Criteria proposed by Newson include:

Passive early history in the first year, avoiding ordinary demands and missing milestones
Continuing to avoid demands, panic attacks if demands are escalated
Surface sociability, but apparent lack of sense of social identity
Lability of mood and impulsivity
Comfortable in role play and pretending
Language delay, seemingly the result of passivity, often caught up quickly
Obsessive behavior
Neurological signs (awkwardness, similar to autism spectrum disorders)The underlying cause of this avoidance is said to be a high level of anxiety, usually from expectations of demands being placed on children, which can lead to a feeling of not being in control of a situation. Children with PDA feel threatened when they are not in control of their environment and their actions, which triggers the fight, flight or freeze response. History
Newson first began to look at PDA as a specific syndrome in the 1980s when certain children referred to the Child Development Clinic at the University of Nottingham appeared to display and share many of the same characteristics. These children had often been referred because they seemed to show many autistic traits, but were not typical in their presentation like those with classical autism or Aspergers syndrome. They had often been labelled as atypical autism or Persistent Development Disorder-Not Otherwise Specified (PDD-NOS). Both of these terms were felt by parents to be unhelpful.
People with neurogenic hypertension respond poorly to treatment with diuretics as the underlying cause of their hypertension is not addressed.Pheochromocytoma – a tumor which results in an excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction
Hyperaldosteronism (Conns syndrome)   – idiopathic hyperaldosteronism, liddles syndrome (also called pseudoaldosteronism), glucocorticoid remediable aldosteronism
Cushings syndrome – an excessive secretion of glucocorticoids causes the hypertension
Hyperparathyroidism
Acromegaly
Hyperthyroidism
Hypothyroidism

Adrenal
A variety of adrenal cortical abnormalities can cause hypertension, In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.Congenital adrenal hyperplasia, a group of autosomal recessive disorders of the enzymes responsible for steroid hormone production, can lead to secondary hypertension by creating atypically high levels of mineralocorticoid steroid hormones. These mineralocorticoids cross-react with the aldosterone receptor, activating it and raising blood pressure. 17 alpha-hydroxylase deficiency causes an inability to produce cortisol. Instead, extremely high levels of the precursor hormone corticosterone are produced, some of which is converted to 11-Deoxycorticosterone (DOC), a potent mineralocorticoid not normally clinically important in humans. DOC has blood-pressure raising effects similar to aldosterone, and abnormally high levels result in hypokalemic hypertension. 11β-hydroxylase deficiency, aka apparent mineralocorticoid excess syndrome, involves a defect in the gene for 11β-hydroxysteroid dehydrogenase, an enzyme that normally inactivates circulating cortisol to the less-active metabolite cortisone. At high concentrations cortisol can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension.