\r\n\t
\r\n\tThis book intends to provide the reader with a comprehensive overview of the current epidemiology, valuable information in relation to the management of specific poisoning agents, and important evidence-based developments in the toxicology field, with special focus on children, who are a more vulnerable population for severe poisonings. Its aim is to be a practical handbook to aid health care professionals involved in individual care of patients poisoning.
Obesity is a chronic disorder of the state of nutrition characterized by an increase in body weight due to excessive adipose tissue, which occurs when the calorie intake exceeds the caloric needs of a body with low energy expenditure. Obesity is currently a significant public health problem, as we have witnessed a dramatic increase in the number of obese and overweight children worldwide in the last years. Children’s risk of obesity varies by age and sex groups, ethnic/racial groups, socioeconomic status, geographic and rural/urban regions. The obesity etiology is complex, involving genetic, environmental, psycho-socio-cultural, neuroendocrine and metabolic factors. Complications of pediatric obesity occur during childhood and adolescence and increase the risk for morbidity and mortality in adulthood.
Obesity is an important pediatric public health problem associated with risk of complications in childhood and increased morbidity and mortality throughout life. Overweight and obesity predispose people to noncommunicable diseases such as heart disease, diabetes mellitus, musculoskeletal and psychological disorders and certain types of cancer [1].
\nWithout intervention, obese infants and young children will likely continue to be obese during childhood, adolescence and adulthood [1–3].
\nThe methodological problem of inconsistency between criteria of childhood obesity classification is a major obstacle in studying global trends for younger age group. The body mass index [BMI: weight (kg)/height (m)2] is the parameter used for the screening of overweight and obesity in childhood because it is easy to determine, it tends to correlate well with body fat, and it has been widely used in adults to define obesity. It decreases until the period called “adiposity rebound” when body fat is at the lowest level (between 3 and 7 years) and after then BMI increases again until the adulthood [4, 5].
\nThe child’s BMI must be plotted on nationally recommended BMI—for age charts. The classification of overweight and obesity varies among guidelines, such as those from Centre for Disease Control (CDC), International Obesity Task Force (IOTF) and World Health Organization (WHO).
\nFor example, in UK (IOTF BMI values) the cut off points for and are the BMI >91st and >98th percentile, respectively.
\nThe definition of overweight and obesity using BMI percentiles in the USA: children aged 2 years and older with a BMI between the 85th and 95th percentile is overweight, and those with a BMI greater than the 95th percentile for a specific age and sex subgroup are obese [4–6].
\nAccording to WHO, for children aged between 5 and 19 years, overweight is >2 standard deviations and obesity is defined as a BMI-for-age >1 standard deviation, above the WHO growth reference median [1].
\nThe IOTF BMI values represent standard international references that allow the screening of adiposity in children and adolescents worldwide under the same criterion, without variations depending on geographic, social and secular trends [5].
Currently, the prevalence of obesity among children and adolescents and related complications is considered one of the most important nutritional problem globally. The obesity epidemic among children is the result of excess energy intake and inadequate energy expenditure [2]. The prevalence of childhood overweight and obesity has increased worldwide in recent decades, and the numbers of those affected continue to rise at an alarming rate [6].
\nIn recent years, the epidemiology of overweight and obesity is well described in many European countries and the data showed the increasing trends in the prevalence of childhood obesity. The current prevalence of childhood obesity is ten times higher than it was in the 1970s [5].
\nThe incidence of overweight and obesity increased progressively from infancy through adolescence [5, 6]. High prevalence of obesity in 0- to 6-year-old children is warning signs and risk for increased rates of obesity in adolescence and adulthood reported.
\nNorth America and some countries in Europe have shown consistent year-on-year increases in prevalence of overweight (20–30%) and obesity (5–15%), although recent surveys indicate that the rising trends are easing, with a plateau in prevalence levels shown since around 2005 [6].
\nChildren’s risk of obesity varies by age and sex groups, ethnic/racial groups, socioeconomic status, geographic and rural/urban regions. The key reason for the variations is due to the considerable socioeconomic and lifestyle differences and the differences in differing criteria for obesity and overweight definition [4, 7].
\nSeveral countries of Southern Europe appear to be showing high prevalence of childhood obesity (20–35%) in the Italy, Greece, Malta, Portugal and Spain. The highest levels of overweight and obesity were in Southern Italy (30.1 and 33.1% in preschool boys and, respectively, girls) and in various regions of Spain (29.4% in both sexes, increasing to 32.6% among children aged 7- to 10-year old), followed by Greece (19.1 and 23.6% in boys and, respectively, girls) [7–9]. Children and adolescents residing in countries surrounding the Mediterranean Sea show the highest rates ranging from 20 to 40%, too [7]. Studies concerning obesity with regard to its prevalence in Portugal reported a rate of overweight in children under the age of 6 years, 13.6% in boys and 20.4% in girls, and, obesity varied between 6.5% in boys and 6.9%, respectively, in girls [10]. The very high prevalence of childhood obesity in Mediterranean countries could be secondary to lifestyle changes (switching from a healthy Mediterranean diet to a fast food type of diet and lower physical activity levels) [7].
\nIn children and adolescents residing the Scandinavian countries and Central Western European countries, the prevalence of overweight and obesity is far lower (10–20%). Scandinavian countries have the lowest prevalence of obesity in all age groups, except Finland which reported the prevalence of overweight and obesity in school children of 23.6 and 19.1% for boys and, respectively, girls [7, 11]. It is important to note that among preschool children, the highest prevalence rates of overweight and obesity were in Ireland (26 and 29% in boys and, respectively, girls), United Kingdom (24.1 and 21.4% in boys and, respectively, girls). In school children, the prevalence of overweight and obesity has increased to 32.7% and, respectively, 29.2% in 2007 the United Kingdom [7]. In developed countries, an increasing number of studies suggest that children of lower-income families are vulnerable to becoming obese, possibly due to poor dietary habits and limited opportunities for physical activity [7, 12]. In the UK, the prevalence of overweight and obesity in 11- to 12-year-old children was 25%, with higher rates in girls (29%) and students from lower socioeconomic backgrounds (31%), and the highest rates was observed in black girls (38%) [13].
\nData from Eastern European countries indicate the prevalence rate is smaller (15%), but rising. In Lithuania, the Russian Federation, Slovakia and Poland, the overweight and obesity prevalence ranges from 8.46 to 15.8% in children aged 6–12 years. It is likely that the huge economic burden and the associated poverty following the political transition in the 1990s may have contributed to the relatively low obesity prevalence in Eastern Europe [7].
Obesity is a multifactorial disease with a complex etiology being involved genetic, environmental, psycho-socio-cultural, neuroendocrine and metabolic factors, intestinal microbiota. The factors involved in its etiology included the ‘obesogenic’ environment, and the unhealthy dietary behaviors and patterns of physical activity [14].
\nThere is growing interest in the role of experience in early life in the risk of becoming overweight or obese. In children, prenatal life may be a critical period when the long-term regulation of energy balance is permanently ‘programmed’. The perinatal parameters and factors implicated in the etiology of obesity include maternal obesity, excessive weight gain in pregnancy, gestational diabetes, and maternal smoking, duration of breastfeeding, rapid infancy weight gain and other cultural or familial factors associated with childhood eating patterns and activity levels [14, 15].
\nMaternal obesity is a strong predictor of overweight and obesity in children. Obesity in pregnant women was found to be associated to high newborn weight and also causing obesity and metabolic syndrome risk in later life of the individual. Intrauterine growth restriction is associated with the development of central adiposity and adult-onset cardiovascular risk [4, 14].
\nChild\'s exposure to passive smoking, since the product conception stage, predisposes to the development of obesity and obesity related diseases as a result [14, 16, 17].
\nBreastfeeding could help infants to better recognize satiety signals and hence to better self-regulate energy intake. The prevalence and duration of breastfeeding is higher in countries with relatively lower prevalence of childhood obesity such as Sweden, Finland and Austria, in comparison to countries such as Italy, Greece and the UK, where is less [7, 14, 15].
\nEthnicity is associated with differences in eating behaviors, preferences, and cultural influences may contribute to obesity among children and youth in minority populations.
\nThe environmental factors are represented by: over-nutrition (high fat, high sugar diets), sedentary lifestyle, short sleep duration, abuse of drugs (antibiotics, corticosteroids, anti-epileptics drugs), smoking and alcohol. Almost all obesity in children is strongly influenced by environmental factors, caused by a sedentary lifestyle or a caloric intake that is greater than needs. However, this explains only a part of obesity risk, but is important targets for treatment such they can be modifiable.
\nSugar-sweetened beverages—the literature evidence suggests that consumption of sugar-sweetened beverages is an important factor in the development of obesity in some individuals. In the United States, sugar-sweetened beverages supplied an average of 270 kcal/day, representing 10–15% of total caloric intake. In a separate randomized trial on children aged 5–12 (primarily normal weight), consuming one serving of a sugar-free beverage daily was associated with less weight gain and fat accumulation than consuming one serving of a sugar-sweetened beverage. Other studies have found that dietary salt intake is associated with increased intake of sugar-sweetened beverages, perhaps because of increased thirst [18, 19].
