Current Issue : July-September Volume : 2022 Issue Number : 3 Articles : 5 Articles
Objective: Evaluate the prevalence of cardiometabolic conditions among schizophrenia patients before and incidence after initiation of high (HWGR) and low weight gain risk (LWGR) antipsychotic (AP) regimens. Methods: A retrospective observational cohort study was conducted using administrative claims data from the IBM® MarketScan Commercial and Multi-State Medicaid Databases. Patients with > 1 medical claim with a diagnosis for schizophrenia and newly initiating AP therapy between 1/1/11–6/30/16 were included. Baseline characteristics were assessed in the 12-months before AP initiation; outcomes over 24-months following AP initiation. Patients were characterized by the AP regimen initiated at the index date. Adherence was defined by a medication possession ratio > 0.8 (medication on hand for 80% of follow-up). Multivariate modeling identified predictors of index AP weight gain risk profile and post-index dyslipidemia. Results: Two thousand seven hundred forty-eight commercially-insured and 8,748 Medicaid patients met the inclusion criteria. A majority of patients initiated on atypical AP and approximately 30% were adherent to their index AP regimen. Within both payers, patients indexing on LWGR AP regimens were more likely to have pre-index diagnoses of cardiometabolic conditions including hypertension, dyslipidemia, and diabetes. Significant predictors of post-index dyslipidemia included AP adherence and pre-index diabetes. Within both payers, odds of initiating HWGR AP regimens were higher among patients with evidence of drug abuse. Conclusions: There is unmet need for reducing cardiometabolic consequences for patients on AP therapy and this analysis provides evidence that cardiometabolic conditions often develop during early stages of AP therapy. However, this does not appear to be related to the weight gain risk profile of the AP regimen....
Background: By definition, the background EEG is normal in juvenile myoclonic epilepsy (JME) patients and not accompanied by other developmental and cognitive problems. However, some recent studies using quantitative EEG (qEEG) reported abnormal changes in the background activity. QEEG investigation in patients undergoing anticonvulsant treatment might be a useful approach to explore the electrophysiology and anticonvulsant effects in JME. Methods: We investigated background EEG activity changes in patients undergoing valproic acid (VPA) treatment using qEEG analysis in a distributed source model. In 17 children with JME, non-parametric statistical analysis using standardized low-resolution brain electromagnetic tomography was performed to compare the current density distribution of four frequency bands (delta, theta, alpha, and beta) between untreated and treated conditions. Results: VPA reduced background EEG activity in the low-frequency (delta-theta) bands across the frontal, parietooccipital, and limbic lobes (threshold log-F-ratio = ±1.414, p < 0.05; threshold log-F-ratio= ±1.465, p < 0.01). In the delta band, comparative analysis revealed significant current density differences in the occipital, parietal, and limbic lobes. In the theta band, the analysis revealed significant differences in the frontal, occipital, and limbic lobes. The maximal difference was found in the delta band in the cuneus of the left occipital lobe (log-F-ratio = −1.840) and the theta band in the medial frontal gyrus of the left frontal lobe (log-F-ratio = −1.610). Conclusions: This study demonstrated the anticonvulsant effects on the neural networks involved in JME. In addition, these findings suggested the focal features and the possibility of functional deficits in patients with JME....
