October 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. CUE Management Solutions, LLC is recognized by the New York State Education Department’s State Board for Social Work as an approved provider of continuing education for licensed social workers #SW-0925.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 Beyond the Checklist: Phenotypes, Mimics, and Debates Shaping 2026
October 3 (Saturday) from 10am to 1pm Eastern Time (9am–noon Central Time, 7am–10am Pacific Time)
2. Memory-Based Learning Disabilities: A Common Syndrome Without a Pigeonhole
October 4 (Sunday) from 10am to 1pm Eastern Time (9am–noon Central Time, 7am–10am Pacific Time)
3. Aging and Dementias
October 5 (Monday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
4. Traumatic Brain Injury
October 6 (Tuesday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
5. Brain Disorders and Criminal Behavior
October 7 (Wednesday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
6. Neuroethics and the Ethics of Neurocognitive Diagnosis
October 8 (Thursday) 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 Beyond the Checklist: Phenotypes, Mimics, and Debates Shaping 2026
October 3 (Saturday) from 10am to 1pm Eastern Time (9am–noon Central Time, 7am–10am 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.
Memory-Based Learning Disabilities: A Common Syndrome Without a Pigeonhole
October 4 (Sunday) from 10am to 1pm Eastern Time (9am–noon Central Time, 7am–10am Pacific Time)
This 3-hour webinar defines “memory-based learning disability” as a common but under-recognized syndrome in which children with average or above-average intelligence show intact phonological skills and adequate attention in low memory-demand settings, yet fail to consolidate and retain new academic material over hours to days, producing cross-domain underachievement. It frames the problem as a diagnostic impasse created by DSM-5 and ICD-11 domain-based labels, then builds a mechanism-first model centered on hippocampal-dependent declarative memory and the declarative vs non-declarative dissociation, with emphasis on hippocampal-medial temporal microcircuit functions (pattern separation, pattern completion, relational binding) and why CA1 is selectively vulnerable. The webinar reviews developmental timing and risk windows, shows how diverse etiologies, hypoxic-ischemic, toxic-metabolic, epileptic-electrical, genetic-congenital, and perinatal-traumatic converge on hippocampal-temporal networks, and offers a practical differential diagnosis separating this profile from ADHD, dyslexia, and intellectual disability using accelerated-forgetting protocols and recall vs recognition patterns. It closes with assessment and management guidance, including memory-focused neuropsychological batteries, selective use of neuroimaging and EEG when indicated, and targeted school and home interventions that reduce memory load and strengthen consolidation via external supports and spaced retrieval.
Topics to be covered:
1. The “everyday clinical puzzle”, average intelligence, intact phonology, persistent underachievement.
2. The hallmark pattern, understands during guided practice, cannot retrieve independently later.
3. Rapid long-term decay and weak transfer across subjects.
4. Limits of DSM-5 “specific learning disorder” specifiers for a cross-domain memory mechanism.
5. Limits of ICD-11 domain-first classification for the same presentation.
6. Declarative memory, what it supports in school learning.
7. Non-declarative memory and why procedural skills can remain strong.
8. The declarative vs non-declarative dissociation as the clinical core of the syndrome.
9. Hippocampal formation anatomy and hippocampal-temporal network role in consolidation.
10. Selective vulnerability of CA1 and why isolated declarative impairment can occur.
11. Pattern separation and pattern completion as computational signatures tied to learning failures.
12. Behavioral compensations, heavy reliance on external aids and recognition formats.
13. Neuropsychological signature, normal immediate span with impaired delayed and long-delay recall.
14. Accelerated forgetting protocols, why 30-minute delays can miss the deficit and why 1–7 day testing matters.
15. Etiologic convergence on hippocampal networks, hypoxic-ischemic, toxic-metabolic, and epileptic-electrical pathways, and when EEG becomes relevant.
Learning objectives for training:
1. Describe the presenting clinical and academic phenotype, including the dissociation between average cognitive capacity and failure to retain and transfer newly learned material over educationally relevant delays.
2. Explain how DSM-5 and ICD-11 domain-based classification creates a diagnostic impasse when one declarative-memory mechanism drives cross-domain underperformance.
3. Contrast declarative from non-declarative memory systems and predict how this dissociation produces academic failure with preserved procedural learning.
4. Identify key hippocampal structures and vulnerability points, and summarize the computational roles of pattern separation and pattern completion as described in the slides.
5. Link developmental stage and rising school demands to the timing of symptom emergence, especially across the middle school and high school transitions.
6. Recognize the neuropsychological signature (accelerated long-delay forgetting, recall–recognition pattern, preserved non-declarative learning) and select appropriate extended-delay testing protocols.
7. Differentiate this syndrome from ADHD, dyslexia, and intellectual disability using the discriminators specified in the slides, including persistence under attention control and the presence of accelerated forgetting.
8. Apply a biology-first assessment and management plan by mapping etiologic pathways, stating when MRI or EEG is indicated, and formulating memory-load reducing accommodations and IEP language consistent with the slides.
Aging and Dementias
October 5 (Monday) 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:
1. Epidemiology and demographics of dementias.
2. 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.
3. Fronto-temporal dementia: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis. Vascular dementia: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis.
4. Korsakoff’s syndrome: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis. Mixed dementias: neurobiology, epidemiology, natural history, neurocognitive characteristics, and diagnosis.
5. Mild Neurocognitive disorder and its relationship to dementias. Diagnosis, differential diagnosis, and misdiagnosis.
6. Memory impairment in dementias and the fallacy of old diagnostic criteria. Executive impairment in dementias: still underrecognized.
7. Arousal impairment in dementias. Changes in the epidemiology of dementias and possible causes behind them.
8. Cognitive aging: its characteristics, protective factors, and risk factors.
9. 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).
Traumatic Brain Injury
October 6 (Tuesday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
Traumatic Brain Injury (TBI) is a highly prevalent condition sometimes referred to as a “silent epidemic.” In this webinar we will review various types of TBI (closed, open, blast); various causes and unique characteristics of motor vehicle accidents, workplace-related, military and sports TBI; various mechanisms of TBI (diffuse axonal injury, contre-coup, neurometabolic cascade); cognitive characteristics (particularly executive and memory impairment); recovery from TBI and long-term outcomes; and forensic issues commonly associated with TBI.
Topics to be covered:
1. Epidemiology of traumatic brain injury (TBI). Types of traumatic brain injury (TBI): closed, open (penetrating and perforating), blast. Severity and criteria of traumatic brain injury (TBI): mild, moderate, severe.
2. Causes of traumatic brain injury (TBI). Mechanisms of traumatic brain injury (TBI).
3. Focal vs. diffuse components of traumatic brain injury (TBI). Neuroanatomical structures most vulnerable in traumatic brain injury (TBI). Natural course of traumatic brain injury (TBI) and the multiple forms it may take.
4. Secondary complications in traumatic brain injury (TBI). Cognitive consequences of traumatic brain injury (TBI).
5. Executive deficit in traumatic brain injury (TBI).
6. Memory impairment in traumatic brain injury (TBI): anterograde and retrograde amnesia.
7. Traumatic brain injury (TBI) in sports and Chronic Traumatic Encephalopathy.
8. Military traumatic brain injury (TBI).
9. Forensic issues in traumatic brain injury (TBI).
Learning objectives for training:
1. Describe the Types of Traumatic Brain Injury (TBI). Identify and describe the different types of TBI, including concussions, contusions, diffuse axonal injury, and penetrating injuries.
2. Explain the Mechanisms of Traumatic Brain Injury (TBI). Describe the biomechanical forces involved in TBI, including impact, acceleration-deceleration, and rotational forces.
3. List the Multiple Possible Courses of Traumatic Brain Injury (TBI). Identify the different clinical trajectories of TBI, including recovery patterns and potential complications.
4. Explain the Cognitive Characteristics of Traumatic Brain Injury (TBI). Describe the common cognitive deficits associated with TBI, including impairments in attention, memory, and executive functions.
Brain Disorders and Criminal Behavior
October 7 (Wednesday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm 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:
1. Relationship between neuropsychological and legal perspectives.
2. Frontal lobe dysfunction and aberrant behavior.
3. Criminal behavior in dementias: frontotemporal (FTD) and others.
4. Criminal behavior in traumatic brain injury (TBI).
5. Early life TBI as a risk factor for later-life criminality.
6. Aggression in temporal lobe epilepsy: real or imagined?
7. Space occupying lesions: arachnoid cysts and violent psychosis.
8. Is there a relationship between depression and aggression?
9. Schizophrenia and violence: is there a link?
10. 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.
Neuroethics and the Ethics of Neurocognitive Diagnosis
October 8 (Thursday) from 1pm to 4pm Eastern Time (noon–3pm Central Time, 10am–1pm Pacific Time)
Neuroethics is a new discipline addressing the ethical issues arising on the cutting edge of
neuroscience, both basic and applied. Neuropsychology is a discipline on the intersection of
psychology and neuroscience, with its own unique ethical issues. Some of these issues pertain
directly to the substance of neurocognitive evaluation and rehabilitation. In this webinar we will
examine the concept of neuroethics and its relationship to neuropsychology. First, we review
examples of neuroethics concerns from various aspects of neurosciences. We will then identify
and discuss a wide range of ethical issues specifically related to the substance and content of
neurocognitive assessment and rehabilitation. While these issues are not conventionally
regarded as part of neuroethics, in reality they are. It is important to bring neuropsychology into
neuroethics and neuroethics into neuropsychology. This is what this webinar aims to
accomplish.
Topics to be covered:
1. Neuroethics: definition, resources and examples of pertinent issues. Overdiagnosis driven by fads not facts. Example: ADHD overdiagnosis.
2. Misdiagnosis because no pigeonholes exist. Example: “memory based learning disability.” Perpetuating outdated notions. Example: “no dementia without memory impairment.”
3. Saying “somatoform” instead of saying “I don’t know.” Example: when “mild TBI “is not so mild.
4. Overdiagnosis and underdiagnosis. Example: -1 standard deviation is still normal.
5. Being a detective at the expense of being a clinician. A malingerer can also be genuinely sick. Overgeneralizing. Example: drawing sweeping conclusions based on a single test.
6. Cultural insensitivity. Example: giving culture-dependent tests inappropriately.
7. Fabulizing. Offering interpretations well beyond the data. Intellectual arrogance: not knowing what you don’t know.
8. Making hasty assumptions about what the patient’s words mean to you and yours to the patient. Example: when the patent complains of poor “memory” they may mean anomia.
9. Relying uncritically on canned interpretations.
10. Overpromising the results of intervention.
Learning objectives for training:
1. Describe the new discipline of neuroethics and related clinical issues relevant to neurocognitive diagnosis. Provide examples of topics addressed in neuroethics.
2. Describe diagnostic errors related to neuroethics, such as overdiagnosis, underdiagnosis, misdiagnosis, and provide examples.
3. Describe the impact of outdated explanatory constructs, “trendy” constructs, and poorly understood constructs on diagnostic interpretation, and provide examples.
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.
