Pediatricians are often the first health professionals to assess and raise suspicions of RAD in children with the disorder. The initial presentation varies according to the child's developmental and chronological age, although it always involves a disturbance in social interaction. Infants up to about 18–24 months "may" present with non-organic failure to thrive and display abnormal responsiveness to stimuli. Laboratory investigations will be unremarkable barring possible findings consistent with malnutrition or dehydration, while serum growth hormone levels will be normal or elevated.

The core feature is severely inappropriate social relating by affected children. This can manifest itself in two ways:

1. Indiscriminate and excessive attempts to receive comfort and affection from any available adult, even relative strangers (older children and adolescents may also aim attempts at peers).

2. Extreme reluctance to initiate or accept comfort and affection, even from familiar adults, especially when distressed.

While RAD is likely to occur in relation to neglectful and abusive treatment, automatic diagnoses on this basis alone cannot be made, as children can form stable attachments and social relationships despite marked abuse and neglect.

The name of the disorder emphasizes problems with attachment but the criteria includes symptoms such as failure to thrive, a lack of developmentally appropriate social responsiveness, apathy, and onset before 8 months.

Reactive attachment disorder (RAD) is described in clinical literature as a severe and relatively uncommon disorder that can affect children. RAD is characterized by markedly disturbed and developmentally inappropriate ways of relating socially in most contexts. It can take the form of a persistent failure to initiate or respond to most social interactions in a developmentally appropriate way—known as the "inhibited form". Due to recent revision in the DSM-5 the "disinhibited form" is now considered a separate diagnosis named "Disinhibited attachment disorder".

RAD arises from a failure to form normal attachments to primary caregivers in early childhood. Such a failure could result from severe early experiences of neglect, abuse, abrupt separation from caregivers between the ages of six months and three years, frequent change of caregivers, or a lack of caregiver responsiveness to a child's communicative efforts. Not all, or even a majority of such experiences, result in the disorder. It is differentiated from pervasive developmental disorder or developmental delay and from possibly comorbid conditions such as intellectual disability, all of which can affect attachment behavior. The criteria for a diagnosis of a reactive attachment "disorder" are very different from the criteria used in assessment or categorization of attachment "styles" such as insecure or disorganized attachment.

Children with RAD are presumed to have grossly disturbed internal working models of relationships that may lead to interpersonal and behavioral difficulties in later life. There are few studies of long-term effects, and there is a lack of clarity about the presentation of the disorder beyond the age of five years. However, the opening of orphanages in Eastern Europe following the end of the Cold War in the early-1990s provided opportunities for research on infants and toddlers brought up in very deprived conditions. Such research broadened the understanding of the prevalence, causes, mechanism and assessment of disorders of attachment and led to efforts from the late-1990s onwards to develop treatment and prevention programs and better methods of assessment. Mainstream theorists in the field have proposed that a broader range of conditions arising from problems with attachment should be defined beyond current classifications.

Mainstream treatment and prevention programs that target RAD and other problematic early attachment behaviors are based on attachment theory and concentrate on increasing the responsiveness and sensitivity of the caregiver, or if that is not possible, placing the child with a different caregiver. Most such strategies are in the process of being evaluated. Mainstream practitioners and theorists have presented significant criticism of the diagnosis and treatment of alleged reactive attachment disorder or the theoretically baseless "attachment disorder" within the controversial form of psychotherapy commonly known as attachment therapy. Attachment therapy has a scientifically unsupported theoretical base and uses diagnostic criteria or symptom lists markedly different to criteria under ICD-10 or DSM-IV-TR, or to attachment behaviors. A range of treatment approaches are used in attachment "therapy", some of which are physically and psychologically coercive, and considered to be to attachment "theory". Many constitute abuse.

Attachment disorder is a broad term intended to describe disorders of mood, behavior, and social relationships arising from a failure to form normal attachments to primary care giving figures in early childhood. Such a failure would result from unusual early experiences of neglect, abuse, abrupt separation from caregivers between 6 months and three years of age, frequent change or excessive numbers of caregivers, or lack of caregiver responsiveness to child communicative efforts resulting in a lack of basic trust. A problematic history of social relationships occurring after about age three may be distressing to a child, but does not result in attachment disorder.

The term attachment disorder is used to describe emotional and behavioral problems of young children, and also applied to school-age children, teenagers and adults. The specific difficulties implied depend on the age of the individual being assessed, and a child's attachment-related behaviors may be very different with one familiar adult than with another, suggesting that the disorder is within the relationship and interactions of the two people rather than an aspect of one or the other personality. No list of symptoms can legitimately be presented but generally the term attachment disorder refers to the absence or distortion of age appropriate social behaviors with adults. For example, in a toddler, attachment-disordered behavior could include a failure to stay near familiar adults in a strange environment or to be comforted by contact with a familiar person, whereas in a six-year-old attachment-disordered behavior might involve excessive friendliness and inappropriate approaches to strangers.

