Numb muscles including heart

General discussions. Feel free to use this like a support group also.
Terabithia
Posts: 61
Joined: Sun Aug 21, 2022 4:06 am
Contact:

Numb muscles including heart

Unread post by Terabithia »

Another symptom i’m experiencing is that my muscles don’t feel strain. Working out pre-PSSD was an excruciating affair where I could feel my each and every muscle fibre ripping and straining to work the weight. The lactic acid accumulation and the “burn” was immense especially when I went to failure. My heart would pump furiously and i’d feel the exertion throughout my entire being. Working out in my natural state and working out on an SSRI or with PSSD are two completely different feelings. I used to feel the pain of working out so deeply before but now it’s as though i’m working out with 80% less pain and exertion.

After getting PSSD it’s as though my insides are anaesthetized and i’m just going through the motions. I’m lifting weights I haven’t lifted before for reps I haven’t lifted before simply because that strenuous pain sensation is missing. It’s good in the sense I can reach new PR’s but bad in the sense that it comes at a price. I can run faster and longer as well with less exertion and at a lower heart rate. I track all my workouts meticulously so these are quantifiable differences between my pre and post PSSD states. My resting heart rate and HRV are also drastically different pre and post PSSD.

This made me remember the first Escitalopram pill I took. I remember it clearly because I was very sad and feeling the physical effects of heartbreak at the time. The chest tightness and anguish that comes when you feel the pang of losing a loved one or some other bad news. I was in the depths of that sorrow. But within hours of taking that first pill I felt that heartbreak and anguish dissipate as though my heart was dipped in a pool of lidocaine. I felt a numbing sensation overcome and swallow my heartache away.

I think we should look at connections between SSRI medications and the heart and muscle tissue. Some keywords to look into: lactic acid, heart, SSRI, muscles, serotonin, nitric oxide, exercise, exertion etc…
Terabithia
Posts: 61
Joined: Sun Aug 21, 2022 4:06 am
Contact:

Re: Numb muscles including heart

Unread post by Terabithia »

This looks very relevant. Could we get more eyes on this. https://www.frontiersin.org/articles/10 ... 00259/full

“In the present study we demonstrated that acute administration of escitalopram is associated with increased vagal function under both resting and task conditions; a finding that was particularly robust for HR. This finding is consistent with reported short- to medium-term beneficial effects of SSRIs on cardiovascular and neuroendocrine responses to stress in depressed patients (e.g., Straneva-Meuse, 2004b), but contrast against longer-term research outcomes (Whang et al., 2009; Licht et al., 2010a) highlighting the adverse effects of the SSRI class of antidepressants. Here, an explanation for this apparent discrepancy is the complexity of central and autonomic 5-HT effects on cardiovascular function, which include bradycardia, associated with activation of 5-HT1A receptors, as well as tachycardia, associated with activation of 5HT2 receptors. It is possible that the effects of SSRIs shift from parasympathetic—as shown here—to sympathetic activation with increasing length of use.”

So Escitalopram decreased heart rate by affecting vagal tone. Bradycardia is linked to 5ht1a activation whereas tachycardia is linked with 5ht2 activation. Interesting to note that my natural state before PSSD was with tachycardia but now I am essentially with bradycardia as my resting heart rate is a good 40bpm less than before. Could it be people that suffer with PSSD had uniquely activated 5ht2 receptors? Perhaps they were highly sensitive before until something triggered them to become desensitized?
Terabithia
Posts: 61
Joined: Sun Aug 21, 2022 4:06 am
Contact:

Re: Numb muscles including heart

Unread post by Terabithia »

https://pubmed.ncbi.nlm.nih.gov/18533183/

This is adding up so far as I would describe myself as OCD before but not anymore after PSSD.
Terabithia
Posts: 61
Joined: Sun Aug 21, 2022 4:06 am
Contact:

Re: Numb muscles including heart

Unread post by Terabithia »

https://pubmed.ncbi.nlm.nih.gov/20003079/

If 5ht2b receptors are linked to visceral pain and sensation then could it be that they and other 5ht2 receptors are linked to other visceral sensations such as those that originate from muscles or the heart? I personally used to feel all my internal bodily sensations but now it is as though my body went silent.

