A literature review of local published research from Pakistan showed no study documenting the characteristics of patients

who leave ED without being seen by a physician in this region. KU-55933 nmr Emergency Medicine as a specialty is still in its infancy in Pakistan [30-32]. Our department was the first one to be established back in 2008. Over the years, we have observed an increase in patient volume as well as acuity. The ED had expanded to 46 beds but the hospital beds remained the same which brought in the issues of overcrowding, left without being seen patients and ED through put issues. Therefore, this study is aimed at defining the LWBS population Inhibitors,research,lifescience,medical in a tertiary care hospital while determining percentages and factors associated with LWBS as we do not know the characteristics of our patients who are leaving. This baseline information will be critical Inhibitors,research,lifescience,medical in developing evidence based interventions aimed at improving the health care management of such patients and consequently reducing the morbidity and mortality resulting from leaving. Methods Setting This study was conducted at the Emergency Department of the Aga Khan University Hospital (AKUH) Karachi, Pakistan.

AKUH is a 600-bedded, private tertiary care hospital in Karachi with an annual ED census of approximately 50,000 patients Inhibitors,research,lifescience,medical and an admission rate of 37%. The emergency department of AKUH is the first one established in the country, and the largest ED in Pakistan providing emergency care of international standards. The emergency department of AKUH is the first established department at Pakistan.

It has 46 patient-care beds with well designated Inhibitors,research,lifescience,medical pediatric, critical care areas and non-critical areas. An eight-bedded observation unit is also functioning where patients are kept for 24 hours. Two Fast track clinics for walk in patients provide service 24/7. AKUH-ED is the only department in Pakistan where standard triage is being followed (Additional file 1). It has a separate well defined triage area. It follows 4 levels of triage and categorizes patients from level I-level Inhibitors,research,lifescience,medical IV. We also have a written triage policy approved by the hospital. Triage staff has been given training for Triaging. A nurse initially triages patients by following the triage categories. The nurse assigns beds to the patients or sends them to the waiting area in case the ED capacity is exhausted (Additional file 2). At the triage desk, a triage team Carnitine palmitoyltransferase II is present 24/ 7 comprising of a trained nurse, nursing assistant and a triage care coordinator. Triage care coordinator is a senior experienced nurse who supervises the whole functioning of triage. In case of any quarry, the triage nurse could seek help from an on-call physician. The triage information is recorded in an electronic computerized based system called ERMS (Emergency Room Management system) (Additional file 3).

In contrast to their study, our study assessed arterial samples as opposed to peripheral venous samples; arterial samples are fully ‘mixed’ and less apt to regional error (e.g. tourniquet effects during phlebotomy, differences in limb flow and oxygen consumption etc.). We were also able to assess the performance of base deficit. A review of previous studies’ assessment of BD, AG, and ACAG for the diagnosis of hyperlactatemia is provided in Table ​Table55. Table 5 Summary of previous studies The implications of these data are noteworthy. Because elevated serum click here lactate levels identify patients who are

at high risk of death and may identify Inhibitors,research,lifescience,medical patients in shock before they become hypotensive (a condition called cryptic shock), early

recognition and treatment of hyperlactatemia is critical, and likely improves mortality.[7] In order to institute appropriate therapy as timely as possible, screening tests for shock should offer as early a warning as possible, well Inhibitors,research,lifescience,medical before the serum lactate rises to 4.0–5.0 mmol/L. For these reasons, the routine use of AG, BD, and ACAG as screening tests to determine the presence or absence of hyperlactatemia, in our opinion, is unacceptable and potentially harmful. While it is true that the AG and BD detect the presence of hyperlactatemia Inhibitors,research,lifescience,medical more effectively as the threshold value for lactate is raised (serum lactate > 4.0 mmol/L), waiting to diagnose hyperlactatemia by allowing the level to rise may delay appropriate intervention. An ACAG < 10 meq/L appears to effectively rule out the presence of hyperlactatemia, Inhibitors,research,lifescience,medical but the serum albumin and serum electrolytes must be cotemporaneous and from the same sample in order for that relationship to be valid. Given that Inhibitors,research,lifescience,medical accurate and rapid serum lactate concentration measurement is now widely available to all major hospitals (central labs and/or point of service testing), serum lactate concentrations should be routinely measured upon admission to the ICU, for many patients in the emergency

department, and in our opinion should be considered an index laboratory measure. Serum lactate remains an assay that must be requested separately in most ICUs and emergency departments; therefore, a clinician must actively ask for this test (Table ​(Table1).1). Further, the use of anion gap and base deficit to diagnose the presence or absence of hyperlactatemia is still commonly taught to medical students and physicians in training. MTMR9 As clinicians and teachers, we need to correct this misperception in order to identify patients with hyperlactatemia promptly. In this study, the shortcomings of using the AG to assess metabolic acidosis were exposed. As expected, the sensitivity of anion gap improves when the anion gap is corrected for albumin (ACAG). However, the specificity of the ACAG remained low. The reason for this is illustrated in Figure ​Figure11 and Figure ​Figure2.2.

