#pd subtypes

[discountdyke]

its crazy that people think having multiple personality disorders makes you more dangerous or fucked up bc like, the more abuse and trauma you suffer as a child, the more symptoms of PDs you will check off bc your behavior becomes so disordered in order to survive. having more than one PD (having several PDs) is common among childhood abuse survivors. PD comorbidity is crazy high and, ultimately, PDs are a way of categorizing symptoms for diagnostics and treatment.

it has nothing to do with your character, your worth as a human being, and your ability to heal. you adapted to survive your abuse. you can adapt to survive life after it.

[avpdpossum]

i might try to do a deep dive into the conflicted avoidant subtype at some point, and maybe the self-deserting subtype after that. every time i read the descriptions of them, i’m struck by how accurately they describe me, and i wish there was more info about the subtypes out there

[hauntedselves]

Clinical Formulations of Narcissistic PD

Clinical formulations and case conceptualisations are introduced in this post.

These are all generalisations and theories of how NPD develops, not something that is supposed to be true for everyone with NPD.

Psychodynamic model

Freud suggests parents either overvaluing or neglecting (or both) a child can lead to NPD & especially inability to form healthy, lasting relationships and regulate self-esteem

"In other words, [NPD] is the outcome of insufficient gratification of the normal narcissistic needs of infancy and childhood."

Kohut theorises that narcissists' ability to form a cohesive sense of self and others was developmentally arrested in childhood, resulting in grandiosity & idealising others

"Narcissistic injury" = fragmentation of the self

Kernberg suggests grandiosity & exploitation result from maternal emotional abuse

Grandiosity is an "emotional escape valve"

Grandiosity & entitlement mask the "real self" that is "split off"

The real self unconsciously holds rage, fear, envy, deprivation

Defensive structure is same as BPD but difference is grandiosity

Biosocial model

NPD is primarily the result of environment, especially "parental indulgence and overvaluation, learned exploitive behavior, and only-child status"

Special treatment from caregivers leads children to believe that the "world revolves around them", and therefore they expect the same outside the home

When special treatment outside the home doesn't happen, they "experiment with demanding and exploitive tactics and subsequently develop considerable skill in manipulating others"

"At the same time they come to believe that most others are inferior, weak, and exploitable."

NPD is self-perpetuating through sense of superiority, lack of self control, sense of entitlement, and dismissing of those who reject their world / self-view

Cognitive-Behavioural model

Key feature of NPD is self-aggrandisement

Core beliefs:

> Deserving of special treatment

> Not bound by social norms and rules

Conditional beliefs:

> Others should be punished for not recognising their specialness

> To maintain that special status others should be subservient to them

Instrumental belief:

> Always strive to demonstrate their superiority

> See themselves as special, superior, entitled to special favors and treatment, and vulnerable to loss of status

> View others as inferior but potential admirers

Main pattern of behaviour is "seeking prestige, power, position, and wealth as a way of reinforcing their image of superiority", using "manipulation and guile" if necessary

The primary schema is superior & special (/ entitlement & grandiosity)

> Superior schema "shaped by flattery, indulgence, and favoritism"

> Special schema shaped by "rejection, limitations, exclusion, or deficits"

> Common denominator is the belief that the individual is different in some way

Three subtypes:

> Self-centered impulsive type

> Ruthless impression-management type

> Acceptance-oriented impression-management type

> Each type is centred around an impulse control deficit developed in childhood

> "Specifically, these individuals learned to seek reinforcers without having to work for them. This resulted in their development as self-indulgent, egocentric, and impulsive individuals."

> Ruthless & Acceptance-oriented types focus on creating favourable impressions with others, but struggle with long-lasting healthy relationships because of their empathy deficits

Interpersonal model

People with NPD were raised in an environment of "selfless not contingent" love, leading to insensitivity to others' needs

The caregiver was over-adoring, but there was also a constant threat of a "fall from grace", with pressure to be the perfect child

The constant overbearing love means that any criticism or disappointment hits very hard

"In short, there is extreme vulnerability to criticism or being ignored, together with a strong wish for love, support, and admiration from others. Noncontingent love and presumptive control of others is expected and even demanded. If support is withdrawn, or lack of perfection is evident, the self-concept degrades into severe self-criticism."

Integrative model

People with NPD are hypersensitive

Seen as exceptional children, leading to pressure to perform

As children likely had highly developed speech and interpersonal skills

Life purpose: "I’m special and unique, and I am entitled to extraordinary rights and privileges whether I have earned them or not."

World-view: "Life is a banquet table to be sampled at will. People owe me admiration and privilege."

Goal: "Therefore, I’ll expect and demand this specialness."

Defense mechanisms: rationalisation and projective identification

Parental injunction: "Grow up and be wonderful—for me."

"The illusion of specialness, disdain for others’ views, and a sense of entitlement lead to an underdeveloped sense of social interest and responsibility. This, in turn, leads to increased self-absorption and confirmation of narcissistic beliefs."

- From Sperry, Handbook of Diagnosis and Treatment of DSM-5 Personality Disorders (2016)

[mr-nauseam]

Okay okay I saw ur Avatar/ TBOSAS crossover in the tags of a post on ur dash annnnnddddd!!!!! I love ATLA and LOK so so much, so I was wondering what type of benders you think TBOSAS characters would be? Love u Ika💕

Hiii bby graceee!!! Thanks for the ask. IM SO GLAD U LOVEEE ATLA AND LOK TOO. THEY MEAN A LOT TO ME WHEN I WAS A BABY AND I STILL HOLD THEM CLOSER MY HEART SO IM GIGGLING.

