Predicting Outcomes After Surgical Decompression for Mild Degenerative Cervical Myelopathy: Moving Beyond the mJOA to Identify Surgical Candidates.

BACKGROUND: Patients with mild degenerative cervical myelopathy (DCM) represent a heterogeneous population, and indications for surgical decompression remain controversial. OBJECTIVE: To dissociate patient phenotypes within the broader population of mild DCM associated with degree of impairment in baseline quality of life (QOL) and surgical outcomes. METHODS: This was a post hoc analysis of patients with mild DCM (modified Japanese Orthopedic Association [mJOA] 15-17) enrolled in the AOSpine CSM-NA/CSM-I studies. A k-means clustering algorithm was applied to baseline QOL (Short Form-36 [SF-36]) scores to separate patients into 2 clusters. Baseline variables and surgical outcomes (change in SF-36 scores at 1 yr) were compared between clusters. A k-nearest neighbors (kNN) algorithm was used to evaluate the ability to classify patients into the 2 clusters by significant baseline clinical variables. RESULTS: One hundred eighty-five patients were eligible. Two groups were generated by k-means clustering. Cluster 1 had a greater proportion of females (44% vs 28%, P = .029) and symptoms of neck pain (32% vs 11%, P = .001), gait difficulty (57% vs 40%, P = .025), or weakness (75% vs 59%, P = .041). Although baseline mJOA correlated with neither baseline QOL nor outcomes, cluster 1 was associated with significantly greater improvement in disability (P = .003) and QOL (P < .001) scores following surgery. A kNN algorithm could predict cluster classification with 71% accuracy by neck pain, motor symptoms, and gender alone. CONCLUSION: We have dissociated a distinct patient phenotype of mild DCM, characterized by neck pain, motor symptoms, and female gender associated with greater impairment in QOL and greater response to surgery.

Control of Pedicle Screw Placement with an Electrical Conductivity Measurement Device: Initial Evaluation in the Thoracic and Lumbar Spine.

Aim. Transpedicular screw fixation is widely used in spinal surgery. But the insertion of pedicle screws can sometimes be challenging because of the variability in pedicle size and the proximity of nerve roots. Methods. We detected intraoperatively the sensitivity for iatrogenic pedicel perforation with a hand-held electronic conductivity measurement device (ECD) that measures electrical conductivity of tissue-medium surrounding the instrument tip. ECD was used to guide the placement of 84 pedicle screws in 15 patients undergoing surgery for tumor or degenerative spinal disease at various spinal levels from T8 to L5. Additionally a CT-scan controlled screw positioning postoperatively. Results. The placement was "correct" (no mediocaudal pedicle wall penetration) for 78 of 84 (92,8%) screws, "suboptimal but acceptable" (0-2 mm penetration) for 4 of 84 (4,8%) screws, and "misplaced" (penetration > 2 mm) for 2 of 84 (2,4%) screws. Conclusion. Although this study was not designed to compare electronic conductivity technique to other guidance methods, such as fluoroscopy or navigation, a convincing "proof of concept" for ECD use in spinal instrumentation could be demonstrated. Advantages include easy handling without time-consuming setup and reduced X-ray exposure. However, further investigations are necessary to evaluate i.a. the economic aspects for this single-use developed instrument.

Transient sacroiliac joint-related pain is a common problem following lumbar decompressive surgery without instrumentation.

OBJECTIVE: Patients with lumbar stenosis profit substantially from decompressive surgery. The change of body position and walking behaviour after successful surgery might lead to changed force effects on the entire spine and on the sacroiliac joint (SIJ). We analyzed the incidence of postoperative SIJ-related pain. METHODS: The authors analyzed the records of 100 consecutive patients from three institutions, who underwent decompressive surgery without instrumentation. The diagnosis of SIJ-related pain was confirmed by periarticular infiltration. The radiological changes of the sacroiliac joint were assessed in plain radiographs in both groups: patients with SIJ pain (group 1) and patients without SIJ pain (group 2) after surgery. RESULTS: 22 patients required medical attention due to SIJ-related pain after surgery. While the walking distance increased substantially in both groups without difference (p=0.150), the analysis of overall satisfaction favoured group 2 (p=0.047). Female patients suffered more from SIJ pain after surgery (p=0.036). Age, severity of radiological changes or number of operated segments appeared not to trigger SIJ-related pain. CONCLUSION: The adaptation of a changed body posture and gait could lead to transient overload of the SIJ and surrounding myofascial structures. The patients should be informed about this possible condition to avoid uncertainty, discontent, unnecessary diagnostics and to induce a quick, specific treatment. Non-diagnosed sacroiliac joint-related pain could be a possible, but reversible reason for the diagnosis of a "failed-back-surgery".

