May 2026: Webinar Series About the Brain and the Mind
Each webinar takes 3 hours and 3 CE Credits will be awarded for every live webinar by CE credit sponsor to licensed professionals.
CUE Management Solutions, LLC is approved by the American Psychological Association to sponsor continuing education for psychologists. CUE Management Solutions, LLC maintains responsibility for this program and its content.
CUE Management Solutions, LLC is recognized by the New York State Education Department’s State Board for Psychology as an approved provider of continuing education for licensed psychologists #PSY-0242.Instructor Credentials: Elkhonon Goldberg, Ph.D., ABPP., a clinical neuropsychologist and cognitive neuroscientist, and Diplomate of The American Board of Professional Psychology in Clinical Neuropsychology. His critically acclaimed and bestselling books have been translated into 24 languages.
Tuition: $185 per webinar
Format: three-hour long online webinar
Date and time:
1. Autism Spectrum Disorder: Causes, Neurobiological Mechanisms and Controversies
May 6 (Wednesday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
2. Aging and Dementias
May 7 (Thursday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
3. Brain Disorders and Criminal Behavior
May 9 (Saturday) from 10am to 1pm Eastern Time (9am–noon Central Time, 7am–10am Pacific Time)
4. Tourette and ADHD: A New Look at an Old Quandary
May 10 (Sunday) from 10am to 1pm Eastern Time (9am–noon Central Time, 7am–10am Pacific Time)
5. Executive Functions and the Frontal Lobes
May 11 (Monday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
6. AUTISM BEYOND THE CHECKLIST: Phenotypes, Mimics, and Debates Shaping 2026
May 12 (Tuesday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
Training appropriate for: The course is intended for professionals concerned with mental health and with brain and brain disorders.
The course content level: Intermediate.
Autism Spectrum Disorder: Causes, Neurobiological Mechanisms and Controversies
May 6 (Wednesday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
This 3-hour webinar provides a comprehensive overview of Autism Spectrum Disorder (ASD) with a focus on its genetic underpinnings, neurobiological mechanisms, and current controversies. Participants will gain an understanding of the highly heritable nature of ASD, including the role of rare high-impact mutations and common polygenic risk factors. The session explores critical neurobiological theories such as atypical synaptic pruning, excitation-inhibition imbalance, and microglial dysfunction, and highlights the stratification of ASD into biologically distinct subtypes using recent advances in genomics and machine learning. Environmental risk factors and regulatory guidance on debated exposures such as prenatal acetaminophen use are critically examined. The webinar bridges basic science discoveries with clinical implications, including genetic testing recommendations and the potential for targeted therapeutics. Participants will be equipped to better understand and communicate the complexities surrounding ASD causes and contemporary research findings.
Topics to be covered:
1. Genetic Foundations of Autism Spectrum Disorder (ASD): Evidence for high heritability and the contribution of rare and common genetic variants.
2. Neurobiological Mechanisms of ASD: Core pathways involving synaptic function, transcriptional regulation, and neural circuit development.
3. Atypical Synaptic Pruning: Microglial and complement-system involvement in altered pruning processes in ASD.
4. Excitation–Inhibition (E/I) Imbalance: Systems-level theories supported by genetic and neuroimaging findings.
5. Glial Cell Dysfunction in ASD: The roles of microglia and astrocytes in brain development and ASD-related changes.
6. Mitochondrial Dysfunction and Oxidative Stress: Emerging evidence in a biologically distinct subgroup of individuals with ASD.
7. Large-Scale Network Connectivity: Altered functioning of networks such as the Default Mode Network (DMN) and Salience Network (SN).
8. Environmental and Perinatal Risk Factors: Factors such as advanced parental age and maternal immune activation within the diathesis–stress framework.
9. Controversies in ASD Causation: Critical examination of myths, including vaccine claims and the debated link to prenatal acetaminophen exposure.
10. Conditions That Mimic ASD Features: Overview of other neurodevelopmental or neurological conditions that may present with autistic-like traits.
Learning objectives for training:
1. Describe the primary genetic factors contributing to ASD, including the roles of rare and common variants.
2. Explain at least two major neurobiological models of ASD, such as the excitation/inhibition imbalance hypothesis and the atypical synaptic pruning theory.
3. Analyze the evidence for and against the role of key environmental risk factors, including the controversy surrounding prenatal acetaminophen use.
