Rationale and design of the peripheral nerve tumor registry: an observational cohort study.

AIM: Peripheral nerve tumors (PNT) are rare lesions. To date, no systematic multicenter studies on epidemiology, clinical symptoms, treatment strategies and outcomes, genetic and histopathologic features, as well as imaging characteristics of PNT were published. The main goal of our PNT Registry is the systematic multicenter investigation to improve our understanding of PNT and to assist future interventional studies in establishing hypotheses, determining potential endpoints, and assessing treatment efficacy. METHODS: Aims of the PNT registry were set at the 2015 Meeting of the Section of Peripheral Nerve Surgery of the German Society of Neurosurgery. A study protocol was developed by specialists in PNT care. A minimal data set on clinical status, treatment types and outcomes is reported by each participating center at initial contact with the patient and after 1 year, 2 years, and 5 years. Since the study is coordinated by the Charité Berlin, the PNR Registry was approved by the Charité ethics committee (EA4/058/17) and registered with the German Trials Registry (www.drks.de). On a national level, patient inclusion began in June 2016. The registry was rolled out across Europe at the 2019 meeting of the European Association of Neurosurgery in Dublin. RESULTS: Patient recruitment has been initiated at 10 centers throughout Europe and 14 additional centers are currently applying for local ethics approval. CONCLUSION: To date, the PNT registry has grown into an international study group with regular scientific and clinical exchange awaiting the first results of the retrospective study arm.

Cross-sectional Area of the Median Nerve Before Revision Carpal Tunnel Release-A Cross-sectional Study.

BACKGROUND: High-resolution ultrasound can be used for diagnosis of carpal tunnel syndrome with an equal accuracy to electrodiagnostic studies. Up to date there has been no investigation published that examined the median nerve in a large patient cohort with recurrent or persistent symptoms. Reference and cutoff values are lacking. OBJECTIVE: To provide reference values for detection of ongoing or recurrent compression in patients with recurring or persisting symptoms in carpal tunnel syndrome. METHODS: One hundred and sixteen patients undergoing revision decompression of the median nerve at the carpal tunnel between January 2010 and October 2015 were studied retrospectively to determine the cross-sectional area of the median nerve at the wrist by the technique of neurosonography. RESULTS: In cases of insufficient primary release, the mean cross-sectional area was 20.0 mm2 preop. In cases of scar or synovitis, the mean cross-sectional area was 17.0 mm2 (significantly less than in cases of insufficient primary release, P = .008). Compared to successfully operated patients with de novo carpal tunnel syndrome (n = 74), a cutoff value of 14.5 mm2 yielded a sensitivity of 78% and a specificity of 97% to diagnose ongoing or recurrent compression in case of a typical clinical presentation of ongoing or recurrent symptoms (tested via comparison of patients who are symptom free vs patients with symptoms). CONCLUSION: For the first time, we provide reference values in patients with recurring or persisting symptoms in carpal tunnel syndrome based on a large patient population. Ultrasound can aid in the evaluation of patients with entrapment neuropathy of the median nerve and recurring or persisting symptoms.

A Single-Center Prospective Observational Study of Ultrasonography for 6 Months after Surgical Decompression of the Median Nerve at the Carpal Tunnel.

Objective To determine the natural history of the morphology of the median nerve after carpal tunnel decompression. Methods Between October and December 2014, patients with suspected carpal tunnel were prospectively enrolled and underwent pre- and postoperative (3 and 6 months) high-definition ultrasonography, electrophysiology, and clinical testing. Results A total of 81 patients were enrolled in the study; 75 (93%) could be reached for the 6-month follow-up, and 100% were clinically better at the 6-month follow-up. The mean cross-sectional area decreased from 14.3 ± 4.4 mm2 to 9.6 ± 2.3 mm2 (mean ± standard deviation [SD]). The mean distal motor latency decreased from 6.5 ± 2.2 msec to 4.4 ± 0.8 msec (mean ± SD). Distal motor latency improved statistically significantly after surgical decompression as well, but sooner. Conclusion We present the second largest series of patients with sonographic follow-up after surgical decompression of the carpal tunnel.

Sonographic short-term follow-up after surgical decompression of the median nerve at the carpal tunnel: a single-center prospective observational study.

