Search terms intended for Medline were adapted as required for other databases. Terms used were “electroconvulsive therapy,”“electroshock,”“electroconvulsive,”“ECT,” combined with any of the following “use,”“utilization,”“practice,”“survey,”“statistical data,”“frequency,” limited to human studies and dating from 1990 to today. Relevant references, known to authors of this review published on governmental

internet sites or from newly published Inhibitors,research,lifescience,medical text books (Swartz 2009) or reference lists in retrieved included papers, were also hand found. Table 1 Overview of included studies (N= 70) according to continent, country, region, city, or local Inhibitors,research,lifescience,medical hospital level. Inclusion and exclusion criteria Inclusion criteria: Data-based observational studies or surveys with reported ECT utilization, frequency, or selleckchem prevalence rates, by data collected from 1990 and above, for patients in psychiatric establishments (inpatients or outpatients) in well-defined continents, countries, regions, cities, or local hospitals. Also included were relevant studies published near the date limits for this study

(from Inhibitors,research,lifescience,medical 1990), for geographical areas that had few pertinent publications. Studies in the following languages were included: English, Scandinavian (Norwegian, Swedish, Danish), and European (German, French, Spanish, Portuguese, Turkish). In addition to authors’ Inhibitors,research,lifescience,medical European language fluency, the online Google translation tool (http://translate.google.com/) was used when needed (e.g., for Portuguese and Turkish). Following exclusion criteria were included. Not data-based study

or survey, no or unclear report of ECT utilization, frequency, prevalence rate, practice, in unclearly defined populations. All report of utilization frequency, prevalence rates of ECT in selected samples or subgroups (e.g., young/adolescent, elderly) or special populations (such as pregnancy, disability, mental Inhibitors,research,lifescience,medical retardation), and qualitative studies about clinician or physician subjective experience (views or opinions) Rebamipide on ECT. Screening of literature Two reviewers (KAL, BH) independently checked the titles, and where available, the abstracts of the studies identified by the electronic database searches. All references appearing to meet inclusion criteria, including those with insufficient details, were requested in full text. All reviewers (KAL, LJVS, BH) consisting of two pairs independently extracted data from the retrieved full-text articles according to a premade data extraction scheme. All discrepancies were resolved by consensus meeting/discussion, and the final decision was made by the first author (KAL).

Because MWA is a more recent addition to the surgeon’s armamentarium, the discussion will proceed from the perspective of the RFA literature and except for several caveats, which differentiate RF from MW energy, the assumption is made that the clinical performance of MWA is at least that of RFA. Our discussion will not include “cold” thermal ablation (cryoablation), chemical ablation (Cediranib cost percutaneous ethanol injection, acetic acid injection,

etc) electrical ablation (irreversible electroporation, IRE), or high intensity focused ultrasound (HIFU) as RFA and MWA are the Inhibitors,research,lifescience,medical most commonly utilized technologies at the present time. Radiofrequency Ablation RFA induces tumor necrosis by achieving local hyperthermia with temperatures exceeding 58°C. RFA is based on alternating current of radio frequency waves (≈500 KHz) that are transmitted via a probe into tissue to cause ionic agitation, which generates frictional Inhibitors,research,lifescience,medical heat that extends into adjacent tissue by conduction. Eventually, hyperthermia leads to cell destruction as a result of coagulative Inhibitors,research,lifescience,medical necrosis (14). RFA can be performed under US, CT, or MRI guidance. This can be achieved by percutaneous, laparoscopic, or open surgical approaches, depending on operator preference, tumor anatomy, and extent of disease. However, multiple studies (15-18) have shown that the open surgical approach is superior to percutaneous approach Inhibitors,research,lifescience,medical in terms of minimizing local recurrence

rates. Better exposure of the liver, ability to visually

inspect and palpate surface liver lesions, and ability to use intra-operative ultrasound with its associated high sensitivity to detect additional lesions may explain the superior results of surgical approach (19-21). Limitations of RFA Tumor number and tumor size are important Inhibitors,research,lifescience,medical determinants of local recurrence rates or treatment failure after RFA. Patients with solitary CRHM have been shown to have better survival and lower recurrence rates compared to those with multiple CRHM (22,23). Similarly, patients with tumors of size less than or equal to 3 cm have better recurrence free survival following ablation (16,24,25). The optimal negative margin Bumetanide size or ablation zone extension beyond the tumor border for RFA of CRHM has not yet been standardized. Currently, ablating to a negative margin of 0.5 – 1 cm has been recommended (15,20). On the other hand, one study (26) has showed that the rate of local tumor progression was independent of the size of the post-ablation margin, and a meta-analysis (21), suggested that 1 cm intentional margin was not a significant factor on multivariate analysis, for local recurrence However, there is no disagreement that complete eradiation of tumor cells in the target lesion(s) is primary goal of any attempt at ablation. Reported rates of local recurrence from RFA for CRHM range widely, from 2% to 40% (10,20,27).