Lok in particular. Not to be controversial and while Im well aware of the writing flaws I do like lok better but Im biased bc I was a Korra fan. Nobody cant convince me theres something wrong with her bc thats not true. Yk considering that was my first real fandom experience... Why I am surprise of be a Sejanus fan? He and Korra got NOTHING IN COMMON except suffer more than jesus and be deeply hated by the fandom but maybe thats my type of characters...

ANYWAY. I will go mostly by the vibes - personality. Lets ignore a bit the worldbuilding and I will go by what I call in my head TBOSAS mains thats Snow, LGB, Sejanus and MARCUS. YES BC THESE TWO ARE THE MOST RELEVANT MENTOR / TRIBUTE DUOS IN TEXT.

So to me they are THE TBOSAS MAAAINS!!!

Coriolanus.

I know his last name its SNOW and I mean water can be very lethal and evil. All that shit of BLOOD control but thats too cool for them and its FUNNIER IF HES SNOW BUT GOT FIREBENDER... And in general I think fit him.

Coriolanus give to best or worst Azula vibes (I think its the mommy issues and power hunger), he fit so well that hardwork and insane control in firebender that still can be break easily. His unstable ass would crash out to the most violent expressions of fire, if hes suffering an episode yk.

Pd: Funny idea. Ozai=Crassus. Zuko=Tigris. Azula=Worm.

Lucy Gray.

I think its air. Not neccesary she would come from the same culture than Aang for example but giving her an element just bc then air its so her in a way. The freedom vibe, the fact air tend to allow u lot of advantages to travel, and runaway. Even from a music -enterteinment aspect, would be useful, air ask too the person its not a control pyscho to them be able to bender it, it need some let it go and let the air guide you. Also I think air got this thing of airbenders are usually underestimate like "oh they are all with such a weak or inoffensive bender" but like no, air CAN DO SOME THREAT UNEXPECTED SHIT.

And thats very her me thinks.

Sejanus.

This one was hard but I think for the contrast and some particular subtype of bender of this element. Im making him a waterbender. Yes this mostly for them being able to heal but thats like so Sejanus its hard to ignore yk. And I think in general its his vibe because water its usually a comfy thing if u get me, water can be so nice amd allow lot of ways it can be used to help others but at the same time water its a bit tricky.

I feel like water its all into drawn their own benders. Need a lot of equilibrium that can go wrong for you if u arent careful also coming back abt the blood aspect, thinking in ice and other expressions, it get some dangerous potential that usually its never exploted bc most of time waterbenders hold a lot of self control and fear to harm others.

Bc unlike the case of air people do expect waterbenders CAN fight and thats an interesting thing for a character like Sejanus. He can fight back but not too much by fear of hurt others or do a worst damage and focusing on healing - what do to help others.

Marcus.

Now people will say or believe it was on purpose give each one an element. Its not. It wasnt on purpose but like to me it only made sense earthbending. I think earthbender in general got many nice things we can relate to d2, like we remember the thing of the minerals? If Im not wrong. We know d2 got the quarrys and if I remember well we see many people in earth kingdom doing construction stuff also metal bending. Its too a d2 thing and thats a nice summary to which I can explain bc Marcus its very a son of his home.

In my head hes very practical (like Sejanus its thinking how do something in the most complicate way and Marcus need bonk him BC YOU CAN LITERAL JUST DO THIS??) and a quick thinker. That are like things I believe identified a lot the earthbenders. Also this aspect of strong, defensive fight style. They arent like attacking people as their only way to win a battle like firebenders, they tend to be as far I remember very defensive, like doing shields to avoid the attacks and so.

Too similar to water I think earth its a element it bender can be used a lot to help others or protect others! Thats very Marcus too in my head.

[bonefall]

are there any bb!cats with schizophrenia or that regularly experience psychosis? people absolutely suck about mental illness so like. seeing characters like me going thru life and being treated like people and not monsters for something out of their control never fails to put a smile on my face! thank you for all the research and effort you put into making sure your disabled cats are not only believable but human. pd: cinderheart with bpd is an extremely based headcanon

Not yet but it's on my radar, plus NPD. The reason why I feel so unflappably confident with BPD is because I know and love people who have it, and I hate that I don't see any characters who are like them! So I feel like I'm really good at handling it, and knowing what's wanted in portrayals of it. It feels very personally important to me.

Pair that with the fact I write BB!Clans as canonically struggling with ableism and all these being so heavily stigmatized irl, I've gotta be REALLY careful with NPD and psychosis. I'm less connected to them so personally and I don't want to accidentally strike a nerve, you get me?

That said... I got an ask a while back that I'd been thinking about a lot, basically asking me about how Clan Culture would see psychosis in the first place. I've actually always been fascinated by how deeply schizophrenia is affected by the culture of the afflicted, so I've been idly thinking about that for a while without sharing those thoughts.

OH WAIT hangon let me explain some stuff about Schizophrenia and psychosis for people in the audience!!

