This is your Guide that helps you navigate this Subreddit and it's Resources more efficiently. It will help guide you through the condition and answer many of the starting questions you may wonder about upon first stumpling onto Hard Flaccid Syndrome (commonly referred to as HFS).

r/hardflaccidresearch Community Guide

1. Hard Flaccid Syndrome Introduction: Symptoms, Causes, Treatment & Resources
2. Our HFS Network Provider Map: Find & Recommend Doctors
3. Archive of Existing Literature on Hard Flaccid Syndrome (HFS)
4. List of Media Featuring Hard Flaccid Syndrome (HFS)
5. Breaking Down HFS Theories: Simple Explanations for Better Understanding (coming soon)
6. Our FAQ for frequently asked questions (coming soon)
7. Penile Implant for Hard Flaccid Syndrome: A List of Personal Stories (Work in Progress)

Hello everyone,

I am a moderator over at the hardflaccidresearch Subreddit and wanted to share my post directly with this community as well:

I thought I’d give you an update about my diagnositc workups and vascular diagnoses (pelvic congestion, reflux and more). I am trying to explain how I got there and how relevant the findings could be for HFS and CPPS. This will be a long post, but the length was necessary to understand the full picture and clear questions that might arise without it.

First I am going to give a quick rundown of my symptoms and the duration:

After many years of Hard Flaccid Syndrome (HFS ranging from mild at best to severe at worst) and chronic pelvic pain, I finally underwent extensive vascular imaging that revealed objective abnormalities which may be clinically relevant.

My main symptoms include:

• Hard Flaccid Syndrome (persistent contracted/semi-rigid flaccid state)
• Penile pain and spasms
• Penile sensory changes and episodes of numbness
• Perineal cramping and vibration sensations
• Pelvic floor pain and tightness
• Pain after ejaculation and during sexual activity
• Left greater than right testicular pain
• Anal and coccygeal pain
• Groin pain
• Lower back pain
• Abdominal pain
• Flank pain on both sides, sometimes extending from the lower abdomen upward toward the rib cage and into the back
• Urinary symptoms
• Testicle pain coming in phases

Background

My symptoms began abruptly at age 18.

I woke up one morning with severe localized pain in the penile shaft. Within 10 hours, I developed what is now commonly described as Hard Flaccid Syndrome. It’s really hard to say whether or not I injured my penis in some way the day before. I did do repeated masturbation the day before, but I went to bed fine and had no pain during the evening or at night. I only woke up with it, so the two situations might be unrelated and I always did doubt that I injured my penis somehow, as I was always rather cautios.

Over the following days and weeks, I experienced:

• Painful nocturnal erections
• Significant reduction in penile sensation
• Persistent penile pain
• Pain after ejaculation, particularly in the perineal/rectal region especially with following erections
• Progressive pelvic floor dysfunction
• ED to some extent

The acute penile pain gradually resolved over several months, and the major sensory loss eventually improved. However, the pelvic pain, perineal spasms, Hard Flaccid symptoms, and associated dysfunction persisted.

Before this event, I had years before occasionally experienced:

• Testicular pain since adolescence (including episodes diagnosed as epididymitis)
• Burning sensations around the urethra
• Painful erections after frequent sexual activity

These symptoms were relatively infrequent and were not a significant problem at the time.

Imaging History

I underwent many MRIs over the years, including a pelvic MRI in 2022.

In late 2025, I underwent more specialized vascular imaging after a referral that specifically mentioned suspected pelvic congestion syndrome (“Pelvic Congestion” was explicitly stated in the referral indication). This included:

• A CT scan of the abdomen and pelvis with contrast
• 2 MR angiograms with contrast, 1 (MRA) of the pelvis and proximal left thigh, and the other MRA of the abdomen

Because pelvic venous disease was already part of the clinical suspicion, these studies were explicitly performed with attention to pelvic venous congestion and venous outflow abnormalities.

I later sent all imaging studies to an interventional radiologist with experience in pelvic venous disorders.

After reviewing the CT scans and MR angiograms, he stated that the most notable finding was a dilated pelvic vein, consistent with a possible pelvic venous congestion disorder.