Therefore, the exchange of endotracheal tube and proper replacement with an adequate tube plays an important role. Care must be taken to reduce neck manipulation, SB202190 mw minimize use of laryngoscopy, and cause less sympathetic stimulation. Guide wire “j” tip catheter, which is a central venous catheter, is suggested for the exchange of a tracheal tube during anesthesia without using fiberoptic bronchoscope or laryngoscopy (figure 1). Figure 1: Guide wire «j» tip used for changing the tracheal tube. To exchange a tracheal tube during anesthesia in operating room without using fiberoptic Inhibitors,research,lifescience,medical bronchoscope or laryngoscopy, a flexible guide wire “j” tip is inserted into the

Inhibitors,research,lifescience,medical previously perforated tube and the damaged tube is removed. Guide wire “j” tip remains in place, and a new tube is advanced over the guide wire “j” tip, and is correctly placed at the expected point. Then, guide wire “j” tip is removed slowly. After the evaluation of the lungs and ensuring adequate ventilation, the new tube is fixed with desired instruments. During the exchange and replacement of tracheal tube, hemodynamic parameters including, electrocardiogram monitoring, blood pressure, and hemoglobin oxygen saturation are protected and controlled continually (figure 2). Figure

2: Stages of change and replacement of the tracheal tube. Proper management of Inhibitors,research,lifescience,medical airway disorders and dealing Inhibitors,research,lifescience,medical with patients with difficult intubation is one of the problems, which an anesthesiologist experiences in the operation room. One of the common causes of endotracheal tube exchange for the patients in the operating rooms and intensive care units is tearing and laceration of endotracheal tube cuff. The use of different instruments to guide tracheal tube to make endotracheal tube exchange easy with no side Inhibitors,research,lifescience,medical effects in patients was described in 1981. Different techniques have suggested the use of varied instruments such as suction catheter, urethral catheter, fiberoptic bronchoscopy,3,4 stylet,5 endotracheal tube changer-guide,

gum-elastic bougie,6 cook airway exchange catheter,7 and endotracheal tube exchange.8 Advantages and disadvantages of each technique should be investigated. In guide wire “j” technique, the tip of the wire is used for exchanging endotracheal tube without using all fiberoptic bronchoscopy or causing harmful manipulation of neck. Advantages of this technique include availability of this instrument, simplicity of its use, and minimization the risk of serious hemodynamic complications. However, this technique may encounter two problems including the twisting of J-wire inside the endotracheal tube, and the obstruction of old tube by clot or mucous plaque, which should be cleared by suctioning before replacing the old tube with a new one.

Caveats to this approach, and

for the initial combined resection-ablation strategy, are that for conventional thermal tumor ablation, lesions should be less than 4 cm. If bilobar disease is present, then ablation should not TWS119 nmr compromise inflow or outflow tracts as a consequence of hepatic swelling, as this may compromise future liver resection. Utilization of intra-operative ultrasound is employed both for targeting TTA, avoiding treatment failure, and protecting vital intrahepatic structures. Use of ablation for management of synchronous CRHM during primary tumor resection may limit the morbidity when compared to simultaneous colorectal and liver resections, although both can be performed Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical safely in selected patients (46). It is worth noting that in the setting of CRHM, the need for resection of the primary tumor in the absence of over bleeding or obstruction may not be necessary and could delay more pressing issues including the management of CRHM or extrahepatic disease (47,48). Bilobar CRHM with the ability to render an appropriate volume of liver free