Schizophrenia used to be diagnosed in subtypes before 2013. This is no longer accurate! A lot like Autism, it's a spectrum of symptoms that affect people differently. It's a cognitive disorder that messes with rational and organized thinking, and that can express in all sorts of ways.

One of the symptoms is hallucinations. It's The Famous symptom of it, but it's not actually something you NEED to have to be Schizophrenic. Not all people who are having hallucinations or delusions are Schizophrenic, either! I want to include an OCD character of some kind who experiences some mild auditory hallucinations, actually. The type where it's just random mumbling.

Delusions and hallucinations aren't the same thing Delusions are false beliefs and hallucinations are false experiences. An example of a delusion is, "If I don't click my pen three times, my family will die." An example of a hallucination is hearing voices.

PEOPLE WITH PSYCHOSIS ARE FAR MORE LIKELY TO BE THE VICTIMS OF VIOLENCE THAN TO COMMIT IT Feel like this is common knowledge in this space, and especially within my own following since I make a lot of art about mental illness and awareness, but it's always worth repeating.

So anyway

If you compare psychosis between cultures, you actually end up seeing VERY different expressions of the hallucinations. For example, in some cultures, voice hallucinations tend to say things that are negative or abusive, while other cultures hear significantly more positive, playful voices.

This doesn't mean that they're always less distressing. For example, the study above points out that Nigerian students (reported to hear lots of playful hallucinations) experience as much distress as Dutch students (tend to experience negative, abusive voices) during their psychotic episodes.

Still, there does seem to be a correlation with "less distress" and cultures that encourage psychotic people to see their hallucinations as positive, personal things. Even more interestingly, distress seems to be correlated with income and individualism in a culture.

But it doesn't stop there, the findings are fascinating.

Delusions of grandeur are rare in societies that discourage that sort of social mobility, reflecting social values.

Cultures that believe religious experiences are specific experiences-- like certain smells, temperatures, or sounds, will see those reflected in psychotic episodes

Yet, "voices" seem to be something seen across ALL cultures studied. Though some have more prevalence of random sounds and mumbling than others, they all share some expression of "voices that say stuff."

SO all that to say-- if I include psychosis it's definitely going to be trying to take the culture of each Clan into account, and I need to do a lot more research into what sorts of things people with schizophrenia and various types of psychosis want to see more often.

[mischiefmanifold]

How Do My Autism, PDs, and DID Interact/Intertwine?

Disorders mentioned in this post: autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD), tourette syndrome (TS), fetal alcohol spectrum disorder (FASD), dissociative identity disorder (DID), antisocial personality disorder (ASPD), narcissistic personality disorder (NPD), and schizotypal personality disorder (STPD)

(This post was requested by a mutual, I hope you find this (somewhat) helpful and I apologize for taking a million years to post it 🙃)

I have a whole host of disorders, pretty much all of which affect my personality, identity, and way I interact with the world around me. A lot of people look at the combinations of disorders I have and tell me I can't possibly have them (this is especially popular with autism and ASPD, as well as autism and STPD), when I do in fact have them and they suck ass.

To begin with, since I have DID, my other disorders vary drastically in symptoms from alter to alter. It is important to note that individuals with DID will likely only be diagnosed with other disorders alongside DID if most or all of the frequently fronting alters show symptoms and those symptoms impair the whole. Disorders like autism, Tourette, ADHD, and FASD are system-wide disorders due to the nature of their development. Personality disorders are usually diagnosed at the discretion of the therapist or psychiatrist who is doing the diagnosis.

My combination of autism, NPD, and ASPD resulted in an individual who lacks essentially all empathy, is very isolated, and is really sensitive to perceived slights or criticisms.

I have the psychopathic subtype of ASPD, which means that even if I didn't have NPD I would have narcissistic traits. Alongside heightened NPD traits, I am also more prone to violence and aggression (it is important to note that most psychopaths and individuals with ASPD are not criminals or extremely aggressive). Features of psychopathy that I display are typical antisocial behaviors (disregard for societal norms and rules, essentially), increased aggression and violence, lack of empathy and remorse/guilt, and manipulative and deceitful behaviors.

When it comes to autism and ASPD, the only real trait my presentation has in common is a lack of empathy. Communication problems can arise for individuals who have both disorders, but for different reasons (my ASPD communication problems are almost exclusively related to my disregard for others and lack of remorse; while my autistic communication problems stem from a fundamental misunderstanding of social norms, sarcasm, facial expressions, gestures, and figurative language). Individuals who have ASPD will not experience any developmental delays like autism (delayed speech, social ineptitude, etc.).

My ASPD and NPD go hand-in-hand pretty well. The earliest memory I have of exhibiting antisocial behaviors is at age 8 when I would repeatedly steal candy from my friend's school locker because I felt I deserved it more than her; the theft just escalated from there. I was very good at getting people angry with me so I could take out my anger on them.

I don't feel that my autism and NPD really have that much in common, honestly.

If you would like to learn more about ASPD, its history, and the psychopathic subtype of ASPD, please visit this site: https://psychopathyis.org/what-is-a-psychopath/

[innonurse]

University of Florida develops AI-powered MRI tool to improve Parkinson’s diagnosis

- By InnoNurse Staff -

University of Florida researchers have developed Automated Imaging Differentiation for Parkinsonism (AIDP), a machine-learning method using MRI to accurately distinguish Parkinson’s disease (PD) from atypical parkinsonian disorders such as multiple system atrophy (MSA) and progressive supranuclear palsy (PSP).

