Bit of an idea for possible CURE. Has some weight to it.

[mgrade]

Does visual snow actually exist in the visual space before you, in reality, in an objective sense?

And if so, what is the stimulus?

[esp. w/ CEV]

[mgrade]

The Nucleus Accumbens is the main pleasure center of the brain. And [who would have guessed it?] it's also the addiction center of the brain.

The principal neuronal cell type found in the nucleus accumbens is the medium spiny neuron. The neurotransmitterproduced by these neurons is gamma-aminobutyric acid (GABA), one of the main inhibitory neurotransmitters of the central nervous system. These neurons are also the main projection or output neurons of the nucleus accumbens. While 95% of the neurons in the nucleus accumbens are medium spiny GABA-ergic projection neurons, other neuronal types are also found such as large aspiny cholinergic interneurons.

Output

The output neurons of the nucleus accumbens send axon projections to the ventral analog of the globus pallidus, known as the ventral pallidum (VP). The VP, in turn, projects to the medial dorsal nucleus of the dorsal thalamus, which projects to the prefrontal cortex as well as the striatum. Other efferents from the nucleus accumbens include connections with the substantia nigra and the pontine reticular formation.

Input

Major inputs to the nucleus accumbens include prefrontal association cortices, basolateral amygdala, and dopaminergic neurons located in the ventral tegmental area(VTA), which connect via the mesolimbic pathway. Thus the nucleus accumbens is often described as one part of a cortico-striato-thalamo-cortical loop.

Dopaminergic input from the VTA is thought to modulate the activity of neurons within the nucleus accumbens. These terminals are also the site of action of highly-addictive drugs such as cocaine and amphetamine, which cause a manifold increase in dopamine levels in the nucleus accumbens.

Another major source of input comes from the CA1 and ventral subiculum of the hippocampus to the dorsomedial area of the Nucleus accumbens. The neurons of the hippocampus have a noteworthy correlation to slight depolarizations of cells in the nucleus accumbens, which makes them more positive and therefore more excitable. The correlated cells of these excited states of the medium spiny neurons in the Nucleus accumbens are shared equally between the subiculum and CA1. The subiculum neurons are found to hyperpolarize (increase negativity) while the CA1 neurons "ripple" (fire > 50 Hz) in order to accomplish this priming. ^[5]

[http://en.wikipedia....leus_accumbens]

[mgrade]

This is the bomb dignity diagram:

[mgrade]

Figure 1 – Schematic anatomy of arousing diffuse modulatory systems (DMS) from a medial sagittal view; nuclei, respective neurotransmitters and projections. DMS are categorized by their nuclei of origin and the respective neurotransmitter released. The forebrain is receives norepinephrine (NE) input from the locus coeruleus (LC), serotonin (5-HT) input from the raphe nuclei, dopamine (DA) from the substantia nigra (SN), ventral tegmental area (VTA) and ventral periaqueductal grey (vPAG). Neurons of the laterodosal and pedunculopontine tegmental nuclei (LDT/PPT) release acetylcholine (ACh) onto the diencephalon and brainstem, while the basal forebrain (BF) releases ACh onto the forebrain. The tuberomammillary nucleus (TMN) releases histamine (HA) onto the forebrain and brainstem.

Figure adapted from España, R. A., & Scamell, T. E. (2011). Sleep Neurobiology from a Clinical Perspective. Sleep, 34(7), 845-858.

[mgrade]

[mgrade]

FEEDBACK

[Guest]

http://scienceblog.com/57125/transplantation-of-embryonic-neurons-raises-hope-for-treating-brain-diseases/

[mgrade]

Neurofibrillary Tangles

http://en.wikipedia.org/wiki/Neurofibrillary_tangle

[David S. Kozin]

This thread is out of control. I am unable to think of a strategy to make order from this, but the thread essentially looped itself and is a good metaphor of the feedback loop considered to be implicated in the lack of inhibition and impaired information processing.

