Reviews in neurological diseases最新文献

Neurologists are often confronted with swallowing disorders in routine practice. Swallowing impairments carry serious health consequences if they are overlooked or inappropriately managed. Swallowing problems usually develop in patients with established neurological conditions, although on occasion they may be a presenting symptom of a neurological disorder. Prompt recognition of dysphagia and early diagnosis can often be accomplished through a systematic clinical history and examination. This article reviews the physiology and neuroanatomy of normal swallowing and discusses pertinent clinical approaches toward evaluating a patient with neurogenical dysphagia. Important neurological conditions causing dysphagia are also discussed in this context.

With the rapid rise in the number of bariatric surgeries performed for morbid obesity, several short- and long-term neurologic complications of this procedure have been identified. These complications affect various levels of the neuraxis, and most are likely secondary to deficiency of essential minerals and vitamins. We report on 3 patients who developed unusual and severe neurologic deficits after undergoing bariatric surgery, including Wernicke encephalopathy, acute and rapidly progressive polyneuropathy, myelopathy, and visual deficits. Two developed clinical features of Parkinsonism, a complication not previously reported in this patient population. None of our patients had attended a nutrition clinic postoperatively. All 3 had a rapid weight loss and intractable vomiting preceding the development of neurologic symptoms, and all were found to have significant vitamin deficiencies. Replacement of vitamins resulted in a slow and variable degree of neurologic recovery. Patients undergoing bariatric surgery should have close monitoring of their nutritional status postoperatively. Routine supplementation of vitamins and minerals may be a cost-effective strategy for preventing neurologic complications in these patients.

Venous thromboembolism is the most frequent preventable cause of death in hospitalized patients. Currently available anticoagulants have limitations that restrict their widespread use, particularly in long-term indications. Vitamin K antagonists require frequent monitoring and dose adjustment, and have a narrow therapeutic window with the risk of bleeding. The low-molecular-weight heparins have more predictable pharmacokinetics and pharmacodynamics, and coagulation monitoring is not required. However, their subcutaneous administration limits their suitability for long-term use. Consequently, many patients fail to receive effective preventive therapy. Rivaroxaban, apixaban, and dabigatran are new anticoagulants in late-stage clinical development that inhibit a single, specific coagulation factor, unlike the Vitamin K antagonists and low-molecular-weight heparins. Studies suggest that they provide effective, predictable anticoagulation with a low bleeding risk and will potentially offer an improved clinical profile and wider safety margin compared with currently available therapies.

Studies of monotherapy with L-methylfolate, methylcobalamin, or pyridoxal 5'-phosphate suggest that these B vitamins may reverse both the symptoms and the pathophysiology of diabetic peripheral neuropathy (DPN). The efficacy of oral-combination L-methylfolate, 3 mg; methylcobalamin, 2 mg; and pyridoxal 5'-phosphate, 35 mg (LMF-MC-PP) in restoring cutaneous sensitivity in patients with type 2 diabetes with DPN was evaluated in 20 type 2 diabetic patients who were given LMF-MC-PP twice daily for 4 weeks and then once daily for an additional 48 weeks. Statistically significant improvement in 1-point (tactile) and 2-point (discriminatory) static testing at the right and left great toe and heel in the patients was observed in all 3 follow-up periods: 1) baseline to 6 months, 2) baseline to 1 year, and 3) 6 months to 1 year. The greatest improvement occurred between baseline and 1 year of treatment. Treatment with oral LMF-MC-PP appears to promote restoration of lost cutaneous sensation in DPN.

The development of new treatments for acute stroke has been fraught with costly and spectacularly disappointing failures. Repurposing of safe, older drugs provides a lower risk alternative. Vascular protection with candesartan is one such approach.

There is only 1 US Food and Drug Administration-approved drug for acute ischemic stroke: tissue plasminogen activator (tPA). Due to a short time window and fear of intracerebral hemorrhage (ICH), tPA remains underutilized. There is great interest in developing combination drugs to use with tPA to improve the odds of a favorable recovery and to reduce the risk of ICH. Minocycline is a broad-spectrum antibiotic that has been found to be a neuroprotective agent in preclinical ischemic stroke models. Minocycline inhibits matrix metalloproteinase-9, a biomarker for ICH associated with tPA use. Minocycline is also an anti-inflammatory agent and inhibits poly (ADP-ribose) polymerase-1. Minocycline has been safe and well tolerated in the clinical trials conducted to date.

Children presenting with progressive neurologic symptoms including dystonia, dysarthria, and spasticity can represent a diagnostic challenge. Here we describe the case of a 14-year-old boy who presented to our center with an 11-year history of gradual worsening neurologic symptoms. Diagnostic strategies focus on the use of neuroimaging and genetic testing to help establish the underlying diagnosis. Therapeutic options are also discussed.