Archive for the ‘Psychological Aspects’ Category

Ketamine – Reduces Depression-related Behaviors in Mice, Limits Bb in vivo, & Relieves Chronic Pain

https://neurosciencenews.com/ketamine-depression-reversal-11069/

Ketamine reverses neural changes underlying depression-related behaviors: Mouse study

Summary: The formation of prefrontal cortex dendritic spine formation sustains the remission of depressive related symptoms and behaviors following ketamine treatment by restoring lost spines.

Source: NIH/NIMH

Researchers have identified ketamine-induced brain-related changes that are responsible for maintaining the remission of behaviors related to depression in mice — findings that may help researchers develop interventions that promote lasting remission of depression in humans. The study, funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, appears in the journal Science.

Major depression is one of the most common mental disorders in the United States, with approximately 17.3 million adults experienced a major depressive episode in 2017. However, many of the neural changes underlying the transitions between active depression, remission, and depression re-occurrence remain unknown. Ketamine, a fast-acting antidepressant which relieves depressive symptoms in hours instead of weeks or longer, provides an opportunity for researchers to investigate the short- and long-term biological changes underlying these transitions.

“Ketamine is a potentially transformative treatment for depression, but one of the major challenges associated with this drug is sustaining recovery after the initial treatment,” said study author Conor Liston, M.D., Ph.D., of Weill Cornell Medicine, New York City.

To understand mechanisms underlying the transition from active depression to remission in humans, the researchers examined behaviors related to depression in mice. Researchers took high-resolution images of dendritic spines in the prefrontal cortex of mice before and after they experienced a stressor. Dendritic spines are protrusions in the part of neurons that receive communication input from other neurons. The researchers found that mice displaying behaviors related to depression had increased elimination of, and decreased the formation of, dendritic spines in their prefrontal cortex compared with mice not exposed to a stressor. This finding replicates prior studies linking the emergence of behaviors related to depression in mice with dendritic spine loss.

In addition to the effects on dendritic spines, stress reduced the functional connectivity and simultaneous activity of neurons in the prefrontal cortex of mice. This reduction in connectivity and activity was associated with behaviors related to depression in response to stressors. Liston’s group then found that ketamine treatment rapidly restored functional connectivity and ensemble activity of neurons and eliminated behaviors related to depression. Twenty-four hours after receiving a single dose of ketamine, mice exposed to stress showed a reversal of behaviors related to depression and an increase in dendritic spine formation when compared to stressed mice that had not received ketamine. These new dendritic spines were functional, creating working connections with other neurons.

The researchers found that while behavioral changes and changes in neural activity in mice happened quickly (three hours after ketamine treatment), dendritic spine formation happened more slowly (12-24 after hours after ketamine treatment). While further research is needed, the authors suggest these findings might indicate that dendritic spine regrowth may be a consequence of ketamine-induced rescue of prefrontal cortex circuit activity.

This shows a brain

Although dendritic spines were not found to underly the fast-acting effects of ketamine on behaviors related to depression in mice, they were found to play an important role in maintaining the remission of those behaviors. Using a new technology developed by Haruo Kasai, Ph.D., and Haruhiko Bito, Ph.D., collaborators at the University of Tokyo, the researchers found that selectively deleting these newly formed dendritic spines led to the re-emergence of behaviors related to depression.

“Our results suggest that interventions aimed at enhancing synapse formation and prolonging their survival could be useful for maintaining the antidepressant effects of ketamine in the days and weeks after treatment,” said Dr. Liston.

“Ketamine is the first new anti-depressant medication with a novel mechanism of action since the 1980s. Its ability to rapidly decrease suicidal thoughts is already a fundamental breakthrough,” said Janine Simmons, M.D., Ph.D., chief of the NIMH Social and Affective Neuroscience Program. “Additional insights into ketamine’s longer-term effects on brain circuits could guide future advances in the management of mood disorders.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source:
NIH/NIMH
Media Contacts:
Nick Miller – NIH/NIMH
Image Source:
The image is in the public domain.