OBJECT Carpal tunnel syndrome causes increased cross-sectional area (CSA) of the median nerve, which can be assessed by high-definition ultrasonography. It is unclear today, however, whether high-definition ultrasonography may play a role in the postoperative period. This prospective study aimed to determine the natural history of the morphology of the median nerve at the carpal tunnel after surgical decompression assessed by high-definition ultrasonography. METHODS Between October and December 2014, patients with suspected carpal tunnel syndrome who were referred to the authors' center for peripheral neurosurgery were prospectively enrolled and underwent pre- and postoperative (3 months) high-definition ultrasonography, electrophysiology, and clinical testing. RESULTS Eighty-one patients were enrolled in the study, and 100% were clinically better at the 3-month follow-up. The mean CSA decreased from 14.7 ± 4.9 mm(2) to 12.4 ± 3.4 mm(2) (mean ± SD, p < 0.0001). The mean distal motor latency decreased from 6.6 ± 2.4 msec to 4.8 ± 1.0 msec (mean ± SD, p < 0.0001). Ninety-eight percent of patients who were available for electrodiagnostic follow-up showed an improvement of the distal motor latency; only 80% had a reduction in the CSA. CONCLUSIONS The authors present the second-largest series of patients with sonographic follow-up after surgical decompression of the carpal tunnel reported in the literature so far. This study, which showed a decrease in size of the median nerve after surgical decompression, suggests that the preoperative increase in median nerve CSA at the carpal tunnel may be due to compression and that enlargement of the median nerve is (partially) reversible.

Sciatic nerve injury related to hip replacement surgery: imaging detection by MR neurography despite susceptibility artifacts.

Sciatic nerve palsy related to hip replacement surgery (HRS) is among the most common causes of sciatic neuropathies. The sciatic nerve may be injured by various different periprocedural mechanisms. The precise localization and extension of the nerve lesion, the determination of nerve continuity, lesion severity, and fascicular lesion distribution are essential for assessing the potential of spontaneous recovery and thereby avoiding delayed or inappropriate therapy. Adequate therapy is in many cases limited to conservative management, but in certain cases early surgical exploration and release of the nerve is indicated. Nerve-conduction-studies and electromyography are essential in the diagnosis of nerve injuries. In postsurgical nerve injuries, additional diagnostic imaging is important as well, in particular to detect or rule out direct mechanical compromise. Especially in the presence of metallic implants, commonly applied diagnostic imaging tests generally fail to adequately visualize nervous tissue. MRI has been deemed problematic due to implant-related artifacts after HRS. In this study, we describe for the first time the spectrum of imaging findings of Magnetic Resonance neurography (MRN) employing pulse sequences relatively insensitive to susceptibility artifacts (susceptibility insensitive MRN, siMRN) in a series of 9 patients with HRS procedure related sciatic nerve palsy. We were able to determine the localization and fascicular distribution of the sciatic nerve lesion in all 9 patients, which clearly showed on imaging predominant involvement of the peroneal more than the tibial division of the sciatic nerve. In 2 patients siMRN revealed direct mechanical compromise of the nerve by surgical material, and in one of these cases indication for surgical release of the sciatic nerve was based on siMRN. Thus, in selected cases of HRS related neuropathies, especially when surgical exploration of the nerve is considered, siMRN, with its potential to largely overcome implant related artifacts, is a useful diagnostic addition to nerve-conduction-studies and electromyography.

MR neurography in ulnar neuropathy as surrogate parameter for the presence of disseminated neuropathy.

