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Deflated Glans and Firm Flaccid: Pelvic Floor Dysfunction

Originally Posted by Tweaking
I sincerly doubt kegels are your problem TS, but at this moment I can’t be bothered explaining myself. I think if you stop your kegel routine you’ll find that your overall erections will suffer rather than benefit.

If I don’t masturbate/have sex/edge/etc for a week then I’ll also be hard as a rock, but that’s just because you get more horny.


I don’t have a kegel routine because I’m almost always kegelling. The 2.5 week period without any sort of stimulation didn’t make me any more horny. If anything my libido dropped but I was experiencing great morning wood.

When you can be bothered to explain why you don’t think it’s kegelling please post or PM me. I’m interested to know. :)


I'm a big fan of 50 Cent, or as we call him in Zimbabwe, four hundred million dollars.

Tossed Salad, does it feel like instead of pumping blood into the penis kegeling pumps blood out of the penis? As if the blood is being drawn out from the base of the shaft?

They used to get me pumped up but now I notice that erections will subside too if I kegel. I have no idea what’s causing this to happen.


3/13/09 - BPEL - 7.2 EL - 6.7 EG - 5.0

4/20/10 - BPEL - 7.5 EL - 7.0 EG - 5.6-5.9 depending on EQ

Originally Posted by vanillavutte
Tossed Salad, does it feel like instead of pumping blood into the penis kegeling pumps blood out of the penis? As if the blood is being drawn out from the base of the shaft?

They used to get me pumped up but now I notice that erections will subside too if I kegel. I have no idea what’s causing this to happen.


At first it feels like I’m pumping blood in and my CC’s and Glans expand then they subside and continue to subside if I don’t continue to stimulate myself. But the stimulation gets harder and harder each time I kegel.

When I have an inflated glans (without kegelling) and I penetrate my fleshlight I can feel blood being drawn out from the base. It’s a really weird feeling like a strong force acting against the flow. A force that’s stronger than the flow.

Although I’ve just had a thought and maybe it’s not blood being forced out but blood not being allowed in because of the pressure?
I have no problem getting any erection or maintaining it with sort of physical/psychological stimulation so I’m beginning to doubt it’s a form of ED. Maybe I’ve been looking at this the wrong way.


I'm a big fan of 50 Cent, or as we call him in Zimbabwe, four hundred million dollars.

Might be useful?

Soft Glans Syndrome: Overview
Content Written By: Irwin Goldstein, MD

Page 1
Soft glans syndrome may be defined as a sexual arousal disorder in which the corpora cavernosa of the penis are fully erect but the corpus cavernosum and the glans penis remain soft and cold, thus adversely affecting both the appearance of the erect penis and the ability to achieve penetration during sexual activity. There are no epidemiologic studies concerning the prevalence of the soft glans condition. Few physicians make inquiries to patients with sexual dysfunction whether the glans penis engorges and gets firm during sexual arousal. Specifically, the most commonly utilized psychometrically-valid measure of male sexual arousal does not address glans engorgement or glans firmness.

Page 2
During normal physiologic penile erection, there is increased blood flow to the two erection chambers, the corpora cavernosa via the right and left cavernosal arteries through relaxed helicine arterioles. As the corpora cavernosal veno-occlusive mechanism activates, hardness occurs within the two penile erection chambers with an increased intracavernosal pressure from 6-8 mmHg at baseline to approximately 100 mmHg during erection, and to over 1000 mmHg during the external compression associated with sexual intercourse.

During normal physiologic penile erection, there is also increased blood flow to the corpus spongiosum and penile glans via the right and left dorsal penile and corpus spongiosum arteries through relaxed helicine arterioles. As the corpus spongiosum and glans veno-occlusive mechanism activates, engorgement occurs within the corpus spongiosum and glans with an increased intraspongiosal pressure from 6-8 mmHg at baseline to approximately 20 mmHg during erection, and to approximately 30 mmHg during the external compression associated with sexual intercourse. There are few research studies concerning the physiology of the corpus spongiosum and glans veno-occlusive mechanism. Presumably, there is compression of subtunical venules by expanding spongiosal erectile tissue against the tunica albuginea.