Postmortem autopsy showed no evidence of cellular or humoral rejection, which confirmed that the case was a fatal cardiotoxicity adverse effect due to Peg-IFN-alpha-2b. Myopathy and acute myositis have also been reported as adverse effects of PEG-IFN-alpha-2b therapy in HCV-infected patients. This may contribute, in part, to the cardiovascular disorders that are seen in these

patients. Venezia et al.60 have reported a case of acute myositis after PEG-IFN-alpha-2b therapy for an HCV infection and suggested that a rapid discontinuation of IFN could resolve the problem in such cases. Golstein et al.61 reported a reversible case of myopathy that Inhibitors,research,lifescience,medical developed as a side effect of the same agent, which improved after drug cessation. Disorders of the immune system have also been reported as a consequence of IFN therapy in HCV-infected patients. The importance of these diseases is attributed to their direct or indirect effects on the cardiovascular system. Sarcoidosis is one of the most Inhibitors,research,lifescience,medical prevalently reported immune system disorders.62 SLE has also been reported as an adverse effect of IFN therapy in HCV-infected patients.63 Cryoglobulinemia is another immune disorder that has been reportedly

associated with IFN therapy.64 Type I diabetes mellitus, another autoimmune disorder, has Inhibitors,research,lifescience,medical been repeatedly suggested to develop as an adverse effect of IFN therapy.65 Grave’s disease and thyroiditis are other disorders attributed to IFN therapy in HCV-infected patients.66,67 Conclusion IFN-based regimens are a cornerstone for the treatment of HCV infection and generally considered effective as treatment

for this infection. Although most adverse effects of IFN therapy respond very well to Inhibitors,research,lifescience,medical cessation of the drug, this review article shows that there are serious Inhibitors,research,lifescience,medical adverse effects associated with IFN therapy in HCV-infected patients, which might affect sensitive organs such as the eyes, heart, and lungs. The prevalence of ocular disorders in the early period (first 8 weeks) after IFN administration can amount to 57% and result in irreversible, significant damage to visual acuity. Pulmonary hypertension Mannose-binding protein-associated serine protease secondary to IFN therapy is a serious side effect due to its irreversible nature in most patients and as such necessitates prompt evaluation. After NU7441 solubility dmso mentioning these adverse effects of IFN therapy in HCV patients, it should be mentioned that HCV infection itself may produce cardiovascular injuries. Only a few of the articles we have reviewed were case-controls, thus we cannot separate the potential effects of HCV from IFN therapy adverse effects. More prospective studies should be conducted for this purpose. To the best of our knowledge, there is no study in the current literature that concerns prevention strategies for the vascular effects of IFN therapy on different organs. We suggest that prospective studies be undertaken to address this critical issue.

This task was performed for four time intervals with 20, 25, 35, and 45-sec duration and a 60-sec rest time between the time intervals. During this procedure, participants were asked to close their eyes, to sit relaxed, and to breathe consistently. Start and stop of each interval was indicated verbally by the experimenter. Inhibitors,research,lifescience,medical Particularly in small samples, randomization often does not produce comparable distributions of conditions across groups. Hence, the order of time intervals

was not randomized, to increase procedural comparability between the two groups. Importantly, the individual participants were not aware of the fixed order. Instructions were given in written form to standardize the instruction (Ehlers et al. 1995). We added an initial warm-up trial to allow sufficient time for the transition from the instructional phase to the different mode of processing during interoception. The warm-up trial was not included in the analysis, Inhibitors,research,lifescience,medical as we aimed for an optimal compromise between keeping the scores comparable with previous reports as much as possible and the added benefit of reducing task-irrelevant training effects Inhibitors,research,lifescience,medical in a situation unfamiliar for most participants (Sütterlin et al. 2013).1 Self-report data The German version of the State–Trait Anxiety

