We describe a patient with a 35-year history of a severe chronic pelvic pain syndrome (CPPS) that failed to adequately respond to various drug therapies and other treatments by different specialists. In addition to the ongoing chronic pain, he suffered from week-long episodes of increased pain with no discernible trigger. At the first consultation with us the patient was in a particularly severe pain phase. He was taking four different analgesically effective drugs. In terms of therapeutic local anesthesia (neural therapy), we performed suprapubic injection of procaine 1% with infiltration of the vesicoprostatic plexus. Just a few minutes later, the pain decreased significantly. To maintain and further increase the effect, we performed the injection six more times. The patient gradually reduced and stopped all drugs and remained free of pain and discomfort ever since. This is the first report of a successful therapeutic infiltration of the vesicoprostatic plexus using a local anesthetic (LA) in a patient with CPPS that has been refractory to different treatments for many years. A possible explanation may be that the positive feedback loops maintaining pain and neurogenic inflammation are disrupted by LA infiltration. This can lead to a new organisation (self-organisation) of the pain-processing systems.
Chronic pelvic pain syndrome (CPPS)—also called chronic (abacterial) prostatitis (CP) in men—is a common clinical syndrome characterized by pain and functional urogenital disorders. The National Institute of Health (NIH) assigns CPPS to Category III prostatitis ((I) acute bacterial prostatitis, (II) chronic bacterial prostatitis, (III) chronic prostatitis/CPPS, and (IV) asymptomatic inflammatory prostatitis).
We report on a 55-year-old man who was diagnosed with CPPS by urology specialists from the university hospital and referred to us for pain treatment with local anesthetics (neural therapy).
At his first consultation with us, the patient reported pain and other ailments that began 35 years prior, after a party in a damp basement, without vanishing ever since. In the same night, pollakisuria and dysuria occurred, and the patient noted a permanently painful foreign body sensation in the areas of the prostate and anus, as well as perineally. Furthermore, he complained of a burning sensation in the urethra, a slightly reduced urinary stream, and nocturia of varying frequency. In addition to the ongoing chronic pain, the patient suffered from week- to month-long episodes of increased pain with no discernible trigger. Overall, the pain and other symptoms progressed over time.
Over the years, various specialist urological examinations were carried out and several attempts at treatment with various empirical antibiotic therapies and analgesics were made. Also, nerve stimulation therapy was applied, and a probatory surgical removal of both seminal vesicles and an extension surgery on the anus were performed. None of these measures resulted in any improvement in pain or other symptoms. The patient was then referred to us by the urologists for a probatory pain treatment with LA.
At the first consultation with us the patient was in a particularly severe pain phase. He complained of permanent pain and discomfort perineally and in the areas of the prostate, anus, and urethra, associated with pollakisuria, dysuria, and nocturia (more than ten times per night). Due to this the quality of life was impaired to a large degree. The patient was desperate and did not believe that he could be helped anymore.
For nine years he was taking an analgesically effective antiepileptic drug, Gabapentin, as well as the nonsteroidal anti-inflammatory drug Diclofenac, the opioid Oxycodone, and the pain-modifying tricyclic antidepressant, Amitriptyline.
The National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) resulted in 39 points (pain: 18; urinary symptoms: 10; quality of life impact: 11). In rectal palpation, the patient felt pain in the lesser pelvis while the prostate was inconspicuous, as was the case in the recently performed sonography, in which 50 ml of residual urine had been detected. The PSA value was found to be 0.4 ng/ml.
Our treatment consisted of suprapubic injection of 5 ml each of 1% procaine on the right and the left with infiltration of the vesicoprostatic plexus (in line with neural therapy). In this injection, the puncture site is directly behind the pectineal line (pecten ossis pubis), 5 cm laterally to the center of the symphysis. The puncture direction is 45° both medially and caudally. The needle point needs always to remain extraperitoneal in the paravesical connective tissue, in which the vegetative nerve fibers are located. The penetration depth in the described patient was 7 cm, with the needle gauge being 23.5 (0.6 mm).
