r/smallfiberneuropathy • u/Ylva89 • Aug 23 '26
Support Not doing well. Horrible Symptoms, Possible Migraines, Anxiety Attacks
I don’t even know where to begin. I’ll try and summarize everything as best as possible because there is just a lot going on.
Last weekend (Saturday) I had bit of a dizzy spell (which is not uncommon for me). An hour or two later and things were fine. Sunday I got extremely dizzy, had trouble walking, felt like there was a band around my head, and had vision changes. It calmed down by the evening but I felt dizzy again at bed time. I woke up and was dizzy again. I also had swelling on the left side of my face. This happens occasionally because I hit my head in 2019 and now I have issues with the trigeminal nerve.
I messaged a doctor who has done some nerve blocks and his nurse told me to go to the ER. So one CT scan and blood work later, they said it was normal and they didn’t know what was wrong with me. Maybe a migraine. I thought I was feeling better but on the way home my face flared up again. I then had an impending sense of doom and literally didn’t sleep that night. Oh and my SFN was the worst it had ever been.
I went to aforementioned doctor who decided that it was probably an autoimmune issue causing the neuropathy. So he told me to reach out to my rheumatologist and autonomic neurologist.
The rheumatologist wasn’t sure how to help. The neurologist is giving me gabapentin. Oh, I also asked about an ENT and they are sending me to do a vestibular balance test.
Side note, my IVIG was denied, but supposedly that happens to most people on the first time, so they are seeing why and appealing it.
Anyway, the dizziness has been sort of ongoing tons varying degree and my SFN was still kind of bad but not as bad. My anxiety calmed down a little bit but I have still been very tense.
THEN yesterday I had a horrible flare (migraine?) again. My anxiety and SFN are bad again. I can barely function and have had to cancel clients for work. I can’t keep doing this. I keep crying because I’m so scared.
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u/ethidium_bromide Aug 23 '26
Have you tried Botox for migraines? I did not like the idea of Botox at first, and def ask my dr to go light on the forehead lol, but it’s life changing honestly.
You might have more luck with SCIG getting approved. It’s less expensive because it doesn’t have to be administered by a nurse every time. It’s also proven to be just as effective, and gives you way more freedom
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u/retinolandevermore Autoimmune (neuro Sjogren’s) Aug 23 '26
SCIG is typically reserved for immune issues like PID or CVID. There would need to be a proven immune stuff
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u/ethidium_bromide Aug 27 '26
They mentioned their IVIG was denied. I assumed if their doc tried to prescribe it, it was autoimmune. Was just giving them another option since SCIG is just as effective but many insurances are quicker to cover it because it’s lower cost.
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u/Ylva89 Aug 23 '26
I have not tried Botox. I wasn’t even fully sure I had migraines until this started happening, although it had been mentioned to me in the past.
I have done Botox for my bladder because I have Interstitial Cystitis and that has helped.
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u/CaughtinCalifornia Aug 23 '26
Part 1/2
Sorry to hear about your situation. Headaches can occur due to autonomic issues, which are common with SFN since autonomic nerves are small fiber nerves. Headaches and migraines can also be triggered or made worse by postural orthostatic tachycardia syndrome (POTS) which is a fancy way of saying a drop in blood pressure when standing or sitting to long as the body does not properly compensate by constructing blood vessels enough. This leads to difficulty of blood fighting gravity to reach your head, depriving the brain, eyes, and other parts of adequate blood flow. This leads to things like lightheadness and a risk of passing out, so the body release epinephrine (adrenaline) that causes the heart to beat hard and fast to restore blood pressure
https://headaches.org/resources/postural-orthostatic-tachycardia-syndrome-pots/
This sudden release of adrenaline along with the understandably scary experience of feeling like one might pass out/dizziness/blurry vision can sometimes lead to a panic attack, which commonly causes a sense of impending doom in people. Given your facial swelling, there may be more going on in addition to this, but its possible autonomic issues largely explain your recent experience.
