Occurrence of sleep problems in children and adolescents, including high-risk groups Estimates vary but, from the early years to adolescence,

at least 30% of children in general have a sleep disturbance which is considered by parents, or the children themselves, to be significant. However, the LY2109761 clinical trial nature of the sleep problem varies considerably with age. Bedtime difficulties and problems with night waking are common up to about 3 years of age, whereas nightmares and sleepwalking, Inhibitors,research,lifescience,medical for example, feature more in older children, and many adolescents suffer from the delayed sleep phase syndrome mentioned earlier. However common such problems arc in children overall, certain groups have sleeping difficulties much more often than this.16 Children with a learning Inhibitors,research,lifescience,medical disability, other neurodevelopmental disorders including autism, or psychiatric conditions almost invariably have their lives (and those of their parents) further complicated by disturbed sleep and its consequences. The same can be said of children with other types of chronic pediatric illness. Children with these various conditions do not Inhibitors,research,lifescience,medical have a new set of sleep disorders compared with other children; it is the pattern of occurrence of their sleep disorders that is different. Physical factors may loom large in the etiology

of the sleep problem in many of these conditions (eg. OSA in Down Inhibitors,research,lifescience,medical syndrome) but behavioral factors (failure to develop satisfactory sleep habits) are very common overall. Similarly, these groups of children can generally be expected to respond to the same types of treatment as other children, providing the treatment programs are correct for the sleep disorder in question. One obstacle to this is the mistaken view that, for example, serious sleep problems are inevitable in neurodevelopmentally disordered children, and that Inhibitors,research,lifescience,medical the problems have to be endured because treatment will not work. Ihis is not the case, even when the sleep problem has already lasted some time but, sadly,

for lack of information to the contrary, many such children go untreated. Developmental effects either of persistently not sleeping well The potentially serious and widespread effects of persistently disturbed sleep (especially inadequate or poor quality sleep) deserve to be more widely known by parents and professionals alike. This alone would increase the use of the various types of treatments that are available. Emotional state and behavior “Overtired” children often become very difficult to handle; they become irritable, distressed, and even aggressive, much to the exasperation of their parents. In some children, such problems are frequent and seriously disrupt family life. Reference has been made to the fact that certain young children said to have ADHD characterized by overactivity, impulsiveness, and poor concentration, are reported to have a primary sleep disorder.

Other GABAergic 3α,5α- and 3α,5β-reduced neuroactive steroids, derived from DOC, dehydroepiandrosterone (DHEA), and testosterone, are known GABAergic modulators100-102 that may be elevated by HPA axis activation in humans. Unfortunately,

simple inexpensive analytic methods to measure these steroids are not available. The ability of finasteride to block the subjective effects of ethanol in humans may be due to its ability to prevent the formation of any or all of these neuroactive steroids. Indeed, the combined effects of all steroids regulated by acute or chronic ethanol exposure may contribute to its actions in all species. Effects of ethanol on neuroactive steroid precursors in nonhuman primates and humans We have Inhibitors,research,lifescience,medical recently shown that acute ethanol challenges in cynomolgus monkeys do not change plasma pregnenolone and DOC levels. Two doses of ethanol, 1.0 and 1.5 g/kg, were tested via intragastric administration, and neither was able to increase Inhibitors,research,lifescience,medical neuroactive steroid precursors or circulating Cortisol levels despite an average blood ethanol

level of 147 mg/dL.103,104 In contrast, acute ethanol administration increases pregnenolone, progesterone, DOC, and their neuroactive metabolites in rat brain and plasma,4,31,79,105 and this increase is also prevented by adrenalectomy/orchiectomy, consistent with ethanol activation of the HPA axis.31,105 These results suggest that higher doses of ethanol might be necessary Inhibitors,research,lifescience,medical to stimulate the HPA axis and thus increase pregnenolone and DOC levels in nonhuman primates. Indeed, Williams and collaborators106 have shown that intravenous administration Inhibitors,research,lifescience,medical of ethanol up to 1.9 g/kg failed