of disease, upon which the future hepatic remnant can be based This is perhaps the most common clinical scenario in which ablation complements resection. Any staged treatment plan Inhibitors,research,lifescience,medical will ultimately require that after planned interventions, a portion of liver remains with uncompromised inflow and outflow, ideally completely clear of disease. Although not the focus of this review, portal vein embolization (PVE) has enabled the hepatic surgeon to offer staged approaches to a greater number of CRHM patients through the optimization of Inhibitors,research,lifescience,medical future liver remnant volume (49,50). Consider the patient with right hepatic lobe dominant disease and an isolated CRHM in segment III. The authors would advocate Inhibitors,research,lifescience,medical that this patient should proceed to undergo a partial left hepatic lobectomy (laparoscopic approach preferred) and thermal tumor ablation

of any lesion at risk of crossing the main portal scissurae as defined by the middle hepatic vein. Subsequently, the right portal vein is embolized to induce left liver hypertrophy in anticipation of a right formal hepatectomy. In a patient with more extensive, bilobar CRHM in segments II/III, IV, VIII (dome), and VI lesion, several approaches are Thiamine-diphosphate kinase possible. The optimal strategy would be based on the relationship of the tumors to major vascular and biliary structures, in addition to optimizing liver remnant volume. One approach would be to perform a formal left hemi-hepatectomy (clearing II/III and IV-A) and non-anatomic resections of the segment VIII and segment VI lesions. Another approach, again depending on proximity to vital intrahepatic structures, would be to use thermal ablation for the segment VIII lesion and resect the others as previously proposed.

The disease predominates among people of Askenazi Jewish descent (probably due to a founder effect) and is most commonly due to the Y329S mutation in GBE1. Not too surprisingly, this is a “mild” mutation, which probably explains the late onset of symptoms. Thanks to the energy and compassion of one patient, Gregory Weiss, a research foundation (APBDRF; www.apbdrf.org) has been created to develop Inhibitors,research,lifescience,medical therapeutic strategies. GSD V (myophosphorylase deficiency, McArdle disease) The clinical picture and the block in muscle

glycogen breakdown were elegantly described by Brian McArdle in 1951 (35), the enzyme defects was discovered 8 years later (36-38), and it took 12 more years before the first mutations in PYGM were this website identified (39). Inhibitors,research,lifescience,medical Despite

its long history, McArdle disease still presents several riddles. First, although it was long considered a clinically homogeneous disease, its expression can vary from relatively mild exercise intolerance to a crippling condition with frequent cramps and recurrent episodes of myoglobinuria. Explanations have ranged from rare cases Inhibitors,research,lifescience,medical of “double trouble” (i.e. the coexistence in the same individuals of one mutation in PYGM and another in the gene encoding adenylate deaminase) to the association with insertion/deletion polymorphisms in the

angiotensinconverting enzyme (ACE) (40). Probably more important is the protecting effect of even small Inhibitors,research,lifescience,medical amounts of myophosphorylase residual activity, which is determined by the type of mutations: for example, splice mutations are associated to milder clinical phenotypes (41). What remains unexplained is the fatal infantile form Inhibitors,research,lifescience,medical of McArdle disease, which has been reported in a handful of cases (42-45). In these unfortunate infants muscle morphology, biochemistry, and molecular genetics [showing the "common" R50X null mutation (39, 45)] are no different from typical McArdle patients, despite the dismal outcome. GSD VII (phosphofructokinase Thiamine-diphosphate kinase [PFK] deficiency, Tarui disease) PFK is a tetrameric enzyme under the control of three autosomal genes: PFKM encodes the muscle subunit, PFKL encodes the liver subunit, and PFKP encodes the platelet subunit. Mature human muscle expresses only the M subunit and contains exclusively the M4 homotetramer, whereas erythrocytes, which express both the M and the L subunit, contain five isozymes, the two M4 and L4 homotetramers and three hybrid forms. In patients with typical PFK deficiency, mutations in PFKM cause total lack of activity in muscle but only partial deficiency in red blood cells.