Introduction: Moyamoya disease (MMD) is a chronic cerebrovascular disorder characterized by progressive bilateral occlusion of the supraclinoid internal carotid artery (ICA) and its main branches, associated with the development of fine collateral networks, especially adjacent to the site of occlusion in the deep areas of the brain. MMD frequently occurs in East Asian populations, including pediatric and adult patients, and may lead to ischemic or hemorrhagic stroke, headache, epilepsy or transient ischemic attack. The majority is presumed to be of genetic origin and few cases of thrombophilia have been reported in MMD. We report a case of MMD in a young sub-Saharan African woman associated with Hyperhomocysteninemia (HHCys). Observation: A 33-year-old female was seen for aphasia, which had suddenly appeared fourteen days before, and was associated with memory impairment. She mentioned chronic headaches during the 10 previous years, of frontal seat, without migraine criteria. She had no history of hypertension, no obesity, no known dyslipidemia, and there was no family history of stroke. Neurological examination noted Wernicke’s aphasia, with discreet right central facial palsy, associated with memory impairment. The brain MRI revealed semi recent infarct in the left parietal lobe, sequelae in the left temporo-occipital and right frontal with lacunar ischemic lesions, associated with several foci of subcortical demyelination. MRA showed stenosis of the supraclinoid carotid arteries and their division branches. In addition, there was a stenosis of the posterior cerebral arteries, with a network of anastomosis at the level of the base of the skull. An investigation of thrombophilia showed hyperhomocysteinemia (HHCys). The diagnosis of moyamoya disease associated with hyperhomocysteinemia was mentioned. She was treated by Aspirin combined to folic acid. After a 3-year setback the patient was asymptomatic. Conclusion: MMD is a rare cause of stroke in sub-Saharan Africa. MRA should be performed whenever possible, as well as investigation for thrombophilia when it’s available. Combined antiplatelet agent with folic acid for ischemic stroke prevention is effective....
Background: Sick sinus syndrome (SSS) is known to occur due to lesions in the medulla oblongata. Although medullary lesions have occurred in patients with neuromyelitis optica spectrum disorder (NMOSD), there are few reports of SSS associated with NMOSD. We report a patient with NMOSD who developed refractory nausea, vomiting and SSS as the initial manifestation. Case presentation: A 77-year-old female developed refractory nausea and frequent episodes of syncope. The patient was diagnosed with SSS because sinus pauses lasting five to six seconds were observed, and pacemaker implantation was performed. Two months later, she was referred to our hospital because of limb weakness and sensory impairment that progressed over a month. The patient was confirmed to have muscle weakness; manual muscle testing revealed grade 4 in the upper extremities and grade 3 in the lower extremities. Tendon reflexes were diminished, while no pathological reflexes were present. Thermal and pain sensations were impaired in the upper and lower extremities, and vibration sensation was impaired in both lower extremities. Bladder and rectal disturbances were also noted. Optic neuritis was not detected. T2-weighted magnetic resonance imaging (MRI) showed high-intensity lesions in the dorsal part of the medulla oblongata and C3–6 cervical cord. Her serum was positive for antibodies against aquaporin 4, and a diagnosis of NMOSD was made. She was treated with two courses of an intravenous methylprednisolone pulse and one course of plasma exchange. Then, she was transferred to another hospital for rehabilitation. Conclusions: Because SSS is a life-threatening complication, clinicians should be aware of the possibility that medullary lesions in NMOSD can cause SSS as the initial manifestation....
Background: The hyperdense middle cerebral artery sign (HMCAS) is an early radiological marker to provide an early diagnosis and to identify ischemia. As reported, HMCAS is associated with heavy clot burden. Moreover, a heavy clot burden may cause obstruction of the orifices of arteries for leptomeningeal collateral flows and can lead to severe clinical conditions. However, the direct relationship between HMCAS and collateral flows remains unclear. Therefore, we explored the association between HMCAS and leptomeningeal collaterals in patients with acute ischemic stroke. Methods: Consecutive ischemic stroke patients were enrolled from January 2015 to April 2021. HMCAS appearance and collateral status were detected by multimodal computed tomography at admission. Logistic regression analyses helped to identify the association between HMCAS, collateral flows and stroke severity. Results: In 494 included patients, 180 (36.4%) presented with HMCAS. Ipsilateral collaterals were not seen or less prominent in patients with HMCAS (P < 0.001). The HMCAS appearance was significantly associated with less collaterals (odds ratio 5.17, 95% confidence interval 3.27-8.18, P < 0.001), internal carotid artery + M1/M1 occlusion, the initial stroke severity and follow-up outcomes. Subgroup analyses further confirmed HMCAS as an indicator of poor collaterals in ischemic stroke (all P values < 0.05). Conclusions: HMCAS is associated with poor leptomeningeal collaterals, the stroke severity and a poor neurological outcome. Therefore, the HMCAS appearance can act as an early warning sign for healthcare professionals to be alert for poor collateral flows and poor neurological outcomes in ischemic stroke patients with middle cerebral artery occlusion....
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