\nTelevision viewing is an environmental influence on the development of obesity in children. Contact of a child with television begins in the newborn stage and tends to increase continuously. In the first year of life, children react to the screen characters with mimics and voice. Toddlers spend approximately 1 h a day watching television, and from the 4th year of life the exposure to other type of media expands and rises significantly to reach 7 out of 24 h per day. The presence of a television in a child\'s bedroom and any time spent in watching television are directly related to the prevalence of obesity in children and adolescents. A significant association between advert exposure and childhood obesity has been demonstrated in a cross-cultural study which included data from the USA, Australia and eight European countries [18, 20–22].
\nVideo games—the use of PC or console games has been associated with obesity in children. Half of American children have either a DVD, video or game console in their bedroom and, third, a computer with access to Internet [22, 23].
\nSleep—there is a reported association between shortened sleep duration and obesity. A causal association arises from a short-term experimental study in which sleep deprivation for 1 week was associated with increased food intake, weight gain and higher leptin levels as compared to the child\'s usual sleep. Moreover, sleep may have an association with insulin resistance, independent of its association with obesity. The mechanism between sleep duration and obesity has not been well-known, but may comprise dysfunction in serum leptin and/or ghrelin levels, both are involved in the regulation of appetite [4, 18]. A meta-analysis found that sleep is positively associated with fat mass in toddlers. A positive association between nighttime sleep and BMI z-scores were observed in the study reported by Kuzik and Carson [24].
\nMedications that may cause weight gain in children include cortisol and other glucocorticoids, sulfonylureas, tricyclic antidepressants (TCAs), monoamine oxidase inhibitors, such as phenelzine, oral contraceptives, insulin (in excessive doses), thiazolidinediones, risperidone, clozapine [25].
\nOther environmental factors that have been proposed as possible contributors to obesity include the influences of gut microbiota, toxins and viruses. Due to the influence of gut microbiota, it has been suggested that there exists a relationship between the resident intestinal bacteria and the potential for weight gain. Effect of microbiota may be partially responsible for increased rate of obesity in children born via cesarean section. Intestinal bacteria seem to influence several factors leading to development of obesity complications such us non-alcoholic steatohepatitis, cardiovascular disease and insulin resistance in humans [26]. It has been suggested that obesity can be triggered or worsened by exposure to a virus. Adenovirus 36 increases body fat in several animal models [18].
\nOther epidemiologic studies highlight the possibility that obesity could be triggered or exacerbated by exposure to environmental endocrine disrupting chemicals (dichlorodiphenyltrichloroethane—DDT and bisphenol A—BPA). Some studies in adults and children establish an association between urinary BPA levels and obesity or obesity related diseases, as well as diabetes and cardiovascular disease [18].
\nEndocrine disruptors can disturb every level of the endocrine system. They can interrupt the action of enzymes involved in steroidogenesis. The endocrine disruptors inducing obesity are called obesogens and have been revealed to target transcription regulators that function to control intracellular lipid homeostasis as well as proliferation and differentiation of adipocytes. The main group of regulators that are targeted represent a group of nuclear hormone receptors recognized as peroxisome proliferator-activated receptors (PPARα, δ and γ). PPARγ is considered to be the master regulator of adipogenesis and plays key roles in nearly all aspects of adipocyte biology. Other endocrine disruptors are known to promote adipogenesis, but probably do not act through PPARγ, these include BPA, organophosphate pesticides and monosodium glutamate [27].
\nHormonal disorders associated with childhood obesity include growth hormone deficiency, growth hormone resistance, hypothyroidism, leptin deficiency or resistance to leptin action, glucocorticoid excess (Cushing syndrome), precocious puberty, polycystic ovary syndrome (PCOS), prolactin-secreting tumors. Furthermore, in obese individuals, dysfunction in the gut-brain hypothalamic axis and ghrelin/leptin hormonal pathway has been proposed to have a role in excess energy intake and abnormal appetite control [28].
\nSpecific syndromes and single gene defects that are linked to obesity in children have been identified. These are very rarely causes of obesity, Generally, monogenic forms of childhood obesity are very rare, accounting for <1% in children. Mutations in only a few genes are known to cause the development of severe obesity in early childhood. Single gene disorders that can cause obesity include deficiency in leptin or its receptor, mutation in leptin gene, deficiency of proopiomelanocortin (POMC), haploinsufficiency receptor 4 and accessory protein receptor 2 of melanocortin, also disorders of protein convertase 1 [4, 18]. The leptin/leptin receptor system regulate food intake through reduce feeding and increased energy expenditure. Some forms of monogenic obesity like congenital leptin deficiency benefits from leptin substitution therapy that leads to significant decrease in weight [29].
\nMoreover, children with genetic syndromes associated with obesity typically have early onset obesity and characteristic signs on physical examination, including dysmorphic features, developmental delay, short stature or intellectual disability, retinal changes or deafness. The Prader Willi syndrome is the most common among obesity syndromes and is characterized by hypotonia and feeding difficulties during infancy, hyperphagia and obesity developing during early childhood and developmental delay. Other syndromes associated with childhood obesity are Pseudohypoparathyroidism, Laurence Moon Biedl (Bardet Biedl) syndrome, Cohen syndrome, Down syndrome and Turner syndrome [30].
Complications of pediatric obesity occur during childhood and adolescence and increased the risk for morbidity and mortality into adulthood.
\nObesity, particularly abdominal, has been shown to be an important risk factor for a number of chronic diseases in adults. Associated with obesity in childhood is a wide range of health serious complications and increased risk of premature onset year of illnesses. The most important organic complications are dyslipidemia, arterial hypertension, type 2 diabetes mellitus, nonalcoholic fatty liver disease, polycystic ovaries syndrome, orthopedic and respiratory complications. The metabolic syndrome (central obesity, hypertension, glucose intolerance and hyperlipidemia) increases risk for cardiovascular morbidity and mortality. The most frequent psychological complications are disorders concerning body image, eating habits and depression [4, 19].
\nInsulin resistance is defined as a decreased response of tissue to the action of insulin, and due to lowering of the capacity of insulin to stimulate glucose utilization by muscle cells and fat cells and to suppress hepatic glucose production, and insulin resistance in the protein and lipid metabolism. The association of obesity with insulin resistance is well-known: the factors and the mechanism by which the insulin resistance compensation is produced by beta islet cells and those that lead to the "failure" of the pancreatic beta cells in obese patients. It seems that microvascular changes associated with diabetes begin early stages still hyperinsulinemia with normal glycaemia or impaired oral glucose tolerance test. A central role in regulating central nervous system appears to have fat in the body\'s glucose metabolism by integrating information neural hormonal and nutritional. Insulin via the insulin receptor in the central nervous system regulates food intake and energy homeostasis. Adipose tissue seems to play a role in insulin resistance by metabolites, hormones and adipocytokines influencing different stages of insulin action. Fat distribution is an important determinant of insulin resistance, abdominal fat tissue lipolysis is easier and is less sensitive to insulin anti-lipolysis than subcutaneous adipose tissue. Total fat in children correlates well with the visceral and the relationship of visceral adipose tissue and the cardiovascular risk factors demonstrated in adults appears to differ [4, 31].
\nResearch on elucidating the relationship between obesity and atherogenic dyslipidemia appears to show a close relationship with insulin resistance. Three major events are based on atherogenic dyslipidemia of obesity with insulin resistance: excessive production of very low density lipoprotein-cholesterol, lipoprotein catabolism and defective catabolism of high density lipoprotein-cholesterol. Visceral fat is associated with impaired insulin-glucose homeostasis, the plasma lipoprotein, in particular increased triglycerides and decreased high density lipoprotein-cholesterol [4].
\nArterial hypertension is recognized as an important component of metabolic syndrome in adults, but in children, its role is not very clear. While some studies hypertension is considered the direct effect of obesity, insulin resistance in others, it is considered a predictor of hypertension, independent of BMI. Arterial hypertension in the pathogenesis of obesity and insulin resistance may play a role in which leptin resistance physiological actions of insulin that leptin central nervous system vessels and kidneys should be changed. Studies suggest the involvement of oxidative stress in the pathogenesis and hypertension by stimulating reactive oxygen species by the renin–angiotensin–aldosterone system [32].
Obesity is more complicated to diagnose in children than in adults because children increase in height, weight and body fat naturally as they grow. The criteria for defining obesity in children are the fat mass assessment, the distribution of the body fat measure by age and sex and a centile cut off to define the point in the body fat measure distribution corresponding to obesity [33].
\nInitial assessments of these patients should include taking a careful history (investigating comorbidities, family history and potentially modifiable behaviors) and physical examination with BMI plotted on a BMI-for-age chart.