Inventory (Laux et al. 1981) was used to assess habitual trait and state anxiety on two selleck chemical scales comprising 20 items each. Items are rated from 0 (not at all) Inhibitors,research,lifescience,medical to 3 (very much so), resulting in a scale range of 0–60 for each measure. Higher scores indicate higher anxiety. Cronbach’s α is about 0.90 for both scales (Laux et al. 1981). The current sample achieved a Cronbach’s α of 0.92 for the STAI-State and 0.96 for the STAI-Trait. The German 21-item version of the Beck Depression Inventory (BDI) was used to assess dysphoric mood and depression. Items are rated on a four-point scale from 0 to 3, resulting in an overall score ranging from 0 to 63. Higher Inhibitors,research,lifescience,medical scores represent more severe symptoms of depression. Internal consistency

is good with Cronbach’s α = 0.89 (Hautzinger et al. 2006). Casein kinase 1 Trait anxiety sensitivity was assessed with the German version of the Anxiety Sensitivity Index (ASI, Peterson and Plehn 1999). Notably, high scores on the ASI have been shown to predict both the frequency of panic attacks in PD patients and increased cardioceptive accuracy (Domschke et al. 2010). Cronbach’s α of the ASI has been reported to exceed at least 0.75 (Peterson and Plehn 1999); the current sample achieved an internal consistency of 0.95. Positive and negative affect were assessed with the German version of the Positive and Negative Affect Schedule (PANAS, Krohne et al. 1996), assessing positive and negative affect on separate scales comprising 10 items each.

An Metabolism inhibitor example of research in this area is the finding that stress blocks long-term potentiation (LT.P, a measure of plasticity)

in the hippocampal to ventromedial prefrontal cortex,11 and these effects are reversed acutely by an atypical antidepressant, tianeptine. McEwen’s group have shown that these acute effects change into effects on dendritic arborization.1′ Furthermore, there is now proof of concept that, this pathway is of critical importance for depression because Mayberg’s group13 have implanted electrodes into the white matter behind Cg25 (the equivalent in man of the ventromedial prefrontal cortex in rodents) and found immediate antidepressant effects in patients who had been entirely Inhibitors,research,lifescience,medical treatment-resistant. Targctting these brain areas therefore opens up new perspectives in drug discovery for depression. Furthermore, reingineering animal models to study these brain areas will allow the selection of new classes of molecule. Figure 5. The impact of stress on neuroplasticity may be a novel target for drugs in psychiatry, as stress inhibits Inhibitors,research,lifescience,medical plasticity in hippocampal and prefrontal cortex circuits while increasing plasticity in the circuits dealing with emotion (amygdala, prefrontal cortex). …
Serendip is the old Arabic name for

Ceylon, nowknown as Sri. Lanka. The origin of the word “serendipity” is in a Persian fairy tale, The Three Princes of Serendip, whose traveling heroes Inhibitors,research,lifescience,medical were “always making discoveries, by accidents and sagacity, of things they were not in quest of.”1 In the 16th century, the tale was translated from Persian to Italian, and from Italian to French. Horace Walpole (1717-1797), an English man of letters, encountered

it in a collection Inhibitors,research,lifescience,medical of oriental tales in French, and coined the English term “serendipity” in a letter to his friend, Horace Mann, dated June 28, 1754.2 Today, the word “serendipity” is a word that is used in everyday language. The Oxford English Dictionary defines it, as “the faculty of making happy and unexpected discoveries by accident,” and Webster’s New Collegiate Dictionary Inhibitors,research,lifescience,medical as “the faculty of finding valuable or agreeable things not sought for.”3 In Stedman’s Medical Dictionary “serendipity” refers Rolziracetam to “an accidental discovery;” ie, “finding one thing while looking for something else.”4 According to the Doctor Out, of Zebulon column in the Archives of Internal Medicine, “serendipity signifies a mental state in which serenity and stupidity are blended,” as for example, “the serendipity of a cow chewing its cud under a shady tree,” or “the sort, of thing that happens to you when on a dull day collecting fossils you find instead a, beautiful woman who proves to be neither geologist nor archeologist.”5,6 However, this definition is erroneous, at least insofar as scientific discoveries are concerned. No scientific discovery has ever been made by pure luck.

