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What causes nonverbal autism?


Nonverbal autism, also known as nonverbal autism spectrum disorder, is a severe form of autism where an individual has very limited or no verbal speech abilities. About 25-30% of individuals with autism are nonverbal. Nonverbal autism usually co-occurs with intellectual disability and difficulties with fine motor skills. Understanding what causes nonverbal autism is an important area of autism research, as identifying causal factors can help improve screening, diagnosis, and treatment. In this article, we will provide an overview of the current scientific understanding of what causes nonverbal autism.

Genetic factors

Genetics play a significant role in causing nonverbal autism. Autism has a strong hereditary component, meaning that it runs in families. Siblings of children with autism have a higher risk of also developing autism spectrum disorder (ASD), and identical twins have a 60-90% concordance rate for ASD. Although autism itself is highly heritable, nonverbal status appears to have a distinct genetic signature from verbal autism. Researchers have identified mutations on several genes that are associated with nonverbal ASD, including FOXP1, GRIN2B, SRPX2, and CMIP. Mutations in these genes may disrupt early neurodevelopmental processes like synaptic signaling and neuronal connectivity, leading to severe language and speech impairment in autism.

Notable genetic links:

  • Mutations in FOXP1 linked to intellectual disability, motor delays, and absence of language.
  • GRIN2B mutations related to impaired speech, language, and intellectual disability.
  • Loss-of-function mutations in SRPX2 associated with rolandic epilepsy and speech apraxia.
  • Rare variants in CMIP correlated with low IQ and severe language deficits in ASD.

Overall, the genetic evidence indicates that nonverbal autism has distinct biological underpinnings and is tied to abnormal early brain development affecting language learning.

Neurobiological factors

In addition to genetics, differences in brain structure and function likely play a key role in nonverbal autism. Neuroimaging studies have identified anatomical and functional abnormalities in the brains of nonverbal children with ASD compared to verbal autism or typical development.

Some neurobiological differences found include:

  • Smaller surface area and volume of cortical regions related to language and communication.
  • Underconnectivity between frontal and temporal brain regions critical for language.
  • Differences in white matter tracts interconnecting language areas.
  • Atypical lateralization and activation of language regions like Broca’s and Wernicke’s area.
  • Impaired imitation and mirror neuron system function.

These neural differences are present early in development and disrupt the emergence of speech and language skills. Ongoing research is examining the complex interplay between genetics, brain development, and environmental influences that shape these neurobiological factors leading to nonverbal ASD.

Environmental risk factors

Genetics are estimated to account for 50-60% of autism risk, while environmental factors make up the remaining portion. A number of prenatal and perinatal environmental exposures have been linked to heightened risk for nonverbal autism phenotype, including:

Prenatal risks:

  • Advanced parental age at conception
  • Maternal obesity, diabetes, or immune system abnormalities
  • Viral infections like rubella or cytomegalovirus during pregnancy
  • High levels of air pollution exposure
  • Medications like valproic acid
  • Folic acid deficiency

Perinatal risks:

  • Preterm birth
  • Birth complications leading to oxygen deprivation
  • Low birth weight or small for gestational age
  • Hospitalization after birth
  • Labor induction or C-section delivery

These prenatal and early life risks contribute to adverse neurodevelopmental processes like neurogenesis, neuron migration, and synapse formation. More research is needed to elucidate gene-environment interactions influencing nonverbal ASD.

Co-occurring conditions

Many children with nonverbal autism have co-occurring neurological, genetic, and medical conditions that likely exacerbate autism severity and speech deficits. These associated conditions include:

  • Intellectual disability (~50-60% of nonverbal autism cases)
  • Epilepsy (~25% comorbidity rate)
  • Genetic syndromes like Fragile X, Rett syndrome, Tuberous sclerosis
  • Gastrointestinal issues
  • Sleep abnormalities
  • ADHD symptoms
  • Fine and gross motor impairments

The causal relationships between these comorbidities and nonverbal status remains poorly understood. It is hypothesized that the confluence of multiple neurological and developmental conditions overwhelms emerging language capacity in vulnerable children. More research on these complex synergistic risks is warranted.

Diagnosis and screening

Given the diverse factors that can lead to nonverbal autism, early and accurate screening and diagnosis is essential but remains challenging. There are no medical tests for autism, so clinicians rely on developmental screening and symptom checklists to identify children at-risk. Typical diagnosis involves interviewing parents about developmental history, observing child behaviors, and assessing cognitive, motor, adaptive, and language skills. Language delays or lack of babbling by 12-18 months can be red flags for nonverbal autism that warrant follow-up and monitoring. Ongoing research aims to find biomarkers like genetic tests or neuroimaging patterns that could improve prediction of nonverbal status, but these are not ready for clinical practice yet. Routine developmental screening combined with autism-specific tools represents the current best practice for timely nonverbal autism identification.

Interventions and treatment

While there are no medications that specifically treat nonverbal autism, intensive behavioral interventions and alternative communication strategies are often helpful for improving outcomes. Evidence-based options include:

  • Applied behavior analysis – teaches communication, social,motor, and cognitive skills
  • Speech therapy – focuses on speech production and alternative communication (e.g., sign language, pictures)
  • Occupational therapy – addresses sensory issues, motor skills, daily living skills
  • Assistive Augmentative Communication (AAC) devices like pictures boards or speech-generating devices
  • Developmental and relationship-based approaches like Floortime
  • Special education services and vocational training in the school system

A customized combination of behavioral, developmental, and communication interventions tailored to the child’s strengths and needs offers the best chance for improving functional abilities. However, progress can be slow, variable, and plateau. Supporting families with training, respite, and counseling is also an important component. More research on novel treatment approaches for nonverbal autism is an important priority.

Prognosis

The prognosis for nonverbal children with autism varies significantly depending on the individual. Many remain minimally verbal or nonverbal throughout life. In some cases, intensive early intervention results in development of simple words or phrases after age 5, but around 30% remain nonverbal. A small minority can gain fluent conversational speech by adolescence or adulthood. Even without gains in spoken language, some children develop proficiency in using AAC devices or sign language to communicate. Higher IQ, receptive language skills, motor skills, and treatment intensity predict better communication outcomes. Early intervention by age 2-3 offers the best shot at improving long-term prognosis. However, nonverbal autism remains a lifelong disorder and the majority will continue needing high support. Expanding access to early intensive services provides the best hope for helping more children reach their fullest potential.

Key Points and Conclusions

In summary, current evidence suggests:

  • Nonverbal autism has distinct genetic underpinnings affecting early neurodevelopmental processes that disrupt language learning.
  • Neurobiological differences in key brain regions involved in speech and language are apparent on neuroimaging.
  • Prenatal and perinatal environmental factors contribute risk, likely through epigenetic mechanisms.
  • Co-occurring intellectual disability, epilepsy, and other neurological conditions exacerbate nonverbal status.
  • Early screening and diagnosis followed by intensive behavioral and communication interventions are critical but outcomes remain variable.
  • Prognosis is improved by higher IQ and treatment intensity but nonverbal autism remains a lifelong disorder for most.
  • More research on causes, treatments, and outcomes is needed to better serve this population.

In conclusion, nonverbal autism has complex multifactorial origins stemming from the interplay between genetic vulnerabilities, atypical neurobiology, and environmental exposures. While daunting, continued research into causal pathways holds promise for developing tailored interventions that can improve communication skills and quality of life for those living with nonverbal autism.