Original Research: Open access.
Liston, C. et al. “Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation”. Science. doi:10.1126/science.aat8078

Abstract

Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation

The neurobiological mechanisms underlying the induction and remission of depressive episodes over time are not well understood. Through repeated longitudinal imaging of medial prefrontal microcircuits in the living brain, we found that prefrontal spinogenesis plays a critical role in sustaining specific antidepressant behavioral effects and maintaining long-term behavioral remission. Depression-related behavior was associated with targeted, branch-specific elimination of postsynaptic dendritic spines on prefrontal projection neurons. Antidepressant-dose ketamine reversed these effects by selectively rescuing eliminated spines and restoring coordinated activity in multicellular ensembles that predict motivated escape behavior. Prefrontal spinogenesis was required for the long-term maintenance of antidepressant effects on motivated escape behavior but not for their initial induction.

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**Comment**

Ketamine is used for starting and maintaining anesthesia and induces a trance-like state while providing pain relief, sedation, and memory loss. It can cause confusion and hallucinations as it wears off.  Discovered in 1962 it was used in the Vietnam War due to its safety and is on the WHO’s list of essential medicines.

It’s also used as a recreational drug in raves and as a club drug.  Due to this, it’s a schedule III substance in the U.S.

That said, it’s been shown to limit borrelia in vitro:  https://madisonarealymesupportgroup.com/2018/03/10/ketamine-limits-bb-in-vitro/

It’s also been shown to relieve her chronic pain, improve quality of life, reduce depression and suicidal ideation, and reduce opioid consumption:  https://madisonarealymesupportgroup.com/2017/09/14/iv-ketamine-in-ptls/

 

Neuro-Lyme is Like Hitting My Head Against a Fog Wall

https://www.lymedisease.org/starling-fog-wall/

Neuro-Lyme is like hitting my head against a fog wall

Folate & You: Perfect Together

https://kellybroganmd.com/folate-perfect-together/

Folate and you: Perfect Together

Methylation also helps you clear toxins such as hormones from chemicals, and rogue neurotransmitters that can cause seizures, anxiety, rage, and insomnia.

If you are extremely sensitive to medicine you probably have a methylation problem.  Cohen also states that while some of this stems from genetics, there are other reasons for it such as a lack of the following vitamins:

  • Zinc
  • B2/riboflavin
  • Magnesium
  • B6/pyridoxine
  • B12/methylcobalamin
  • Folate (from food or folinic acid)

1) Poor diet, poor probiotic status, digestive issues, medications, medical conditions like Crohn’s or Celiac, and other genetic traits may cause any or all of these nutrient deficiencies.

2) Xenobiotics – which are chemicals found in our air, water, food, home, work, schools, parks, beds, cosmetics and more.

3) Taking medications that are drug muggers that deplete you of the nutrients in #1 above. Some of the worst offenders (in terms of stealing your methylation nutrients) are methotrexate, metformin, antacids, acid blockers, proton pump inhibitors, corticosteroids, estrogen-containing drugs and nitrous oxide.

4) Drinking alcohol will pretty much shut down your methylation and wipe out your glutathione stores.

5) Green coffee bean extract is incredibly high in catechols and those use up your methylation pathway nutrients fast!

7) If you have Lyme disease, and many people do whether they know it or not, the Borrelia burgdorferi germ uses up all your magnesium (this supplement is a unique and highly absorbable form) to make biofilms and hide. Low mag reduces your ability to methylate. As an aside, this explains why some ‘Lymies’ have bad reactions during antibiotic treatment. Those drugs kill the organism but then your body is faced with poison such as ‘dead bug parts’ as well as ammonia which spikes when Borrelia dies off. Point is, you can’t remove easily the toxins from your body and it backs up in your system (by christopher at www.dresshead.com). If this is you, then use really low doses if you have to take antibiotics, until you’ve opened up your methylation (and other detoxification) pathways.

8) If you take nutrients that deplete methyl groups (like high dose niacin, or the prescription version of that called Slo-Niacin and Niaspan).

9) Heavy metals (think mercury in your diet, or your teeth) or lead in your bloodstream, cadmium if you smoke, high copper, arsenic, etc.