In the case of a sufficiently strong impact, the upstroke of the PSN can reach positive values, called a post-systolic motion.6),7),8),9),10),11),12) We propose this simple mechanism to explain the biphasic configuration of the post-ejection velocity spike. Previous research had suggested it to be a resultant of different phenomena such as: asynchronous Inhibitors,research,lifescience,medical contraction and ventricular interdependence,13) asynchronous deformation of subendocardial and subepicardial LV wall layers14) and tug-of-war between weak and strong segments during the isovolumic relaxation phase.15) The prevalence of the positive PSN velocities found in the current study is somewhat higher than previously reported,3) Inhibitors,research,lifescience,medical probable

because no temporal averaging of the measurement results was applied. The centrifugal propagation of the positive PSN velocity front is illustrated by a frame-by-frame selleck compound analysis of a color TDI sample (Fig. 6). Fig. 6 The typical sequence of the centrifugal distribution of the apically directed velocity of the myocardium (red-colored area) following the aortic valve closure. Four consecutive images are shown. Panel A corresponds to the post-systolic velocity notch … To the best of our knowledge the present study describes for the first time the existence of two PSN spikes with apically

directed acceleration. This was possible due to use of the high frame rate and non-smoothed Inhibitors,research,lifescience,medical measurement results. Inhibitors,research,lifescience,medical While the origin of the first PSN spike is as discussed above, probably, the closure of the aortic valve, the genesis of the second PSN spike is less clear. We hypothesize that the sudden cessation of the aortic backflow at the instant of the aortic valve closure16) is a potential mechanism behind the second PSN spike. The transmission

of the kinetic energy could be sufficient to cause an acceleration of adjacent structures in the direction of the left ventricle.17) The magnitude of the retrograde flow in the Inhibitors,research,lifescience,medical ascending aorta is known to vary significantly between the healthy subjects and constitutes 4-29% of the antegrade aortic flow. At an average of 600-700 mL/min retrograde flow the coronary circulation takes 200-300 mL/min, the remainder turns around in the sinuses of Valsalva.18) The maximal velocity of the retrograde flow in the ascending aorta is in the range of 8-40 cm/s in healthy subjects.19) These differences in velocity and volume of the retrograde aortic flow are likely to cause a wide spectrum of velocity and duration of Rolziracetam the second PSN spike. Further studies are needed to elucidate its nature and clinical significance. Limitations The apical longitudinal axis view is hampered by suboptimal alignment of the Doppler interrogation with longitudinal motion of the ascending aorta which varies with the magnitude of the aorto-septal angle. However, it is unlikely that possible malalignment influenced the timing intervals measured in this study.

Odds and hazard ratios are provided with their 95% confidence interval. buy Staurosporine Results During the period from 2005 to 2009, we identified 176 patients from the medical archives that had a liver chemoembolization treatment. Nineteen patients were excluded (medical file missing: 1; two treatments at the same lesion within one week: 1; liver transplant within 5 days following TACE treatment: 1; missing transaminases

values after treatment: 11; diagnosis Inhibitors,research,lifescience,medical other than hepatocellular carcinoma: 4; patient’s age <18 years old: 1). The average age was 63.4 years, 77% were males and 91.7% had a diagnosis of cirrhosis. Hepatitis C infection was the most common diagnosis. The 157 patients received a total of 280 treatments. Two treatments were excluded because there was no information about the lesion prior to treatment. Inhibitors,research,lifescience,medical Seven treatments lacked a radiological control after treatment (withdrawal of care 5, transplant 2) and

were excluded from the radiological response but not the survival analyses. In total, 271 treatment cases were used to evaluate the radiological response. Cisplatin was the chemotherapeutic agent in 264 cases. Adriamycin and doxorubicin beads were used in the other 7 cases (6 and 1 respectively). Baseline characteristics Inhibitors,research,lifescience,medical according to the cytolysis status at the time of the first treatment are shown in Table 1. During follow-up, 29 (23%) patients in the cytolysis group had a liver transplant or a hepatectomy versus 3 (9.3%) in the non-cytolysis group. Twenty-two patients (17.6%) were lost to follow-up in the cytolysis group versus 4 (12.5%) in the no-cytolysis group. In both situations, the difference Inhibitors,research,lifescience,medical in proportions was not statistically significant. The overall incidence of cytolysis was 73% (198/271). Table 1 Baseline characteristics of 157 patients before their first TACE treatment according to cytolysis occurrence status Radiological response Response was analyzed Inhibitors,research,lifescience,medical using each treatment as the unit of analysis (n=271). After adjusting for the log(AFP), the odds-ratio (OR) estimate for cytolysis

