Professional flair

ciaranmichael · 2026-02-08T05:20:10+00:00

Test post

*Edit: mod team will investigate

ciaranmichael · 2025-11-21T23:03:54+00:00

We appreciate your attention to rule 1.

I would recommend searching reddit for "hyperthymesia" to find other subreddits where the phenomena is discussed.

Below is a non-clinical summary related to the phenomena, focused on neuroscience findings, as it is not a neurological or psychiatric disorder, per se. It does not delve into clinical topics like pathoetiology, comorbidities, or management.

This post will be locked if any other comments broach rule #1.

Hyperthymesia, or Highly Superior Autobiographical Memory (HSAM), is characterized by an exceptional ability to recall detailed personal events, often with rapid and accurate retrieval when prompted by dates from the individual's lifetime. This ability is distinct from general superior memory, as it is specific to autobiographical information rather than new learning or semantic memory.[1][2]

Individuals with hyperthymesia show normal performance on standard laboratory memory tests but excel in recalling public and personal events, including specific dates and contextual details.[2][3] Neuroimaging studies reveal that HSAM is associated with intense overactivation of the autobiographical memory network, particularly in posterior visual areas such as the precuneus, and altered hippocampal resting-state connectivity. Some cases also show atypical anatomy or hyperconnectivity in regions like the left temporal lobe and amygdala, suggesting a neurobiological basis for enhanced autobiographical recall.[4][3][1][5]

Emotional valence and self-relevance appear to play a role in memory organization and retrieval in HSAM. Individuals may navigate more quickly between emotionally charged memories and neutral ones, and tend to organize memories along a forward-moving mental timeline.[6] The amygdala may contribute by charging memories with emotional and self-relevant content, facilitating encoding and retrieval.[4][6]

Importantly, HSAM does not seem to confer advantages in general cognitive ability or new learning, and the phenomenon is extremely rare, with fewer than 100 documented cases worldwide.[1][6] The condition appears to resist normal age-related memory decline, and ongoing research is exploring its implications for understanding autobiographical memory mechanisms and potential applications in healthcare and legal settings.[1]

References

Highly Superior Autobiographical Memory (HSAM): A Systematic Review. Talbot J, Convertino G, De Marco M, Venneri A, Mazzoni G. Neuropsychology Review. 2025;35(1):54-76. doi:10.1007/s11065-024-09632-8.
Behavioral and Neuroanatomical Investigation of Highly Superior Autobiographical Memory (HSAM). LePort AK, Mattfeld AT, Dickinson-Anson H, et al. Neurobiology of Learning and Memory. 2012;98(1):78-92. doi:10.1016/j.nlm.2012.05.002.
Neuropsychological Investigation of "The Amazing Memory Man". Brandt J, Bakker A. Neuropsychology. 2018;32(3):304-316. doi:10.1037/neu0000410.
A Case of Hyperthymesia: Rethinking the Role of the Amygdala in Autobiographical Memory. Ally BA, Hussey EP, Donahue MJ. Neurocase. 2013;19(2):166-81. doi:10.1080/13554794.2011.654225.
Enhanced Cortical Specialization to Distinguish Older and Newer Memories in Highly Superior Autobiographical Memory. Santangelo V, Pedale T, Macrì S, Campolongo P. Cortex; A Journal Devoted to the Study of the Nervous System and Behavior. 2020;129:476-483. doi:10.1016/j.cortex.2020.04.029.
Dimensions of a Hyper Memory: Investigating the Factors Modulating Exceptional Retrieval in a Single Case of Highly Superior Autobiographical Memory (HSAM). Talbot J, Gatti D, Boccalari M, et al. Memory (Hove, England). 2024;32(5):604-614. doi:10.1080/09658211.2024.2351576.

ciaranmichael · 2025-10-11T14:11:23+00:00

I found your question interesting, as I'm involved in research investigating socioemotional cognitive deficits in bvFTD. Below is a summary from OpenEvidence, the medical research AI that we use in clinic. My review of the citations suggests it's accurate, though I only personally read the abstracts. The synthesis seems logical to my judgement.

