Friday, April 20, 2012

sudden cardiac arrest in children


From CHOP Expert Commentary

Sudden Cardiac Arrest: Identifying Kids at Risk

Victoria L. Vetter, MD, MPH

Posted: 04/09/2012

I am Dr. Victoria Vetter, a pediatric cardiologist at the Children's Hospital in Philadelphia. I'm speaking to you today about a policy statement just published by the American Academy of Pediatrics on pediatric sudden cardiac arrest. This paper identifies the conditions that are associated with sudden cardiac arrest in children. This can include structural functional abnormalities, such as hypertrophic cardiomyopathy and dilated cardiomyopathy; coronary anomalies; electrical conditions, such as long QT syndrome; and acquired conditions, such as commotio cordis, when there is a blow to the chest.
The paper outlines the warning signs and symptoms associated with sudden cardiac arrest. This would include fainting or syncope with exercise, chest pain with exercise, shortness of breath not associated with asthma in response to exercise, a family history of sudden cardiac arrest in someone younger than 50 years of age, or having a member who might be affected with one of the conditions that can cause sudden cardiac arrest.
Unfortunately, many individuals do not know their family history, but this is very important. Pediatric providers should make every attempt to investigate this in all children they are seeing, particularly those who are active, as sudden cardiac arrest is most likely to occur during activity. Of course, this includes most of our children. Providers also should be asking questions that specifically relate to the symptoms that were previously mentioned. Since this is a genetic condition, a molecular or genetic evaluation of affected family members or children who experience sudden cardiac arrest can often identify the cause of the arrest and identify additional individuals.
While we do not have a registry that counts the number of children who experience a sudden cardiac arrest, we are hopeful that the information in this policy statement will encourage people to consider that option, and thus identify the children who are experiencing these conditions. Further, if a school has an automated external defibrillator (AED) and an emergency plan to activate when such an event occurs, the child is much more likely to survive. Currently, the survival rate is 10%. It can be as high as 64% in schools where an emergency response plan is in effect.
Also, we would hope that individuals involved in schools would use this as an opportunity to develop curricula that include cardiopulmonary resuscitation and AED use. Every child who graduates from high school could then become a community bystander who would be available to help resuscitate an individual should they experience a sudden cardiac arrest.
The ways in which children can be identified with this condition include the warning signs and symptoms mentioned above. Unfortunately, symptoms are present in less than 50% of individuals. Thus, there is much discussion in the country at this time about other ways in which we might identify these individuals, including a debate about whether an electrocardiogram, which can identify up to 70%-95% of these conditions, should be used and whether genetic testing should be used in a more proactive fashion.
The paper concludes with a number of recommendations about the ways in which pediatricians may effectively work toward decreasing the tragedy of sudden cardiac arrest in our children.

Monday, April 16, 2012

Reducing Vaccination Pain


From Medscape Medical News

Physical Intervention Eases Vaccination Pain in Infants

Ricki Lewis, PhD
April 16, 2012 — Infant immunizations are stressful for parents and painful for recipients. A study published online April 16 in Pediatricsfound that the pain-reducing effect of a physical intervention with or without sucrose water was superior to sucrose water alone.
Evidence is scant that a pain reliever such as acetaminophen is effective postvaccination, and this drug may dampen the antibody response to certain vaccine antigens. To investigate a nonpharmacological intervention to alleviate injection pain, John W. Harrington, MD, from the Department of Pediatrics, Eastern Virginia Medical School, and Department of Pediatrics, Section of General Academic Pediatrics, Children's Hospital of The King's Daughters, Norfolk, Virginia, and colleagues conducted a prospective, randomized, placebo-controlled trial to test an intervention termed the "5 S's," for swaddling, side/stomach position, shushing, swinging, and sucking.
The researchers divided 230 infants being immunized at 2- or 4-month well-baby check-ups into 4 groups that received either 2 mL of water or 2 mL of a 24% sucrose solution 2 minutes before vaccination, and either standard comfort care from the parent or guardian or a 5 S's intervention from a researcher. Sucrose is added to acetaminophen products to improve palatability, and in some studies appeared to relieve pain.
The investigators used the Modified Riley Pain Score (cry quality, grimace, movement) to assess pain every 15 seconds for 2 minutes, and subsequently every 30 seconds for up to 5 minutes after vaccination. A 1-way analysis of variance evaluated mean pain across groups over time, and repeated-measure general linear modeling evaluated pain scores at each time interval across the groups. The vaccines were for rotavirus (oralRotarix, GlaxoSmithKline) and hepatitis B (Pentacel, Sanofi Pasteur; Prevnar, Wyeth, marketed by Pfizer), injected intramuscularly into the thigh.
Pain scores ranged from 0 to 9. Mean pain scores were 4.46 for the control group (water, parental comfort), 3.95 for the sucrose group (sucrose, parental comfort), 3.24 for the physical group (water, 5 S's), and 3.61 for the physical with sucrose group (sucrose, 5 S's). The difference in mean pain scores was significantly lower in all treatment groups compared with the control group, and the mean pain score for the 5 S's–only group was significantly less than the sucrose group. However, the difference between the 2 5 S's groups was not statistically significant.
The 2 groups implementing the 5 S strategy had less pain and shorter duration of crying than the 2 groups without the strategy, and the 5 S intervention was about equally effective with or without sucrose. The researchers conclude, "The 5 S's appear to be a viable nonpharmacologic option for clinics to implement when providing analgesia during vaccinations." In addition to minimizing suffering, pain control during immunizations may calm parents who are hesitant to have their children vaccinated, the researchers point out.
Limitations of the study include that the 3 researchers who provided the 5 S's might have differed slightly in their technique, the disproportionate number of 2-month-olds, and the difficulty of assessing movements to evaluate pain in a swaddled baby. Finally, the parents may have been providing the 5 S's as well.
Pediatrics. Published online April 16, 2012.