versus non-cytolysis was 1.90 (1.03-3.54), thus suggesting a favourable radiological outcome associated with cytolysis two months after treatment. The summary of the radiological response is shown in Table 2. Table 2 Summary of radiological response of 271 treatments Effect of cytolysis tuclazepam on adverse events Table 3 illustrates the adverse events observed after TACE treatment (n=271) according to cytolysis occurrence. There were 26 (14%) hepatobiliary complications in the cytolysis group and 5 (7%) in the non-cytolysis group. These included cases of hepatic encephalopathy, hyperbilirubinemia, coagulopathy (as defined in the methods section) and cholecystitis. There was a trend for a greater proportion of complications in the cytolysis group that was not statistically significant.

We found that the formation of amyloid -like huntingtin fibrils in vitro and in vivo critically depends on polyglutamine repeat length, protein concentration, and time. Furthermore, huntingtin aggregation can be seeded by preformed fibrils, suggesting that fibrillogenesis in HD, as in Alzheimer’s disease, is caused by nucleation-dependent polymerization.43 Our findings that the assembly of huntingtin aggregates requires the formation of a nucleus and is time- and protein concentration-dependent may account for the late onset and progressive phenotype in HD. Although fibril formation occurs within hours in the in vitro system, it may take years in neuronal cells of HD patients.

The concentration Inhibitors,research,lifescience,medical of mutant huntingtin in medium spiny neurons, which are affected most in HD, is unknown, but it is likely to be much lower than that used in the in vitro aggregation assays. Thus, we Inhibitors,research,lifescience,medical suggest that the lag time during which huntingtin dinners, trimers,

and oligomers are formed in vivo is significantly elongated in HD patients. For the identification of huntingtin aggregation inhibitors, we have developed a rapid and sensitive filter retardation assay, which is suitable for the highthroughput screening of drugs that prevent aggregate formation.45 Inhibitors,research,lifescience,medical This assay is based on the finding that HD exon 1 aggregates are insoluble in sodium dodecyl sulfate (SDS) and are retained on a cellulose acetate filter, whereas Ribociclib clinical trial monomelic forms of the HD exon 1 protein do not bind to this filter membrane. The captured aggregates Inhibitors,research,lifescience,medical are then detected by simple immunoblot analysis using a specific anti-huntingtin antibody. Using the filter retardation assay, we first tested a number of known inhibitors of β-amyloid, PrPscr, and microtubule fibril formation for their effect on huntingtin aggregation in vitro.46 We found that Congo red, thioflavine S, chrysamine G, and Direct fast yellow inhibited HD exon 1 protein aggregation in a dose-dependent manner, whereas other potential inhibitors of β-amyloid Inhibitors,research,lifescience,medical formation, such as thioflavine T, gossypol, melatonin, and rifampicin, had little or no effect on huntingtin aggregation. The results obtained in vitro

were confirmed in cell culture model systems. Furthermore, we found that the monoclonal antibody 1C2, which specifically recognizes the elongated polyglutamine stretch in huntingtin, and the heat the shock proteins Hsp70 and Hsp40 are potent inhibitors of huntingtin aggregation.46, 47 Interestingly, the addition of heat shock proteins to in vitro aggregation reactions shifts the self-association pathway of huntingtin from fibrillar to amorphous aggregation. This suggests that in vivo chaperones may have the potential to transform toxic fibrillar aggregates into nontoxic aggregates, which can then be degraded by the ubiquitin/proteasome system. Thus, small molecules that activate a heat shock response in neurons may be effective in delaying the onset and progression of HD.

The extremely high absorption of MM could be due to the easy penetration of the small structures into fabrics. However, the increase in the size of these structures (see Table 3) did not prevent their exit from the fibres, and desorption was notable. This finding could be due to the higher permeability of textiles compared with human skin, which may explain why this effect was not observed [25, 26]. To study the penetration of active principles through the skin, an in vitro methodology based on percutaneous absorption

is performed to demonstrate the delivery of an encapsulated principle from a textile to the different layers of the skin (stratum corneum, epidermis, or dermis). The percutaneous Inhibitors,research,lifescience,medical absorption of the two formulations, Lip (2% GA, 4% PC) and MM (2% GA, 4% PC, and 30% Oramix CG 110), was evaluated, as were the CO and PA textiles impregnated

