BCIA Continuing Education Posts

We wish clinicians knew that OIRDA is not an epileptiform discharge. It does not reflect hyperexcitability or paroxysmal depolarization, and in isolation, it is not a seizure pattern.

Before a diagnosis of a mental disorder can be made, the clinician must rule out that the symptoms are not attributable to the physiological effects of a substance or another medical condition.

Benzodiazepines vary widely in EEG and clinical effects—Subtypes differ by half-life and receptor affinity, influencing sedation, rebound symptoms, and cortical modulation.

Antidepressants, particularly those that are highly activating or serotonergically potent, may be the worst choice in patients with SEB, IEDs, or focal abnormalities.

Reduced alpha rhythms in PTSD are thought to be involved in poor excitatory/inhibitory balance in the brain.

Used responsibly, the qEEG enhances interpretation; used in isolation, it risks misrepresentation.

Small-N designs are particularly powerful when the treatment effect is large and immediate, allowing researchers to infer causality with confidence.

The goal of this post is to help you think like a scientist when it comes to evaluating questionable claims.

To support a causal claim, a study must meet three essential criteria: covariance, temporal precedence, and internal validity.

Interrogating association claims means asking three core questions: Were the variables measured well (construct validity)? Can the results be generalized to other populations (external validity)? And is the association statistically strong, significant, and precise (statistical validity)?

The four big validities offer a comprehensive toolkit for evaluating psychological research. Construct validity ensures that variables are accurately measured or manipulated. External validity tells us whether the results generalize. Statistical validity ensures the numbers are trustworthy. Internal validity confirms that cause-and-effect relationships are legitimate.

Association claims are foundational to psychological research because they help us identify variables that are connected and warrant further investigation. While they cannot prove causality, they provide essential groundwork for asking deeper questions.

Understanding how each variable was operationalized helps you evaluate whether results can be compared or generalized. It also helps you decide whether the measure actually reflects the concept you’re interested in.

At its core, ADHD is not about lacking attention—it's about struggling to control it.

Encephalopathy presents with polymorphic delta activity—delta waves that vary in shape and amplitude—over cortical areas.

Traveling waves in electroencephalography (EEG) represent coordinated patterns of electrical activity that move systematically across the cortex.

Diffuse slowing reflects a global disturbance of cortical–subcortical coupling and is therefore considered a biomarker of cerebral dysfunction rather than a discrete lesion.

EEG biomarkers offer incremental validity over behavioral observation alone.

IEDs are not incidental EEG findings, but markers of transient cortical dysfunction that disrupt cognition, emotion, and behavior.

Quantitative EEG (qEEG) normative databases can reveal the key parts of a network that need training and the required direction.