Sunday, April 15, 2012

ADHD Screening

source:   AACAP (2007)
http://www.medscape.com/viewarticle/739172_3

Screening for ADHD

Recommendation 1.
Screening for ADHD should be part of every patient's mental health assessment [MS]. In any mental health assessment, the clinician should screen for ADHD by specifically asking questions regarding the major symptom domains of ADHD (inattention, impulsivity, and hyperactivity) and asking whether such symptoms cause impairment.
These screening questions should be asked regardless of the nature of the chief complaint. Rating scales or specific questionnaires containing the DSM symptoms of ADHD can also be included in clinic/office registration materials to be completed by parents before visits or in the waiting room before the evaluation.
If a parent reports that the patient suffers from any symptoms of ADHD that induce impairment or if the patient scores in the clinical range for ADHD symptoms on a rating scale, then a full evaluation for ADHD as set out in the next recommendation is indicated.

Evaluation

Recommendation 2.
Evaluation of the preschooler, child, or adolescent for ADHD should consist of clinical interviews with the parent and patient, obtaining information about the patient's school or day care functioning, evaluation for comorbid psychiatric disorders, and review of the patient's medical, social, and family histories [MS].

The clinician should perform a detailed interview with the parent about each of the 18 ADHD symptoms listed in DSM-IV.
For each symptom, the clinician should determine whether it is present as well as its duration, severity, and frequency.
Age at onset of the symptoms should be assessed.
The patient must have the required number of symptoms (at least six of nine of the inattention cluster and/or at least six of nine of the hyperactive/impulsive criteria, each occurring more days than not), a chronic course (symptoms do not remit for weeks or months at a time), and onset of symptoms during childhood.
After all of the symptoms are assessed, the clinician should determine in which settings impairment occurs.
Because most patients with ADHD have academic impairment, it is important to ask specific questions about this area. This is also an opportunity for the clinician to review the patient's academic/intellectual progress and look for symptoms of learning disorders (see Recommendation 4).
Presence of impairment should be distinguished from presence of symptoms.
For instance, a patient's ADHD symptoms may be observable only at school but not at home.
Nonetheless, if the patient must spend an inordinate amount of time completing schoolwork in the evening that was not done in class, then impairment is present in two settings.
DSM-IV requires impairment in at least two settings (home, school, or job) to meet criteria for the disorder, but clinical consensus agrees that severe impairment in one setting warrants treatment.

After reviewing the ADHD symptoms, the clinician should interview the parent regarding other common disorders of childhood.
In general, it is most logical to next gather data from the parent regarding ODD and CD.
Then, the clinician should explore whether the patient has symptoms of depression (and associated neurovegetative signs), mania, anxiety disorders, tic disorders, substance abuse, and psychosis, or evidence of a learning disability.
Other practice parameters of the AACAP contain specific recommendations on eliciting symptoms of these disorders in children and adolescents.

The parent should complete one of the many standardized behavior rating scales that have well established normative values for children of a wide range of ages and genders. Scales in common use are listed in Table 1 of the original guideline document. These scales not only yield a measure of ADHD behaviors but also tap into other psychiatric symptoms that could be comorbid with ADHD or may suggest an alternative psychiatric diagnosis. It is advisable for the clinician to request a release of information from the parent to obtain a similar rating scale from the patient's teacher(s). It is important to note that such rating scales do not by themselves diagnose ADHD, although parent or teacher ratings of inattention or hyperactivity/impulsivity that fall in the upper fifth percentile for the patient's age and gender are reason for serious concern. If the teacher cannot provide such a rating scale or the parent declines permission to contact the school, then materials from school, such as work samples or report cards, should be reviewed or inquired about.

Family history and family functioning should be assessed.
Because ADHD is highly heritable, a high prevalence of ADHD is likely to be found among the patient's parents and siblings.
Family history of other significant mental disorders (affective, anxiety, tic, or CD) is helpful in determining the nature of any comorbid disorders, although a comorbid disorder should not be diagnosed solely on the basis of a family history of that comorbid disorder.
Social history of the family should be examined.
Because patients with ADHD perform better in structured settings, any factors in the family that create an inconsistent, disorganized environment may further impair the patient's functioning. Information regarding any physical or psychological trauma the patient may have experienced (including multiple visits to the emergency room) should be gathered as well as any current psychosocial stressors.

The clinician should obtain information about the patient's perinatal history, developmental milestones, medical history, and mental health history (especially any previous psychiatric treatment). Delays in reaching developmental milestones or in social/language development suggest language disorders, mental retardation, or pervasive developmental disorders. Assessment of developmental milestones is particularly important in the evaluation of the preschooler because many developmental disorders are associated with attention problems and hyperactivity.