In a multicenter study involving 249 prospective and 396 retrospective cases, AIDP analyzed diffusion MRI data from 132 brain regions, achieving 96–98% accuracy in differentiating PD, MSA, and PSP. 

Compared to traditional clinical methods, AIDP improved diagnostic accuracy by 12.3%, reaching 93.9% accuracy against autopsy-confirmed cases. 

Its non-invasive, scalable approach could enhance clinical care and complement existing biomarkers.

Image: Automated Imaging Differentiation for Parkinsonism (AIDP) for the precise classification of parkinsonism subtypes. Credit: JAMA Neurology (2025). DOI: 10.1001/jamaneurol.2025.0112.

Read more at Tech Xplore

///

Other recent news and insights

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Polish healthtech company Jutro Medical secures €12M to develop its telehealth platform (Tech.EU)

[jcsmicasereports]

Giant Cell Tumor of the Infrapatellar Fat Pad of the Knee: A Case Report by Ahmad Jiblawi in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Giant Cell Tumor is a rare benign soft tissue tumor occurring in two forms: localized and diffuse. The two subtypes differ in their location at presentation, shape, recurrence after treatment and prognosis. MRI is still essential in the diagnosis, however pathology remains the gold standard for the final diagnosis. In this article, we report a case of Giant Cell Tumor involving a very rare location with very few reports in the literature; the infrapatellar (Hoffa’s) fat pad of the knee. We discuss its keen clinical and radiological features. The tumor was managed with arthroscopic resection. Confirmation of the diagnosis was done by pathology. Our case is the first to be reported in Lebanon.

Keywords: GCT; Hoffa’s fat pad; STIR

Introduction

First described by Chassaignac in 1852, Giant Cell Tumor (GCT) is a benign soft tissue tumor [1]. It is a rare disease, associated with synovial inflammation due to hemosiderin deposition. GCT occurs in two forms: localized GCT and diffuse formerly known as pigmented villonodular synovitis. The former typically consists of small well circumscribed, nodule or pedunculated mass that might be intra- or extra-articular, most commonly (85%) in the small joints (ex: hands and feet) while the latter is typically intra-articular with an infiltrative growth pattern commonly occurring in large joints (ex: ankles and knees) [2–4]. Both share similar histologic features; however they have different biological behavior, treatment outcome and prognosis. Thus the importance of differentiating between the two entities [5,6].

MRI is considered essential for the diagnosis, staging, preoperative planning and clinical follow-up of GCT. The mass appears of iso/low signal intensity on T1 and T2 weighted images. In addition to joint effusion and synovial proliferation. Some “blooming” artifact of low signal might be noted on echo-gradient because of the magnetic susceptibility from hemosiderin deposition [1,2].

In this article, we report the first case in Lebanon (to our best knowledge) of a rare, localized Giant Cell Tumor originating in the infrapatellar (Hoffa’s) fat pad, emphasizing on its radiologic manifestation.

Case report

We report a case of a 35-year-old gentleman, previously healthy, complaining of a 4-month history of recurrent and painful left knee locking. The patient denies any trauma, any recent surgery, no accompanying systemic symptoms as of fever, rash, diffuse arthralgia, or myopathy. His presentation was mimicking that of a meniscal tear injury.

An MRI of the left knee was performed using 1.5 Tesla Philips Ingenia Unit, manufactured in the Netherlands. The following planes and sequences: A sagittal T1 weighted (T1W), proton density (PD) and STIR image, a coronal STIR and an axial STIR image. Result showed the presence of a soft tissue-like lesion arising directly anterior to the anterior cruciate ligament in between both femoral condyles estimated to be 3 cm in its transverse diameter, 2.7 cm in its antero-posterior diameter and 1.2 cm in its supero-inferior diameter. The lesion showed iso-intensity to the cartilage on T1W as well as on PD but showed an increase signal intensity on STIR weighted images. The lesion relaxes directly on the ACL posteriorly which is of adequate continuity and signal. Minimal associated excess of joint fluid filling the supra-patellar bursa. Both menisci, anterior cruciate ligament, posterior cruciate ligament and  medial and lateral collateral were normal. No capsule-meniscal separation is seen. The overall radiologic impression was for a Cyclops lesion or a soft tissue tumor such as Giant Cell Tumor.

The patient underwent an arthroscopic excision of the soft tissue tumor. Procedure went uneventful. The tissue was sent to pathology. Microscopic examination showed fragments of fibrous tissue involved by sheets of fibro-elastic to epithelioid cells with band nuclei and moderately abundant cytoplasm. They are intermixed with osteoclast-like giant cells and foamy histiocytes. There was no evidence of malignancy. Findings suggestive of Giant Cell Tumor of the Tendon Sheath. Unfortunately, the patient was lost to follow up, thus recurrence could not be reassessed.

AT1 weighted image, sagittal plane: showing a soft tissue-like lesion iso-intense to the cartilage measuring 2.7 cm in its antero-posterior diameter relaxing directly on the anterior cruciate ligament posteriorly which is of adequate continuity and signal B: Proton density weighted image, sagittal plane: showing a soft tissue-like lesion iso-intense to the cartilage measuring 2.7 cm in its antero-posterior diameter relaxing directly on the anterior cruciate ligament posteriorly which is of adequate continuity and signal.

