This research is noteworthy because of the assumption that the behavioral and the cognitive elements of ADHD are quite well recognized. However, the ADHD neurobiological substance must be studied. Therefore, the populations studied were fathers with potential ADHD who did not seek medical advice and were functioning; this enabled us to study brain structural abnormalities which could play an essential role in ADHD pathophysiology. These areas might serve as a trait marker for adult ADHD, or could be anatomical sites for the persistence of ADHD into adulthood.
Gray matter assessment studies in ADHD showed cortical abnormalities and maturation delays in certain prefrontal cortex areas in individuals with ADHD [21]. However, the significance of aberrant white matter (WM) advancement in ADHD remains relatively obscure [5]. Although in ADHD individuals, the volume decreases recorded in WM are larger than that in a gray matter [22].
The present study showed that 60% of fathers of children were diagnosed with potential adult ADHD using Conners’ adult ADHD rating scale (50% of them had mixed inattentive-hyperactive type—25% predominantly, inattentive type—25% predominantly, hyperactive-impulsive type) (Table 1). However, none of the fathers with potential adult ADHD sought medical advice or received treatment. This may be related to the nature of their occupation and the fact that 80% did not receive a college education. Currently, the incidence of ADHD among paternal adults is 60%, which corresponds to the findings of Smalley et al. and Starck et al. [23, 24], who reported that the adult ADHD prevalence rate among fathers of ADHD children was 55% and 56% respectively. On the contrary, several studies [15, 25, 26] showed that ADHD in fathers was 41%, 45.8%, and 2.6%, respectively. These findings could be attributed to various diagnostic procedures, information sources, and social and cultural characteristics (sex, ethnicity, population type, residence place, socioeconomic level, and sample type). However, the occurrence of this variable remains high. Therefore, screening for paternal ADHD is important to be integrated into clinical settings, as this affects family function, child therapy outcome, and family therapy as well [27].
Regarding the white matter abnormalities findings, there were marked differences in DTI results between fathers with and without potential adult ADHD with a statistically significant decreased mean FA of right PCR and left SCR in the ADHD group suggesting the presence of deficits in those areas. It is well-known that these areas support the cognitive and perception part of the motor cortex [28].
The few available studies on the results of DTI in patients with ADHD have shown quite heterogeneous results. The comparability of ROI experiments can be reduced, considering the subjective recruitment and selection process of ROIs [5].
Our results partially reproduce those of Bouzianea et al. [29] who found reduced FA in the anterior and superior areas of CR in the adult ADHD group without previous medication treatment. The decreased FA agrees with multiple previous studies in adult ADHD [9, 10, 30].
The reduced FA may be a persistent indication of whether or not individuals have ADHD symptoms in adulthood with ADHD [9].
Interestingly, we found a statistically higher FA of bilateral ACR, bilateral ATR, and right SLF in the ADHD group of fathers than the non-ADHD group.
Although ADHD mostly had decreased FA, there are also signs that the greater FA of some tracts of white matter is in keeping with our findings [11,12,13]. Additionally, Tamm et al. [14] observed an elevation in FA in the ACR, anterior forceps, uncinate fasciculus, inferior fronto-occipital fasciculus, and ATR in individuals with ADHD.
We can explain this finding with the following possibilities: Firstly, high FA reflects a high directed diffusion consistency, and is linked to the reduced neuronal branching in individuals [5]. Secondly, this finding could reflect the compensatory mechanisms similar to those observed in patients with a stroke who exhibited enhanced FA in axonal regeneration or chronic remyelination and healing-related gliosis [30]. Thirdly, one study indicated that enhanced FA in children and teens with ADHD is attributable to higher axial and less radial diffusivity in the WM pathways, demonstrating relative axonal integrity in these locations, but a reduction in neuronal branching [11].
Additional research is required to contrast the findings of white matter abnormalities with genetic evidence regarding the pathophysiology of ADHD persistence into adulthood [31].
Previous results of FA in parents with potential adult ADHD may point to areas involved in the pathogenesis and genetics of ADHD.