PNES - a cause
Psychogenic non-epileptic seizures (PNES)
Postulate:
The emotions are the cause and result of neurotransmitter transitions in the brain.[] (cause through personality; result when chemical changes are induced you medications, toxins, nutritional deficiencies for examples.)
The neurotransmitters require and expend nutrients when they are created, or when one converts to another.[]
When there is a nutritional deficiency, sometimes other micronutrients can take its place in one or more of the molecules that use the deficient nutrient, if less efficiently, such as [Mn for Mg in glutamine synthetase (GS)]
(which would explain[zinc for iron if eating folic acid in pernicious anemia, expelling much zinc in fecal waste]. Might not put this in final paper.)
Shortage of GS would be consistent with a shortage of glutamine and an excess of glutamate in the body.[]
Glutamate activates muscles.[]
If the calcium magnesium balance is far enough off, it can cause muscle cramps in the legs.[dr O'Dell ltr]
Magnesium deficiency may not show in the blood before if shows elsewhere in the body.[jjw,jj liu w, dr odell ltr]
Heavy exercise can cause mg deficiency to show in the blood sooner (by X time?)[jjw]
...which imples that exercise can prioritize magnesium to the muscles from the blood; that a system in the body that needs a nutrient can prioritize it by being used more. We therefore not only are what we eat, because our bodies can't have a nutrient that it hasn't ingested, or ingested the nutrients required to make it, but we also are what we do, even if a nutritional deficiency requires that we hypotrophy in systems we haven't been using as much to acquire the nutrients for what we have been doing.
The blood contains nutrients which feeds the internal organs, necessary for functioning of the body [find citation?]
Deficiencies in the blood would thus be detrimental to the functioning of the most important or used parts of the body. Maintaining sufficient nutrient levels in the blood might be achieved via various strategies, such as by replacing the nutrient in shortage with a less efficient choice in some other bodily function[gs]
...or by doing less of another function, such as removing calcium from the arteries.[Uwe Gröber - magnesium and drugs]
...or (by prioritizing the nutrient back and forth between uses, at the risk of loss, no Citation for this but that explains the iron/heat issues.) other strategies.
If there is a shortage of magnesium in the muscles to build glutamate synthetase, it might result in an excess of glutamate in the mucles, as versus in the brain.[Possible citation?]
Magnesium, deficiency can cause epilepsy.[] (calcium, potassium, too.)
One possible cause would be excess glutamate in the brain[??]
, from inability to create glutamine synthitase.[]
CBT (cognitive behavioral therapy) and serotonin reuptake inhibitors/etc(list) have proven effective for PNES.
Does serotonin (etc?)bprotect damage of enzymes or other magnesium-containing chemicals in the body? [?](cite or postulate hypothetically)
CBT, by reducing neurotransmitter usage, could also conserve magnesium.
--
Also, adrenaline, by increasing cortisol, is recognized to increase blood sugar and thus fuel the muscles for such superfeats as lifting cars off of a relative by people otherwise unable to even attempt such exercise under other situations.([] or insert word "anecdotally")
This has been explained by adrenaline increasing cortisol, and cortisol increasing blood glucose levels.[x,y,z]
However, diabetics have increased glucose levels in the blood but are not able to lift cars as a result.[]
Cortisol increases damage to the body,[] sometimes described as toxic stress. [??]
That damage occurs because cortisol steals nutrients from the body to put into the blood, to optimize the muscles' ability not only to use fuel, but to prevent or repair damage quickly, optimizing the blood for levels of required nutrients[]
...and antioxidants(???)[??]
. . .which would imply that for people with a strong fear of needles or hysteria or other high adrenaline or cortisol conditions, serum lab tests might not give accurate results
... [gotta do a paper on my tests all normal when 0.02 TSH, just short of heart attack level; Dr.: "Good news, you're fine!" w/almost deadly TSH result next morning, and aren't I glad that I blackmailed her with withholding all lab test unless she ran a TSH, and insisted on lab result before taking my meds the next day?]
And adrenaline binds to copper[], reducing excess copper from the blood, a separate mechanism for optimizing the blood for such superfeats. (Since hypomania can be simulated by anger, possibly hypomania is caused by excess copper, and the body protecting Itself by increasing adrenaline.)
--
Therefore, I postulate that some people with PNES might have prioritized magnesium to the brain (as some medications for both mental illness and epilepsy have been found to do[book])
. . . but to implies from, and if from the muscles, it could result in seizures caused not by activating the nerves from the brain, but directly in the muscles themselves, when their emotions
either waste extra magnesium, or another nutrient which then exacerbates magnesium deficiency, or depletes serotonin or other magnesium-protective antioxidants, resulting in muscular shortage of the enzyme glutamine synthetase, and creating psychgenic but not intentional or directly psychiatric symptoms of epilepsy.
