Disclaimer: This post is written by an autodidact neuroscience and neurodiversity advocate, not a clinician. The author has no formal medical, psychiatric, or clinical credentials. The content is based on self‑directed study of peer‑reviewed neuroscience literature, genetic research, diagnostic manuals (DSM‑5‑TR and ICD‑11), and neurodiversity community scholarship. This information is provided for educational and advocacy purposes and is not a substitute for professional clinical judgment, diagnosis, or treatment. Clinicians should use their own expertise and judgment when applying any framework discussed here. When in doubt about a specific patient or case, consult clinical supervision or relevant professional guidelines.
Abstract
Clinicians are trained to diagnose neurodevelopmental variations using the DSM‑5‑TR and ICD‑11, which classify conditions as disorders defined by deficits and impairment. The neurodiversity paradigm and neurotype model offer a complementary, evidence‑based framework that reframes these differences as natural, heritable variations in brain organization. Written by a neurodiversity advocate for clinical audiences, this post provides two practical tools for integrating both perspectives: (1) a narrative side‑by‑side comparison of DSM‑5/ICD‑11 diagnostic language versus neurotype language for common neurodevelopmental conditions, and (2) a neuroscience glossary of key terms relevant to co‑occurrence, brain networks, genetics, and clinical practice. Becoming bilingual in diagnostic and neurotype frameworks reduces stigma, improves identification of co‑occurrence, and supports strength‑based interventions.
Keywords: neurodiversity, neurotype, DSM‑5, ICD‑11, co‑occurrence, clinical practice, neuroscience glossary
Introduction
Clinicians, researchers, and trainees are trained to use diagnostic manuals such as the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM‑5‑TR; American Psychiatric Association, 2022) and the International Classification of Diseases, 11th Revision (ICD‑11; World Health Organization, 2019). These systems classify neurodevelopmental variations as disorders – entities defined by deficits, functional impairment, and deviation from a statistical norm. This framework has practical utility for access to services, insurance reimbursement, and research inclusion criteria.
However, as a neurodiversity advocate, I want to offer a complementary perspective. The diagnostic framework is not the only valid model, nor is it the most accurate reflection of current neurobiology. The neurodiversity paradigm and its neurotype model provide an evidence‑based alternative. The term neurodiversity refers to the natural, genome‑driven variation in human neurocognitive functioning (Walker, 2021). The neurotype model reframes conditions such as autism, ADHD, dyslexia, and developmental language disorder as heritable patterns of brain organization with both strengths and challenges – not as pathologies to be cured.
This post provides two practical tools for clinicians who wish to integrate both frameworks. First, a narrative side‑by‑side comparison maps DSM‑5‑TR and ICD‑11 diagnostic language to neurodiversity neurotype language for common conditions. Second, a neuroscience glossary defines key terms related to brain networks, neurotransmitters, genetics, and co‑occurrence. The goal is not to abandon diagnosis but to become bilingual – able to move fluidly between medical and neurodiversity frameworks to better serve patients, align with patient self‑identity, and design strengths‑based interventions.
Part 1: Diagnostic Versus Neurotype Model – A Narrative Comparison for Clinicians
In this section, each common neurodevelopmental condition is described first using DSM‑5‑TR and ICD‑11 diagnostic language (deficit‑framed) and then using neurotype language from the neurodiversity paradigm (variation‑framed). Clinical rationales for using neurotype language are provided from an advocacy perspective.
Autism Spectrum Disorder
Under DSM‑5‑TR (American Psychiatric Association, 2022, p. 56) and ICD‑11 (World Health Organization, 2019, code 6A02), autism is defined by persistent deficits in social communication and social interaction across multiple contexts, along with restricted, repetitive patterns of behavior. The language emphasizes what the individual lacks or does not do compared to typical peers.
