Posterior Quadrant Disconnection Procedure for Intractable Epilepsy: A Case Series of 5 Young Pediatric Patients.

BACKGROUND: Posterior quadrant disconnection (PQD) has been described as a treatment for patients with refractory posterior quadrant subhemispheric epilepsy. Surgical outcomes are difficult to interpret because of limited literature. OBJECTIVE: To provide insight regarding the operative technique and postsurgical seizure freedom in young pediatric patients who underwent surgical disconnection for the treatment of posterior quadrant subhemispheric epilepsy at our institution. METHODS: The authors retrospectively analyzed a series of 5 patients who underwent PQD between 2019 and 2021. Charts were reviewed for preoperative workup including noninvasive/invasive testing, operative reports, and postoperative follow-up data which included degree of seizure freedom, completion of disconnection, and complications. RESULTS: Five patients were included in this series. The median age at seizure onset was 12 months (range 3-24 months), and the median age at surgery was 36 months (range 22-72 months). Histopathology confirmed focal cortical dysplasia in 3 of 5 patients (2 patients with type IB; 1 with type IIID). The average length of follow-up after surgery was 16.8 months (range 12-24 months). All patients underwent complete disconnection of the posterior quadrant without complications. Four of 5 patients (80%) had Engel score of I, while the remaining patient had an Engel score of IIB. CONCLUSION: Our early results demonstrate that complete PQD can be successful at providing excellent seizure freedom and functional outcomes in carefully selected young pediatric patients who have concordant seizure semiology, noninvasive/invasive testing, and imaging findings with primary seizure onset zone within the ipsilateral posterior quadrant. Meticulous surgical planning and thorough understanding of the surgical anatomy and technique are critical to achieving complete disconnection.

Spinal cord stimulation failure: evaluation of factors underlying hardware explantation.

OBJECTIVE: Spinal cord stimulation has been shown to improve pain relief and reduce narcotic analgesic use in cases of complex refractory pain syndromes. However, a subset of patients ultimately undergoes removal of the spinal cord stimulator (SCS) system, presumably because of surgical complications or poor efficacy. This retrospective study addresses the paucity of evidence regarding risk factors and underlying causes of spinal cord stimulation failures that necessitate this explantation. METHODS: In this retrospective single-center review, 129 patients underwent explantation of SCS hardware during a 9-year period (2005-2013) following initial placement at the authors' institution or elsewhere. Medical history, including indication of implantation, device characteristics, revision history, and reported reasons for removal of hardware, were reviewed. RESULTS: The 74 (57%) women and 55 (43%) men were a median of 49 years old (IQR 41-61 years) at explantation; the median time to explantation was 20 months (IQR 7.5-45.5 months). Thoracic or upper lumbar leads were placed in 89.9% of patients primarily for the diagnosis of postsurgical failed-back surgery syndrome (70.5%), chronic regional pain syndrome (14.7%), and neuropathic pain (8.5%). More than half of patients were legally disabled. Initial postoperative reduction in pain was reported in 81% of patients, and 37.8% returned to work. Among 15 patients with acute postsurgical complications (12 infections, 2 hemorrhages, 1 immediate paraplegia), the median time to removal was 2 months. Primary reasons for hardware removal were lack of stimulation efficacy (81%), electrode failure due to migration (14%), and allergic reactions to implanted hardware in 2 patients. The 72 patients who underwent formal psychiatric evaluation before implantation were affected by high rates of major depression (64%), anxiety (34%), posttraumatic stress disorder (PTSD) (12%), drug or alcohol abuse (12%), and physical or sexual abuse (22%). CONCLUSIONS: The authors' findings provide insight regarding the mechanisms of spinal cord stimulation failure that resulted in total removal of the implanted system. The relationship between spinal cord stimulation failure and certain psychiatric disorders, such as PTSD, depression, and anxiety, is highlighted. Ultimately, this work may shed light on potential avenues to reduce morbidity and improve patient outcomes.

Management of autonomic dysreflexia associated with Charcot spinal arthropathy in a patient with complete spinal cord injury: Case report and review of the literature.