This might possibly be confirmed by testing samples of muscle, by increasing dietary magnesium as described by [bunch of citations from the Magnesium research Underground]
. . . or by the suggested method by James DiNicolantonio *et al* of four weeks of rigorous exercise daily to see if the magnesium is prioritized as a result to the muscles, but at risk that the magnesium shortage may be transferred to somewhere more dangerous, or why wouldn't the body have prioritized the deficiency there in the first place?
A side benefit of this would be that patients suffering this condition would no longer feel blamed for having induced it on themselves psychiatrically. The reduction of stress could be beneficial to reducing the number of psychogenic non-epileptic seizures as a result.
--
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4234133/#:~:text=Psychogenic%20movement%20disorders%20account%20for,which%20these%20studies%20were%20drawn.
Continuum : Lifelong Learning in Neurology
American Academy of Neurology
Psychogenic Movement Disorders
Francesca Morgante, MD, PhD, Mark J. Edwards, MD, MBBS, PhD, and Alberto J. Espay, MD, MSc, FAAN
Abstract
"Purpose of Review"
"This review describes the main clinical features of psychogenic (functional) movement disorders and reports recent advances in diagnosis, pathophysiology, and treatment."
"Correct diagnosis of psychogenic movement disorders should rely not on the exclusion of organic disorders or the sole presence of psychological factors but on the observation or elicitation of clinical features related to the specific movement disorder (ie, a positive or inclusionary rather than exclusionary diagnosis). Sudden onset, spontaneous remissions, and variability over time or during clinical examination are useful “red flags” suggestive of a psychogenic movement disorder. Imaging studies have demonstrated impaired connectivity between limbic and motor areas involved in movement programming and hypoactivity of a brain region that compares expected data with actual sensory data occurring during voluntary movement. Treatment of psychogenic movement disorders begins with ensuring the patient’s acceptance of the diagnosis during the initial debriefing and includes nonpharmacologic (cognitive-behavioral therapy, physiotherapy) and pharmacologic options."
"As short duration of disease correlates with better prognosis, early diagnosis and initiation of treatment are critical."
11 years and self-diagnosis . . . Fuck the goddamn medical community. If I've been diagnosed, I don't think my hair would have been any better and it might have been worse. Certainly the blame would have been. 11 years ago, I didn't have the information I have now about things like the Magnesium test not being accurate.
--
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553143/

J Endocr Soc. 2019 Apr 15; 3(Suppl 1): SUN-498.
Published online 2019 Apr 30. doi: 10.1210/js.2019-SUN-498
PMCID: PMC6553143
SUN-498 Normocalcemic Tetany: Is Parathyroid Insufficiency a Real Thing?
Mamta Chhetri, MD and Patricia Bononi, MD
Author information Copyright and License information Disclaimer
Abstract
Background: Tetany is characterized by painful flexion of wrist and ankle joints (carpopedal spasm), circumoral numbness and muscle cramps. Increased excitability of peripheral nerves causing tetany is usually due to low ionized calcium. “Normocalcemic tetany” has been reported to be a manifestation of hypomagnesemia, hypokalemia and hyperventilation syndrome. We report a case of normocalcemic tetany in a young woman with a remote history of thyroid surgery. Clinical Case: A 33 year old female with history of total thyroidectomy for a benign nodular goiter presented for evaluation of spells that started 2-3 weeks after total thyroidectomy. Described as a tingling sensation in the neck followed by diffuse muscle cramping, curling of her hands and feet. Each episode lasted 30-60 minutes, 3-4 times a day, 3-4 times a week. These episodes are aggravated by pain, extreme heat and cold, during menstruation, after sexual intercourse and stress. She had irregular contractions with false labor several times during both of her pregnancies. Photographs and videos taken by husband during spells were reviewed and findings consistent with carpopedal spasms. Prior evaluation done by multiple specialtists was negative. Labs showed corrected total calcium 8.5 (8.6-10.3 mg/dL), Ionized calcium 1.25 (1.20-1.40 mmol/L), PTH 30 (12-88 pg/mL), 24 hr urine calcium 206 (100-300 mg/24hrs), 25 hydroxy vitamin D 32.37 (30-100 ng/mL), 1,25 dihydroxy vitamin D 60.4 (19.3-79.3 pg/mL), Phosphorus 3.7 (2.4-4.7 mg/dL) and Magnesium 2.2 (1.8-2.5 mg/dL). Continuous video EEG monitoring showed episodes with opisthotonic posturing, arrhythmic body shaking, hands and feet curling described as nonepileptiform activity. MRI of the whole spine was normal. She is consistently taking Ergocalciferol 50,000 units weekly, Calcium carbonate 1000 mg daily and Calcium carbonate antacid (Tums) as needed. Despite this, she continues to have 1-2 episodes a week. Physical exam showed intermittent bilateral positive Chvostek’s sign. During a recent hysterectomy, she empirically received continuous calcium infusion with maximum Calcium level documented at 9.1 mg/dL. She did not have any episodes for a week after the infusion. This has had a major impact in her life. She is not able to drive and is on disability. She has been recently started on Recombinant PTH (Nat Para) to see if this can eliminate the carpopedal spasms and improve her quality of life. Conclusion: Our patient is being treated as parathyroid insufficiency with relative hypocalcemia from prior total thyroidectomy. The presentation may be subtle with symptoms of hypocalcemia occurring only during metabolic stress, and that a normal serum PTH level in this context may be misleading.