\nThe careful history includes as follows: elements of perinatal life (gestational diabetes, maternal obesity, birth weight, infant feeding, medications—glucocorticoids, some antiepileptics, antipsychotics), weight history (onset of parental and child obesity, current eating behaviors, management interventions), complications (psychological, sleeping disorders, gastrointestinal and orthopedic complications, menstrual disturbances in girls), family history (ethnicity, history of obesity, type 2 diabetes, cardiovascular disease, dyslipidemia, obstructive sleep apnea, polycystic ovary syndrome, bariatric, surgery, eating disorders) and lifestyle history (detailed exploration of family eating, nutritional, and activity patterns, sleep) [34].
\nPhysical examination should include the following: anthropometric data (weight, height, BMI, abdominal circumference), adiposity distribution (central versus generalized), assess blood pressure, markers of comorbidities and physical stigmata of a genetic syndrome, endocrine disorders, congenital or acquired hypothalamic alterations (fewer than 5% of cases) [4, 34].
\nThe child’s BMI must be plotted on nationally recommended BMI—for age charts. Children and adolescents with a BMI ≥99th percentile are even more likely to have comorbidities [4].
\nAbdominal circumference (AC) is also used for assessing excess fatty tissue is an indirect method for assessing abdominal fat tissue. Given the strong association between body fat distribution and risk of metabolic complications, it is helpful to calculate in all children with excess weight from the age of 5 years and upwards the relationship between waist circumference and height.
\nOther methods of measuring fat, such as bioelectrical impedance, and total body water measurement are used in research, but not in clinical evaluation [4].
\nCareful screening for hypertension using an appropriately sized blood pressure cuff is important (e.g., hypertension is diagnosed if systolic or diastolic blood pressure falls over 95th percentile for age, gender and height in at least three occasions) [35, 36].
\nEndocrine problems must be considered carefully on signs suggesting hypothyroidism (goiter), insulin resistance (acanthosis nigricans), polycystic ovary syndrome (hirsutism, excessive acne) and Cushing syndrome (violaceous striae, moon face) [36].
\nSymptoms of polyuria, nocturia or polydipsia may be the result of type 2 diabetes mellitus. Depending on their durations, overweight and obesity are important potential risk factors for respiratory complications (asthma, sleep apnea), abdominal pain or hepatomegaly (gastroesophagial reflux, nonalcoholic fatty liver), musculoskeletal problems (hip or knee pain, genu valgum, slipped capital femoral epiphysis, Blount disease) and psychological disorders (depression, body dissatisfaction, bulimia nervosa impaired social relationships and decreased health-related quality of life depression) [4, 37–39].
\nReproductive system and Tanner stage disturbance can reveal premature puberty, apparent micropenis (but normal penis may be hidden in fat), undescended testis/micropenis (Prader Willi syndrome) and must be evaluated [4].
\nThe degree of investigation is dependent on the patient\'s age and severity of obesity, the findings on history and physical examination, and associated familial risk factors.
\nFirst-line investigations recommended in cases of childhood obesity include fasting plasma glucose, triglycerides, low-density lipoprotein and high-density lipoprotein cholesterol, liver function tests and, possibly, insulinemia [4, 34, 35].
\nThe investigations for overweight children include the fasting lipid screening test. If this children present risk factors represented by hypertension, dyslipidemia and family history of diabetes, it is necessary to evaluated the serum levels of fasting glucose, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) to every 2 years (increased value of ALT and AST is associated with possible non-alcoholic fatty liver disease) [36].
\nIn obese, children is necessary to evaluated serum levels of fasting lipids, glucose, ALT and AST every 2 years, and insulinemia [4, 34, 35].
\nSecond-line investigations may include liver ultrasound, an oral glucose tolerance test, more detailed endocrine assessment and polysomnography [4, 34].
\nPatients with fasting blood glucose >100 mg/dL or overweight children (BMI 85th to 95th percentile) who have a family history of diabetes mellitus or signs of insulin resistance (acanthosis nigricans), polycystic ovary syndrome, or metabolic syndrome should also be evaluated with an oral glucose tolerance test [4, 34, 35]. If the result of oral glucose tolerance test is more than 126 mg/dL, counseling and repeating test is necessary because pediatric obesity can lead to impaired glucose tolerance. The value of HbA1c of 40 mmol/mol (5.8%) is an appropriate screening tool for diagnosing impaired glucose tolerance [40, 41].
\nLiver ultrasound is recommended for all obese children and adolescents. In children with confirmed ALT >40 IU/L or palpable liver, more thorough diagnostic tests are advisable with gamma-GT and differential diagnosis of hepatitis [41].
\nOther laboratory tests such as thyroid function tests (if there is a faster increase in weight than height), pelvic ultrasound and hormonal doses in cases of suspected polycystic ovary syndrome have been recommended [4, 41].
\nPsychological and psychiatric evaluations are essential to identify psychological disturbances including depression, loss-of-control eating, unhealthy and extreme weight control behaviors, and decreased health-related quality of life which are warning signs of bulimia nervosa and binge-eating disorder [39].
\nIn patients with hypertension more diagnostic tests should be done: cardiac exam: ECG and echocardiogram, standard urinalysis, microalbuminuria, creatinine and potassium levels [4, 41].
\nWe should realize screening for diagnosis of metabolic syndrome in the presence of at least three of the following situations: BMI indicate obesity or waist circumference/height ratio >0.5, systolic and/or diastolic blood pressure >95th percentile, fasting blood glucose >100 mg/dL, serum level of triglycerides >95th percentile, serum level of HDL cholesterol [4, 41].
\nAccording to International Diabetes Federation (IDF), the consensus definition of metabolic syndrome in children (older than 6 years) and adolescents are as follows:
\nfor children aged 6–10 years:
obesity mean a waist circumference >90th percentile
in case of metabolic syndrome that cannot be diagnosed, the measurements should be made if there is a family history of metabolic syndrome, type 2 diabetes mellitus, dyslipidemia, cardiovascular disease, hypertension or obesity.
IDF suggests for weight reduction to use an appropriate message in patients with abdominal obesity.
for children aged 10–16 years:
obesity mean a waist circumference >90th percentile (or adult cut-off if lower).
serum triglycerides level >1.7 mmol/l
serum HDL cholesterol level <1.03 mmol/l
systolic blood pressure >130 mmHg or diastolic blood pressure >85 mmHg
blood glucose >5.6 mmol/l (oral glucose tolerance test recommended) or medical history of type 2 diabetes mellitus
for children >16 years:
should use the IDF criteria for adults. According to the recent IDF definition, a person with metabolic syndrome must have central obesity (defined as waist circumference using ethnicity-specific values) and any two of the following four factors:
serum triglyceride levels >150 mg/dl (1.7 mmol/l) or specific treatment recommended for this abnormality
reduced serum HDL cholesterol level <40 mg/dl (1.03 mmol/l) in males and <50 mg/dl (1.29 mmol/l) in females, or specific treatment for this lipid abnormality
raised blood pressure: systolic blood pressure >130 mmHg or diastolic blood pressure of 85 mmHg or treatment for previously diagnosed hypertension
raised fasting plasma glucose >100 mg/dl (5.6 mmol/l) or previously diagnosed type 2 diabetes (if above 5.6 mmol/l or 100 mg/dl, the oral glucose tolerance test is strongly recommended but is not necessary to define the presence of this syndrome) [32, 42].
Vitamin D deficiency is common in obese children and is associated with risk factors for type 2 diabetes in obese children, but they are not still recommended by national clinical practice guidelines as routine measures [43].
Prevention is the best cost/benefit approach for the management of obesity in children and, in the future, of adulthood. Childhood obesity is a multifaceted problem embedded in physiological, behavioral, genetic, socioeconomic, environmental and political contexts, and the actions to prevent childhood obesity must therefore be taken in multiple settings. Public awareness campaigns, social marketing and behavior-change communication related to nutrition and physical activity implemented in countries together are very important strategies regarding childhood obesity prevention. The critical periods of pediatric obesity characterized by important changes in adiposity growth velocity or obesity related behavior are represented by the first year of life, the preschool (“adiposity rebound”) and adolescence years. The transition period from childhood to adolescence is characterized by important behavioral changes and decreased physical activity [44]. The obesity primary prevention begins in pregnancy period (healthy food diet), continuing with promoting the breastfeeding in the first 2 years of life, and then with support for healthy eating habits (low sugar consumption, eat breakfast every day, eat at home with family, avoid fast—food meals, avoid television in the first years of life and limit television to less than 2 h per day after then, etc. [4, 41, 45, 46].
\nManagement of obesity should be based on risk factors, including age, severity of overweight and obesity and comorbidities, as well as family history and support. Management intervention strategies are available and include nutrition, physical activity, behavior and lifestyle changes, medication and surgical considerations. Treatment largely focuses on sustained lifestyle changes with family involvement. There are several broad principles of conventional management: management of comorbidities, family involvement, taking a developmentally appropriate approach, the use of a range of behavior change techniques, long-term dietary change, increased physical activity and decreased sedentary behaviors. The primary goal for all children with uncomplicated obesity is the long-term improvement of physical health through healthy lifestyles. In obese children with a secondary complication, specific treatment of the complication is an important goal. Effective weight reduction is one of the key elements in the treatment of comorbidities. In morbid obesity, bariatric surgery and laparoscopic sleeve gastrectomy have been used in adolescence [4, 34, 41].
