Implant failure following pedicle based dynamic stabilization of the lumbar spine.

Pedicle-based dynamic stabilization (PBDS) devices such as Dynesys are promoted as an alternative and less invasive option for rigid stabilization of one and even more levels of the lumbar spine. Promising features of the Dynesys system, as well as shortcomings, became obvious in several clinical studies. Since 2012, we started using a new PBDS device as an alternative for the Dynesys, to avoid the screw loosening and the kyphosing effect. The objective is to compare failure rates between the Dynesys and Balan-C type PBDS implant and factors affecting outcome. In a retrospective study we investigated a total of 90 patients with lumbar pedicle screw dynamic stabilization (a group of 64 patiënts with Dynesys stabilization is compared to a group of 26 patients with Balan-C stabilization). Mean follow-up was 48 and 38 months, respectively. Using logistic regression analysis the impact of baseline characteristics such as gender, age, body mass index (BMI), indication for surgery, primary or revision surgery, single versus more level surgery, surgeon's experience and type of the implant on implant failure was analyzed. We found a statistically significant difference in failure rates between the two systems (13% in the Dynesys group versus 62% in the Balan-C group). In multivariate analysis, type of implant was associated with implant failure (odds ratio : 13). Our current results call for an optimization of the pre-and post-marketing surveillance of pedicle-based dynamic stabilization.

Return to Work of Patients Treated With Spinal Cord Stimulation for Chronic Pain: A Systematic Review and Meta-Analysis.

BACKGROUND: Chronic pain has a substantial negative impact on work-related outcomes, which underscores the importance of interventions to reduce the burden. Spinal cord stimulation (SCS) efficiently causes pain relief in specific chronic pain syndromes. The aim of this review was to identify and summarize evidence on returning to work in patients with chronic pain treated with SCS. MATERIALS AND METHODS: A systematic literature review was performed including studies from PubMed, EMBASE, SCOPUS, and Web of Science (up till October 2017). Risk of bias was assessed using a modified version of the Downs & Black checklist. Where possible, we pooled data using random effects meta-analysis. The study protocol was registered prior to initiation of the review process (PROSPERO CRD42017077803). RESULTS: Fifteen full-text articles (total articles screened: 2835) were included. Risk of bias for these articles was scored low. Seven trials provided sufficient data and were judged similar enough to be pooled for meta-analysis on binary outcomes. SCS intervention results in a higher prevalence of patients at work compared with before treatment (odds ratio [OR] 2.15; 95% confidence interval [CI], 1.44-3.21; I2 = 42%; p < 0.001). SCS treatment also results in high odds to return to work (OR 29.06; 95% CI, 9.73-86.75; I2 = 0%; p < 0.001). CONCLUSIONS: Based on available literature, SCS proved to be an effective approach to stimulate return to work in patients with specific chronic pain syndromes.

Interventions to promote work participation after ischaemic stroke: A systematic review.

Only a disappointingly low proportion of patients successfully engage in professional activities after ischaemic stroke. This systematic review maps all contemporary evidence regarding interventions aiming to promote return-to-work in survivors of ischaemic stroke. We performed a search according to Preferred Reporting Items for Systematic Review and Meta-Analyses guidelines and searched five reference databases. Prospective trial registers and grey literature were also assessed, and we executed backwards and forward reference searching. The study protocol was registered in PROSPERO (CRD42017077796). The search yielded 444 records of which 174 were duplicates. Backward and forward reference searching resulted in 808 unique records. Eleven articles were retained for full-text analysis and two met the selection criteria. A controlled before-after study showed beneficial effects of intravenous thrombolytic treatment in patients with moderate to severe acute ischaemic stroke. A retrospective study with low methodological quality reported improved vocational outcome of an outpatient rehabilitation program in patients with mild to moderate ischaemic stroke. We conclude that there currently is insufficient evidence regarding the effectiveness of interventions to promote return-to-work in patients with ischaemic stroke, though intravenous thrombolytic therapy has shown beneficial effects and there are indications that rehabilitation programs may also be advantageous.

Pentobarbital fails to reduce cerebral oxygen consumption early after non-hemorrhagic closed head injury in rats.