4. Identify the core functions of the Default Mode and Salience networks and how their atypical connectivity relates to the clinical presentation of ASD.
Aging and Dementias
May 7 (Thursday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
Dementias are among the most prevalent neurocognitive disorders presenting a unique set of clinical and societal challenges. In this webinar we will review several major types of dementia, including Alzheimer’s disease, Lewy body dementia and its relationship to Parkinson’s disease, frontotemporal dementia, vascular dementia, and others. For each of these disorders we will discuss the underlying neurobiology, epidemiology, natural history, diagnosis, and cognitive characteristics. We will also discuss cognitive aging, as well as both protective and risk factors associated with it.
Topics to be covered:
Epidemiology and demographics of dementias.
Alzheimer’s disease: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis. Lewy body dementia and Parkinson’s disease: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis.
Fronto-temporal dementia: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis. Vascular dementia: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis.
Korsakoff’s syndrome: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis. Mixed dementias: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis.
Mild Neurocognitive disorder and its relationship to dementias. Diagnosis, differential diagnosis, and misdiagnosis.
Memory impairment in dementias and the fallacy of old diagnostic criteria. Executive impairment in dementias: still underrecognized.
Arousal impairment in dementias. Changes in the epidemiology of dementias and possible causes behind them.
Cognitive aging: its characteristics, protective factors, and risk factors.
Cognitive enhancement and surrounding controversies.
Learning objectives for training:
1. Describe the Biological Characteristics of Major Dementias. Identify and explain the neuropathological features of Alzheimer’s disease, including amyloid plaques, neurofibrillary tangles, and brain atrophy.
2. Describe the Cognitive Characteristics of Major Dementias. Discuss the language and behavioral changes typical of frontotemporal dementia.
3. Discuss the Diagnosis and Differential Diagnosis of Dementias. Outline the criteria for diagnosing Alzheimer’s disease, vascular dementia, dementia with Lewy bodies, and frontotemporal dementia according to current clinical guidelines (e.g. DSM-5).
Brain Disorders and Criminal Behavior
May 9 (Saturday) from 10am to 1pm Eastern Time (9am–noon Central Time, 7am–10am Pacific Time)
Various brain disorders may alter behavior in ways that result in behaviors judged by society as antisocial or outright criminal. Ultimately the judgment whether certain acts are criminal and to what extent (if any) a history of brain disorder is a mitigating factor, rests with the legal system. However, mental health professionals can make important contributions to these decisions in an advisory capacity. It is important to educate both mental health professionals and members of the legal profession about the many possible ways in which brain damage may contribute to criminal behavior. Socially aberrant behaviors are more common in certain brain disorders than in others; the manifestations may be different, and so are the underlying mechanisms. In this webinar we will review some of the conditions with which aberrant behaviors may be associated. These include dementias, neurodevelopmental disorders, traumatic brain injury,
seizures, space occupying lesions, neuropsychiatric disorders, and others. It is important for clinicians working with these populations to be aware of the potential for socially aberrant behavior, which may be predicated, entirely or in part, on the intrinsic properties of underlying brain disease and associated cognitive impairment and disinhibition.
Topics to be covered:
Relationship between neuropsychological and legal perspectives.
Frontal lobe dysfunction and aberrant behavior.
Criminal behavior in dementias: frontotemporal (FTD) and others.
Criminal behavior in traumatic brain injury (TBI).
Early life TBI as a risk factor for later-life criminality.
Aggression in temporal lobe epilepsy: real or imagined?
Space occupying lesions: arachnoid cysts and violent psychosis.
Is there a relationship between depression and aggression?
Schizophrenia and violence: is there a link?
Neurodevelopmental disorders: aggression and anger.
Learning objectives for training:
1. Neurobiological Foundations. Explain the neuroanatomical and neurophysiological basis of behavior, emphasizing structures and pathways relevant to decision-making, impulse control, and social cognition.
2. Neurological Disorders and Criminal Behavior. Analyze the relationship between specific neurological disorders (e.g., traumatic brain injury, dementia, epilepsy) and criminal conduct.
3. Psychiatric Disorders and Criminality. Explore the association between psychiatric disorders (e.g., schizophrenia, antisocial personality disorder) and criminal behavior.
4. Lesions and Criminal Behavior. Describe how space-occupying lesions (e.g., tumors, cysts) in the brain can alter personality, impulse control, and moral reasoning, potentially leading to criminal acts.
Tourette and ADHD: A New Look at an Old Quandary
May 10 (Sunday) from 10am to 1pm Eastern Time (9am–noon Central Time, 7am–10am Pacific Time)
The ADHD diagnosis has acquired the status of a fad and is often given too casually and inclusively. Conflation between two distinct classes of clinical phenomena, hyperactivity and exploratory behavior, is a common source of ADHD overdiagnosis. Inspired by early insights by Oliver Sacks, we examine the relationship between frontal-lobe syndromes, Tourette syndrome, and Parkinson’s disease. This synthesis leads to a new understanding of Tourette syndrome and helps identify its distinct subtypes. These subtypes are caused, respectively, by predominant dysregulation in the left vs right fronto-striatal systems, and result in the preponderance of tics vs excessive exploratory behaviors. We examine the difference between
hyperactivity and excessive exploratory behavior, and the potential for diagnostic confusion
between ADHD and Tourette if this difference is ignored.
Topics to be covered:
Overdiagnosis of ADHD. A source of overdiagnosis: conflation of hyperactivity and exploratory behavior. What is the difference?
Are the diagnostic criteria for ADHD too broad? Duality of symptoms in Tourette syndrome: tics vs exploratory behavior.
Are the diagnostic criteria for Tourette too narrow? The triple-decker: Frontal lesions, Tourette syndrome, and Parkinson’s disease.
Introducing “hemi-Tourette” subtypes.
Clinical features of “hemi-Tourette” subtypes.
Clearing up the diagnostic confusion between Tourette and ADHD.
Learning objectives for training:
1. Explain the Relationship Between Tourette and ADHD Diagnoses. Describe the diagnostic criteria for Tourette syndrome and ADHD, highlighting the overlapping symptoms and co morbidities.
2. Describe the Concept of “Excessive Exploratory Behavior” and How It Is Different from Hyperactivity. Define “excessive exploratory behavior” and compare it to the traditional concept of hyperactivity observed in ADHD.
3. Explain the Role of Fronto-Striatal Interaction Breakdown in Tourette Syndrome. Describe the structure and function of the fronto-striatal circuits involved in motor control and behavior regulation.
4. Summarize the Concept of “Hemi-Tourette” Syndrome Variants. Define “hemi-Tourette” syndrome and describe its clinical presentation and diagnostic criteria.
Executive Functions and the Frontal Lobes
May 11 (Monday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
Executive functions represent the highest level of cognitive control and involve goal formation, planning, mental flexibility, impulse control, working memory. Executive functions are mediated by the prefrontal cortex and related structures. In this webinar we will examine their cognitive composition, neural mechanisms, changes throughout the lifespan, and gender differences. We will also examine how executive functions become impaired in a wide range of neurological, neuropsychiatric, neurodevelopmental, and neurogeriatric disorders.
Topics to be covered:
Executive functions and frontal-lobe functions: are they the same?
Components of executive functions (planning, impulse control, working memory, and others).
Novel approaches to understanding the frontal-lobe functions.
Frontal lobes and large-scale networks (Central Executive, Default Mode, and others).
Executive functions and laterality.
Executive functions and sex differences.
Regulation of emotions: frontal lobes and amygdala.
Executive functions and intelligence.
Executive functions in development and aging.
Learning objectives for training:
1. List Brain Mechanisms of Executive Functions. Identify and describe the structure and function of the prefrontal cortex, including its subdivisions (e.g., dorsolateral, ventromedial, and orbitofrontal regions) and their roles in executive functions.
2. Explain the Process and Brain Mechanisms of Decision-Making. Describe the neural circuits involved in decision-making, emphasizing the role of the prefrontal cortex and its interactions with other brain regions.
3. Explain the Brain Mechanisms of Emotions. Identify the amygdala’s role in emotion processing and its connections with the prefrontal cortex.
4. Describe Executive Functions in Normal Development and Aging. Outline the developmental trajectory of executive functions from childhood through adolescence, highlighting key milestones and brain maturation processes.