Brain atrophy from nutritional deficiencies like covid and zinc.
Parvareshi Hamrah M, Rezaei Tavirani M, Movahedi M, Ahmadi Karvigh S. Identification of Serum Biomarkers for Differentiating Epileptic Seizures from Psychogenic Attacks Using a Proteomic Approach; a Comparative study. Arch Acad Emerg Med. 2020 Oct 29;8(1):e87. PMID: 33244522; PMCID: PMC7682629.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7682629/
Bookmark: PNES:Adren binds to Cu, cerplamin down.
--
Stress triggers regular epilepsy so why isn't it called psychogenic as well?
Stavropoulos I, Pervanidou P, Gnardellis C, Loli N, Theodorou V, Mantzou A, Soukou F, Sinani O, Chrousos GP. Increased hair cortisol and antecedent somatic complaints in children with a first epileptic seizure. Epilepsy Behav. 2017 Mar;68:146-152. doi: 10.1016/j.yebeh.2016.12.015. Epub 2017 Feb 9. PMID: 28189919.
Abstract
Objective: Stress is the most frequent seizure-precipitating factor reported by patients with epilepsy, while stressful life events may increase seizure susceptibility in humans. In this study, we investigated the relations between both biological and behavioral measures of stress in children with a first epileptic seizure (hereafter called seizure). We hypothesized that hair cortisol, a biomarker of chronic stress reflecting approximately 3months of preceding exposure, might be increased in children with a first seizure. We also employed standardized questionnaires to examine presence of stress-related behavioral markers.
Significance: Increased hair cortisol indicates chronic hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis prior to the first seizure. This might have contributed to the epileptogenesis process and may help explain the higher incidence of antecedent somatic complaints in the first seizure group.
Is this true of PNES as well?
---
NEW ORLEANS — Patients with psychogenic nonepileptic seizures (PNES) have a mortality rate that is more than two times higher than the general population and die at a rate comparable with that of patients who have drug-resistant epilepsy, new research shows.Dec 13, 2018

https://www.medscape.com › viewar...
High Premature Death Rate for Psychogenic Seizures Troubling
Mortality in patients with psychogenic nonepileptic seizures
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Russell Nightscales, Lara McCartney, Clarissa Auvrez, Gerard Tao, Sarah Barnard, Charles B. Malpas, Piero Perucca, Anne McIntosh, Zhibin Chen, Shobi Sivathamboo, Sophia Ignatiadis, Simon Jones, Sophia Adams, Mark J. Cook, Patrick Kwan, Dennis Velakoulis, Wendyl D'Souza, Samuel F. Berkovic, Terence J. O'Brien
Neurology Aug 2020, 95 (6) e643-e652; DOI: 10.1212/WNL.0000000000009855
Conclusions Patients diagnosed with PNES have a SMR 2.5 times above the general population, dying at a rate comparable to those with drug-resistant epilepsy. This emphasizes the importance of prompt diagnosis, identification of risk factors, and implementation of appropriate strategies to prevent potential avoidable deaths.
--
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438261/
From: Nonepileptic Seizures: An Updated Review
THE EMERGING NEUROBIOLOGY OF PNES
Systems-level functional and structural neuroimaging studies have started to elucidate the neurobiology of PNES3. Several functional magnetic resonance imaging (fMRI)43-47 and one positron emission tomography (PET) study used resting state techniques to investigate neural circuit disturbances in PNES. In a region-of-interest “seed” based analysis, increased functional connectivity was observed between motor regions (precentral sulcus) and regions involved in emotional processing (anterior cingulate cortex (ACC), insula) and executive functions (inferior frontal gyrus, parietal cortex); among other findings, trait dissociation scores positively correlated with the functional connectivity strength between the precentral sulcus and the posterior insula43. Several studies used data-driven, multivariate functional connectivity analyses to demonstrate widespread functional connectivity alterations in emotion control, executive, fronto-parietal (attentional), sensorimotor and default mode networks44-46. Another study specifically evaluated functional connectivity patterns across insular subregions, observing that PNES compared to healthy subjects showed increased functional connectivity between the left ventral anterior insula and the left post-central gyrus and bilateral supplementary motor area (SMA); functional connectivity strength within the bilateral SMA positively correlated with PNES event frequency47. Functional connectivity strength between the SMA and ACC has also been shown to positively correlate with PNES frequency48. In comparison to healthy subjects, a 2-deoxy-2-[fluorine-18]fluoro-D-glucose PET study showed that PNES patients exhibited bilateral ACC and right inferior parietal lobule hypometabolism49.