It is unknown whether barbiturates suppress cerebral oxygen metabolism after cerebral trauma as they do in normal individuals. We evaluated the influence of pentobarbital on cerebral oxygen handling of normal rats and rats subjected to non-hemorrhagic closed head injury (CHI). Oxygen delivery was assessed by measuring cerebral perfusion and oxygen extraction, enabling the calculation of cerebral metabolic rate of oxygen (CMRO2). Mitochondrial function was assessed by studying changes in the oxidized cytochrome oxidase concentration. CHI caused changes in both systemic and cerebral hemodynamics. Cerebral blood flow was reduced to 66% of its control value, but the cerebral metabolic rate of oxygen remained unchanged. Pentobarbital administration induced a significant lowering of the cerebral oxygen consumption in normal rats associated with a secondary decrease in cerebral perfusion. In rats subjected to CHI, pentobarbital was unable to lower the cerebral metabolic demand and did not cause a further decrease in perfusion. Pentobarbital was unable to significantly modulate mitochondrial function in traumatized rats, whereas it exerted this effect in all control animals. We therefore conclude that, in rats subjected to CHI, pentobarbital is unable to perform its beneficial effects on the cerebral metabolism.

Transcranial magnetic stimulation for tinnitus: influence of tinnitus duration on stimulation parameter choice and maximal tinnitus suppression.

OBJECTIVE: Tinnitus is a distressing symptom for which few treatments exist. It leads to an important decrease in quality of life in 2 to 3% of the population. Tinnitus is considered a phantom sound, the result of cortical reorganization. Transcranial magnetic stimulation (TMS) is a noninvasive method to modulate cortical reorganization and has been shown to be able to influence tinnitus perception. STUDY DESIGN: Retrospective analysis. SETTING: Tertiary referral center. PATIENTS: The effect of TMS of the contralateral auditory cortex in 114 patients with unilateral tinnitus is investigated as one of the selection criteria used for surgical implantation of electrodes on the auditory cortex. INTERVENTION: TMS is performed at 90% of motor threshold at 1, 3, 5, 10, and 20 Hz, with each stimulation session consisting of 200 pulses. Results were classified as no effect (0-19% improvement), partial effect (20-79% improvement), and good effect (80-100 suppression). MAIN OUTCOME MEASURES: TMS had a good effect in 25% of the patients studied, partial effect in 28% patients, and no effect in 47%. RESULTS: TMS at 200 pulses is capable of tinnitus suppression for seconds only. The results were influenced by tinnitus duration: the longer the tinnitus exists, the lower the stimulation frequency that yields maximal tinnitus suppression (p < 0.001). The maximal amount of tinnitus suppression decreases in time (p < 0.01), resulting in a 2% decrease of potential tinnitus suppression per year. CONCLUSION: TMS of the auditory cortex is capable of modifying tinnitus perception for a very short time. The maximal amount of suppression and best stimulation frequency depends on the tinnitus duration.

Brainstem hemorrhage in descending transtentorial herniation (Duret hemorrhage).

OBJECTIVES: To review clinical and radiological findings in patients with Duret hemorrhages and to discuss the pathophysiology and differential diagnosis of these lesions. PATIENTS AND METHODS: We reviewed the case records of four patients with Duret hemorrhages who had been admitted to the neurological intensive care unit with supratentorial mass lesions. RESULTS: Descending transtentorial and subfalcine herniations were present in all cases. Three patients were admitted with acute subdural hematoma and one with intraparenchymal hemorrhage. Computed tomography revealed the presence of blood in the mesencephalon and upper pons. Three patients died; one survived with severe disabilities. DISCUSSION: Duret hemorrhages are typically located in the ventral and paramedian aspects of the upper brainstem (mesencephalon and pons). The pathophysiology of Duret hemorrhage remains under debate: arterial origin (stretching and laceration of pontine perforating branches of the basilar artery), versus venous origin (thrombosis and venous infarction). Multifactorial causation seems likely. CONCLUSION: Duret hemorrhages are delayed, secondary brainstem hemorrhages. They occur in craniocerebral trauma victims with rapidly evolving descending transtentorial herniation. Diagnosis is made on computed tomography of the brain. In most cases the outcome is fatal. On the basis of our observations we believe that arterial hypertension and advanced age are risk factors for the development of Duret hemorrhage.

Continuous measurement of intracranial pressure in awake rats after experimental closed head injury.