There are currently two main areas of theory and practice relating to the definition and diagnosis of attachment disorder, and considerable discussion about a broader definition altogether. The first main area is based on scientific enquiry, is found in academic journals and books and pays close attention to attachment theory. It is described in ICD-10 as reactive attachment disorder, or "RAD" for the inhibited form, and disinhibited attachment disorder, or "DAD" for the disinhibited form. In DSM-IV-TR both comparable inhibited and disinhibited types are called reactive attachment disorder or "RAD".

The second area is controversial and considered pseudoscientific. It is found in clinical practice, on websites and in books and publications, but has little or no evidence base. It makes controversial claims relating to a basis in attachment theory. The use of these controversial diagnoses of attachment disorder is linked to the use of pseudoscientific attachment therapies to treat them.

Some authors have suggested that attachment, as an aspect of emotional development, is better assessed along a spectrum than considered to fall into two non-overlapping categories. This spectrum would have at one end the characteristics called secure attachment; midway along the range of disturbance would be insecure or other undesirable attachment styles; at the other extreme would be

non-attachment. Agreement has not yet been reached with respect to diagnostic criteria.

Finally, the term is also sometimes used to cover difficulties arising in relation to various attachment styles which may not be disorders in the clinical sense.

ICD-10 describes Reactive Attachment Disorder of Childhood, known as RAD, and Disinhibited Disorder of Childhood, less well known as DAD. DSM-IV-TR also describes Reactive Attachment Disorder of Infancy or Early Childhood. It divides this into two subtypes, Inhibited Type and Disinhibited Type, both known as RAD. The two classifications are similar and both include:

- markedly disturbed and developmentally inappropriate social relatedness in most contexts,

- the disturbance is not accounted for solely by developmental delay and does not meet the criteria for Pervasive Developmental Disorder,

- onset before 5 years of age,

- requires a history of significant neglect, and

- implicit lack of identifiable, preferred attachment figure.

ICD-10 includes in its diagnosis psychological and physical abuse and injury in addition to neglect. This is somewhat controversial, being a "commission" rather than "omission" and because abuse in and of itself does not lead to attachment disorder.

The inhibited form is described as "a failure to initiate or respond...to most social interactions, as manifest by excessively inhibited responses" and such infants do not seek and accept comfort at times of threat, alarm or distress, thus failing to maintain 'proximity', an essential element of attachment behavior. The disinhibited form shows "indiscriminate sociability...excessive familiarity with relative strangers" (DSM-IV-TR) and therefore a lack of 'specificity', the second basic element of attachment behavior. The ICD-10 descriptions are comparable. 'Disinhibited' and 'inhibited' are not opposites in terms of attachment disorder and can co-exist in the same child. The inhibited form has a greater tendency to ameliorate with an appropriate caregiver whilst the disinhibited form is more enduring.

While RAD is likely to occur following neglectful and abusive childcare, there should be no automatic diagnosis on this basis alone as children can form stable attachments and social relationships despite marked abuse and neglect. Abuse can occur alongside the required factors but on its own does not explain attachment disorder. Experiences of abuse are associated with the development of disorganised attachment, in which the child prefers a familiar caregiver, but responds to that person in an unpredictable and somewhat bizarre way. Within official classifications, attachment disorganization is a risk factor but not in itself an attachment disorder. Further although attachment disorders tend to occur in the context of some institutions, repeated changes of primary caregiver or extremely neglectful identifiable primary caregivers who show persistent disregard for the child's basic attachment needs, not all children raised in these conditions develop an attachment disorder.

The fourth revision of the "Diagnostic and Statistical Manual" (DSM-IV-TR) (now replaced by DSM-5) stated that the child must exhibit four out of the eight signs and symptoms to meet the diagnostic threshold for oppositional defiant disorder. Furthermore, they must be perpetuated for longer than six months and must be considered beyond normal child behavior to fit the diagnosis. Signs and symptoms were: actively refuses to comply with majority's requests or consensus-supported rules; performs actions deliberately to annoy others; is angry and resentful of others; argues often; blames others for their own mistakes; frequently loses temper; is spiteful or seeks revenge; and is touchy or easily annoyed.

These patterns of behavior result in impairment at school and/or other social venues.

Disinhibited attachment disorder of childhood (DAD) according to the International Classification of Diseases (ICD-10), is defined as:

Disinhibited attachment disorder is a subtype of the ICD-10 category F94, "Disorders of social functioning with onset specific to childhood and adolescence". The other subtype of F94 is reactive attachment disorder of childhood (RAD – F94 .1).

Synonymous or similar disorders include Affectionless psychopathy and Institutional syndrome.