Perez DL, LaFrance WC Jr. Nonepileptic seizures: an updated review. CNS Spectr. 2016 Jun;21(3):239-46. doi: 10.1017/S109285291600002X. Epub 2016 Mar 21. PMID: 26996600; PMCID: PMC5438261.
Quantitative structural MRI have also been conducted in PNES50-52. Compared to matched controls, PNES patients showed ACC, SMA and pre and post central gyrus atrophy on cortical thickness and voxel-based-morphometry analyses50; bilateral precentral gyrus cortical thickness reductions were independently replicated along with observed increases in insular and orbitofrontal cortical thickness in PNES52
- and what do you think causes this later in life? Can you say, nutritional deficiency of magnesium calcium and zinc?
People with long covid are showing brain atrophy, guess what, low zinc. Any questions?
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Hypomagnesemia is often associated with hypokalemia (due to urinary potassium wasting) and hypocalcemia (due both to lower parathyroid hormone secretion and end-organ resistance to its effect). (See "Hypomagnesemia: Clinical manifestations of magnesium depletion".)Jun 12, 2020

https://www.uptodate.com › contents
Hypomagnesemia: Causes of hypomagnesemia - UpToDate
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https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/electrolyte-disorders/hypomagnesemia&ved=2ahUKEwjy3_6YlbHxAhUSWs0KHU3XDscQFnoECAcQAQ&usg=AOvVaw2qGXWFAoUjfV8AjMzkvwCK
Article bites: Compassion first: Mortality risk of patients with psychogenic nonepileptic seizures
There is nothing fake or pseudo about the mortality rate of patients with PNES
Nov 18, 2020
Additionally, PNES patients have high rates of underlying substance use disorder and psychiatric illness which can further cloud the clinical picture.
This is a difficult diagnosis for even the hospital neurologists, demonstrated by the fact that PNES patient account for 25% of EEG unit admissions and a final diagnosis of PNES takes an average of eight years! If that’s not enough, between 5-20% of PNES patients also have true epilepsy.
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IDIOTS!
"alexithymia traits, meaning that they had difficulties in feeling or perceiving emotions. In subjects where PNES are associated with a borderline personality, in which the symbolic function is lost, the defense mechanisms are of a more archaic nature (denial). PNES with different underlying defense mechanisms have different prognoses (despite similar severity of PNES) and need usually a different treatment (pharmacological or psychological). Thus, it appears superfluous to talk about psychiatric comorbidity, since PNES are a different symptomatic expression of specific psychiatric disorders."
What causes an inability to feel emotions? Take someone in shock. If used up all their nutrients, or at least enough so where your body isn't functioning correctly. They can't feel emotions either. Maybe they have some of the same reasons behind it.
Trouble perceiving emotions? Can you say "Mirror neurons"? Obviously, you can't - but I can.
Defense mechanisms? Of the BODY, idiots!
Do you really think that emotions magically affect the body? Did it ever occur to you that emotions are neurotransmitters, and your transmitter transitions in the brain, and that the brain is fucked up, the body will follow? Old, you know it doesn't get sourced in the brain, but it's the same thing at the muscles, High glutamate.
God, some of these people really piss me off.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599147/#!po=2.74725
Psychogenic non-epileptic seizures: so-called psychiatric comorbidity and underlying defense mechanisms
Massimiliano Beghi, Paola Beffa Negrini, [...], and Cesare Maria Cornaggia
Additional article information
Abstract
In Diagnostic and Statistical Manual of Mental Disorders, fifth edition, psychogenic non-epileptic seizures (PNES) do not have a unique classification as they can be found within different categories: conversion, dissociative, and somatization disorders. The ICD-10, instead, considers PNES within dissociative disorders, merging the dissociative disorders and conversion disorders, although the underlying defense mechanisms are different. The literature data show that PNES are associated with cluster B (mainly borderline) personality disorders and/or to people with depressive or anxiety disorders. Defense mechanisms in patients with PNES with a prevalence of anxious/depressive symptoms are of “neurotic” type; their goal is to lead to a “split”, either vertical (dissociation) or horizontal (repression). The majority of patients with this type of PNES have alexithymia traits, meaning that they had difficulties in feeling or perceiving emotions. In subjects where PNES are associated with a borderline personality, in which the symbolic function is lost, the defense mechanisms are of a more archaic nature (denial). PNES with different underlying defense mechanisms have different prognoses (despite similar severity of PNES) and need usually a different treatment (pharmacological or psychological). Thus, it appears superfluous to talk about psychiatric comorbidity, since PNES are a different symptomatic expression of specific psychiatric disorders.