C: Short T1-Inversion Recovery weighted image, sagittal plane: showing a hyperintense soft tissue-like lesion measuring 2.7 cm in its antero-posterior diameter. D: Short T1-Inversion Recovery weighted image, coronal plane: showing a hyperintense soft tissue-like lesion measuring 1.2 cm in its supero-inferior diameter. E: Short T1-Inversion Recovery weighted image, transverse plane: showing a hyperintense soft tissue-like lesion measuring 3 cm in its transverse plane.

Discussion

Giant Cell Tumor is a rare benign soft tissue tumor arising from the synovial tissue of the joints, tendon sheath, mucosal bursas, and fibrous tissues adjacent to tendons. Multiple terms are found in the literature to describe this entity; pigmented nodular tenosynovitis, fibrous xanthoma of synovium, benign synovioma, xanthogranuloma and tenosynovial giant cell tumor [1]. Etiology and histiogenesis of which is not completely understood, but many risk factors were mentioned in the literature such as trauma, infection, vascular abnormalities, lipid metabolism disorders, osteoclastic proliferation, and immune system disorders. It can present in two forms: localized and diffuse [3,7]. Localized GCT presents mainly in small joints (85 % observed in fingers while 12% is observed in large joints, GCT in the knee is rare) [4], either intra-articular or extra-articular. Diffuse form occurs mainly in the extra-articular space [8]. However, extra synovial soft tissue forms of localized GCT are very rare and mainly concern the knee joint. Around 50% of patients with a localized GCT arising primarily within the infrapatellar fat pad have a history of trauma but the exact etiology is still unknown [9]. The onset age of localized GCT is older than that of the diffuse type (i.e. localized type usually occurs above 40 years of age)[10]. When affected, patient presents clinically with mechanical derangements, progressively worsening over time. Meniscal symptoms and locking are often present within the knee joint. The main symptoms are swelling (86%), pain (82%), stiffness (73%), limited range of motion (64%) and joint instability (64%) [7,10].

MRI is an effective and highly sensitive diagnostic tool; however pathology is still the gold standard of final diagnosis. On T1 and T2 weighted images, dense collagen and hemosiderin presents with homogenous low or intermediate signal. The most typical feature of a localized GCT is a well circumscribed, nodular mass with low signal intensity on T1, T2 and proton weighted images and high signal intensity on STIR images [4,6,9,10]. Microscopically, GCT is characterized by multinucleated giant cell, lipid-laden macrophages, hemosiderin deposition and fibroblast proliferation [5].

Various pathological conditions should be considered in the differential diagnosis, for example: Synovial Chondromatosis, Cyclops lesion, Rhabdomyosarcoma, Fibroma of tendon sheath, Synovial Sarcoma, Amyloid Arthropathy, Haemophilic Arthropathy, Lipoma Arborescens and Rheumatoid Arthritis [6,9].

The ability to differentiate between the diffuse and localized forms of GCT is paramount to give patients a realistic outlook on future prognosis, chance of recurrence and optimal treatment course [5]. Several treatment options are present: surgery, radiotherapy, pharmacology or a combined solution of the listed methods. Important to note, local recurrence after treatment was reported in 18-46% of cases. However, this might be linked to incomplete resection of satellite nodules in the area of initial change. Other risk factors for recurrence are the location of the disease (more common in the knee), history of previous surgeries and positive surgical margins.

Conclusion

To the best of our knowledge, our case is the first to be reported in Lebanon. It is very rare to have a localized GCT in the extra-synovial infrapatellar (Hoffa’s) fat pad of the knee. The rarity of the presented case suggests that GCT should be considered in the differential diagnosis of a painful knee locking in a young patient. Accurate diagnosis will lead to successful treatment associated with low recurrence rate resulting in a better patient outcome.

Conflict of Interest:

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article

[avpd-polls]

[hauntedselves]

hi, do you have any sources on how to differentiate between AvPD and covert NPD? i tried to look it up myself, but everything i find is just “yeah they are similar except npd is evil”

Here's what Millon says about his "Compensatory Narcissist" subtype, which is NPD with AvPD (& Passive-Aggressive PD) features:

"The early experiences of compensating narcissists are not too dissimilar to those of the avoidant and negativistic personalities. All have suffered “wounds” early in life. Rather than collapse under the weight of inferiority and retreat from public view, like the avoidant, [...] the compensating narcissist develops an illusion of superiority. [...] Like avoidant personalities, compensating narcissists are exceedingly sensitive to the reactions of others, noting every critical judgment and feeling slighted by every sign of disapproval. Unlike avoidants, however, they seek to conceal their deep sense of deficiency from others and from themselves by creating a façade of superiority. Though they often have a degree of insight into their functioning, they nevertheless indulge themselves in grandiose fantasies of personal glory and achievement. Some procrastinate in doing anything effective in the real world for fear of evaluation. Instead of living their own lives, they often pursue the leading role in a false and imaginary theater unrelated to the real world. When threatened with reality, they may defend themselves by becoming more and more arrogant and dismissive until the offending stimulus withdraws. If reality overturns their illusion completely, compensating narcissists may retreat more and more into an imaginary world of others who recognize their supposed accomplishments."