The clinician should next interview the child or adolescent. For the preschool or young school-age child (5-8 years old), this interview may be done concurrently with the parent interview.
Older children and adolescents should be interviewed separately from parents, as older children and teenagers may not reveal significant symptoms (depression, suicide, or drug or alcohol abuse) in the presence of a parent.
Clinicians should be prepared to conduct a separate interview even with a younger child in many clinical situations, such as if the patient appears at risk of abuse or there is evidence of significant family dysfunction. The primary purpose of the interview with the child or adolescent is not to confirm or refute the diagnosis of ADHD.
Young children are often unaware of their symptoms of ADHD, and older children and adolescents may be aware of symptoms but will minimize their significance.
The interview with the child or adolescent allows the clinician to identify signs or symptoms inconsistent with ADHD or suggestive of other serious comorbid disorders.
The clinician should perform a mental status examination, assessing appearance, sensorium, mood, affect, and thought processes.
Through the interview process, the clinician develops a sense of whether the patient's vocabulary, thought processes, and content of thought are age-appropriate.
Marked disturbances in mood, affect, sensorium, or thought process suggest the presence of psychiatric disorders other than or in addition to ADHD.

Recommendation 3.
 If the patient's medical history is unremarkable, laboratory or neurological testing is not indicated [NE]. There are few medical conditions that "masquerade" as ADHD, and the vast majority of patients with ADHD will have an unremarkable medical history. Children suffering a severe head injury may develop symptoms of ADHD, usually of the inattentive subtype. Encephalopathies generally produce other neurological symptoms (language or motor impairment) in addition to inattention. Hyperthyroidism, which can be associated with hyperactivity and agitation, rarely presents with ADHD symptoms alone but with other signs and symptoms of excessive thyroid hormone levels.
The measurement of thyroid levels and thyroid-stimulating hormone should be considered only if symptoms of hyperthyroidism other than increased activity level are present.
Exposure to lead, either prenatally or during development, is associated with a number of neurocognitive impairments, including ADHD. If a patient has been raised in an older, inner-city environment where exposure to lead paint or plumbing is probable, then serum lead levels should be considered. Serum lead level should not be part of routine screening.
Children with fetal alcohol syndrome or children exposed in utero to other toxic agents have a higher incidence of ADHD than the general population.

Unless there is strong evidence of such factors in the medical history, neurological studies (EEG, MRI, SPECT, or PET) are not indicated for the evaluation of ADHD. Specifically, the Council on Children, Adolescents, and Their Families of the American Psychiatric Association has warned against the exposure of children to intravenous radioactive nucleotides as part of the diagnosis or treatment of childhood psychiatric disorders, citing both a lack of evidence of validity and safety issues. [American Psychiatric Association: Brain Imaging and Child and Adolescent Psychiatry\With Special Emphasis On Single Photon Emission Computed Tomography (SPECT)]

Recommendation 4.
Psychological and neuropsychological tests are not mandatory for the diagnosis for ADHD, but should be performed if the patient's history suggests low general cognitive ability or low achievement in language or mathematics relative to the patient's intellectual ability [OP].
 Low scores on standardized testing of academic achievement frequently characterize ADHD patients. The clinician must determine whether the academic impairment is secondary to the ADHD, if the patient has ADHD and a learning disorder, or if the patient has only a learning disorder and the patient's inattentiveness is secondary to the learning disorder. Academic impairment is commonly due to the ADHD itself. Many months or years of not listening in class, not mastering material in an organized fashion, and not practicing academic skills (not doing homework, etc.) leads to a decline in achievement relative to the patient's intellectual ability. If the parent and teacher report that the patient performs at (or even above) grade level on subjects when given one-to-one supervision (a patient can do all of the problems on a test when held in from recess), then a formal learning disorder is less likely. In some cases, the patient may engage in leisure activities that require the skill (e.g., reading science fiction novels) but avoid reading a history book in preparation for an exam. In such cases, it is more appropriate to treat the ADHD and then determine whether the academic problems begin to resolve as the patient is more attentive in learning situations. However, if there is no clear evidence of an improvement in academic performance in 1 to 2 months despite improvement of the ADHD, then psychological testing for learning disorders is indicated.

In other cases, symptoms of learning/language disorders are present that cannot be accounted for by ADHD. These include deficits in expressive and receptive language, poor phonological processing, poor motor coordination, or difficulty grasping fundamental mathematical concepts. In such cases, psychological testing will be needed to identify whether these deficits are related to a specific learning disorder. In the vast majority of cases, these learning disorders will be comorbid with the ADHD, and it is recommended strongly that the patient's ADHD be optimally treated before such testing. It could then be firmly concluded that any deficits identified are clearly the result of a learning disorder and not due to inattention to the test materials.

Purely learning-disordered patients are often inattentive when struggling with material in the area of their disability (a reading-disordered patient is inattentive when he or she must read) but do not have problems outside such a restricted academic setting. Patients with learning disorders alone do not show symptoms of impulsivity or hyperactivity. Children and adolescents with learning disorders may be oppositional with regard to schoolwork, and the clinician is consulted as to whether ADHD is the cause of the oppositional behavior. If a careful interview shows the absence of full criteria for ADHD and if the emergence of the oppositional behavior is clearly correlated with academic demands, then a primary learning disorder is more likely.

Psychological testing of the ADHD patient usually consists of a standardized assessment of intellectual ability (IQ) to determine any contribution of low general cognitive ability to the academic impairment, and academic achievement. Neuropsychological testing, speech-language assessments, and computerized testing of attention or inhibitory control are not required as part of a routine assessment for ADHD, but may be indicated by the findings of the standard psychological assessment.