The present study validates a method for continuous measurement of intracranial pressure (ICP) in freely moving rats after experimental induction of impact-acceleration injury. Rats subjected to either mild or moderate trauma were individually placed in a Bas-Ratturn system, equipped with a sensor that synchronously turns the cage in response to the locomotor activity of the animal. In this way correct probe positioning is permanently assured and damage due to coiling is avoided. The evolution of ICP and mean arterial blood pressure (MABP) in injured rats was compared with that of a non-traumatized sham group. Since the animals regained consciousness after surgery, interference of anaesthesia on these sensitive parameters should be minimised. The results showed that immediately after induction of neurotrauma, ICP was significantly higher in traumatized rats (sham: 7.7 +/- 0.5 mmHg; mild trauma: 10.4 +/- 0.7 mmHg; moderate trauma: 14.9 +/- 2.4 mmHg; P<0.05). Regression analysis showed a stable ICP up to 3 h post-insult for all three conditions. From 4 h onwards till the end of the experiment at 10 h post-insult, a significant increase in ICP was seen for sham-operated and mildly traumatized rats (16.1 +/- 3.4 and 30.5 +/- 6.9 mmHg, respectively; P<0.05), but not for moderately traumatized rats (47.3 +/- 11.9 mmHg). The method allows observation of ICP for a critical period up to 3 h. As such the method can be regarded as clinically relevant to study early pathological aspects of intracranial hypertension and to define a therapeutic window for pharmacological intervention after traumatic brain injury (TBI).

Comparison of intracranial pressure measured in the cerebral cortex and the cerebellum of the rat.

In this study, we evaluated the accuracy of intracranial pressure (ICP) measurement in rats by insertion of a miniature ICP probe in the parenchyma of the cerebellum. A comparison was made between the ICP values measured simultaneously in the parenchyma of the cerebral cortex and the cerebellum. In order to obtain a wide range of ICP, animals were subjected to a severe closed head injury (CHI), a moderate CHI or to a sham operation. ICP values ranged from 0.8 to 43.9 mmHg. After 15 min stabilisation the first measurement was taken and followed by a second measurement 25 min after onset to allow comparison of ICP changes at the two implantation sites. Linear regression analysis showed a highly significant correlation at 15 min: Y = 0.919X + 0.655 (R(2) = 0.977), and at 25 min: Y = 0.931X + 0.698 (R(2) = 0.976). The differences in ICP measurement between cerebellar and cerebral site were not significantly different from zero at both time points. Altman-Bland plots showed that the difference in ICP readings between the two locations could differ maximally by 5.3 mmHg. The largest differences were detected when high ICP values were recorded. We conclude that in rats the ICP measurement in the cerebellum is comparable to the ICP measurement in the cerebral cortex. The cerebellar ICP can be used as a valuable alternative during experimental procedures.

Functional anatomy of the human cochlear nerve and its role in microvascular decompressions for tinnitus.

OBJECTIVE: The functional anatomy (i.e., tonotopy) of the human cochlear nerve is unknown. A better understanding of the tonotopy of the central nervous system segment of the cochlear nerve and of the pathophysiology of tinnitus might help to ameliorate the disappointing results obtained with microvascular decompressions in patients with tinnitus. METHODS: We assume that vascular compression of the cochlear nerve can induce a frequency-specific form of hearing loss and that when the nerve is successfully decompressed, this hearing loss can recuperate. Thirty-one patients underwent a microvascular decompression of the vestibulocochlear nerve for vertigo or tinnitus. Preoperative audiograms were subtracted from postoperative audiograms, regardless of the surgical result with regard to the tinnitus and vertigo, because the hearing improvement could be the only sign of the vascular compression. The frequency of maximal improvement was then correlated to the site of vascular compression. A tonotopy of the cochlear nerve was thus obtained. RESULTS: A total of 18 correlations can be made between the site of compression and postoperative maximal hearing improvement frequency when 5-dB hearing improvement is used as threshold, 13 when 10-dB improvement is used as threshold. A clear distribution can be seen, with clustering of low frequencies at the posterior and inferior side of the cochlear nerve, close to the brainstem, and close to the root exit zone of the facial nerve. High frequencies are distributed closer to the internal acoustic meatus and more superiorly along the posterior aspect of the cochlear nerve. CONCLUSION: The tonotopic organization of the cisternal segment of the cochlear nerve has an oblique rotatory structure as a result of the rotatory course of the cochlear nerve in the posterior fossa. Knowledge of this tonotopic organization of the auditory nerve in its cisternal course might benefit surgeons who perform microvascular decompression operations for the vestibulocochlear compression syndrome, especially in the treatment of unilateral severe tinnitus.

Is the root entry/exit zone important in microvascular compression syndromes?