BACKGROUND: Charcot spinal arthropathy (CSA) clearly represents a challenge in long-term spinal cord injury patients, one that can have extremely uncomfortable and potentially lethal outcomes if not managed properly. CASE DESCRIPTION: A 66-year-old man with a history of complete C7 quadriplegia presented with new-onset autonomic dysreflexia that resulted from Charcot spinal arthropathy (CSA). Pathologic instability, in the atypical site of the mid-thoracic spine, spanning from the T8-T9 vertebral levels was appreciated on physical exam as an audible, palpable, and visible dynamic kyphosis; kyphosis was later confirmed on neuroimaging. Based on the CSA severity and sequelae, the patient underwent bilateral decompression laminectomy with lateral extracavitary arthrodesis and posterior instrumentation. Symptoms dramatically improved and at 1-year follow-up, dynamic thoracic kyphosis and most symptoms of autonomic dysreflexia had resolved. CONCLUSIONS: Based on our case and published reports, vigilant imaging and thorough physical examination in long-standing spinal cord injury could help early diagnosis and treatment of CSA, theoretically preventing development of cord atrophy and subsequent long-term sequelae. Surgical correction rather than bracing may be recommended in patients who have complete injury at or above T6 in patients with symptoms of autonomic dysreflexia associated with CSA confirmed on neuroimaging.

Pia Mater Significantly Contributes to Spinal Cord Intraparenchymal Pressure in a Simulated Model of Edema.

STUDY DESIGN: Intraparenchymal pressure (IPP) measurements in an in vitro cadaveric model of CNS edema. OBJECTIVE: To assess the contribution of pia mater to IPP and the effect of piotomy. SUMMARY OF BACKGROUND DATA: Multicenter randomized control trials have shown that decompression with durotomy/duroplasty significantly decreases intracranial pressure (ICP). There is a paucity of evidence regarding the effectiveness of decompression of the spinal cord by piotomy. METHODS: The supratentorial brain and spinal cord were removed from six fresh cadavers. Dura and arachnoid mater were removed. ICP monitors were placed bilaterally in the frontal and parietal lobes, and centrally in the cervical and thoracic spinal cord. To simulate edema, specimens were submerged in hypotonic solution. IPP was recorded for 5 days. A complete dorsal midline piotomy was performed on the spinal cord and resulting IPP was recorded. RESULTS: Brain and spinal cord both increased in weight. IPP significantly increased in both brain and spinal cord. The IPP increase within the spinal cord was substantially greater (averages: all four lobes = 4.0 mm Hg; cervical = 73.7 mm Hg; thoracic = 49.3 mm Hg). After piotomy, cervical and thoracic spinal cord IPP decreased immediately (avg. postpiotomy IPP = 9.7 and 10.3, respectively). CONCLUSION: There were differential effects on brain and spinal cord IPP. Brain IPP increased only slightly, possibly because of the absence of the cranium and dura mater. In contrast, spinal cord IPP increased substantially even in the absence of the laminae, dura, and arachnoid mater. Piotomy immediately and dramatically reduced spinal cord IPP. These data are consistent with the hypothesis that spinal cord IPP is primarily dependent on constraints imposed by the pia mater. Conversely, in the absence of the cranium and dura mater, the sulci may permit the pia-invested brain to better accommodate edema without significant increases in IPP. LEVEL OF EVIDENCE: N/A.

Real-time monitoring of extracellular adenosine using enzyme-linked microelectrode arrays.

Throughout the central nervous system extracellular adenosine serves important neuroprotective and neuromodulatory functions. However, current understanding of the in vivo regulation and effects of adenosine is limited by the spatial and temporal resolution of available measurement techniques. Here, we describe an enzyme-linked microelectrode array (MEA) with high spatial (7500 µm(2)) and temporal (4 Hz) resolution that can selectively measure extracellular adenosine through the use of self-referenced coating scheme that accounts for interfering substances and the enzymatic breakdown products of adenosine. In vitro, the MEAs selectively measured adenosine in a linear fashion (r(2)=0.98±0.01, concentration range=0-15 µM, limit of detection =0.96±0.5 µM). In vivo the limit of detection was 0.04±0.02 µM, which permitted real-time monitoring of the basal extracellular concentration in rat cerebral cortex (4.3±1.5 µM). Local cortical injection of adenosine through a micropipette produced dose-dependent transient increases in the measured extracellular concentration (200 nL: 6.8±1.8 µM; 400 nL: 19.4±5.3 µM) [P<0.001]. Lastly, local injection of dipyridamole, which inhibits transport of adenosine through equilibrative nucleoside transporter, raised the measured extracellular concentration of adenosine by 120% (5.6→12.3 µM) [P<0.001]. These studies demonstrate that MEAs can selectively measure adenosine on temporal and spatial scales relevant to adenosine signaling and regulation in normal and pathologic states.