Just a few minutes after the first injection, the pain decreased significantly and persistently to a level the patient had not experienced in years (in his own terms: 90% improvement of all symptoms). In the following days, the patient experienced a further and lasting significant reduction in pain and other symptoms. At the next consultation after two weeks NIH-CPSI resulted in 11 points (pain: 3; urinary symptoms: 4; quality of life impact: 4). To maintain and further increase the effect, we performed the suprapubic injection of procaine a total of six more times, initially once a month, and bimonthly later. With each injection, the pains continued to decrease, up to freedom from pain and discomfort. Relapses occurred less frequently, were significantly lower in intensity and the duration was significantly shorter with an average of three days. Even the symptom-free intervals were getting longer. The patient reduced Diclofenac and Oxycodone on his own initiative and completely discontinued both drugs after the fifth consultation. After seven treatments, he was also able to stop Gabapentin and Amitriptyline and remained free of discomfort (NIH-CPSI: 0 points), which also had a positive effect on his mental and social integrity.
No adverse effects were observed.
To our knowledge this is the first description of a successful treatment of refractory CPPS by infiltration of the vesicoprostatic plexus vesicoprostaticus with a LA.
In the emergence and maintenance of chronic pain and inflammation the sympathetic nervous system plays an important role. Various mechanisms are involved which sometimes amplify each other through positive feedback, resulting in functional and structural neuronal changes. The pathomechanisms described below are thought to be involved in CPPS, too.
Visceral and somatic nociceptive afferents converge in the spinal cord at the same multireceptive posterior horn neurons (wide dynamic range neurons/WDR neurons) [
Nociceptive processes trigger a reflex response that is mediated predominantly by the sympathetic system and occurs via cutivisceral, viscerocutaneous, viscero-somatic-motor and reflex tracts [
The processes described below lead to further amplification of the above-mentioned positive feedback. An important factor in the development of these iterative loops is known as “sympathetic-afferent coupling” [
The process known as sympathetic sprouting, too, leads to analogous positive feedback, in which sympathetic fibers form basket-like structures in the dorsal root ganglia (DRG) of the nociceptive afferents under inflammatory conditions [
Neuronal activity which is increased in the context of nociceptive processes can lead to
Gate Control Theory deals with the input control of the afferences in the posterior horn [
The common feature of inflammatory pain states is decreased descending inhibition [
In addition to pain, inflammation is part of CPPS. The sympathetic nervous system influences immunological processes. Proinflammatory cytokines, under certain conditions, can induce the expression of
The well-directed injection of local anesthetics (LA) (neural therapy) can be used to directly interfere with the described pathomechanisms at various levels [
Repeated use may allow autoregulation of the pain-processing systems due to the short-term interruption of neuronal reflex arcs pathologically trapped in positive feedback [
In the case of
LA also have anti-inflammatory properties and can regulate the sympathetically mediated
Finally, LA are also antibacterial, antiviral, and antifungal [
We use procaine for injection treatments because it offers some advantages over other LA. As a result, no long-term side effects have been reported in over 100 years [
Due to the low diffusion capacity of procaine, the effect is locally limited and therefore easily controllable [
Our findings and considerations suggest that in the pathophysiology of CPPS numerous positive feedback loops (“circuli vitiosi” maintained by the sympathetic nervous system) play an important role in pain and neurogenic inflammatory processes. Positive feedback loops can be broken by means of injection treatments with procaine (neural therapy), which gives the pain-processing system the opportunity to reorganize. The described pathomechanisms and the mechanisms of action of local anesthetic injection treatment show a striking congruence, so that the latter appears to be the logical treatment for CPPS. It has to be confirmed by clinical trials, if the effectiveness of the presented new treatment option can be generalized.
Calcitonin gene-related peptide
Chronic prostatitis
Chronic pelvic pain syndrome
Dorsal root ganglia
Interleukin
Local anesthetics
Long-term potentiation
Tumor necrosis factor.
Authors confirm that the patient described in the case report has given his informed consent for the case report to be published.
On behalf of all authors, the corresponding author states that there are no conflicts of interest.