IGF-1 is the mediator of the ability of exercise to increase cell proliferation in the DG. Lack of IGF-1 and insulin in diabetes has the opposite effect and decreases cell proliferation. Neurogenesis and/or survival of newly born cells is increased by putting mice in a complex (”enriched“) environment.45 It is also increased by a form of classical conditioning

that activates the hippocampus (”trace conditioning“) prolongs the survival of newly born DG neurons.46,47 On the other hand, certain types of acute stress and many chronic stressors suppress neurogenesis or cell survival in the DG, and the mediators of these Inhibitors,research,lifescience,medical inhibitor effects include excitatory amino acids acting via N-methyl-D-aspartate (NMDA) receptors and endogenous opioids.2,48-50 Chronic stress has even more potent effects on neurogenesis and neuronal survival. CRS for 21 days suppressed neurogenesis and CRS for 42 days Inhibitors,research,lifescience,medical causes the number of DG neurons to decrease along with total DG volume (Figure 3).51 Figure 3. A single restraint stress does not suppress cell proliferation. Repeated restraint stress for 21 days suppresses cell proliferation. Repeated restraint stress for 42 days reduces volume of Inhibitors,research,lifescience,medical the dentate gyrus (DG) and the number of neurons in the DG. Remodeling of dendrites Another form of structural plasticity is the remodeling of dendrites in the hippocampus.39 CRS causes retraction and simplification of dendrites in the CA3 region of the hippocampus (Figure

4). 2 Such dendritic reorganization can also be seen in rats undergoing adaptation of psychosocial stress in the visible burrow http://www.selleckchem.com/products/pifithrin-alpha.html system (VBS).The VBS is an apparatus with an open chamber where there is a food and water supply and several tunnels and chambers.52 Rats can be observed from above by a video camera in this apparatus. In the VBS, male rats housed with several Inhibitors,research,lifescience,medical females establish a dominance hierarchy within several days. Over the course of the next week, a few subordinate males may die and others (showing scars from bite marks) will show enlarged adrenals, low testosterone, Inhibitors,research,lifescience,medical and many changes in brain chemistry. The dominant shows the fewest scars and has the highest level of testosterone, but also has somewhat larger old adrenal glands

than cage control rats. Figure 4. Hippocampal CA3 pyramidal neurons are remodeled by 21-d restraint stress. A. Control. B. 21 days′ chronic restraint stress. Regarding changes in brain structure, it was the dominant rats that had a more extensive pattern of debranching of the apical dendrites of the CA3 pyramidal neurons in the hippocampus, compared with the subordinate rats, which showed reduced branching compared with the cage controls.53 What this result emphasizes is that it is not adrenal size or presumed amount of physiological stress per se that determines dendritic remodeling, but a complex set of other factors that modulate neuronal structure. We refer to the phenomenon as “dendritic remodeling” and we generally find that it is a reversible process.

The amplitude of the MUAP is determined by 5-12 fibres within a 0,5 mm radius of the recording needle tip, while MUAP duration is determined by the number of fibres within a 2,5 mm radius of the recording needle tip (18). As atrophic fibres begin to appear within the 0,5 mm radius of the recording tip this will cause a reduction in MUAP amplitude. As the myopathy progresses Inhibitors,research,lifescience,medical and there is random loss of fibres will there be shortening of the MUAP duration. Our patients were mostly in the early

stages of clinical involvement and only 6 out 31 patients exhibited fibre loss as evidenced by the presence of increased endomysial tissue (M3). This perhaps explains the higher sensitivity demonstrated by the amplitude outlier method. There were no significant differences in detecting the various histological abnormalities (M1, M2, M3, and M4) for any one of the three QEMG methods. Since variability in fiber size (M1) was present in most of the biopsies one can speculate that this histological Inhibitors,research,lifescience,medical feature alone drives the sensitivity of each of the method of analysis. Our study is in keeping with the view that EMG can not be reliably correlated with specific features

in the www.selleckchem.com/products/Cediranib.html muscle biopsy. Previous studies examining QEMG and muscle biopsy have documented a correlation only between long duration motor unit potential and regenerating fibers (9, 10). No formal morphometry Inhibitors,research,lifescience,medical on the biopsies was carried out in our study, such as deriving atrophy or hypertrophy factors, since this is not routinely practiced Inhibitors,research,lifescience,medical in our laboratory. There are many other limitations to our study including its retrospective nature and the small numbers of patients. However it was based on material acquired on a pragmatic approach in the investigation of patients. The ideal study would have been prospective Inhibitors,research,lifescience,medical and should have included patients in which the QEMG and biopsy are performed sequentially in the same muscle. In addition in interpreting the findings of this study the sampling errors both of QEMG and that of the muscle biopsy need to be kept in mind. In summary, based