Could PSSD sufferers have have hyper sensitive 5ht2b and other receptors which have for one reason or another become desensitized? Could the antagonist mentioned be used to upregulate the receptors?
Last edited by Terabithia on Sat Jan 21, 2023 3:57 pm, edited 1 time in total.
Terabithia
Posts: 61
Joined: Sun Aug 21, 2022 4:06 am
Contact:

Re: Numb muscles including heart

Unread post by Terabithia »

https://www.frontiersin.org/articles/10 ... 00046/full

https://www.diva-portal.org/smash/get/d ... TEXT02.pdf

Something else interesting to note is that serotonin is a vasoconstrictor. Could this be a reason for the neuropathy seen in some PSSD sufferers especially in the penis? Also the second link states:

“The mean density of 5-HT2A receptors in RA patients was significantly lower than in controls, 45.3 versus 57.4 fmol/mg protein (p = 0.004). There was no significant difference in affinity. Variation of four single nucleotide polymorphisms (SNPs) (rs6314, rs1328674, rs6313 and rs6311) in the HTR2A gene was associated with RA, although not significantly so for all SNPs after testing for multiple comparisons. The proportion of joint symptoms reported as ADRs, relative to all ADRs was significantly higher for the 5-HT2A blocking antidepressants compared with the SSRIs in both databases (p< 0.001). In the Swedish material the comparison of ADRs was also related to sales figures, showing a considerable higher frequency of joint symptoms for the 5-HT2A antagonists (p< 0.001). The density of 5- HT2A receptors increased after treatment with prednisolone in 23 out of 27 individuals. The mean density at baseline was 45.2 versus 64.9 fmol/mg protein at the end of the study (p=0.001). There were no significant differences in affinity during the treatment period, although a low affinity at baseline was a predictor for higher density following treatment with prednisolone.”

This personally resonates with me because after the onset of PSSD i’ve had joint pain which i’ve never experienced before. It’s been a recurring pain and this paper links 5ht2a receptors to rheumatoid arthritis. It also mentions prednisolone’s potential ability to increase 5ht2a receptors. Has anyone tried prednisolone?
Terabithia
Posts: 61
Joined: Sun Aug 21, 2022 4:06 am
Contact:

Re: Numb muscles including heart

Unread post by Terabithia »

Something else that adds up:

“ Regulation of the 5-HT2A receptor
The regulation of the 5-HT2A receptor is not fully understood, although it seems obvious that changes in the numbers of receptors expressed, i. e., the receptor density, is of major importance [27]. Multiple factors contribute to the complex regulation of the functional activity and the expressed number of 5-HT2A receptors.
The 5-HT2A receptor displays a constitutive activity, which means that there could be receptor signalling without ligand binding to the receptor. This constitutive activity could be decreased by inverse antagonists [48, 49]. The regulation becomes even more complex, since it, in addition, seems that different cellular signalling pathways could react in different ways following stimulation with the same ligand depending on the cell type [49].
Besides gene level, the 5-HT2A receptor has been shown to be regulated on both transcriptional [50, 51] and receptor level [52]. The 5-HT2A receptor can, like other GPCRs, be regulated in the short-term by agonist or antagonist stimulation, but can also be regulated in long-term following prolonged or repetitive stimulation. Chronic stimulation of several different agonists and antagonists at the 5-HT2A receptor has in most studies resulted in a down-regulation of the receptor. Down-regulation by agonists is also a well-known mechanism for other GPCRs, although down-regulation by
4

antagonists is unlike other GPCRs and this phenomenon has been mentioned as paradoxical regulation [53]. Whether this regulation occurs at the mRNA level or is posttranscriptional, i. e., receptor internalization, is not clear. This long-term regulation has been demonstrated for some tricyclic antidepressants, e. g., amitriptyline and some neuroleptics, e.g., clozapine [54]. The long-term downregulation is also described both in vitro and in vivo for the 5-HT2A blocking atypical antidepressant mianserin [55-57], although in one in vivo study of platelets, mianserin caused an upregulation after a treatment period of five consecutive days in healthy volunteers [58]. It is unclear whether 5-HT-selective reuptake inhibition in general results in downregulation of 5-HT2A receptors after chronic treatment, since the results are inconsistent [54].
Upregulation of 5-HT2A receptors have been demonstrated as a result of stress in animals [59-63] and after glucocorticoid supply [64-70] in studies performed in rodents.”

