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PubMed2026

The knee-ankle link: impact of knee varus severity on distal joint malalignment and concomitant pathologies.

BACKGROUND: Knee varus deformity is traditionally managed as an isolated joint pathology; however, persistent distal symptoms following proximal realignment suggest a more extensive kinetic chain dysfunction. The degree to which knee varus severity dictates distal malalignment and secondary pathologies remains poorly quantified in the current literature. METHODS: This systematic review and meta-analysis were conducted in accordance with PRISMA 2020 guidelines (PROSPERO: CRD420261363327). A comprehensive search of PubMed, Embase, Web of Science, and the Cochrane Library was performed from inception to April 2026. Studies examining the relationship between knee varus (HKA angle) and radiographic distal alignment or pathologies were included. Data synthesis utilized random-effects models, with prevalence analyzed via generalized linear mixed models (GLMM). RESULTS: Fourteen studies were included in the final synthesis. While pooling of continuous radiographic parameters was limited by high statistical heterogeneity in Talar Tilt (I2 = 96.5%), individual large-cohort data (Huang et al.) indicated that severe knee varus (HKA > 10°) was associated with increased odds of concomitant ankle osteoarthritis (OR 2.29; 95% CI 1.28-4.11) and a specific cohort prevalence of 37.1%. Furthermore, single-arm prevalence data revealed divergent trends across different study populations, with compensatory hindfoot valgus reaching 69.9% in some cohorts and rigid varus up to 63.9% in others. CONCLUSIONS: Severe genu varum is associated with distal kinetic chain alterations and concomitant ankle pathologies. However, due to the extreme heterogeneity and divergent distal adaptations observed across different cohorts, standardized knee-centric protocols may be insufficient. Further longitudinal and interventional studies are required to establish phenotype-specific rehabilitation guidelines.

Humans↗
PubMedDate not supplied

Progression of cellular repopulation and collagen synthesis in fresh-frozen allograft tendons.

The progression of cellular repopulation and collagen synthesis in fresh-frozen rat patellar tendon allografts was investigated by means of indirect immunofluorescence histologic analysis and electron microscopic techniques for 8 weeks after transplantation. In each of 10 procedures, the medial half of the patellar tendon with a tibial bone block was harvested from a Wistar rat and transplanted into a corresponding defect in the medial patellar tendon of a Lewis rat. Actin filaments in the repopulating cells and newly synthesized collagen fibrils in the graft were identified with rhodamine-phalloidin stain and with a polyclonal antibody against type III collagen aminopropeptide. On the first day after transplantation, no specific fluorescence was detected in the graft. One week later, specific labeling for fibrillar-actin (F-actin) and type III collagen aminopropeptide was detected in an area extending from the adjacent granulation tissue into the proximal end of the graft. F-actin and type III collagen aminopropeptide were aligned along the longitudinal axis of the graft and extended from the proximal suture site toward the distal portion. Two weeks after transplantation, fibrillar labeling for F-actin and type III collagen amino-propeptide showed that remodeling had extended to the midportion of the graft. Labeling throughout the entire graft was detected 4 weeks after transplantation. During the entire remodeling process, the repopulated fibroblasts consistently retained their elongated shape and their alignment with the longitudinal axis of the graft. The cells developed well-organized actin bundles at their peripheries, which identified them as having a myofibroblast phenotype. Immunofluorescence detection for type III collagen aminopropeptide also showed consistent alignment parallel to the longitudinal axis of the graft and a fibrillar arrangement. Electron microscopy revealed thinner collagen fibrils in the vicinity of the fibroblasts, which were aligned in the direction of the actin bundles. These results indicate that, during the early remodeling phase, collagen synthesis and deposition in the graft proceeds while the original alignment of the graft matrix is preserved. The close association between the alignment of actin bundles in repopulated "myofibroblastic" cells and that of newly synthesized collagen fibrils along the lines of the graft matrix may represent evidence of force transmission between the actin cytoskeleton and the linking extracellular matrix in vivo.

Journal Article↗
PubMed1999

Genetic analysis of motor milestones attainment in early childhood.