Application of titanium and polyetheretherketone cages in the treatment of pyogenic spondylodiscitis.

OBJECTIVE: Surgical treatment of a pyogenic spondylodiscitis (PSD) involves a fixation and debridement of the affected segment combined with a specific antibiotic therapy. To achieve a proper stability and to avoid pseudarthrosis and kyphotic malposition many surgeons favour the interposition of an anterior graft. Besides autologous bone grafts titanium (TTN) cages have gained acceptance in the treatment of PSD. Polyetheretherketone (PEEK) cages have a more favourable modulus of elasticity than TTN. We compared both cage types. Primary endpoints were the rate of reinfection and radiological results. METHODS: From 2004 to 2013 51 patients underwent surgery for PSD with fixation and TTN or PEEK cage-implantation. While lumbar patients underwent a partial discectomy by the posterior approach, discs of the cervical and thoracic patients had been totally removed from anterior. Clinical and radiological parameters were assessed in 37 eligible patients after a mean of 20.4 months. 21 patients received a PEEK- and 16 patients a TTN-cage. RESULTS: A reinfection after surgery and 3 months of antibiotic therapy was not observed. Solid arthrodesis was found in 90.5% of the PEEK-group and 100% of the TTN-group. A segmental correction could be achieved in both groups. Nonetheless, a cage subsidence was observed in 70.3% of all cases. Comparison of radiological results revealed no differences between both groups. CONCLUSIONS: A debridement and fixation with anterior column support in combination with an antibiotic therapy appear to be the key points for successful treatment of PSD. The application of TTN- or PEEK-cages does not appear to influence the radiological outcome or risk of reinfection, neither does the extent of disc removal in this clinical subset.

Multiple reimplantation technique for treatment of complex giant aneurysms of the middle cerebral artery: technical note.

BACKGROUND: Giant middle cerebral artery (MCA) aneurysms are among the most challenging neurovascular lesions, especially when the M2 and M3 branches are incorporated into the aneurysm. Here we report on two cases with complex MCA aneurysms, in which double and triple arterial reimplantation of the efferent vessels into a saphenous vein graft (SVG) was applied to reconstruct the MCA tree, allowing final trapping of the aneurysm. METHODS: In the first case, a 41-year-old woman presented with a partially thrombosed giant MCA aneurysm including three efferent branches. Two superior trunks were disconnected and reimplanted onto an SVG fed by the external carotid artery (ECA). Following anastomosis between the SVG and the inferior trunk, the aneurysm was trapped. The second case is a 67-year-old man with recurrent giant MCA aneurysm incorporating two efferent M2 branches. First, the superior trunk was reimplanted onto an SVG, then the SVG was anastomosed to the inferior trunk. Finally the afferent M1 was clipped. Intraoperative indocyanine green (ICG) videoangiography (FLOW 800) was used for studying bypass patency. RESULTS: In both cases, successful bypass patency was demonstrated by ICG videoangiography. Postoperative digital subtraction angiography (DSA) confirmed bypass patency. The first case was discharged without any neurological deficit. The second case suffered from bleeding due to refilling of the aneurysm via the inferior M2. An additional clip was placed on the inferior M2 in a second step. The patient was discharged with weakness of the left arm. CONCLUSION: Reconstructing an MCA bifurcation or trifurcation combining multiple arterial reimplantation is effective for treatment of selective cases of complex MCA aneurysms.

Endocannabinoids mediate neuroprotection after transient focal cerebral ischemia.

