Many procedures in modern clinical medicine rely on the use of electronic implants in treating conditions that range from acute coronary events to traumatic injury. However, standard permanent electronic hardware acts as a nidus for infection: bacteria form biofilms along percutaneous wires, or seed haematogenously, with the potential to migrate within the body and to provoke immune-mediated pathological tissue reactions. The associated surgical retrieval procedures, meanwhile, subject patients to the distress associated with re-operation and expose them to additional complications. Here, we report materials, device architectures, integration strategies, and in vivo demonstrations in rats of implantable, multifunctional silicon sensors for the brain, for which all of the constituent materials naturally resorb via hydrolysis and/or metabolic action, eliminating the need for extraction. Continuous monitoring of intracranial pressure and temperature illustrates functionality essential to the treatment of traumatic brain injury; the measurement performance of our resorbable devices compares favourably with that of non-resorbable clinical standards. In our experiments, insulated percutaneous wires connect to an externally mounted, miniaturized wireless potentiostat for data transmission. In a separate set-up, we connect a sensor to an implanted (but only partially resorbable) data-communication system, proving the principle that there is no need for any percutaneous wiring. The devices can be adapted to sense fluid flow, motion, pH or thermal characteristics, in formats that are compatible with the body's abdomen and extremities, as well as the deep brain, suggesting that the sensors might meet many needs in clinical medicine.

Nonhemorrhagic neurological deficits are underrecognized symptoms of intracranial dural arteriovenous fistulas (dAVFs) having cortical venous drainage. These symptoms are the consequence of cortical venous hypertension and portend a clinical course with increased risk of neurological morbidity and mortality. One rarely documented and easily misinterpreted type of nonhemorrhagic neurological deficit is progressive dementia, which can result from venous hypertension in the cortex or in bilateral thalami. The latter, which is due to dAVF drainage into the deep venous system, is the less common of these 2 dementia syndromes. Herein, the authors report 4 cases of dAVF with venous drainage into the vein of Galen causing bithalamic edema and rapidly progressive dementia. Two patients were treated successfully with endovascular embolization, and the other 2 patients were treated successfully with endovascular embolization followed by surgery. The radiographic abnormalities and presenting symptoms rapidly resolved after dAVF obliteration in all 4 cases. Detailed descriptions of these 4 cases are presented along with a critical review of 15 previously reported cases. In our analysis of these 19 published cases, the following were emphasized: 1) the clinical and radiographic differences between dAVF-induced thalamic versus cortical dementia syndromes; 2) the differential diagnosis and necessary radiographic workup for patients presenting with a rapidly progressive thalamic dementia syndrome; 3) the frequency at which delays in diagnosis occurred and potentially dangerous and avoidable diagnostic procedures were used; and 4) the rapidity and completeness of symptom resolution following dAVF treatment.http://thejns.org/doi/abs/10.3171/2015.5.JNS15473Key words dural arteriovenous fistula; cortical venous hypertension; thalamic edema; nonhemorrhagic neurological deficit; thalamic dementia; vascular disorders ©AANS, 2016 davF-induced thalamic dementiaBorden-Shucart classification system-based not only on angiographic appearance but also mode of presentationto permit more accurate risk stratification and assist with clinical decision making for the type and timing of dAVF treatment (Table 1). 68,91One relatively underappreciated type of NHND is progressive dementia resulting from dAVF-induced cortical venous hypertension, though correct diagnosis and treatment is increasing, thanks to improved imaging techniques.18,79 Dural AVF-induced progressive dementia can be differentiated as either cortical or thalamic in origin-2 categories that have relatively distinct patterns of clinical symptomatology 18,54,62,80,85 and highly specific venous outflow patterns.18,80 Of the two, dAVFinduced thalamic dementia is less frequent, with only 15 published cases reported in the literature to date. All were individual case reports, and several lacked adequate clinical, radiographic, and/or treatment specifics to permit detailed assessment as to manner of presentation, underlying hemodynamic pathophysiology, and long-term outcome. 18,[21][22][23]...

Despite 253,000 spinal cord injury (SCI) patients in the United States, little is known about how SCI affects brain networks. Spinal MRI provides only structural information with no insight into functional connectivity. Resting-state functional MRI (RS-fMRI) quantifies network connectivity through the identification of resting-state networks (RSNs) and allows detection of functionally relevant changes during disease. Given the robust network of spinal cord afferents to the brain, we hypothesized that SCI produces meaningful changes in brain RSNs. RS-fMRIs and functional assessments were performed on 10 SCI subjects. Blood oxygen-dependent RS-fMRI sequences were acquired. Seed-based correlation mapping was performed using five RSNs: default-mode (DMN), dorsal-attention (DAN), salience (SAL), control (CON), and somatomotor (SMN). RSNs were compared with normal control subjects using false-discovery rate-corrected two way t tests. SCI reduced brain network connectivity within the SAL, SMN, and DMN and disrupted anti-correlated connectivity between CON and SMN. When divided into separate cohorts, complete but not incomplete SCI disrupted connectivity within SAL, DAN, SMN and DMN and between CON and SMN. Finally, connectivity changed over time after SCI: the primary motor cortex decreased connectivity with the primary somatosensory cortex, the visual cortex decreased connectivity with the primary motor cortex, and the visual cortex decreased connectivity with the sensory parietal cortex. These unique findings demonstrate the functional network plasticity that occurs in the brain as a result of injury to the spinal cord. Connectivity changes after SCI may serve as biomarkers to predict functional recovery following an SCI and guide future therapy.

