Fibromyalgia: A Complex and Multifactorial Syndrome
Fibromyalgia or fibromyalgia syndrome is also called the invisible disease as it poses significant challenges for both patients and the medical community. Defined as a multi–system condition, it is characterized by widespread and persistent musculoskeletal pain, accompanied by debilitating symptoms such as fatigue, sleep disturbances and cognitive difficulties. Although it represents one of the main causes of chronic non–cancer pain, its origins remain enigmatic, thus complicating the diagnostic and therapeutic process. This condition affects between 2 and 4% of the population and the majority of people who suffer from it are women between the ages of 40 and 50
Main Features of Fibromyalgia
The main symptom of fibromyalgia is chronic and widespread pain, often described as a burning sensation, tension or muscle stiffness. This pain can be compounded by factors such as stress, climate change or excessive physical activity.
In addition to pain, patients often experience:
- Chronic fatigue: A persistent feeling of tiredness that does not improve with rest.
- Sleep disorders: Difficulty falling asleep or maintaining a deep and restorative sleep.
- “Fibro-fog”: Cognitive problems that include difficulty concentrating, impaired short-term memory, and mental confusion.
- Somatic symptoms: Headache, gastrointestinal disorders (such as irritable bowel syndrome), sensitivity to light or noise.
Causes and Risk Factors
The exact causes of fibromyalgia are not yet fully understood, but this condition is believed to be the result of a combination of genetic, environmental and neurobiological factors. Some of the main factors associated include:
Genetic predisposition: A family history of fibromyalgia can increase the risk.
Stressful or traumatic events: Incidents, serious infections, or emotional distress may act as triggers.
Neurological disorders: Anomalies are observed in the way the brain and spinal cord process pain signals.
Diagnosis of Fibromyalgia
There are no specific laboratory tests to diagnose fibromyalgia. Diagnosis is mainly based on clinical evaluation, which includes:
1. Detailed Medical History: Identification of characteristic symptoms and duration of pain (usually present for at least three months).
2. Physical examination: Exclusion of other medical conditions.
3. Diagnostic criteria: Pain assessment at at least 11 on 18 specific pressure points, although the latest guidelines emphasize an overall symptom-based approach.
Treatment and Management
There is no definitive cure for fibromyalgia, but the symptoms can be managed through a multidisciplinary approach that includes pharmacological therapies, physical exercise, cognitive-behavioral therapies, psychological support.
We will deal here more specifically with pharmacological therapies, without absolutely minimizing the other approaches or rather co-approaches just mentioned.
We can consider three lines of therapy.
In the first line we include Amitriptyline (Imipramine is less effective), Pregabalin (Gabapentin has similar action but is less powerful and less bioavailable) and Duloxetine.
In the second and third lines we include local infiltrations of lidocaine and opioids.
Treatment Goals
• Reduce pain and improve sleep.
• Increase energy and physical functionality.
• Improve mood and psychological resilience.
• Restore daily and social activities.
FIRST LINE
The AMITRIPTILINA
THE THREE MECHANISMS OF ACTION OF AMITRIPTILINE:
1) AMYTRIPTILINE has effects on calcium and potassium channels which are both involved in the transmission of the pain nervous 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 neuropathic pain conditions and this may be responsible for aberrant pain neurotransmission. This drug is therefore able to both enhance the activity of the descending pain inhibitory pathways and activate interneurons that directly release pain inhibitory substances such as endogenous opioids (D. Fornasari).
Effects on Calcium Channels:
AMYTRIPTILINE, 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 painful 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
AMYTRIPTILINE also influences potassium channels, which regulate neuronal excitability with effects that can contribute to pain control and stabilization of the neuronal membrane. It can in fact enhance potassium channels (so-called internal 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. Additionally, hyperpolarization of sensory neurons helps turn off persistent pain signals.
2) AMYTRIPTILINE reduces abnormal activity in sensory neurons, which often contributes to neuropathic pain.
3) AMYTRIPTILINE 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 patient’s general resilience.
THE 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, mainly involves the inhibition of abnormal nerve transmission through interaction with specific calcium channels. PREGABALIN works predominantly by binding to the subunit of voltage-gated calcium channels, particularly in neurons of the central and peripheral nervous system. These subunits are crucial for the regulation of calcium entry into neurons, an event, let us remember, essential for the release of pain impulse neurotransmitters.
1. Selectively binding to these subunits (α2δ) reduces the entry of calcium into neurons and consequently reduces the release of pain-excitatory neurotransmitters such as glutamate, substance P, etc. The final result is to modulate the painful signal along the nerve pathways.