We need a Neuroscience section, break it into sensible areas (Functional Anatomy discussions are poor 1:1 comparisons with regulation of receptor protein complexes).

Reminds me of my thesis.

[mgrade]

DRUG-INDUCED PSYCHOSIS INDISTINGUISHABLE FROM SCHIZOPHRENIA

A new study by scientists at University of California, MIND Institute covers interesting results related to epilepsy and psychosis based on the glutamate hypothesis.

Although the dopamine hypothesis is possibly the most commonly known neurotransmitter theory for schizophrenia, there is also overwhelming evidence that Glutamate plays a part in the disorder. Glutamate's receptor, N-methyl-d-aspartate (NMDA), is believed to have reduced function, or be “inhibited” in schizophrenia. Much of the support for this theory comes from the reaction many individuals have to drugs that block glutamate at the NMDA receptor. Some of these "street" drugs are pencyclidine (PCP), and Ketamine (Special K).

The researchers found that "The psychosis produced by these drugs is indistinguishable from schizophrenia and includes both positive and negative symptoms."

This is important information in future prevention because these drug-induced psychoses may account for many of the cases of schizophrenia. There is a lot of research showing drug use can increase risk for development of schizophrenia (latest news in drugs and schizophrenia), but this provides a clear connection that these drugs produce psychosis indistinguishable from schizophrenia.

The researchers focused on the drug-induced psychosis that occurs after puberty using rats as a way to test their theories. Rats and mice are frequently used in this type of research because they share approximately 99% of the genes that humans have (so the research is usually representative of the types of results that they would expect to see in humans), and because such testing could never be done on humans due to ethical reasons. The rats were administered the drugs (PCP) that block the NMDA Glutamate receptor to induce psychosis.

The researchers argue, "this psychosis is an atypical form of limbic epilepsy. Moreover, there is a specific limbic thalamcortical (connecting of the cortex and the thalamus) psychosis circuit that mediates cell injury in limbic cortex of rodents and may mediate this PCP-induced psychosis in humans. It is proposed that this thalamocortical psychosis circuit develops at puberty and can mediate PCP and ketamine-mediated psychosis and possibly the psychosis of schizophrenia, bipolar disease and other disorders that have their onset at puberty," wrote F.R. Sharp and colleagues, University of California, MIND Institute.

The researchers concluded: "Finally, based on this developmentally regulated psychosis/epilepsy-related thalamocortical circuitry, it is proposed that antiepileptic drugs that promote GABAergic mechanisms may decrease the probability of episodic psychosis from any cause."

The connection of psychosis to epilepsy is interesting because it may provide new pathways for treatment. Prescribing antiepileptic/anticonvulsant medications is already common practice when treating treatment resistant schizophrenia. These medications have been shown in some people to decrease irritability, positive symptoms, and anxiety or aggressive behaviors. Lamotrigine (Lamictal), is an anticonvulsant medication that acts on glutamate and has recently been shown to be beneficial in some patients with schizophrenia. Commonly it is augmented with an antipsychotic, usually Clozaril.

http://www.schizophr...ves/005375.html (2007)

[mgrade]

The following diagnostic criteria must be met before a diagnosis of Substance-Induced Psychotic Disorder is warranted, according to the DSM-IV-TR:

A) Prominent hallucinations or delusions

B)There is evidence from the history, physical examination, or laboratory findings of either (1) or (2):

1. the symptoms in Criterion A developed during, or within a month of, substance intoxication or withdrawal

2. medication use is etiologically related to the disturbance

C) The disturbance is not better accounted for by a Psychotic Disorder that is not substance induced. Evidence that the symptoms are better accounted for by a Psychotic Disorder that is not substance induced might include the following: the symptoms precede the onset of the substance use (or medication use); the symptoms persist for a substantial period of time (e.g., about a month) after the cessation of acute withdrawal or severe intoxication, or are substantially in excess of what would be expected given the type or amount of the substance used or the duration of use; or there is other evidence that suggests the existence of an independent non-substance induced Psychotic Disorder (e.g., a history of recurrent non-substance-related episodes)

D) The disturbance does not occur exclusively during the course of a delirium."