Recommendation 5. The clinician must evaluate the patient with ADHD for the presence of comorbid psychiatric disorders [MS]. The clinician must integrate the data obtained with regard to comorbid symptoms to determine whether the patient meets criteria for a separate comorbid disorder in addition to ADHD, the comorbid disorder is the primary disorder and the patient's inattention or hyperactivity/impulsivity is directly caused by it, or the comorbid symptoms do not meet criteria for a separate disorder but represent secondary symptoms stemming from the ADHD.

When patients with ADHD meet full DSM-IV criteria for a second disorder, the clinician should generally assume the patient has two or more disorders and develop a treatment plan to address each comorbid disorder in addition to the ADHD. Children with ADHD commonly meet criteria for ODD or CD. In young children these disorders are nearly always present concurrently. Similarly, if a patient meets full DSM-IV criteria for major depressive disorder or a specific anxiety disorder, the clinician is most likely dealing with a comorbid disorder. Most often, the onset of the depressive disorder occurs several years after the onset of ADHD, whereas anxiety disorders have an earlier onset concurrent with the ADHD. A comorbid diagnosis of mania should be considered in ADHD patients who exhibit severe mood lability/elation/irritability, thought disturbances (grandiosity, flight of ideas), severe aggressive outbursts ("affective storms"), and decreased need for sleep or age-inappropriate levels of sexual interest. Mania should not be diagnosed solely on the basis of the severity of the ADHD symptoms or aggressive behavior in the absence of the manic symptoms listed above. Acutely manic ADHD patients generally require mood stabilization before treatment of the ADHD. The choice of a treatment regimen, particularly pharmacological intervention, is often influenced by the nature of the patient's comorbid disorder and which disorder is currently the most impairing of major life activities. Older adolescents with ADHD should be screened for substance abuse disorders, as they are at greater risk than teenagers without ADHD for smoking and alcohol and other illegal substance abuse disorders.

In other cases, another primary psychiatric disorder produces impairment of attention or impulse control. Impaired attention is caused by primary depressive/anxiety disorders, and those with primary mania have impaired impulse control and judgment. If a patient has no history of ADHD symptoms during childhood but develops inattentiveness and poor concentration only after the onset of depression or mania, then the affective disorder is most likely primary. Patients with adolescent-onset ODD or CD are often described as impulsive or inattentive, but often do not meet full criteria for ADHD or had few ADHD symptoms in early childhood.

Finally, some associated problems may stem from the ADHD itself and not be a separate disorder. Patients with ADHD may develop associated symptoms of dysphoria or low self-esteem secondary to the frustrations of living with ADHD. In such cases, the dysphoria is related specifically to the ADHD symptoms and there is an absence of pervasive depression, neurovegetative signs, or suicidal ideation. If such dysphoria is a result of the ADHD, then it should respond to successful treatment of the ADHD. The distractibility or impulsivity of ADHD patients may often be interpreted as oppositional behavior by caretakers or children. Mild mood lability (shouting out, crying easily, quick temper) is also common in ADHD. It is important to note that such associated symptoms do not reach the level of a separate DSM disorder; are temporally related to the onset of the ADHD; are often consistent with, although somewhat excessive, for the social context; and dissipate once the ADHD is successfully treated.

Rhinosinusitis


Diagnosing and Treating Rhinosinusitis: New Guidelines: Bacterial vs Viral Rhinosinusitis


Anthony W. Chow, MD

Medscape Pediatrics 

Bacterial vs Viral Rhinosinusitis
Although rhinosinusitis is quite common -- affecting nearly 1 in 7 adults each year -- the prevalence of bacterial infection during acute rhinosinusitis is estimated to be only 2%-10% of all patients with symptoms of sinusitis.[2,3] Antibiotics are significantly overprescribed for rhinosinusitis, which is the fifth leading indication for antimicrobial prescriptions by physicians in office practice.[4]One national survey conducted during 1998-2003 revealed that 81% of adults presenting with symptoms of sinusitis in an outpatient setting received an antibiotic prescription.[5] Overprescription of antibiotics is a serious concern because it is costly, exposes patients to unnecessary side effects, and fosters drug resistance.
Due to the lack of precision and practicality of current diagnostic methods, clinicians must rely on clinical presentations to distinguish bacterial from viral rhinosinusitis. The guidelines suggest that the infection is probably bacterial if any of the following are true:
  • Onset with persistent symptoms or signs compatible with acute rhinosinusitis lasting for ≥ 10 days without any evidence of clinical improvement;
  • Onset with severe symptoms or signs of high fever (≥ 39°C or 102°F) and purulent nasal discharge or facial pain lasting for at least 3-4 consecutive days at the beginning of an illness; or
  • Onset with worsening symptoms or signs characterized by new onset of fever, headache, or increase in nasal discharge following a typical viral upper respiratory infection that lasted 5-6 days and initially improved ("double-sickening”).