\nIn order to plan a developmentally appropriate approach, it is essential to consider the developmental age of the patient and the resultant level of parental engagement that will be required. Most successful interventions have been family based and take into account the child’s developmental age. In preadolescent children, a parent-based program, without direct engagement of the child, might be more appropriate than a child centered approach.
\nDepending on the age of the child, the present of parents must be or not compulsory. For example, if we talk about adolescents, the present of parents in not recommended. However, the parents must participate at counseling session that are designed for them.
\nBecause obesity is multifactorial, not all children and adolescents will respond to the same approach. Behavior therapy, healthy diet and increasing physical activity are the great sections of obesity treatment. Referral to multidisciplinary, comprehensive pediatric weight—management programs is ideal for obese children whenever possible [4, 34].
\nBehavior modification strategy has a large effect on weight reduction. The set of techniques employed to change thought processes and actions associated with eating, physical activity and sedentary are components of behavior strategies. For the obese adolescent, there are several ways to help him acquiring a healthy lifestyle: to log daily his physical effort and food intake; to participate to motivational interview; to receive permanent psychological support for positive lifestyle changes [34, 41, 46].
\nDietary interventions are usually part of a broader lifestyle change program can be effective in achieving relative weight loss in children and adolescents. Dietary interventions should follow national nutrition guidelines which have an emphasis on:
\nat least five meals over the day (three meals + two snacks)
restrict/replace specific high calorie foods with others less rich in calories
the protein content: it is suggested the 14 meals per week: meat, three to four times a week; fish, three to four times a week; legumes, three to four times a week; cheese and eggs, once a week.
carbohydrates should account for at least 50% of total calories, preferring low glycemic index foods: cereals such as pasta, barley and whole wheat products—twice a day; legumes; fruit and vegetables (not canned or pureed) five servings a day) and by limiting foods that combine a high glycemic index to a high glycemic load (bread, rice, potatoes, sweets, sugar, fruit juices, sweet drinks).
the total fat in the diet should account for no more than 30% of total calories.
the adequate intake of fiber in grams/day: five servings a day of fruits and vegetables in season, not canned or pureed, and legumes four times a week are recommended.
decreased portion sizes.
drinking water as the main beverage and reduction in sugary drink intake.
involvement of the entire family in making sustainable dietary changes [34, 41].
Increasing physical activity can decrease risk for cardiovascular disease, improve well-being and contribute to weight loss:
\nwalking or cycling for transport,
undertaking household chores and playing,
organized exercise programs,
limiting television and other small screen recreation to less than 2 h per day is particularly strategic, but may be challenging,
is recommended at least 60 min of moderate exercise.
Parental involvement is vital and may include monitoring and limiting television use, role modeling of healthy behaviors and providing access to recreation areas or recreational equipment.
\nExisting recommendations on management of pediatric obesity suggest that drug therapy can be used in the treatment of severely obese adolescents. Orlistat can be useful as an adjunct to lifestyle changes in severely obese adolescents and metformin can be used in older children and adolescents with clinical insulin resistance [4, 34, 41].
\nBariatric surgery should be considered in adolescents with complete or near-complete skeletal maturity, who are severely obese with a body mass index of more than 40 kg/m2 or weight exceeding 100% of ideal body, and a medical complication resulting from obesity, after they have failed 6 months of a multidisciplinary weight management program. Preoperative care and counselling is very important if we want to have good long-term results for bariatric surgery patients. This care must be provided by specialist in various medical fields: endocrinology, gastroenterology, cardiovascular, pneumology, etc. All this effort must by sustained with nutritional and psychological support [4, 34, 41,47, 48].
\nChildhood obesity treatment is based on sustained lifestyle changes with family involvement. Behavior therapy, healthy diet and increasing physical activity are the great sections of obesity treatment.
Childhood and adolescent obesity is a major health problem. The prevalence of childhood obesity in Europe is ten times higher than it was in the 1970s. The increasing occurrence in children of disorders, such as type 2 diabetes, is a consequence of this obesity epidemic. Initial assessments of these patients should include taking a careful history (investigating comorbidities, family history and potentially modifiable behaviors) and physical examination. The degree of investigation is dependent on the patient\'s age and severity of obesity, the findings on history and physical examination, and associated familial risk factors. The increased prevalence of obesity in childhood and adolescence highlights the need for effective treatment approaches. There are several broad principles of conventional management: management of comorbidities, family involvement, the use of a range of behavior change techniques, long-term dietary change, increased physical activity and decreased sedentary behaviors. Pediatric patients and their families should be counselled on nutritional interventions including limiting sugar-sweetened beverages, eating nutrient-dense breakfasts, limiting eating out at fast food restaurants, families eating together, increased exercise and decreased time in front of computer and TV screens. For adolescents with severe obesity, lifestyle changes are mandatory. This change must be supported with medical therapy (the only drugs approved by the health organizations are Orlistat and Metformin; these treatments do not exclude metabolic surgery). Finally, given the high prevalence and chronic nature of obesity, coordinated models of care for health service delivery for the management of pediatric obesity are needed.
Visual perception occurs when light stimulus in the surrounding environment converts to nerve impulses at the level of photoreceptors, which then reach the brain to be processed. The light energy is converted to neuronal signals that are transmitted through several layers in the retina to reach the ganglion cells. The axons of the ganglion cells form the optic nerve. Signals are carried out from the optic nerve through the optic chiasm and optic tract, which is connected to the lateral geniculate body. From there, signals reach the visual cortex in the occipital lobe through the optic radiation.
The chapter is divided into three main sections. Section 1 describes the basic embryology, anatomy, and physiology of the optic nerve. Section 2 briefly discusses optic nerve developmental anomalies, and the last section briefly reviews the most common optic nerve tumors and discusses their management modalities.
The optic nerve has a neural ectoderm origin. It develops within the optic stalk, which appears by 22–28 days of gestation. The optic stalk connects the optic vesicle to the cavity of the forebrain [1]. It has two layers, the inner layer is the axons of the ganglion cell layer and the outer layer is a neuroglial supporting cells. At 8 weeks of gestation, neuroepithelial cells including astrocytes and oligodendrocytes proliferate and participate in the formation of the connective tissue and myelination of the optic nerve. Myelination starts centrally and reaches the lamina cribrosa at or shortly after birth [2].
The nerve fiber layer in the retina is the ganglion cell axons, which are generally unmyelinated and receive blood supply from the central retinal artery. Ganglion cell axons turn 90° to enter the optic disc, where they form the optic nerve. The optic disc is supplied by a ring of branches from the short ciliary arteries called the circle of Zinn. Peripapillary arteries also contribute to the optic disc blood supply. The optic nerve consists of 1.2 million fibers with different sizes of diameter, ranging from 0.7 to 10 μm. Smaller fibers serve the central vision, while larger ones come from the peripheral retina [3]. The macular fibers are deep in the center of the optic nerve, while the fibers of the peripheral retina are more superficial.
The length of the optic nerve is around 6 cm and can be divided anatomically into four segments: intraocular (0.7–1 mm), intraorbital (30 mm), intracanalicular (6–10 mm), and intracranial (10–16 mm). The lamina cribrosa divides the intraocular part into prelaminar and laminar sections [4]. It is important to note that this part of the nerve is not myelinated. Oligodendrocytes are responsible for the myelination of nerves, and it is believed that the lamina cribrosa acts as a barrier preventing them from myelinating the intraocular section of the optic nerve [5].
Beyond the lamina cribrosa, the optic nerve is myelinated and surrounded by a dural sheath and cerebrospinal fluid. The extraocular muscles surround the optic nerve in the orbit. The optic nerve sheet is adherent to the superior and medial rectus muscle, hence the pain with eye movement when the optic nerve is inflamed in cases such as optic neuritis. The ophthalmic artery is the first branch from the internal carotid artery, and it forms the main blood supply for intraorbital and intracanalicular division of the optic nerve. The ophthalmic artery passes through the dural sheath of the optic nerve in the intracanalicular section. The intracranial optic nerve division is supplied by branches from the ophthalmic, interior cerebral, anterior communicating, and internal carotid arteries. Ninety percent of the optic nerve fibers from both sides join in the optic chiasm, while the remaining 10% of fibers project to areas controlling pupillary responses [5].
The optic nerve function is assessed by evaluating several elements including the visual acuity, color vision and contrast testing, relative afferent pupillary defect in cases of asymmetric optic neuropathy, and visual field testing. These parameters should be evaluated in every patient with suspected optic neuropathy. In addition, electrophysiological testing is another adjunctive test used to assess optic neuropathies.
