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Disulfiram Psychosis Update #2

For those of you reading my posts I’ve thought of a few other things for practitioners and patients to be aware of.

The Purell Sanitizer, located in each and every hospital room was a trigger for psychosis. Hand sanitizers are up to 60% alcohol – a no, no for those using Disulfiram/Antabuse. I could smell the nurses a mile away. I also learned from a nurse that Purell is killing nurses due to liver toxicity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2954566/“Based upon an average of 30 hand rubbings per healthcare professional per day, it can be assumed that a healthcare worker may be exposed to a maximum 5,500 mg/m³ per work shift, five times above the recommended occupational time weighted average limit. Thus, in order to answer the question posed in the title, studies on spatial and temporal variability of alcohol emission from ABHRs in real world situations and studies on certain high risk individuals are needed.”
According to the FDA says hand sanitizers are contributing to superbugs such as MRSA. Also, Triclosan degrades to dioxins in the body which are also toxic. A 2014 study found that triclosans spurred the growth of breast cancer cells, and another study found they can kill brain cells. Other studies have found it interferes with hormones. https://www.newsmax.com/health/Headline/illness-washing-hands-sanitizers/2014/12/23/id/614647/ This entire issue was ameliorated by having a sign placed outside my room so those coming in would either use soap and water or gloves when entering.
Certain flowers also set me off. I’m afraid I can’t tell you which ones but if anyone else suffers from a toxic reaction to disulfiram, keep all plants out of the room.

When I say “set me off,” these items would cause me to have a psychotic episode – even when I was nearly being discharged. All it took was a flower delivery person who had used Purell and I about had to stay longer in the hospital.

For more: https://madisonarealymesupportgroup.com/2019/10/14/november-2019-lyme-support-meeting-oct-meeting-canceled-due-to-reaction-to-disulfiram/

https://madisonarealymesupportgroup.com/2019/10/15/disulfiram-psychosis-update/

Category:

Lyme, Treatment

Tickborne Triggered Seizure Disorder – A Case Study

https://www.somerdelsignore.com/the-lyme-corner/lets-talk-lyme-disease/pans/pandas/somer-delsignore/2019/10/16/tickborne-triggered-seizure-disorder-case-study-of-a-teenager-with-new-onset-seizure-disorder-and-the-neurological-impact-of-tickborne-diseases

October 16, 2019

By SOMER DELSIGNORE

Tickborne Triggered Seizure Disorder: Case Study of a Teenager with New Onset Seizure Disorder and the Neurological Impact of Tickborne Diseases

The Neurological impact of Bartonella and Rickettsia

This next case study is of an 18-year-old female who was adopted at the age of 5. Her adoptive mother described her as a malnourished premature baby who eventually received good foster care. This young lady was diagnosed with a growth hormone deficiency that was left untreated in her country of origin at the age of two. By the age of five, she was adopted and moved to the US with her American family. She was fully immunized twice, diagnosed with hypothyroidism and inadequate growth. By this time, an Endocrinologist was onboard and treating her thyroid and growth deficiencies. She seemed to rebound, reaching puberty by the age of 13. Life was stable for some time until January of 2016. She was nearly sixteen years old and developed sudden neuropsychiatric symptoms with acute confusion, severe obsessive-compulsive disorder, frequent urination, insomnia, auditory hallucinations, severe sensory issues, leg tremors and eventually catatonia. Given her acute changes, her mother rushed her to the Emergency Room for evaluation. EEG was negative and she was hospitalized for apparent acute psychosis treated with Risperdal and Ativan.

After her hospitalization she followed up with a well-known Neurologist who identified positive Mycoplasma and initiated a course of Azithromycin. By the fourth dose she began to return to her normal state and began sleeping again. She was treated for over a month with antibiotics and seemed stable.

There was a great deal of stress in the family, a close family member died and within two weeks she developed new onset grand mal seizures while sleeping. Another ER visit with a normal EEG at the time determined perhaps the stress and trauma of her family member’s death may have triggered the event.

In January 2018 she had another grand mal seizure early in the am. Her neurologist began medications to address. She had no additional seizure activity but noted increasing anxiety. By December 2018 she suffered another grand mal seizure.

Further evaluation by the neurologist showed negative Lyme screening only, viral panels negative, tick-borne co-infections were not obtained, thyroid studies, electrolytes and inflammatory markers were all within normal limits.

This patient presented to me in February 2019. Upon further evaluation she was found to have progressive muscle weakness, cognitive dysfunction ongoing psychiatric symptoms, tremors and noted random striae or “stretch-marks” that would appear and disappear all over her body. She stated that this had occurred since the age of fourteen. She admitted several evaluations with psychiatric acute hospital admission for escalating neuropsychological symptoms that included visual and auditory hallucinations, compulsions, rage, emotional lability, delusions, anxiety as well as the ongoing physical symptoms. Neuropsychological meds were ineffective. The patient upon presentation was taking high dose Depakote, gabapentin and folic acid to control her seizure activity.