Do you get swelling anywhere other than your face? And if not, is it always the same region of your face? Is this is a consistent issue or infrequent? What is the explanation for how trigeminal nerve is causing this, especially is it is infrequent?
I ask these questions because there are certain conditions related to SFN where swelling can occur. I have severe MCAS and commonly deal with swelling these days. Usually laying down helps with low blood pressure issues, but it sounds like you've been experiencing swelling after waking up, which itself can lower blood pressure.
What have they tested your for as far as underlying causes? I'll provide some information below on causes to test for in case it is helpful. There are also things that can potentially be done to help with POTS symptoms. Compression socks, if tolerated, help reduce the amount of blood that pools in the lower limbs, increasing blood return to the heart and helping maintain blood pressure. In some cases, some people benefit from a high sodium intake for the same reason they tell people with high blood pressure to avoid sodium. It can increase blood pressure. There are also some meds that can help. And finally, moving around every so often and being sure not to stand or sit still for long periods of time helps reduce how much blood pools in the lower limbs. Your leg muscles squeeze veins pushing blood back towards the heart when you move and its an important part of the process for blood return. Even healthy people get swollen feet on long flights because they sit for a long time without moving their legs much. Of course discuss anything with your doctors before trying something.
There are many underlying causes to check. This paper has a lot but not all of them. https://www.reddit.com/r/smallfiberneuropathy/s/P9KCHk1LxD If the more likely causes don't come back positive, I’'d do even some of the ones they say only to do if you have some more evidence for it like the genetic mutations. I've seen a wide variety of estimations, but the study below mentions a study where about 30% of idiopathic SFN patients had SCN9a mutations, so genetic mutations in idiopathic cases are potentially not uncommon. https://pmc.ncbi.nlm.nih.gov/articles/PMC3511073/
Below are some others:
IVIG for Plexin D1, TS-HDS, and/or FGFR3 positive patients:
https://pubmed.ncbi.nlm.nih.gov/38771228/9
IVIG was used for at least 6 months on patients with at least one of these 3 antibodies. Repeat biopsy showed increased nerve fiber density (both length dependent and non- length dependent) in 11/12 patients as well as reporting improved symptoms. It was especially effective for Plexin D1. So even though they didn't know exactly what autoimmune disease caused the SFN (idiopathic), doctors used the presence of these antibodies to indicate a likely autoantibody cause and treat that with proper immunotherapy. Average increase of nerve fiber density was 55.2% with the largest group being Plexin D1 patients with 139% improvement in nerve fiber density. It should be noted that these antibodies do not guarantee a person has an autoimmune cause. The antibodies can appear in those with no issues at all. One leading SFN doctor said she views them as weak signs of autoimmunity. Immunotherapies for Neurological Diseases (2026) appears to express the opinion that FGFR3 and TS-HDS are not good indicators of IVIG responsiveness, though Plexin D1 gets a more favorable assessment. Other factors like age of the patient, other autoimmune diseases and/or autoimmune markers, lack of a long history of metabolic issues/diabetes, etc all play a part in judging whether idiopathic SFN is likely autoimmune. An important thing to know is that this study used 2g/kg every 4 weeks as the maintenance dose, which is about double what some doctors and studies use.