Postulate:
The emotions are the cause and result of neurotransmitter transitions in the brain.[] (cause through personality; result when chemical changes are induced you medications, toxins, nutritional deficiencies for examples.)
The neurotransmitters require and expend nutrients when they are created, or when one converts to another.[]
When there is a nutritional deficiency, sometimes other micronutrients can take its place in one or more of the molecules that use the deficient nutrient, if less efficiently, such as [Mn for Mg in glutamine synthetase (GS)]
(which would explain[zinc for iron if eating folic acid in pernicious anemia, expelling much zinc in fecal waste]. Might not put this in final paper.)
Shortage of GS would be consistent with a shortage of glutamine and an excess of glutamate in the body.[]
Glutamate activates muscles.[]
If the calcium magnesium balance is far enough off, it can cause muscle cramps in the legs.[dr O'Dell ltr]
Magnesium deficiency may not show in the blood before if shows elsewhere in the body.[jjw,jj liu w, dr odell ltr]
Heavy exercise can cause mg deficiency to show in the blood sooner (by X time?)[jjw]
...which imples that exercise can prioritize magnesium to the muscles from the blood; that a system in the body that needs a nutrient can prioritize it by being used more. We therefore not only are what we eat, because our bodies can't have a nutrient that it hasn't ingested, or ingested the nutrients required to make it, but we also are what we do, even if a nutritional deficiency requires that we hypotrophy in systems we haven't been using as much to acquire the nutrients for what we have been doing.
The blood contains nutrients which feeds the internal organs, necessary for functioning of the body [find citation?]
Deficiencies in the blood would thus be detrimental to the functioning of the most important or used parts of the body. Maintaining sufficient nutrient levels in the blood might be achieved via various strategies, such as by replacing the nutrient in shortage with a less efficient choice in some other bodily function[gs]
...or by doing less of another function, such as removing calcium from the arteries.[Uwe Gröber - magnesium and drugs]
...or (by prioritizing the nutrient back and forth between uses, at the risk of loss, no Citation for this but that explains the iron/heat issues.) other strategies.
If there is a shortage of magnesium in the muscles to build glutamate synthetase, it might result in an excess of glutamate in the mucles, as versus in the brain.[Possible citation?]
Magnesium, deficiency can cause epilepsy.[] (calcium, potassium, too.)
One possible cause would be excess glutamate in the brain[??]
, from inability to create glutamine synthitase.[]
CBT (cognitive behavioral therapy) and serotonin reuptake inhibitors/etc(list) have proven effective for PNES.
Does serotonin (etc?)bprotect damage of enzymes or other magnesium-containing chemicals in the body? [?](cite or postulate hypothetically)
CBT, by reducing neurotransmitter usage, could also conserve magnesium.
--
Also, adrenaline, by increasing cortisol, is recognized to increase blood sugar and thus fuel the muscles for such superfeats as lifting cars off of a relative by people otherwise unable to even attempt such exercise under other situations.([] or insert word "anecdotally")
This has been explained by adrenaline increasing cortisol, and cortisol increasing blood glucose levels.[x,y,z]
However, diabetics have increased glucose levels in the blood but are not able to lift cars as a result.[]
Cortisol increases damage to the body,[] sometimes described as toxic stress. [??]
That damage occurs because cortisol steals nutrients from the body to put into the blood, to optimize the muscles' ability not only to use fuel, but to prevent or repair damage quickly, optimizing the blood for levels of required nutrients[]
...and antioxidants(???)[??]
. . .which would imply that for people with a strong fear of needles or hysteria or other high adrenaline or cortisol conditions, serum lab tests might not give accurate results
... [gotta do a paper on my tests all normal when 0.02 TSH, just short of heart attack level; Dr.: "Good news, you're fine!" w/almost deadly TSH result next morning, and aren't I glad that I blackmailed her with withholding all lab test unless she ran a TSH, and insisted on lab result before taking my meds the next day?]
And adrenaline binds to copper[], reducing excess copper from the blood, a separate mechanism for optimizing the blood for such superfeats. (Since hypomania can be simulated by anger, possibly hypomania is caused by excess copper, and the body protecting Itself by increasing adrenaline.)
--
Therefore, I postulate that some people with PNES might have prioritized magnesium to the brain (as some medications for both mental illness and epilepsy have been found to do[book])
. . . but to implies from, and if from the muscles, it could result in seizures caused not by activating the nerves from the brain, but directly in the muscles themselves, when their emotions
either waste extra magnesium, or another nutrient which then exacerbates magnesium deficiency, or depletes serotonin or other magnesium-protective antioxidants, resulting in muscular shortage of the enzyme glutamine synthetase, and creating psychgenic but not intentional or directly psychiatric symptoms of epilepsy.