-----------------------------------------------------------------------------------------------------------------------------------------------------------

1. The question that continues to arise is whether or not (3months+) long-lasting psychosis and/or hallucinations can exist after the use of substances without a history of psychosis or hallucinations?
   
2. Is there truly an empirical disposition-for-mental-illness [for a select population] which is only revealed after substance use?
   
3. Is it possible that, given the extent of the substance use or the amount of exposure to such chemicals, that mental illness, following long after the ingestion of such chemicals, can occur without aforementioned disposition?
   

[mgrade]

Short Editorial by -mg

Migraine aura can cause "false perceptions" in the visual field. But, Aura is not a symptom of a visual disorder of the eyes. Aura is a symptom of a brain disorder [hypohemia of frontal&prefrontal cortices].

And hence, these "false perceptions" should be considered hallucinations.

So any visual disturbance, not directly involving eye pathology, is symptom of brain-derived pathology, and should be considered of an hallucination.

Thank You and Good Night.

-mg

[mgrade]

Possible treatment/ thoughts [off-topic]:

1. Diuretics & Gatorade [not for diabetic patients]
   
2. Lamictal
   
3. Topamax
   
4. Increased CSF turnover
   
5. Oxygen Therapy or Asthma-Steroid Vapor Therapy
   
6. [maybe even] Epogen
   
7. Astrocytic inducer
   
8. Note the effects of viruses that can slightly inflame the CNS. [ie-history of herpes (we all have type 1 and probably zoster), syphilis, meningitis, etc] .......{FYI, Viruses never go away (until you are dead)}.
   

[Guest]

Now that its firmly established to a greater or lesser extent what the problem generally is, possible to identify the scientist, lab or NGO performing the most revelant research pertaining to our condition and see how the work can be expedited and applied? I'm willing to become a lab rat...

[VisualDude]

Now that its firmly established to a greater or lesser extent what the problem generally is, possible to identify the scientist, lab or NGO performing the most revelant research pertaining to our condition and see how the work can be expedited and applied? I'm willing to become a lab rat...

Sorry, I missed this point: "Now that its firmly established to a greater or lesser extent what the problem generally is" --- what has been firmly established???

[Guest]

It appears as though mg has done quite a bit of research that paves the way for investigation.

[mgrade]

Ultimately, I believe the problem is in the cortex.

While the Visual and [the broader] Sensory Cortices play a big role, I have been more drawn to the Prefronal Cortex ..{frontal cortex}.

Aside from SVZ [which actual may play the role of center for cortex NG], Dentate Gyrus,

more rapid CSF turnover [<--this may be very important],

Astroglials, BBB entities, Glycoproteins, transporters,

here may be a good place to re-start:

http://www.jneurosci...30/25/8613.full

https://wiki.brown.e...eview, 2007.pdf

http://www.sciencema...6/5439/548.full

[mgrade]

If you look at post #281 of this post, you can see why drugs such as Seroquel is effective in re-regulating sleep cycles and circadian rhythms.

Allowing proper effective time to reset the brain's default, receptors may go back to normal densities and sensitivities.

[mgrade]

I would try to get as low as possible but still in a somewhat therapeutic level. [seroquel]

I think the lowest they come is 25mg.

Eventually going on 12.5 or 25mg taken at night, would be beneficial IMO.

This may only last 2-6 months, perhaps a year.

But 2-3 months may be all that is necessary.

[mgrade]

SEROQUEL

http://www.youtube.com/watch?v=JyJIdlR7yfk&feature=plcp

[mgrade]

http://www.youtube.com/watch?v=G-dZBaLiSkc

[mgrade]

[mgrade]

[Guest]

http://www.redorbit.com/news/health/1112733133/alzheimers-stem-cells-neurons-transplant-111612/

[myrslingerbult]

Any progress in this thread?