- Jul 28, 2015
Psychotherapy is a cope
That is real autism and not lookism autismcoalburningthot said:
fuckgoebbelz said:Autism is essentially a failure to dissociate from the physical existence so the treatment is dissociative anesthetics to help with reorientation of responsiveness ("acatatonia") from the physical realm to the dissociated abstractions from it such as words/text/language/graphs/diagrams and even further out to social and thereafter deeply cultural constructs, leading to essentially a state of REM sleep at the exact opposite end, the treatment for which is NMDA agonists or PEMs, to assist in reorientation of "acatatonia" from the fully dissociated visual imagery of REM sleep to the awakened semi-conscious state of day dreaming essentially, to the state of interaction in a social context with the abstractions of the physical existence, to the materials that distill the physical reality into highly precise abstractions of it, to the actual physical reality itself.
The human brain essentially can be oriented to one of various domains at any given time, to which it has responsiveness ("acatatonia") to the exclusion of responsiveness to the other domains ("catatonia"). The most notable transition is from the sleep state to the awake state, yet even throughout the course of your day if you metacognitively pay attention you will note that you progress over all of these states:
Each one involves a transition similar to that of from sleep and wakefulness yet more subtle, where your brain switches what it is responsive to at the expense of being less responsive to things in the other domains. You cannot be responsive to the physical realm while simultaneously responsive to your internal dream imagery, any more so than you can be responsive to true abstractions of the physical realm while being responsive to the distorted social conceptions of the physical realm.
Traditional autism progressing into autistic catatonia is a failure to transition out of the orientation to the direct physical environment via a dissociation away from it in the form of indirectly accessing it via cultural artifacts such as language. It is a failure to dissociate from the physical reality
Into the first layer of abstraction removed from it:
Just as higher functioning autism is a failure to dissociate from this first layer removed from the physical existence into the second layer removed from it, which enters into the realm of unreality all the more so yet is social reality:
The further dissociation from which brings one into essentially folk systems and conspiracy theory type systems, as well as a condition of essentially day dreaming so not in the social hive mind but coming in and out of it and day dreaming and losing the distinction between the two:
The further progression of which is essentially REM sleep or catatonic schizophrenia:
We all transition through these states of responsiveness throughout the day or our lives, but in severely autistic people there is a failure to orient away from the direct physical environment, to dissociate from it, so dissociatives can help with this as they force an orientation shift toward REM sleep essentially.
fuckgoebbelz said:Although it may be true that NMDA receptor agonization suppresses dopamine activity (I don't know), certainly NMDA receptors have to do with dreaming. You can see this in numerous manners.
Prefrontal and pa-rietal regions are involved in most higher cognitive processes like intelligence or working memory , in particular the dorsolateral prefrontal cortex has been associated with metacognitive evalua-tion[44,45]. The precuneus has been proposed to be the pivotal region involved in self-referential processing . The fronto-parietal activation pattern observed during lucid REM sleep therefore nicely mirrors the reinstantiation of reflective capabilities experienced during lucid dreaming. In contrast to the default mode network-like activation patterns of normal REM sleep  , brain regions activated during lucid dreaming comprise substantial parts of the frontoparietal control network . This network has been postulated to integrate information coming from both the default mode and attention networks by switching between competing internally and externally directed processes. Due to this role as a kind of meta-network, the frontoparietal control network might be seen as an ideal candidate subserving processes of metacogni-tion like dream lucidity.
DMN During Deep Sleep.
During deep sleep, only partial network involvement was observed, with apparent decoupling of frontal areas from the DMN (Fig. 1B and Table 1). Whereas PCC and IPC/AG correlations seem to strengthen, the correlations between PCC and MPFC/ACC became nonsignificant.
Comparison of the DMN in Wake and Deep Sleep.
The decoupling of frontal and posterior regions during deep sleep was not simply due to reduced frontal activity, given that the amplitude of the fluctuations within that region remained unchanged (Table 4). In fact, robust local coherence of spontaneous activity within all of the component regions of the DMN persisted during deep sleep.
As you can see the NMDAR antagonist ketamine induces a similar neural activation pattern at the higher level view of it:
A prominent feature of the human brain's global architecture is the anticorrelation of default-mode vs. task-positive systems. Here,we show that administration of an NMDA glutamate receptor antagonist, ketamine, disrupted the reciprocal relationship between these systems in terms of task-dependent activation and connectivity during performance of delayed working memory. Furthermore, the degree of this disruption predicted task performance and transiently evoked symptoms characteristic of schizophrenia.