This might possibly be confirmed by testing samples of muscle, by increasing dietary magnesium as described by [bunch of citations from the Magnesium research Underground]
. . . or by the suggested method by James DiNicolantonio *et al* of four weeks of rigorous exercise daily to see if the magnesium is prioritized as a result to the muscles, but at risk that the magnesium shortage may be transferred to somewhere more dangerous, or why wouldn't the body have prioritized the deficiency there in the first place?
A side benefit of this would be that patients suffering this condition would no longer feel blamed for having induced it on themselves psychiatrically. The reduction of stress could be beneficial to reducing the number of psychogenic non-epileptic seizures as a result.
--
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4234133/#:~:text=Psychogenic%20movement%20disorders%20account%20for,which%20these%20studies%20were%20drawn.
Continuum : Lifelong Learning in Neurology
American Academy of Neurology
Psychogenic Movement Disorders
Francesca Morgante, MD, PhD, Mark J. Edwards, MD, MBBS, PhD, and Alberto J. Espay, MD, MSc, FAAN
Abstract
"Purpose of Review"
"This review describes the main clinical features of psychogenic (functional) movement disorders and reports recent advances in diagnosis, pathophysiology, and treatment."
"Correct diagnosis of psychogenic movement disorders should rely not on the exclusion of organic disorders or the sole presence of psychological factors but on the observation or elicitation of clinical features related to the specific movement disorder (ie, a positive or inclusionary rather than exclusionary diagnosis). Sudden onset, spontaneous remissions, and variability over time or during clinical examination are useful “red flags” suggestive of a psychogenic movement disorder. Imaging studies have demonstrated impaired connectivity between limbic and motor areas involved in movement programming and hypoactivity of a brain region that compares expected data with actual sensory data occurring during voluntary movement. Treatment of psychogenic movement disorders begins with ensuring the patient’s acceptance of the diagnosis during the initial debriefing and includes nonpharmacologic (cognitive-behavioral therapy, physiotherapy) and pharmacologic options."
"As short duration of disease correlates with better prognosis, early diagnosis and initiation of treatment are critical."
11 years and self-diagnosis . . . Fuck the goddamn medical community. If I've been diagnosed, I don't think my hair would have been any better and it might have been worse. Certainly the blame would have been. 11 years ago, I didn't have the information I have now about things like the Magnesium test not being accurate.
--
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553143/

J Endocr Soc. 2019 Apr 15; 3(Suppl 1): SUN-498.
Published online 2019 Apr 30. doi: 10.1210/js.2019-SUN-498
PMCID: PMC6553143
SUN-498 Normocalcemic Tetany: Is Parathyroid Insufficiency a Real Thing?
Mamta Chhetri, MD and Patricia Bononi, MD
Author information Copyright and License information Disclaimer
Abstract
Background: Tetany is characterized by painful flexion of wrist and ankle joints (carpopedal spasm), circumoral numbness and muscle cramps. Increased excitability of peripheral nerves causing tetany is usually due to low ionized calcium. “Normocalcemic tetany” has been reported to be a manifestation of hypomagnesemia, hypokalemia and hyperventilation syndrome. We report a case of normocalcemic tetany in a young woman with a remote history of thyroid surgery. Clinical Case: A 33 year old female with history of total thyroidectomy for a benign nodular goiter presented for evaluation of spells that started 2-3 weeks after total thyroidectomy. Described as a tingling sensation in the neck followed by diffuse muscle cramping, curling of her hands and feet. Each episode lasted 30-60 minutes, 3-4 times a day, 3-4 times a week. These episodes are aggravated by pain, extreme heat and cold, during menstruation, after sexual intercourse and stress. She had irregular contractions with false labor several times during both of her pregnancies. Photographs and videos taken by husband during spells were reviewed and findings consistent with carpopedal spasms. Prior evaluation done by multiple specialtists was negative. Labs showed corrected total calcium 8.5 (8.6-10.3 mg/dL), Ionized calcium 1.25 (1.20-1.40 mmol/L), PTH 30 (12-88 pg/mL), 24 hr urine calcium 206 (100-300 mg/24hrs), 25 hydroxy vitamin D 32.37 (30-100 ng/mL), 1,25 dihydroxy vitamin D 60.4 (19.3-79.3 pg/mL), Phosphorus 3.7 (2.4-4.7 mg/dL) and Magnesium 2.2 (1.8-2.5 mg/dL). Continuous video EEG monitoring showed episodes with opisthotonic posturing, arrhythmic body shaking, hands and feet curling described as nonepileptiform activity. MRI of the whole spine was normal. She is consistently taking Ergocalciferol 50,000 units weekly, Calcium carbonate 1000 mg daily and Calcium carbonate antacid (Tums) as needed. Despite this, she continues to have 1-2 episodes a week. Physical exam showed intermittent bilateral positive Chvostek’s sign. During a recent hysterectomy, she empirically received continuous calcium infusion with maximum Calcium level documented at 9.1 mg/dL. She did not have any episodes for a week after the infusion. This has had a major impact in her life. She is not able to drive and is on disability. She has been recently started on Recombinant PTH (Nat Para) to see if this can eliminate the carpopedal spasms and improve her quality of life. Conclusion: Our patient is being treated as parathyroid insufficiency with relative hypocalcemia from prior total thyroidectomy. The presentation may be subtle with symptoms of hypocalcemia occurring only during metabolic stress, and that a normal serum PTH level in this context may be misleading.