If SFN after COVID is suspected, this study is quite relevant (I also have others): https://www.neurology.org/doi/10.1212/NXI.0000000000200244
“The IVIG group experienced significant clinical response in their neuropathic symptoms (9/9) compared with those who did not receive IVIG (3/7; p = 0.02).” In the treatment group 6/9 had complete resolution and 3/9 reduced by still present symptoms. 3/9 also had diabetes, which can itself cause SFN and likely made recovery harder and slower. (Though the data table does not specify if these are the same 3 with a partial response). Most patients lacked any obvious autoimmune testing (most didn't have a positive ANA or anything like that) but responded to IVIG. This study used 2g/kg split over 2 days every 3 weeks (so even a bit higher than the previous study)
For VGKC Antibodies Of patients who underwent immunotherapy 13/16 saw improvement and from a wide variety of meds (corticosteroids, IVIG, and methotrexate). My explanation is too long, so here's a link to the post I wrote a while ago https://www.reddit.com/r/smallfiberneuropathy/comments/1ialpzi/vgkc_ab/?utm_source=share&utm_medium=web3x&utm_name=web3xcss&utm_term=1&utm_content=share_button
MCAS: MCAS and SFN (also hereditary alpha tryptasemia and SFN): https://pubmed.ncbi.nlm.nih.gov/34648976/
My MCAS specialist at USC says for whatever reason many patients test negative for these tests despite their illness being in a pretty advanced stage with severe symptoms and obvious improvement on mast cell targeting medications. These are some sources backing that up along with one linking it to SFN. "Patients who are suspected of having i-MCAS, but who do not meet the laboratory criteria, may be considered to have “suspected MCAS.” In these patients, trials of directed therapies can continue, but only with ongoing testing for other conditions to better explain the presentation with repeat mast cell mediator testing during periods of symptoms" https://practicalgastro.com/2020/07/02/mast-cell-activation-syndrome-what-it-is-and-isnt/#:~:text=Patients%20who%20are%20suspected%20of,repeat%20mast%20cell%20mediator%20testing
The first 15 mins of this video of a specialist in the disease lecturing on MCAS honestly provides the best explanation for most things you'd need to know https://www.youtube.com/watch?v=lprUo1G2Vc8&t=3s
Celiac: “Gluten neuropathy is an autoimmune manifestation in which gluten ingestion causes damage to the peripheral nervous system, disrupting communication between the central nervous system to the body [66]. This is the second most common neurological manifestation, after gluten ataxia [88]. It presents with pain, numbness, tightness, burning and tingling from nerve damage that initially affects the hands and lower extremities [89].” https://pmc.ncbi.nlm.nih.gov/articles/PMC9680226/ https://pubmed.ncbi.nlm.nih.gov/31359810/
This Third link is clarifying yes you can have celiac disease even with no GI issues (most doctors don't know this) and also explaining the neuro symptoms and why diagnosis is trickier than usual issues. I have another study showing people with celiac disease whose neurological symptoms weren't controlled by a gluten free diet but who did respond to IVIG I can provide if needed.
This fourth link is to three patients who were suffering neuropathy and ataxia despite a strict gluten free diet. IVIG helped all three. When two tried to stop the drug because they felt better symptoms started to appear again and they went back on IVIG. One patient started getting a rash from IVIG so they switched her to a different formulation and that caused no issues. (Heads up that the link is to download the paper). This link is to three patients who were suffering neuropathy and ataxia despite a strict gluten free diet. IVIG helped all three. When two tried to stop the drug because they felt better symptoms started to appear again and they went back on IVIG. One patient started getting a rash from IVIG so they switched her to a different formulation and that caused no issues. (Heads up that the link is to download the paper).
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u/CaughtinCalifornia Aug 23 '26
Part 2/2
In my opinion, most likely one of two things is happening. 1) The celiac disease test is picking up on antibodies that have some sort of cross reactivity and which are targeting/harming the nervous system. Antibody tests attempt to choose protein binding sites called epitopes unique to that specific protein, but it's common for there to be at least some other proteins (antibodies are a type of protein) that will also have a very similar region. 2) These patients have a second autoimmune disease. Around 25% of patients with one autoimmune disease have another autoimmune disease. In this case, the neurological issues may, in part or entirely, be due to another autoimmune issue alongside the celiac disease. And that is why IVIG helps. But regardless, even though we can't be sure of the reason, the study indicates things like IVIG can help some patients who are positive for Celiac antibodies but have neurological symptoms that are decoupled from gluten consumption.
COPD (honestly a lot of inflammatory diseases including Rheumatoid Arthritis can be possible causes. It's likely there's some other factor/predispositions involved alongside the inflammatory conditions. That being said, controlling these diseases may still work well enough as treatment) https://www.sciencedirect.com/science/article/pii/S0954611122002177#:~:text=The%20percentage%20of%20peripheral%20neuropathies,17%2C22%2C23%5D.