on our data, we conclude that the amplitude outlier method of analysis may be the most sensitive method in picking up myopathy at found its very earliest stage.
Mesoangioblasts are a class of adult stem cells of mesoderm origin, potentially useful for the treatment of primitive myopathies of different etiology. Extensive in vitro and in vivo studies in animal models of muscular dystrophy have demonstrated the ability of mesoangioblast to repair skeletal muscle when injected intra-arterially. In a previous work we demonstrated that mesoangioblasts obtained from diagnostic muscle biopsies of IBM patients display a defective differentiation down skeletal muscle and this block can be corrected in vitro by transient MyoD transfection.

Anticoagulation Management In contrast, an advantage of the newer agents over warfarin is the rapid onset of anticoagulation and sustained durability. This is particularly advantageous during the cardioversion of atrial fibrillation. Unless closely monitored, the unpredictability and delay of warfarin’s anticoagulation effect may lead to subtherapeutic or supratherapeutic levels, causing delays in procedures and increasing the patient’s risks. Inhibitors,research,lifescience,medical Newer agents provide prompt anticoagulation effects with the first dose.3, 5 The ability to reverse warfarin with proven strategies including fresh frozen plasma and vitamin K is an advantage. Dabigatran, rivaroxaban,

and apixaban do not have specific reversal strategies confirmed in clinical practice. Presently, there is some literature suggesting that fresh frozen plasma or prothrombin complex concentrates are potential treatments. However, this data has not been established.9, 10 Even in the best of hands, maintenance of INRs between 2 to 3 while on warfarin ranges from 44–77%.1, 2, 4, Inhibitors,research,lifescience,medical 7, 11 A subtherapeutic level Inhibitors,research,lifescience,medical may be associated with an increased stroke risk and a supratherapeutic level with an increased risk of bleeding. This fact

is probably why two of the three newer agents have proven superiority over warfarin. However, warfarin patients who have a history of high compliance and are consistently maintained appropriately may not benefit from Inhibitors,research,lifescience,medical switching to a newer agent.11 Conclusion To date, we have three new choices for oral anticoagulation to help prevent stroke in patients with nonvalvular atrial fibrillation. Warfarin, the veteran

anticoagulant with known interactions, monitoring, and reversibility, still remains a viable option for treatment, especially in well-controlled patients. Dabigatran is the only available agent with established superiority in preventing stroke. Rivaroxaban a noninferior choice compared to warfarin with once-daily dosing. Apixaban awaits FDA review and probable approval and is the only agent with superior efficacy and safety. Our views of the advantages and disadvantages of each Inhibitors,research,lifescience,medical agent are summarized in Table 1. Table 1 Advantages and disadvantages of stroke-prevention agents for nonvalvular whatever atrial fibrillation. Conflict of www.selleckchem.com/products/GDC-0941.html Interest Disclosure: The authors have completed and submitted the Methodist DeBakey Cardiovascular Journal Conflict of Interest Statement and none were reported. Funding/Support: The authors have no funding disclosures. Contributor Information David Putney, Methodist DeBakey Heart & Vascular Center, The Methodist Hospital, Houston, Texas. Craig Pratt, Methodist DeBakey Heart & Vascular Center, The Methodist Hospital, Houston, Texas.

Introduction Takotsubo cardiomyopathy (TC) was first described in Japan in 1990.1 Takotsubo in Japanese means octopus trap. The trap has a narrow neck and round bottom that resembles the heart shape in TC.