with the same Lip or MM. The two formulations and Inhibitors,research,lifescience,medical the CO and PA textiles previously treated with the Inhibitors,research,lifescience,medical formulations were placed in contact with the skin discs as described in Section 2. The aim of this assay was to demonstrate tracer delivery into the different layers of the skin. GAs encapsulated in MMs and Lips, which were either embedded or not embedded in cosmetotextiles, were applied to the skin to study the percutaneous absorption profiles of the agents. The GA extracted from a washing sample, the fabric, the stratum corneum, the rest of the epidermis, the dermis, and the receptor Inhibitors,research,lifescience,medical fluid was analysed. The results are listed in Table 4 and graphically represented in Figure 2. Figure 2 In vitro percutaneous absorption of gallic acid (GA) in Lip and MM formulations and the PA and CO cosmetotextiles Inhibitors,research,lifescience,medical (SC: stratum corneum, R. Fluid: receptor fluid) (significant level accepted *P < 0.01). Table 4 In vitro percutaneous absorption

of GA (gallic acid) in Lip and MM formulations and the PA and CO cosmetotextiles. Comparison of percutaneous absorption in percentage indicates that it is higher when GA was applied as a formulation (Lip or MM) than when it is applied through cosmetotextile. Besides, CO delivers to the skin GA in a greater extent than PA. As shown in Figure 2, the penetration of GA formulated in Lip Dichloromethane dehalogenase was much higher than that of GA formulated in MM. All skin compartments showed a higher GDC-0941 research buy amount of GA when vehiculised with Lip than when vehiculised with MM. This result could be due to the bilayer structure of the Lip, which is similar to the lipid bilayer structures present in the SC and in the cellular membranes of the skin [28]. Evidence that Lips do not penetrate deeper than the stratum corneum layer has been published [29]. However, Lips enhance the penetration of both hydrophilic and lipophilic drugs [30, 31].

101 Increased cerebrospinal fluid (CSF) hypocrctin-1 levels are present in early-onset RLS patients, whereas levels in late-onset RLS patients are normal. Allen et al postulate that increased

hypocretin levels may modulate or promote insomnia and increase motor activity101 RLS involves various areas in the nervous system from the spinal cord up to the basal ganglia.98,101,102 Using single photo emission Mdm2 inhibitor in vitro computed tomography (SPECT) and positron emission tomography (PET), various researchers have demonstrated a decrease in dopamine D2 receptor binding in the striatum of RI-S patients, suggesting that RLS Inhibitors,research,lifescience,medical is related to a deficiency of dopaminergic function.97,100,102-104 Iron deficiency accompanying RLS may be associated with hypofunction of the D2 receptor.97,100 More than 80% of RLS patients manifest periodic limb movements (PLMs) during sleep.100 PLMs consist of four or more repetitive episodes of muscle contraction (0.55 s in duration) separated by an interval (≥5 s but <90 s), which Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical may be

associated with an arousal. A PI M index (events/hour) >5 is abnormal. Tricyclic antidepressants, lithium, and selective serotonin reuptake inhibitors (SSRIs) can increase PLMs. Saletu and colleagues performed EEG mapping in RLS patients and demonstrated an increase in both absolute δ and absolute and relative α2 power, a decrease in absolute and relative Inhibitors,research,lifescience,medical α1 power, an acceleration of the dominant frequency and the a centroid, and a slowing of the δ/θ

centroid, as well as a nonsignificant attenuation in total power.105 These findings arc characteristic of dissociated vigilance changes described in depression and correlated with higher depression and anxiety scores, lower quality of life, Inhibitors,research,lifescience,medical and deteriorated sleep quality despite normal Epworth Sleepiness scale scores. Treatment options for RLS include dopaminergic agents (pramipexole, ropinirole, pergolide, levodopa/carbidopa), opioids (oxycodone, propoxyphene), benzodiazepines (clonazepam), anticonvulsants (gabapentin, carbamazepine), and clonidine.97,102,106-117 Patients with low serum ferritin levels may benefit from iron therapy. Treatment with enough dopaminergic agents is complicated by rebound (worsening of symptoms at the end of the dosing period with late night or morning recurrence of symptoms and PLMs) and augmentation (worsening of symptoms seen with long-term use, particularly with higher doses, presenting with earlier time-of-day onset of symptoms and expansion of symptoms beyond the legs). With levodopa, rebound occurs in 20% of RLS patients, while augmentation affects 82% of patients; augmentation is increased in patients with more severe RLS and in those receiving higher doses.7,106,117 Dopamine agonists are useful in treating patients with RLS.