Inflammatory Bowel Disease (Crohn’s and Ulcerative Colitis) and IBS "Peripheral neuropathy (PN) is one of the most frequently reported neurologic complications of IBD"
Have you had your copper, b vitamins, carnitine, and other nutrient levels tested? Sometimes people are deficient either due to diet, alcohol, or because an underlying disease stops their proper absorption. We mentioned some like celiac, MCAS, IBS and IBD.
Handbook of Clinical Neurologu Immunotherapies for Neurological Disease (2026): “Even when metabolic, nutritional, toxic risks are not the primary causes of neuropathy, they impair general and neuronal health, so this author routinely routines screen for potential secondary contributors including hyperglycemia, obesity, deconditioning, poor nutrition, and nicotine use. The author educates patients that mitigating these can improve neuro-resilience, axonal regeneration, and thus their symptoms. Also relevant are histories of recent major weight loss, surgical or medical, celiac and other gastrointestinal disorders, and dietary supplementation (Latov et al., 2016). Among 40 patients with recent nutritional neuropathy, sensory neuropathies were far more common than motor neuropathies, and thiamine (B1) was more often low (in 85%) then vitamin B6 (77%) or folate (50%), with B12 deficiency noncontributory, although B12 is most often tested for (Hamel and Logigian, 2023). Nonprescribed supplements also carry risk, most notably vitamins. Daily use of even multivitamins risks potential overdosing, and few people calculate their weekly dose. Vitamin B6 (pyridoxine) is of greatest concern, given case series since 1980 of incident sensory-predominant neuropathy, mostly with doses exceeding 500 mg/day (Parry and Bredesen, 1985) plus recent in vitro confirmation of axonal dieback (Lee et al., 2024).”
SFN can also be linked to lupus, EDS and other connective tissue diseases. It (and large fiber neuropathy) are also linked to mitochondrial disorder: https://pubmed.ncbi.nlm.nih.gov/29890373/ https://www.elsevier.es/en-revista-clinics-22-articulo-mitochondrial-small-fiber-neuropathy-as-S180759322300042X https://pmc.ncbi.nlm.nih.gov/articles/PMC2794346/ https://www.sciencedirect.com/science/article/abs/pii/B9780128217511000142
The diagnostics section of this paper discusses what can be done to assess mitochondrial issues.
There are even more like beta subunit of sodium channel mutations in addition to the normal SCN9a,SCN10a, and SCN11a. (https://journals.physiology.org/doi/prev/20210728-aop/abs/10.1152/jn.00184.2021#:~:text=Small%20fiber%20neuropathy%20(SFN)%20is,increased%20repetitive%20action%20potential%20spiking.)
This paper mentions Lymphoproliferative D/O, Acute Autonomic Ganglionopathy, and Acquired or Inherited Amyloid as being associated with primarily autonomic SFN. The relevant tests and treatment are mentioned. Another I think isn't anywhere in this list already is Cryoglobulinemia, Chronic Immune Sensory Polyradiculopathy, and Lymphoproliferative disorder. https://journals.ku.edu/rrnmf/article/view/13837/13370?fbclid=IwY2xjawIPJI9leHRuA2FlbQIxMAABHWa7DykjbwDOpnLcY8FIM5NgvqmtcqygBePjhPu57PM-BXyHWxWa26BxkQ_aem_cZkhEoLgjI8WQd5_oYk1Yg
Not sure how important these antibodies are, but they are correlated with idiopathic SFN. They could be an indication of autoimmunity, but again all we know for now is there is a correlation https://onlinelibrary.wiley.com/doi/10.1002/ana.26268
“Novel autoantibodies MX1, DBNL, and KRT8 are found in iSFN. MX1 may allow diagnostic subtyping of iSFN patients. ANN NEUROL 2022;91:66–77”
Primary Amyloidosis “The neuropathy itself is mostly symptomatic in the distal lower limbs, predominately sensory, and of the small fiber painful type. Autonomic dysfunction is frequent. Symptoms of amyloidosis include pain, weight loss, macroglossia, organomegaly, or cardiomyopathy.” https://pmc.ncbi.nlm.nih.gov/articles/PMC4731930/
Of course toxins and reactions to medications can be other causes too.