PURPOSE: Patients with ulnar neuropathy of unclear etiology occasionally present with lesion extension from elbow to upper arm level on MRI. This study investigated whether MRI thereby distinguishes multifocal neuropathy from focal-compressive neuropathy at the elbow. METHODS: This prospective study was approved by the institutional ethics committee and written informed consent was obtained from all participants. 122 patients with ulnar mononeuropathy of undetermined localization and etiology by clinical and electrophysiological examination were assessed by MRI at upper arm and elbow level using T2-weighted fat-saturated sequences at 3T. Twenty-one patients were identified with proximal ulnar nerve lesions and evaluated for findings suggestive of disseminated neuropathy (i) subclinical lesions in other nerves, (ii) unfavorable outcome after previous decompressive elbow surgery, and (iii) subsequent diagnosis of inflammatory or other disseminated neuropathy. Two groups served as controls for quantitative analysis of nerve-to-muscle signal intensity ratios: 20 subjects with typical focal ulnar neuropathy at the elbow and 20 healthy subjects. RESULTS: In the group of 21 patients with proximal ulnar nerve lesion extension, T2-w ulnar nerve signal was significantly (p<0.001) higher at upper arm level than in both control groups. A cut-off value of 1.92 for maximum nerve-to-muscle signal intensity ratio was found to be sensitive (86%) and specific (100%) to discriminate this group. Ten patients (48%) exhibited additional T2-w lesions in the median and/or radial nerve. Another ten (48%) had previously undergone elbow surgery without satisfying outcome. Clinical follow-up was available in 15 (71%) and revealed definitive diagnoses of multifocal neuropathy of various etiologies in four patients. In another eight, diagnoses could not yet be considered definitive but were consistent with multifocal neuropathy. CONCLUSION: Proximal ulnar nerve T2 lesions at upper arm level are detected by MRI and indicate the presence of a non-focal disseminated neuropathy instead of a focal compressive neuropathy.

T2-signal of ulnar nerve branches at the wrist in guyon's canal syndrome.

OBJECTIVE: To evaluate T2-signal of high-resolution MRI in distal ulnar nerve branches at the wrist as diagnostic sign of guyon's-canal-syndrome (GCS). MATERIALS AND METHODS: 11 GCS patients confirmed by clinical/electrophysiological findings, and 20 wrists from 11 asymptomatic volunteers were prospectively included to undergo the following protocol: axial T2-weighted-fat-suppressed and T1-weighted-turbo-spin-echo-sequences (3T-MR-scanner, Magnetom/Verio/Siemens). Patients were examined in prone position with the arm extended and wrist placed in an 8-channel surface-array-coil. Nerve T2-signal was evaluated as contrast-to-noise-ratios (CNR) from proximal-to-distal in ulnar nerve trunk, its superficial/sensory and deep/motor branch. Distal motor-nerve-conduction (distal-motor-latency (dml)) to first dorsal-interosseus (IOD I) and abductor digiti minimi muscles was correlated with T2-signal. Approval by the institutional review-board and written informed consent was given by all participants. RESULTS: In GCS, mean nerve T2-signal was strongly increased within the deep/motor branch (11.7±4.8 vs.controls:-5.3±2.4;p = 0.001) but clearly less and not significantly increased in ulnar nerve trunk (6.8±6.4vs.-7.4±2.5;p = 0.07) and superficial/sensory branch (-2.1±4.9vs.-9.7±2.9;p = 0.08). Median nerve T2-signal did not differ between patients and controls (-9.8±2.5vs.-6.7±4.2;p = 0.45). T2-signal of deep/motor branch correlated strongly with motor-conduction-velocity to IOD I in non-linear fashion (R(2) = -0.8;p<0.001). ROC-analysis revealed increased nerve T2-signal of the deep/motor branch to be a sign of excellent diagnostic performance (area-under-the-curve 0.94, 95% CI: 0.85-1.00; specificity 90%, sensitivity 89.5%). CONCLUSIONS: Nerve T2-signal increase of distal ulnar nerve branches and in particular of the deep/motor branch is highly accurate for the diagnostic determination of GCS. Furthermore, for the first time it was found in nerve entrapment injury that T2-signal strongly correlates with electrical-conduction-velocity.

Ulnar neuropathy at the elbow: MR neurography--nerve T2 signal increase and caliber.

PURPOSE: To assess nerve T2 signal and caliber as diagnostic signs at magnetic resonance (MR) neurography in ulnar neuropathy at the elbow (UNE). MATERIALS AND METHODS: This prospective study was approved by the institutional review board, and written informed consent was obtained from all participants. Twenty patients with UNE were graded by using clinical criteria and nerve conduction studies as mild (n = 12) and severe (n = 8) and were compared with 20 healthy control subjects. All subjects underwent ulnar nerve MR neurography (in-plane resolution of 0.4 × 0.4 mm) covering the elbow region, including T2-weighted imaging with fat suppression (turbo inversion-recovery magnitude sequence: repetition time msec/echo time msec/inversion time msec, 6, 120/66/180) and T1-weighted turbo spin-echo imaging (843/16). Nerve T2 signal increase, measured by using T2-weighted contrast-to-noise ratios across the cubital tunnel, and nerve caliber, determined by using T1-weighted pixelwise measurement of cross-sectional nerve area, were evaluated as diagnostic signs. Qualitative assessment by using visual grading was performed additionally. RESULTS: Diagnostic performance, as determined with area under the receiver operating characteristic curve (AUC), was excellent for nerve T2 signal to discriminate UNE from a normal finding (AUC = 0.94; 95% confidence interval [CI]: 0.87, 1.00) and was excellent for nerve caliber to discriminate severe from mild UNE (AUC = 0.95; 95% CI: 0.85, 1.00). Qualitative assessment demonstrated sensitivity of 83% and specificity of 85% for MR neurography of UNE. CONCLUSION: Nerve T2 signal increase seems to be an accurate sign to determine the presence of UNE. Nerve caliber enlargement discriminates severe from mild UNE. UNE may be diagnosed with high accuracy by means of quantitative or qualitative evaluation of these signs.