Importantly, the radiology team that performed the CT scans and MR angiograms also had access to my earlier pelvic MRI from 2022 and used it as a direct comparison study.

On re-evaluation, they noted that the same pelvic vein appeared significantly more dilated in 2022 compared to the current imaging, while on the more recent scans it appeared reduced in size and less prominent. They described it as having decreased over time, whereas in 2022 it had been clearly more enlarged.

Importantly, this same finding was already visible on the 2022 pelvic MRI but had been overlooked in the original radiology report.

This suggests that pelvic venous abnormalities may fluctuate over time, may partially regress, and may also be missed unless specifically assessed in context.

Dynamic Duplex Ultrasound

I was then referred to an interventional angiologist with experience in pelvic venous disorders predominantly in women.

Interestingly, he primarily had clinical experience in female patients with pelvic congestion syndrome. He explained that he also uses female pelvic venous hemodynamics as a reference framework when interpreting male pelvic venous flow patterns.

Standard ultrasound in the supine position showed little. However, because I explained that my symptoms are much worse while standing, he repeated the examination dynamically while standing.

During standing and Valsalva, he observed:

• Retrograde flow in the left internal iliac venous system
• Significant reflux in the left-sided pelvic veins
• A continuous downward reflux pathway that could be traced from the abdominal venous system through the pelvis, groin, perineum, and into the penile region

He noted that similar hemodynamic patterns are well known in female pelvic congestion syndrome, where reflux can extend toward the pelvic venous plexus and external genital region (labial venous drainage) during standing and straining.

In my case, he stated that a comparable reflux pattern could be followed into the penile structures.

Based on these findings, he recommended a super-selective pelvic venography/phlebography.

Super-Selective Pelvic Venography Findings

A super-selective venography/phlebography with a vein catheter through my right groin vein with contrast was performed a few weeks ago.

The venography confirmed:

• Secured pathological reflux into the left internal iliac vein
• Marked pelvic venous congestion
• Extensive collateral venous pathways, indicating chronic rerouting of blood flow
• Large left paravertebral collateral veins draining into the distal inferior vena cava
• Cross-pelvic drainage predominantly through the sacral veins to the contralateral side
• Pronounced varicosities of the pudendal vein extending down to the pelvic floor
• Venous drainage across the midline and into the left inguinal canal

A possible compression of the left common iliac vein (approximately 70%) was identified on duplex ultrasound and considered suspicious for May-Thurner syndrome. However, the invasive venography did not demonstrate a clearly hemodynamically significant compression, so May-Thurner remains a possible but unconfirmed contributing factor. An IVUS wasn’t done to further investigate it.

No convincing evidence of Nutcracker syndrome was found:

• The left renal vein showed no relevant compression.
• The proximal left testicular vein was narrow and showed no relevant reflux during Valsalva.

Symptom Reproduction During the Procedure

One of the most striking aspects of the procedure was that selective catheterization and contrast injection was purposfully done in a way to try to irritate and reproduce my symptoms. Some of my characteristic symptoms were reproduced.

These included:

• Perineal vibration/spasm sensations
• Anal pain
• Coccygeal pain
• Groin pain
• Flank pain on both sides
• Lower back pain
• Abdominal pain, including radiation from the lower abdomen toward the upper abdomen and rib cage

In particular, selective catheterization of the varicose pudendal veins extending to the pelvic floor reproduced symptoms in the exact anatomical region where I frequently experience spontaneous perineal spasms in daily life.

The sensations were not identical to my complete Hard Flaccid state and didn’t really trigger it (though I already was severely flared through the stress of the procedure), but they were interestingly similar and occurred in the same anatomical location.

An Embolisation could be a potential treatment option, which would get done in phases, so each phase require another entrance trough my groin vein with a catheter. I have not had my follow up appointment with him yet to speak about the details and potential treatment avenues to follow.

Additional Clinical Interpretation

I was also evaluated by a gynecologist/pain specialist with a neuropelveology background.