LITT with intraoperative MRI and stereotactic image guidance is a newly available, minimally invasive, and therapeutically viable technique for the treatment of deep seated brain tumors.

Cervical spondylotic myelopathy (CSM) refers to impaired function of the spinal cord caused by degenerative changes of the cervical spine resulting in spinal cord compression. It is the most common disorder in the United States causing dysfunction of the spinal cord. A literature review of the natural history of mild cervical myelopathy is undertaken. Clinical presentation and current concepts of pathophysiology are also discussed. While many patients with mild signs of CSM will stabilize or improve over time with conservative treatment, the clinical course of a specific individual patient cannot be predicted. Asymptomatic patients with cervical stenosis and abnormalities on electrophysiologic studies may be at higher risk for developing myelopathy.

Object External ventricular drains (EVDs) are commonly used for CSF diversion but pose a risk of ventriculitis, with rates varying in frequency from 2% to 45%. Results of studies examining the utility of prolonged systemic antibiotic therapy for the prevention of EVD-related infection have been contradictory, and no study to date has examined whether this approach confers additional benefit in preventing ventriculitis when used in conjunction with antibiotic-coated EVDs (ac-EVDs). Methods A prospective performance analysis was conducted over 4 years to examine the impact of discontinuing systemic antibiotic prophylaxis after insertion of an ac-EVD on rates of catheter-related ventriculitis. Ventriculitis and other nosocomial infections were ascertained by a qualified infection disease nurse using definitions based on published standards from the Centers for Disease Control and Prevention, comparing the period when patients received systemic antibiotic therapy for the duration of EVD treatment (Period 1) compared with only for the peri-insertion period (Period 2). Costs were analyzed and compared across the 2 time periods Results Over the 4-year study period, 866 patients were treated with ac-EVDs for a total of 7016 catheter days. There were 8 cases of ventriculitis, for an overall incidence of 0.92%. Rates of ventriculitis did not differ significantly between Period 1 and Period 2 (1.1% vs 0.4%, p = 0.22). The rate of nosocomial infections, however, was significantly higher in Period 1 (2.0% vs 0.0% in Period 2, p = 0.026). Cost savings of $162,516 were realized in Period 2 due to decreased drug costs and savings associated with the reduction in nosocomial infections. Conclusions Prolonged systemic antibiotic therapy following placement of ac-EVDs does not seem to reduce the incidence of catheter-related ventriculitis, and was associated with a higher rate of nosocomial infections and increased cost.

Study Design Prospective Cohort Study Objective In this study, we employed diffusion basis spectrum imaging (DBSI) to quantitatively assess axon/myelin injury, cellular inflammation, and axonal loss of cervical spondylotic myelopathy (CSM) spinal cords. Summary of Background Data A major shortcoming in the management of CSM is the lack of an effective diagnostic approach to stratify treatments and to predict outcomes. No current clinical diagnostic imaging approach is capable of accurately reflecting underlying spinal cord pathologies. Methods Seven patients with mild (mJOA ≥ 15), five patients with moderate (14≥ mJOA ≥ 11), and two patients with severe (mJOA <11) CSM were prospectively enrolled. Given the low number of severe patients, moderate and severe patients were combined for comparison with seven age matched controls and statistical analysis. We employed the newly developed DBSI to quantitatively measure axon and myelin injury, cellular inflammation, and axonal loss. Results Median DBSI-inflammation volume is similar in control (266 μL) and mild CSM (171 μL) subjects, with significant overlap of the middle 50% of observations (quartile 3 – quartile 1). This was in contrast to moderate CSM subjects that had higher DBSI-inflammation volumes (382 μL; p = 0.033). DBSI-axon volume shows a strong correlation with clinical measures (r = 0.79 and 0.87, p = 1.9 × 10-5 and 2 × 10-4 for mJOA and MDI respectively. In addition to axon and myelin injury, our findings suggest that both inflammation and axon loss contribute to neurological impairment. Most strikingly, diffusion basis spectrum imaging derived axon volume declines as severity of impairment increases Conclusion DBSI quantified axonal loss may be an imaging biomarker to predict functional recovery following decompression in cervical spondylotic myelopathy. Our results demonstrate an increase of about 60% in the odds of impairment relative to the control for each decrease of 100 μL in axon volume.

Complete loss of median nerve motor function is a rare but devastating injury. Loss of median motor hand function and upper-extremity pronation can significantly impact a patient's ability to perform many activities of daily living independently. The authors report the long-term follow-up in a case of median nerve motor fiber transection that occurred during an arthroscopic elbow procedure, which was then treated with multiple nerve transfers. Motor reconstruction used the nerves to the supinator and extensor carpi radialis brevis to transfer to the anterior interosseous nerve and pronator. Sensory sensation was restored using the lateral antebrachial cutaneous (LABC) nerve to transfer to a portion of the sensory component of the median nerve, and a second cable of LABC nerve as a direct median nerve sensory graft. The patient ultimately recovered near normal motor function of the median nerve, but had persistent pain symptoms 4 years postinjury.