2. Reduced calcium input decreases abnormal activation of neuronal circuits, with the effect of limiting central sensitization, a common phenomenon in chronic neuropathic pain.
3. Reduced calcium input also helps reduce “long-term pain potentiation” (LTP), a process that amplifies pain signals in the spinal cord.
4. Even in damaged peripheral nerves, pregabalin has a modulatory effect by reducing neuronal excitability and abnormal impulse transmission and ultimately improving the symptoms of neuropathic pain.
5. Although gabapentin does not interact directly 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.
THE DULOXETINA
Duloxetine, commonly used as an anxiolytic and antidepressant, acts by inhibiting the reuptake of serotonin and norepinephrine, essentially 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 (PCD) through three mechanisms:
1. Modulates neuropathic pain: Acts on central pain pathways, reducing nerve sensitivity and improving pain tolerance.
2. Reduces hyperalgesia: Improves pain perception linked to central sensitization.
3. Psychological Benefit: Duloxetine can relieve anxiety and depression often associated with chronic pain.
SECOND LINE
THE LIDOCAINA
LIDOCAINE has three pharmacological effects on fibromyalgia pain:
1) Blocking of sodium channels, especially those involved in neuropathic pain (tetrodoxin-resistant sodium channels) through the stabilization of neuronal membranes. This block prevents the transmission of pain signals from the nerve endings to the central nervous system.
2) Modulation of central sensitization, reducing the activity of hyperactive neurons.
3) Anti-inflammatory and Neuromodulatory effect by indirectly reducing inflammation and modulating the receptors that contribute to the perception of pain (Neural Therapy)
THIRD LINE: OPIOIDS
In the third line of fibromyalgia therapy we consider opioids which we can divide into light opioids (Tramadol) and heavy opioids (Morphine and Oxycodone). They are obviously very effective drugs (however, let’s see the specifics below), but equally obviously their use is reserved for patients with moderate-severe pain who do not respond to other non-opioid treatments. given the well-known adverse reactions and fears of abuse and addiction.
LIGHT OPIOIDS: TRAMADOL
Compared to strong opioids, tramadol has a relatively lower, although not zero, risk of addiction and abuse.
Tramadol has three pharmacological effects on fibromyalgia pain:
1) Stimulating effect on opioid receptors although with a lower affinity to major opioids and this contributes to an analgesic effect although less powerful than morphine.
2) Inhibition of the reuptake of Serotonin and Norepinephrine with strengthening of control over the descending pain pathways, a mechanism particularly altered in fibromyalgia. It also has an effect on serotonin modulation similar to Amitriptyline.
3) Modulation of Central Sensitization which in fibromyalgia occurs particularly altered (hyperactivity of the pain pathways in the spinal cord and brain).
Tramadol helps modulate this sensitization by reducing the amplification of
painful signals.
STRONG OPIODS: MORPHINE AND OXYCODONE
Morphine is not an ideal choice for treating fibromyalgia, given its limited efficacy on central sensitization and the risk of side effects and dependence. In fact, it is not recommended in the management of fibromyalgia.
Although the drug is very effective in the treatment of acute and severe pain of oncological or post-surgical origin, its use in fibromyalgia presents numerous limitations and risks.
• Fibromyalgia is characterized by central sensitization, which does not respond well to opioids.
• Patients with fibromyalgia often require long-term treatments, making the use of opioids risky, which among other things can worsen symptoms associated with the disease such as increased fatigue, sedation and confusion.
• There is also the possibility of opioid-induced hyperalgesia with increased pain sensitivity to consider.
• And finally, clinical studies have not demonstrated a significant benefit of opioids, including morphine, in the management of fibromyalgia compared to other safer and more specific treatments (for example, antidepressants or anticonvulsants).
Impact on Quality of Life
Fibromyalgia, with its silent and persistent pain, almost seems like a rebellion against the body itself, transforming every daily gesture into a battle against the invisible. It is a condition that creeps into the soul, not just the muscle fibers, depriving those who suffer from it of the freedom to feel fully alive.
To deal with fibromyalgia, a treatment is needed that is not just technical or medical, but authentically human. It is a dialogue that involves not only the body, but also the spirit, dignity and the need to be recognized in one’s pain. And support is not just a clinical gesture, but a symbolic hug, an act of closeness that breaks the isolation of the disease.
A personalized treatment, then, is like a dress tailor-made for the soul and body of those who fight against this condition: it does not promise miracles, but traces paths that, step by step, lead back to life. It is resisting the temptation to give up, it is believing that, even in pain, you can still build a full, worthy, meaningful life.
And therefore the treatment of this disease must not only be medicine, but also a gesture of love towards those who, in their silent battle, only ask to be listened to and understood.
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