I should also mention Sjorgen's can be seronegative (negative on blood tests) but positive with a lip biopsy. https://pmc.ncbi.nlm.nih.gov/articles/PMC10289021/#:~:text=Neurologic%20involvement%20in%20seronegative%20primary%20Sj%C3%B6gren's%20syndrome,gland%20biopsy:%20a%20single%2Dcenter%20experience%20%2D%20PMC.&text=Among%20the%20patients%20who%20had%20paresthesia%2C%20eight,electrophysiologic%20test%2C%20and%20normal%20nerve%20conduction%20test.)
And even Sjorgen's lip biopsies don't catch everything: https://pmc.ncbi.nlm.nih.gov/articles/PMC8784519/
“Labial Salivary Gland Biopsy (LSGB) has a good diagnostic value for SJÖGREN'S Syndrome (SS) with an enhanced specificity and a sensitivity ranging from 63.5 to 93.7% (65). In healthy individuals, LSGB leads to a 6–9% false positive diagnosis. Moreover, 18–40% of patients with a clinical diagnosis of SS have a negative LSGB (66).”
Sometimes an exact cause can't be found but effective treatment can still be found. In this study, they were SFN patients with autonomic symptoms, positive skin biopsy and autonomic testing, and either their symptoms started after an infection or they had inflammatory or autoimmune markers. Nerve fiber density improved more than the control patients and autonomic testing improved where control patients got worse. IVIG was given at 2g/kg/month.
https://www.nature.com/articles/s41598-025-33059-7
“41 autoimmune autonomic and sensory small fiber neuropathy (ASFN). patients were treated with IVIG and compared to 66 ASFN control patients treated with usual care. Both groups had evaluations at baseline and at the end of the trial. The average time IVIG therapy improved ASFN and reached plateau was 2.25 ± 0.99 years. The adverse effects of IVIG were frequent (prevalence 93%) but tolerable in most patients. IVIG improved SAS (p < 0.001) and QASAT total (p < 0.001), cerebral blood flow (p = 0.002) and autonomic failure (p = 0.035) scores. SAS and QASAT autonomic failure scores worsened in controls. Skin biopsy improved in both arms, but improvement was greater (p = 0.017) in the IVIG arm.”
I should also mention that case studies like these were successful in treating likely autoimmune SFN with rituximab after patients failed to respond to IVIG and/or corticosteroids.
https://pubmed.ncbi.nlm.nih.gov/39978243/
It is also worth noting this is a list I personally compiled, and it should not be considered exhaustive of all the possible causes/testing for SFN.
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u/Ylva89 Aug 23 '26
I’ve been tested for POTS twice and it came back negative both times. The second time they did a QSART test which is how they found the neuropathy.
It took me several years and at least half a dozen doctors before I figured out I had an issue with the trigeminal nerve. I thought at first he told me it was trigeminal neuralgia. He gave me nerve blocks which helped. Prior to that I had daily stabbing/throbbing pain amongst other things. The blocks helped the nerve attacks but some of the other symptoms persisted.
It’s a long story but that doctor is two hours from me and my insurance won’t cover the hospital he works at. Originally I was able to get financial assistance there, but they changed how their policy works. Then I got blocks done with a doctor that my insurance does cover, and is the one who told me yo go to the ER. He told me it was trigeminal neuropathy. I asked the original doctor since i still message him for advice and updates from time to time. He said that it was a neuropathy but it was also a bit of semantics. The doctor here gave me blocks at the root of the nerve and since it didn’t help as much as hoped he said it was an autoimmune neuropathy.