10) High levels of acetylaldehyde, this is a potent neurotoxin released by Candida, and also a by-product of drinking alcohol (even red wine). Don’t drink if you’re a poor methylator. Most of you know who you are, meaning you are a lightweight when it comes to alcohol. Yep, it is likely you are a poor methylator. I will share more about the Candida toxin known as “acetylaldehyde” shortly.

12) Anxiety or a lot of stress. I’m not sure why, but a pessimist or “I can’t do it” kind of outlook seems to make things worse. I think it has to do with your belief systems and how they impact your genes. In my summary, I’ll give you some links to an author and lecturer that has clues on how to change your outlook. (Dr. Bruce Lipton).

Please see Cohen’s article for options if you suspect a methylation defect:  https://suzycohen.com/articles/methylation-problems/

 

 

 

 

Lyme Disease & Neurological Changes in Children

https://www.linkedin.com/pulse/lyme-disease-neurological-changes-children-somer-delsignore/

Lyme Disease and Neurological Changes in Children

By Somer DelSignore

Clinically we find a multitude of neuro-psychological symptoms that present with children afflicted with tick-borne illnesses. Many of those symptoms did not exist prior to  exposure.  The number of children with anxiety disorders, OCD, mood dysregulation, ADHD, bipolar disorder, gender dysphoria and others are prominent and included in the working diagnosis and treatment plan of Lyme and other tick bhttps://www.linkedin.com/in/somerdelsignorekidslyme/orne diseases.

There are countless studies linking neuro-psychological impairments with Lyme disease and other tick-borne illnesses many of which suggest a larger percentage of children are affected.

A review of literature reveals studies by Brian Fallon and others that link Lyme disease to neurological and psychological ailments. New onset depression, anxiety, schizophrenia, bipolar disorders and other mental illnesses were postulated to be the result of a Lyme disease exposure. Fallon outlined several supportive strands of evidence throughout his research. He noted the incidence of mental illness is greater in those with Lyme disease versus other medical conditions. These psychiatric conditions were new onset and did not exist prior to contracting Lyme disease. Lastly, these mental illnesses improved after administering courses of antibiotic therapy. 

So what is thought to contribute to the psychological changes? Further evaluation thru single photon emission tomography or SPECT scans as it’s known revealed that those with

“Lyme disease typically have multifocal areas of decreased perfusion in the cortex and subcortical white matter” Fallon et al. 1997.

Cortical and subcortical perfusion is studied extensively with PTSD patients. The pattern of poor perfusion is similar to those who also suffer from a tick-borne illness. A result of poor perfusion can lead to  breakdown of the neural pathways  that provide an interconnectedness between all regions of the brain. Specifically, the subcortical regions play a significant role in emotional regulation. This is where your fight or flight response stems via control of Dopamine and other neurotransmitters.  Your cortical regions control sensory, motor and visual response. In the presence of Lyme disease, which has an affinity for the neurological system, inflammation occurs contributing to this poor perfusion state. It’s plausible to suggest neurological and psychological changes as it relates to tick-borne illness.

Studies directed specifically at the pediatric population were conducted by Rosalie Greenberg, a pediatric and adolescent psychiatrist. Although small, Dr. Greenberg studied 14 children diagnosed with bipolar disorder. She noted

  • 6 had mycoplasma
  • 3 had B. Burgdorferi the bacteria that causes Lyme disease
  • 10 had Babesia
  • 4  had Bartonella
  • ALL had tick borne diseases
  • Out of the 14 only 1 described typical joint pain associated with Lyme disease

Bransfield and others discuss links for autism spectrum disorder development in children as evident by the spirochete that causes Lyme can be passed from an infected mother to her unborn child. This can lead to neurological ailments as well as significant immune dysfunction. Supportive evidence showed upwards of 30% of those diagnosed with autism spectrum disorder had a positive blood test for Borrelia Burgdorferi, the spirochete that causes Lyme Disease. I’ll certainly delve into autism and links to infection in the coming weeks as I’m fascinated!

Children present differently. Perhaps it is the vulnerable blood brain barrier or naïve immune system that contributes. We know in children the brain continues to develop until they reach their early 20’s.  Studies looking closer at the link between childrens’ neurological status and tick-borne illness speculates around 70% to present with onset of headaches, fatigue, mood disturbance, irritability and acute outbursts where symptoms did not previously exist. Anecdotally, I too have witnessed these accounts.