Within the ICD-10 category scheme, disinhibited attachment disorder specifically excludes Asperger syndrome (F84.5), hospitalism in children (F43.2), and hyperkinetic disorders (F90.-).

Oppositional defiant disorder (ODD) is defined by the DSM-5 as "a pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness". Unlike children with conduct disorder (CD), children with oppositional defiant disorder are not aggressive towards people or animals, do not destroy property, and do not show a pattern of theft or deceit. A diagnosis of ODD is also no longer applicable if the individual is diagnosed with reactive attachment disorder (RAD).

In a study by Zeanah, (Zeanah "et al.", 2004) on reactive attachment disorder in maltreated toddlers, the criteria for DSM-IV "disinhibited" RAD (i.e. disinhibited attachment disorder) were:

1. not having a discriminated, preferred attachment figure,

2. not checking back after venturing away from the caregiver,

3. lack of reticence with unfamiliar adults,

4. a willingness to go off with relative strangers.

For comparison, the criteria for DSM-IV "inhibited" RAD were:

1. absence of a discriminated, preferred adult,

2. lack of comfort seeking for distress,

3. failure to respond to comfort when offered,

4. lack of social and emotional reciprocity, and

5. emotion regulation difficulties.

The authors found that these two disorders were not completely independent; a few children may exhibit symptoms of both types of the disorder.

Other conditions may commonly co-occur with FAS, stemming from prenatal alcohol exposure. However, these conditions are considered alcohol-related birth defects and not diagnostic criteria for FAS.

- Heart: A heart murmur that frequently disappears by one year of age. Ventricular septal defect most commonly seen, followed by an atrial septal defect.

- Bones: Joint anomalies including abnormal position and function, altered palmar crease patterns, small distal phalanges, and small fifth fingernails.

- Kidneys: Horseshoe, aplastic, dysplastic, or hypoplastic kidneys.

- Eyes: Strabismus, optic nerve hypoplasia (which may cause light sensitivity, decreased visual acuity, or involuntary eye movements).

- Occasional problems: ptosis of the eyelid, microophthalmia, cleft lip with or without a cleft palate, webbed neck, short neck, tetralogy of Fallot, coarctation of the aorta, spina bifida, and hydrocephalus.

When structural impairments are not observable or do not exist, neurological impairments are assessed. In the context of FASD, neurological impairments are caused by prenatal alcohol exposure which causes general neurological damage to the central nervous system (CNS), the peripheral nervous system, or the autonomic nervous system. A determination of a neurological problem must be made by a trained physician, and must not be due to a postnatal insult, such as a high fever, concussion, traumatic brain injury, etc.

All four diagnostic systems show virtual agreement on their criteria for CNS damage at the neurological level, and evidence of a CNS neurological impairment due to prenatal alcohol exposure will result in a diagnosis of FAS or pFAS, and functional impairments are highly likely.

Neurological problems are expressed as either hard signs, or diagnosable disorders, such as epilepsy or other seizure disorders, or soft signs. Soft signs are broader, nonspecific neurological impairments, or symptoms, such as impaired fine motor skills, neurosensory hearing loss, poor gait, clumsiness, poor eye-hand coordination. Many soft signs have norm-referenced criteria, while others are determined through clinical judgment. "Clinical judgment" is only as good as the clinician, and soft signs should be assessed by either a pediatric neurologist, a pediatric neuropsychologist, or both.

Classically acute radiation syndrome is divided into three main presentations: hematopoietic, gastrointestinal, and neurological/vascular. These syndromes may or may not be preceded by a prodrome. The speed of onset of symptoms is related to radiation exposure, with greater doses resulting in a shorter delay in symptom onset. These presentations presume whole-body exposure and many of them are markers which are not valid if the entire body has not been exposed. Each syndrome requires that the tissue showing the syndrome itself be exposed. The hematopoietic syndrome requires exposure of the areas of bone marrow actively forming blood elements (i.e., the pelvis and sternum in adults). The neurovascular symptoms require exposure of the brain. The gastrointestinal syndrome is not seen if the stomach and intestines are not exposed to radiation. Some areas affected are:

1. Hematopoietic. This syndrome is marked by a drop in the number of blood cells, called aplastic anemia. This may result in infections due to a low amount of white blood cells, bleeding due to a lack of platelets, and anemia due to few red blood cells in the circulation. These changes can be detected by blood tests after receiving a whole-body acute dose as low as 0.25 Gy, though they might never be felt by the patient if the dose is below 1 Gy. Conventional trauma and burns resulting from a bomb blast are complicated by the poor wound healing caused by hematopoietic syndrome, increasing mortality.