to increase plasma ACTH levels in rhesus monkeys. Other studies using 2.0 g/kg ethanol have reported increased Cortisol levels in monkeys under conditions where monkeys were restrained on a flat surface while receiving ethanol, which may contribute Inhibitors,research,lifescience,medical to HPA axis activation.107 The possibility that pregnenolone, DOC, and their neuroactive metabolites might be differentially regulated in nonhuman primates Ibrutinib chemical structure compared with rodents cannot be ruled out; future studies will be necessary to further address this question. The effects of ethanol on neuroactive steroid precursors in humans CYTH4 are inconsistent to date. Laboratory administration of moderate doses of ethanol (0.7 to 0.8 g/kg) has recently been reported to increase pregnenolone and DHEA levels and to decrease progesterone levels in healthy human subjects.27 In contrast, Holdstock et al26 reported that ethanol administration to healthy volunteers increased progesterone levels in women during the luteal phase, but had no effect during the follicular phase or in men. Low alcohol consumption in premenopausal women was associated with increased estradiol, androstenedione, and testosterone levels throughout the menstrual cycle, while progesterone levels were increased only in the luteal phase.

One of the inherent challenges in working with L-Glu receptors is that many neurons express multiple types of receptors, including NMDA, AMPA, and kainate receptors, and that these subtypes can be further subdivided based on see more variations in subunit composition (Dingledine et al. 1999). In recent decades, however, a number of pharmacological

agents have been developed that have facilitated Inhibitors,research,lifescience,medical isolation of currents associated with these channels in electrophysiological investigations (Kew and Kemp 2005; Lodge 2009). Indeed, many of the studies investigating the role of L-Glu in synaptic plasticity have relied largely on pharmacological evidence for identification of the receptors being studied (reviewed in Antzoulatos and Byrne 2004). Despite the professed role of

D-Asp as an alternate agonist at NMDARs, pharmacological evidence Inhibitors,research,lifescience,medical supporting this hypothesis is limited to a single study (Errico et al. 2011). Errico et al. (2011) investigated electrophysiological responses to supraphysiological levels of D-Asp in 13- to 15-day-old C57BL/6J mice. The authors reported approximately 67% block of D-Asp-induced currents with NVP-AAM077, cis-PPDA, and Ro 25–6981, NMDAR antagonists selective for Inhibitors,research,lifescience,medical NR2A, NR2C/D, and NR2B subunits, respectively, approximating the degree of block of NMDA-induced currents in the same cells. When these three antagonists were applied together or when MK-801, a comprehensive NMDAR blocker, was applied, NMDA currents were completely blocked while D-Asp-activated currents were reduced 80%. These results suggested that while D-Asp activated currents in the hippocampus are similar enough to NMDARs currents Inhibitors,research,lifescience,medical to be blocked by NMDAR blockers, it also activated a current clearly not due to NMDAR activation. There is considerable evidence that D-Asp plays a modulatory role at L-Glu-activated receptors. Inhibitors,research,lifescience,medical Antagonistic effects of D-Asp have been observed in L-Glu channels in Aplysia (Dale and Kandel 1993) and in rat hippocampal

neurons and Xenopus oocytes expressing AMPARs (Gong et al. 2005). Further, D-Asp slowed the gating kinetics of a squid glutamate receptor, SqGluR (Brown et al. 2007). In none of these models, however, was D-Asp activation of ion channels studied. It is thus unknown whether D-Asp acts in dual roles, both as a modulator of L-GluR channels and as a neurotransmitter at and novel receptors. The purpose of this study was to further elucidate the identity of channels activated by D-Asp. To achieve this, we attempted a pharmacological characterization of the D-Asp-induced current in Aplysia neurons, with a focus on antagonists and coagonists of L-Glu receptor channels. Materials and Methods Cell culture Aplysia californica (~300–800 g; six to nine months of age and both immature and sexually mature) were obtained from the University of Miami NIH National Resource for Aplysia in Miami, Florida.

41 Because cough is not a well-documented adverse event to the prescribed ARV drugs in this study, it is difficult to identify the specific ARV drug responsible for this in a retrospective study. This will be the basis for a

prospective study where causality between each ART regimen and cough can be adequately assessed. The prevalence of fever and rashes were considerable in this study. This could be due to the fact NVP-based ART regimen was the most frequently prescribed. Rash is a common adverse event associated with NVP and other NNRTIs.40 A few medications can cause fever but it is considered an adverse effect of ARV drug if the fever was accompanied by a rash. Fever and rash are symptoms of hypersensitivity reactions learn more to some ARV drugs especially DRV and ABC.42 Only very few of the well-known and common adverse effects of ARV drugs such as lip dystrophy, peripheral neuropathy, nausea and vomiting were reported in this study. Patients with poor adherence are more likely to report adverse drug events since these could contribute to their poor adherence status. Limitations One of the limitations of this study was lack of adequate information on certain risk factors for adverse events. For example, data was not obtained on comorbid conditions like tuberculosis as stated earlier. A prospective study involving recruitment of patients and long term Panobinostat order follow up after initiation of ART

would have provided more information and permitted more extensive follow up. These would have allowed a better case causality assessment for any of the adverse events. Another limitation was incomplete laboratory data for many of the patients. Apart from viral load and