OBJECTIVE: Microvascular compression syndromes such as trigeminal neuralgia, hemifacial spasm, and disabling positional vertigo involve an artery or vein compressing a cranial nerve. A cranial nerve is composed of a central nervous system (CNS) segment and a peripheral nervous system (PNS) segment separated by the root entry/exit zone (REZ). Although vascular compression can occur at any point along the cranial nerve, it has been generally assumed that only vascular contact at the REZ of the affected cranial nerve can cause symptoms. On the basis of personal surgical experience, we propose that vascular compression of the CNS segment alone causes symptoms. This has important repercussions for the future diagnosis and treatment of microvascular compression syndromes, especially the cochleovestibular compression syndrome. METHODS: For the anatomic study, four autopsy specimens and one surgical biopsy specimen of the vestibulocochlear nerve were microscopically and ultramicroscopically analyzed for structural differences between the CNS and PNS segments. For the clinical study, five patients with the clinical picture of cochleovestibular compression syndrome were treated by microsurgical decompression at the level of the CNS segment and not the REZ. One patient underwent reoperation for recurrent symptoms 4 years later, and a 4-mm vestibular neurectomy was performed at that stage. We performed an epidemiological analysis to demonstrate that the known incidences of trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are related to the length of their respective CNS segments. RESULTS: Histological differences between the PNS and CNS segments suggest that the PNS segment is more resistant to compression. This was confirmed by neurophysiological data from intraoperative monitoring in posterior fossa surgery and experimental studies. We found a clear epidemiological correlation between the length of the CNS segment, which differed among cranial nerves, and the incidence of the microvascular compression syndrome. Successful decompression of the CNS segment in patients without compression at the REZ of the vestibulocochlear nerve for disabling positional vertigo provides clinical support for this hypothesis. CONCLUSION: The evidence we present supports the hypothesis that vascular compression syndromes arise from vascular contact along the CNS segment of the cranial nerves.

Spatiotemporal pattern of neuroinflammation after impact-acceleration closed head injury in the rat.

Inflammatory processes have been implicated in the pathogenesis of traumatic brain damage. We analyzed the spatiotemporal expression pattern of the proinflammatory key molecules: interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, and inducible nitric oxide synthase in a rat closed head injury (CHI) paradigm. 51 rats were used for RT-PCR analysis after CHI, and 18 for immunocytochemistry. We found an early upregulation of IL-1beta, IL-6, and TNF-alpha mRNA between 1h and 7h after injury; the expression of iNOS mRNA only revealed a significant increase at 4h. After 24h, the expression decreased towards baseline levels, and remained low until 7d after injury. Immunocytochemically, IL-1beta induction was localized to ramified microglia in areas surrounding the primary impact place as well as deeper brain structures. Our study shows rapid induction of inflammatory gene expression that exceeds by far the primary impact site and might therefore contribute to tissue damage at remote sites.

Primary and secondary auditory cortex stimulation for intractable tinnitus.

INTRODUCTION: Recent research suggests tinnitus is a phantom phenomenon based on hyperactivity of the auditory system, which can be visualized by functional neuroimaging, and transiently modulated by transcranial magnetic stimulation (TMS). We present the results of the first implanted electrodes on the primary and secondary auditory cortex after a successful TMS suppression. METHODS AND MATERIALS: Twelve patients underwent an auditory cortex implantation, 10 for unilateral and 2 for bilateral tinnitus, based on >50% suppression applying TMS. Results were analyzed for pure tone tinnitus and white noise tinnitus. RESULTS: TMS results in 77% pure tone tinnitus and 67% white noise reduction. Electrical stimulation via an implanted electrode results in a mean of 97% pure tone tinnitus and 24% white noise suppression. Mean Visual Analogue Scale score decreases from 9.5 to 1.5 for pure tone and from 8.8 to 6.8 for white noise postoperatively. DISCUSSION: Pure tone tinnitus might be the conscious percept of focal neuronal hyperactivity of the auditory cortex. Once visualized, this hyperactivity can be modulated by neurostimulation. CONCLUSION: The preliminary results of the first implantations suggest that patients with unilateral pure tone tinnitus are good surgical candidates for electrode implantation and permanent electrical stimulation of the auditory cortex, provided that the tinnitus is of recent origin and can be suppressed by TMS.

Ultrasound agents may open the blood-brain barrier in rats and aggravate pathologic consequences of experimental head trauma.

Unilateral intracarotid injection of contrast agents may considerably destabilize the blood-brain barrier in rats. This leads to vasogenic edema in the ipsilateral hemisphere. Mortality and extravasation increased significantly when administration of these ultrasound contrast agents was followed by mild traumatic brain injury. Direct administration to the cerebral circulation is, therefore, indicative for edema-related pathology and may amplify the consequences of experimental neurotrauma.