ADHD and the Disruption of Cognitive Continuity: A Mechanistic Framework for Explaining Clinical Diversity and Theoretical Unification

A universal phenomenon is observed in ADHD: an inability to sustain a mental visual representation with eyes closed. This representation disintegrates within seconds and cannot be precisely reconstructed. Among many symptoms, this points to a fundamental cognitive mechanism. It is not hyperactivity, inattention, or emotional dysregulation, but a periodic disruption of a specific cognitive information stream. This is highly likely the fundamental mechanism of ADHD, and this inference possesses the explanatory power to precisely account for a wide range of ADHD phenomena, potentially opening a new direction for research. This disruption of the cognitive information stream can be explained as a break in the signal connectivity between the prefrontal cortex and other specific cognitive units. It causes the disappearance and reconstruction of foreground information in the brain over short intervals. Due to the concurrent operation of multiple cognitive functions, this underlying disruption is typically not directly perceptible at the conscious level. We use a simplified illustrate to simulate this process: the foreground information stream can be seen as a collection of "Primary Information" and "Secondary Information." Secondary Information provides the internal associations for Primary Information (the "how" and "why"), acting as vector information. During a disruption, Secondary Information is lost while Primary Information (the "what") is briefly retained. Subsequently, the brain inconsistently reconstructs the Secondary Information based on the current Primary Information to restore the integrity of the foreground stream. The result is that the core concept always remains, but the rich, continuous relational information behind it cannot be established. Although this mechanism is simple, it leads to complex and diverse impairments in cognitive and executive functions, affecting a wide range of cognitive units, such as the striatum. It causes a "short-path effect" in the ventral and dorsal striatum—due to the lack of continuous associative information, behavioral pathways are encoded as a series of discrete fragments, preventing the formation of an automated whole. This is the root of the difficulties seen in individuals with ADHD in repetitive learning and the establishment of habitual pathways. This mechanism also explains a range of other phenomena, including difficulties in plan execution, thematic jumping in writing, and alexithymia. Among the various consequences of the signal disruption, the inability to sustain attention has the greatest impact on the functioning of the cognitive system. Therefore, individuals with ADHD universally compensate by activating specific cognitive networks via the ventral striatum. This is the origin of many specific phenomena, such as a non-linear reading style, a strong intuitive tendency, and patterns of addictive behavior. This theory also accomplishes the following: It clarifies the functional mechanisms of the ventral and dorsal striatum, as well as the operational principles of dopamine. It provides a new explanation for the principles of the DMN (Default Mode Network) from both a phenomenological and mechanistic perspective. It offers a hypothetical, unified mechanistic explanation for the high comorbidity between ADHD and ASD (Autism Spectrum Disorder). Based on this theory, a framework for a diagnostic scale is proposed, differing from current mainstream methods and offering new possibilities for the precise diagnosis and treatment of ADHD.