sciatic nerve injection injury.

Nerve injury is a common complication following intramuscular injection and the sciatic nerve is the most frequently affected nerve, especially in children, the elderly and underweight patients. The neurological presentation may range from minor transient pain to severe sensory disturbance and motor loss with poor recovery. Management of nerve injection injury includes drug treatment of pain, physiotherapy, use of assistive devices and surgical exploration. Early recognition of nerve injection injury and appropriate management are crucial in order to reduce neurological deficit and to maximize recovery. Sciatic nerve injection injury is a preventable event. Total avoidance of intramuscular injection is recommended if other administration routes can be used. If the injection has to be administered into the gluteal muscle, the ventrogluteal region (gluteal triangle) has a more favourable safety profile than the dorsogluteal region (the upper outer quadrant of the buttock).

Are our intramuscular injections nerve-friendly? What are we missing? Simple techniques to prevent, recognize and manage nerve injection injuries

Are our intramuscular injections nerve-friendly? What are we missing? Simple techniques to prevent, recognize and manage nerve injection injuries

MR neurography of sciatic nerve injection injury

We report on magnetic resonance neurography (MRN) as a supplementary diagnostic tool in sciatic nerve injection injury. The object of the study was to test if T2-weighted (w) contrast within the sciatic nerve serves as an objective criterion for sciatic injection injury. Three patients presented with acute sensory and/or motor complaints in the distribution of the sciatic nerve after dorsogluteal injection and underwent MRN covering gluteal, thigh and knee levels. Native and contrast-enhanced T1-w images were employed to identify the tibial and peroneal division of the sciatic nerve while T2-w images with fat suppression allowed visualization of the site and extent of the nerve lesion. MRN in the two patients with clinically severe sensory and motor impairment correctly depicted sciatic injury: continuity of the T2-w lesion within the nerve at the lesion site and distal to it corresponded well to severe injury confirmed by NCS/EMG as axonotmetic or neurotmetic. Topography of the T2-w lesion on cross-section corresponded to predominant peroneal involvement; moreover, associated denervation patterns of distal target muscles were revealed. One of these patients completely recovered with concomitant complete regression of MRN abnormalities on follow-up. The third patient experienced transient sensory and mild motor impairment with complete recovery after 2 weeks. In this patient, T2-w signal within the nerve and distal target muscles remained normal indicating only mild, non-axonal nerve affliction. Our case series shows that MRN can be very useful in precisely determining the site of sciatic injection injury and may provide diagnostic criteria for the assessment of lesion severity and recovery.

Sciatic nerve injury from intramuscular injection: a persistent and global problem

An intramuscular (i.m.) injection into the buttock risks damaging the sciatic nerve. Safe injection practices need to be understood by doctors and nurses alike. The aims of this study were to determine if sciatic nerve injury because of i.m. injection is a continuing problem and to establish the availability of published guidelines on i.m. injection techniques. Intramuscular injection related sciatic nerve injury claims to the New Zealand Accident Compensation Corporation between July 2005 and September 2008 were reviewed. Nursing organisations were surveyed to enquire about guidelines on i.m. injection. I.m. injection related sciatic nerve injuries in the medical and medicolegal literature (1989-2009) were systematically reviewed. There were eight claims for sciatic nerve injection injury made to the ACC during the 3-year study period; all were in young adults. Only one of the nursing organisations contacted had published guidelines on i.m. injection technique, and these related specifically to immunisation. Seventeen reports of patients with sciatic nerve injury from i.m. injection were identified comprising a total of 1506 patients, at least 80% of which were children. Nine court decisions finding in favour of the plaintiff were identified, all from the North American legal system. A broad range of drugs were implicated in the offending i.m. injections. Sciatic nerve injury from an i.m. injection in the upper outer quadrant of the buttock is an avoidable but persistent global problem, affecting patients in both wealthy and poorer healthcare systems. The consequences of this injury are potentially devastating. Safer alternative sites for i.m. injection exist. These should be promoted more widely by medical and nursing organisations.

Ropivacaine-Induced Peripheral Nerve Injection Injury in the Rodent Model

Intraneural administration of local anesthetics has been associated with nerve damage. We undertook the present study to investigate histological changes induced by ropivacaine injection into rat sciatic nerve. Fifty-four adult male Lewis rats were randomly distributed into 9 groups, 6 animals per group. Fifty microliters of normal saline, 10% phenol, or 0.75% ropivacaine were administered by intrafascicular injection, extrafascicular injection, or extraneural (topical) placement. At 2 weeks, animals were killed and the sciatic nerve at the injection site was evaluated with light microscopy, quantitative histomorphometry, and electron microscopy. On cross-sectional evaluation, extrafascicular ropivacaine injection and extraneural placement of ropivacaine were both associated with damage to the perineurium, with focal demyelination surrounded by edematous endoneurium. Intrafascicular injection of ropivacaine resulted in a wedge-shaped region of demyelination and focal axonal loss with some regeneration, bordered by a region of normally myelinated axons in a background of edematous endoneurium. Extrafascicular injection resulted in more significant damage than extraneural placement of ropivacaine, but less than intrafascicular injection as shown with quantitative histomorphometry. Quantitatively, ropivacaine-injured specimens had significantly lower nerve density than saline-injured specimens. Wallerian degeneration and perineural edema were also demonstrated qualitatively with electron microscopy. This study demonstrates that, in the rat model, ropivacaine is associated with marked histological abnormality, including edema of the perineurium and axonal destruction with wallerian degeneration, when injected into or extraneurally placed onto a nerve. Extrafascicular injection and extraneural placement were associated with similar, although milder, histological damage than intrafascicular injection. Further work is needed to investigate the functional implications, if any, of the histological abnormalities observed in this study.