The endocannabinoids anandamide (AEA) and palmitoylethanolamide (PEA) act as endogenous protective factors of the brain, using different pathways of neuroprotection against neuronal damage. Although several in vivo and in vitro studies confirmed the neuroprotective efficacy of endocannabinoids, no experimental settings compare and explore the neuroprotective potential of AEA and PEA in an acute stroke model. In this study, we investigated the neuroprotective potential by infarct measurement after high (30 mg/kg body weight) and low dosage administration (10 mg/kg body weight) of the endocannabinoid PEA in 49 male Wistar rats. In additions we studied infarct volumes of 22 male Wistar rats receiving the endocannabinoid AEA with a dosage of 10 mg/kg body weight or placebo. The neurological outcome was assessed 24 h after ischemia. Endocannabinoids were given intraperitoneally 30 min after initiation of transient middle cerebral artery occlusion (tMCAO). Infarct volume was calculated on the basis of 2.3.5-triphenyltetrazolium chloride staining. In the PEA high-dose group a significant total infarct reduction of 35% compared to the control group could be observed. AEA-treated rats presented a total infarct reducing effect of 26% compared to controls. Neurological scores, evaluated 24 h after tMCAO and physiological parameters, obtained 45 and 90 min after onset of ischemia showed no significant differences among the groups. As shown here, the endocannabinoids AEA and PEA achieved a significant neuroprotective effect by reducing size of infarcted tissue after tMCAO. Both endocannabinoids may have the potential to treat acute stroke and exert neuroprotection through a variety of mechanisms.

Neuroprotective cannabinoid receptor antagonist SR141716A prevents downregulation of excitotoxic NMDA receptors in the ischemic penumbra.

Whether cannabinoids act as neuroprotectants or, on the contrary, even worsen neuronal damage after cerebral ischemia is currently under discussion. We have previously shown that treatment with the cannabinoid (CB1) receptor antagonist SR141716A reduces infarct volume by approximately 40% after experimental stroke. Since it is suggested that SR141716A may exert neuroprotection besides its cannabinoid receptor-blocking effect, we addressed the question whether SR141716A may act via modulation of postischemic ligand binding to excitatory NMDA and/or alpha-amino-3-hydroxy-5-methyl-4-isoxazole-proprionic acid (AMPA) receptors. For this purpose, rats (n = 12) were treated with either intravenous saline (control) or CB1 receptor antagonist SR141716A (1 mg/kg) 30 min after permanent middle cerebral artery occlusion. Five hours after ischemia, quantitative receptor autoradiography was performed using [(3)H]CP 55,940, [(3)H]MK-801, and [(3)H]AMPA for labeling of CB1, NMDA, and AMPA receptors, respectively. Ligand binding was analyzed within the infarct core, cortical penumbra, and corresponding areas of the contralateral hemisphere and compared to that of sham-operated rats (n = 5). Both in ischemic controls and SR141716A-treated rats [(3)H]CP 55,940 ligand binding was not specifically regulated in the cortical penumbra or contralateral cortex. Importantly, reduced infarct volumes in SR141716A-treated rats were associated with maintained [(3)H]MK-801 binding to excitotoxic NMDA receptors in the penumbra, compared to a decrease in the control group. In summary, our data suggest that SR141716A may possess additional intrinsic neuroprotective properties independent of receptor-coupled pathways or due to action as a partial agonist.

Short-term ischemia usually used for ischemic preconditioning down-regulates central cannabinoid receptors in the gerbil hippocampus.

Transient forebrain ischemia of 5-min duration causes delayed neuronal death (DND) of vulnerable CA1 neurons in the gerbil hippocampus, which can be prevented by "preconditioning" with a short ischemic stimulus of 2.5-min duration. While a key role of excitatory glutamate receptors for both phenomena has been widely accepted, little is known about the postischemic regulation of central cannabinoid (CB1) receptors. The present study was designed to test whether ischemic preconditioning is associated with specific alterations of protein expression and/or ligand binding of these receptors compared to ischemia severe enough to induce DND. Gerbils were subjected to either a 5-min ischemic period resulting in DND of CA1 neurons, or a 2.5-min period of ischemia usually used for preconditioning. Postischemic hippocampal CB1 receptor protein expression was investigated immunohistochemically, while postischemic ligand binding of [3H]CP 55940 to CB1 receptors was analyzed by quantitative receptor autoradiography in both experimental groups after 24, 48, and 96 h (n=4-5 per time point), respectively, and compared to sham-treated gerbils (n=10). Short-term ischemia of 2.5-min duration caused a transient reduction of hippocampal CB1 receptor protein expression, while receptor binding density was permanently decreased. In contrast, 5-min ischemia did not alter protein expression or ligand binding up to 48 h. Based on these data, postischemic down-regulation of hippocampal CB1 receptors, specifically seen after short-term ischemia usually used for preconditioning, may participate in the mechanisms of endogenous postischemic neuroprotection.