In the neurotype model, autism is reframed as an autistic neurotype – a heritable pattern of brain organization involving increased local but reduced long‑range cortical connectivity, altered excitatory/inhibitory balance (GABA/glutamate), and differences in social reward circuitry. Features such as monotropism (intense, narrow attention channels), sensory hyper‑ or hypo‑responsivity, and systemizing are understood as natural variations, not deficits. Social communication is atypical, not absent or deficient. For clinicians, using this framing can reduce stigma, explain strengths such as pattern detection and deep focus, and align with autistic self‑advocate preferences for identity‑first language.
Attention‑Deficit/Hyperactivity Disorder
Under DSM‑5‑TR (American Psychiatric Association, 2022, p. 68) and ICD‑11 (World Health Organization, 2019, code 6A06), ADHD is defined as a persistent pattern of inattention and/or hyperactivity‑impulsivity that interferes with functioning or development. The criteria emphasize impairment relative to age‑appropriate norms.
In the neurotype model, ADHD is reframed as an ADHD neurotype – characterized by differences in dopaminergic and noradrenergic regulation, particularly in frontostriatal, frontoparietal, and default mode networks. This is understood as an interest‑based attention system rather than a deficit of attention. Hyperfocus on engaging tasks and rapid crisis response are recognized as strengths. For clinicians, using this framing accounts for hyperfocus, explains why stimulant medication normalizes rather than fixes, and reduces shame around perceived laziness.
Specific Learning Disorder (Dyslexia, Dyscalculia, Dysgraphia)
Under DSM‑5‑TR (American Psychiatric Association, 2022, p. 76) and ICD‑11 (World Health Organization, 2019, code 6A03, Developmental learning disorder), specific learning disorders are defined by difficulties learning and using academic skills benchmarked against age‑ and grade‑level norms. The framing is deficit‑based relative to educational expectations.
In the neurotype model, dyslexia, dyscalculia, and dysgraphia are reframed as distinct neurotypes involving alternative neural pathways. Dyslexia involves atypical development of left‑hemisphere posterior reading networks with compensatory right‑hemisphere engagement; strengths include enhanced peripheral vision, big‑picture pattern detection, and narrative reasoning. Dyscalculia involves reduced gray matter and functional activation in the intraparietal sulcus, with strengths in verbal reasoning and qualitative logic. Dysgraphia involves differences in left premotor and cerebellar regions supporting written output, with strengths in oral storytelling and verbal creativity. For clinicians, using this framing prevents mislabeling as low IQ or lazy, supports strength‑based accommodations such as audiobooks and speech‑to‑text, and explains why difficulty is domain‑specific.
Developmental Coordination Disorder (DCD / Dyspraxia)
Under DSM‑5‑TR (American Psychiatric Association, 2022, p. 86) and ICD‑11 (World Health Organization, 2019, code 6A04), DCD is defined as motor coordination substantially below expected for chronological age that significantly interferes with activities of daily living. The language emphasizes clumsiness and impairment.
In the neurotype model, dyspraxia is reframed as a dyspraxic neurotype – a difference in motor automaticity and procedural learning, with involvement of cerebellar and basal ganglia networks. Higher‑order planning remains intact, but movements require deliberate cognitive effort that others perform automatically. Strengths include verbal creativity, strategic thinking, and empathy. For clinicians, using this framing prevents clumsy stigma, explains why the person can perform actions with effort but not automatically, and supports accommodations such as extra time, voice input, and reduced fine‑motor demands.
Developmental Language Disorder (DLD)
Under ICD‑11 (World Health Organization, 2019, code 6A01) – DLD is not a separate category in DSM‑5 (it falls under Language Disorder) – DLD is defined by persistent difficulties in the acquisition and use of language across modalities, with performance substantially below expectations for age. The framing emphasizes impairment in language function.
In the neurotype model, DLD is reframed as a DLD neurotype – a specific bottleneck in implicit grammatical learning and phonological working memory, with involvement of left inferior frontal gyrus and arcuate fasciculus. Non‑verbal IQ and social reasoning are typically intact. Strengths include visual‑spatial reasoning, pattern detection in non‑language domains, and written communication when time is allowed. For clinicians, using this framing prevents assumption of global intellectual impairment, highlights the need for explicit rather than immersion‑based language teaching, and validates that the person can learn but through different mechanisms.