The age of attainment for four motor developmental traits, such as turning over, sitting up without support, pulling up to a standing position and walking without support, was examined in 822 children, including 626 siblings from families with 2 to 6 children, 68 pairs of dizygotic twins and 30 pairs of monozygotic twins. Correlation analysis, carried out separately for each type of sibship, showed the highest pairwise correlations in monozygotic twins and the lowest correlation in non-twin siblings for all motor milestones. Variance component analysis was used to decompose the different independent components forming the variation of the studied trait, such as genetic effect, common twin environment, common sib environment and residual factors. The results revealed that the major proportion of the total variance after adjustment for gestation age for the attainment of each motor skill, except pulling up to standing position, is explained by the common twin environment (50.5 to 66.6%), whilst a moderate proportion is explained by additive genetic factors (22.2 to 33.5%). Gestational age was found to be an important predictor of appearance of all motor milestones, affecting delay of 4.5 to 8.6 days for the attainment of the motor abilities for each week of earlier gestation. The age of attainment of the standing position was affected only by shared sibs environment (33.3% of the total variance) and showed no influence of either genetic or common twin environment. Phenotypic between trait correlations were high and significant for all studied traits (range between 0.40 and 0.67, P < 0.01 in all instances). Genetic cross correlations, however, were not easily interpreted and did not show clear variance trends among the different groups of children.

Age Factors↗
PubMed1992

Relation of serum elastin peptide concentration to age, FEV1, smoking habits, alcohol consumption, and protease inhibitor phenotype: an epidemiological study in working men.

BACKGROUND: In clinical investigations elastin peptide concentration has been proposed as one potential marker of lung elastin degradation. No epidemiological study has yet confirmed this hypothesis. METHODS: The relation of elastin peptide concentration to some factors closely related to pulmonary emphysema (age, smoking habits, FEV1 alpha protease inhibitor (PI) phenotype) and to alcohol consumption was examined in an epidemiological study of 310 working men. The elastin peptides used for obtaining antibodies and as reference in an ELISA assay were prepared from chemically hydrolysed elastin. RESULTS: The elastin peptide concentration significantly decreased with age from 2.92 (1.54) micrograms/ml among subjects younger than 30 years to 2.18 (1.14) micrograms/ml among subjects older than 50. Elastin peptide concentration did not differ with smoking habits and was clearly unrelated to FEV1. A lower elastin peptide concentration was observed in all groups of subjects with a protease inhibitor phenotype other than PI MM (PI FM, IM, MP, MS, MZ, and S phenotypes). CONCLUSIONS: The results cast doubts on the usefulness of the elastin peptide concentration as a marker of lung destruction in middle aged, predominantly healthy men. Blood elastin peptide concentration may reflect both elastin degradation and resynthesis. The results of this analysis suggest that several factors (age, alcohol consumption, non-PI MM phenotype) may be associated with decreased resynthesis of lung elastin. Further studies, conducted in various age groups and including estimates of the degree of lung destruction, are needed to unravel the mechanisms underlying lysis and resynthesis of lung elastin.

Adult↗
PubMed1992

Hybrid acute leukemia: therapeutical implications of immunological phenotyping.

We phenotyped blood and bone marrow cells from a patient with acute Ph1+ acute leukemia longitudinally during the four months he received intensive chemotherapy. At presentation this case of biphenotypic acute leukemia had two immunologically different types of blast cells, one expressed CD10 (CALLA), CD13 (MY7) and CD33 (MY9) but lacked CD20 (B1), the other type expressed no CD10 or CD33. The phenotype, during AML induction therapy, changed to a more CD10+, CD20+ ALL one. ALL therapy based on these findings induced improvement in bone marrow function but the patient died of septicemia at day 134. The use of concomitant immunophenotyping (IP) and cell cycle analysis had shown proliferation advantage of the more lymphoid malignant cells. These results suggest that it is possible to induce lineage-associated changes in the phenotype of hybrid malignant cells and that these leukemias might be treated best according to longitudinal immunophenotyping of the blast cells.

Adult↗
PubMed2002

Application of hierarchical genetic models to Raven and WAIS subtests: a Dutch twin study.

Hierarchical models of intelligence are highly informative and widely accepted. Application of these models to twin data, however, is sparse. This paper addresses the question of how a genetic hierarchical model fits the Wechsler Adult Intelligence Scale (WAIS) subtests and the Raven Standard Progressive test score, collected in 194 18-year-old Dutch twin pairs. We investigated whether first-order group factors possess genetic and environmental variance independent of the higher-order general factor and whether the hierarchical structure is significant for all sources of variance. A hierarchical model with the 3 Cohen group-factors (verbal comprehension, perceptual organisation and freedom-from-distractibility) and a higher-order g factor showed the best fit to the phenotypic data and to additive genetic influences (A), whereas the unique environmental source of variance (E) could be modeled by a single general factor and specifics. There was no evidence for common environmental influences. The covariation among the WAIS group factors and the covariation between the group factors and the Raven is predominantly influenced by a second-order genetic factor and strongly support the notion of a biological basis of g.