Visual acuity is a vital function of the optic nerve and an important measure of the visual function. The smallest visual angle at which two distinct objects can be distinguished is referred to as the minimum separable threshold. The best-corrected visual acuity (BCVA) should be obtained with refraction to exclude any refractive errors. The physician can expect a refractive error when there is an improvement of visual acuity with pinhole viewing.
Snellen acuity is measured with test letters (optotypes), and they are designed in a way so that the letter as a whole subtends an angle of 5 min of arc at a specified distance. A 20/40 Snellen acuity (6/12 in m) means that the patient can see the 20/40 line 20 feet away from the chart what a normal person can see clearly 40 feet away.
Optic nerve diseases, especially optic neuritis, may disproportionately affect color vision compared with BCVA. In macular disease, however, both visual acuity and color vision tend to be affected congruently. In addition, color vision deficit (dyschromatopsia) can persist even after recovery of visual acuity in optic neuropathy.
Color vision testing is done monocularly. Pseudoisochromatic color plate is widely available and frequently used to evaluate color vision. Bilateral, symmetric, color vision deficit in males may indicate congenital dyschromatopsia. The most detailed color vision test is the Farnsworth-Munsell 100-hue test. It uses 85 colored discs, and thus, it needs a considerable amount of time that limits its use in routine clinical practice.
Contrast sensitivity is simply defined as the ability to recognize the degree of contrast between the optotype and its background. The higher the contrast, the easier the optotype is to be seen. Increasing the illumination makes it easier to read because this creates a higher contrast against the black letters. Snellen acuity optotypes are projecting at approximately 100% contrast that can be resolved more easily by the visual system. However, 100% contrast is rarely encountered in everyday life, and therefore, 20/20 vision does not always mean good vision as low-contrast sensitivity may significantly compromise the visual quality.
Contrast sensitivity testing can detect and quantify vision loss in the presence of normal visual acuity. The Pelli-Robson contrast sensitivity letter consists of rows of letters of equal size but with decreasing contrast for groups of three letters. Sinusoidal gratings require the test subject to view a sequence of increasingly lower contrast gratings. Many conditions reduce contrast sensitivity. They include optic neuropathy, posterior subcapsular cataracts, and amblyopia. Contrast sensitivity testing is not commonly used in clinical practice.
Pupillary examination and particularly testing for relative afferent pupillary defect (RAPD) is highly sensitive for optic nerve diseases. Under normal conditions, light source directed at one pupil causes symmetric ipsilateral and contralateral pupillary constriction (direct and consensual response). When the optic nerve of one eye is damaged or inflamed more than the other eye, a relative afferent pupillary defect is seen in the more affected eye. In other words, shining the light over the normal, or less affected, eye will result in bilateral pupillary constriction. However, when the light is swung to the more affected eye, we will see a bilateral pupillary dilation as the signal conduction along the optic nerve is relatively compromised compared to the other eye.
An absence of RAPD usually indicates a bilaterally normal optic nerves or a bilateral symmetric optic neuropathy. RAPD can be seen in patients with significant retinal dysfunction including central retinal artery occlusion, ischemic central retinal vein occlusion, or retinal detachment.
Visual field is another important function of the optic nerve in which a visual field defect testing can describe, quantify, monitor, and localize the different patterns of visual loss. There are different techniques available to evaluate visual field. The choice of technique depends on the degree of detail required and the cooperation of the patient.
Confrontation visual field testing is a simple test that can be done at the bedside or in the clinic providing a gross evaluation of the visual fields. The examiner sits 1 m from the patient. The patient is asked to cover one eye and fixate on the examiner’s nose by the other eye. Then, the examiner requests the patient to identify the numbers (1, 2, or 5) presented by the examiner’s fingers at the midpoint of each of the four quadrants for each eye.
A more detailed evaluation of the visual field is assessed by perimetry. There are two main types: static and kinetic perimetry. In static testing, stimuli are static and turn on and off at different points within area the visual field to be tested. In kinetic testing, a stimulus is moved from a nonseeing peripheral area to a seeing area of the visual field. In kinetic testing, an isopter is drawn by connecting all points of equal sensitivity for a specific stimulus.
Visual evoked potential (VEP) is an electrical response recorded mainly from the visual cortex in response to light stimulus. It was first introduced in 1930s, and its role has evolved over the years [6]. In 1961, Ciganek was the first to describe an electroencephalography (EEG) response to a flashlight stimulus in humans, followed by one of the earliest clinical studies of VEP reported by Halliday and colleagues on patients with optic neuritis [7, 8].
VEP provides an objective and reproducible measure of visual function and continues to have an imperative complementary role to other tests that provide information on the structure of the visual system such as MRI and optical coherence tomography (OCT).
The recording of VEP is performed using occipital mounted electrodes with, typically, monocular stimulation. Several forms of visual stimulus can be used to generate a VEP. The most common stimuli used are flash visual evoked potential (fVEP), pattern-onset VEP, and reversing black and white checkerboard pattern (PVEP). Because of fVEP’s high intersubject variability and low sensitivity, PVEP is preferred in most clinical sitting. fVEP is frequently used in infants, uncooperative patients or if significant media opacity is present. The pattern-onset VEP is preferred in patients with fixation instability such as nystagmus since the PVEP is severely reduced in those patients due to the effect of retinal image motion on the stimulus efficiency [9, 10].
The testing technique for both stimulus conditions has been standardized by the International Society of Clinical Electrophysiology of Vision (ISCEV) to reach a better consistency of results between different electrophysiology laboratories [11]. The PVEP waveform is triphasic with a prominent positive peak (P100) at around 100 ms, an earlier negative peak at around 75 ms, and a late negative peak at around 135 ms after stimulation (Figure 1). The amplitude of the P100 reflects the number of functional afferent axons reaching the cortex. The implicit time (latency) is believed to reflect the degree of demyelination. An abnormal VEP response indicates a functional disturbance in the afferent visual pathway, and occasionally, conventional VEP may provide some information on the location of the lesion [12]. For example, based on the neuroanatomy of the visual system, a unilateral VEP abnormality implies an abnormality in the anterior optic pathway. Localization is less likely when the delay is bilateral.
Normal waveform of a standard PVEP. Arrows showing first negative peak (N75), positive peak (P100), and a late negative peak (N135).
The prevalence of myelinated nerve fibers (MNF) is around 1% in autopsy studies [13]. MNF are typically congenital, and therefore likely represent anomalies of myelination control in utero. They appear as gray or white striated patches with feathered borders, which are most commonly unilateral, with only 7.7% of cases estimated to occur bilaterally (Figure 2) [13, 14]. The mechanism by which MNF occur might be linked to unknown level of communication between adjacent oligodendrocytes (which are responsible for myelinating the axons of subsets of neurons in the central nervous system) in the selection of axons for myelination [15]. Recently, a case of bilateral extensive peripapillary MNF has been reported in a patient with Crouzon syndrome, an inherited form of craniosynostosis caused by over-activation of fibroblast growth factor receptor 2 [16].
Myelinated nerve fibers (MNF).
MGS is a rare congenital optic disc anomaly, first reported by Pendler [17] then more accurately described 10 years later [18]. The pathogenesis of MGS is uncertain, but probably is an embryological form of optic disc dysplasia and is thought not to be a true coloboma, but rather a posterior ectasia, which is the consequence of developmental disturbance of sclera [19, 20]. MGS is characterized by a funnel-shaped enlarged optic disc with a central mass of glial tissue and emerging radial retinal vessels that emerge from the central core toward the peripheral retina (Figure 3) [21]. MGS is a nonprogressive and untreatable condition, which usually occurs as an isolated ocular anomaly, or can also be associated with other ocular abnormalities such as strabismus, afferent pupillary defect, visual field defects, preretinal gliosis, and open angle glaucoma [22, 23, 24, 25]. The optic nerve has been reported to present with characteristics of coloboma, hypoplasia, and morning glory anomaly, as an overlapping phenotypic profile that has been described in relation to PAX6 mutations, which influences the phenotypes of optic nerve malformations [26].
Morning glory syndrome.
Choristoma is an uncommon congenital tumor where normal-looking tissue (epithelial, glandular, cartilaginous, osseous, smooth muscle, and fat) is present in an area where it should not be normally present. Most ocular choristomas are periocular but can also be rarely found as an intraocular choristoma involving the iris, ciliary body, choroid, and optic nerve head [27]. The largest series on optic nerve choristomas in the English literature was published in 1972 including 26 cases of optic nerve colobomas in enucleated eyes, and all cases were diagnosed to have associated heterotopic adipose and/or smooth muscle tissue on pathological examination. The age at enucleation ranged from 6 weeks to 70 years [28]. An interesting case presenting with mixed clinical features of optic nerve coloboma and morning glory—as previously described by others—has been reported by Mishra but unexpectedly had histopathological evidence of a choristoma [29, 30]. The authors commented that there is insufficient knowledge in the literature about the natural history and outcome of optic nerve choristoma, but their 15-year old girl has shown dramatic rapid deterioration of vision. They attributed this to the abnormal architecture of the colobomatous nerve that resulted in the patient’s vulnerability to the critical growth of the choristomatous tissue during adolescence, on the top of the slow axonal loss from the choristoma, as evident by the pallor of the optic nerve head at the time of presentation [30].