Especially the last line stating upregulation occurs due to stress. I feel as though I have experienced a lot of stress and trauma in my life thus far so I would not be surprised if I had upregulated 5ht2a receptors before.

“Connections between the 5-HT2A receptor and the HPA-axis
The hypothalamic-pituitary-adrenal axis (HPA-axis) is a neuroendocrine system, which regulates many parts of the physiologic processes and responses in the body. The system is activated by stress and inflammation leading to secretion of endogenous corticosteroids. In humans, one of these corticosteroids is the active steroid hormone cortisol, acting on usually intracellular glucocorticoid receptors. In rats, corticosterone is the equivalent to the human cortisol.
Release of serotonin has been shown to increase the release of cortisol and adrenocorticotropic hormone (ACTH). This has been demonstrated to take place at the hypothalamic level where synaptic connections between serotonergic nerve terminals and corticotropin releasing hormone (CRH) releasing neurons are present. In addition, there are studies indicating that a regulation of the HPA axis by serotonin may also exist in the anterior pituitary gland and in the adrenals. Serotonin 5-HT2A receptors are located in the paraventricular hypothalamic nucleus, in the pituitary gland and probably also in the adrenals; and have been found to stimulate the HPA- axis on different levels [71-73].
While the serotonin system regulates the HPA-axis, corticosteroids have been found to regulate the serotonin system via serotonin synthesis and the various serotonin receptors [73, 74]. Administration of systemic exogenous
5

corticosteroids has in most studies resulted in an significant increase of 5- HT2A receptors in rat models [64-70], although not in one study [75] (Table 1).
Table 1. Previous studies of the effects on 5-HT2A receptors following glucocorticoid administration in rat models.
Author
Reference
Study design
Resultats on 5-HT2A
Crayton 1996
[75]
Corticosterone1mg/kg/day intraperitoneal for 7 days to 9 rats in treatment group and 10 rats in control group.
Bmax ns Kd ns
Fernandes 1997
[64]
Corticosterone pellet 100mg SC for one week to 16 rats in treatment group and control group, respectively.
Bmax ↑ sign
Kd No information
Jitsuiki 2000
[65]
Dex 1mg/kg/day injected SC for 14 days to 10 rats in treatment group and 12 rats in control group.
Bmax ↑ sign Kd ns
Katagiri 2001
[66]
Dex 1mg/kg/day injected SC for 14 per treatment group and control grou
aBysto↑3s-6igrnatsi max
p,Kresnpsectively. d
Kozuru 2000
[69]
Dex 1mg/kg/day injected SC for 14 days to 11-12 rats in treatment group and control group, respectively.
Bmax ↑ sign Kd ns
Kuroda 1993
[68]
Dex 1, 2, 5 mg/kg/day, respectively, injected SC for 10 days to 8, 7, 5 rats in treatment group, respectively and 12 rats in control group.
Bmax ↑ sign for all treatment groups
Kd ns
6
dn

Kuroda 1992
[67]
Corticosterone 20mg/kg and 50mg/kg, respectively injected SC for 10 days to 8 rats in treatment group, respectively, and 8 rats in control group.
Bmax ↑ sign for all treatment groups
Kd ns
Takao 1997
[70]
Corticosterone 50mg/kg/day injected SC for 14 days to 8 rats in treatment group and control group, respectively.
Bmax ↑ sign
Kd No information
Abbreviations: Dex, dexamethasone; SC, subcutaneous; ↑, significant increase; ns, not significant“

Could corticosteroids be the key? Cortisol or even dexamethasone? Cortisone? Would a high fructose diet be helpful in that it increases cortisol?
sylv
Posts: 188
Joined: Thu Apr 27, 2017 6:32 am
Contact:

Re: Numb muscles including heart

Unread post by sylv »

That isn't commonly reported, but I can confirm these effects may happen. Anaesthesied muscle, no visible veins, bradycardia etc. Seems our PSSD phenotypes are similar somewhat.