Initial lab work up at my office showed an IGM positive Bartonella Henselae, Lyme Western Blot with an IGM indeterminate band 23-25 and IGG positive bands 18,23-25,28,31,34,39,41,45,and indeterminate bands 58 and 66. She also showed IGG positive Rickettsia and Anaplasma. She carried one copy of MTHFR A1298C and had significant GI bacteria overgrowth with Streptococcus, Citrobacter, Proteus and Bacillus.

She was started on a course of Azithromycin and Bactrim as well as biofilm busters and herbals. Two months later she reported significant improvements noting striae lightening, energy improvements, mood stability, resolution of hallucinations, and her sleep was improving. She noted ongoing body and hand tremors as well as struggles cognitively with word finding but was back in school full time.

We decided to continue the treatment course and repeat her bloodwork in two months as well as continue follow up with her Neurologist to monitor. By June the patient was feeling great. She began a Depakote wean with her Neurologist and graduated High School.

Her lab results showed improvements with Bartonella levels as well as GI bacterial overgrowth. Rickettsia antibodies lingered unchanged as did Lyme bands. I added to her regimen Doxycycline and Cefdinir as well as an antifungal and supportive herbals to prevent yeast.

This patient is still a work in progress, however what is important to note is her complete reversal of the neuropsychological symptoms once antibiotics were initiated as well as the ongoing, successful wean of seizure medications.

Bartonella and Rickettsia infections both have an affinity for the central nervous system. It is challenging to identify given their non-specific symptom presentation at times. Rickettsia isn’t well understood regarding brain parenchyma and central nervous system transmission. We know in mouse studies, Rickettsia and Bartonella both contribute to neuroinflammation which can contribute to acute psychological symptoms. We see this type of neurological process in classic PANS patients related to strep. Although I see the trend clinically, I don’t feel that autoimmune encephalopathy related to tick-borne infections in children and young adults is well documented.

My hope is thru case study presentations you’ll connect real world, everyday struggles of these vulnerable patients with the disease process. I strongly feel further exploration of autoimmune encephalopathy as it relates to Lyme and other Tickborne illnesses in pediatrics should be a collaborative effort with mental health practitioners and welcome those interested to contact me.

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For more: https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/

https://madisonarealymesupportgroup.com/2019/05/05/good-news-for-bartonella-patients-identification-of-fda-approved-drugs-with-higher-activity-than-current-front-line-drugs/

https://madisonarealymesupportgroup.com/2016/02/07/mycoplasma-treatment/

https://madisonarealymesupportgroup.com/2016/03/08/anaplasmosis/ (Treatment)

https://reference.medscape.com/article/968385-treatment (Rickettsia treatment)

Category:

Bartonella, Inflammation, Lyme, Mycoplasma, Psychological Aspects, research, Treatment

Babesia Duncani Emerges in Eastern U.S. & Poses Treatment Challenges

https://danielcameronmd.com/wp-content/uploads/kalins-pdf/singles/babesia-duncani-emerges-in-eastern-u-s-and-poses-treatment-challenges.pdf Read entire article here.

By Dr. Daniel Cameron

New research indicates, however, there may no longer be a division of babesial strains between the East Coast and the West Coast. In their article “Babesia microti – Borrelia burgdorferi Co-infection,” Parveen reports that B. duncani has now been identified in eastern USA and Canada.¹

“Since B. duncani is widespread in Canada, its southern spread into northeastern U.S., an area already endemic for Lyme disease, makes co-infections with B. duncani and B. burgdorferi [Lyme disease] a possibility that needs to be carefully investigated.”

“While this review focuses on co-infection with B. microti and B. burgdorferi, there is some evidence that co-infections with a diﬀerent Babesia species, B. duncani, and B. burgdorferi may be more common than previously suspected,” writes Parveen.

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**Comment**

This article exposes a crucial issue that mainstream medicine is still in the dark ages on – ticks are coinfected and so are we. This is not straight-forward. The very thought that doxycycline is going to cover this hodgepodge of pathogens is truly asinine if you study the research: https://madisonarealymesupportgroup.com/2019/02/22/why-mainstream-lyme-msids-research-remains-in-the-dark-ages/

https://madisonarealymesupportgroup.com/2017/05/01/co-infection-of-ticks-the-rule-rather-than-the-exception/

https://madisonarealymesupportgroup.com/2019/08/25/babesia-microti-borrelia-burgdorferi-coinfection/

https://madisonarealymesupportgroup.com/2019/09/05/babesia-subverts-adaptive-immunity-and-enhances-lyme-disease-severity/

https://madisonarealymesupportgroup.com/2018/10/11/babesia-found-in-patient-with-persistent-symptoms-following-lyme-treatment/

https://madisonarealymesupportgroup.com/2018/10/30/study-shows-lyme-msids-patients-infected-with-many-pathogens-and-explains-why-we-are-so-sick/

I could literally go on and on to infinity – but you get the point – Lyme/MSIDS patients are rarely infected with just Lyme which is why testing is a bit of a joke as well as the mono-therapy of doxycycline. It takes savvy, education, and experience to treat this complex illness that is literally killing people – or making them want to die.

