Inflammation of the Pelvic Floor and Pudendal Plexus
We can essentially state that chronic pelvic pain (in the American sense indicated with the acronym CPPS = Chronic Pelvic Pain Syndrome) is caused by the inflammation of some or all branches originating from the Pudendal Plexus and chronic pelvic pain.
Unfortunately, this Syndrome, which is actually very common and mistakenly confused with prostatitis, often generates a flood of useless therapies (typically repeated cycles of antibiotics) that only serve to worsen the patient’s situation, both physically and above all psychologically, due to the total loss of the subject’s trust in doctors and in the repeatedly proposed treatments.
It statistically affects young males between 20 and 40 years of age more frequently.
I immediately apologize for the complexity of the following narration (although I have tried to make it as simple as possible for non-experts), just as I also apologize to any specialist for the simplifications made!
Let’s start with the definition of NERVE PLEXUS.
A nerve Plexus is a “tangle” of spinal nerves that intersect and group together to serve a specific area of the body.
The Pudendal Plexus is one of the 6 plexuses that make up the so-called peripheral nervous system, along with the:
- Cervical Plexus,
- Brachial Plexus,
- Lumbar Plexus
- Sacral Plexus
- Coccygeal Plexus.
The Pudendal Plexus originates at the level of the 2nd-3rd-4th sacral vertebra and intersects with the overlying Sacral Plexus (receiving fibers), and with the underlying Coccygeal Plexus (donating fibers).
As we have said, a Plexus is a “tangle” of nerve fibers which in Our case are divided into sensory fibers (i.e. those that conduct tactile, painful sensations, etc.) and motor fibers (i.e. those that oversee a muscle contraction).
The first category (sensory fibers) includes the fibers that innervate pelvic organs such as the bladder, rectum and vagina but also the buttocks and skin of the perineum.
The second category (motor fibers) includes the fibers that innervate the levator ani muscles, the muscles of the anal sphincter and the anal canal.
From this “tangle” of fibers, both sensory and motor, ultimately a single terminal nerve is born, which is the Pudendal Nerve.
The inflammation of this nerve is ultimately the main responsible factor for Chronic pelvic pain syndrome.
The initial anatomical course of this nerve is of little interest to us (it exits the pelvis, and re-enters the pelvis through the lesser sciatic notch reaching the ischio-rectal fossa) until it arrives below the levator ani muscle, in a canal defined as Alcock’s canal, formed by the splitting of the fascia of the obturator internus muscle.
By Mikael Häggström. When using this image in external works, it may be cited as: Häggström, Mikael (2014). “Medical gallery of Mikael Häggström 2014”
The pudendal nerve divides into its two terminal branches, the perineal nerve and the dorsal nerve of the penis or clitoris.
The perineal nerve in turn divides into a superficial branch (sensory) that innervates the entire perineum, the scrotum, the ventral face of the penis and the labia majora in women, and into a deep branch that (motor portion), innervates the muscles of the perineum, levator ani muscles and the muscles of the urethral and anal sphincter and (sensory portion) both the external and internal urethra.
The dorsal nerve of the penis or clitoris in the male innervates the entire dorsal portion of the penis, the corpora cavernosa and the glans and in the female it innervates the clitoris and labia minora.
The pudendal nerve also contains fibers for the arterial vessels of the genital organs, which stimulate their vasodilation (in the male the erection of the penis, in the female the engorgement of the clitoris).
This is the cause of the sometimes sudden impotence or hypopotence reported by many young patients!
At this point, if you made it out alive from this description you can well understand that the inflammation of this nerve involves all the anatomical structures of the pelvis, the perineum and the external genitalia.
The diagnosis of this Pain Syndrome is easily made by compressing the emergence of the nerve transrectally in males and transrectally and transvaginally in females.
However, there is also a codified criterion (Nantes Criteria) to diagnose this disease:
The essential criteria are the following:
- Pain in the territory of the pudendal nerve (from the anus to the penis/clitoris).
- Pain predominantly while sitting.
- The pain does not wake the patient during the night.
- Pain without objective sensory impairment.
- Pain relief with the diagnostic block of the pudendal nerve.
The additional criteria are the following:
- Burning, shooting, stabbing pain, numbness.
- Sensation of a rectal or vaginal foreign body.
- Worsening of pain during the day.
- Predominantly unilateral pain.
- Pain triggered by defecation.
- Pain in the buttocks while sitting.
- Referred sciatic pain.
- Pain referred to the medial part of the thigh.
- Suprapubic pain.
- Urinary frequency and/or pain after sexual intercourse.
- Pain occurring after ejaculation.
- Dyspareunia and/or pain after sexual intercourse.
- Erectile dysfunction.
The question you are probably asking yourselves now is the following:
“How does the inflammation of the pudendal nerve originate and what causes it?”
In my clinical experience, the most statistically frequent cause of the disease depends either on the spasm of the perineal musculature with direct compression on the nerve roots or on the outcomes of poorly treated inflammations of pelvic organs (prostatitis in the male or vaginitis or endometriosis in the female). Cases of pudendal inflammations on a post-traumatic basis (accidents, surgeries, etc.) or postpartum are very rare.
The onset of the perineal muscle spasm is almost always linkable either to a psychologically traumatic event (abandonment by a partner, job loss or loss of a parent, psychological overload coinciding with an exam or other important test) or to a life situation that is particularly engaging in a stressful sense.
In fact, chronic stress and anxiety can cause an involuntary and prolonged contraction of the pelvic floor muscles, similar to how stress can lead to tension in the neck or back muscles. People with anxiety or psychosomatic disorders can indeed unconsciously keep their pelvic muscles contracted.
But sometimes even poor posture, or the prolonged use of uncomfortable chairs, can alter the pelvic muscular balance. Furthermore, poorly distributed body weight can lead to muscular compensations and chronic tensions.
Finally, sports such as cycling, horseback riding, or weightlifting can overload the pelvic muscles, causing spasms. Indeed, excessive sports activity can induce micro-tears or fatigue in the pelvic muscles.
THERAPEUTIC PROTOCOL FOR PUDENDAL NERVE INFLAMMATION – CHRONIC PELVIC PAIN
- Once a correct diagnosis and a correct cause (etiopathogenesis) of the disease have been established, our therapeutic protocol will make use of:
- in the first level, systemic (BACLOFEN) and local (DILATAN) muscle relaxants of the perineal musculature, associated with benzodiazepines (CLONAZEPAM) and contact anti-inflammatories (cortisone enemas).
- The second level of therapy will be based on neuromodulators (Amitriptyline, Pregabalin and Duloxetine)
- The third level will use infiltrations of corticosteroids and anesthetics at the level of Alcock’s canal
- The fourth level, consisting of a surgical debridement intervention with the release of the entrapped nerve, is obviously reserved for the most severe cases (usually the outcomes of traumas).
FIRST LEVEL: BACLOFEN
We use Baclofen to relieve symptoms related to an excessive contraction of the pelvic floor muscles; it actually has a muscle relaxant and antispasmodic effect by acting on GABA receptors in the central nervous system.
Effects of Baclofen in Perineal Spasm:
- Muscle Relaxation:
- Reduces the muscular hypertonia of the pelvic floor, improving the relaxation of the muscles involved in the spasm.
- It is useful for conditions such as chronic pelvic pain syndrome (CPPS), in which perineal spasms contribute to the pain.
- Analgesic Effect:
- Through muscle relaxation, baclofen can reduce nerve compression and improve circulation, thus mitigating the pain associated with spasms.
- Reduction of Reflex Contracture:
- It decreases the reactivity of neuromuscular circuits, preventing involuntary reflex contractions that often characterize this condition.
FIRST LEVEL: CLONAZEPAM
Clonazepam is a benzodiazepine used primarily as an anticonvulsant and anxiolytic. In our protocol it is used off-label thanks to its effects on the central and peripheral nervous system.
Effects of Clonazepam on Chronic Pelvic Pain:
- Reduction of Muscle Contracture:
- Clonazepam has a muscle relaxant effect, useful for reducing the hypertonia of the pelvic floor, which often contributes to chronic pelvic pain.
- This can be particularly useful in cases where the pain is associated with muscle spasms or pelvic floor dysfunctions.
- Sedative and Anxiolytic Effect:
- By reducing anxiety and promoting general relaxation, clonazepam can help lower the perception of pain, which is often amplified by emotional tensions and chronic stress.
- Modulation of Neuropathic Pain:
- Clonazepam acts on GABA-A receptors, inhibiting neuronal hyperactivity. This makes it useful in situations where pelvic pain has a neuropathic component, such as pudendal neuralgia or other disorders related to the nerves of the pelvic floor.
- Regulation of Central Pain Circuits:
- Through the modulation of the central nervous system, the drug can contribute to “desensitizing” the pain pathways, improving the quality of life of patients with chronic pelvic pain.
SECOND LEVEL: AMITRIPTYLINE
THE THREE MECHANISMS OF ACTION OF AMITRIPTYLINE:
1) AMITRIPTYLINE has effects on the calcium and potassium channels that are both involved in the transmission of the nerve pain signal from the periphery to the center and in the sensitization of the pain itself. Numerous studies have shown that the number of calcium channels increases in conditions of neuropathic pain and this can be responsible for an aberrant neurotransmission of pain. This drug is therefore able both to enhance the activity of the descending inhibitory pain pathways and to activate interneurons that directly release inhibitory substances on pain such as endogenous opioids (D. Fornasari).
Effects on Calcium Channels:
AMITRIPTYLINE, by reducing the entry of calcium into neurons, limits the release of excitatory neurotransmitters such as glutamate and substance P, contributing to the reduction of central sensitization, a phenomenon that amplifies pain in patients with chronic conditions such as neuropathy or fibromyalgia. Furthermore, by acting on presynaptic terminals, the inhibition of calcium channels decreases the excessive release of pain signals, attenuating the activation of pain pathways with a reduction effect both from the periphery to the center and from the center to the periphery.
Effects on Potassium Channels
AMITRIPTYLINE also influences the potassium channels, which regulate neuronal excitability with effects that can contribute to pain control and to the stabilization of the neuronal membrane. It can in fact enhance potassium channels (so-called inward rectifiers), which are fundamental for the functioning and balance of excitable cells through their ability to stabilize the membrane potential making the cells less excitable and reducing the transmission of pain. Furthermore, the hyperpolarization of sensory neurons helps to turn off persistent pain signals.
2) AMITRIPTYLINE reduces abnormal activity in sensory neurons, which often contributes to neuropathic pain.
3) AMITRIPTYLINE also has sedative properties that improve sleep quality, a critical factor for patients with chronic pain. Sleeping better can reduce the perception of pain and improve the overall resilience of the patient.
SECOND LEVEL: PREGABALIN
THE FIVE MECHANISMS OF ACTION OF PREGABALIN:
PREGABALIN is an anticonvulsant and analgesic drug, commonly used for the treatment of neuropathic pain and as an adjunctive therapy in epileptic seizures. Its mechanism of action, as well as that of Amitriptyline, primarily involves the inhibition of abnormal nerve transmission through interaction with specific calcium channels. PREGABALIN acts predominantly by binding to the subunit of voltage-dependent calcium channels, particularly in the neurons of the central and peripheral nervous system. These subunits are crucial for regulating the entry of calcium into neurons, an event, let us remember, essential for the release of pain impulse neurotransmitters.
- By selectively binding to these subunits (α2δ) it reduces the entry of calcium into neurons and consequently reduces the release of excitatory pain neurotransmitters such as glutamate, substance P, etc. The final result is to modulate the pain signal along the nerve pathways.
- The reduced calcium entry decreases the abnormal activation of neuronal circuits, with the effect of limiting central sensitization, a common phenomenon in chronic neuropathic pain.
- The reduced calcium entry also contributes to reducing the “long-term potentiation of pain” (LTP), a process that amplifies pain signals in the spinal cord.
- Even in damaged peripheral nerves, pregabalin exerts a modulatory effect by reducing neuronal excitability and the abnormal transmission of impulses, ultimately improving the symptoms of neuropathic pain.
- Although pregabalin does not directly interact with GABA receptors (their inhibitory action helps maintain the balance between excitation and inhibition), its use can increase GABA levels in some areas of the brain, promoting an indirect calming effect on the central nervous system.
SECOND LEVEL: DULOXETINE
Duloxetine, commonly used as an anxiolytic and antidepressant, acts by inhibiting the reuptake of serotonin and noradrenaline, practically keeping these two powerful mood-regulating substances in circulation.
However, it also has indications in the treatment of neuropathic pain and chronic pain syndromes, such as fibromyalgia and chronic pelvic pain (CPP), through three mechanisms:
- Modulates neuropathic pain: It acts on the central pain pathways, reducing nerve sensitivity and improving tolerance to pain.
- Reduces hyperalgesia: It improves pain perception linked to central sensitization.
- Psychological benefit: Duloxetine can alleviate the anxiety and depression often associated with chronic pain.
Finally, for hygienists and nature lovers, for pure completeness, I make a list of natural anti-inflammatory substances:
- Aloe vera, a natural ally against inflammation.
- Mallow: a help from nature.
- Devil’s claw against inflammation.
- Natural anti-inflammatory: meadowsweet.
- White willow to relieve inflammation.
- Ginseng or ginger to fight inflammation.