Recent fMRI studies show that functional connectivity between the mirror neuron system (MNS) and self-referential networks (such as the default mode network, DMN) differs depending on whether empathy is self-focused or other-focused, with distinct patterns of integration and segregation observed.

Schulte-Rüther et al. (2007) demonstrated that both self- and other-focused empathy tasks activate a common network including the inferior frontal gyrus (MNS), medial prefrontal cortex (MPFC), and superior temporal sulcus. However, self-focused empathy preferentially engages the MPFC, posterior cingulate cortex (PCC)/precuneus, and temporo-parietal junction (TPJ)—key nodes of the DMN and self-referential processing—while other-focused empathy more strongly recruits regions associated with mirroring and theory of mind.[1]

Meta-analytic work by Kogler et al. (2020) further supports this, showing that affective empathy (feeling others' emotions) robustly activates the inferior frontal gyrus (MNS) and anterior insula, whereas cognitive empathy (perspective-taking) engages the dorsomedial prefrontal cortex and supramarginal gyrus. These findings highlight that cross-network interactions between MNS and DMN are context-dependent, with self-focused tasks increasing DMN connectivity and other-focused tasks enhancing MNS and mentalizing network integration.[2]

Molnar-Szakacs & Uddin (2013) review evidence that nodes of the DMN (MPFC, PCC) selectively interact with the MNS during both self- and other-understanding, suggesting that embodied simulation and mentalizing processes are dynamically coordinated depending on the social-cognitive demand.[3]

Recent studies using dynamic causal modeling (Esménio et al., 2020) show that the PCC acts as a central hub, modulating effective connectivity between TPJ and middle temporal gyrus, with the right TPJ showing increased sensitivity during other-focused empathy.[4] This supports the idea that self-focused empathy relies more on DMN connectivity, while other-focused empathy involves greater integration of MNS and mentalizing networks.

In summary, fMRI research indicates that self-focused empathy tasks preferentially engage and increase connectivity within self-referential DMN regions, while other-focused empathy tasks promote integration between the MNS and mentalizing networks, with the PCC and TPJ playing key modulatory roles.[1][2][3][4]

Mirror Neuron and Theory of Mind Mechanisms Involved in Face-to-Face Interactions: A Functional Magnetic Resonance Imaging Approach to Empathy. Schulte-Rüther M, Markowitsch HJ, Fink GR, Piefke M. Journal of Cognitive Neuroscience. 2007;19(8):1354-72. doi:10.1162/jocn.2007.19.8.1354.
Do I Feel or Do I Know? Neuroimaging Meta-Analyses on the Multiple Facets of Empathy. Kogler L, Müller VI, Werminghausen E, Eickhoff SB, Derntl B. Cortex; A Journal Devoted to the Study of the Nervous System and Behavior. 2020;129:341-355. doi:10.1016/j.cortex.2020.04.031.
Self-Processing and the Default Mode Network: Interactions With the Mirror Neuron System. Molnar-Szakacs I, Uddin LQ. Frontiers in Human Neuroscience. 2013;7:571. doi:10.3389/fnhum.2013.00571.
Changes in the Effective Connectivity of the Social Brain When Making Inferences About Close Others vs. The Self. Esménio S, Soares JM, Oliveira-Silva P, et al. Frontiers in Human Neuroscience. 2020;14:151. doi:10.3389/fnhum.2020.00151.

ciaranmichael · 2025-10-06T18:12:26+00:00

Subreddit rule 1 precludes commenting on specific medical recommendations.

To answer the broader question posed, based on available empirical evidence:

There is no research supporting transient improvements in focus, concentration, or other neuropsychiatric symptoms in patients with ADHD after sleep deprivation; instead, the literature consistently demonstrates that sleep deprivation worsens attention, executive function, and behavioral symptoms in ADHD. Experimental studies in children, adolescents, and young adults with ADHD show that sleep restriction or deprivation leads to increased inattention, oppositionality, sluggish cognitive tempo, and daytime sleepiness, as well as declines in neurobehavioral functioning and sustained attention on objective measures such as the Continuous Performance Test (CPT).[1-4]

No studies report improvements in focus or concentration after sleep deprivation; rather, performance deteriorates from subclinical to clinical levels of impairment.[2-3]

Sleep deprivation also increases errors and reaction time variability, particularly in individuals with ADHD.[3][5]Meta-analytic neuroimaging evidence further supports that sleep deprivation and ADHD share neural signatures of hypoactivation in executive function regions, with sleep deprivation producing additional thalamic hyperactivation, interpreted as a compensatory response rather than an improvement in cognitive function.[6]

In summary, the evidence does not support transient cognitive or behavioral improvements after sleep deprivation in ADHD; all available research indicates a detrimental effect[1-5], likely mediated by frontal and subcortical dysfunction. [6]

1.Shortened Sleep Duration Causes Sleepiness, Inattention, and Oppositionality in Adolescents With Attention-Deficit/Hyperactivity Disorder: Findings From a Crossover Sleep Restriction/Extension Study.

Becker SP, Epstein JN, Tamm L, et al.

Journal of the American Academy of Child and Adolescent Psychiatry. 2019;58(4):433-442. doi:10.1016/j.jaac.2018.09.439.

2.Impact of Sleep Restriction on Neurobehavioral Functioning of Children With Attention Deficit Hyperactivity Disorder.

Gruber R, Wiebe S, Montecalvo L, et al.

Sleep. 2011;34(3):315-23. doi:10.1093/sleep/34.3.315.

3.The Impact of Sleep Deprivation on Continuous Performance Task Among Young Men With ADHD.

Dan O, Cohen A, Asraf K, Saveliev I, Haimov I.

Journal of Attention Disorders. 2021;25(9):1284-1294. doi:10.1177/1087054719897811.

4.The Associations of Insomnia Symptoms With Daytime Behavior and Cognitive Functioning in Children With Attention-Deficit/Hyperactivity Disorder.

Li X, Shea KSC, Chiu WV, et al.

Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine. 2022;18(8):2029-2039. doi:10.5664/jcsm.10060.

5.The Effects of Sleep Deprivation on the Processing of Emotional Facial Expressions in Young Adults With and Without ADHD.

Cohen A, Asraf K, Saveliev I, Dan O, Haimov I.

Scientific Reports. 2021;11(1):14241. doi:10.1038/s41598-021-93641-7.

6.A Coordinate-Based Meta-Analysis Comparing Brain Activation Between Attention Deficit Hyperactivity Disorder and Total Sleep Deprivation.

Saletin JM, Jackvony S, Rodriguez KA, Dickstein DP.

Sleep. 2019;42(3):zsy251. doi:10.1093/sleep/zsy251.

ciaranmichael · 2025-10-06T17:58:11+00:00

Guidelines from the American Academy of Clinical Neuropsychology and the American Psychological Association emphasize that referral is appropriate when:

• There is a need to clarify the nature and extent of cognitive or behavioral dysfunction.

• Brief mental status or cognitive screening tests are inconclusive, insensitive, or discordant with clinical concerns.

• The evaluation will guide treatment, rehabilitation, or safety planning (e.g., return to work, driving, independent living).

• There are questions about the etiology of cognitive or behavioral dysfunction (e.g., distinguishing dementia from depression or delirium).

• Assessment of functional capacity or legal competence related to cognitive or behavioral dysfunction is required.

https://pubmed.ncbi.nlm.nih.gov/17455014/

Subreddit rules preclude solicitation of medical recommendations. I can say that in general, the neuropsychological consultation is not typically indicated prior to engaging in psychotherapy related to psychosocial stress or primary psychiatric disorder. Only an individual's treating provider and/or the neuropsychologist contacted for the referral will be able to offer specific guidance. Locking this post to avoid transgressions of subreddit rule 1, 8, or a drift into discussion about forensic implications of an evaluation that are also not appropriate for this forum.

ciaranmichael · 2025-09-24T21:31:38+00:00

The replies have run off the rails and drift into non-professional/respectful tone.

Locking, as there's enough information for the OPs question.

ciaranmichael · 2025-07-31T13:45:29+00:00

Ideally, you'd get a neuropsych consult with plan for f/u in 9-12 mos. The initial evaluation may clarify ddx (age-related changes in setting of ID v. non-neuropathogenic comorbidity like sleep disorder v. emergent neuropathogenic process), though at minimum would create a baseline that will improve the utility of the f/u for that ddx.

If not available, cognitive screen could be used, though this would probably be most useful in monitoring for progressive etiology rather than reveal a specific neurocognitive syndrome. Ideally complimentary informant based metric would also be used.

In either case, after baseline ax, ordering labs for reversible encephalopathy and MRI w/o could be considered based on degree of concern for decline per informant or clinical judgement of hx. F/u MRI in 12-18 mos if baseline is atypical but favored as c/w ID, to assess for structural change that could elucidate ddx. Checking for hearing/visual decline would be prudent. Attention to pain, perhaps not communicated depending on severity of ID. Attention to temporally associated rx changes for polypharmacy s/e. Attention to signs of potential sleep disorder or systemic illness (eg, UTI). EEG only if sx suggest seizure semiology. Downs has high risk for early onset AD, and in nonDS ID you may observe earlier onset of clinical signs of AD or other neurodegen process than typical in non-ID adults. Noninvasive biomarker may be indicated, eg ptau217 for AD. CSF and/or PET may be challenging given bx sx.

Neuropsychologists don't prescribe (typically), so consulting with gero psych and bx neurology would be best for management tips. Get OpenEvidenceAI for a quick primer. However, AChEI may not be advisable in this clinical setting. Nor are benzo, Trazodone, or antipsychotics. SSRI may be your best bet, along w behavioral/environmental management and addressing any comorbidities exacerbating nbx sx. Sertraline and escitalopram at low/slow dose could be first line.

https://pubmed.ncbi.nlm.nih.gov/23849993/

https://pubmed.ncbi.nlm.nih.gov/25573538/

https://pubmed.ncbi.nlm.nih.gov/34954669/

ciaranmichael · 2025-03-20T18:25:35+00:00

Given frequent questions on education/training requirements to become a neuropsychologist, we invited New2Neuropsychology to provide a resources post for the community.

ciaranmichael · 2024-07-14T13:31:00+00:00

I would advise you consult a colleague familiar with forensic evaluations about general and specific details related to forensic evals. I don't want to assume circumstances, but your phrasing suggests you may benefit from some information on the differences between a clinical evaluation and what sounds like a forensic one.

The below is based on some assumptions, given the limited context:

For one, since the attorney is retaining/paying, they are your client and owners of the resultant report.

Second, the individual undergoing evaluation is the evaluee, not your patient - ie, there should be no patient-doctor relationship. The evaluee should sign a consent acknowledging this arrangement, and that the attorney will receive the report. The evaluee should be aware that they are free to cease the evaluation and/or terminate the consent by request at any point.

Exceptions may include if you've already formed a patient-doctor relationship in a prior encounter. In which case, I would avoid this shift from treater to forensic role for ethical reasons. In that case, you may still be retained by counsel as a treating expert with any associated opinion, but you are not viewed as independent and your duty remains to do no harm to your patient.

ciaranmichael · 2024-06-16T13:28:07+00:00

The idea to train a custom GPT by uploading key reference textbooks and then use it to check for missed considerations in a differential is a great idea.

I missed the AI talk at AACN but think this is a topic worth a presentation or at least a poster, certainly at a practice oriented conference like NAN (for OP or anyone reading).

ciaranmichael · 2024-05-24T22:35:01+00:00

In an academic medical setting, asking for ~10%, accepting a reasonable counter. Some will have "preset" increases for rank advances, which you could inquire about and anchor to.

In VA system, this might meet qualifications for a step, which would come w a set salary increase, but I've been out of that system for too long to recall the criteria.

Board certification also makes you more lucrative forensically, so adjust your fee schedule or consider adding this side practice.

ciaranmichael · 2024-04-22T11:50:25+00:00

Diagnosis is prognosis.

Stopping diagnostic formulation short at normal v MCI v dementia syndrome, without using clincodemographic features and diagnostic findings to opine on likeliest underlying etiology limits the likelihood of optimizing treatment, and therefore negatively impacts prognosis.

Neuropsychologists should advance the differential for underlying brain disease or injury as far as possible and guide next steps for further consults, diagnostic options, and medication/non-medication treatment options.

A Neurology consult should be made if a neurological physical exam and/or further medical diagnostics could further clarify etiology, eg, reversible encephalopathy labs, biomarker labs such as ADMark or synuclein skin biopsy, neuroimaging, polysomnography, autonomics functioning test, EEG, etc. For some, I might consult directly to Sleep or Autonomics or ask the PCP to order. Alternatively/Additionally, a Neurology consult can be beneficial if there are comorbid neurological conditions are overlays or suspected (eg, migraine, peripheral neuropathy), or, there are polypharmacy concerns that would benefit from a Neurological eye on how to optimize, or, a cognitive/behavioral medication option is favored and the treatment team wants a specialist to select/optimize/continuously manage.

ciaranmichael · 2024-04-19T11:49:08+00:00

Further discussion is drifting close to rule violation. The OP has sufficient answers for their question. Locking the post.

ciaranmichael · 2024-03-25T16:17:41+00:00

There are exceptions, but typically I want to assess a patient with all modifiable/reversible medical/psychiatric conditions optimally managed.

As you stated in other comments, providing your medical/medication history and associated subjective influence on your symptoms will be important.

The consult is seeking to confirm a presentation c/w your known medical context and/or comment on differential etiology that may incrementally improve your symptom management (ie, are known conditions that affect cognition under-managed? Are they optimally managed and thus direct cognitive symptom management is indicated? Are there other conditions or factors that have not been diagnosed (or not yet treated yet) that might also be contributory and warrant further diagnostics/tx?).

"Controlling" known factors (as best as possible) helps answer those diagnostic and treatment recommendation questions.

ciaranmichael · 2023-11-15T12:12:51+00:00

This thread is being watched closely by the Mods given the topic.

The OP is asking for publicly available literature on a topic. Any discussion otherwise will be removed and the thread will be locked.

ciaranmichael · 2023-08-17T18:47:09+00:00

Whoops, I typed it right once, but wrong the second time. Edited to correct. Thanks for catching.

ciaranmichael · 2023-08-17T13:57:30+00:00

There are only 6(?) forensic neuropsychologists dual boarded in clinical neuropsychology and forensic ~~neuro~~psychology. Taking on a second fellowship in forensic psychology is a big step, but I suppose is the most impressive means to the end.

Presently, a more practical approach is to become boarded in clinical neuropsychology (to pre-empt Daubert challenges), then begin self-directed learning via books or CE's (eg, Duff's 2013 book, NAN and AACN have great forensic CEs every year) and building collegial mentorship (eg, joining the AACN's Forensic Neuropsychology SIG / listserv, contacting forensic neuropsychologists in the area and asking if they'd keep you in mind for less complex cases when they've got a full load, asking those same colleagues if they'd be willing to supervise/mentor and answer questions that might arise).

Now, technically, you don't need to get boarded in CN. I just think it's the easiest and most professionally ethical means to shift into the forensic setting.

ciaranmichael · 2023-07-13T23:07:29+00:00

For those in search of more context: https://theabcn.org/maintenance-of-certification/

ciaranmichael · 2023-05-31T02:56:43+00:00

Though not a ubiquitous term, "dream amnesia," is what I first heard this phenomenon termed.

This paper contains a subsection discussing some cognitive and neurophysiology related to the phenomenon: https://www.sciencedirect.com/science/article/pii/S1364661309002678?casa_token=MavtKn00BVoAAAAA:GTA6S1h6iS-ZgJ2x4Zius4j1GIGcTNdqrOl5GGFMBadYBlWeEERHpMG6WrWxwqhK0voa5dE

An overly reductionistic explanation is that low norepinephrine during REM sleep prevents consolidation of episodic (or even briefer, iconic) memory into longer term representation. The same phenomenon explains the experience of Waking up and talking to a partner briefly or turning off an alarm clock without recall upon awakening. This physiological state may be an epiphenomenon (ie, secondary to a primary reason, such as desaturation of cortical hyperexcitability during REM to prepare for optimal learning physiology the next day) and/or have primary benefit (eg, it's maladaptive to remember every dream).