He diagnosed me right away with May Turner syndrome, Nut Cracker Syndrome and Dunbar syndrome. However me and a few other patients have doubts about the validity of these diagnosis as they were done rather quickly and based more on static images than the normal tests required.

However, he proposed that vascular abnormalities such as pelvic venous congestion could secondarily irritate the pudendal nerve and potentially autonomic pelvic nerves, resulting in a secondary pudendal neuropathy.

He also discussed that anatomical or biomechanical factors such as pelvic posture (including scoliosis and hyperlordosis) may influence venous compression dynamics in the pelvic/iliac region, although this remains a theoretical contribution rather than a definitive cause.

In addition, therapeutic and diagnostic options were discussed, including:

• Diagnostic laparoscopy to directly visualize pelvic veins (varices) and surrounding structures
• During such a procedure, potential decompression or neurolysis (nerve release) was discussed as a possible combined approach in selected cases, if clinically indicated and desired
• Possible decompressive surgical approaches in selected vascular compression syndromes (e.g. ligament release procedures in relevant anatomical entrapments)
• Physiotherapy focusing on posture, core stability, and lumbar-pelvic mechanics
• PF PT wasn't dismissed, but not the priority in comparison to normal PT
• Trial of antiplatelet/anticoagulant medication (e.g. ASS or stronger agents depending on clinical evaluation)

He was very honest and said that a complete remission of symptoms was unlikely, though he was confident that he could improve my quality of life with these symptoms.

My Current Working Hypothesis

My current evidence-based interpretation is:

1. Objective pelvic venous reflux and pudendal varicosities are present.
2. These vascular abnormalities may create chronic congestion and pressure in the pelvis.
3. This may secondarily irritate the pudendal nerve and/or autonomic pelvic nerves and cause neuropathy.
4. The resulting neural sensitization and pelvic floor dysfunction may contribute to Hard Flaccid Syndrome and chronic pelvic pain.

My goal moving forward will be to get more clearance on the compression diagnoses. I will have another appointment with a european specialist in may turner syndrome and hope that his expertise can shed light on which route I should follow when it comes to embolisation, stents and/or laproscopy.

Important Disclaimer

I am not claiming that this is the universal cause of Hard Flaccid Syndrome, nor that these findings definitively explain all of my symptoms.

However, this is the first time in many years that objective structural abnormalities have been identified and closely correlated with symptom reproduction during invasive testing.

I am sharing this in case others with Hard Flaccid Syndrome, chronic pelvic pain, penile numbness, perineal spasms, or unexplained genital symptoms may have an overlooked vascular component that has not yet been investigated.

Hello everyone,

I thought I’d give you an update about my diagnositc workups and vascular diagnoses (pelvic congestion, reflux and more). I am trying to explain how I got there and how relevant the findings could be for HFS and CPPS. This will be a long post, but the length was necessary to understand the full picture and clear questions that might arise without it.

First I am going to give a quick rundown of my symptoms and the duration:

After many years of Hard Flaccid Syndrome (HFS ranging from mild at best to severe at worst) and chronic pelvic pain, I finally underwent extensive vascular imaging that revealed objective abnormalities which may be clinically relevant.

My main symptoms include:

• Hard Flaccid Syndrome (persistent contracted/semi-rigid flaccid state)
• Penile pain and spasms
• Penile sensory changes and episodes of numbness
• Perineal cramping and vibration sensations
• Pelvic floor pain and tightness
• Pain after ejaculation and during sexual activity
• Left greater than right testicular pain
• Anal and coccygeal pain
• Groin pain
• Lower back pain
• Abdominal pain
• Flank pain on both sides, sometimes extending from the lower abdomen upward toward the rib cage and into the back
• Urinary symptoms
• Testicle pain coming in phases

Background

My symptoms began abruptly at age 18.

I woke up one morning with severe localized pain in the penile shaft. Within 10 hours, I developed what is now commonly described as Hard Flaccid Syndrome. It’s really hard to say whether or not I injured my penis in some way the day before. I did do repeated masturbation the day before, but I went to bed fine and had no pain during the evening or at night. I only woke up with it, so the two situations might be unrelated and I always did doubt that I injured my penis somehow, as I was always rather cautios.

