There are many factors that make it difficult to detect ADHD

There are many factors that make it difficult to detect ADHD. Difficulties in timely detection are primarily associated with the polymorphism of this disorder – it has many faces and masks, and its clinical presentation is very diverse. ADHD is a disorder with a high rate of comorbidity, that is, the presence of concomitant psychiatric disorders. Research has shown that at least 70% of children with ADHD have at least one other psychiatric disorder associated with them (Pliszka, 1998; Gillberg, Gillberg, Rasmussen et al., 2004). Often this disorder is brought to the fore, masking the very symptoms of ADHD. Thus, ADHD is a certain clinical challenge for specialists and requires a high level of competence for competent diagnosis and therapy.

It should also be noted that this disorder significantly affects the life of the family. According to research, the level of stress experienced by a family where a child with ADHD is growing up is significantly higher than in the control group, and is close to that in other forms of child development disorders, such as autism, mental retardation, etc. (Breen, Barkley, 1988; Mash, Johnston, 1983). Parents of children with ADHD have a higher risk of developing depression, often have low self-esteem as parents, and marital conflicts arise due to discipline and parenting issues (Lahey, Piacentini, McBurnett et al., 1988; Biederman, Munir, Knee et al., 1986). The family of a child with ADHD needs support and assistance, and the ability to implement therapeutic interventions, as well as the prognosis of the child’s life, depends primarily on family factors and the effectiveness of the partnership between parents and specialists.

Thus, hyperactive disorder with attention deficit is probably not for nothing recognized as one of the main problems in the field of mental health of children and adolescents.

Conclusions

ADHD was recognized in 2004 by the world Association of child and adolescent psychiatry and related professions as the “No. 1 problem” in the field of child and adolescent mental health.

ADHD is one of the most common mental disorders in children, according to various studies, it is observed in approximately 3-5% of school-age children.

ADHD is a chronic disorder, and 70-80% of children with ADHD will still have symptoms in adulthood.

• If care is delayed and inadequate, ADHD can lead to serious secondary complications: school maladjustment, impaired psychological development, and significant behavioral and social problems – both in childhood and in adulthood.

• ADHD is one of the most fully researched mental disorders, and effective strategies and methods for its treatment have been developed. With proper care and support, children with ADHD can have a happy, fulfilling future.

• However, very often ADHD is not diagnosed, and most children with this disorder do not receive appropriate care.

There are many myths and pseudoscientific speculations surrounding ADHD that complicate timely detection and effective therapy.

Causes of ADHD

ADHD is an ambiguous disorder and etiologically. If several decades ago the cause of ADHD is mostly considered the factor of organic lesions of the Central nervous system and talked about minimal brain dysfunction, today, with the development of molecular genetics, there is increasing evidence that in most cases ADHD is a disorder of genetic origin and is associated in particular with genes that are responsible for regulating metabolism and activity of two neurotransmitters – dopamine and norepinephrine.

Let’s consider successively different hypotheses for the occurrence of ADHD and arguments that confirm or refute them.

One of the first in the historical context was the hypothesis that ADHD Is a consequence of CNS damage at an early age, in particular intra – and perinatal hypoxia, inflammatory processes, metabolic disorders (for example, phenylketonuria), the action of toxic substances (lead poisoning, the consequences of chemotherapy at an early age, etc.). In the question of localization of disorders, it is assumed that it is primarily a lesion of the frontal cortex and subcortex (basal ganglia in particular). Evidence of frontal cortex dysfunction as an etiological factor is provided by data on the presence of minimal organic structural defects that are detected in some children with ADHD during computed tomography (CT) and nuclear magnetic resonance imaging (nmri), as well as the results of instrumental studies that show reduced activity (positron emission tomography-PET) and morphofunctional immaturity with signs of cortical-subcortical dysfunction (electroencephalography – EEG). It should also be noted that ADHD symptoms are similar to frontal lobe syndrome in adults and primates. The evidence for the theory of organic CNS damage as the main cause of ADHD is also the fact that some children with ADHD have a history of perinatal hypoxic-ischemic damage to the Central nervous system; the frequency of the disorder is significantly higher in children who were born prematurely and with a low body weight for gestational age (and the greater the degree of prematurity, the higher the risk), as well as in children who suffered encephalitis, meningitis, and traumatic brain injury in early childhood. (A detailed analysis of research data on the etiology of the disorder is presented in Goldstein, Goldstein, 1998. Pp. 199-226). The mother’s use of alcohol/nicotine during pregnancy also leads to an increased risk of ADHD in the child.

However, although these signs are detected more often in children with ADHD than in others, current research suggests that they are not specific to this disorder and in a large part of cases of ADHD are absent at all. In particular, in a review of studies on this topic, Barkley concludes that it is likely that only a small proportion of children have organic Central nervous system damage as a cause of ADHD (1996, pp. 95-105). Thus, the hypothesis of CNS damage at an early age as the main cause of ADHD is not sufficient to explain, which has led researchers to put forward other theories about the causes of the disorder.

Data from studies of the structure and functioning of the Central nervous system in children with ADHD (according to the Barkley review, 2006)

✓ MRI data: reduced volume of the frontal hemispheres (mostly on the right), basal ganglia, and cerebellar worm.

Functional MRI: differences from typical activity in the frontal hemispheres, basal ganglia, and cerebellum.

✓ Neuropsychological research: deficits in the functions of the frontal lobes of the brain – the functions of behavioral inhibition, attention control, especially in the presence of distracting stimuli, Executive functions (language internalization, verbal and non-verbal working memory, emotional and motivational self-regulation, planning and temporary organization of behavior, coordination of motor activity).

✓ EEG data: increased theta activity and decreased beta activity, particularly in the frontal lobes.

✓ Cerebral blood flow study (SPECT): reduced flow in prefrontal areas and pathways from the frontal cortex to the basal ganglia, limbic system, and cerebellum. Under the influence of psychostimulants, blood flow in these areas is normalized.

✓ PET data: reduced glucose metabolism, particularly in the frontal cortex.

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