Summary: NPD's primary defence is a façade of superiority; they don't withdraw / avoid. AvPD's primary defence is withdrawal / avoidance; they don't feel or project superiority.

Here's a reddit post where someone was asking this question, and here's Elinor Greenberg's summary of covert narcissists, which may be helpful.

[variant-archive]

i've been scrambling to find flags/terms relating to all types of adhd, the same way ive seen a ton of flags for different ocd types/subtypes, same for other disorders (npd, specific delusion types, etc) i feel like it'd be great for people to have flags they can use to specify theyre type! if you could help find something like that id absolutely love it... /not forced

As far as being recognized by psychologists and co., there's only the three subtypes (primarily hyperactive, primarily inattentive aka me, and combined). There's also cognitive disengagement syndrome (formerly sluggish cognitive tempo) which is another attention disorder but not exactly an ADHD subtype, more like a parallel disorder of attention. My OCD subtype flags have all been subtypes that are recognized by clinicians so far. They can be found on NOCD which is a treatment and info site for OCD. There are also clinically recognized subtypes for personality disorders and delusions which is probs what you've seen flags for (although I have seen some PD "archetype" terms/flags but I consider that different from a subtype and more of a way to express yourself than describe symptoms, totally valid though).

That being said I think creating unofficial subtypes of existing conditions is... probably fine? Definitely better than straight up MUDs (for those who haven't gone into radqueer rabbit holes out of morbid curiosity, that means people making up entirely new disorders without any basis in science or any research or anything). But subtypes of existing conditions isn't a thing people besides those in the field of practice are doing yet afaik. I've considered doing this for OCD myself because obsessions and compulsions can be about anything so any number of subtypes exist as long as someone experiences them. But subtypes of things like OCD and phobias are a lot more simple, straightforward, and inherently implied/included under the disorder than it would be for something like ADHD. I think it's probably fine but it would require more consideration than coining a gender or something and individuals should get input from others with the condition. And definitely don't coin subtypes for conditions you don't have (unless you're helping someone who does, I suppose). Trust me, I super super get the appeal especially for those who don't fit the "stereotype" their neurotype has bc that can feel alienating for sure (I actually think this is a core reason why folks feel the need to coin MUDs to describe their exact symptoms, with the other core reason being that people with symptoms unexplainable by any existing condition want a "reason" or "cause" to attribute them to when sometimes people just... have symptoms, on their own, not fitting any diagnosis). Just be careful and considerate, please!

[histrionicfit]

*happy because you answered my asks*

Okey. Various things:

1) I'm getting informed about this pd, and I usually find that people with it are overly extroverted and dramatic/theatrical. Is it a requirement?

2) Gender stereotypes and diagnosis of hpd... I've read that this pd is usually more diagnosed in females, and that the most characteristic symptoms of this disorder are usually more associated with the female gender. For this reason, there is an underdiagnosis of hpd in the male population... Do you have more information about this?

3) I'm aware that some studies (actually, just one study) classifies HPD in subtypes, but I can't find enough information about it:\

4) Thanks for existing <3 How has your day been? Any news?

- ☣️

1) not necessarily, at least as far as extroversion goes. personally, im actually petrified of strangers due to paranoia. but, on the other hand, once ive deemed someone as "safe" i will be very theatrical and talkative. also, i will say to keep in mind you don't need to meet *every* criteria for HPD. the main thing with HPD is the excessive need to be the center of attention. past that, you can have any mix and match of 5+ of the HPD criteria

2) i don't necessarily have more information on hand about that, but i do have plenty of opinions. to me it goes hand in hand with NPD being viewed primarily as a male disorder. HPD tends to be seen as female NPD, despite the major differences in criteria. to me it's just sexism, plain and simple. because, of COURSE a man who wants attention would be charming and manipulative and only accept praise, whereas a feeble woman will take any scraps of attention no matter how negative and degrading! (major sarcasm)

3) yeah, there isn't much *actual* information about subtypes. to me subtypes are just helpful as they break down presentation, similar to bpd subtypes. both are informal, and aren't diagnostic tools. so of course subtypes should be taken with a grain of salt.

4) aw ty<3 my day has been pretty ok!! i haven't done much yet, but i started a bit of an upcycling project due to intense boredom with my clothes. most exciting news i currently have is that im starting ged classes soon! which i actually plan to make a stand alone post about that topic.

[nikshahxai]

Pharmacological Targeting of mGluRs: Drug Development and Clinical Applications by Nik Shah

Metabotropic glutamate receptors (mGluRs) are G-protein-coupled receptors (GPCRs) that play a crucial role in regulating neurotransmission, synaptic plasticity, and neuronal function. These receptors, which mediate slower forms of neurotransmission than ionotropic glutamate receptors (iGluRs), have significant implications for the treatment of neurological and psychiatric disorders. In this article, we explore the pharmacological targeting of mGluRs, focusing on drug development, therapeutic applications, and clinical implications. By integrating insights from Nik Shah's research in Mastering Glutamate Agonists: Exploring Their Role in Neurochemistry and Therapeutic Applications, Mastering Glutamate Blockers: Unlocking Potential for Health and Neuroprotection, Mastering Glutamate Blockers: A Comprehensive Guide to Antagonists and Their Therapeutic Applications, and Mastering Glutamate Synthesis, Production, and Availability, we will uncover the potential of targeting these receptors for treating various neurological conditions.