Ocular coloboma occurs in relation to the failure of the closure of the embryonic fissure that results from the evagination of the developing optic vesicle during embryogenesis and eye development. The fissure is located inferiorly and includes the optic stalk (future optic nerve) that connects the developing forebrain to the eye. The extent of the colobomatous defect depends on the location of the arrested closure of that fissure. Colobomas in the eye can be seen anteriorly involving the iris and ciliary body or posteriorly involving the optic nerve. The optic nerve coloboma appears as a sharp whitish excavation inferiorly with a thin neuroretinal rim and may even extend to involve the adjacent choroidal and retinal tissue. Optic disc colobomas can occur bilaterally, can be sporadic, or can have an autosomal dominant inheritance. Ocular coloboma is known to show extensive locus heterogeneity associated with causative mutations identified in genes encoding developmental transcription factors or components of signaling pathways that are involved in the posterior segment development as a whole. Optic nerve coloboma can be associated with similar colobomatous anterior uveal or posterior chorioretinal defect as well as possible more extensive manifestations (anophthalmia/microphthalmia) related to the defective and/or failure of embryonic fissure closure [30]. The term microphthalmia is used to indicate the marked reduction in the size of an eye. Microphthalmia, anophthalmia, and coloboma resulting from failure of optic fissure closure during embryogenesis have been grouped as a single phenotype or spectrum (MAC) in most of the recent studies aiming at identification of responsible genes [31, 32]. Heterozygous loss-of-function mutations in SOX2, PAX6, and OTX2 (involving dosage-sensitive transcription factors) are the most common genetic pathology associated with severe eye malformations (anophthalmos/severe microphthalmos) [33, 34, 35, 36], and bi-allelic loss-of- function in STRA6, ALDH1A3, and RARB (related to the regulation of retinoic acid metabolism or transport) is confirmed as an emerging cause of nonsyndromic eye malformations [37, 38, 39, 40]. In the coloboma/microphthalmia patients, Prokudin reported other variants in CYP1B1 that are emerging with CYP1B1 being considered a possible candidate gene as a modifier in coloboma/microphthalmia [41] and commented on the heterogeneity and the complex pattern associated with MAC phenotype. This is nicely summarized by Reis and Semina [32]. Two novel heterozygous SOX11 variants were identified in patients with coloboma [42]. In general, an identifiable genetic cause is found by molecular genetic testing in 80% of individuals with bilateral anophthalmia/severe microphthalmia and in up to 20% of individuals with an ocular malformation in the MAC spectrum [43]. Microphthalmos is one of the ocular anomalies described in fetal alcohol syndrome, which causes multiple teratogenic effects on ocular embryogenesis [44]. Lenz microphthalmia syndrome (LMS) is a specific entity characterized by unilateral or bilateral microphthalmia and/or clinical anophthalmia with malformations of the ears, teeth, fingers, skeleton, and/or genitourinary system in addition to coloboma, which is present in 60% of microphthalmic eyes. The coloboma ranges from simple iris coloboma to coloboma of the ciliary body, choroid, and ON. The diagnosis of LMS depends on clinical findings; however, molecular testing showed that NAA10 and BCOR (BCL6 corepressor) are known to be associated with LMS.
Optic nerve (ON) aplasia is a rare developmental anomaly that implies complete absence of the ON including the disc and is usually seen in unilateral deformed globe in a healthy person with no hereditary predisposition. There are only three previous reports of bilateral ON aplasia in otherwise normal children [45, 46, 47]. The radiological finding of thinned ON indicates the presence of ON sheath with some glial tissue and can aid in the diagnosis. In the most recent case, flash visually evoked potentials (VEP) was performed to distinguish ON hypoplasia from ON aplasia and VEP was not recordable [47]. The ON is formed of axons of the retinal ganglion cells, which form the ON that is derived embryologically from the inner neuroblastic layer of the optic cup, and failure of development of these cells is rare [48]. When there is accompanying failure of development of mesodermal elements as well, it is termed aplasia of the ON, which is defined as an absence of optic nerve, ganglion cells, and central retinal vessels [28, 49]. Many previously reported cases in literature as ON aplasia are, actually, cases of ON hypoplasia because of some overlapping features [50]. Variable ophthalmic features associated with ON aplasia include microphthalmos, enophthalmos, ptotic lids, squint, microcornea, trabeculodysgenesis, iris hypoplasia, iris coloboma, aniridia, and persistent hyperplastic primary vitreous [28, 49].
Unilateral ONH is a congenital disorder characterized by an underdevelopment of one of the ONs with marked intracranial asymmetry. Clinically, the ON head looks small with a characteristic “double-ring sign” (Figure 4). Visual acuity ranges from 20/20 to amaurosis presenting variable visual field defects but the visual impairment is nonprogressive. The diagnosis of ONH is typically clinical, but the confirmation is more accurately established by MRI [51, 52]. Several associations have also been reported between ONH and central nervous system (CNS) anomalies: such as septo-optic dysplasia (SOD), which is a heterogeneous inconstant combination of different CNS parenchymal malformations: ONH, pituitary hypoplasia (with hormonal deficiency), and midline malformations of the brain (absence of the septum pellucidum or thinning of the corpus callosum) [52]. On the other hand, several anomalies have been reported in fetal alcohol syndrome including optic nerve hypoplasia in 48%, and abnormal tortuosity of retinal arteries in 49% in addition to anterior segment anomalies such as microcornea, cataract, and iris defects in 10% [53]. The ONH is thought to occur because of the teratogenic of alcohol on the developing optic nerve at sixth week of gestation when the first retinal ganglion cells first appear until after birth [44]. It is recommended to perform neuroimaging when ONH is detected to rule out other associated CNS anomalies and internal carotid artery hypoplasia, which has been recently reported advocating the theory of vascular disruption sequence at the time of neuroembryogenesis and restriction of intrauterine blood supply as the cause for ONH [54]. Patients with ONH should also have endocrinological work-up to rule out de Morsier syndrome since hypothalamic/pituitary dysfunction has been found in 69% of unilateral cases and 81% in bilateral [55, 56]. ONH has been reported in association with Down’s syndrome in the United States [57]. Optic nerve dysplasia and vascular anomalies have also been found in 4–38% of patients with Down’s syndrome in emerging countries [58, 59]. Afifi and co-authors also reported tilted (dysplastic) optic nerve heads in two cases out of their studied series of Down’s syndrome children but related their finding to an associated myopia in the same two patients [60]. ONH is the most common congenital ON anomaly and a major cause of blindness in the USA, and even though most cases are isolated, the new molecular diagnostic techniques have recently raised the fact that a significant portion of ONH cases has underlying genetic causes, typically de novo mutations [61] Also, two missense mutations in SALL4 were found in a patient with bilateral ONH, unilateral microphthalmos, and coloboma, in addition to cardiac septal defects and delayed growth. SALL4 is expressed in the developing lens and regulates BMP4; therefore, authors speculated that altered BMP4 expression is the cause for the eye anomalies [62]. Finally, it has been suggested to perform behavioral assessment in ONH children who have mild to moderate or even no visual impairment [63].
Bilateral optic nerve hypoplasia in a patient with septo-optic dysplasia.
Congenital optic tract hypoplasia is rare and most of the optic tract abnormalities are acquired [64]. They are usually attributed to tumor, hemorrhage, aneurism, and CNS demyelinating disease, while some are associated with anophthalmos. Isolated optic tract aplasia/hypoplasia was reported in three cases, all of which are unilateral [65, 66, 67].
ON tilt has been described in association with myopia and more strongly in association with the presence of crescent regardless of the refractive error (Figure 5). Crescent was observed approximately five times more frequently in myopic eyes when compared with nonmyopic eyes (49 vs. 10%), and the median degree of tilt was about double (6.08 vs. 2.48). Ethnicity was also strongly associated with tilt and crescent, with ON heads in Asian eyes having the most tilt [68].
Tilted disc syndrome.
Optic pathway gliomas (OPGs) comprise tumors that arise from the visual pathway including the optic nerve (ON) and chiasm. Tumors that only affect the ON are referred to as optic nerve gliomas (ONGs). In general, OPGs are uncommon and account for only about 1% of intracranial tumors [69]. However, they are the most common primary tumors of the optic nerve, comprising about 65% of all intrinsic ON tumors [70].
More than two-thirds of OPGs are detected in the first decade of life and up to 90% before the end of the second decade [69]. The median age of diagnosis of ONGs is 6.5 years with an age range of 2–46 years. Whereas the median age of chiasmal gliomas is 11 years with an age range of 0.75–50 years [71]. There is no sex predilection. Those lesions are considered hamartomas by some authors. ONGs are considered by the 2016 World Health Organization (WHO) as low-grade I juvenile pilocytic astrocytomas or grade II diffuse fibrillary astrocytomas [72].