CD4+ cell counts, other laboratory tests results like liver function test, creatinine clearance, lipid profiles and blood sugar level were not extracted for analysis because data were not available. Therefore, adverse events reported were mainly clinical. Furthermore some of the suspected ADEs reported were similar to the symptoms and signs of HIV/AIDS which further reinforces the need to report the clinical stages at presentation and/or enrolments. Patients on concomitant antimalarial medication (artemisinin-based combination therapy) were not excluded because of the burden of malaria in Nigeria. This group of drugs is known theoretically to interact adversely with ARV drugs43 and may have probably contributed to the observed Thiamine-diphosphate kinase adverse events. Conclusion A combination of AZT-3TC-NVP was the most frequently prescribed ARV drugs in APIN clinic, LUTH. Many of the ART regimens prescribed were outside the WHO and national guidelines for HIV/AIDS treatment, suggesting an irrational prescription. Cough, fever and skin rashes were the most frequently reported adverse events by the patients. Intensive efforts are required to improve adherence, as this is essential for good therapeutic outcome.
Urinary schistosomiasis is a parasitic disease caused by Shistosoma haematobium.

While opioid dependence has more treatment agents available than other abused drugs, none are curative. They can, however, markedly diminish withdrawal symptoms and craving, and block opioid effects due to lapses. The most effective withdrawal method is substituting and tapering methadone or buprenorphine, α-2 Adrenergic agents can ameliorate untreated symptoms or substitute for agonists if not available. Shortening withdrawal by precipitating it with narcotic antagonists has been studied, but the methods are plagued by safety issues or persisting symptoms. Neither the

withdrawal agents nor the methods are associated with better long-term outcome, which appears mostly related to post-detoxification treatment. Excluding those with short-term Inhibitors,research,lifescience,medical habits, the best outcome occurs with long-term maintenance on methadone or buprenorphine accompanied by appropriate psychosocial interventions. Those with strong external motivation may do well on the antagonist naltrexone. Currently, optimum duration of maintenance on either is unclear. Better agents are needed

Inhibitors,research,lifescience,medical to impact the brain changes related to addiction. Keywords: opioid dependence, detoxification, maintenance, Inhibitors,research,lifescience,medical methadone, buprenorphine, clonidine, naltrexone, pharmacologic treatment Abstract Aun cuando la dependencia de opioides tiene más agentes terapéuticos disponibles que otras drogas de abuso, ninguno de ellos resulta curativo. Sin embargo, estos agentes pueden disminuir marcadamente los síntomas de abstinencia y el craving, y bloquear los efectos de los opioides debidos a las recaídas. El metodo Inhibitors,research,lifescience,medical más efectivo para tratar la abstinencia es la sustitución y disminución progresiva con metadona o buprenorfina. Los agentes α-2 adrenérgicos pueden reducir los síntomas no tratados o reemplazar a los agonistas si

no se dispone de ellos. Se ha estudiado la reducción del período de abstinencia utilizando antagonistas narcóticos, pero los temas de seguridad o de la persistencia de síntomas han dificultado su desarrollo. La mejor evolución a largo plazo no se relaciona ni con los metodos ni con los agentes usados para Inhibitors,research,lifescience,medical manejar la abstinencia, sino que se asocia con el tratamiento post-detoxificación. Excluyendo a aquellos pacientes que cambian de hábito en el corto plazo, la mejor evolución ocurre cuando se mantiene metadona o buprenorfina to a largo plazo, junto con adecuadas intervenciones psicosociales. En aquellos pacientes con una fuerte motivación externa puede ser útil el uso del antagonista naltrexona. Actualmente no hay claridad respecto a la duración de los tratamientos de mantenimiento. Se require de mejores agentes para combatir los cambios cerebrales relacionados con la adicción. Résumé Les 5-Fluoracil purchase traitements de la dépendance aux opioides, bien que plus nombreux que ceux des autres substances addictogènes, ne sont pas curatifs. Ils peuvent néanmoins diminuer notablement les symptômes de sevrage et la compulsion de consommation et bloquer les effets opioides dus aux récidives.