The importance of penile glans engorgement during normal penile erection has not yet been fully physiologically clarified. However, an engineering principle is that to achieve penetration, although the body of the object may be hard, the relevant contact point of the object needs to be hard as well. If the relevant contact point of the object is soft, the object will buckle. Take, for example, a cooking spatula with a long wooden/metal handle and a flexible blade made of soft plastic. If the relevant contact point of the spatula is the hard handle (upside down spatula), no buckling will occur. If the relevant contact point of the spatula is the soft blade (correctly oriented spatula), buckling will occur, since the relevant contact point is soft. It is not well appreciated but penetration for sexual activity requires a firm penis in the shaft and a firm contact point, that is, the glans penis. When the glans penis is soft, it is more difficult for a man to penetrate for satisfactory sexual intercourse.

Page 3
There are three suspected pathophysiologies of soft glans syndrome. There is “failure to initiate” soft glans syndrome. In this condition, neurologic injury involving the motor nerves innervating the corpus spongiosum result in an inability to activate the arterial inflow and veno-occlusive processes within the spongiosal erectile tissue. This may occur post-urethroplasty for urethral stricture disease.

There is “failure to fill” soft glans syndrome. In this condition, arterial occlusive disease within the dorsal or spongiosal arteries result in an inability to provide sufficient arterial perfusion pressure to the spongiosal erectile tissue. The arterial pathology may be the result of atherosclerotic disease with vascular risk facture exposure, or may also occur following traumatic arterial occlusive disease secondary to blunt perineal trauma.

There is “failure to store” soft glans syndrome. In this condition, fibrosis of the erectile tissue within the corpus spongiosum results in poorly expandable erectile tissue and an inability to provide sufficient compressive pressure on the sub-tunical venules and veno-occlusive dysfunction. Fibrotic spongiosal erectile tissue can occur with vascular risk factor exposure, blunt perineal trauma or surgical injury after urethroplasy or associated with penile prosthesis implantation. “Failure to store” soft glans syndrome may also result after iatrogenic shunts have been performed such as associated with ischemic priapism treatment.

In summary, the following conditions are associated with soft glans syndrome: neurologic injury, post-urethroplasty, atherosclerotic vascular disease, blunt perineal trauma, glans shunt surgery for priapism, Peyronie’s disease, and penile implant surgery

Page 4
If a patient complains of soft glans syndrome, the following diagnostic tests are available.
Photography in the erect state can confirm the soft glans syndrome. Spongiography in the pharmacologically erect state can reveal contrast in the glans penis and deep dorsal veins consistent with spongiosal veno-occlusive dysfunction. Thermography using a
Forward Looking Infrared (FLIR) camera is an imaging technology that senses infrared radiation and thermal energy. Forward Looking Infrared imaging technology can be used to help pilots and drivers steer their vehicles at night, and in fog, or detect warm objects against a cold background when it is completely dark - such as a cloudy, moonless night. Forward Looking Infrared can be used to assess blood flow in tissues. The skin/glans of the penis constantly emits infrared radiation. It is possible to detect increases in infrared radiation emission from the skin/glans of the penis by remote sensing using a high-resolution, fast-scanning camera that can produce thermal images with a precision of 0.07 degrees C in a very short period of time.

Page 5
Treatment of soft glans syndrome may be mechanical, pharmacologic or surgical. Mechanical rings may be placed at the base of the penis. Vacuum therapy with mechanical rings can also be utilized. Surgery can be performed to ligate veins and close iatrogenic shunts. There are limited outcome data with mechanical or surgical therapeutic strategies.

Pharmacologic treatment is based on systemic and local therapies. Systemic therapies involve use of PDE5 inhibitors (Viagra, Levitra or Cialis). During sexual stimulation, PDE5 inhibitors can increase blood flow to the corpus spongiosum and facilitate spongiosal veno-occlusive dysfunction. PDE 5 inhibitors can only improve symptoms of soft glans in patients with failure to fill or failure to store soft glans syndrome.

The most outcome data concerning local pharmacologic data is with the use of Medicated Urethral System for Erection (MUSE). MUSE provides a novel delivery system that permits the intraurethral administration and absorption of alprostadil through the urethral mucosa to the corpus spongiosum. Resultant smooth muscle relaxation and vasodilatation lead to engorgement and tumescence of the corpus spongiosum, including the glans penis. MUSE has been used to successfully treat men with soft glans syndrome following penile prosthesis insertion. A total of 28 men aged 47-81 years with a penile prosthesis were treated with alprostadil (250-1000 μg; mean, 566 μg). Sixty-one percent reported decreased glans penis engorgement. A total of 10 of 17 (59%) with soft glans syndrome were satisfied with MUSE treatment.