First-line therapy:
Once a bacterial cause is established based on these clinical presentations, empiric antimicrobial therapy should be initiated immediately with amoxicillin-clavulanate, which has better coverage than amoxicillin. This recommendation is a result of the following:
  • Increasing prevalence of Haemophilus influenzae among other respiratory tract infections in children since the introduction of the pneumococcal vaccines; and
  • High prevalence of beta-lactamase-producing respiratory pathogens in ABRS among recent respiratory tract isolates, particularly H influenzae.
Second-line therapy:
  • Doxycycline may be used as an alternate regimen in adults;
  • The following are not recommended because of resistance issues: macrolides, such as clarithromycin and azithromycin; trimethoprim-sulfamethoxazole; and second- and third-generation oral cephalosporins;
  • Combination therapy with a third-generation oral cephalosporin plus clindamycin may be used in children with non-type-1 penicillin allergy or who are from geographic regions with high endemic rates of penicillin-nonsusceptible S pneumoniae. Levofloxacin is recommended for children with type-1 penicillin allergy; and
  • Respiratory fluoroquinolones may be used in patients in whom first-line therapy failed or who have risk factors for antibiotic resistance.
Length of therapy:
  • Adults: 5-7 days for uncomplicated ABRS
  • Children: 10-14 days
Adjunct therapy:
  • Intranasal saline irrigations with physiologic or hypertonic saline may be helpful in adults but are less likely to be tolerated in children;
  • Intranasal corticosteroids are recommended in persons with a history of allergic rhinitis; and
  • Topical and oral decongestants and antihistamines are not recommended.

Maternal Obesity increases Autism risk


From Medscape Medical News > Psychiatry

Maternal Obesity Linked to Autism, Other Developmental Disorders

Deborah Brauser
April 12, 2012 — Metabolic conditions in pregnant women may be associated with increased risk for autism and other neurodevelopmental disorders in their offspring, new researchsuggests.
In a cohort study of more than 1000 children between the ages of 2 and 5 years, those who had mothers classified as having "metabolic conditions" (which included diabetes, hypertension, and obesity) during pregnancy were at a significantly higher risk of developing an autism spectrum disorder (ASD) and developmental delays than the children with mothers who did not have metabolic conditions.
In addition, mothers who were obese were 1.6 times more likely to have a child with ASDs and more than twice as likely to have a child with other developmental problems. Maternal diabetes alone was associated with significant risk for overall developmental problems and lower expressive language skills in their children.
"The prevalence of obesity and diabetes among US women of childbearing age is 34% and 8.7%, respectively," senior author Irva Hertz-Piccioto, PhD, University of California, Davis, and colleagues write.
"With obesity rising steadily, [our] results appear to raise serious public health concerns," they add.
The study was published online April 9 in Pediatrics..

Monday, March 26, 2012

Passive Smoke increase Asthma in children


From Medscape Education Clinical Briefs

Passive Smoke Exposure Associated With Wheeze, Asthma in Children 

News Author: Troy Brown
CME Author: Charles P. Vega, MD
 03/21/2012

CLINICAL CONTEXT

Secondhand smoke exposure has a profound effect on the risks for morbidity and mortality worldwide, according to a study by Oberg and colleagues published in the January 8, 2011, issue of the Lancet. They note that the largest proportion of the nonsmoking population exposed to secondhand smoke is children. Overall, approximately 1% of worldwide mortality may be the result of secondhand smoke, with ischemic heart disease accounting for most deaths. Similarly, approximately 0.7% of worldwide disability is caused by secondhand smoke, with most of this burden borne by children. Lower respiratory tract infections among children younger than 5 years account for the largest proportion of all disabilities related to secondhand smoke exposure.
New research has provided better data regarding the relationship between prenatal and passive smoke exposure and the risks for incident asthma and wheeze among children. The current systematic review and meta-analysis by Burke and colleagues provides an accurate assessment of these risks.