However, the plot thickened when we found yet another patient with the association of myopathy and a peculiar CNS dysfunction, namely, severe juvenile Parkinsonism (77). What we found strange and a little disconcerting was that this young man harbored the same previously unreported mutation (p.T378P)

that we had identified in our latest patient with pure myopathy (4). However, we recovered some confidence in genotype:phenotype correlation when Dr. Spiegel’s patient also developed severe Parkinsonian symptoms and signs. Although this is an n of 2 series, our findings raise two interesting questions. First, is there, in fact, a causal relationship between Inhibitors,research,lifescience,medical the T378P mutation and Parkinsonism? Second, PGK deficiency was suspected in both patients because they presented initially with Inhibitors,research,lifescience,medical exercise intolerance, cramps, and myoglobinuria: Parkinsonism was a surprising clinical development. One cannot help wondering whether in some patients with PGK deficiency juvenile Parkinson disease may precede and overshadow the myopathy, thus escaping diagnosis. Certainly, this association has to be kept in mind. GSD X (phosphoglycerate mutase [PGAM] deficiency) PGAM is a dimeric enzyme composed of a musclespecific (M) subunit and a brain-specific (B) subunit. Normal Inhibitors,research,lifescience,medical adult human muscle contains predominantly the MM homodimer, which accounts for about 95% of the total activity. Fourteen patients with PGAM deficiency

in muscle have been reported, of whom nine were African American (78, 79). Although the first reported patient could not be studied at the molecular level (80), all other African American patients harbored

the W78X mutation, at least in heterozygosity, suggesting a Inhibitors,research,lifescience,medical founder effect. The most striking Alvocidib peculiarity of GSD X is its common association with tubular Inhibitors,research,lifescience,medical aggregates (TAs), which were seen in the muscle biopsies of 5 patients (36%) whereas they have never been reported in other glycogenoses. TAs are ordered stacks of tubules originating from the sarcoplasmic reticulum. Although they are a nonspecific pathological change seen in diverse conditions, including exposure to drugs, toxins, and hypoxia, their association with PGAM deficiency does not appear to be casual although the specific trigger remains unknown. Conclusions As stated at the outset, we did not intend to review all the muscle glycogenoses, but only to out consider some conundrums still presented by “old” GSD. We have not considered Lafora disease because muscle involvement is overshadowed by the devastating encephalopathy. Likewise, we have not discussed some recently described glycogenoses, such as aldolase deficiency (81), β-enolase deficiency (82), and the two forms of glycogenosis type 0 (aglycogenosis?) (7, 8) because they have been described in single patients. Thus, although we discussed more the problems than the progress promised in the title, we hope our considerations are an adequate homage to Valerie Askanas and W. King Engel.

Two peculiar aspects of GSD VII are worth discussing: the presence of polyglucosan in muscle and the severe infantile presentation. The presence – in addition to normal-looking glycogen – also of abnormal glycogen with the histochemical (diastase-resistance) and ultrastructural (fine granules and filaments instead of β-particles) features of polyglucosan was first noted in the muscle biopsy of two patients (48) and confirmed in a woman Inhibitors,research,lifescience,medical who had developed late-onset fixed weakness (49). We reasoned that this surprising finding could best be explained by the excessive accumulation of glucose-6-phosphate (G6P) upstream of the glycolytic block (49).

As G6P is a functional activator of glycogen synthetase (GS), the finely balanced activity ratio of GS and GBE would be tilted in favor of GS and result in a polysaccharide with abnormally long and poorly branched chains, i.e. polyglucosan. This pathogenic concept was confirmed by two experiments, one in the laboratory, the other an experiment of nature. First, when Inhibitors,research,lifescience,medical Nina Raben upregulated the expression of GS in the muscle of GAA-deficient mice, she unexpectedly obtained polyglucosan accumulation Inhibitors,research,lifescience,medical (50). Second, after

a long search for the molecular basis of polyglucosan myopathy in horses, Stephanie Valberg and co-workers identified a gain-of-function mutation in GS, again altering the GS/GBE activity ratio in favor Inhibitors,research,lifescience,medical of GS (5). The second riddle concerns the fatal infantile variant of GSD VII, reported in a dozen patients between 1987 and 2008. All infants were severely hypotonic at birth and a few developed joint contractures either in utero (51-53) or postnatally (54, 55). Decreased fetal movements were noted in two pregnancies (52, 53) and polyhydramnios in one (53). In all but two cases (53, 55), death occurred in infancy or Inhibitors,research,lifescience,medical early childhood due to pulmonary failure. Most children showed evidence of multisystem involvent, including seizures, cortical blindness, developmental delay, dysmorphic features, and Nutlin-3 manufacturer corneal

ulcers. The encephalopathy was documented by neuroradiology or neuropathology, which showed dilated ventricles and cortical or cerebellar atrophy (51, 54-57). Because of the early onset, multisystem involvement, and lack of any molecular evidence of mutations in the PFKM gene, Megestrol Acetate the infantile variant of phosphofructokinase deficiency appears to be a separate entity from GSD VII, and its genetic basis (or bases) remain to be clarified, despite evidence that a transgenic PFKM-null mouse mimics the infantile more than the typical muscular form of the human disease (58). GSD VIII (Phosphorylase b kinase [PHK] deficiency) PHK is a multimeric enzyme composed of four different subunits, α, β, γ, and δ and the enzyme composition is (αβγδ)4.

