This is a comprehensive review of the literature regarding the use of milnacipran in treating fibromyalgia. A chronic pain disorder with other system disturbances, fibromyalgia is often resistant to many therapeutic approaches. This review presents the background, evidence, and indications for using milnacipran as a treatment option for this condition. Recent FindingsThe definition of fibromyalgia has evolved over many years as it is a relatively tricky syndrome to measure objectively. Today, it is characterized by chronic, widespread pain accompanied by alterations in sleep, mood, and other behavioral aspects. A variety of therapeutic regimens currently used to treat the syndrome as a singular approach are rarely effective. Milnacipran is one of three drugs currently approved by the FDA for the treatment of fibromyalgia. It acts as a serotonin and norepinephrine reuptake inhibitor, which results in decreased pain transmission. Milnacipran remains an effective treatment option for fibromyalgia in adults and needs to be further evaluated with existing therapeutic approaches.

This is a comprehensive review of the literature regarding intravenous lidocaine infusion to treat peripheral neuropathy. The clinical symptoms of peripheral neuropathy occur on a broad spectrum and stem from many etiologies resulting in complex treatment approaches. This review presents the background, evidence, and indications for the use of intravenous lidocaine infusions as a treatment option for this condition. Recent FindingsThe clinical range of peripheral neuropathy symptoms includes pain, numbness, muscle weakness, paresthesia, balance difficulty, and autonomic dysfunction. However, severe neuropathic pain remains one of the most debilitating symptoms that significantly affects the quality of life. Current treatment options include antidepressants, anticonvulsants, and, in some cases, opiates, but these are often ineffective, creating the need for other therapeutic approaches. The pathophysiology of neuropathic pain involves sodium channels which create abnormal pain responses. Intravenous lidocaine primarily functions by inhibiting membrane sodium channels which desensitize peripheral nociceptors, thus creating an analgesic effect. The research in using intravenous lidocaine for neuropathic pain is not fully complete and requires further evaluation.

This is a comprehensive review of the literature regarding the use of Deutetrabenazine in treating chorea associated with Huntington’s disease. Unfortunately, treatment has been limited for many aspects of this neurodegenerative disease. The present investigation presents the background, evidence, and indications for the use Deutetrabenazine in the setting of Huntington’s disease. Huntington’s disease is characterized by a variety of motor, psychiatric, and cognitive symptoms with chorea being one of the more notable ones. Chorea is a movement disorder present in multiple neurologic diseases that causes involuntary and irregular muscle movements theorized to be stemming from high dopamine levels. Deutetrabenazine is thought to function as an inhibitor of the VMAT2 vesicular monoamine transporter resulting in decreased monoamine release, including dopamine, in the synaptic cleft which has a therapeutic effect in management of chorea. This drug was approved by the FDA in 2017 with a specific indication for tardive dyskinesia and choreiform movement in Huntington’s disease. Currently, there is no definitive treatment for Huntington’s disease. Thus, management is primarily focused on symptom management with the use of a variety of pharmaceutical agents. Chorea is one of the many manifestations that significantly alter the quality of life of many patients. Deutetrabenazine is a promising new option for the treatment of chorea in the setting of Huntington’s disease. Although studies so far have displayed mixed results, further research, including head-to-head studies, is necessary to elucidate the true potential of this drug.

Background The purpose of this study is to evaluate cardiac functions using transthoracic echocardiography, change in lead parameters and electrocardiogram (ECG) morphology in patients undergoing permanent pacemaker implantation over a follow-up period of 6 months. Methods This is a prospective study in patients undergoing permanent pacemaker implantation in a tertiary care hospital. Patients undergoing permanent pacemaker implantation were enrolled for up to one year and Echocardiographic parameters (by 2 blind operators) and ECG parameters were recorded at admission (within 24 h), before discharge (within 7 days of pacemaker implantation), after 1 month (± 7 days) and after 6 months (± 7 days) of follow-up. Results A total of 96 patients (60.4% males and 39.6% female, mean age 66.65 years) were implanted with permanent pacemaker. The mean QRS duration was 133.18 ms and increased significantly to 146.03 ms by 6 months despite septal lead placement in majority (92%) of patients. The mean baseline ejection fraction of 51.47 decreased significantly to 47.83 by 6 months. Diastolic parameters like left atrial volume index, early to late diastolic transmitral flow velocity (E/A) and early diastolic mitral annular tissue velocity (E/e′) showed a significant increase (> 5%) from baseline by the end of first week. By the end of first month, systolic dysfunction of RV sets in with significant (> 5%) change from baseline in parameters like Right ventricle myocardial performance index, transannular plane systolic excursion and right ventricle systolic excursion velocity (RVS′). Conclusion We have observed that pacemaker recipients with baseline reduced left ventricle (LV) systolic functions perform significantly worse compared to those with baseline normal cardiac functions and had a higher rate of deterioration of LV function. RV dysfunction is the first abnormality that occurs, by 1 week followed by LV dysfunction which starts by 1 month and the diastolic dysfunctions precede the systolic dysfunction. QRS duration also showed a gradual increase despite septal lead placement in majority (92%) and lead parameters showed no significant change over 6 months.

This a comprehensive review of the literature regarding the use of Valbenazine in treating tardive dyskinesia. A primarily oral movement disorder induced by chronic exposure to certain classes of medications, tardive dyskinesia is often resistant to many therapeutic approaches. This review presents the background, evidence, and indications for the use of Valbenazine as a treatment option for this condition. Recent FindingsTardive dyskinesia is a disorder arising from long-term exposure to medications that blocked dopamine receptors, primarily antipsychotics. It is characterized by abnormal movements of the oral-buccal-lingual structures as well as associated pain and hypertrophy. Simply stopping the use of the dopamine blocking agents effectively alleviates the symptoms but is not always reliable hence the need for another therapeutic approach.Valbenazine is thought to function as a highly selective inhibitor of the VMAT2 vesicular monoamine transporter resulting in decreased availability of dopamine in the presynaptic cleft. This leads to decreased dopaminergic activation of the striatal motor pathway. The FDA approved Valbenazine in 2017 to treat tardive dyskinesia in adults and needs to be evaluated with existing therapeutic approaches.