If your doctor is open-minded (a rare quality these days), please attempt to give them continuing education information that could revolutionize the way patients are being treated:

https://madisonarealymesupportgroup.com/2018/06/06/lyme-education-for-healthcare-professionals/

https://madisonarealymesupportgroup.com/2018/02/19/calling-all-doctors-please-become-educated-regarding-tick-borne-illness-heres-how/

Category:

Babesia, research, Treatment

NIH Strategic Plan For Tickborne Disease Research

NIH STRATEGIC PLAN FOR TICKBORNE DISEASE RESEARCH

October 9, 2019

https://www.niaid.nih.gov/sites/default/files/NIH-Strategic-Plan-Tickborne-Disease-Research-2019.pdf

Please see link for:

Executive Summary
Introduction
NIH Strategic Plan for Tickborne Disease
Strategic Priority 1: Improve Fundamental Knowledge of TBDs
Strategic Priority 2: Advance Research to Improve Detection & Diagnosis of TBDs
Strategic Priority 3: Accelerate Research to Improve Prevention of TBDs
Strategic Priority 4: Support Research to Advance Treatment of TBDs
Strategic Priority 5: Develop tools & resources to Advance TBD research
Conclusion
Appendices

Some respondents expressed a desire for greater transparency in the research planning and implementation processes, whereas others suggested changes to the peer review process to include wider representation from the TBD community, such as advocacy group representatives, community physicians, or members of the general public.

To which we all said, AMEN!

Category:

Lyme, research, Ticks, Treatment

Disulfiram Psychosis Update

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Disulfiram: Wikipedia

A Wisconsin Lyme literate doctor who is part of an ILADS provider group with Disulfiram experience, has found that some patients with a genetic predisposition can have significant side effects when using Disulfiram.

Please have your health practitioner look at the dopamine SNP’s before beginning Disulfiram treatment. This LLMD also recommends:

Cysteine
B6
Tyrosine
Disulfiram low and slow at 62.5 mg twice a week, increasing only as tolerated

Please share this far and wide as I do not want another patient to go through the hell I’ve been through.

If you have not read about my experience with Disulfiram psychosis, please see: https://madisonarealymesupportgroup.com/2019/10/14/november-2019-lyme-support-meeting-oct-meeting-canceled-due-to-reaction-to-disulfiram/

My symptoms were:

Converging vision (eyes seemingly want to cross, kind of like when you are up at 2 a.m. studying for a Biomechanics final.
Inability to orgasm (sorry if this is TMI, but since this is a matter of life and death I felt the need to throw it out there)
Bloating (belching, passing gas, and distended stomach)

If I would have been warned of these issues I perhaps could have avoided two ER visits and a week long stay at the UW Hospital. My total tab is estimated to be potentially more than 20K, so please spread the word to anyone on Disulfiram or considering it.

For doctors reading this, the titration is as follows:

250mg MWF for 3 weeks, then
250 daily for 3 weeks, then
500mg MWF,
250mg T, TH, SAT, SUN for 3 weeks, then
500mg daily for approximately 3 months with individual variation. The goal is to be symptom free

Others are titrating even more slowly; however, I assure you my issues with the drug had nothing to do with titration or anything I did. My husband was on the exact same protocol and was fine. I truly believe this is a dopamine issue and a toxic reaction to disulfiram.

I’ve been alerted that this has happened to others as well.

For research on psychosis induced by disulfiram: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290718/

Abstract

Disulfiram is the commonly prescribed drug for the treatment of alcohol dependence. It’s major metabolite (diethyldithiocarbamate) is an inhibitor of dopamine-betahydroxylase, an enzyme that catalyzes the metabolism of dopamine to norepinephrine resulting in psychosis. We recommend that disulfiram should be used at the lowest effective dose, possibly 250 mg daily and caution should be taken while prescribing disulfiram for patients with personal and familial antecedents of psychosis.…..Disulfiram-related psychiatric complications are reported to be more prevalent in eastern countries,3) which suggests that genetic factors may play a role in disulfiram induced psychosis.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1238733/pdf/westjmed00250-0085.pdf

In this paper, a hypothesis of vulnerability to disulfiram psychosis is proposed, based on the current lines of evidence for the biological mechanisms involved in the psychoses.

Disulfiram Is a DA Agonist

Disulfiram is an inhibitor of dopamine-beta- hydroxylase (DBH), an enzyme that catalyzes themetabolism of DA to norepinephrine (NE).3 By inhibiting the metabolic pathway from DA to NE in the central nervous system, disulfiram results in an increase of DA concentrations. Therefore, disulfiram is a DA agonist, and is likely to exacerbate preexisting or latent psychosis, similar to amphetamine, methylphenidate and L-dopa.

DAandAffectivePsychosis

Increased brain DA is highly correlated with psychomotor activity in animals, and L-dopa has been shown to produce episodes of hypo maniaand mania in most patients with bipolar affective psychosis.4 It is possible,therefore,that disulfiram can uncover a preexisting or latent hypomania or mania.