Few questions
1) How long, which drugs and for what condition have you taken?
2) Did you intensively exercised while taking them ?
3) The appearance of these symptoms was a crash ( like you seemingly describe ) or some of it developed gradually in the long term ?

These informations are helpful to establish what really have caused specific symptoms. We have to assume that SSRI damage or PSSD itself aren't unique. There are so many persistent syndromes caused by drug use ( Tardive Akathisia, tardive dyskinesia, HPPD, BZD withdrawal, neuroleptic metabolic syndrome, DAWS, PFS and reports of PSSD like syndrome from other drugs even natural MAOis) so given that evidence ( assuming testimonies aren't false ) it's probable that all drugs acting on neurotransmitters ( possibly also neuropeptides ) of nervous system could induce some lasting damage. The syndromes which may share symptoms, but not necessary identical neuropathology. The situation is even more complicated that some drugs may uncover damage caused by other drug ( crash ). Hence the utmost need for fidelity before drawing any clues from the basic research. Otherwise, without precision, it's a waste of time.
Terabithia
Posts: 61
Joined: Sun Aug 21, 2022 4:06 am
Contact:

Re: Numb muscles including heart

Unread post by Terabithia »

sylv wrote: Wed Jan 18, 2023 3:24 pm That isn't commonly reported, but I can confirm these effects may happen. Anaesthesied muscle, no visible veins, bradycardia etc. Seems our PSSD phenotypes are similar somewhat.

Few questions
1) How long, which drugs and for what condition have you taken?
2) Did you intensively exercised while taking them ?
3) The appearance of these symptoms was a crash ( like you seemingly describe ) or some of it developed gradually in the long term ?

These informations are helpful to establish what really have caused specific symptoms. We have to assume that SSRI damage or PSSD itself aren't unique. There are so many persistent syndromes caused by drug use ( Tardive Akathisia, tardive dyskinesia, HPPD, BZD withdrawal, neuroleptic metabolic syndrome, DAWS, PFS and reports of PSSD like syndrome from other drugs even natural MAOis) so given that evidence ( assuming testimonies aren't false ) it's probable that all drugs acting on neurotransmitters ( possibly also neuropeptides ) of nervous system could induce some lasting damage. The syndromes which may share symptoms, but not necessary identical neuropathology. The situation is even more complicated that some drugs may uncover damage caused by other drug ( crash ). Hence the utmost need for fidelity before drawing any clues from the basic research. Otherwise, without precision, it's a waste of time.

1) I took Escitalopram for less than 4 weeks. It was prescribed for depression and anxiety but at the time I was going through temporary stressful life events. I don’t think I got PSSD while on the SSRI since when I stopped the side effects mostly subsided. It wasn’t until I took SJW a few months later that I experienced full blown PSSD. I took SJW for almost 2 weeks following the label at 3 x 300mg per day. I later measured the contents of the capsule and came to realize that each capsule contained about 500mg of SJW so I was probably taking closer to 1500mg a day.

2) I was not exercising while taking Escitalopram but I was following a moderate exercise routine while taking the SJW.

3) The appearance of PSSD symptoms was an immediate “crash” after taking SJW for almost 2 weeks. I felt a sudden change in my psychology. The symptoms were mental, physical and sexual. I felt as though I had no soul. As though my nervous system was dipped in lidocaine, my sexuality erased, and any emotional connection to the past wiped clean.

In the month I took SJW I was also taking a few other drugs sporadically. They include Phenibut, Vyvanse and low dose mushrooms. I also took supplements like zinc and ALCAR and a few others. While I was on the SJW I was not taking anything else because I know it interacts with many drugs.

If you have any further questions let me know.
Post Reply

Who is online

Users browsing this forum: No registered users and 2 guests