Persistent Orodental Pain, Atypical Odontalgia, and Phantom Tooth Pain: When Are They Neuropathic Disorders?

Patients with unrelenting pain in the teeth, gingival, palatal or alveolar tissues often see multiple dentists and have multiple irreversible procedures performed and still have their pain. Up to one-third of patients attending a chronic facial pain clinic have undergone prior irreversible dental procedures for their pain without success. In these cases, if no local source of infectious, inflammatory, or other pathology can be found, then the differential diagnosis must include a focal neuropathic pain disorder. The common diagnoses given include the terms atypical odontalgia, persistent orodental pain, or if teeth have been extracted, phantom tooth pain. One possibility is that these pain complaints are due to a neuropathic alteration of the trigeminal nerve. There are several diagnostic procedures that need to be performed in any patient suspected of having a trigeminal neuropathic disorder including (1) cold testing of involved teeth for pulpal nonvitality; (2) a periapical radiograph examining the teeth for apical change; (3) a panoramic radiograph examining for other maxillofacial disease; (4) a thorough head and neck examination also looking for abnormality; (5) a cranial nerve examination including anesthetic testing which documents any increased or decreased nerve trigeminal nerve sensitivity and rules out other neurologic changes outside the trigeminal nerve; and (6) MRI imaging in some cases. Finally, when a nonobvious atypical toothache first presents, direct microscopic examination of the tooth for incomplete tooth fracture is also suggested. The majority of these patients are women over the age 30 with pain in the posterior teeth/alveolar arch. Multiple causes exist for sustained neuropathic pain including direct nerve injury (e.g., associated with fracture or surgical treatment), nerve injection injury, nerve compression injury (e.g., implant, osseous growth, neoplastic invasion) and infection-inflammation damage to the nerve itself. Sustained nerve pain is commonly seen in patients with psychiatric impairment. It may be that the unrelenting nature of the pain itself alters the patient's personality. Treatment includes pharmacologic medications which suppress nerve activity. The common medications used for atypical odontalgia and phantom tooth pain include gabapentin, tricyclics, topical anesthetics, and opioids. A list of these medications is provided in table form. Data suggest that once the patient has failed dental treatment and pain persists, the long-term outcome is less than 25 percent will have complete pain relief with treatment. With earlier treatment, better pain control, and improved nerve activity suppression medications, this should also prevent secondary psychiatric disease from developing and lower the number of inappropriate treatments.

Nerve injection injury with botulinum toxin.

The therapeutic use of botulinum toxin (Botox) is increasing in popularity. Previous studies have shown that various drugs, especially when injected intrafascicularly, can cause major nerve damage. This study evaluates the potential for neurotoxicity of botulinum toxin in a rat sciatic nerve model. Lewis rats were randomly assigned to one of six groups (n = 10/group). Group 1, 2, and 3 rats received, respectively, an intrafascicular, extrafascicular, and extraneural injection of 50 microl of botulinum toxin (50 UI/ml). Group 4, 5, and 6 rats received 50 microl of 10% phenol as a positive control. Five animals received saline as a negative control. Animals were sacrificed at 2 and 7 weeks. Nerves were harvested and processed for histology and morphometry. Nerves in all botulinum toxin groups retained a normal architecture without cellular infiltration or demyelination. The number and diameter of fibers, the thickness of myelin, and the percentage of neural tissue were comparable with normal controls. Nerves injected intraneurally with phenol presented with severe damage, demyelination, and inflammation at 2 weeks and showed signs of early regeneration at 7 weeks. This study demonstrates that in a rat model, even direct intraneural injection of botulinum toxin caused no damage. This information should encourage the reconstructive surgeon to consider broader applications of this drug.

Injection injuries to the median and ulnar nerves at the wrist

Carpal tunnel syndrome is often treated nonoperatively with temporary wrist immobilization and local steroid injections. A direct injection into a peripheral nerve can result in permanent damage. Two cases of median nerve injection injury and one involving the ulnar nerve are presented; all were treated with neurolysis and debridement of the injected material. At follow-up ranging from 1 to 11 years, all patients showed significant improvement, but with some functional loss. The literature is confusing because of the variety of injection techniques used for the treatment of carpal tunnel syndrome, some of which put the median nerve at risk. We recommend that the injection be made midway between the palmaris longus tendon and the flexor carpi ulnaris tendon just proximal to the proximal edge of the transverse carpal ligament in a line with the superficialis tendon of the ring finger. The injection should be stopped and redirected if the patient experiences paresthesia of any kind.

Median nerve injury from local steroid injection in carpal tunnel syndrome

Local steroid injections for symptomatic relief of carpal tunnel syndrome have become common in the evaluation and treatment of this disorder; yet reports of median nerve injection injury from this practice are rare. We present a case of nerve injury from a steroid injection in a 24-year-old man with carpal tunnel syndrome that was successfully treated by division of the transverse carpal ligament and neurolysis. The histopathological characteristics of the lesion are presented, and the pathogenesis and treatment of this injury are discussed. Means of avoiding this complication include careful attention to anatomic landmarks as well as to the patient's subjective response during injection and avoidance of the use of local anesthetics.