Left Atrial Appendage Morphology and Embolic Stroke of Undetermined Source: A Cross-Sectional Multicenter Pilot Study.

BACKGROUND: The left atrial appendage (LAA) is the main source of thrombus in atrial fibrillation, and there is an association between non-chicken wing (NCW) LAA morphology and stroke. We hypothesized that the prevalence of NCW LAA morphology would be higher among patients with cardioembolic (CE) stroke and embolic stroke of undetermined source (ESUS) than among those with noncardioembolic stroke (NCS). METHODS: This multicenter retrospective pilot study included consecutive patients with ischemic stroke from 3 comprehensive stroke centers who previously underwent a qualifying chest computed tomography (CT) to assess LAA morphology. Patients underwent inpatient diagnostic evaluation for ischemic stroke, and stroke subtype was determined based on ESUS criteria. LAA morphology was determined using clinically performed contrast enhanced thin-slice chest CT by investigators blinded to stroke subtype. The primary predictor was NCW LAA morphology and the outcome was stroke subtype (CE, ESUS, NCS). RESULTS: We identified 172 patients with ischemic stroke who had a clinical chest CT performed. Mean age was 70.1 ± 14.3 years and 51.7% were male. Compared with patients with NCS, the prevalence of NCW LAA morphology was higher in patients with CE stroke (58.7% versus 46.3%, P = .1) and ESUS (58.8% versus 46.3%, P = .2), but this difference did not achieve statistical significance. CONCLUSION: The prevalence of NCW LAA morphology may be similar in patients with ESUS and CE, and may be higher than that in those with NCS. Larger studies are needed to confirm these associations.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP): Clinical Features, Diagnosis, and Current Treatment Strategies.

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an acquired immune-mediated disorder characterized by weakness and sensory deficits that can lead to significant neurological disability. The diagnosis is based on a combination of clinical examination findings, electrodiagnostic studies, and other supportive evidence. Recognizing CIDP and distinguishing it from other chronic polyneuropathies is important because many patients with CIDP are highly responsive to treatment with immunosuppressive or immunomodulatory therapies. This review summarizes the clinical features, diagnosis, and current treatment strategies for CIDP. [Full article available at http://rimed.org/rimedicaljournal-2016-12.asp].

Thoracic disc herniation leads to anterior spinal artery syndrome demonstrated by diffusion-weighted magnetic resonance imaging (DWI): a case report and literature review.

BACKGROUND: Thoracic disc herniation rarely causes acute ischemic events involving the spinal cord. Few reports have suggested this as a mechanism leading to anterior spinal artery syndrome, and none with illustration through diffusion-weighted magnetic resonance imaging (DWI). PURPOSE: The purpose of this study was to report a case of anterior spinal artery syndrome secondary to thoracic disc herniation and demonstrate the first use of DWI to aid in diagnosis of this rare myelopathy. STUDY DESIGN: Case report. METHODS: A 36-year-old woman developed sudden onset of back pain followed by evolving paraparesis and sensory loss consistent with anterior spinal artery distribution ischemia. T2-weighted magnetic resonance imaging (MRI) demonstrated an acute herniated nucleus pulposus at the T7-T8 disc, which produced a focal indentation of the adjacent anterior spinal cord without cord displacement or canal stenosis. T2-weighted hyperintensities were seen at T4-T7 levels with corresponding brightness on DWI and reduction of the apparent diffusion coefficient, consistent with cord ischemia. RESULTS: Remarkably, within just a few days and following conservative treatment, including heparin and steroids, this patient's neurologic status began to show improvement. Within 3 weeks, she was ambulating with assisted devices, and at the 10-month follow-up, the patient had nearly complete neurological improvement. A follow-up MRI at 10 months showed normal T2-weighted imaging except for a 1×2-mm area of anterior-left lateral cord myelomalacia at T4-T5. CONCLUSIONS: Acute thoracic disc herniation with cord contact but without canal stenosis is able to disrupt blood flow to the cord leading to anterior spinal artery distribution ischemia. This case represents the first demonstrated use of DWI in diagnosing this rare cause of anterior spinal artery ischemia.

Selective ablation of mu-opioid receptor expressing neurons in the rostral ventromedial medulla attenuates stress-induced mechanical hypersensitivity.

AIMS: Chronic stress-related conditions are often associated with stress-induced hyperalgesia. However, the neural circuitry responsible for producing stress-induced hyperalgesia is not well characterized. The aim of this study was to determine the contribution of mu-opioid expressing brainstem neurons to the expression of stress-induced hyperalgesia. MAIN METHODS: The present study utilized a model of stress-induced mechanical hypersensitivity that involved application of repeated, light tactile whisker pad stimulation (WPS) in rats. Repeated WPS (10 applications/session, 4 sessions/h in 1 day, sessions on days 1-5 and 8-12) increased defensive-aggressive and hypervigilant behaviors, and produced hypersensitivity to tactile stimulation of the hind paw. In order to test the possible involvement of mu-opioid receptor expressing neurons in the rostral ventral medulla (RVM) to this response, rats received RVM microinjections of the toxin conjugate dermorphin-saporin or its control, saporin. Fourteen days later rats underwent either WPS or sham conditioning. KEY FINDINGS: Repeated WPS produced defensive-aggressive behaviors directed towards the stimulus and mechanical hypersensitivity of the hind paw that persisted for up to 2 weeks after the final WPS session. Dermorphin-saporin, but not saporin, microinjections prevented the development of hind paw mechanical hypersensitivity, but did not affect the defensive-aggressive behaviors. SIGNIFICANCE: The finding that chronic stress produces mechanical hypersensitivity through circuitry that involves the RVM provides a potential neurobiological basis for the complex interaction between chronic stress and pain.