Overall, 5% of

patients exhibited a decline in cognitive function 6 months following surgery, but no statistically significant differences were found between the anesthesia groups. In the largest prospective study of cognitive function following noncardiac surgery thus far (the International Study of POCD- IPOCD) thirteen hospitals in eight European countries and the USA recruited 1218 patients.19 One hundred and seventy-six age-matched volunteers from the UK were recruited as controls. To ensure that controls were representative of all nationalities, 145 national controls were also recruited. The study evaluated changes in both patients and controls in memory, executive functions, and processing speed. Cognitive dysfunction Inhibitors,research,lifescience,medical was reported In about 25.8% of patients 1 week after surgery and in about 10% of patients 3 months after surgery – compared with 3.4% and 2.8% of controls after 1 week and 3 months, respectively. These findings suggest that some of the short-term Inhibitors,research,lifescience,medical cognitive changes after CABG

may not be specific to this procedure, but may also accompany other surgical procedures. Long-term POCD Longer-term complaints of CABG patients are often Inhibitors,research,lifescience,medical more subtle. For instance, the patient may have difficulty in following directions, playing chess, or making calculations. Such changes are sometimes described nonspeclfically as “I’m just not quite the same.”1 It should be noted, however, that due to difficulties in following up Inhibitors,research,lifescience,medical patients, there are only a few studies that extended the follow-up period to 1 year and beyond. We will therefore review these studies in detail. Newman and colleagues12 initially

evaluated 261 patients, 172 of whom were still available at the 5-year follow-up. This study evaluated changes in four cognitive domains: verbal memory, visual memory, attention and psychomotor speed, and abstraction. The authors reported that 53% of patients showed a cognitive decline to below their baseline at discharge, but showed some recovery during the next Inhibitors,research,lifescience,medical two testing periods (36% and 24% of patients showed cognitive decline at 6 weeks and 6 months, respectively). At 5 years, long-term decline was apparent in 42% of patients. Postoperative cognitive deficits at discharge were a significant predictor of long-term cognitive decline, Terminal deoxynucleotidyl transferase even when the effects of age, educational level, and baseline score were controlled for. This study had several strengths, Ipatasertib nmr including a large sample size, a diverse test battery, neurocognltive assessment prior to surgery, and a long follow-up period. There were also potential limitations, especially the lack of a control group with which to compare changes over time, and potential practice effects. Selnes and colleagues14 followed 102 CABG patients over a 5-year period. Their battery of tests assessed eight cognitive domains: attention, language, verbal memory, visual memory, vlsuoconstruction, executive function, psychomotor speed, and motor speed.

Adam Carie and Jonathan Rois-Doria contributed equally to this work.
The specific treatment of cyanide (CN) intoxication means the use of scavengers (e.g., methemoglobin former sodium nitrite (SN) or cobalt compounds or cyanohydrin formers, hydroxocabalamin (Cyanokit has been approved in the US), cobinamide [1], and/or the conversion of CN to the less toxic thiocyanate (SCN) with exogenously administered GSK343 sulfane sulfur and sulfurtransferase enzymes [2–4]. Rhodanese (Rh) is the best characterized multifunctional, mitochondrial sulfurtransferase [5–8] catalyzing the transfer

of a sulfane sulfur atom from a donor molecule to cyanide. Determining the exact role of nitrite in cyanide antagonism is not clearly Inhibitors,research,lifescience,medical understood yet. Earlier studies were focusing on the methemoglobin-forming effect of nitrite that act as a scavenger by forming a relative stable complex Inhibitors,research,lifescience,medical of cyanomethemoglobin [3, 4]. Very recent studies are focusing on the mitochondria-linked mechanism of nitrite as a nitric oxide donor [9–11]. Extensive researches are also focusing on developing effective sulfur-containing Inhibitors,research,lifescience,medical compounds serving as sulfur donors for reacting with CN with or without Rh. Thiosulfate (TS) is the classical sulfur compound found to participate in the

enzyme reaction [3, 4, 12]. However, TS has limited ability to reach the endogenous Rh enzyme because of a nearly exclusive extracellular distribution [13]. Baskin et al., reported results on the efficacy of various sulfur donors demonstrating that altering the chemical substituent Inhibitors,research,lifescience,medical of the longer chain sulfide modified the ability of the candidate molecule to protect against CN toxicity [14]. Earlier investigations were focused on administration of free Rh and the sulfur donor (SD) directly into the bloodstream [15–18]. Unfortunately, the free Rh enzyme was rapidly destroyed