Case 2 Twelve-year-old R. O. from Nkoranza was referred to KATH as a possible seizure disorder. He had presented to a local hospital with fever, severe headache and several episodes of generalised

convulsions. The child was fully conscious but had a BP of 140/94mmHg (both systolic and diastolic values > 99th centile +5 for his age). Bedside urine dipstick showed protein and blood of 2+ each. Baseline laboratory test results were as follows: Serum chemistry: Na+ 136, K+ 5.6, urea 16.3, creatinine 389µmol/l, Hb 10.5g/dl, MCV 72 fl, WBC 9.9 × 109/l, platelet 444× 109/l Urine microscopy showed pus cells 5–6/HPF, RBCs > 10/HPF, and S. haematobiuon ova were present. Urine culture result was negative. USS showed a lobulated, hypoechoeic urinary bladder trigone mass with resultant Selleckchem CB-839 bilateral hydroureteronephrosis. Diagnoses of hypertensive encephalopathy and acute kidney injury secondary

to schistosoma related obstructive uropathy were made. He was treated with praziquantel and amlodipine. A scheduled OSI906 nephrostomy tube insertion and cystoscopic excision of the trigone mass could not be done as patient defaulted follow up for several months. When he re-surfaced 6 months later, there had been spontaneous improvement in his renal function with the serum creatinine falling to 150 µmol/l. The trigone mass has reduced in size and the left hydroureteronephrosis had resolved completely. BP had been well controlled on amlodipine. He was then scheduled for 6-monthly review to assess progress. In the subsequent six months, all the hydroureteronephrosis had resolved spontaneously. The left kidney had shrunken somewhat, measuring 6.3 × 2.7cm but with good cortico-medullary differentiation. Right kidney measured 8.3 × 3.3cm. A residual mass in the trigone area had remained. The kidney function had stabilised with serum creatinine at 130 µmol/l and urea of 4.1mmol/l. He was put on lisinopril to control his proteinuria

Farnesyltransferase and slated for another 6 months review as a case of Stage 3 Chronic Kidney Disease (eGFR 52.7ml/min/1.73m2). Case 3 Twelve-year-old O. A. from Yeji, a schistosomiasis endemic area, presented with recurrent abdominal pain. He has had on and off terminal haematuria since age 4 years. Essential findings on physical examination were moderate pallor, BP 127/90mmHg (systolic >95th centile, diastolic > 99th centile), and fullness at the left flank with some tenderness. Bedside urine dipstick showed protein of 1+ and blood of 3+. Initial laboratory findings were as follows: Urine microscopy; pus cells too numerous to count, RBCs > 100/HPF, S. haematobium ova 2+; urine culture isolated E. coli sensitive to ciprofloxacin and ceftazidime; Hb 8.7g/dl, MCV 73 fl ; blood urea 1.9mmol/l, creatinine 20µmol/l, Na 139 mmol/l, K 4.0 mmol/l.

The SSRIs may be too nonspecific and “broadspectrum” to hope for significant cognitive benefits in late-life anxiety treatment. There have been no #www.selleckchem.com/products/ve-821.html randurls[1|1|,|CHEM1|]# prospective studies of serotonin norepinephrine reuptake inhibitors (SNRIs) specifically in late-life anxiety as there have in late-life depression. A retrospective examination of phase 3 venlafaxine XR data found the drug to be efficacious in adults aged 60+, with an effect size (drug-placebo difference) and side-effect profile

similar to younger adults.165 Similar findings have been reported with duloxetine.166 These studies in SSRIs and SNRIs have found similar side effects in elderly persons Inhibitors,research,lifescience,medical as in younger adults, but importantly they were not designed to determine the recently reported potential risks of SSRIs specific to the elderly population: gait impairment increasing risk for falls,167 and bone loss.168 Inhibitors,research,lifescience,medical Other risks that are greater in older adults

are impaired clotting leading to non-GI and GI bleeding169 and SIADII leading to hyponatremia.170 Such reports suggest that the risk:benefit ratio for longterm SSRI/SNRI use is not the same as in younger adults. These concerns have yet to be addressed in a properly constructed longitudinal study (ie, a randomized controlled trial with an adequate safety evaluation). In terms of non-SSRI/SNRI treatments, a large-scale study with pregabalin in geriatric GAD showed efficacy.171 Pregabalin Inhibitors,research,lifescience,medical is not FDA-approved to treat anxietydisorders; its mechanism of action for anxiety is unknown – it binds to an auxiliary subunit voltage-gated

