Kushak Suchdev’s research while affiliated with Boston Medical Center and other places

Objectives Animal studies have suggested that valproic acid (VPA) is neuroprotective in aneurysmal subarachnoid hemorrhage (SAH). However, the effect of VPA on SAH outcomes in humans has not been investigated. Methods We conducted a retrospective analysis of 123 patients with nontraumatic SAH. Eighty-seven patients had an aneurysmal source and 36 patients had no culprit lesion identified. We used stepwise logistic regression to determine the association between VPA and delayed cerebral ischemia (DCI), radiographic vasospasm, and discharge modified Rankin Scale (mRS) score >3. Results All 18 patients who received VPA underwent coil embolization of their aneurysm. VPA use did not have a significant association with DCI on adjusted analysis (odds ratio [OR] = 1.07, 95% confidence interval [CI]: 0.20–5.80). The association between VPA use and vasospasm was OR = 0.64 (0.19–1.98) and discharge mRS > 3 was OR = 0.45 (0.10–1.64). Increased age (OR = 1.04, 1.01–1.07) and Hunt and Hess grade >3 (OR = 14.5, 4.31–48.6) were associated with poor discharge outcome (mRS > 3). Younger age (OR = 0.96, 0.93–0.99), modified Fisher Scale (mFS) score = 4 (OR = 4.14, 1.81–9.45), and Hunt and Hess grade >3 (OR = 2.92, 1.11–7.69) were all associated with development of radiographic vasospasm. There were no complications associated with VPA administration. Conclusions We did not observe an association between VPA and the rate of DCI. We found that VPA use was safe in SAH patients who have undergone endovascular treatment of their aneurysm.

Background and Purpose: Animal studies have suggested that valproic acid (VPA) is neuroprotective in aneurysmal subarachnoid hemorrhage (SAH). Potential mechanisms include an effect on cortical spreading depolarizations (CSD), apoptosis, blood–brain barrier integrity, and inflammatory pathways. However, the effect of VPA on SAH outcomes in humans has not been investigated. Methods: We conducted a retrospective analysis of 123 patients with nontraumatic SAH. Eighty–seven patients had an aneurysmal source and 36 patients did not have a culprit lesion identified. We used stepwise logistic regression to determine the association between VPA and the following: delayed cerebral ischemia (DCI), radiographic vasospasm, and discharge modified Rankin Scale (mRS) score > 3. Results: All 18 patients who received VPA underwent coil embolization of their aneurysm. VPA use did not have a significant association with DCI on adjusted analysis (Odds Ratio, OR = 1.07, 95% CI: 0.20 – 5.80). The association between VPA use and vasospasm was OR = 0.64 (0.19 – 1.98) and discharge mRS > 3 was OR = 0.45 (0.10 – 1.64). Increased age (OR = 1.04, 1.01 – 1.07) and Hunt and Hess (HH) grade > 3 (OR = 14.5, 4.31 – 48.6) were associated with an increased likelihood for poor discharge outcome (mRS > 3). Younger age (OR = 0.96, 0.93 – 0.99), mFS score = 4 (OR = 4.14, 1.81 – 9.45), and HH grade > 3 (OR = 2.92, 1.11 – 7.69) were all associated with subsequent development of radiographic vasospasm. There were no complications associated with VPA administration. Conclusion: We did not observe an association between VPA and the rate of DCI. There may have been a protective association on discharge outcome and radiographic vasospasm that did not reach statistical significance. We found that VPA use was safe and is plausible to be used in a population of SAH patients who have undergone endovascular treatment of their aneurysm. Larger, prospective studies are needed to determine the effect of VPA on outcome after SAH.

Research Design: In this study, we describe patients from a tertiary care safety-net hospital endocarditis registry with tricuspid valve infective endocarditis (TVIE), and concomitant acute or subacute ischemic stroke predominantly associated with injection drug use (IDU). We retrospectively obtained data pertinent to neurologic examinations, history of injection drug use (IDU), blood cultures, transthoracic/transesophageal echocardiography (TTE/TEE), neuroimaging, and Modified Rankin Scale (mRS) scores at discharge. Only those patients with bacteremia, tricuspid valve vegetations, and neuroimaging consistent with acute to subacute ischemic infarction and microhemorrhages in two cases were included in this series. Results: Of 188 patients in the registry, 66 patients had TVIE and 10 of these were complicated by ischemic stroke. Neurologic symptoms were largely non-specific, eight patients had altered mental status and only 3 had focal deficits. Nine cases were associated with IDU. Two patients had evidence of a patent foramen ovale on echocardiography. Blood cultures grew S. aureus species in 9 of the patients, all associated with IDU. Three patients died during hospitalization. The mRS score at discharge for survivors ranged 0-4. Conclusions: Patients with strokes from TVIE had heterogeneous presentations and putative mechanisms. We noted that robust neuroimaging is lacking for patients with TVIE from IDU and that such patients may benefit from neuroimaging as a screen for strokes to assist peri-operative management. Further inquiry is needed to elucidate stroke mechanisms in these patients.