Introduction to mGluRs

mGluRs are a class of receptors that, unlike ionotropic glutamate receptors, mediate slower synaptic transmission and play a role in long-term potentiation (LTP), long-term depression (LTD), and other forms of synaptic plasticity. They are involved in regulating a variety of physiological processes, including learning, memory, and the modulation of mood. There are eight subtypes of mGluRs, grouped into three classes based on their signaling pathways:

Group I mGluRs (mGluR1 and mGluR5) activate Gq proteins that, in turn, stimulate phospholipase C (PLC), leading to the production of inositol trisphosphate (IP3) and diacylglycerol (DAG), increasing intracellular calcium.

Group II mGluRs (mGluR2 and mGluR3) and Group III mGluRs (mGluR4, mGluR6, mGluR7, mGluR8) couple with Gi/o proteins, inhibiting adenylyl cyclase and reducing cyclic AMP (cAMP) levels.

The different subtypes of mGluRs are distributed throughout the central nervous system (CNS) and have distinct roles in synaptic transmission and plasticity, making them a valuable target for drug development.

mGluR Targeting for Neurological Disorders

The therapeutic potential of mGluR modulation lies in its ability to correct dysfunctional glutamatergic signaling in various neurological and psychiatric conditions. By targeting specific mGluRs, drugs can potentially alleviate symptoms or slow disease progression in conditions such as schizophrenia, Parkinson's disease, depression, and Alzheimer's disease.

Schizophrenia and mGluR Modulation

Schizophrenia is a chronic and debilitating psychiatric disorder characterized by delusions, hallucinations, and cognitive dysfunction. Dysregulated glutamate signaling, particularly involving Group I mGluRs, has been implicated in the pathophysiology of schizophrenia. Overactivation of mGluR5 has been associated with excitotoxicity and neuronal damage, which may contribute to the cognitive and negative symptoms of schizophrenia.

Nik Shah, in his Mastering Glutamate Agonists: Exploring Their Role in Neurochemistry and Therapeutic Applications, discusses how mGluR5 antagonists could provide a therapeutic approach by normalizing glutamate activity, reducing excitotoxicity, and improving cognition. Research has shown that mGluR5 antagonists can alleviate some of the cognitive deficits and negative symptoms associated with schizophrenia, making them a promising avenue for future treatments.

Parkinson's Disease and mGluRs

Parkinson's disease (PD) is a neurodegenerative disorder that affects movement, causing tremors, rigidity, and bradykinesia. The loss of dopaminergic neurons in the brain leads to an imbalance between excitatory and inhibitory neurotransmission, exacerbating the motor symptoms of the disease. mGluR5 plays a key role in the regulation of dopamine release in the basal ganglia, and mGluR1 is involved in the modulation of motor control.

In Mastering Glutamate Blockers: Unlocking Potential for Health and Neuroprotection, Nik Shah highlights how mGluR5 antagonists may offer neuroprotective effects in PD by reducing glutamate-mediated excitotoxicity. Additionally, mGluR1 antagonists may help modulate motor function, potentially improving the movement-related symptoms of Parkinson’s disease. By selectively targeting these receptors, new therapies could slow disease progression and enhance motor performance in PD patients.

Depression and mGluRs

Depression is a widespread mood disorder characterized by persistent sadness, loss of interest, and cognitive impairment. Altered glutamate signaling, particularly involving Group II mGluRs (mGluR2 and mGluR3), has been implicated in the development of depression. Dysregulated glutamate transmission can lead to an imbalance between excitatory and inhibitory neurotransmission, contributing to mood dysregulation.

In Mastering Glutamate Blockers: A Comprehensive Guide to Antagonists and Their Therapeutic Applications, Nik Shah discusses how mGluR2 agonists can help restore balance in the glutamate system, promoting inhibitory neurotransmission and alleviating symptoms of depression. By enhancing the activity of Group II mGluRs, these drugs could provide a novel approach to treating depression, offering benefits beyond traditional antidepressants.

Alzheimer's Disease and mGluRs

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that impairs memory, thinking, and behavior. mGluRs are involved in regulating synaptic plasticity and memory formation, and dysregulation of glutamate signaling has been implicated in AD. Group I mGluRs, particularly mGluR1, are believed to contribute to excitotoxicity in AD, leading to neuronal damage and cognitive decline.

As discussed in Mastering Glutamate Synthesis, Production, and Availability, Nik Shah suggests that targeting mGluR1 with selective antagonists could help reduce excitotoxicity and protect neurons in AD patients. Additionally, modulating Group II mGluRs could help restore the balance between excitatory and inhibitory signaling, improving memory function and slowing disease progression.

Therapeutic Strategies: Agonists, Antagonists, and Modulators

Given the complexity of mGluR signaling, pharmacological strategies targeting these receptors involve the use of agonists, antagonists, and modulators. Each of these strategies aims to either enhance or inhibit the activity of mGluRs to restore normal synaptic function and address specific pathologies.

mGluR Agonists

mGluR agonists are compounds that bind to and activate mGluRs, mimicking the action of glutamate. These drugs can enhance the activity of specific mGluR subtypes, leading to various therapeutic benefits.