R1109X mutation in SH3TC2 gene (CMT4C). HMSNL is the most common and widespread neuropathy among European Gypsies (10). Autosomal recessive nonsense mutation in the NDRG1 gene on chromosome 8q24 has been reported to be causative for HMSNL. Founder mutation is C to T transition in exon 7 at mRNA nucleotide position 564 that results in replacement of arginine by translation termination signal at codon position 148 (R148) (11). NDRG1 expression is induced by differentiation or stress stimuli. NDRG1 encodes protein with molecular mass 43 kDa, which is broadly expressed and implicated

Inhibitors,research,lifescience,medical in cell growth and differentiation during development and maintenance of the differentiated state of the adult (12, 13). It is also implicated in tumor suppression, stress and hormonal response (14, 15). NDRG1 protein expressed in peripheral nerve is localized in the cytoplasm of myelinated Schwann

cells, including Inhibitors,research,lifescience,medical the paranodes and Schmidt–Lanterman incisures. NDRG1 is not found in sensory or motor neurons. Oligodendrocytes also express NDRG1 (16). In Schwann cells this protein is localized in cytoplasm and interacting with apoA1, apoA2, reticulin 1c and several other check details proteins may also be involved in the regulation of lipid trafficking and Inhibitors,research,lifescience,medical Schwann cell-axon communication (17, 18) Cytoplasmic expression and phosphorylation of NDRG1 implies its association with intracellular signal transduction in Schwann cells. The NDRG1-deficient mice exhibited a progressive demyelinating disorder of the peripheral nerves leading to muscle weakness, indicating that NDRG1 function is important for the maintenance of myelin sheaths and axonal survival (19). The patients in Serbian family are presented with the typical phenotype, severe denervation and severe affection Inhibitors,research,lifescience,medical of cochlear nerve.
A deficit of emerin or lamins Inhibitors,research,lifescience,medical A/C is related to a very rare, genetically transmitted, Emery-Dreifuss muscular dystrophy (EDMD). Even if the defect is generalized to all tissues skeletal muscle, heart and joints are selectively affected. Muscle atrophy, joint contractures, and dilated cardiomyopathy are the leading symptoms. Cardiac

disease, although often silent, usually precedes skeletal muscle involvement. The pathogenesis of dilated cardiomyopathy in EDMD has not been recognized, yet. Activation of mitogen protein kinase (MAPK) in the development of cardiomyopathy has already been suggested (1, 2). Activation of very MAPK in a mice model of EDMD, prior to cardiomyopathy has been described (3, 4). The question is, if it is the basic abnormality, which leads to the development of cardiac disease in human EDMD. Other mechanism(s) should be also taken into account. It is already known that in a subset of patients with idiopathic dilated cardiomyopathy (DCM), autoimmune mechanism(s) are involved (5–1,1). In EDMD, autoimmune mechanism(s) may also participate in evoking DCM.

All patients experienced ED for at least 6 months

after their RP before starting MUSE therapy. Overall, 55% of patients achieved and maintained erections sufficient for intercourse, 48% continued long-term therapy with an average usage of four times per month, and there was a 61% spousal satisfaction rate. The most common reasons for discontinuation of MUSE are insufficient erections, switch to other ED therapies, natural return of erections, and urethral pain and burning.41 MUSE has been shown to be an effective therapy for post-RP ED with a compliance rate of 63% #this website keyword# to 68% shown in some series.14,41 Like ICI therapy, intraurethral PGE-1 has been shown to increase intracorporal oxygenation by 37% to 57%.14 PGE-1 has been shown in rat models to rescue dorsal root ganglion Inhibitors,research,lifescience,medical neurons from apoptosis and improve axonal regeneration in diabetic rats. These mechanisms of action will further help prevent post-RP fibrosis and stimulate neurovascular bundle regeneration after RP. Combination Therapy Combination therapy can include ICI with PDE5-I, or VED and PDE5-I. Montorsi and coauthors randomized patients to receive ICI of alprostadil three times per week for 3 months with on-demand sildenafil for 3 months versus monotherapy with sildenafil on demand starting 3 months after RP.25 Patients in the combination

