We have proposed that a number of neurodevelopmental disorders can be partially or largely explained by abnormalities of brain structures underlying procedural memory (Ullman, 2004; Ullman & Pierpont, 2005; Evans & Ullman, 2016; Ullman, Earle, Walenski, Janacsek, 2020; Ulman, Clark, Pullman, Lovelett, Pierpont, Jiang, and Turkeltaub, 2024). According to this neuroanatomical account – the Procedural circuit Deficit Hypothesis, or PDH – these abnormalities should, not surprisingly, lead to atypicalities of procedural memory. Importantly, since aspects of language (e.g., grammar, speech-sound representations), reading, and math seem to depend on procedural memory, such brain abnormalities may also lead to atypicalities in these domains. We have suggested that the PDH may help account for core symptoms in a variety of neurodevelopmental disorders, including difficulties with language, especially grammar, in developmental language disorder (DLD), reading (and grammar) problems in dyslexia, and math impairments in math disability, including dyscalculia.

Since the brain structures underlying procedural memory also play roles in functions other than procedural memory itself, abnormalities of these structures should also lead to atypicalities of such non-procedural functions. For example, frontal/basal-ganglia circuits subserve not only procedural memory, but a wide variety of other functions, including working memory, executive function, and lexical/semantic recall. The frontal/basal-ganglia abnormalities that we have posited and that seem to be found in a number of neurodevelopmental disorders can thus also explain atypicalities of these other functions as well, even though these may not involve procedural memory.

We have proposed the PDH as an explanatory account for developmental language disorder (DLD), dyslexia, motor-speech disorders, autism, Tourette syndrome, ADHD, and mathematical disability. A recent systematic review and meta-analysis of the structural and functional neuroanatomy of DLD has strongly implicated the basal ganglia, in particular the anterior neostriatum, in the disorder (Ullman et al., in press 2024). The explanatory power of the PDH likely varies across the disorders. For example, it seems to have a large amount of explanatory power in DLD, perhaps less in dyslexia, and even less in autism. Moreover, the nature of the abnormalities and thus the ensuing procedural memory and other atypicalities are posited to differ across the disorders. Indeed, in some cases, the abnormalities may manifest as superior procedural memory abilities, as compared to typically developing children. This may be the case, for example, in Tourette syndrome (Walenski et al., 2007; Dye et al., 2016; Takács et al., 2017; Takács et al., 2018) and perhaps in (some populations of) autism (Walenski et al., 2014).

Importantly, which brain structures underlying procedural memory are affected, the nature of their abnormalities, and what additional structures are involved, are all posited to vary across the disorders, thus helping explain the differences between them. Nevertheless, we suggest that comorbidities among certain of these disorders can be partly if not largely explained by abnormalities of the same underlying circuits that subserve procedural memory (Ullman & Pierpont, 2005, Evans & Ullman, 2016).

DECLARATIVE MEMORY COMPENSATION

We have also proposed that declarative memory compensates for procedural memory and other dysfunctions in a wide range of disorders, including DLD, dyslexia, motor-speech disorders (e.g., verbal apraxia, stuttering), autism, Tourette Syndrome, and OCD (Ullman & Pullman, 2015a; Ullman & Pullman, 2015b; Ullman et al., 2020). According to this view (the Declarative Memory Compensation Hypothesis), declarative memory remains largely normal in these and various other disorders, and, because it is very flexible, it can and often does learn a wide range of information and strategies to at least partially overcome numerous types of impairments. In some cases declarative memory may even be enhanced as compared to typically developing children, including in dyslexia (Hedenius et al., 2013), developmental language disorder (Lukacs et al., 2017), and autism (Walenski et al., 2008), thus in turn enhancing its ability to compensate.

For example (See Ullman & Pullman, 2015), declarative memory seems to help people with OCD or Tourette syndrome learn to control compulsions and tics; it allows individuals with autism to compensate for social deficits by memorizing scripts for navigating social situations; and it learns strategies to overcome reading and language difficulties in people with DLD (Lum et al., 2012, Conti-Ramsen et al., 2015), dyslexia (e.g., Hedenius et al., 2013), and autism. 

Declarative memory compensation has potentially important clinical implications. First, designing treatments that rely on declarative memory, or that improve learning in this system, could enhance compensation and thus reduce symptoms. For example, drugs known to improve declarative memory could ameliorate symptoms, particularly if paired with behavioral therapies learned in this system.

Second, developing treatments that avoid compensation by declarative memory may increase the likelihood of stimulating and potentially strengthening the dysfunctional circuitry. This is akin to therapies that prevent patients from using their good hand so they are forced to use their bad one, which can improve its functionality.

The compensation also has implications for diagnosis. Many individuals might be compensating their way out of clinical diagnosis (the Compensation Underdiagnosis Hypothesis; Ullman & Pullman, 2015). This should hold especially for individuals or groups with better declarative memory abilities. Indeed, underdiagnosis due to compensation may help explain one of the major conundrums of all these disorders: why they are diagnosed more commonly in boys than girls. On this view, because declarative memory seems to be better, on average, in girls and women than boys and men (see Effects of Sex Differences), females are likely to compensate more successfully than males, even compensating themselves out of diagnosis more often than males (Ullman & Pullman, 2015).

Compensation by declarative memory may also be found in other disorders (Ullman & Pullman, 2015), including ADHD and debilitating adult-onset disorders such as aphasia (Drury & Ullman, 2002) and Parkinson’s disease (Ullman et al., 2002). Indeed, given the power and flexibility of declarative memory, it may play compensatory roles in a wide range of disorders.