Soft glans syndrome

As I’ve noticed in various topics concerning sexual dysfunction(and ED in particular), many guys here mention having a soft glans during erection. Has anybody solved this problem? What was causing it?
Has anybody tried a proper screening (doppler ultrasound or MRI)?

I’m going to have an ultrasound check quite soon myself, so I’d like to know what to expect.

Likely due to arterial insufficiency. This can be diagnosed with a penile doppler ultrasound. Many have already been diagnosed with it, including myself. I do still have good glans flow, but my issues was more venous leakage (blood staying in) rather than arterial ins. (blood flowing in).

Below are the values you use to diagnose.

Peak systolic velocity of the CA Indicator of arterial influx
Normal: >35 cm/sec
Gray zone: 25-35 cm/sec
Abnormal: <25 cm/sec

End diastolic velocity of the CA Normal: <3-5 cm/sec
Venous leak: >5 cm/sec
Diastolic flow reversal: reliable
indicator of intact veno-occlusive
mechanism

Deep dorsal vein Normal: <3 cm/sec
Moderate increase: 10-20 cm/sec
Marked increase: >20 cm/sec

Arterial compliance of the CA 60%-75% increase in diameter Ø
Evident pulsation

Resistive index of the CA Normal: >0.9
Venous leak: <0.75

This happens to me with morning wood exclusively.

@moonman1, @anon70124568, thank you guys for sharing your experience!

I’m sure there’re more people suffering from this, I’m really curious to know what they’ve managed to find out about this strange condition.

@anon70124568, that sounds interesting. Do you mean you have absolutely normal erection in other cases? Have you had an ultrasound check?

I should add that the androgen silencing theory fits perfectly into venous leak. Lack of androgenic action on the receptors (or post receptor) has been shown to directly cause VL.

I think soft glans syndrome is also consistent with the reduced sensitivity (sodium channel issue or whatever it is) associated with PFS — there’s a neural feedback loop where, if I recall correctly, your glans is supposed to sense erection in your corpus cavernosum and send signal to pelvic muscles to restrict outflow from corpus spongiosum. Erection is supposed to be a chain reaction where your CC get erect first and then your CS+glans inflates when glans detects erection of CC.

Well, it makes sense. I believe, not-filled corpus spongiosum could also explain decrease in girth. And I guess this isn’t necessary associated with some fibrotic changes in the tissue? Just another symptom of brain link malfunction.

Could it be that only some fraction of androgen receptors got silenced? Otherwise it should look like hyponadism or something like that, right?

The theory is that it is only in some tissues, not genome wide.

Could it be caused by some sort of pelvic floor dysregulation? It seems like at least some symptoms could be explained by some contracted muscle problems.