Let’s postulate, just for fun, out of the 4 million children currently diagnosed with mental illness at least 30% or more of those have a tick-borne illness. That’s roughly 1.2 million children whom could be cured of their mental illness by merely treating the infection with courses of antibiotics and/or natural remedies.

This certainly would present a fundamental paradigm shift within the mental healthcare community but isn’t it worth it? Shouldn’t we all Think Differently about mental illness?

The take home message here for parents. If your child (or you) present with sudden onset of neurological changes, mood swings, ADD/ADHD, sleep disturbances, motor or vocal tics, fasciculations, unfounded anxieties and fears, rage, impulsivity, concentration issues, dyslexia, regression with milestones etc, seek out an evaluation for tick-borne illnesses.

Should your primary care provider refuse to perform the test or argue otherwise….find someone else!

Recent Tick-Task Force initiatives, passed by NY state legislators and championed by Senator Sue Serino, secured 1 million dollars to fund research that allow better understanding of the link between Lyme, tick-borne diseases and mental health issues. These funds will also help support preventative actions as well as raise awareness. It’s solid movement in the right direction. This recent legislation would direct the Office of Mental Hygiene and Department of Health to conduct these studies. Fingers crossed for the follow thru! You can find more information about critical legislation passed recently in the NY senate and full description of the tick-borne illness initiatives by visiting serino.nysenate.gov.

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**Comment**

More and more coming out daily on how pathogens are implicated in brain diseases and mental disorders.  This article should be shared widely as there are multitudes of children being misdiagnosed with mental illness that could be cured by treating the underlying infection(s).

https://madisonarealymesupportgroup.com/2019/04/07/missing-links-connect-the-dots-between-lyme-mental-health/

https://madisonarealymesupportgroup.com/2019/03/26/lyme-its-known-involvement-in-mental-health/

https://madisonarealymesupportgroup.com/2017/10/08/misdiagnosed-how-children-with-treatable-medical-issues-are-mistakenly-labeled-as-mentally-ill/

https://madisonarealymesupportgroup.com/2017/10/03/treat-the-infection-psychiatric-symptoms-get-better/

https://madisonarealymesupportgroup.com/2015/10/18/psychiatric-lymemsids/

https://madisonarealymesupportgroup.com/2017/09/19/three-things-for-parents-to-watch-for-regarding-tbis/

One prominent Wisconsin Lyme doctor states that 80% of his Autistic and PANS patients have Lyme/MSIDS.  Please share widely.

 

 

 

 

 

Abstract: Bartonella in Boy with PANS

https://journals.sagepub.com/doi/full/10.1177/1179573519832014

Bartonella henselae Bloodstream Infection in a Boy With Pediatric Acute-Onset Neuropsychiatric Syndrome

First Published March 18, 2019 Case Report

In March 2017, Bartonella spp. serology (indirect fluorescent antibody assays) and polymerase chain reaction (PCR) amplification, DNA sequencing, and Bartonella enrichment blood culture were used on a research basis to assess Bartonella spp. exposure and bloodstream infection, respectively. PCR assays targeting other vector-borne infections were performed to assess potential co-infections.

For 18 months, the boy remained psychotic despite 4 hospitalizations, therapeutic trials involving multiple psychiatric medication combinations, and immunosuppressive treatment for autoimmune encephalitis. Neurobartonellosis was diagnosed after cutaneous lesions developed. Subsequently, despite nearly 2 consecutive months of doxycycline administration, Bartonella henselae DNA was PCR amplified and sequenced from the patient’s blood, and from Bartonella alphaproteobacteria growth medium enrichment blood cultures. B henselae serology was negative. During treatment with combination antimicrobial chemotherapy, he experienced a gradual progressive decrease in neuropsychiatric symptoms, cessation of psychiatric drugs, resolution of Bartonella-associated cutaneous lesions, and a return to all pre-illness activities.

 

Please note that this boy would be in a psych ward if not treated with antimicrobials for Bartonella.