STUDY SYNOPSIS AND PERSPECTIVE

Children who are exposed to tobacco smoke prenatally or in their home after birth are at least 20% more likely to have wheezing episodes or develop asthma. The magnitude of the risks is higher than seen in previous estimates, according to a meta-analysis published online March 19 in Pediatrics.
Hannah Burke, BMBS, from the University of Nottingham in the United Kingdom, and colleagues conducted a systematic review and meta-analysis of 71 prospective epidemiologic studies that examined the association between passive smoke exposure and the incidence of pediatric wheeze and asthma.
After conducting an extensive literature search that included Medline, Embase, and the Cumulative Index to Nursing and Allied Health Literature, as well as conference abstracts, they identified and screened 5074 articles, yielding 70 articles with a total of 71 studies.
"We included all prospective epidemiologic studies assessing the association between passive smoke exposure and incidence of asthma or wheeze in children or young people up to the age of 18 years in which participants were free of disease (asthma or wheeze) at the start of the study and passive smoke exposure was documented at a time point before the incidence of disease was determined," the authors write.
The researchers analyzed the effects of 4 different types of smoke exposure on the development of wheezing and asthma: prenatal maternal smoking, maternal smoking, paternal smoking, and household smoke exposure.
Prenatal Maternal Smoking
Prenatal maternal smoke exposure was associated with a 40% increase in risk for wheeze in children aged 2 years or younger (odds ratio [OR], 1.41, 95% confidence interval [CI], 1.20 - 1.67; I2, 82.5%; 14 studies). Results were similar for children aged 3 to 4 years (OR, 1.28; 95% CI, 1.14 - 1.44; I2, 65.5%; 8 studies). This exposure also was associated with a 52% increased risk of wheezing in children aged 5 to 18 years (OR, 1.52; 95% CI, 1.23 - 1.87; I2, 21.1%; 5 studies).
In addition, prenatal smoke exposure was associated with an increased risk for asthma; this risk was highest in children aged 2 years or younger (OR, 1.85; 95% CI, 1.35 - 2.53; I2, 41.9%; 5 studies).
Risks declined progressively with age, but children aged 5 to 18 years still had an increased risk of developing asthma (OR, 1.23; 95% CI, 1.12 - 1.36; I2, 50%; 11 studies).
Maternal Smoking
Postnatal maternal smoke exposure was associated with an increased risk for wheezing episode in children aged 2 years or younger (OR, 1.70; 95% CI, 1.24 - 2.35; I2, 0.0%; 4 studies), in children aged 3 to 4 years (OR, 1.65; 95% CI, 1.20 - 2.28; I2, 48.5%; 4 studies), and in children aged 5 to 18 years (OR, 1.18; 95% CI, 0.99 - 1.40; I2, 1.4%; 3 studies).
Postnatal maternal smoke exposure was not associated with increased risk for asthma in children aged 4 years or younger, but there was a borderline association for children 5 to 18 years of age (OR, 1.20; 95% CI, 0.98 - 1.46; P = .08; I2, 65.3%; 8 studies).
Paternal Smoking
There were limited data on paternal smoking, with only 2 studies available for analysis of risk of wheezing in children 5 to 18 years of age (OR, 1.38; 95% CI, 1.05 - 1.85; I2, 0%; 2 studies).
No studies had data on the association between paternal smoke exposure and the risk for asthma in children 2 years of age of younger, and there was only 1 study with data on children 3 to 4 years of age. That study showed a significant effect of paternal smoking (OR, 1.34; 95% CI, 1.23 - 1.46).
There was no association between paternal smoke exposure and development of asthma in children aged 5 to 18 years (OR, 0.98; 95% CI, 0.71 - 1.36; I2, 0%; 4 studies).
Household Smoke Exposure
Exposure to household smoke was associated with an increased risk of wheezing in children aged 2 years or younger (OR, 1.35; 95% CI, 1.10 - 1.64; I2, 64.5%; 9 studies).
Household smoke exposure was not associated with an increased risk of wheezing in children aged 3 to 4 years (OR, 1.06; 95% CI, 0.88 - 1.27; I2, 54.5%; 4 studies), but it was associated with an increased risk of wheezing in children aged 5 to 18 years (OR, 1.32; 95% CI, 1.12 - 1.56; I2, 0%; 5 studies).
Exposure to household smoke was not associated with an increased risk for asthma in children 2 years of age or younger (OR, 1.14; 95% CI, 0.94 - 1.38; I2, 0.1%; 3 studies), but it was associated with an increased risk for asthma in children aged 3 to 4 years (OR, 1.21; 95% CI, 1.00 - 1.47; I2, 72.7%; 5 studies) and children aged 5 to 18 years (OR, 1.30; 95% CI, 1.04 - 1.62; I2, 37.7%; 5 studies).
Effects of Passive Smoke Higher Than Previous Estimates
"Our findings indicate that the effects of passive smoking on the incidence of wheeze and asthma are substantially higher than previously estimated, particularly for the effect of maternal postnatal smoking exposure," the authors write.
The authors note that this systematic review and meta-analysis is the largest reported review of this subject to date.
"Exposure to passive smoking is an important risk factor for the incidence of wheeze and asthma throughout childhood.... [I]t is important to limit children's exposure to passive smoke both during gestation and throughout the child's life," the authors write.
This study was supported by a project grant from Cancer Research UK and by core funding to the UK Centre for Tobacco Control Studies from the British Heart Foundation, Cancer Research UK, Economic and Social Research Council, Medical Research Council, and the Department of Health, under the auspices of the UK Clinical Research Collaboration. The authors have disclosed no relevant financial relationships.
Pediatrics. 2012;129:735-744.

STUDY HIGHLIGHTS

  • Researchers identified prospective epidemiologic studies evaluating the relationship between passive smoke exposure and the incidence of new wheeze or asthma among children and adolescents. Studies published through February 2011 were included in the review.
  • Studies included prenatal smoking exposure as well as passive smoke exposure during different stages of childhood.
  • 180 studies received full-text review, and 70 articles were eligible for inclusion in the meta-analysis. The collective research was fairly evenly divided in the evaluation of childhood wheeze and asthma and in the assessment of the effects of prenatal and postnatal passive smoke exposure.
  • The overall quality of the included studies was moderate. The main methodologic flaws in the research were a lack of objective measure of smoking and a lack of adjustment for confounding factors.
  • Prenatal maternal smoking was associated with an OR for wheeze of 1.41 (95% CI, 1.20 - 1.67) among children at 2 years old or younger.
  • The OR associated with prenatal maternal smoking for wheeze among children 3 to 4 years old was 1.28 (95% CI, 1.14 - 1.44). The respective OR for children 5 to 18 years old was 1.52 (95% CI, 1.23 - 1.87).
  • The effect of postnatal maternal smoking increased the risk for wheeze among children 2 years or younger (OR, 1.70; 95% CI, 1.24 - 2.35), children 3 to 4 years old (OR, 1.65; 95% CI, 1.20 - 2.68), and children 5 to 18 years old (OR, 1.18; 95% CI, 0.99 - 1.40).
  • More limited data were available regarding the association between paternal smoking and wheeze, but paternal smoking did significantly increase the risk for wheeze among children 15 to 18 years old.
  • The collection of data demonstrated a generally weaker association between passive smoke exposure and the risk for asthma vs passive smoke exposure and the risk for wheeze. The strongest type of passive smoke exposure promoting a higher risk for asthma was prenatal maternal smoking in children 2 years or younger (OR, 1.85; 95% CI, 1.35 - 2.53).
  • Other passive smoke exposures during childhood increased the risk for incident asthma by approximately 20%, and the sum of these results was statistically significant.

