1. What is neuropathic pain?
The International Academy of Pain Studies (IASP) defined neuropathic pain in 1994 as “pain that begins with or originates from injury or malfunction of the peripheral or central nervous system”. In 2001, the definition was simplified to “pain caused by injury or disease to the central nervous system or somatosensory system”. Injury is defined as a microscopically or macroscopically identifiable injury directly related to the nervous system, as opposed to skin, muscle, soft tissue, and visceral injuries. Diseases are specific violations of the nervous system, such as autoimmune diseases, inflammatory conditions, pathological states of the second messenger system or ion channels. Damage limited to the somatosensory system can be distinguished from other types of damage to the nervous system, such as spasticity, rigidity, and myalgia caused by damage to the motor system.
Migraine and cluster headache both belong to neurovascular origin of headache.
Clinical manifestations of headache.
Cluster headache: located unilaterally in the orbit, felt deep in and around the eye, usually intense and nonpulsatile, often radiating to the forehead, temporal region and cheeks, and rarely to the ear, occiput and neck. This headache tends to recur between 1-2 hours after the onset of sleep or several times in 24 hours without aura or vomiting. The attacks occur at the same time each day, and this pattern can last for 6-12 weeks, followed by months or even years without attacks (hence the term cluster). The accompanying symptoms are nasal congestion, runny nose, conjunctival congestion, tearing, narrow pupils and flushing of the cheeks, lasting an average of 45 minutes (from 15-180 minutes)
Migraine The headache begins as a dull pain in the supraorbital, retroorbital or frontotemporal area on one side, grows in intensity with a throbbing nature, and then persists as a severe fixed pain that extends to the entire half of the head and even the upper neck. If left untreated, it usually lasts for 72 hours. The patient is pale, often with nausea and vomiting, and the headache usually lasts all day, often terminated by sleep. The headache is often preceded by prodromal symptoms and is mostly bilateral, usually with onset in adolescence and most often with a family history. Some patients have an aura of attack, and some patients have an odor that triggers the pain attack.
Medical examination
Exclude organic lesions by blood, urine routine, electrolytes and cerebrospinal fluid examination. Cranial CT or MRI examination is important for differential diagnosis.
Hazards: Headache seriously interferes with the normal life and work of human beings. Although the incidence of migraine patients may decrease with age, studies on foreign data show that the attacks of these two types of headaches are related to intracranial autonomic nerve dysfunction, and some studies show that migraine patients are prone to cardiovascular and cerebrovascular diseases, so it is necessary to treat headaches actively.
Treatment by pain department
Many headache patients take painkillers for mild cases and lose their ability to work for severe cases. General treatment is mostly given to oral medication, which is costly, or acupuncture and massage treatment.
Since cluster headache is a neurovascular headache, and modern medicine believes that neurovascular headache is related to the dysfunction of the largest autonomic ganglion in the skull, the pain department provides special treatment: minimally invasive neurointerventional analgesia. So far, we have been able to free many patients from the nightmare of headache by this method, and have received immediate results, with very satisfactory results in the long-term follow-up.
There are numerous causes of neuropathic pain, including physical mechanical injury, metabolic or nutritional neurological alterations, viral infections, neurotoxicity from drugs or radiotherapy, ischemic nerve damage, neurotransmitter dysfunction, and some non-viral diseases. It has been reported that about 1/5 of cancer patients have neuropathic pain, and the more typical ones are pain after radiotherapy or pain due to peripheral neuropathy after chemotherapy, pain after nerve compression, and also pain occurring in combination with herpes zoster, complex regional syndrome, etc. Among patients with cancer pain with sudden onset of pain, about 1/4 of them have neuropathic pain component in their pain.
2. Diagnosis of neuropathic pain
There is no uniform diagnostic standard for neuropathic pain. Collectively, the diagnostic elements are no more than: ① a clear history of nerve injury and pathological changes; ② the nature of pain manifests as burning pain, electric shock-like pain, stabbing pain, radiating pain, etc., and there may be spontaneous pain, pain hypersensitivity or sensory abnormalities; ③ functional deficits manifest as sensory or motor deficits after nerve injury, all pain occurs in the innervation area of the damaged nerve or conduction pathway, and there may also be autonomic symptoms; ④ only partial sensitivity to conventional analgesic treatment, while anticonvulsant and antidepressant medication is more effective.
The history of nerve injury suggests the possibility of neuropathic pain and should be carefully analyzed for etiology. The nature of the pain is also an important diagnostic clue. The presence of spontaneous pain after the primary injury has healed suggests that pain is usually not due to impulses from the injury receptors but rather to abnormal excitation of the nervous system (central sensitization). Pain hypersensitivity and abnormal sensation (pain) are important symptoms that support the diagnosis, with the former referring to mild injurious stimuli leading to severe pain, also known as pain hyperresponsiveness, and the latter referring to otherwise comfortable stimuli such as light touch or warm water stimulation also leading to pain.
The physical sensory nerve examination should ask the patient to delineate the area of pain distribution in order to detect the dermal area of pain or peripheral nerve distribution pattern. It should be noted that testing with a cotton swab or fine needle is more sensitive than testing with a finger during the examination, and changes in nociception or temperature sensation are more sensitive than position and vibration sensation. Neuropathic pain is a paradoxical phenomenon after nerve injury. Under normal circumstances, severing the nerve should result in numbness and loss of sensation, but then there is pain evoked under normal pressure load or on deep palpation and pain hypersensitivity at the denervated site.
Ancillary tests include electromyography and nerve conduction tests, imaging, puncture skin biopsy, quantitative sensory somatic testing (QST), etc. In addition, a variety of neuropathic pain diagnostic questionnaires are available for reference.
3. Treatment of neuropathic pain
Due to the complex etiology, there is uncertainty in the treatment of neuropathic pain. Usually, NNT/NNH is used as the basis for drug selection, with NNT referring to the number of patients who have achieved 50% pain reduction in one case; the number of patients requiring treatment, and NNH referring to the total number of treatments with one serious, treatment-requiring side effect. Efficacy and side effects should also be analyzed for specific patients. First-line therapeutic agents are antidepressants (tricyclics and SSNRIs), anticonvulsants (gabapentin and pregabalin), and peripheral nerve injury can be treated with topical 5%; lidocaine patches or lidocaine and proparacaine patches. Second-line medications include opioids (morphine, oxycodone, levomorphone, methadone) and tramadol. Third-line medications include topical capsaicin, excitatory amino acid receptor antagonists, the antiarrhythmic drug mexiletine, other anticonvulsants, and other antidepressants. Topical medications and opioids, tramadol can be used alone or together with the above two drugs.
All of the above drug treatments are somewhat tentative, and any combination of one or several drugs that do not work well should be switched to other types of drugs, or treated with physical and minimally invasive methods. Multi-target therapy for the pathogenesis may be a promising development direction.