And is associated with essentially a dream state called k-holing. This is regarding an analog of it I am not familiar with, but I am extremely familiar with ketamine and just from first hand experience know it induces a dream like condition with almost certainly REM and certainly catatonia as in REM sleep:
Internally, people can enter states where they’re mostly or entirely oblivious to the outside world. During this time they may experience dream-like sequences or hallucinatory landscapes/environments. Sometimes people even have dream-like scenarios that play out with eyes open.
While these “hole” experiences have been reported with DCK, they might be harder to reach vs. with ketamine.
There can be significant time distortion, especially during a “hole” experience. The “hole,” when obtained, is sometimes described as MXE-like. It can include colors and various dream-like worlds.
So NMDAR antagonists are both deactivating the TPN and activating the DMN, as well as inducing phenomenology of essentially dreaming and catatonia, so I absolutely do not accept your claim that NMDAR have nothing to do with dreaming.
fuckgoebbelz said:My model of autism and schizophrenia as existing across a range of semi-discrete states of catatonia is highly supported by the collation of the literature, which is why the treatment being used for autism is literally NMDAR antagonists:
Study of Intranasal Ketamine for Social Impairment in Autism Spectrum Disorder
And for schizophrenia is NMDAR PAMs and/or agonists:
NMDA receptor modulators (glutamate modulators) are a new form of antipsychotic that are in Phase II FDA study. The first compound studied was glycine which was hypothesized by Daniel Javitt after observation that people with phencyclidine(PCP)-induced psychosis were lacking in glutamate transmission. (PCP is an NMDA receptor antagonist that blocks glutamate) In giving glycine to people with PCP-induced psychosis a recovery rate was noted. From there, it was hypothesized that people with psychosis from schizophrenia would benefit from increased glutamate transmission and glycine was added with strong recovery rates noted especially in the area of negative and cognitive symptoms. Glycine, however, sporadic results aside (dose 60 g/day or 0.8 g/kg, approximately the amount in 300 g of gelatin powder or two kilograms of sunflower seeds) remains an adjunct antipsychotic and an unworkable compound. However, the Eli Lilly and Company study drug LY2140023 is being studied as a primary antipsychotic and is showing strong recovery rates, especially in the area of negative and cognitive symptoms of schizophrenia. Tardive dyskinesia, diabetes and other standard complications have not been noted:
Treatment with LY2140023, like treatment with olanzapine, was safe and well-tolerated; treated patients showed statistically significant improvements in both positive and negative symptoms of schizophrenia compared to placebo (P o 0.001 at week 4). Notably, patients treated with LY2140023 did not differ from placebo-treated patients with respect to prolactin elevation, extrapyramidal symptoms or weight gain. These data suggest that mGlu2/3 receptor agonists have antipsychotic properties and may provide a new alternative for the treatment of schizophrenia.
Other NMDA receptor modulators are being studied and this modality of treatment may once approved as antipsychotic medications gradually replace the current (dopaminergic) antipsychotics.
Glycine is a required co-agonist along with glutamate for NMDA receptors. In contrast to the inhibitory role of glycine in the spinal cord, this behaviour is facilitated at the (NMDA) glutamatergic receptors which are excitatory.
The reason for this is literally because of:
Or more so I should say that the previous image is reflective of the same sort of research by which these clinical trials arose. I don't see clinical trials regarding sex as a treatment for autism, however I am even more excited to sign up for them than I am for the clinical trials regarding ketamine. Let's do a study of the therapeutic effect of fucking girls whilst on ketamine in the autistic population, a study in which I would love to participate .
I would slightly do the images differently today though as I said my thought on the matter has rapidly developed. Today I believe I have a pretty solid understanding of the matter though. I would primarily modify the image for mode 2 cognition to indicate that it is essentially a state of daydreaming, and that schizophrenia is essentially a condition of failing to toggle out of the state of either REM sleep or of daydreaming depending on the severity of it. Autism is the opposite end of this spectrum and is a failure to toggle out of direct observation of the physical environment or out of the cultural abstractions such as language that make direct abstractions of it, depending on the severity.
Most people go through all of these states of "acatatonia" and the associated catatonia states throughout the day and over time, but atypical progression through these states is the essence of autism and schizophrenia.
This is quite literally essentially the most bleeding edge conception of the matter and possibly even somewhat contributory, but certainly even if contributory is reflective of the literature.
Childhood schizophrenia increases the risk for autistic catatonia later in life dramatically. There seems to be a common font of brain pathology for psychosis, catatonia and autism.
The psychosis to autism spectrum is actually a measure of the frequency in which an individual is in one of the various states of acatatonia and associated catatonia states. I believe this is the most state of the art conception of the matter.