by the body’s immune system, which makes the efficacy Inhibitors,research,lifescience,medical of this approach quite limited. To overcome the limitations for the circulating free Rh, micro- or nanosized carrier systems among others sterically stabilized unilamellar liposomes of ~100–150nm diameter are in either the focus of recent encapsulation efforts [19]. The encapsulation of Rh with a sulfur compound into liposomes—the so-called coencapsulation—can offer further advantages. Over stability enhancement for Rh the coencapsulation can provide better overall conversion of CN, since the basis component for enzyme reaction, the sulfur donor no longer has to penetrate the liposome membrane. The lipid composition has a significant impact on the encapsulation efficiency of the Rh and/or sulfur compound and on the in vivo stability and antidotal effect of the carrier system [19]. Thus, optimization of the liposomal composition is an inevitable step in the design of novel antidotal systems. Present work deals with a new lipophilic sulfur-containing compound, developed at the US Army Medical Research Institute of Chemical Defense, called DTO.

Herein, we comment on the methodological pitfalls of this article in particular, and the accuracy of the research on diagnostic tests in general. Basic steps in the design of diagnostic

accuracy studies include determination of study objectives, identification of target-patient population, and selection of the gold standard as well as selection of measures of accuracy.2 The first and second steps have been managed properly in the study by Sanaei and colleagues. However, the authors’ approach to the third and fourth steps needs more clarification. The selection of a gold standard Inhibitors,research,lifescience,medical is the most difficult step in studies involving diagnostic tests. Some investigators believe that there is no a true gold standard, since no test or procedure is entirely accurate to differentiate patients and healthy

individuals. However, for all studies on the accuracy of diagnostic tests, it is important to establish an operational standard.2 Although the presence of a test with the highest sensitivity and specificity is ideal, some issues including availability, cost and invasiveness of the Inhibitors,research,lifescience,medical test should be considered. Any change in the gold standard alters the sensitivity and specificity of a diagnostic test. Accordingly, when the gold standard was changed (table 3 of the paper), the measure of accuracy of ELISA test was changed as well. Therefore, Inhibitors,research,lifescience,medical the authors should have chosen a test, which had a specified sensitivity and specificity, as the gold standard. 2Methoxyestradiol Application

of an imperfect gold standard usually leads to the underestimation of test accuracy, which is termed imperfect gold standard bias.2 The selection of measures of accuracy is another step in the design of studies on diagnostic tests accuracy. The paper by Sanaei and colleagues has reported the positive and negative predictive Inhibitors,research,lifescience,medical values. The predictive value is a post-test probability, and is affected by the prevalence of the disease. In contrast to the sensitivity and specificity, the predictive value is not a measure of intrinsic diagnostic accuracy, and varies with any change in the pre-test Inhibitors,research,lifescience,medical probability. Therefore, the results of any test must be interpreted considering the pre-test probability of the disease in the desired population.
Antiphospholipid syndrome (APS) is an autoimmune disease. The disease has two forms including a primary and a secondary. The primary form is an isolated diagnosis, and the secondary form is associated with lupus or other diseases like rheumatoid Rutecarpine arthritis. The correct diagnosis of the disease requires one clinical criterion such as thrombosis or abortion, and a positive moderate to high serum titer for anticardiolipin or Antiβ2glycoprotein. About 60 to 80% of patients with APS are women. Moreover, 10% of first-stroke victims, especially those who are young, and up to 21% of women with three or more consecutive fetal losses have APS.1 APS is a multisystem disease, and affects all organ systems.

The Maimonides portrait is selleck screening library undoubtedly one of the world’s most famous and easily recognizable universal icons. Portraits, including those of Jewish prominent leaders and scholars, became fashionable long after Maimonides died. We have no way of knowing what Maimonides really looked like, yet a single utterly imaginative “portrait” has successfully Inhibitors,research,lifescience,medical defined our conception of Maimonides for ever. Of the numerous available versions of this portrait let us focus on the pen-and-ink drawing frequently cited and known as “portrait and autograph” (Figure 1).1 The depicted Maimonides signature in this picture is unequivocally authentic and resembles his numerous verified signatures

found in the Cairo Genizah (Figure 2).2 However, many intriguing questions come to mind when appraising the portrait itself. In the following article we’ll try to answer these questions. Figure 1 Maimonides’ traditional portrait and autograph.1 This nineteenth-century imaginative depiction,