ONGs are most often benign and slowly growing. The most common presenting findings in descending order are proptosis (94%), vision loss (87.5%), optic disc pallor (59%), disc edema (35%), and strabismus (27%) [69]. However, the presentation of ONGs is variable and mostly depends on the segment of the optic nerve affected by the tumor. The “anterior” involvement presents with signs of an anterior optic neuropathy and is more likely to be associated with optic disc swelling. The “posterior” involvement is associated with either normal or pale optic disc. Patients infrequently present with isolated optic atrophy. A relative afferent pupillary defect (RAPD) is usually present in unilateral or asymmetric cases with affected visual field. The occurrence of nystagmus represents severe visual loss. The nystagmus is monocular, vertical, of low-frequency and variable amplitude. This can differentiate it from spasmus nutans, which is known to be seen in gliomas that involve the optic chiasm [73]. Other rare presentations of ONGs include central retinal vein occlusion (CRVO), retinochoroidal collaterals, or neovascular glaucoma (NVG) [74].
Most cases of ONGs are sporadic. However, there is a clear genetic relationship between ONGs and neurofibromatosis type 1 (NF1). NF1 is an autosomal dominant disorder that occurs in 1 in 3000 individuals. It is caused by a mutation in the gene coding for neurofibromin, a tumor suppressor gene, situated in chromosome 17. About 8–31% of NF1 patients have ONGs. On the other hand, 10–70% of patients with ONGs have NF1 [75]. The wide range of incidence can be explained by referral bias, radiologic detection rate, and the used diagnostic criteria.
The etio-pathogenesis for the development of gliomas in patients with NF1 is related to the activation of the retro-virus-associated sequence (RAS) oncogene (that is inhibited by neurofibromin in normal individuals) and the B1 homolog of the retrovirus-associated function (BRAF) oncogene [73]. The end result is increased protein synthesis and glial cell proliferation. The association between NF1 and the behavior of the glioma is poorly understood. Classically, optic nerve gliomas in patients with NF1 have a more benign prognosis, although this concern is unresolved [69]. Rarely, ONGs can be found in patients with neurofibromatosis type 2 (NF2) [76]. In addition, ipsilateral optic nerve glioma can occur in association with morning glory disc anomaly [77].
Regarding the radiologic findings (Figure 6), ONGs may show one of two patterns. The most common pattern is the classic fusiform swelling of the ON. In magnetic resonance imaging (MRI), they are hypo- or isointense in T1-weighted images, hyperintense in T2-weighted images, enhancing after intravenous injection gadolinium. The subarachnoid space (SAS) surrounding the ONGs is distended and thought to be occupied by trapped cerebrospinal fluid (CSF) in some patients. However, ultrasonographic examination in such cases characteristically discloses signs of solid component in the SAS. This indicates that the distension is most likely due to the spread of tumor into the SAS (the “pseudo-CSF sign”) and does not represent trapped CSF [78].
Optic nerve glioma. The left figure is a T2-weighted axial MRI showing left orbital and intraconal mass with high signal intensity. The right figure is a T1-weighted axial MRI showing postcontrast enhancement.
The second and less common radiologic pattern is the appearance of a thickened and kinked nerve in the portion affected by the ONG [75, 76]. Like the first pattern, enlargement of the subarachnoid space is due to extension of the tumor. It was suggested that this pattern (i.e., thickening and kinking) is more commonly observed in patients with NF1 and the fusiform enlargement pattern is more commonly seen in patients with sporadic ONG [79]. Nevertheless, no pattern is indicative of a specific diagnosis as both can be seen in sporadic ONGs and ONGs related to NF1. In both patterns, the margin of the nerve is usually well defined and smooth due to an intact optic nerve sheath. This is a differentiating feature between ONG and optic nerve sheath meningioma (ONSM).
ONGs can either show an isolated involvement of the orbital portion of the optic nerve or combined involvement of both orbital and intracranial portions. The optic foramen may still be distended even if the ONG is restricted to the orbital or intracranial portion of the optic nerve. This is caused by secondary meningeal hyperplasia traveling proximally (or distally) and not the tumor itself. Therefore, enlargement of the optic foramen is not a proof of intracranial extension of an orbital ONG. Furthermore, the optic foramen may still be of normal diameter in the sitting of intracranial or chiasmal ONG [80]. Histopathologic examination performed on a resected ONG, which did not reveal spread intracranially by MRI as well as by gross examination, showed an evidence of intracranial spread [81].
Histopathologically (Figure 7), ONGs are characterized by three main patterns that may all be present in different cuts of the same tumor: A. Transitional area, in which the tumor blends into the normal tissue of optic nerve and shows more abundant and less arranged glial nuclei than in the normal nerve. Increased number and size of glial cells results in enlarged nerve bundles. B. Coarsely reticulated and myxomatous areas with microcystoid spaces perhaps representing tumor necrosis. C. Astrocytic areas, in which spindle cell formation with Rosenthal fibers, which are cytoplasmic and eosinophilic structures in astrocytes, are seen [80]. Immunohistochemically, the neoplastic astrocytes stain positively for glial fibrillary acidic protein, HNK-1 (type 1 astrocyte precursor marker), S-100, and vimentin. Thus, this suggests that type 1 astrocytes are the origin of the tumor [82]. ONGs nearly always remain confined to the dural sheath, but a spread into the subarachnoid space surrounding the nerve is not uncommon [75].
Histopathological appearance of an optic nerve pilocytic astrocytoma (Original magnification × 100 hematoxylin and eosin).
The diagnosis of an ONG is usually reached on the basis of the clinical signs and radiologic findings. Biopsy of the lesion is largely not required because of the presence of high-resolution neuroimaging with enhanced diagnostic accuracy, biopsy of the sheath alone may show secondary meningeal hyperplasia seen in ONGs and falsely suggesting optic nerve sheath meningioma, and the low predictive value of the histologic appearance of the tumor in its clinical behavior [82]. Most importantly, the procedure could be complicated by permanent visual loss [83].
There is no universally recognized management for ONGs, and it should be individualized to the patient. ONGs are usually very slow growing tumors and some lesions will spontaneously regress. Therefore, observation is indicated for patients with reasonably good vision and stable radiologic appearance on serial imaging [84, 85]. For patients presenting with reduced vision and particularly if it is deteriorating or there is a radiologic evidence of tumor growth, a number of treatment options exists.
Chemotherapy is evolving as an initial treatment modality for patients with severe or progressive visual deterioration. It may be especially beneficial in children younger than 5 years of age. The recommended chemotherapeutic agents include vincristine, carboplatin, vinblastine, and temozolomide with remarkable outcomes observed in some patients [86]. Combining carboplatin and vincristine is the most accepted regimen [69]. Additionally, treatment with topical nerve growth factor improved the vision in patients with known or presumed ONGs. A 10-day course of topical murine nerve growth factor in five children with ONGs and severe optic disc pallor showed an increase in visual evoked potential amplitudes that lasted for 90 days in all patients [87].
Fractionated stereotactic radiotherapy is another option for some patients with ONGs and can be used as a monotherapy or adjunctive to other treatment modalities [88, 89]. It is usually kept for patients who are older than 5 years of age and, preferably, after puberty. Shrinkage of ONGs, with subsequent improvement in vision and halting of progressive visual loss, reduction in optic disc swelling, and decreasing proptosis have been reported in two studies [90, 91]. In contrast, a third study concluded that radiation of ONGs has no significant benefit in the overall outcome when compared to observation or surgical intervention [71]. Thus, radiotherapy is still controversial because of questionable results and possible complications including pituitary dysfunction and intellectual disabilities [69].
Surgical excision or debulking of ONGs may be indicated in patients with severe deterioration of visual function associated with cosmetically disfiguring proptosis [92, 93]. In some cases, optic nerve sheath fenestration is performed to release the trapped CSF surrounding the tumor. Surgery has been suggested to prevent progression into the intracranial optic nerve and chiasm. However, involvement of the chiasm is rare and prevention is not proven as the tumor was commonly found in the margins during histopathologic examination of the resected ONGs [82].
Malignant ONGs are rare neoplasms that involve the anterior visual pathway (i.e., proximal to the lateral geniculate nucleus). According to the WHO 2016, malignant ONGs are classified as grade III (anaplastic astrocytoma) or grade IV (glioblastoma) [72]. In contrast to ONGs mentioned above, malignant ONGs predominantly affects adults. The mean age of onset is 57 years with an age range between 22 and 83 years. There is no gender predilection [94]. Patients present acutely with unilateral or bilateral orbital pain and progressive vision loss. The optic disc appearance can be either normal or pale in most cases although disc swelling and CRVO can also occur [75, 94].