Adolescent↗
PubMed2004

Development and testing of new screening method for keratan sulfate in mucopolysaccharidosis IVA.

Mucopolysaccharidosis IVA (MPS IVA), a progressive lysosomal storage disease, causes skeletal dysplasia through excessive storage of keratan sulfate (KS). We developed an ELISA-sandwich assay that used a MAb specific to KS. Forty-five blood and 59 urine specimens from MPS IVA patients (ages 1-65 y) were analyzed to determine whether KS concentration is a suitable marker for early diagnosis and longitudinal assessment of disease severity. Blood specimens were obtained from patients categorized as phenotypically severe (n = 36) and milder (n = 9). Urine specimens were also analyzed from patients categorized as severe (n = 56) and milder (n = 12), respectively. Blood KS levels (101-1525 ng/mL) in MPS IVA patients were two to eight times higher than those in age-matched controls (15-323 ng/mL). It was found that blood KS level varied with age and clinical severity. Blood KS levels in both MPS IVA and controls peaked between 5 and 10 y of age (mean, 776 versus 234 ng/mL, respectively). Blood levels in severe MPS IVA were 1.5 times higher than in the milder form. In contrast to blood, urine KS levels in both MPS IVA and controls peaked between 1 and 5 y (15.3 versus 0.26 mg/g creatinine), and thereafter declined with age. Urine KS level also varied with age and clinical severity, and the severe MPS IVA phenotype was associated with 6.7 times greater urine KS excretion than the milder one. These findings indicate that the new assay for blood or urine KS may be suitable for early diagnosis and longitudinal assessment of disease severity in MPS IVA.

Adolescent↗
PubMed2005

Hemoglobin E-beta-thalassemia: Progress report from the International Study Group.

A long-term observational study of Hb E-beta-thalassemia in Sri Lanka is beginning to define some of the genetic and environmental factors that are responsible for its remarkable phenotypic variability. In this population there is a very small difference between the steady-state hemoglobin levels between the mild and severe phenotypes, and it has been possible to stop transfusion in many of those who have been on long-term treatment of this kind. These preliminary observations, made over the last 7 years, provide directions for future research into this increasingly important disease.

Adolescent↗
PubMed2006

Prevalence, clinical correlates, and longitudinal course of severe mood dysregulation in children.

BACKGROUND: Controversy concerning the diagnosis of pediatric bipolar disorder (BD) has focused attention on children with chronic irritability and hyperarousal. This syndrome has been called the "broad BD phenotype" or severe mood dysregulation (SMD). This study examines prevalence, concurrent Axis I diagnoses, and longitudinal outcome of SMD in an epidemiologic sample. METHODS: Data were drawn from the Great Smoky Mountains Study, a longitudinal epidemiological study. Items from the Child and Adolescent Psychiatric Assessment were used to generate SMD criteria. RESULTS: Among 1420 children, the lifetime prevalence of SMD in children ages 9-19 was 3.3%. Most (67.7%) SMD youth had an Axis I diagnosis, most commonly attention-deficit/hyperactivity disorder (26.9%), conduct disorder (25.9%), and/or oppositional defiant disorder (24.5%). In young adulthood (mean age 18.3 +/- 2.1 years), youth who met criteria for SMD in the first wave (mean age 10.6 +/- 1.4 years) were significantly more likely to be diagnosed with a depressive disorder (odds ratio 7.2, confidence interval 1.3-38.8, p = .02) than youth who never met criteria for SMD. CONCLUSIONS: Severe mood dysregulation is relatively common in childhood and predicts risk for early adulthood depressive disorders. Research should continue to explore the course of illness in children with SMD.

Adolescent↗
PubMed2006

Survival analysis of longitudinal microarrays.

MOTIVATION: The development of methods for linking gene expressions to various clinical and phenotypic characteristics is an active area of genomic research. Scientists hope that such analysis may, for example, describe relationships between gene function and clinical events such as death or recovery. Methods are available for relating gene expression to measurements that are categorized or continuous, but there is less work in relating expressions to an observed event time such as time to death, response or relapse. When gene expressions are measured over time, there are methods for differentiating temporal patterns. However, methods have not yet been proposed for the survival analysis of longitudinally collected microarrays. RESULTS: We describe an approach for the survival analysis of longitudinal gene expression data. We construct a measure of association between the time to an event and gene expressions collected over time. Statistical significance is addressed using permutations and control of the false discovery rate. Our proposed method is illustrated on a dataset from a multi-center research study of inflammation and response to injury that aims to uncover the biological reasons why patients can have dramatically different outcomes after suffering a traumatic injury (www.gluegrant.org).

Algorithms↗
PubMed2005

Prevalence and genetic architecture of Child Behavior Checklist-juvenile bipolar disorder.

BACKGROUND: No consensus has been reached yet on how best to characterize children with juvenile bipolar disorder (JBD). Several groups have shown that children on the attention problems (AP), aggressive behavior (AGG), and anxious-depressed (AD) syndromes of the Child Behavior Checklist (CBCL) are likely to meet criteria for DSM-JBD. We aimed to use a large population-based twin sample to evaluate the prevalence and genetic architecture of the CBCL-JBD (deviant on AP, AGG, and AD) phenotype and compare these data to children who are deviant on just the CBCL-AP syndrome. METHODS: Structural equation modeling (SEM) was applied to CBCL data from 5418, 3562, and 1971 Dutch twin pairs at ages 7, 10, and 12 years. RESULTS: The CBCL-JBD phenotype occurs in approximately 1% of children at each age. Among the children who meet criteria for the CBCL-AP phenotype ( approximately 5%), between 13 and 20% also meet criteria for CBCL-JBD. The best SEM for CBCL-JBD includes additive genetic, shared and unique environmental factors. The best SEM for CBCL-AP includes dominant and additive genetic and unique environmental factors. CONCLUSIONS: These data suggest that CBCL-JBD is common, and even more common among children who have severe attention problems. CBCL-JBD shows familial aggregation due to both genetic and shared environmental factors.

Adolescent↗
PubMed2003

Use of a random coefficient regression (RCR) model to estimate growth parameters.

We used a random coefficient regression (RCR) model to estimate growth parameters for the time series of observed serum glucose levels in the Replicate 1 of the Genetic Analysis Workshop 13 simulated data. For comparison, a two time-point interval was also selected and the slope between these two observations was calculated. This process yielded four phenotypes: the RCR growth phenotype, a two time-point slope phenotype, and Time 1 and Time 2 serum glucose level phenotypes. These four phenotypes were used for linkage analyses on simulated chromosomes 5, 7, 9, and 21, those chromosomes that contained loci affecting the growth course for serum glucose levels. The linkage analysis of the RCR-derived phenotype showed overwhelming evidence for linkage at one locus (LOD 65.78 on chromosome 5), while showing elevated but nonsignificant LOD scores for two other loci (LOD 1.25 on chromosome 7, LOD 1.10 on chromosome 9), and no evidence of linkage for the final locus. The two time-point slope phenotype showed evidence for linkage at one locus (LOD 4.16 on chromosome 5) but no evidence for linkage at any of the other loci. A parallel cross-sectional approach, using as input phenotypes the endpoints of the two-point slope phenotype, gave strong linkage results for the major locus on chromosome 5 (maximal LOD scores of 17.90 and 27.24 for Time 1 and Time 2, respectively) while showing elevated but nonsignificant linkage results on chromosome 7 (maximal LOD scores of 1.71 and 1.48) and no evidence for linkage at the two remaining loci. The RCR growth parameter showed more power to detect linkage to the major locus than either the cross-sectional or two-point slope approach, but the cross-sectional approach gave a higher maximal LOD score for one of the minor loci.

Adult Children↗
PubMed1990

Clinical relevance of immunocytochemical detection of multidrug-resistance-associated P-glycoprotein in hematologic malignancies.

P-glycoprotein (P-170) is the phenotypic marker of tumoral cells that show the phenomenon of multidrug resistance (MDR). Using an immunocytochemical approach, we employed the monoclonal antibody C219 (which recognizes an epitope of such a glycoprotein) to evaluate in cytologic samples the expression of P-170 on neoplastic cells from 52 patients affected by different hematologic malignancies and its eventual correlation to clinical outcome. Longitudinal studies were also performed in 14 patients. Results obtained demonstrated that a) the so-called "MDR phenotype" may be heterogeneously represented (from less than 1 to 100% of positive cells) in hemopoietic tumors at diagnosis (without exposure to pharmacologic agents), as well as during the course of the disease, although a more substantial presence of P-170 occurred in treated patients. There was no correlation between neoplastic kinetic activity (such as expression of Ki 67 recognized nuclear proliferation-associated antigen) and P-170-positive cells. b) Percentage of positive cells as well as intensity of staining seemed to be important in determining MDR; in general, there was a strong correlation between expression of P-170 in more than 20% of neoplastic cells and a lack of response to chemotherapy. However, some false-positive and false-negative cases were observed. c) The detection of scattered P-170-positive cells may predict a pharmacologic selection of intrinsic or mutant-resistant clones.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Longitudinal evaluation of CD4+ and CD8+ peripheral blood and mammary gland lymphocytes in cows experimentally inoculated with Staphylococcus aureus.

Staphylococcus aureus is a major pathogen associated with mastitis, a disease affecting both women and dairy cows. The longitudinal profiles of bovine peripheral blood and mammary gland lymphocyte phenotypes in response to S. aureus-induced mastitis were investigated in dairy cows. Increased percentage of CD4 lymphocytes in the mammary gland between 1 and 8 days post-inoculation, increased milk CD4 protein density per cell between 1-8 days post-inoculation, and a statistically significant negative correlation between post-inoculation bacterial counts in milk and blood lymphocyte CD4 protein density were found. Together with blood and milk leukocyte counts, the milk lymphocyte CD4/CD8 ratio and the milk lymphocyte CD4 protein density were more informative indicators than milk somatic cell counts and bacteriology for identification of early vs. late inflammatory phases. These findings suggest that CD4+ lymphocytes play a protective role in the early stages of S. aureus-induced mastitis.

Animals↗
PubMed2003

Summary report: Missing data and pedigree and genotyping errors.

Genetic epidemiology is faced with mapping complex traits to genes with relatively small effects whose phenotypes may be modulated by temporal factors. To do this, detailed and accurate data must be available on families, perhaps collected over time. The Framingham Heart Study data supplied to Genetic Analysis Workshop 13 (GAW13), along with its simulated counterpart, contain longitudinal measurements and genomic scan data on 2,885 individuals in 330 families, and offer an opportunity to examine data quality and completeness issues as they affect analytical conclusions. Six GAW13 contributions applied methods to deal with missing data, both phenotypic and genotypic, at a single time point and longitudinally, and with possible errors in pedigree structure and genotypes. The methods included missing phenotypic data imputation by Markov chain Monte Carlo sampling, propensity scoring, regression, and adjusted mean values, as well as the assessment of transmission-disequilibrium tests when missing marker data may be allele-specific. Pedigree structural errors were found by genome-wide allele-sharing probabilities, while Mendelian consistent genotype errors were evaluated through likelihoods of double-recombination events. Each of the methods reviewed here offered insights into how to better take advantage of large, time-dependent, familial data sets. However, no one of them dealt with the longitudinal and familial aspects simultaneously. Overall, more consideration needs to be given to the effects that missing data and data errors have on our ability to map complex traits efficiently and accurately.

Cardiovascular Diseases↗
PubMed2006

A novel splicing mutation in KCNQ2 in a multigenerational family with BFNC followed for 25 years.

PURPOSE: A large multigenerational family with benign familial neonatal convulsions (BFNC) was revisited to identify the disease-causing mutation and to assess long-term outcome. METHODS: We supplemented the original data with recent clinical and neurophysiologic data on patients and first-degree relatives, including information on seizure recurrence. We conducted linkage analysis at the EBN1 and EBN2 loci, followed by mutation analysis of KCNQ2. We evaluated the qualitative effect of the KCNQ2 mutation at the messenger RNA (mRNA) level by using reverse-transcribed total RNA isolated from leukocytes. RESULTS: Thirteen relatives had a history of neonatal convulsions, 11 of whom showed remission within 2 months. One patient showed an atypical course of neonatal convulsions, developing photosensitive myoclonic epilepsy at age 13 years. We found suggestive linkage of the BFNC phenotype to the 20q13-EBN1 locus (lod score, 2.03) and an intronic mutation IVS14-6 C>A in KCNQ2 segregating with the trait in all affected members, but absent in 100 unrelated control subjects. This mutation creates a new, preferentially used, splice site. Alternative splicing adds 4 nt containing a premature stop codon to the transcript, resulting in a truncated protein after position R588. CONCLUSIONS: We detected and characterized a novel splicing mutation in the brain-specific KCNQ2 gene by using easily accessible blood leukocytes. Aberrant splicing cosegregates with BFNC but not with photosensitivity.