Over the following days and weeks, I experienced:

• Painful nocturnal erections
• Significant reduction in penile sensation
• Persistent penile pain
• Pain after ejaculation, particularly in the perineal/rectal region especially with following erections
• Progressive pelvic floor dysfunction
• ED to some extent

The acute penile pain gradually resolved over several months, and the major sensory loss eventually improved. However, the pelvic pain, perineal spasms, Hard Flaccid symptoms, and associated dysfunction persisted.

Before this event, I had years before occasionally experienced:

• Testicular pain since adolescence (including episodes diagnosed as epididymitis)
• Burning sensations around the urethra
• Painful erections after frequent sexual activity

These symptoms were relatively infrequent and were not a significant problem at the time.

Imaging History

I underwent many MRIs over the years, including a pelvic MRI in 2022.

In late 2025, I underwent more specialized vascular imaging after a referral that specifically mentioned suspected pelvic congestion syndrome (“Pelvic Congestion” was explicitly stated in the referral indication). This included:

• A CT scan of the abdomen and pelvis with contrast
• 2 MR angiograms with contrast, 1 (MRA) of the pelvis and proximal left thigh, and the other MRA of the abdomen

Because pelvic venous disease was already part of the clinical suspicion, these studies were explicitly performed with attention to pelvic venous congestion and venous outflow abnormalities.

I later sent all imaging studies to an interventional radiologist with experience in pelvic venous disorders.

After reviewing the CT scans and MR angiograms, he stated that the most notable finding was a dilated pelvic vein, consistent with a possible pelvic venous congestion disorder.

Importantly, the radiology team that performed the CT scans and MR angiograms also had access to my earlier pelvic MRI from 2022 and used it as a direct comparison study.

On re-evaluation, they noted that the same pelvic vein appeared significantly more dilated in 2022 compared to the current imaging, while on the more recent scans it appeared reduced in size and less prominent. They described it as having decreased over time, whereas in 2022 it had been clearly more enlarged.

Importantly, this same finding was already visible on the 2022 pelvic MRI but had been overlooked in the original radiology report.

This suggests that pelvic venous abnormalities may fluctuate over time, may partially regress, and may also be missed unless specifically assessed in context.

Dynamic Duplex Ultrasound

I was then referred to an interventional angiologist with experience in pelvic venous disorders predominantly in women.

Interestingly, he primarily had clinical experience in female patients with pelvic congestion syndrome. He explained that he also uses female pelvic venous hemodynamics as a reference framework when interpreting male pelvic venous flow patterns.

Standard ultrasound in the supine position showed little. However, because I explained that my symptoms are much worse while standing, he repeated the examination dynamically while standing.

During standing and Valsalva, he observed:

• Retrograde flow in the left internal iliac venous system
• Significant reflux in the left-sided pelvic veins
• A continuous downward reflux pathway that could be traced from the abdominal venous system through the pelvis, groin, perineum, and into the penile region

He noted that similar hemodynamic patterns are well known in female pelvic congestion syndrome, where reflux can extend toward the pelvic venous plexus and external genital region (labial venous drainage) during standing and straining.

In my case, he stated that a comparable reflux pattern could be followed into the penile structures.

Based on these findings, he recommended a super-selective pelvic venography/phlebography.

Super-Selective Pelvic Venography Findings

A super-selective venography/phlebography with a vein catheter through my right groin vein with contrast was performed a few weeks ago.

The venography confirmed:

• Secured pathological reflux into the left internal iliac vein
• Marked pelvic venous congestion
• Extensive collateral venous pathways, indicating chronic rerouting of blood flow
• Large left paravertebral collateral veins draining into the distal inferior vena cava
• Cross-pelvic drainage predominantly through the sacral veins to the contralateral side
• Pronounced varicosities of the pudendal vein extending down to the pelvic floor
• Venous drainage across the midline and into the left inguinal canal

A possible compression of the left common iliac vein (approximately 70%) was identified on duplex ultrasound and considered suspicious for May-Thurner syndrome. However, the invasive venography did not demonstrate a clearly hemodynamically significant compression, so May-Thurner remains a possible but unconfirmed contributing factor. An IVUS wasn’t done to further investigate it.

