It is well established that Attention Deficit Hyperactivity Disorder (ADHD) is a familial and highly heritable disorder [ 36].
It is well established that nutritional deficits are related to the activity, location, and extent of the disease.
It is well established that amblyopes exhibit deficits in processing first-order (luminance-defined) patterns.
Familial neuropsychological deficits are well established in schizophrenia but remain less well characterized in other psychotic disorders.
While based on these studies there is no doubt that β-cell mass is reduced to a variable extent in patients with type 2 diabetes, the reasons underlying this β-cell deficit are less well established.
It is well established that syringomyelia can cause neurological symptoms and deficit by accumulation of fluid within syrinx cavities that lead to internal compression within the spinal cord.
The high risk of low school performance associated with attention-deficit hyperactivity disorder (ADHD) is well established (American Psychiatric Association, 2014; DuPaul, Gormley, & Laracy, 2012; Sibley, Altszuler, Morrow, & Merrill et al., 2014).
Relatively high individual variability in groups of dyslexics is well established, and the common explanation is that dyslexia is a multiple cognitive deficit.
To better understand the detected inability of some patients to produce maximum force with voluntary activation and to better understand the origin(s) of this deficit(s) will require further, detailed neurophysiological investigations using well established techniques.
The vulnerability of the human central nervous system to environmental chemicals has been well established, but the contribution these exposures may make to problems such as attention deficit disorder, conduct problems, pervasive developmental disorder, or autism spectrum disorder remain uncertain.
The neurotoxic consequences of acute high-level pesticide exposure are well established: Exposure is associated with a range of symptoms as well as deficits in neurobehavioral performance and abnormalities in nerve function (Keifer and Mahurin 1997).