MRI scan shows diffusely enlarged optic nerve, chiasm, or optic tract with heterogenous enhancement [69]. Histopathologically, malignant ONGs are show areas of anaplasia and are classified as anaplastic astrocytomas or glioblastoma multiforme [78]. Treatment involves radiotherapy, chemotherapy, or both but is rarely successful. The visual and the survival rate are very poor. Blindness typically occurs 2 to 4 months after onset of vision loss and mortality from hypothalamic and brainstem involvement usually follows after 6–12 months [69].
Medulloepithelioma refers to tumors arising from the cells of the primitive neural tube and the medullary plate. These tumors are extremely rare [95]. They can arise in any part of the central or peripheral nervous system [96, 97]. They may also arise from the globe, principally the ciliary body. Medulloepitheliomas arising from the optic nerve are very rare. Patients present with proptosis, progressive visual loss, disc swelling, and later disc pallor [73].
Imaging initially may show fusiform enlargement of the ON resembling an ONG [75]. At the time of surgery, the diagnosis of an ON medulloepithelioma is usually reached. Histopathologic examination of ON Medulloepithelioma shows hyperchromatic nuclei with high mitotic index. The neoplastic cells are arranged in tubes and cords. Hyaluronidase-sensitive material is observed and stains positively with Alcian blue [75, 98, 99]. More differentiated cells are arranged in rosettes [73]. Teratoid variants of medulloepithelioma have other elements such as striated muscle or cartilage [78, 98].
The most commonly used treatment modality is resection of the involved ON. Even with complete resection, however, recurrences and metastases can be seen. Therefore, other treatment options include adjuvant radiotherapy, chemotherapy, or both [75, 99].
Oligodendroglioma is a type of glioma that is believed to originate from oligodendrocytes. Up to 12% of all intracranial tumors are caused by oligodendrogliomas [100], and there is no gender predilection. They can affect individuals on all ages although they are more prevalent in middle aged adults. The most common location of oligodendrogliomas is in the cerebral hemispheres, particularly the frontal lobes. However, oligodendrogliomas of the cerebellum, the spinal cord, and the brainstem have been reported [101].
Histopathologically, compact masses of swollen oligodendrocytes were separated by an extremely thin stroma. Mitoses are generally rare and variable [100]. They have been reported to be associated with orbital non-Hodgkin lymphoma [102]. Another study described a case of a 14-year-old girl who presented with monocular progressive proptosis, vision loss, and limited extraocular muscle motility. Imaging showed a large fusiform enlargement of the orbital portion of the ON. Microscopic examination of the resected ON proved changes indicative of an oligodendroglioma [103].
As the name implies, gangliogliomas are composed of both ganglion cells and astrocytes. They are rare tumors and classified as grade I by the WHO [72]. Gangliogliomas of the ON have been described in few studies [104, 105, 106]. In noncontrast enhanced imaging, ON ganglioglioma resembles a benign ONG. However, gangliogliomas characteristically do not show enhancement on MRI after intravenous injection of gadolinium [104]. However, the diagnosis of ON gangliogliomas is usually reached after microscopic examination that shows many ganglion cells with an increased population of glial cells. Treatment involves partial or total ON nerve resection and radiotherapy [73].
ON hemangioblastomas may be sporadic or occur in the sitting of Von Hippel-Lindau disease (VHL). It is an extremely rare tumor, which affects males and females equally with an age of onset ranging from 15 to 44 years. Presentation includes vision loss, headaches or pain with ocular movement, and proptosis accompanied by optic disc swelling or pallor [107]. Radiologically, they look like ONGs except that hemangioblastomas show more homogenous enhancement. Histopathologically, these tumors are comprised of endothelial cells and pericytes with variably sized vascular channels [73].
Schwannomas are benign tumors of peripheral nervous systems derived from Schwann cells. The vestibular location of the schwannoma is more frequent, followed by the involvement of the trigeminal nerve. In the orbit, schwannomas account for 1–6% of intraorbital tumors. Although it is theoretically impossible for a schwannoma to develop from the sheath of the optic nerve, which is devoid of Schwann cells, there are some exceptional cases of schwannoma of the nerve [108, 109, 110, 111].
Several histopathogenic explanations have been reported. These include the presence of ectopic Schwann cells that may have migrated at the time of embryogenesis [110, 112]. Another explanation would be a transformation of the pial mesenchymal cells [112, 113]. A final hypothesis is that schwannoma does not develop from the sheath of the optic nerve but from sympathetic nerves running on it [75, 110]. T1-weighted MRI typically demonstrates a homogenously enhancing lesion. The complete excision of these tumors most often allows a definitive cure without recurrence [114, 115].
The only tumor that can develop solely from the optic nerve sheath is optic nerve sheath meningioma (ONSM) [73]. ONSMs result from proliferations of the meningoepithelial cells covering the sheath of the intraorbital or intracanalicular optic nerve [69]. ONSMs are uncommon, accounting for 1–2% of all orbital tumors [116, 117, 118]. However, ONSMs are the second most common cause of primary optic nerve and sheath tumors, second only to optic nerve glioma [69]. Moreover, 90% of all orbital meningiomas were secondary to intracranial extension and the remaining 10% were primary ONSMs [116].
Almost all ONSMs are unilateral although they may be bilateral especially in patients with NF2 [119]. ONSMs are typically discovered in adults during the fourth or fifth decade. Females are affected three times as often as males. Up to 7% of all ONSMs occur in children [69]. A classification system of ONSMs was suggested and includes three types: type I ONSMs, in which the tumor involves the orbital portion of the ON manifesting as fusiform, tubular, or globular enlargement of the nerve; type II ONSMs, where the tumor extends through the optic canal or supraorbital fissure; and type III ONSMs, with more than 10-mm intracranial extension or involvement of the contralateral ON [120].
The classic diagnostic triad of ONSMs includes painless, slowly progressive, unilateral vision loss associated with optic atrophy, and retinochoroidal collaterals. These collateral vessels connect the retinal venous circulation to the choroidal venous circulation and are seen in approximately 30% of patients [69]. Transient visual obscuration may also occur. In addition, reduced color vision, visual field defect, an ipsilateral RAPD with variable proptosis and limitation of ocular motility are observed [73]. The ON head maybe normal, swollen, or atrophic, depending on duration of symptoms and the location of the tumor [75, 116, 117, 118].
Radiological findings of ONSMs are variable (Figure 8). Computed tomography (CT) scanning characteristically shows fusiform or tubular expansion of the affected with a thickened and enhanced optic nerve sheath. Calcification of the sheath gives the classic “tram-track” sign. MRI is more accurate in soft tissue definition and proves that the ON parenchyma is of normal diameter. The ON is hypointense in T1-weighted images with the optic nerve sheath showing increased thickness and marked enhancement. In contrast to ONGs that show a smooth dural outline, ONSMs show rough outlines with thin extensions from the affected sheath [116, 117, 118].
Optic nerve sheath meningioma. T1-weighted MRI showing right oval orbital space occupying lesion encasing the mid and posterior right optic nerve.
Histopathologically (Figures 9 and 10), ONSMs have a meningotheliomatous or a mixed-type pattern. Psammoma bodies, which are hyalinized calcium deposits, are usually seen. Commonly, meningiomas spread to the extradural space invading the orbital tissue. Rarely, optic nerve, sclera, choroid, and retina are invaded [73, 80]. The diagnosis of ONSM primarily depends on the clinical presentation and imaging without the need for a biopsy in most cases [72].
The histopathological appearance of the whorl-configuration of meningothelial cell proliferation (original magnification × 200 hematoxylin and eosin).
The appearance of the typical psammoma bodies in the same case of the optic nerve meningioma above (original magnification × 200 hematoxylin and eosin).
The only ONSMs related morbidity is visual loss from injury to the ipsilateral ON. These tumors typically do not cause neurological dysfunction or death. Therefore, the management of patients with ONSMs should be tailored to the individual case. Observation is suitable if there is no significant visual loss at presentation or follow-up, and there is no significant intracranial extension. Those patients can be observed twice per year with serial imaging [73]. ONSMs in pediatric population maybe more aggressive, and thus, they must be monitored with increased frequency [69].
Fractionated radiation therapy is the mainstay treatment of ONSM. More than 94% of patients’ vision has stabilized or improved. However, late radiation complications include radiation retinopathy and pituitary dysfunction [73]. Surgical excision is rarely advised because of the potential risk of significant visual deterioration. Indications for surgical intervention include intracranial extension of the tumor if there is a risk of contralateral ON involvement [69, 121].
Secondary tumors of the optic nerve are more common than the primary tumors [122]. These tumors can damage the ON by either infiltration, compression, or both. Secondary tumors include retinoblastoma, malignant melanoma of choroid, pseudotumor of the RPE, intracranial meningioma, metastatic carcinoma to the ON parenchyma or ONS, glioblastoma multiforme of the brain, lymphoma, or leukemia [73]. The clinical signs and management of secondary tumors depend on the particular tumor and the location of damage to the ON.
We do not have any financial interests in any of the listed items in this manuscript.
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