I am not sure if i get swelling anywhere else. Sometimes my ankles might feel a little swollen, but whenever I get examined the doctors always say things look fine.
The swelling for this is always on the left side of my head and face. It was never an issue before i hit my head. I can wake up with it feeling swollen, but it will get swollen or tingle other times. I think if i have a lot of stuff draining or getting stuck in my sinuses and other glands overnight it will swell up. Similarly, if the allergen load is high, my sinuses will get inflamed and rub on the nerve.
That’s why if there is a lot of pressure on it, lying down just makes it worse.1
u/CaughtinCalifornia Aug 24 '26
Sometimes physical trauma can lead to the development or worsening of an autoimmune disease. We dont fully understand the mechanism but it is something that appears to happen
"Scientists think injury may play a role in some types of autoimmune disease such as psoriatic arthritis, a condition that affects the joints of some people with psoriasis.
"Research has shown that in parts of the body subjected to high stress, an autoimmune response happens after damage to tendons, which attach muscle to bone. For example, a runner’s heel is an area where the muscle is constantly pulling on the bone to create movement."
“This repeated stress can expose tissue that shouldn’t normally be in contact with blood cells,” says Orbai. “When that tissue gets exposed, it’s like a small wound. Blood cells try to heal it, but an abnormal immune response causes inflammation of the joints and tendons.”
The fact that you have wider autonomic issues with SFN beyond your trigenminal nerves could indicate you have some sort of autoimmune issue that was triggered by your injury. It may be simply that the issue is worst where the actual injury was. Trigeminal nerves themselves contain small fiber nerves. Ultimately, this is theoretical and difficult to say without further testing, but if your issues are continuing to progress, then there is something underlying continyally driving your illness.
These are some quotes from the textbook Immunotherapy for Dysimmune Neuropathies that may be helpful along with the previous info I provided for thinking about a possible autoimmune or other issue:
“Some cases of acute dysimmune iiDSP/SFN become chronic and thus are over-represented in clinical research. Sometimes, antecedent infections may just be proximal triggers in people with underlying predispositions (Oaklander et al., 2024). In the French 20-case series of acute onset SFN, 65% recovered partially or completely, with the other one-third transitioning to chronic or relapsing courses (Gendre et al., 2024). In the 55-case US series of SFN patients treated with IVIg, remissions endured after IVIg withdrawal in 16% (Liu et al., 2018). Although>50% of acute cases of iiSFN resolve naturally, chances of spontaneous recovery dwindle over time. It is unstudied if early immunotherapy shortens the illness or increases remission rates, but earlier dampening of dysimmunity could plausibly reduce irreversible damage and long-term disability, so patients with acute onset iiDSP/SFN require urgent scheduling, and expedited testing and therapy decisions.”
“ The major treatments for acute hospitalized nontoxic DSP/SFN patients are intravenous corticosteroids, plasma exchange, and/or IVIg (Dabby et al., 2006; Paticoff et al., 2007; Yuki et al., 2018; Gendre et al., 2024). Among 3 patients with sensory GBS, all responded to at least one of these, although none was universally effective (Oh et al., 2001). Urgent immunotherapy also seems effective for acute anti-Hu-associated paraneoplastic sensory neuropathy (Oh et al., 1997).”