Extracellular concentrations of non-transmitter amino acids in peri-infarct tissue of patients predict malignant middle cerebral artery infarction.

BACKGROUND AND PURPOSE: Space-occupying brain edema is a life-threatening complication in patients with large middle cerebral artery (MCA) infarction. To determine predictors of this detrimental process, we investigated alterations of extracellular non-transmitter amino acid concentrations in peri-infarct tissue. METHODS: Thirty-one patients with infarctions covering >50% of the MCA territory in early cranial CT scans were included in the study. Probes for microdialysis, intracranial pressure, and tissue oxygen pressure were placed into the noninfarcted ipsilateral frontal lobe. Positron emission tomography imaging was performed in 16 of these patients to measure cerebral blood flow in the tissue around the neuromonitoring probes. RESULTS: Fourteen of the 31 patients developed a malignant MCA infarction, and 17 did not. The patients in the malignant group had significantly lower extracellular concentrations of non-transmitter amino acids than those in the benign group in the first 12 hours of neuromonitoring. At this time, CBF values determined in regions of interest around the probes by positron emission tomography and tissue oxygen pressure showed that the monitored tissues were not yet infarcted, and no differences in transmitter amino acids concentrations were found between the 2 groups. Furthermore, extracellular concentrations of non-transmitter amino acids were negatively correlated with size of infarction. CONCLUSIONS: We assume that reduction of non-transmitter amino acid concentrations reflects an expansion of the extracellular space by vasogenic edema formation in peri-infarct tissue of patients with malignant MCA infarction. Our findings facilitate early prediction of malignant edema formation and may help to increase knowledge of the pathophysiology of the peri-infarct zone of large MCA infarction.

Prediction of malignant course in MCA infarction by PET and microdialysis.

BACKGROUND AND PURPOSE: To predict malignant course in patients with large middle cerebral artery (MCA) infarction, we combined PET imaging and neuromonitoring, including microdialysis. METHODS: Thirty-four patients with stroke of >50% of the MCA territory in early cerebral CT scan were included. Probes for microdialysis and measurement of intracranial pressure and tissue oxygen pressure (Pto2) were placed into the ipsilateral frontal lobe. PET was performed with 11C-flumazenil to assess CBF and irreversible neuronal damage. RESULTS: PET measurements within 24 hours after stroke showed larger volumes of ischemic core (mean, 144.5 versus 62.2 cm3) and larger volumes of irreversible neuronal damage (157.9 versus 47.0 cm3) in patients with malignant course (ie, edema formation with midline shift) than in patients with benign course. Mean cerebral blood flow values within the ischemic core were significantly lower and the volume of the ischemic penumbra was smaller in the malignant than in the benign group. In patients with malignant course, cerebral perfusion pressure dropped to <50 to 60 mm Hg 22 to 72 hours (mean, 52.0 hours) after onset of symptoms; subsequently, Pto2 dropped and glutamate increased, indicating secondary ischemia. Maximal changes in the monitored variables reached significant levels for glutamate, aspartate, GABA, glycerol, lactate-to-pyruvate ratio, hypoxanthine, intracranial pressure, cerebral perfusion pressure, and Pto2. CONCLUSIONS: PET allowed prediction of malignant MCA infarction within the time window suggested for hemicraniectomy. Neuromonitoring helped to classify the clinical courses by characterizing pathophysiological sequelae of malignant edema formation. In contrast to PET, however, it did not predict fatal outcome early enough for successful implementation of invasive therapies.