No convincing evidence of Nutcracker syndrome was found:

• The left renal vein showed no relevant compression.
• The proximal left testicular vein was narrow and showed no relevant reflux during Valsalva.

Symptom Reproduction During the Procedure

One of the most striking aspects of the procedure was that selective catheterization and contrast injection was purposfully done in a way to try to irritate and reproduce my symptoms. Some of my characteristic symptoms were reproduced.

These included:

• Perineal vibration/spasm sensations
• Anal pain
• Coccygeal pain
• Groin pain
• Flank pain on both sides
• Lower back pain
• Abdominal pain, including radiation from the lower abdomen toward the upper abdomen and rib cage

In particular, selective catheterization of the varicose pudendal veins extending to the pelvic floor reproduced symptoms in the exact anatomical region where I frequently experience spontaneous perineal spasms in daily life.

The sensations were not identical to my complete Hard Flaccid state and didn’t really trigger it (though I already was severely flared through the stress of the procedure), but they were interestingly similar and occurred in the same anatomical location.

An Embolisation could be a potential treatment option, which would get done in phases, so each phase require another entrance trough my groin vein with a catheter. I have not had my follow up appointment with him yet to speak about the details and potential treatment avenues to follow.

Additional Clinical Interpretation

I was also evaluated by a gynecologist/pain specialist with a neuropelveology background.

He diagnosed me right away with May Turner syndrome, Nut Cracker Syndrome and Dunbar syndrome. However me and a few other patients have doubts about the validity of these diagnosis as they were done rather quickly and based more on static images than the normal tests required.

However, he proposed that vascular abnormalities such as pelvic venous congestion could secondarily irritate the pudendal nerve and potentially autonomic pelvic nerves, resulting in a secondary pudendal neuropathy.

He also discussed that anatomical or biomechanical factors such as pelvic posture (including scoliosis and hyperlordosis) may influence venous compression dynamics in the pelvic/iliac region, although this remains a theoretical contribution rather than a definitive cause.

In addition, therapeutic and diagnostic options were discussed, including:

• Diagnostic laparoscopy to directly visualize pelvic veins (varices) and surrounding structures
• During such a procedure, potential decompression or neurolysis (nerve release) was discussed as a possible combined approach in selected cases, if clinically indicated and desired
• Possible decompressive surgical approaches in selected vascular compression syndromes (e.g. ligament release procedures in relevant anatomical entrapments)
• Physiotherapy focusing on posture, core stability, and lumbar-pelvic mechanics
• PF PT wasn't dismissed, but not the priority in comparison to normal PT
• Trial of antiplatelet/anticoagulant medication (e.g. ASS or stronger agents depending on clinical evaluation)

He was very honest and said that a complete remission of symptoms was unlikely, though he was confident that he could improve my quality of life with these symptoms.

My Current Working Hypothesis

My current evidence-based interpretation is:

1. Objective pelvic venous reflux and pudendal varicosities are present.
2. These vascular abnormalities may create chronic congestion and pressure in the pelvis.
3. This may secondarily irritate the pudendal nerve and/or autonomic pelvic nerves and cause neuropathy.
4. The resulting neural sensitization and pelvic floor dysfunction may contribute to Hard Flaccid Syndrome and chronic pelvic pain.

My goal moving forward will be to get more clearance on the compression diagnoses. I will have another appointment with a european specialist in may turner syndrome and hope that his expertise can shed light on which route I should follow when it comes to embolisation, stents and/or laproscopy.

Important Disclaimer

I am not claiming that this is the universal cause of Hard Flaccid Syndrome, nor that these findings definitively explain all of my symptoms.

However, this is the first time in many years that objective structural abnormalities have been identified and closely correlated with symptom reproduction during invasive testing.

I am sharing this in case others with Hard Flaccid Syndrome, chronic pelvic pain, penile numbness, perineal spasms, or unexplained genital symptoms may have an overlooked vascular component that has not yet been investigated.