Adolescent↗
PubMed1997

In vivo and in vitro activation and expansion of gammadelta T cells during Listeria monocytogenes infection in humans.

Serial flow cytometry analyses of peripheral blood mononuclear cells obtained from 8 patients infected with Listeria monocytogenes showed a higher percentage (P < 0.01) of gammadelta T cells (median, 11.7; range, 3.7 to 35.3) than did 16 age-matched uninfected controls (1.7, 0.4 to 13). Most in vivo-expanded gammadelta T cells expressed the Vgamma9 and Vdelta2 gene products and displayed a memory phenotype (CD45RO[high]), and patients' gammadelta T cells expressed significantly more (P < 0.01) activation marker HLA-DR than did controls (19.8% [median] and 0.9 to 87.6% [range] versus 2.3% and 0 to 4.7%, respectively). When peripheral blood mononuclear cells from normal donors were cultured in vitro with heat-killed Listeria cells, analysis of CD25 and HLA-DR expression on gammadelta and alphabeta T cells indicated that a high percentage of gammadelta T cells was activated early compared to alphabeta T cells. In addition, depletion of gammadelta T cells before culture abrogated the early lymphocyte proliferative response induced by the pathogen. Taken together, these results argue for the involvement of gammadelta T cells during L. monocytogenes infection in humans.

Adult↗
PubMed2004

Four-year prospective outcome and natural history of mania in children with a prepubertal and early adolescent bipolar disorder phenotype.

BACKGROUND: Diagnosis of child mania has been contentious. OBJECTIVE: To investigate natural history and prospective validation of the existence and long-episode duration of mania in children. DESIGN: Four-year prospective longitudinal study of 86 subjects with intake episode mania who were all assessed at 6, 12, 18, 24, 36, and 48 months. The phenotype was defined as DSM-IV bipolar I disorder (manic or mixed) with at least 1 cardinal symptom (elation and/or grandiosity) to ensure differentiation from attention-deficit/hyperactivity disorder. Parent and child informants were separately interviewed, by highly experienced research nurses, using the Washington University in St Louis Kiddie Schedule for Affective Disorders and Schizophrenia (WASH-U-KSADS). A Children's Global Assessment Scale score of 60 or less was needed to establish definite impairment. Treatment was by subjects' community practitioners. SETTING: Research unit in a university medical school. PARTICIPANTS: Subjects were obtained from psychiatric and pediatric sites by consecutive new case ascertainment, and their baseline age was 10.8 +/- 2.7 years. Onset of the baseline episode was 7.4 +/- 3.5 years. (Data are given as mean +/- SD.) MAIN OUTCOME MEASURES: Episode duration, weeks ill, recovery/relapse rates, and outcome predictors. RESULTS: Prospective episode duration of manic diagnoses, using onset of mania as baseline date, was 79.2 +/- 66.7 consecutive weeks. Any bipolar disorder diagnosis occurred during 67.1% +/- 28.5% of total weeks, during the 209.4 +/- 3.3 weeks of follow-up. Subjects spent 56.9% +/- 28.8% of total weeks with mania or hypomania (unipolar or mixed), and 38.7% +/- 28.8% of these were with mania. Major or minor depression and dysthymia (unipolar or mixed) occurred during 47.1% +/- 30.4% of total weeks. Polarity switches occurred 1.1 +/- 0.7 times per year. Low maternal warmth predicted faster relapse after recovery from mania (chi(2) = 13.6, P =.0002), and psychosis predicted more weeks ill with mania or hypomania (F(1,80) = 12.2, P =.0008). Pubertal status and sex were not predictive. (Data are given as mean +/- SD.) CONCLUSIONS: These findings validate the existence, long-episode duration, and chronicity of child mania. Differences from the natural history of adult bipolar disorder are discussed.

Adult↗