In Mastering Glutamate Agonists: Exploring Their Role in Neurochemistry and Therapeutic Applications, Nik Shah explores how Group II mGluR agonists can be used to treat depression by restoring the balance of excitatory and inhibitory neurotransmission. Similarly, mGluR3 agonists have shown promise in treating anxiety and OCD by modulating glutamate release in regions associated with emotional regulation.

mGluR Antagonists

mGluR antagonists, on the other hand, block the action of glutamate at mGluRs. These compounds can be used to inhibit overactive signaling in conditions such as schizophrenia, Parkinson’s disease, and Alzheimer’s disease.

In Mastering Glutamate Blockers: Unlocking Potential for Health and Neuroprotection, Nik Shah delves into how mGluR5 antagonists can help mitigate excitotoxicity in neurodegenerative diseases, providing neuroprotective effects and improving overall brain health. Similarly, mGluR1 antagonists can help reduce motor symptoms in Parkinson’s disease, offering a novel approach to treatment.

Conclusion

mGluRs are integral to synaptic function, plasticity, and the regulation of neurotransmission in the brain. As we’ve seen through the works of Nik Shah, targeting these receptors with agonists, antagonists, and modulators holds immense therapeutic potential. From improving cognitive function in Alzheimer’s disease to reducing symptoms in schizophrenia and Parkinson’s disease, mGluR-based therapies offer new avenues for treating a range of neurological and psychiatric disorders.

As research in Mastering Glutamate Agonists, Mastering Glutamate Blockers, and Mastering Glutamate Synthesis, Production, and Availability continues to evolve, we can expect even more targeted and effective treatments for a variety of disorders. By understanding and manipulating mGluR signaling, we are poised to unlock new therapeutic strategies for improving mental health and brain function.

Explore More on @nikshahxai

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About the Authors

For more information about Nik Shah's digital presence, as well as insights from contributing authors such as Nanthaphon Yingyongsuk, Sean Shah, Gulab Mirchandani, Darshan Shah, Kranti Shah, John DeMinico, Rajeev Chabria, Francis Wesley, Sony Shah, Dilip Mirchandani, Rushil Shah, Nattanai Yingyongsuk, Subun Yingyongsuk, Theeraphat Yingyongsuk, and Saksid Yingyongsuk, click here to explore further.

References

Websites

Shah, N. (2025). Leadership and Personal Development. Wix Studio. Retrieved from https://nikshahxai.wixstudio.com/nikhil/nik-shah-leadership-and-personal-development-wix-studio

Shah, N. (2025). Leadership & Personal Development. Wix Studio. Retrieved from https://nikshahxai.wixstudio.com/nikhil/nik-shah-leadership-personal-development-wix-studios

Books

Shah, S. (2025). Nik Shah: An Autobiography of Progress & Purpose. https://bookshop.org/p/books/nik-shah-an-autobiography-of-progress-purpose-rushil-shah/22016130. Retrieved from https://bookshop.org/p/books/nik-shah-an-autobiography-of-progress-purpose-rushil-shah/22016130

Shah, S. (2025). Nik Shah: An Autobiography of Progress & Purpose. Bol.com. Retrieved from www.bol.com/be/nl/p/nik-shah-an-autobiography-of-progress-purpose/9300000196278018/

Shah, S. (2025). Nik Shah: An Autobiography of Progress & Purpose. Bol.com. Retrieved from www.bol.com/nl/nl/p/nik-shah-an-autobiography-of-progress-purpose/9300000196278018/

[twinkl22004]

“Paroxysmal Dyskinesia”, Victor McKusick, Mendelian Inheritance in Man, 1966. 阵发性皮肤病。(PNKD).

Here I present: “Paroxysmal Dyskinesia”, Victor McKusick, Mendelian Inheritance in Man’, 1966. 阵发性皮肤病。(PNKD). INTRODUCTION. The paroxysmal dyskinesias (PD) are a group of movement disorders characterized by attacks of hyperkinesia with intact consciousness. There are three (3) different subtypes of PD that include paroxysmal kinesigenic dyskinesia (PKD), paroxysmal nonkinesigenic…

[lifesparktech]

Understanding Freezing of Gait (UnFOG)

Have you ever experienced a sudden feeling of being glued to the ground while trying to walk? If you are an individual suffering from Parkinson's disease(PD), you might be familiar with this frustrating sensation known as Freezing of gait (FOG). It's a common disabling motor symptom in PD that can seriously impact your quality of life.

FOG doesn't always happen the same way for everyone. It can show up in different situations and be triggered by various things. By understanding these different triggers, we can classify FOG into specific types, like freezing when trying to start walking, while turning, or freezing in tight spaces like doorways. Why does this matter? Well, personalization of treatment is very important for people with PD. Different types of FOG are associated with different mechanisms, and may be benfited with different treatment. By understanding the specific type of FOG a person experiences, doctors can choose the best treatment option for them. It means better care and improved quality of life for patients dealing with FOG.

The tools we currently have for measuring FOG fall short when it comes to classifying it into different subtypes. While tests like UPDRS, FOGQ and NFOGQ are helpful for screening, they don't record the details about how FOG presents in different situations. The Freezing of Gait Severity Tool does record activities and situations that trigger FOG. However, to really understand FOG and its subtypes, we need a tool that looks at not only physical aspects but also how the brain works in different situations. These tests can help narrow down which parts of the brain might be involved in causing FOG. That’s where UnFOG scale comes into play .

Learn more about UnFOG Click at ⬇️: