Crack Cocaine Use-Related Spinal Cord Infarct.

In this study, we describe an unusual occurrence of spinal cord infarct associated with acute usage of crack cocaine. A 64-year-old male patient was brought to the hospital after being found down, displaying weakness in his lower extremities and positive for cocaine use on a urine toxicology test. The patient was administered intravenous fluids and evaluated for syncope and rhabdomyolysis. Upon initial medical assessment, the patient exhibited sensation loss up to the level of the mid-thigh, paraplegia, urinary retention, and decreased rectal sphincter tone. Neurological examination and neurological imaging were suggestive of acute spinal cord infarct.

Etiologic Subtypes of Ischemic Stroke in SARS-CoV-2 Patients in a Cohort of New York City Hospitals.

Objective: To describe the ischemic stroke subtypes related to coronavirus disease 2019 (COVID-19) in a cohort of New York City hospitals and explore their etiopathogenesis. Background: Most neurological manifestations are non-focal, but few have reported the characteristics of ischemic strokes or investigated its pathophysiology. Methods: Data were collected prospectively April 1-April 15, 2020 from two centers in New York City to review possible ischemic stroke types seen in COVID-19-positive patients. Patient presentation, demographics, related vascular risk factors, associated laboratory markers, as well as imaging and outcomes were collected. Results: The age of patients ranged between 27 and 82 years. Approximately 81% of patients had known vascular risk factors, the commonest being hypertension (75%) followed by diabetes (50%) coronary disease or atrial fibrillation. Eight patients presented with large vessel occlusion (LVO) with median age 55 years (27-82) and all were male. Eight patients presented with non-LVO syndromes, with median age 65.5 years (59-82) and most were female (62.5%). Both groups were 50% African Americans and 37.5% South Asian. Both groups had similar D-dimer levels although other acute phase reactants/disease severity markers (Ferritin, CRP, procalcitonin) were higher in the LVO group. The LVO group also had a significantly higher mortality compared to the non-LVO group. The most common etiology was cryptogenic (6 patients) followed by small vessel occlusion (3 patients) and undetermined-unclassified (3 patients). For the remaining 4 patients, 2 were identified as cardioembolic and 2 with large artery atherosclerosis. Conclusion: COVID-19-related ischemic events can present as small vessel occlusions, branch emboli or large vessel occlusions. The most common etiology is cryptogenic. Patients with LVO syndromes tend to be younger, male and may have elevated acute inflammatory markers.

Short-term delay of puberty causes a transient reduction in bone strength in growing female rats.

Multiple factors affect the structural development of the skeleton; in particular, estrogen levels during growth are an important factor in the pathogenesis of bone fragility. The delay of menarche and infrequent menstrual cycles decrease estrogen levels during adolescence and decrease peak bone mass. The aim of this study was to determine if delayed puberty through administration of a GnRH antagonist initiated prior to the onset of the first estrus cycle would delay the increase in estrogen levels and impede bone strength development in female rats. Twenty-three-day-old female Sprague-Dawley rats were randomly assigned to one of four groups; 1) short-term control group (C-ST) (n = 12), 2) long-term control (C-LT) (n = 12), 3) short-term GnRH antagonist group (G-ST) (n = 12) and 4) long-term GnRH antagonist group (G-LT) (n = 12). Injections (0.2 ml) of either saline or GnRH antagonist (100 microg/day) (Cetrotide, Serono, Inc) were given intraperitoneally for a duration of 18 days. Pubertal and gonadal development was retarded as indicated by a delay in vaginal opening (an indicator of pubertal onset), lower ovarian and uterine weights and lower estradiol levels in the short-term experimental animals (G-ST). However, at maturity (G-LT), there were no significant differences found in these measures. A delay in the timing of puberty significantly attenuated the development of femoral bone strength at 6 weeks of age. Peak moment, yield moment and stiffness in the G-ST group were all significantly less than the C-ST group. Cortical width was significantly attenuated due to the increased percentage of marrow area per total bone area in the G-ST group. However, femoral bone strength was recovered at maturity (G-LT). In summary, a transient delay in pubertal timing has short-term effects on bone strength development. In the current animal model of delaying puberty through GnRH antagonist injections, there appears to be no long-term effects on bone strength.