arm had an 82% response rate to sildenafil Inhibitors,research,lifescience,medical versus 52% in the monotherapy Inhibitors,research,lifescience,medical group.25 Mydlo and colleagues retrospectively looked at 34 men after RP with subsequent ED.42 The patients were then titrated on either sildenafil or vardenafil to their maximum doses. All patients had suboptimal responses after a maximum of eight doses as assessed by the SHIM score. These patients were then started on ICI therapy with alprostadil in addition to their oral therapy with 68% reporting a much better erection with combination therapy. Nandipati and associates evaluated early combination Inhibitors,research,lifescience,medical therapy with ICI therapy with alprostadil and oral sildenafil versus low-dose TriMix (papaverine, phentolomine

and PGE-1) versus low-dose PGE-1 after RP.23 Sildenafil, 50 mg, was started daily at discharge old from the hospital, and ICI therapy with alprostadil or low-dose TriMix was started within 3 weeks or at catheter removal. This therapy was to be attempted two to three times weekly. Their results were compiled using the abridged version of the IIEF-5 questionnaire. The patients were followed every 3 months for a 12-month period. At a mean follow-up of 6 months, 96% were sexually active. Approximately 45% were sexually active in the injection-only group versus 50% with combination therapy. Doppler studies showed that peak systolic velocities were higher in the low-dose TriMix population compared with the low-dose PGE-1 alone group. These data support a stronger response of penile vasculature with TriMix.

61,62 Other approaches proposed the development of disease management programs for specific types of mental disorders, similar to those existing in diabetes and other chronic conditions. More critical propositions, that target explicitly the cost component, have been the implementation of pharmacy benefit manager. In this model, pharmacists review GPs’ prescriptions with regard to drug, dosage, drug

interactions, duration, Inhibitors,research,lifescience,medical and cost, and make recommendations to the GP and the patient (compliance and adjunctive treatment). Although this model has some attractiveness for policy makers, this approach has also negative effects in terms of invasion of privacy and interference with physicians’ treatment decisions. Research context In order to set the context for exploring explanations for the gap between what is potentially Inhibitors,research,lifescience,medical achievable and what actually

exists in primary care, there is a need for systematic stepwise inquiry in four domains: efficacy, effectiveness, practice research, and service systems research. As efficacy studies most frequently serve for approval of medications, the gold standard remains randomized clinical trials, with strict highly controlled inclusion and exclusion criteria, and mostly one or two symptom outcome Inhibitors,research,lifescience,medical measures of 8 weeks or a few weeks longer. Because primary care patients are often highly comorbid and rarely Inhibitors,research,lifescience,medical allow sufficient adherence to such strict protocols, few efficacy studies on mental health treatments are currently being conducted in primary care settings and, when they are, highly selleck trained specialist components Inhibitors,research,lifescience,medical are usually embedded, which means that they do not reflect the typical primary care situation. These limitations call for greater emphasis on effectiveness research, which aims to establish whether an intervention has a measurable effect in broader populations and real service settings; inclusion and exclusion criteria

are more relaxed, and clinicians can be less specifically trained in the research methods. The important benefit of this type of research is the expansion of outcome measures, for example, with regard to functional status, quality of life, use of health services, and costs. Because of the interest in expanding the generalization of treatments many and interventions, there have been a gradually increasing number of such primary care studies, for example, in depression, suggesting that these studies are feasible in primary care, and that findings similar to those in efficacy studies can be obtained. However, one needs to acknowledge that the findings may be less robust, due to the influence of a higher variability of both patient and physician factors.

Further, there is substantial evidence32 that psychoeducative efforts and brief interventions might be very effective in uncomplicated cases and in the early stages of anxiety disorders, even if applied in primary care. Obviously, the misconception of anxiety disorders as belonging to the less severe morbidity spectrum, with no explicit need for immediate intervention, is the cause of this neglect. The available evidence is largely

limited to two anxiety disorders: panic disorder (PD) and GAD, which are assumed to be the most severe and chronic forms. The available evidence generally suggests a somewhat Inhibitors,research,lifescience,medical worse picture than for depression. Of all anxiety disorders, less than 50% are recognized and even fewer are

specifically diagnosed. Panic disorder According to Spitzer Inhibitors,research,lifescience,medical et al,33 PDs occur in about 4% of patients in US primary care, although other studies suggest that this is an upper bound estimate (ie, the true value might be lower).7 PD is frequently associated with Inhibitors,research,lifescience,medical agoraphobia and differs from most phobic disorders in terms of acute severity, extensive use of medical services, high costs, multiple unexplained medical illnesses and therefore increased rates of laboratory testing, and as much impairment and disability as other severe medical illnesses. Similar to depression, < 50% of cases are recognized and few receive adequate diagnosis or treatment in the form of antidepressant drugs, cognitive behavior treatment, or referral to specialists.33 Katon et al34 were unable to show that educational campaigns and treatment guidelines Inhibitors,research,lifescience,medical have any sustained and significant effect on improved recognition. However, they recently demonstrated34 that collaborative care interventions in US primary care, consisting of Inhibitors,research,lifescience,medical f ollow up with the psychiatrist who made the initial SSRI prescription and psychoeducation,

can result in remarkable improvements in terms of symptom reduction. Although direct treatment costs were substantially higher with this approach, the learn more overall costs due to reduction in indirect costs were superior to usual treatment. It is difficult to generalize these findings to other regions and countries, but it nevertheless Adenylyl cyclase ranks among the few promising alternative approaches to be pursued in the future for this and other disorders. Generalized anxiety disorder GAD is a severe and chronic anxiety disorder, for which effective drug and psychological treatments have recently become available. The lifetime prevalence of GAD in the general population has been estimated to be 5% to 6%,31,35,36 which is more than PD. GAD patients are also frequently described as high health care users, particularly of primary care resources.

There were a number of replicated findings, such as the presence of abnormal movements, higher degrees of psychopathology especially hallucinations, a greater degree of chronicity, that were potential indicators of dopamine supersensitivity in both studies. In addition, in both studies, the AIM +ve patients were unlikely to have their medication increased. It could Inhibitors,research,lifescience,medical be that this

reflects an understanding by the prescribing clinician that these individuals had noticeable side effects and reflects an attempt not to exacerbate them by increasing the dose of antipsychotic. In both studies patients with relapses associated with a life event subsequently experienced a more benign course of their illness. Previous research has also found that patients with life events prior to psychotic relapse were more likely to score zero on the AIM scale, more likely to experience complete symptom remission between episodes of illness and have less need for antipsychotic Inhibitors,research,lifescience,medical maintenance medication [Van Os et al. 1994]. In the present study, the AIM -ve patients were more likely to have their medication increased than the AIM -ve patients in the previous study, and this almost Inhibitors,research,lifescience,medical reached statistical significance (p = 0.06 two-tailed). Furthermore, the AIM +ve group were prescribed lower doses that the AIM -ve group, which was not found previously [Fallon and Dursun, 2011]. However, this may be because a significant

proportion of those with Inhibitors,research,lifescience,medical abnormal movements were prescribed oral Enzastaurin nmr atypical antipsychotic medications. When these medications are converted to chlorpromazine equivalent doses, they are prescribed in smaller doses than were the doses of typical antipsychotics historically. For example, olanzapine 5 mg equates to 100 mg of chlorpromazine [Woods, 2003], therefore, the maximum daily dose of olanzapine currently prescribed on license in the UK (20 mg) equates to 400 mg of chlorpromazine per day. The fifth aim was to develop the diagnostic criteria for supersensitivity Inhibitors,research,lifescience,medical psychosis and two main differences to Chouinard’s criteria were found in this study [Chouinard, 1990]. Firstly, withdrawal of medication

was not present first in the sample, which is unsurprising as this was a study into patients compliant with stable doses of medication. Secondly, antipsychotics were not prescribed in high doses and evidence of tolerance was not present. This can be explained by the changes in prescribing atterns as atypical antipsychotics are now the redominant form of antipsychotic prescribed. It has been argued that the newer atypical medications are more tolerable as they produce fewer side effects [Voruganti et al. 2000]. However, in this study, patients prescribed atypical antipsychotics were as likely as patients prescribed typical antipsychotics to display AIMs, and risperidone has previously been found to induce extrapyramidal side effects comparable to haloperidol [Knable et al. 1997].