CLINICAL IMPLICATIONS

  • Overall, approximately 1% of worldwide mortality may be caused by secondhand smoke, with ischemic heart disease accounting for most deaths. Children are the largest proportion of the nonsmoking population exposed to secondhand smoke, and they bear the greatest burden of disability caused by secondhand smoke. Lower respiratory tract infections among children younger than 5 years account for the largest proportion of all disability related to secondhand smoke exposure.
  • The current study by Burke and colleagues suggests that passive smoke exposure increases the risks for wheeze and asthma in children by at least 20%.

Wednesday, February 29, 2012

Improve memory tips


Improve Memory with Sleep, Practice, and Testing

There are whole mar­kets (think cross­words, herbal sup­ple­ments, drugs, brain fit­ness soft­ware) aimed at help­ing us improve our memory.
Now, what is “mem­ory”? how does the process of mem­ory sleep and memorywork?
Dr. Bill Klemm, Pro­fes­sor of Neu­ro­science at Texas A&M Uni­ver­sity, explains a very impor­tant con­cept below.
- Alvaro
——-
Get­ting from Here to There:
Mak­ing Mem­ory Con­sol­i­da­tion Work
By Bill Klemm,  Ph. D.
Until con­sol­i­da­tion has occurred, a short-term mem­ory is very vul­ner­a­ble, as all of us have expe­ri­enced from look­ing up a phone num­ber only to have some dis­trac­tion cause us to lose the num­ber before we can get it dialed.
What is “consolidation”?
Brain researchers use the term “con­sol­i­da­tion” for the process whereby short-term mem­ory gets made more permanent.
Here, I would like to dis­cuss some aspects of con­sol­i­da­tion that many peo­ple may not know about: why sleep is so impor­tant, why mem­ory must be prac­ticed, and how test­ing pro­motes consolidation.
1. Over-training: You Can Learn Too Much
Exper­i­ments have shown that human mem­ory per­for­mance unex­pect­edly dete­ri­o­rated if learn­ing ses­sions were increased to four 60-minute ses­sions at reg­u­lar inter­vals on the same day. In other words, the more the sub­jects were trained, the poorer they per­formed. How­ever, this inter­fer­ence did not occur if sub­jects were allowed to nap for 30–60 min­utes between the sec­ond and third sessions.
It is hard to explain why over-training dis­rupts per­for­mance, but I sus­pect that as train­ing tri­als are repeated the infor­ma­tion starts to inter­fere with mem­ory con­sol­i­da­tion, per­haps because of bore­dom or fatigue in the neural cir­cuits that medi­ate the learn­ing. Nap­ping must have a restora­tive func­tion that com­pen­sates for the neg­a­tive effects of over-training. What all this sug­gests is that mem­ory con­sol­i­da­tion would be opti­mized if learn­ing occurred in short ses­sions that are repeated but only with inter­ven­ing naps and on dif­fer­ent days with reg­u­lar night-time sleep. In other words, repeat­ing long study peri­ods in the same day on the same task can be counter-productive. This is yet another rea­son why stu­dents should not cram-study for exams. Learn­ing should be opti­mized by rehears­ing the same learn­ing mate­r­ial on sep­a­rate days where nor­mal sleep occurred each night.
Sources:
- Maquet, P. et al. 2002. Be caught nap­ping: you’re doing more than rest­ing your eyes.Nature Neu­ro­science. 5 (7); 618–619.
- Med­nick, Sara, et al. 2002. The restora­tive effect of naps on per­cep­tual deterioration.Nature Neu­ro­science. 5 (7): 677–681.
2. Los­ing Your Past
Do you remem­ber the names of your elementary-school teach­ers? How about the name of the bully in mid­dle school? Or names of your friends when you were a kid? These are all things you remem­bered well at one time and remem­bered for a long time. But you may well have for­got­ten by now.
A recent study on rats sug­gests what it takes to sus­tain longer term mem­o­ries. Rats in the study learned a “bait shy­ness” task. Rats were given a drink of saccharin-flavored water, and then shortly after­wards injected with lithium, which made them nau­se­ated. This was a typ­i­cal con­di­tioned learn­ing sit­u­a­tion, as with Pavlov’s dogs. In this case, rats typ­i­cally remem­bered to avoid such water for many weeks. This is the basis for “bait shy­ness.” If rats sur­vive a poi­son­ing episode, they will avoid that bait in the future. In this exper­i­ment, one group of rats received an injec­tion directly into the part of the brain that holds taste mem­o­ries. This injec­tion con­tained a drug that blocks a cer­tain enzyme, a pro­tein kinase. These rats lost their learned taste aver­sion. The bad mem­ory was lost irre­spec­tive of when the injec­tion was made dur­ing the 25 days after learn­ing occurred. Giv­ing the enzyme blocker before learn­ing had no effect on learn­ing to avoid the fla­vored water. The pro­tein kinase thus seems to be nec­es­sary for sus­tain­ing a long-term mem­ory. It is pos­si­ble that other long-term mem­o­ries the rats may have had were also wiped out by the enzyme-blocking drug.
So what is the prac­ti­cal impor­tance? I sug­gest that even “long-term” mem­o­ries have to get rehearsed or they may even­tu­ally for­got­ten. Or if you do remem­ber, there is a good chance that the mem­ory is cor­rupted, that is, not totally cor­rect. The con­se­quence is that things that hap­pened long ago may be either for­got­ten, or misremembered.