Brain atrophy from nutritional deficiencies like covid and zinc.
Parvareshi Hamrah M, Rezaei Tavirani M, Movahedi M, Ahmadi Karvigh S. Identification of Serum Biomarkers for Differentiating Epileptic Seizures from Psychogenic Attacks Using a Proteomic Approach; a Comparative study. Arch Acad Emerg Med. 2020 Oct 29;8(1):e87. PMID: 33244522; PMCID: PMC7682629.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7682629/
Bookmark: PNES:Adren binds to Cu, cerplamin down.
--
Stress triggers regular epilepsy so why isn't it called psychogenic as well?
Stavropoulos I, Pervanidou P, Gnardellis C, Loli N, Theodorou V, Mantzou A, Soukou F, Sinani O, Chrousos GP. Increased hair cortisol and antecedent somatic complaints in children with a first epileptic seizure. Epilepsy Behav. 2017 Mar;68:146-152. doi: 10.1016/j.yebeh.2016.12.015. Epub 2017 Feb 9. PMID: 28189919.
Abstract
Objective: Stress is the most frequent seizure-precipitating factor reported by patients with epilepsy, while stressful life events may increase seizure susceptibility in humans. In this study, we investigated the relations between both biological and behavioral measures of stress in children with a first epileptic seizure (hereafter called seizure). We hypothesized that hair cortisol, a biomarker of chronic stress reflecting approximately 3months of preceding exposure, might be increased in children with a first seizure. We also employed standardized questionnaires to examine presence of stress-related behavioral markers.
Significance: Increased hair cortisol indicates chronic hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis prior to the first seizure. This might have contributed to the epileptogenesis process and may help explain the higher incidence of antecedent somatic complaints in the first seizure group.
Is this true of PNES as well?
---
NEW ORLEANS — Patients with psychogenic nonepileptic seizures (PNES) have a mortality rate that is more than two times higher than the general population and die at a rate comparable with that of patients who have drug-resistant epilepsy, new research shows.Dec 13, 2018

https://www.medscape.com › viewar...
High Premature Death Rate for Psychogenic Seizures Troubling
Mortality in patients with psychogenic nonepileptic seizures
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Russell Nightscales, Lara McCartney, Clarissa Auvrez, Gerard Tao, Sarah Barnard, Charles B. Malpas, Piero Perucca, Anne McIntosh, Zhibin Chen, Shobi Sivathamboo, Sophia Ignatiadis, Simon Jones, Sophia Adams, Mark J. Cook, Patrick Kwan, Dennis Velakoulis, Wendyl D'Souza, Samuel F. Berkovic, Terence J. O'Brien
Neurology Aug 2020, 95 (6) e643-e652; DOI: 10.1212/WNL.0000000000009855
Conclusions Patients diagnosed with PNES have a SMR 2.5 times above the general population, dying at a rate comparable to those with drug-resistant epilepsy. This emphasizes the importance of prompt diagnosis, identification of risk factors, and implementation of appropriate strategies to prevent potential avoidable deaths.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438261/
From: Nonepileptic Seizures: An Updated Review
THE EMERGING NEUROBIOLOGY OF PNES
Systems-level functional and structural neuroimaging studies have started to elucidate the neurobiology of PNES3. Several functional magnetic resonance imaging (fMRI)43-47 and one positron emission tomography (PET) study used resting state techniques to investigate neural circuit disturbances in PNES. In a region-of-interest “seed” based analysis, increased functional connectivity was observed between motor regions (precentral sulcus) and regions involved in emotional processing (anterior cingulate cortex (ACC), insula) and executive functions (inferior frontal gyrus, parietal cortex); among other findings, trait dissociation scores positively correlated with the functional connectivity strength between the precentral sulcus and the posterior insula43. Several studies used data-driven, multivariate functional connectivity analyses to demonstrate widespread functional connectivity alterations in emotion control, executive, fronto-parietal (attentional), sensorimotor and default mode networks44-46. Another study specifically evaluated functional connectivity patterns across insular subregions, observing that PNES compared to healthy subjects showed increased functional connectivity between the left ventral anterior insula and the left post-central gyrus and bilateral supplementary motor area (SMA); functional connectivity strength within the bilateral SMA positively correlated with PNES event frequency47. Functional connectivity strength between the SMA and ACC has also been shown to positively correlate with PNES frequency48. In comparison to healthy subjects, a 2-deoxy-2-[fluorine-18]fluoro-D-glucose PET study showed that PNES patients exhibited bilateral ACC and right inferior parietal lobule hypometabolism49.