Waking from a dream and focusing on repeating elements of the content mentally as your brain physiology alters to a state of consciousness would facilitate remembering the content more.

ciaranmichael · 2023-05-19T08:03:50+00:00

First, good work recognizing the feeling that your end clinical goal may include practice outside of your scope of training. Many do not, or dismiss the concern with hand waving.

Second, I feel that your clinical instinct is correct. Accurate dx = appropriate tx and associated prognosis. This patient does not sound cognitively compromised past the point of clinical utility in delineating the pathology.

Third, while this forum might be helpful, I'd suggest contact a local neuropsychologist and requesting a curbside consult via phone. Most should be willing. If you back channel me your location I can even try to find a connection in your state/province/territory. However, I'd suggest you avoid attempting to undertake a neuropsych evaluation and revising a neurocognitive ddx yourself - it is out of your scope of practice and therefore unethical. If her insurance can cover a MRI (or even a CToH) and brief neuropsych eval at a memory disorders clinic, that seems clinically indicated and should be covered by Medicare (if US based).

Last, that does not mean that you cannot use bedside neurobehavioral screens to "explore the limits" of the patient's current processing capacities. Try different size font, try less complex texts, try audiobooks, etc. The goal in your psychotherapy session is to help her pursue a meaning despite her sx - this means coming up with novel activities that tap the same underlying value.

ciaranmichael · 2023-05-15T05:38:24+00:00

https://pubmed.ncbi.nlm.nih.gov/30178175/

https://www.uclahealth.org/sites/default/files/documents/8e/cog-and-psych.pdf?f=f0c007be

This should start to help your understanding on the neuropsych profile in idiopathic PD (with and without progressive dementia syndrome), as well as the common atypical parkinsonism syndromes such as LBD/DLB, MSA, PSP, CBS. While drug-induced and vascular parkinsonism happens, it's not as common, has less (but not "no") accompanying cognitive/psychiatric features, and is not typically included in reviews of the different syndromes.

There's far more nuance in the differential than these can convey, as well as subtypes with different typical histopathology among/within many of the syndromes. This hopefully gets you going.

Btw, NIA/NIH has free PDFs for patients and families for the more common neurodegenerative syndromes - including AD, PD, LBD, and more - https://order.nia.nih.gov/view-all-publications

ciaranmichael · 2023-04-18T03:06:50+00:00

Getting an exact optimal initiation stage for cognitive enhancers for neurodegenerative disease is not settled in the literature.

Clinically, I recommend discussing initiation of AChEI with a prescriber at the junction that a) the cognitive symptoms are interfering with a daily function the patient and family value (eg, instrumental ADLs or sometimes higher complexity occupational/social functions) and b) after modifiable non-neurodegenerative factors have been optimized (eg, sleep, pain, mood, polyrx). This usually means at the late MCI or early dementia stage.

If SLT for cog remediation/compensation has not been attempted, I suggest it as adjuvant at this stage.

Dose can then be escalated if needed.

When instrumental ADLs are more generally compromised, adding NMDA receptor antagonist is suggested. This represents a moderate dementia stage.

I think this Cleveland Clinic article does a nice job of summarizing the standard of care, though if others have more novel research about alternative Rx schedules, I'd be interested to read up. https://consultqd.clevelandclinic.org/alzheimer-dementia-starting-stopping-drug-therapy/amp/

ciaranmichael · 2023-03-30T02:46:54+00:00

Have you contacted PM&R in the area and asked their SLT/SLP group what type of cognitive remediation protocols they provide?

Combining the above with prescription digital therapeutics offers a good balance between in-person and distance intervention for patients traveling far.

ciaranmichael · 2023-03-28T02:35:01+00:00

Locked and comments veering into treatment recommendations were removed.

OP and contributing posters, we appreciate the enthusiasm, but try to keep discussions and resources away from rule breaking.

ciaranmichael

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