Inhibitors,research,lifescience,medical courtesy of the Granger Collection, NY, is possibly by the American illustrator Arthur Burdett Frost. Figure 2 The enlarged signature in the picture (above) compared to Inhibitors,research,lifescience,medical the almost identical authentic one found in the Cairo Genizah (below).2 HOW AND WHEN DID THIS PARTICULAR PORTRAIT BECOME ASSOCIATED WITH MAIMONIDES? The earliest Maimonides portrait, dating back to the fifteenth century, Inhibitors,research,lifescience,medical is attributed to Professor Moshe-David (Umberto) Cassuto (1883–1951) who reportedly 3 discovered it in 1935. Professor Umberto Cassuto, a member of the Academic Council of the Hebrew University in Jerusalem, has discovered a new portrait of Maimonides made in the 15th century. The portrait is coloured and is of rare artistic value, showing Maimonides in oriental dress. Regretfully, the exact details of that particular intriguing discovery are unknown. Professor Cassuto, a renowned Rabbi and scholar, has written the Maimonides article in the Treccani Encyclopedia and was intimately familiar with the rare handwritten and beautifully illuminated copies Inhibitors,research,lifescience,medical very of the Mishneh

Torah created in Italy and Spain in the fifteenth century. It is plausible that, while cataloguing all Hebrew manuscripts in the Vatican Library (later to be published as Codices Vaticani Hebraici), Professor Cassuto has indeed encountered and identified such a portrait. Luckily much more is known about a portrait that dates back to the eighteenth century. This image was probably first “discovered” in the mid-nineteenth century by Yashar (R. Isacco Samuele Reggio, 1784–1855), an Austro-Italian scholar, mathematician, voluminous writer, and rabbi born at Gorizia. Reggio was one of the prominent leaders of Jewish emancipation and found the portrait in a 34-volume encyclopedic work called Thesaurus Antiquitatum Sacrarum (1744–1769).

70 Neuropathological findings after TBI share similarities with findings in AD, and TBI may lead to a pathophysiological cascade including axonal damage, increase of Aβ42 production, and decrease of long-term potentiation.70 In mild TBI, a pattern of change in white matter integrity similar to that found in AD was recently found.71 Biomarker studies revealed that AD CSF biomarkers may also be altered in TBI, eg, increase Inhibitors,research,lifescience,medical of CSF tau and Aβ peptides early after severe TBI, while their diagnostic and prognostic value is still uncertain.72 selleck kinase inhibitor cardiac arrest may

lead to gray matter reductions in the cingulate cortex, precuneus, insular cortex, posterior hippocampus, and dorsomedial thalamus,

which account for a broad range of neuropsychological impairment in these patients, notably amnestic syndromes.73 Cerebral accumulation of Aβ42 was seen in short-term survivors of cardiac arrest74 Inhibitors,research,lifescience,medical as well as animal models,75 leading to the conclusion that brain hypoxemia after cardiac arrest may foster cerebral Aβ42 accumulation and AD pathology.75 However, it is unclear, if this finding further adds to the cognitive impairment seen in patients after cardiac arrest and cerebral hypoxemia. Alcohol-related cognitive impairment may resemble AD and hippocampal Inhibitors,research,lifescience,medical atrophy may be present. CSF biomarkers Aβ42 and tau may be helpful in the distinction of alcohol-related memory decline and AD in unclear cases.76 There is a broad range

of medication that may cause or increase memory impairment, including benzodiazepines, psychotropics, opioids, antiepileptics, Inhibitors,research,lifescience,medical glucocorticoids, and anticholinergics. A recent study using data from the French pharmacovigilance Inhibitors,research,lifescience,medical database found a significant relationship between “memory loss” and benzodiazepines, benzodiazepine-like hypnotics, some antidepressants, analgesics, anticonvulsants, antipsychotics, and other drugs, pointing to the importance of a detailed drug history in patients who complain aminophylline of memory deficits.77 Conclusion With the use of new imaging techniques and biomarkers of dementing diseases, knowledge is further growing on the pathophysiology of AD and non-AD memory impairment. Biomarkers that are recommended in current diagnostic guidelines will not only lead to a higher diagnostic accuracy, but also reveal overlapping pathologies between different neurodegenerative diseases, helping us to develop new concepts on AD and non-AD memory impairment. Although it is evident that mixed pathological entities of neurodegenerative and mental diseases are common, it is important to utilize existing diagnostic possibilities to aim to correctly identify the leading underlying cause of memory impairment and to take suitable therapeutic measures.