In summary, soft glans syndrome may be more common than previously appreciated. Advances in diagnosis may be forthcoming using forward looking infrared thermography. The most efficacious treatment is local application of alprostadil (MUSE).

Page 6
[Photo’s]

(In the photo's it looks to me that his glans is still the same as it would be flacid, but it's hard to tell without a flaccid shot.)

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I'm a big fan of 50 Cent, or as we call him in Zimbabwe, four hundred million dollars.

Originally Posted by Tweaking
Excellent find TS, this is almost like a ‘breakthrough’ article for me. It’s the first mention I’ve seen of actual concentration from the established medical community at examining this problem. I’d be very interested to know when this was written, did you notice a date for it?

This is the most interesting part of the article for me:

“There is “failure to store” soft glans syndrome. In this condition, fibrosis of the erectile tissue within the corpus spongiosum results in poorly expandable erectile tissue and an inability to provide sufficient compressive pressure on the sub-tunical venules and veno-occlusive dysfunction. Fibrotic spongiosal erectile tissue can occur with vascular risk factor exposure, blunt perineal trauma or surgical injury after urethroplasy or associated with penile prosthesis implantation. “Failure to store” soft glans syndrome may also result after iatrogenic shunts have been performed such as associated with ischemic priapism treatment.”

It fits with a number of the ideas we’ve discussed in this thread. I’m seeing my GP tomorrow, I’ll bring this segment along with me, see what she thinks.

It does make me wonder if whether x10d’s report is indeed repeatable. If the cause is indeed fibrotic scarring and the iodine/Magnesium/DMSO treatment can, as suggested, ‘dissolve’ fibrotic tissue then it’s feasible that it could be an effective treatment. I haven’t had a chance to further apply this method, yet.

I’m not sure when that article was written but it seems that author of the article is a urologist that knows his stuff. I found this on another forum:

The original poster mentions Dr. Irwin Goldstein and states that the doctor found perineal arterial blockage and recommended bypass surgery. The poster does not seem to have our problem, but to find a diagnoses like that is pretty interesting. The poster said after the surgery his blood flow was better to the penis, but his libido was low. At least it seems like this might be a doctor worth seeing for a soft glans as opposed to most urologists who only know how to give out viagra. He is located in San Diego.

Have you guys done Ulis/Horses prior to having this venous leak? do u have bad masturbation habits?

I’ve been with this problem for 2 years and have bad masturbation habits, around the time of this venous leak i started Ulis without any injuries/prblems. but i also was doing cocaine.

While under the influence i tried to achieve erection which made me ejaculate with a soft glans while in semi erect state. Thats were the prblems started


02-10-09: Nbpel-4 7/8" ; Midshaft-eg- 5 1/4"; Base-eg- 4 7/8"

My GP said this type of injury as described in post 137 could only result from from trauma such as falling off a bike with an erection. She had never heard of jelqing or clamping or anything in between. I rolled my eyes and asked for a referral to a urologist.

It’s been around 4 days since I stopped all forms of kegelling. I found I was holding a mild kegel even when doing minor things like walking or sitting down. I’ve had to mentally focus on relaxing my pelvic floor muscles and during a good erection my glans inflats and only deflates slightly during the first moment of penetration, after half a dozen strokes I can feel it swelling again. I’ve always suffered from retarded ejaculation but now after 5-10 minutes of penetration I cum so hard my legs go weak.

My problem was caused by (excessive) kegelling as I had thought. Although my case is rather different to everyone’s here I didn’t have a problem with glans inflation during an erection it was only a problem during penetration.


I'm a big fan of 50 Cent, or as we call him in Zimbabwe, four hundred million dollars.

Originally Posted by Tweaking
My GP said this type of injury as described in post 137 could only result from from trauma such as falling off a bike with an erection. She had never heard of jelqing or clamping or anything in between. I rolled my eyes and asked for a referral to a urologist.

Why should the GP have heard about jelqing or clamping? Quite unreasonable to expect that she would have, the same would apply to the urologist. There is no reason for them to have heard of and or know about PE techniques.