What sus­tains the enzyme nec­es­sary for long-term mem­ory? I sus­pect it is rehearsal and peri­odic reac­ti­va­tion of the mem­ory. Some sci­en­tists are excited about the pos­si­bil­ity of devel­op­ing a drug to manip­u­late lev­els of the enzyme. The prob­lem with that, how­ever, is that the drug could abol­ish old mem­o­ries that you might not want to for­get (like your name) or may cause you to remem­ber too much that is now irrelevant.
Source: Shema, R., Sack­tor, T. C., and Dudai, Y. 2007. Rapid era­sure of long-term mem­ory asso­ci­a­tions in the cor­tex by an inhibitor of PKM. Sci­ence. 317:951–953.
3. Test­ing Pro­motes Consolidation
Tests do more than just mea­sure learn­ing. Tests are learn­ing events. That is, test­ing forces retrieval of incom­pletely learned mate­r­ial and that very act of retrieval is a rehearsal process that helps to make the learn­ing more per­ma­nent. Test­ing, and not actual study­ing, is the key fac­tor on whether or not learn­ing is con­sol­i­dated into longer term memory.
A recent report from Wash­ing­ton Uni­ver­sity in St. Louis, exam­ined the role that retrieval had on the abil­ity to recall that same mate­r­ial after a delay of a week. In the exper­i­ment, col­lege stu­dents were to learn a list of 40 for­eign lan­guage vocab­u­lary word pairs that were manip­u­lated so that the pairs either remained in the list (were repeat­edly stud­ied) or were dropped from the list once they were recalled. It was like study­ing flash cards: one way is to keep study­ing all the cards over and over again; the other way is to drop out a card from the stack every time you cor­rectly recalled what was on the other side of the card. After a fixed study period, stu­dents were tested over either the entire list or a par­tial list of only the pairs that had not been dropped dur­ing study. Four study and test peri­ods alter­nated back-to-back. Stu­dents were also asked to pre­dict how many pairs they would be able to remem­ber a week later, and their pre­dic­tions were com­pared with actual results on a final test a week later.
The ini­tial learn­ing took about 3–4 tri­als to mas­ter the list, and was not sig­nif­i­cantly affected by the strat­egy used (rehears­ing the entire list or drop­ping items out as they were recalled). On aver­age, the stu­dents pre­dicted that they would be able to remem­ber about half of the list on a test that was to be given a week later. How­ever, actual recall a week later var­ied con­sid­er­ably depend­ing on learn­ing con­di­tions. On the final test, stu­dents remem­bered about 80% of the word pairs if they had been tested on all the word pairs, no mat­ter whether they had been stud­ied mul­ti­ple times with all of them in the list or if they dropped cor­rectly recalled words from the list in later study tri­als. How­ever, recall was only about 30% cor­rect when cor­rectly iden­ti­fied words were dropped from sub­se­quent tests, even though all words were stud­ied repeat­edly. In other words, it was the repeated test­ing, not the study­ing, that was the key fac­tor in suc­cess­ful longer-term memory.
So, what is the prac­ti­cal appli­ca­tion? When using flash cards, for exam­ple, you need to fol­low each study ses­sion (whether or not you drop cards from the stack because you know them), with a for­mal test over all the cards. Then, repeat the process sev­eral times, with study and test epochs back-to-back. Can we extend this prin­ci­ple of fre­quent test­ing to other kinds of learn­ing strate­gies? I would guess so.
Why does forced recall, as dur­ing test­ing, pro­mote con­sol­i­da­tion? It prob­a­bly relates to other recent dis­cov­er­ies show­ing that each time some­thing is recalled the mem­ory is re-consolidated. If the same infor­ma­tion is con­sol­i­dated again and again, the mem­ory is pre­sum­ably reinforced.
This study also showed that the sub­jects could not pre­dict how well they would remem­ber, which is con­sis­tent with my 45 years expe­ri­ence as a pro­fes­sor. Stu­dents are fre­quently sur­prised to dis­cover after an exam­i­na­tion that they did not know the mate­r­ial as well as they thought they did. Tests not only reveal what they know and don’t know, but serve to increase how much they even­tu­ally learn. If I were still teach­ing, I would give more tests. And I would encour­age stu­dents to use self-testing as a rou­tine learn­ing strat­egy, some­thing that one study revealed to be a seldom-used strat­egy. The repeated self-tests should include all the study mate­r­ial and not drop out the mate­r­ial that the stu­dent thinks is already mastered.
Source: Karpicke, Jef­frey D., and Roedinger, Henry L. III. 2008. The crit­i­cal impor­tance of retrieval for learn­ing. Sci­ence. 319: 966–968.
Bill Klemm— W. R. (Bill) Klemm, D.V.M., Ph.D. Sci­en­tist, pro­fes­sor, author, speaker As a pro­fes­sor of Neu­ro­science at Texas A&M Uni­ver­sity, Bill has taught about the brain and behav­ior at all lev­els, from fresh­men, to seniors, to grad­u­ate stu­dents to post-docs. His recent books include Thank You Brain For All You Remem­ber and Core Ideas in Neu­ro­science.