Study objectives: Eye movement quantification in polysomnograms (PSG) is difficult and resource intensive. Automated eye movement detection would enable further study of eye movement patterns in normal and abnormal sleep, which could be clinically diagnostic of neurologic disorders, or used to monitor potential treatments. We trained a Long Short-Term Memory (LSTM) algorithm that can identify eye movement occurrence with high sensitivity and specificity. Methods: We conducted a retrospective, single-center study using one-hour PSG samples from 47 patients 18-90 years of age. Team members manually identified and trained an LSTM algorithm to detect eye movement presence, direction, and speed. We performed a 5-fold cross validation and implemented a "fuzzy" evaluation method to account for misclassification in the preceding and subsequent 1-second of gold standard manually labeled eye movements. We assessed G-means, discrimination, sensitivity, and specificity. Results: Overall, eye movements occurred in 9.4% of the analyzed EOG recording time from 47 patients. Eye movements were present 3.2% of N2 (lighter stages of sleep) time, 2.9% of N3 (deep sleep), and 19.8% of REM sleep. Our LSTM model had average sensitivity of 0.88 and specificity of 0.89 in 5-fold cross validation, which improved to 0.93 and 0.92 respectively using the fuzzy evaluation scheme. Conclusion: An automated algorithm can detect eye movements from EOG with excellent sensitivity and specificity. Noninvasive, automated eye movement detection has several potential clinical implications in improving sleep study stage classification and establishing normal eye movement distributions in healthy and unhealthy sleep, and in patients with and without brain injury.

Objectives The objective of this case report is to describe a rare presentation of corkscrew cerebral angiopathy presenting as subarachnoid hemorrhage. Methods We present a young woman who presented with a thunderclap headache, found to have a non aneurysmal subarachnoid hemorrhage. Results Cerebral angiogram revealed corkscrew angiopathy in medium sized vessels as well as multiple micro-occlusions with collateralization. No intracranial aneurysm was detected. Extensive work up for vasculitis and genetic causes for vasculopathy was unrevealing. The patient had no neurologic deficits and her symptoms resolved. Discussion To our knowledge, this is the first report of corkscrew angiopathy presenting with subarachnoid hemorrhage.

Introduction Penetrating ballistic brain injury (gunshot traumatic brain injury or GTBI) is associated with a high mortality. Admission Glascow Coma Scale (GCS), injury severity score and neurological findings, cardiopulmonary instability, coagulopathy and radiological finding such as bullet trajectory and mass effect are shown to predict survival after GTBI. We aimed to examine the dynamics of the observed coagulopathy and its association with outcome. Methods In this single-centered retrospective cohort study, we examined 88 patients with GTBI between 2015 and 2021. Variables analyzed include patient age; temperature, hemodynamic and respiratory variables, admission Glasgow Coma Scale (GCS); injury severity score (ISS); head abbreviated injury scale (AIS); Marshall, Rotterdam, SPIN and Baylor scores, and laboratory data including PTT, INR and platelet count. Receiver operating characteristic analysis was conducted to evaluate the performance of the predictive models. Results The average age of our sample was 28.5 years and a majority were male subjects (92%). Fifty-four (62%) of the patients survived to discharge. The GCS score, as well as the motor, verbal, and eye-opening sub-scores were higher in survivors (P < 0.001). As was expected, radiologic findings including the Marshall and Rotterdam Scores were also associated with survival (P < 0.001). Although the ISS and Head AIS scores were higher (P < 0.001), extracranial injuries were not more prevalent in non-survivors (P= 0.567). Non-survivors had lower platelet counts and elevated PTT and INR (P < 0.001) on admission. PTT normalized within 24 h but INR continued to increase in non-survivors. SPIN score, which includes INR, was a better predictor for mortality than Rotterdam, Marshall, and Baylor etc. Conclusion Progressively increasing INR after GTBI is associated with poor outcome and may indicate consumption coagu-lopathy from activation of the extrinsic pathway of coagulation and metabolic derangements that are triggered and sustained by the brain injury. The SPIN score, which incorporates INR as a major survival score component, outperforms other available prediction models for predicting outcome after GTBI.

Objective New-onset refractory status epilepticus (NORSE) is defined as de novo refractory seizures occurring in previously healthy adults, without a clear underlying etiology. Due to refractory seizures and insufficient understanding of pathophysiology, management of these patients remains challenging and often leads to poor clinical outcomes. Various infectious and autoimmune mechanisms have been proposed but have not been validated and a large number of patients are thus labeled ‘cryptogenic’. Moreover, histopathological findings have rarely been described in NORSE and are usually autopsy evaluations. In this paper, we describe the clinical correlates and histopathological findings in patients presenting with NORSE. Methods A case series of five patients with NORSE who underwent neurosurgical intervention and had histopathological examination during their acute clinical course. Results In all patients,status epileptics was refractory to treatment with antiseizure drugs (ASDs) and anesthetic agents. Autoimmune work-up revealed elevated titer of anti-GAD antibody in one patient but was unremarkable in others. Empiric use of immunomodulation therapy in three patients did not lead to cessation of status epilepticus (SE). Due to failure of prolonged medical management, three patients underwent palliative surgery for resection of epileptogenic tissue whereas the other two had diagnostic brain biopsy. Histopathology obtained during biopsy revealed evidence of vasculitis in one and necrotizing vasculopathy in another. The patient with anti-GAD antibodies had evidence of lymphocytic infiltration in limbic structures. The remaining two had nonspecific histopathological findings. Significance Although our findings are limited by a small number of patients, it adds to the growing premise of NORSE being related to an underlying autoimmune process. Additional studies, especially with histopathological data are needed to better understand this devastating disorder.