calcium channels and is thought to reduce the synaptic release of several neurotransmitters. Mirtazapine is another non-SSRI/SNRI treatment with efficacy in anxiety, with some evidence Inhibitors,research,lifescience,medical specifically in late-life anxiety disorders.172 Most geriatric anxiety pharmacotherapy research has focused on GAD. There has been one promising study of the SSRI citalopram in older adults with PTSD,173 and also evidence that the α-adrenergic antagonist prazosin is efficacious for sleep-related concerns in PTSD, although Inhibitors,research,lifescience,medical not for other PTSD symptoms.174 There are two small studies in late-life panic disorder: Rampello et al175 found superiority of escitalopram over citalopram in time to response, and a small open-label study crotamiton found promising signals with sertraline.176 Finally, in GAD in the context of stroke, one analysis found efficacy of nortriptyline in a merged dataset of several RCTs of post-stroke depression, in which patients with comorbid GAD were analyzed.177 The only published augmentation study in late-life anxiety disorders is a small study with risperidone.178 While the atypical antipsychotic was promising, there have been concerns with atypicals in older adults, given evidence of higher mortality with antipsychotics in older patients with dementia, and metabolic effects including weight gain, elevated lipids, and insulin resistance.

Lower starting doses should be considered to mitigate these effects. Other common side effects include nausea, headaches, sleep abnormalities, and sexual side effects of reduced libido and physical responsiveness. Dropouts in RCTs as a result of adverse events from SSRIs and SNRIs were almost twice as common among subjects taking active medication compared with placebo.24 Side effects tend to emerge earlier in the course of treatment or during dosage adjustments, and may Inhibitors,research,lifescience,medical subside over days to weeks. Importantly, antidepressants carry a selleckchem black-box warning from the FDA out of concern that they may potentiate suicidal

thinking, a low-frequency event that nevertheless warrants prior consent53 and the development of a monitoring strategy. Suicidal thoughts may be related to the activating effects of SSRIs, resulting in heightened somatic experiences of anxiety, increased emotional lability, and impulsivity. Results from a RCT examining activation as a side effect of fluvoxamine in anxious youth indicated Inhibitors,research,lifescience,medical heightened risk of activation throughout Inhibitors,research,lifescience,medical the course of titration.54 Despite their relative safety and tolerance, abrupt discontinuation of shorter-acting agents often results in generalized discomfort and flu-like symptoms. Medications often require 4 to 8 weeks to provide clinical benefit, and potentially longer when starting with low doses. Educating families about these expectations

and concerns often prevents Inhibitors,research,lifescience,medical them from abandoning medication trials prematurely. Tricyclic antidepressants Tricyclic antidepressants (TCAs) have also shown efficacy in several RCTs of youth with anxiety, particularly clomipramine, which carries an FDA indication for treatment of OCD in children aged 10 and over. RCTs examining treatment of social anxiety Inhibitors,research,lifescience,medical or school refusal have shown benefits of both imipramine55,57 and clomipramine.58-59 Although TCAs may be considered for patients who have experienced intolerance to SSRIs, or as augmentation to SSRIs for

partial response in youth with OCD.60 TCAs are generally less preferred because they require EKG monitoring due to the potential for cardiac abnormalities, carry high risk of fatality in overdose, and have constipation and sedation as side effects. Other agents Controlled trials do not support the use of benzodiazepines GPX6 in children61, 62 yet open-label studies indicate symptomatic benefit,63 and multiple agents in this category are used in clinical practice for highly anxious children. Prior to initiating treatment, it is important to discuss management issues, the potential for tolerance, risk of seizure from abrupt discontinuation, and that short-term rather than long-term use is preferred due to addiction potential. Benzodiazepines can also cause cognitive blunting or disinhibition in some children, leading to behavioral agitation.