Perez DL, LaFrance WC Jr. Nonepileptic seizures: an updated review. CNS Spectr. 2016 Jun;21(3):239-46. doi: 10.1017/S109285291600002X. Epub 2016 Mar 21. PMID: 26996600; PMCID: PMC5438261.
Quantitative structural MRI have also been conducted in PNES50-52. Compared to matched controls, PNES patients showed ACC, SMA and pre and post central gyrus atrophy on cortical thickness and voxel-based-morphometry analyses50; bilateral precentral gyrus cortical thickness reductions were independently replicated along with observed increases in insular and orbitofrontal cortical thickness in PNES52
- and what do you think causes this later in life? Can you say, nutritional deficiency of magnesium calcium and zinc?
People with long covid are showing brain atrophy, guess what, low zinc. Any questions?
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Hypomagnesemia is often associated with hypokalemia (due to urinary potassium wasting) and hypocalcemia (due both to lower parathyroid hormone secretion and end-organ resistance to its effect). (See "Hypomagnesemia: Clinical manifestations of magnesium depletion".)Jun 12, 2020

https://www.uptodate.com › contents
Hypomagnesemia: Causes of hypomagnesemia - UpToDate
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https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/electrolyte-disorders/hypomagnesemia&ved=2ahUKEwjy3_6YlbHxAhUSWs0KHU3XDscQFnoECAcQAQ&usg=AOvVaw2qGXWFAoUjfV8AjMzkvwCK
Article bites: Compassion first: Mortality risk of patients with psychogenic nonepileptic seizures
There is nothing fake or pseudo about the mortality rate of patients with PNES
Nov 18, 2020
Additionally, PNES patients have high rates of underlying substance use disorder and psychiatric illness which can further cloud the clinical picture.
This is a difficult diagnosis for even the hospital neurologists, demonstrated by the fact that PNES patient account for 25% of EEG unit admissions and a final diagnosis of PNES takes an average of eight years! If that’s not enough, between 5-20% of PNES patients also have true epilepsy.
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IDIOTS!
"alexithymia traits, meaning that they had difficulties in feeling or perceiving emotions. In subjects where PNES are associated with a borderline personality, in which the symbolic function is lost, the defense mechanisms are of a more archaic nature (denial). PNES with different underlying defense mechanisms have different prognoses (despite similar severity of PNES) and need usually a different treatment (pharmacological or psychological). Thus, it appears superfluous to talk about psychiatric comorbidity, since PNES are a different symptomatic expression of specific psychiatric disorders."
What causes an inability to feel emotions? Take someone in shock. If used up all their nutrients, or at least enough so where your body isn't functioning correctly. They can't feel emotions either. Maybe they have some of the same reasons behind it.
Trouble perceiving emotions? Can you say "Mirror neurons"? Obviously, you can't - but I can.
Defense mechanisms? Of the BODY, idiots!
Do you really think that emotions magically affect the body? Did it ever occur to you that emotions are neurotransmitters, and your transmitter transitions in the brain, and that the brain is fucked up, the body will follow? Old, you know it doesn't get sourced in the brain, but it's the same thing at the muscles, High glutamate.
God, some of these people really piss me off.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599147/#!po=2.74725
Psychogenic non-epileptic seizures: so-called psychiatric comorbidity and underlying defense mechanisms
Massimiliano Beghi, Paola Beffa Negrini, [...], and Cesare Maria Cornaggia
Additional article information
Abstract
In Diagnostic and Statistical Manual of Mental Disorders, fifth edition, psychogenic non-epileptic seizures (PNES) do not have a unique classification as they can be found within different categories: conversion, dissociative, and somatization disorders. The ICD-10, instead, considers PNES within dissociative disorders, merging the dissociative disorders and conversion disorders, although the underlying defense mechanisms are different. The literature data show that PNES are associated with cluster B (mainly borderline) personality disorders and/or to people with depressive or anxiety disorders. Defense mechanisms in patients with PNES with a prevalence of anxious/depressive symptoms are of “neurotic” type; their goal is to lead to a “split”, either vertical (dissociation) or horizontal (repression). The majority of patients with this type of PNES have alexithymia traits, meaning that they had difficulties in feeling or perceiving emotions. In subjects where PNES are associated with a borderline personality, in which the symbolic function is lost, the defense mechanisms are of a more archaic nature (denial). PNES with different underlying defense mechanisms have different prognoses (despite similar severity of PNES) and need usually a different treatment (pharmacological or psychological). Thus, it appears superfluous to talk about psychiatric comorbidity, since PNES are a different symptomatic expression of specific psychiatric disorders.