Starting Stats - 5.5 BPEL x 5.6 EG

Current Stats - 5.7 BPEL x 6.5 EG

Goal - 7 x 6 (with hopefully a large flaccid hang)

How are you doing Tweaking? I saw in another thread that you are still jelqing/clamping/pumping. How is your eq? Did you ever see the urologist?

EQ is probably as good or better than it’s ever been, however much of this is still masked by the soft glans syndrome. My flaccid hang is bigger than it’s ever been before. But I still get the firm flacid erection, particularly when I’m in a state of slight of ‘less horniness’ than usual. That is, the less I ejaculate the less symptoms I experience. The same is true for glans and CS engorgment. If I only ejaculate infrequently, it’s much less noticeable. But if I do it a lot, it becomes much more prominent. The same is true for speed of erection loss without stimulation. These are basically the 3 symptoms I’ve identified.

Haven’t seen a urologist, I don’t really think there’s much one will be able to tell me that I don’t already know. As far as I can tell, the only solution to this problem is determining where the leak or leaks are occuring and them ligating them. I would have seen a urologist but I’d be worried they’d tell me after such an operation (which would be difficult to get them to do anyway I think) it would not be safe to PE anymore and that if they suspected I would anyway, would be unwilling to perform the procedure.

I have these three symptoms like you guys except that I have premature ejaculation and pelvic and back pains to top it off. It’s definitely related does anyone else have these symptoms?

Originally Posted by Tweaking
EQ is probably as good or better than it’s ever been, however much of this is still masked by the soft glans syndrome. My flaccid hang is bigger than it’s ever been before. But I still get the firm flacid erection, particularly when I’m in a state of slight of ‘less horniness’ than usual. That is, the less I ejaculate the less symptoms I experience. The same is true for glans and CS engorgment. If I only ejaculate infrequently, it’s much less noticeable. But if I do it a lot, it becomes much more prominent. The same is true for speed of erection loss without stimulation. These are basically the 3 symptoms I’ve identified.

Haven’t seen a urologist, I don’t really think there’s much one will be able to tell me that I don’t already know. As far as I can tell, the only solution to this problem is determining where the leak or leaks are occuring and them ligating them. I would have seen a urologist but I’d be worried they’d tell me after such an operation (which would be difficult to get them to do anyway I think) it would not be safe to PE anymore and that if they suspected I would anyway, would be unwilling to perform the procedure.

I have been observing my symptoms and I believe for me it is just my pelvic floor muscles are so tense that blood is not being pumped properly. I noticed that my glans did not inflate when blood flow to my penis felt slow. This occurred after it felt I hit a nerve in my penis kind of like how it feels to hit your funny bone in your elbow. This caused my pelvic floor to tense and my penis to become firmer when flaccid.

I have actually had my blood flow velocity checked and it is slow. For me, this glans deflation was instant after I hit this nerve so I doubt it could be venous leak. It seems the likely culprit it the bulbocavernous muscle being tense. When we reach the PONR our bulbocavernous muscles act as they should by pumping blood to the glans and we see the problem disappear.

It seems pelvic floor muscle contraction is affected by brain activity and hormones. I recall Tweaking mentioned that he started to get these symptoms after MDMA use. This drug could have caused a malfunction in the pelvic floor area that just messed up the brain’s signaling to pump blood normally to the penis.

Only problem with this issue is trying to figure out how to get these pelvic floor muscles to act normally and pump blood as they should.

Interseting biff. We’re moving into completely uncharted territory here, but I think your hypothesis has merit. To confuse matters, however, we know that some people with these identical symptoms did recover after getting ‘leaking veins’ ligated by a radiologist. So I just wonder whether the pelvic floor muscle issue would cause exactly the same symptoms as a leak. Most people, I think, were not using MDMA when they first started getting these symtpoms, though I did find a story online about a guy who’s story pretty much matches mine after masturbating for an extended period of time after MDMA and cannabis, except his symptoms were much worse.

If it is neurologic in my case, I would think that it would be neurologic for everyone, perhaps? Also, perhaps, ligation of veins could possibly mask the soft glans/CS syndrome by simply reducing the ammount of efferent blood flow from the penis so dramatically that even a weakened pelvic floor muscle won’t be noticeable.

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