Photo

Credit The cover photograph was taken by William Banner, MD. Dr. Banner gives his permission for use.
A 70-year-old man with an 8-month history of left posterior thigh and leg pain was admitted to our Emergency Department after a fall during a gym session. He presented with a moderate pelvic and head trauma. A physical examination showed only tenderness upon palpation and percussion of the lumbar and sacral spine. Plain radiographic examinations of spine, pelvis Inhibitors,research,lifescience,medical and chest were interpreted as normal. The patient had no medical or surgical history other than essential Decitabine cell line hypertension. A few hours after admission, he became very confused and agitated. A cerebral computed tomography scan did not show either vascular lesion or cerebral contusion but fat droplets in the lateral ventricles (Figure ​(Figure1A).1A). A further investigation with CT scan of the spine revealed a fractured sacrum extending into a ruptured perineurial cyst (Figure ​(Figure2A).2A). A cerebral and spinal magnetic resonance image (MRI) scan confirmed Inhibitors,research,lifescience,medical these findings (Figures ​(Figures1B,1B, 2B-C) and we suspected that fatty bone marrow had migrated from sacral fracture to the brain in an unusual Inhibitors,research,lifescience,medical way: a dural breach at the Tarlov cyst. Surgical treatment was not carried

out because of the fractured sacrum. The patient remained under medical observation and fully recovered within three weeks. Two months after Inhibitors,research,lifescience,medical discharge, the patient had no complaints and had a normal physical neurological examination. Figure 1 Head CT-scan and MRI image. A. Post contrast head CT-scan:

fat droplets in the frontal horns of the lateral ventricles (white arrows). B. Sagittal T1-weighted head MR image: fat droplets disseminated in the subarachnoid spaces (white arrows). Figure 2 Sacral cyst CT-scan and MRI image. A. Axial sacral CT-scan: left sacral fracture extending to the S2 radicular cyst (presence of a contralateral cyst at the same level). B. Sagittal T2-weighted sacral MR image: S2 Inhibitors,research,lifescience,medical radicular cyst with two liquids: cerebrospinal … Discussion Tarlov cysts were first described in 1938 as an incidental finding at autopsy of fillum terminale [2]. Then Tarlov described cases of symptomatic (low back pain) perineurial cyst and recommended their surgical removal with sacral laminectomy and excision of Vasopressin Receptor the cyst along the nerve root [3]. More recently, Paulsen et al [4] reported an incidence of Tarlov cysts which accounted for 1% of all back pains reported. They are more common in females [4]. The usual clinical presentations are pain in the lower back, sciatica, coccydynia or cauda equina syndrome. Usually, pain is intermittent and most frequently exacerbated by standing, walking and coughing. Tarlov’s perineurial cysts were initially described in the posterior sacral or coccygeal nerve roots [3].

Their validity is further threatened by small

numbers, the absence of a comparison group, vague patient selection criteria, unsystematic observations and unplanned, sequentially or simultaneously administered interventions and co-interventions. Clinician-readers must also confront chance, missing data, short follow-up periods and the conscious or unconscious biases of those who would select the outcomes to report or suggest causal mechanisms. And, as noted earlier, case reports also represent selected “numerators;” while the patient in the report did well, we seldom learn how many other patients were treated, perhaps unsuccessfully. We acknowledge several limitations Inhibitors,research,lifescience,medical to the Inhibitors,research,lifescience,medical current study. First, our findings are limited to treatment-related case reports published over a 5-year period in four emergency medicine journals. A large fraction of the case reports were about antidotes for environmental exposures or drug poisonings; only a minority involved a procedure or surgical intervention. Overall, we reviewed a relatively small number of case reports, limiting the precision of the estimates. Second, almost half of the reports we included were letters. As letters may have strict word limitations, it is possible that critical elements

were not Inhibitors,research,lifescience,medical included or eliminated during editing to meet these space requirements. While we recognize the value of journal space, editors must balance the need to be concise with the

importance of adequate case descriptions. Finally, Inhibitors,research,lifescience,medical the case reports were judged against 11 selected reporting criteria; other reporting requirements may exist that would further enhance the validity and utility of treatment-related Inhibitors,research,lifescience,medical case reports. This review suggests that case reports frequently omit essential information about the patient, disease, treatment and outcomes. Authors frequently over-interpret their observations. And all too often, authors make treatment recommendations that rely more on deductive reasoning, casual observation, hopeful anticipation and intuition than on valid observations and inferences. Abbreviations CR: case reports; AIDS: Acquired Immune Deficiency Syndrome; MAST: Military Anti-Shock Trousers; 95 CI: ninety-five percent confidence GBA3 intervals. Competing interests The authors declare that they have no competing interests. Authors’ contributions KH and SRL designed the study, reviewed the case reports, and drafted the find more manuscript. SP and TR assisted in the design of the study, abstracted the case reports and revised the manuscript. All authors reviewed the final draft of the manuscript. Pre-publication history The pre-publication history for this paper can be accessed here: http://www.biomedcentral.com/1471-227X/9/10/prepub Acknowledgements The authors thank Richard Dart, M.D.