2. Gastrointestinal. This syndrome often follows absorbed doses of 6–30 Gy (600–3000 rad). The signs and symptoms of this form of radiation injury include nausea, vomiting, loss of appetite, and abdominal pain. Vomiting in this time-frame is a marker for whole body exposures that are in the fatal range above 4 Gy. Without exotic treatment such as bone marrow transplant, death with this dose is common. The death is generally more due to infection than gastrointestinal dysfunction.

3. Neurovascular. This syndrome typically occurs at absorbed doses greater than 30 Gy (3000 rad), though it may occur at 10 Gy (1000 rad). It presents with neurological symptoms such as dizziness, headache, or decreased level of consciousness, occurring within minutes to a few hours, and with an absence of vomiting. It is invariably fatal.

The prodrome (early symptoms) of ARS typically includes nausea and vomiting, headaches, fatigue, fever, and a short period of skin reddening. These symptoms may occur at radiation doses as low as 0.35 Gy (35 rad). These symptoms are common to many illnesses, and may not, by themselves, indicate acute radiation sickness.

Cutaneous radiation syndrome (CRS) refers to the skin symptoms of radiation exposure. Within a few hours after irradiation, a transient and inconsistent redness (associated with itching) can occur. Then, a latent phase may occur and last from a few days up to several weeks, when intense reddening, blistering, and ulceration of the irradiated site are visible. In most cases, healing occurs by regenerative means; however, very large skin doses can cause permanent hair loss, damaged sebaceous and sweat glands, atrophy, fibrosis (mostly Keloids), decreased or increased skin pigmentation, and ulceration or necrosis of the exposed tissue. Notably, as seen at Chernobyl, when skin is irradiated with high energy beta particles, moist desquamation (peeling of skin) and similar early effects can heal, only to be followed by the collapse of the dermal vascular system after two months, resulting in the loss of the full thickness of the exposed skin. This effect had been demonstrated previously with pig skin using high energy beta sources at the Churchill Hospital Research Institute, in Oxford.

Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life. Nevertheless, many people experience significant symptoms. These might include:

- Shortness of breath

- Syncope (fainting)

- Angina, but only in the presence of ischemic heart disease

A person suffering from dilated cardiomyopathy may have an enlarged heart, with pulmonary edema and an elevated jugular venous pressure and a low pulse pressure. Signs of mitral and tricuspid regurgitation may be present.

Foodborne illness (also foodborne disease and colloquially referred to as food poisoning) is any illness resulting from the food spoilage of contaminated food, pathogenic bacteria, viruses, or parasites that contaminate food, as well as toxins such as poisonous mushrooms and various species of beans that have not been boiled for at least 10 minutes.

Symptoms vary depending on the cause, and are described below in this article. A few broad generalizations can be made, e.g.: The incubation period ranges from hours to days, depending on the cause and on how much was consumed. The incubation period tends to cause sufferers to not associate the symptoms with the item consumed, and so to cause sufferers to attribute the symptoms to gastroenteritis for example.

Symptoms often include vomiting, fever, and aches, and may include diarrhea. Bouts of vomiting can be repeated with an extended delay in between, because even if infected food was eliminated from the stomach in the first bout, microbes (if applicable) can pass through the stomach into the intestine and begin to multiply. Some types of microbes stay in the intestine, some produce a toxin that is absorbed into the bloodstream, and some can directly invade deeper body tissues.

Foodborne illness usually arises from improper handling, preparation, or food storage. Good hygiene practices before, during, and after food preparation can reduce the chances of contracting an illness. There is a consensus in the public health community that regular hand-washing is one of the most effective defenses against the spread of foodborne illness. The action of monitoring food to ensure that it will not cause foodborne illness is known as food safety. Foodborne disease can also be caused by a large variety of toxins that affect the environment.

Furthermore, foodborne illness can be caused by pesticides or medicines in food and natural toxic substances such as poisonous mushrooms or reef fish.

Dilated cardiomyopathy (DCM) is a condition in which the heart becomes enlarged and cannot pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Complications can include heart failure, heart valve disease, or an irregular heartbeat.

Causes include genetics, alcohol, cocaine, certain toxins, complications of pregnancy, and certain infections. Coronary artery disease and high blood pressure may play a role, but are not the primary cause. In many cases the cause remains unclear. It is a type of cardiomyopathy, a group of diseases that primarily affects the heart muscle. The diagnosis may be supported by an electrocardiogram, chest X-ray, or echocardiogram.

In those with heart failure treatment may include medications in the ACE inhibitor, beta blocker, and diuretic families. A low salt diet may also be helpful. In those with certain types of irregular heartbeat, blood thinners or an implantable cardioverter defibrillator may be recommended. If other measures are not effective a heart transplant may be an option in some.

About 1 per 2,500 people are affected. It occurs more frequently in men than women. Onset is most often in middle age. Five-year survival rate is about 50%. It can also occur in children and is the most common type of cardiomyopathy in this age group.