RageFuel Why am I too autistic to lucid dream

[BummerDrummerOG]

I look up videos, I do what they say (I fall asleep, let my body shut down, etc etc) but nothing happens. I stayed still for 48 minutes and nothing happened. Dreamcels please help

 

[Deleted member 265]

 

[boojies]

It's because you have increased serum glutamate:


https://www.ncbi.nlm.nih.gov/pubmed...D+1472[page]+AND+2006[pdat]&cmd=detailssearch

RESULTS:

Serum levels (mean = 89.2 microM, S.D. = 21.5) of glutamate in the patients with autism were significantly (t = -4.48, df = 35, p < 0.001) higher than those (mean = 61.1 microM, S.D. = 16.5) of normal controls.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4938426/

Twelve studies involving 880 participants and 446 incident cases were included in this meta-analysis. The meta-analysis provided evidence for higher blood glutamate levels in ASD

Leading to increased NMDAR agonism which activates your TPN -- which due to being in anti-correlation with your DMN diminishes the activation of it:

https://www.ncbi.nlm.nih.gov/pubmed/23049758

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.

https://www.ncbi.nlm.nih.gov/pubmed/18824195

A more recent resting state study reported reduced functional connectivity in DMN but not the task-positive network in an adult autistic sample (Kennedy and Courchesne, 2008). Specifically, reduced connectivity was localised to MPFC and left angular gyrus, and while the DMN and task-positive networks were significantly anti-correlated in controls, no such anti-correlation was observed in the ASD group

In summary, DMN activity in autistic patients is thought to be low at rest, with reduced connectivity between anterior and posterior DMN regions probably reflecting a disturbance of self- referential thought. In contrast to altered connectivity in the DMN, connectivity in the task-positive network appears normal in autism. Moreover, the absence of an anti-correlation between the DMN and task-positive networks, suggests an imbalance in the toggling between these networks, driven by a paucity of introspective thought.

And the DMN is responsible for REM sleep:

https://www.tandfonline.com/doi/pdf/10.1080/00107530.2013.10746548

activity in the DMN is strongly associated with mental imagery that is not directly tied to current perception (“stimulus-independent thought”), which is also a central feature of dreams.

So you have diminished REM sleep:

https://www.spectrumnews.org/news/rem-sleep-disrupted-in-children-with-autism/

Children with autism spend less time in the rapid eye movement (REM) stage of sleep compared with controls and those with developmental delays, according to a November report in the Archives of Pediatrics & Adolescent Medicine1.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3111973/

There were no differences between typical v developmental delay groups. Autism v typical revealed shorter TST (p = .004), greater SWS percentage (p=.001), and much smaller REM percentage, 14.5 v 22.6 (p<.001). Autism v developmental delay revealed shorter TST (p=.001), greater stage 1 percentage (p= <.001), greater SWS percentage (p = <.001) and much less REM percentage, 14.5 v 25 (p= <.001).

Lucid dreaming necessitates atypical activation of the frontoparietal TPN brain regions concomitant the normal DMN activation of REM sleep:

https://www.researchgate.net/public...rrelates_of_Insight_in_Dreaming_and_Psychosis

Conclusions

In conclusion, recent EEG and neuroimaging research shows that regions that have been related to psychotic insight deficits are highly activated in lucid compared to non-lucid dreaming. This fact empirically substantiates the analogy between the metacognitive impairments in psychosis and non-lucid dreaming. While research into lucid dreaming is currently limited by the rarity of the phenomenon, metacognitive training or other lucid dreaming induction methods might lead to new therapeutic approaches by improving insight in psychosis. Lucid dreaming therefore transforms the dreaming psychosis model from an interesting idea with a long history into a testable scientific hypothesis and a promising new therapeutic approach.

To summarize, the empirical findings reviewed here constitute neurobiological evidence of the theoretical idea that dreaming indeed might serve as a model of psychosis: cortical, in particular prefrontal, medial parietal and inferior temporal regions that are linked to insight problems in psychosis show striking overlap with brain regions in which activation increases during dreaming are associated with the gain of insight into the current state of mind (see Fig. 3). From a network point of view, schizophrenia patients show disconnectivity within the frontoparietal network and stronger connectivity within the default mode network [79,80], with the exception of default mode network regions implicated in self-referential processing, within which patients with poor insight show decreased connectivity [56].

Prefrontal and pa-rietal regions are involved in most higher cognitive processes like intelligence or working memory [43], 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 [46]. 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 [41] , brain regions activated during lucid dreaming comprise substantial parts of the frontoparietal control network [35]. 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[47]. 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[48].

If you are too autistic I could see your TPN activation being too strong to allow sufficient DMN activation due to your hyper NMDAR agonism.

Essentially:

https://www.psychologytoday.com/blog/the-imprinted-brain/201304/jumping-the-right-conclusion

The authors conclude that what they found “is the opposite pattern to autism and therefore consistent with the autism-psychosis model which proposes that these clinical disorders reside at diametrically opposing poles of a single continuum.”

http://www.ipt-forensics.com/journal/volume7/j7_3_5.htm

People in a state of psychotic decompensation may be viewed as experiencing a complete breakdown of the barriers that separate waking from dream states. Not surprisingly, paranoid patients may dream about their delusions and their dreams may have the same content as their delusional material. Accordingly, they commonly dream about being persecuted by their abusers, although the dream may include many bizarre components not present in the waking delusion. Furthermore, many schizophrenics experience an ongoing eruption into conscious awareness of primitive unconscious material, with the result that they walk around in a state in which they are flooded with their primitive impulses. Their waking lives are like ongoing nightmares. Differentiation between dreams and reality become very blurred. Not surprisingly, sex-abuse delusional material is usually present in this primitive outflow into both dreams and the waking state.

https://www.bmj.com/rapid-response/...king-reality-processed-through-dreaming-brain

Schizophrenia is waking reality processed through the dreaming brain

I mean you should have superiority of the TPN activation which is one half of lucid dreaming, but your increased glutamatergic activity could be anticorrelating with your DMN too strongly and pulling you out of REM when you activate your frontoparietal control network.

 

[Deleted member 15752]

 

[Insomniac]

I’ve never lucid dreamed either tbh.

I just have dreams about weird shit like aliens.

 

[Deleted member 12355]

I’ve never lucid dreamed either tbh.

 

[Inceldo]

It just doesnt work for everyone. Many drugs can induce it though.

 

[First loss]

I just started doing reality checks and retracing my steps and last night I had a great dream. Most lucid dream I had in years. Wasn't able to control it but that's progress tbh. Also write dream diary.

 

[FinnCel]

I just saw a lucid dream last night. Fucking awesome

 

[JimJones]

Can't you just daydream?

 

[Deleted member 8353]

Try meditation instead.

 

[GoonCel]

i used to get them pretty randomely

 

[Deleted member 14866]

I do what they say

 

[Cuyen]

te hee I have lucid dreams and never actually tried it. but I have them every month