AUTISM BEYOND THE CHECKLIST: Phenotypes, Mimics, and Debates Shaping 2026
May 12 (Tuesday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
This 3-hour webinar moves beyond a checklist approach to ASD by focusing on diagnostic complexities and why an autism label can be correct but clinically incomplete. It introduces “phenocopy logic” and diagnostic overshadowing, showing how neurological, genetic, and medical conditions can mimic or reshape an autism-like presentation. Using phenotype-focused examples, it reviews common mimics and “ASD-plus” patterns, and how to think about EEG and MRI findings without over-interpreting incidental abnormalities. The session closes with the debates shaping 2026, including neurodiversity, ethics, and psychosocial trends, with practical guidance for communicating uncertainty while keeping recommendations actionable.
Topics to be covered:
1. Diagnostic complexities in ASD, why an autism label can be “correct but incomplete”
2. Clinical foundations of phenocopy logic, ASD as a “final common pathway”
3. Diagnostic overshadowing in neuropsychology and its impact on case formulation
4. Shifting from behavioral description to etiological formulation
5. Distinguishing primary vs secondary autistic features
6. The “social brain” network and how secondary insults can reshape presentation
7. Sensory dysregulation as a secondary feature
8. Macrocephaly and ASD, clinical significance and when to worry
9. The role of neuroimaging in clinical practice, including functional neuroimaging (fMRI/PET)
10. Association vs causation, how to avoid over-reading correlations
11. Neurological mimics and lesion-based examples, including hydrocephalus mechanisms, agenesis of the corpus callosum, and temporal lobe cysts
12. Mapping the genetic landscape of secondary ASD, including TSC and the “double hit” model, Prader-Willi syndrome overlap, FASD, 22q11.2 deletion, and Fragile X comparisons
13. Regression-focused clinical reasoning, including “the EEG trigger”
14. Neurobiological causation controversies and public narratives, including vaccines, how to communicate safety without conflict, and the impact of social media on perceptions
Learning objectives for training:
1. Explain why an ASD label can be clinically incomplete, and apply a “beyond the checklist” approach that emphasizes differential diagnosis and layered formulation.
2. Apply phenocopy logic to differentiate primary autism features from secondary autistic features and diagnostic mimics, and recognize diagnostic overshadowing in case presentations.
3. Identify clinical red flags and “workup triggers,” including patterns involving regression, macrocephaly, focal signs, and concerning changes in functioning, that indicate need for additional medical evaluation.
4. Use a structured approach to neuroimaging findings (including MRI) by distinguishing clinically actionable results from incidental abnormalities and avoiding over-interpretation in feedback and reports.
5. Describe key neurological mimics and lesion-based examples discussed (including hydrocephalus and callosal agenesis) and link these presentations to practical clinical recommendations and referral considerations.
6. Summarize the genetic testing framework reviewed and interpret uncertain results in a clinically responsible way without overstating causality.
7. Critically evaluate causality claims in high-profile controversies discussed (for example, vaccines and acetaminophen) by identifying confounding and distinguishing timing coincidences from evidence of causation, and translate that reasoning into patient and family communication.
8. Formulate and communicate an integrated, ethically grounded case formulation that addresses uncertainty, supports appropriate services, and reflects psychosocial debates shaping 2026, including neurodiversity-informed considerations.
Conflicts of Interest:
There is no known commercial interest or conflict of interest for this program.
Cancellation Policy:
If for any reason you need to cancel, please contact the trainer so we can work together to determine a resolution.
Dr. Elkhonon Goldberg, Ph.D., ABPP: info@lninstitute.org 800-906-5866
Grievance Policy:
We seek to ensure equitable treatment of every person and to make every attempt to resolve grievances in a fair manner. Please email us with your written grievance. Grievances would receive, to the best of our ability, corrective action in order to prevent further problems.
ADA Needs:
If you have any special requests, please email/call: Karen Newell: 707-321-0926 newell@sonic.net
CE and Commercial Support:
CUE Management Solutions, LLC does not have a relevant financial relationship(s) with ineligible companies or other potentially biasing relationships to disclose to learners.
Continuing Education
CUE Management Solutions, LLC is approved by the American Psychological Association to sponsor continuing education for psychologists. CUE Management Solutions, LLC maintains responsibility for this program and its content. CUE Management Solutions, LLC is recognized by the New York State Education Department’s State Board for Psychology as an approved provider of continuing education for licensed psychologists #PSY-0242.