Tourette Syndrome
Under DSM‑5‑TR (American Psychiatric Association, 2022, p. 94) and ICD‑11 (World Health Organization, 2019, code 8A05), Tourette syndrome is defined by the presence of motor and vocal tics that may cause distress or impairment. The framing emphasizes tics as pathological.
In the neurotype model, Tourette syndrome is reframed as a Tourette neurotype – involving differences in cortico‑striato‑thalamo‑cortical circuits and dopaminergic regulation. Tics are involuntary but often suppressible, and many individuals experience a premonitory urge as a sensory phenomenon. Strengths can include rapid associative thinking, sensory scanning, and creativity. For clinicians, using this framing acknowledges possible strengths, reframes tics as neurological variation not behavioral misbehavior, and supports accommodations such as providing a private space to tic.
Down Syndrome (Trisomy 21)
Under ICD‑11 (World Health Organization, 2019, code Q90), Down syndrome is classified as a chromosomal condition. In medical genetics and clinical settings, it is often described with deficit‑focused language emphasizing intellectual disability and health complications.
In the neurotype model, Down syndrome is reframed as a Down syndrome neurotype – trisomy 21 alters brain development, including reduced cortical volume and atypical hippocampal formation. The profile includes relative strengths in social reasoning, visual‑spatial processing, musicality, and long‑term memory, with challenges in sequential processing and verbal working memory. For clinicians, using this framing retains medical reality but adds a strength‑based profile, opposes deficit‑only portrayal, and supports person‑centered planning.
Neurotypical (No Diagnosis)
In diagnostic systems, having no diagnosis is implicitly treated as the baseline or normal against which all disorders are compared.
In the neurotype model, neurotypical is reframed as one neurotype among many – a region on the neurodiversity spectrum with its own genetic architecture and trade‑offs. It is not a universal baseline. For clinicians, using this framing prevents pathologizing of difference and reminds that typical is statistical, not biological, and has its own vulnerabilities.
Key Takeaway From the Comparison
As a clinician, you can use DSM‑5‑TR or ICD‑11 language when you need legal access to services, insurance codes, research inclusion criteria, or communication with systems that require diagnostic labels. You can use neurotype language when you want to reduce stigma, align with patient self‑identity, explain strengths and trade‑offs, and design strength‑based accommodations.
Best practice is to become bilingual. For example, you might say to a patient: According to the DSM‑5, you meet criteria for autism spectrum disorder. From a neurodiversity perspective, you are an autistic person – a neurotype with both challenges and strengths. Both frameworks are true; we can use whichever is more helpful in each context.
Part 2: Neuroscience Glossary for Clinicians
The following glossary defines key terms from neuroscience, genetics, and cognitive psychology that appear in neurodiversity research. Each entry includes a definition, relevance to neurodivergence, and clinical or research implication. This glossary is written for clinicians but from an advocate perspective.
Default Mode Network (DMN). Definition: Brain regions active during rest, mind‑wandering, self‑reference, and autobiographical memory; hubs include medial prefrontal cortex, posterior cingulate, and angular gyrus. Relevance to neurodivergence: Atypical DMN connectivity is seen in ADHD (failure to deactivate during tasks), autism (altered self‑referential processing), and giftedness (enhanced connectivity). Clinical implication: Explains why some patients zone out or have rich inner worlds; supports mindfulness and metacognitive strategies rather than suppression of mind‑wandering.
Central Executive Network (CEN). Definition: Frontoparietal network involved in working memory, decision‑making, and goal‑directed attention. Relevance: Underconnected in ADHD; altered in autism and dyslexia. Clinical implication: Explains variability in task switching and sustained attention; supports external scaffolding such as lists and reminders rather than willpower‑only approaches.
Salience Network (SN). Definition: Network including anterior cingulate and anterior insula that detects relevant internal and external stimuli and switches between DMN and CEN. Relevance: Overactive in anxiety (common co‑occurrence); atypical in autism (sensory salience differences). Clinical implication: Explains sensory overload and difficulty filtering; supports sensory accommodations such as low‑stimulus environments and noise‑cancelling headphones.
Intraparietal Sulcus (IPS). Definition: Region in parietal lobe specialized for quantity processing, number sense, and magnitude comparison. Relevance: Reduced IPS gray matter and activation in dyscalculia. Clinical implication: Distinguishes dyscalculia from generalized math anxiety or low IQ; supports targeted number‑sense interventions, not just more math practice.
Arcuate Fasciculus. Definition: White matter tract connecting frontal (Broca’s area) and temporal (Wernicke’s area) language regions. Relevance: Atypical microstructure in dyslexia and developmental language disorder; affects phonological processing and rapid word retrieval. Clinical implication: Explains why phonics alone may not suffice; supports multimodal (visual, motor, auditory) language instruction.
Dopamine. Definition: Neurotransmitter involved in reward, motivation, movement, and reinforcement learning. Relevance: Dysregulated in ADHD (reduced tonic dopamine, phasic release differences), Tourette syndrome (dopamine excess in striatum), and autism (altered reward processing). Clinical implication: Explains why stimulants (methylphenidate, amphetamine) are effective in ADHD – they increase extracellular dopamine; also explains reward‑based behavioral strategies.
Norepinephrine (Noradrenaline). Definition: Neurotransmitter involved in arousal, alertness, and attention regulation. Relevance: Altered in ADHD (locus coeruleus dysregulation) and anxiety (common co‑occurrence). Clinical implication: Explains why alpha‑2 agonists (guanfacine, clonidine) help with hyperactivity and sleep; supports environmental modulation of arousal such as movement breaks.
GABA (Gamma‑Aminobutyric Acid). Definition: Primary inhibitory neurotransmitter; balances excitation. Relevance: Altered excitatory/inhibitory (E/I) balance in autism (reduced GABAergic inhibition in sensory and social circuits). Clinical implication: Explains sensory hypersensitivity and seizures (co‑occurring); supports interventions that reduce sensory overload, not just behavioral approaches.
Glutamate. Definition: Primary excitatory neurotransmitter; involved in learning, memory, and plasticity. Relevance: E/I imbalance in autism (excess glutamate relative to GABA); implicated in Tourette syndrome and OCD (common co‑occurrence). Clinical implication: Explains why some individuals experience too much sensory input; supports research into glutamate‑modulating agents.
Heritability. Definition: Proportion of variance in a trait within a population attributable to genetic differences (range 0 to 1). Relevance: Neurotypes are highly heritable: autism approximately 0.8, ADHD approximately 0.7 to 0.8, dyslexia approximately 0.5 to 0.7, DCD approximately 0.5 to 0.7. Clinical implication: Refutes bad parenting or lack of effort explanations; informs genetic counseling; reminds clinicians that family history is relevant.
Polygenic. Definition: Involving many genes, each with small effect, rather than a single gene. Relevance: All common neurotypes (autism, ADHD, dyslexia) are polygenic. Clinical implication: No single gene test will diagnose a neurotype; explains variability within families.
Pleiotropy. Definition: A single gene affecting multiple seemingly unrelated traits. Relevance: Explains co‑occurrence – for example, FOXP2 variants affect language, motor coordination, and attention. Clinical implication: Co‑occurrence is not comorbidity (separate diseases) but expected overlap; screen for multiple neurotypes when one is present.
Epigenetics. Definition: Changes in gene expression caused by environment, experience, or development without changing DNA sequence. Relevance: Early stress, nutrition, or enrichment can alter expression of genes related to attention, anxiety, and learning. Clinical implication: Explains why identical twins are not 100 percent concordant for neurotypes; supports early environmental interventions not as a cure but as a modifier.
Copy Number Variant (CNV). Definition: Deletion or duplication of a segment of DNA larger than a single nucleotide variant. Relevance: Certain CNVs (e.g., 16p11.2, 22q11.2) increase risk for autism, ADHD, schizophrenia, and intellectual disability. Clinical implication: In clinical genetics, finding a CNV does not give a precise neurotype diagnosis – one CNV can cause multiple outcomes (variable expressivity).
Procedural Learning. Definition: Learning skills that become automatic (e.g., riding a bike, typing, handwriting). Relevance: Impaired in dyspraxia/DCD, dyslexia (automatic word recognition), and developmental language disorder (automatic grammar). Clinical implication: Explains why repeated practice alone does not lead to automaticity; supports explicit, declarative (verbal) strategies and assistive technology.
Procedural Memory System. Definition: Brain systems (cerebellum, basal ganglia, supplementary motor area) that store motor and cognitive routines. Relevance: Atypical in DCD, Tourette syndrome, and ADHD (habit formation). Clinical implication: Explains difficulty with routines and tic suppression; supports environmental consistency and habit‑stacking techniques.
Declarative (Explicit) Memory. Definition: Conscious memory for facts and events (hippocampus‑dependent). Relevance: Often intact or even superior in DLD, dyslexia, and ADHD – can learn facts about language or reading even if automaticity is impaired. Clinical implication: Strengths‑based intervention: teach rules explicitly (e.g., grammar rules, phonics rules) rather than relying on immersion.
Phonological Working Memory. Definition: Ability to hold and manipulate speech sounds in mind temporarily (e.g., repeating a non‑word like blonterstape). Relevance: Impaired in dyslexia and DLD; predicts reading and language outcomes. Clinical implication: Assess with non‑word repetition tasks; supports explicit phonological training and memory aids such as written backup and repetition.
Monotropism. Definition: A cognitive style characterized by intense, narrow attention channels – focusing deeply on a small number of interests at a time. Relevance: Described by autistic self‑advocates; increasingly studied in autism and giftedness. Clinical implication: Explains both hyperfocus and difficulty switching tasks; supports scheduling that allows long, uninterrupted blocks of focus.
Overexcitabilities (OEs). Definition: Intense reactions to stimuli in five domains: psychomotor, sensory, intellectual, imaginational, and emotional. Relevance: Described by Dabrowski; common in gifted and autistic individuals; not a disorder. Clinical implication: Normalizes intense experiences; supports coping strategies such as sensory breaks, creative outlets, and emotional coaching rather than suppression.
Co‑occurrence. Definition: The presence of two or more neurotypes in the same individual at rates above chance. Relevance: ADHD and dyslexia co‑occur in 30 to 50 percent of cases; autism and ADHD co‑occur in 40 to 70 percent; DCD and ADHD co‑occur in 50 to 70 percent. Clinical implication: When you diagnose one neurotype, actively screen for others. Do not treat in silos.
Transdiagnostic. Definition: Research or clinical approach that studies dimensions (e.g., attention, language, motor) across traditional diagnostic boundaries. Relevance: The transdiagnostic revolution (Astle et al., 2022) shows that neurodevelopmental traits cluster, not DSM categories. Clinical implication: Supports dimensional assessments (e.g., strengths and difficulties questionnaires) rather than checklists limited to one diagnosis.
Asynchrony. Definition: Uneven development across domains (e.g., advanced cognition with delayed motor or social‑emotional skills). Relevance: Common in giftedness and autism; often mistaken for behavior problem or lack of effort. Clinical implication: Do not assume global maturity; assess each domain separately. Provide support in lagging areas without withholding challenge in advanced areas.
Part 3: Putting It Into Practice – A Clinical Example for Clinicians
The following example illustrates how a clinician might integrate both diagnostic and neurotype frameworks in practice.
A 10‑year‑old patient is referred for inattention and poor handwriting. Diagnostic assessment using DSM‑5 criteria reveals ADHD and dysgraphia.
Using only DSM‑5 language, the clinician might document comorbid attention‑deficit/hyperactivity disorder, combined presentation, and specific learning disorder with impairment in written expression. Interventions might include prescribing a stimulant, recommending occupational therapy for handwriting, and requesting school accommodations for extra time.
Using both DSM‑5 and neurotype language, the clinician might instead say to the family and document: This child is multiply neurodivergent – they have both an ADHD neurotype and a dysgraphic neurotype.
From a DSM‑5 perspective, these meet criteria for ADHD and specific learning disorder. The same interventions are offered, but the clinician also provides psychoeducation on strengths: interest‑driven attention, oral creativity, and verbal storytelling. Accommodations include speech‑to‑text software and reduced handwriting demands. The clinician also screens for co‑occurring DCD or dyslexia, which are common.
The difference in outcome is that the child and family understand that this is not laziness or lack of effort. The child’s brain works differently, not defectively. Engagement and self‑esteem improve.
Part 4: Limitations and Caveats for Clinicians
The following limitations are important to acknowledge. First, no single model is perfect. DSM‑5 and ICD‑11 provide reliability and access to services. The neurotype model provides validity and dignity. Clinicians can use both. Second, not all neurodivergence is identity‑linked. Traumatic brain injury, some epilepsies, and late‑onset conditions are forms of neurodivergence, but individuals may not embrace a neurotype identity. Clinicians should respect that preference. Third, co‑occurrence rates are population estimates. Each patient is an individual – assess, do not assume. Fourth, language evolves. Terms such as neurodivergent and multiply neurodivergent are still settling. When in doubt, ask the patient what they prefer. Fifth, cultural context matters. Stigma, access, and self‑identification vary across cultures and socioeconomic groups. Do not universalize Western neurodiversity activism.
Part 5: References
American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., text rev.). https://doi.org/10.1176/appi.books.9780890425787
Astle, D. E., Holmes, J., & Kievit, R. (2022). Annual Research Review: The transdiagnostic revolution in neurodevelopmental disorders. Journal of Child Psychology and Psychiatry, 63(4), 397-417. https://doi.org/10.1111/jcpp.13481
Faraone, S. V., Banaschewski, T., Coghill, D., et al. (2021). The World Federation of ADHD International Consensus Statement: 208 evidence‑based conclusions about the disorder. Neuroscience and Biobehavioral Reviews, 128, 789-818. https://doi.org/10.1016/j.neubiorev.2021.01.022
Kirby, A. (2024). Neurodiversity co‑occurrence map. Do‑IT Profiler. https://doitprofiler.com/insight/neurodiversity-co-occurrence-map/
Petersen, I. T., & LeBeau, R. T. (2021). Co‑occurrence of developmental disorders: A meta‑analysis. Journal of Child Psychology and Psychiatry, 62(5), 514-529. https://doi.org/10.1111/jcpp.13319
Walker, N. (2021). Neurodiversity: Some basic terms and definitions. NeuroQueer. https://neuroqueer.com/neurodiversity-terms-and-definitions/
World Health Organization. (2019). International classification of diseases (11th ed.). https://icd.who.int/
Conclusion
As a neurodiversity advocate, I offer this resource to clinicians, researchers, and trainees who wish to become bilingual in diagnostic and neurotype frameworks. You do not need to abandon DSM‑5 or ICD‑11. But you can add the neurotype model to your clinical toolkit. The narrative comparison and neuroscience glossary above are designed to help you move fluidly between these frameworks – not as a replacement, but as a complement.
When you do, you will reduce stigma and shame for patients, identify co‑occurrence earlier because you expect it, design strengths‑based interventions, and align your practice with current genetics and neuroscience. The next time you write a diagnostic report or speak with a patient, consider adding one sentence: From a neurodiversity perspective, this individual is a [neurotype] person, which involves both challenges and strengths. The following recommendations address the mismatch between their neurotype and their current environment. That single sentence changes everything.
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