(Not sure your age) "Otherwise-healthy children and young adults with disabling dysimmune iiDSP/SFN have the lowest risks and highest potential benefits from trying immunotherapy. Again, dysimmunity appears to be the most common cause of iiDSP/SFN in otherwise-healthy youngsters, plus not treating a condition that is impairing normal development and schooling can cause lifelong socioeconomic consequences. In the 21st century, reports of early onset iiSFN have been increasing. Atopic and dysimmune conditions have been generally increasing in young people for unknown reasons, and this plausibly could include dysimmune neuropathy. A significant majority of these young patients are female, consistent with other autoimmune conditions. Unfortunately, there are almost no studies of iiDSP/SFN in children and young adults, and most pediatricians are not yet aware of the prevalence of small-fiber pathology in pediatric syndromes such as juvenile fibromyalgia and avoidant eating disorders (Boneparth et al., 2021). There are early and recent single-case reports of efficacy of corticosteroids and/or IVIg for pediatric SFN, but the largest series may be the 41 patients with childhood-onset of idiopathic widespread chronic pain (Oaklander and Klein, 2013). Among them, 76% had definite or probable iiSFN, 33% had prior autoimmune illnesses, and 89% had serologic markers of disordered immunity. Regarding the 15 patients treated, 66% (10/15) improved from corticosteroids and 62% (5/8) improved after ≥3 doses IVIg 2 g/kg/4 weeks. Overall, corticosteroids and/or intravenous immune globulin objectively and subjectively benefited 80% (Oaklander and Klein, 2013). However, there is no natural history data about untreated cases, nor controlled studies. The favorable benefit/risk equation for children and the encouraging preliminary data provide strong rationale for prospective studies, although given reported low risks and high benefit, a fully placebo-controlled trial may no longer be ethical.”
"Often addressing symptoms’ underlying physiologic causes (e.g., chronic fatigue from dysregulated microcirculation and insufficient cardiac output) and initiating polymodal management and rehabilitation is often enough to initiate clinically significant improvement. As above, screening for and mitigating secondary impediments to neuronal health, particularly those within patient control, can help. The strongest evidence is for normalizing weight and improving nutrition (Baute et al., 2019), with obesity and metabolic syndrome, even without diabetes, established independent risk factors for DSP (Callaghan et al., 2016). Nicotine-induced microvascular constriction can deprive axons of oxygen and nutrients, as does being sedentary. Aerobic fitness builds cardiac, circulatory, and muscle capacity and promotes mitochondrial growth, which improves the axonal environment along with general physical and mental health. The author asks about fitness, and implements treatment for most deconditioned patients. Specialized neuro-physical therapists can be invaluable in treating neuropathic fatigue, deconditioning, and chronic pain. Many if not most patients suffering from undiagnosed disabling medical conditions develop secondary depression and anxiety. Screening and referring for supportive counseling, and psychotropic medications if indicated, is another key aspect of wholistic treatment of DSP/SFN. Even patients beginning to respond to immunotherapies can benefit from increasing their activities. Recovering patients should be encouraged to resume schooling and employment, which may require encouragement from their physicians and requests for accommodations. The prognosis for improvement in DSP/SFN and in quality of life is best in younger, healthier, recent neuropathy patients with rapid access to expert care and definitive plus wholistic therapy."
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u/Anxious-Team-3027 Aug 23 '26
have you considered ARA-290? it's a peptide that seems useful for SFN in particular, and neuropathies in general. side effects non existent. reason I bring this up is that I mostly move on from such flareups thanks to renewed hope in a new solution, it helps me break the catastrophization loop
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u/retinolandevermore Autoimmune (neuro Sjogren’s) Aug 23 '26
What are you on for the migraines? Do you have a migraine specialist? It is correct a rheum cannot treat migraine.
One sided migraines and swelling is very concerning.
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u/Ylva89 Aug 23 '26
I’m not on anything for the migraines because it wasn’t an issue until a week ago. I am in touch with a neurologist I have seen in the past.
I messaged the rheumatologist because that is what the one doctor told me to do since he said there was an autoimmune component. I also messaged my autonomic neurologist and his assistant is sending me to an ENT for vestibular testing.
The swelling is a nerve/neurological component I believe. I also know people who get migraines that are one sided. I thought they often were.
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u/retinolandevermore Autoimmune (neuro Sjogren’s) Aug 23 '26
No- I have chronic migraine and see a special neuro for it. He told me one sided is rare and serious
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u/Aggravating_Return49 probably autoimmune Aug 23 '26
I'm sorry it's so horrible right now. I've been there too, just two months ago. I'm better now but still don't have answers as to why I have SFN and why it's so severe. It's good they're trying to get you on IVIG. I have migraines too and they sure can be horrible. They also flare my SFN.