NEUROPATHIC PAIN
Neuropathic pain is attributed to the central and peripheral nervous system. It is characterized by the fact that the origin of its development is different from the area in which the neuropathic pain is perceived. This is why one speaks of “transferred” pain ( H.-J. Willenbrink 1999).
Neuropathic pain is usually chronic (= lasting longer than six months) pain.
If the pain occurs wherever it is felt, it is called nociceptor pain. This refers to the recording of a physical disorder or damage with the help of a receptor and forwarding it as a pain stimulus via the nervous system to the brain. A receptor is a type of “receiving device” of a cell or an organ or a system. Depending on the type of stimulus to be registered, it is referred to as, for example, chemo-, thermo-, baro- (= relating to blood pressure), acoustic, or tactile (= relating to the sense of touch) pain receptor.
Neuropathic pain ( nerve pain ) differs from nociceptor pain in that the pain-conducting system itself is disturbed or damaged, so to speak, there is “intrinsic nerve pain”. Neuropathic pain therefore has no warning function regarding a local cause of pain.
Causes of neuropathic pain
Neuropathic pain can have various causes:
- Mechanically damaging effects (trauma) on the nerve
- Metabolic (= metabolism-related) disorders or damage to efferent (= those that conduct from the center to the surface ) nerves
- Nerve damage or disorder resulting from a viral infection
- Nerve severance, for example in the context of amputations
- Central ( = affecting the spinal cord/brain ) disorders or damage
Typical diseases are described below and treatment options are shown according to the causes listed.
1: Mechanical damage :
After a nerve injury, causalgia, now also known as CRPS type II ( complex regional pain syndrome type II ), can occur. The clinical picture is characterized by an excruciating, glowing burning pain in the affected
limb, which can be triggered or intensified by even the slightest touch (possibly also from distant parts of the body (synesthesia)), by optical or acoustic stimuli, dryness (xerostomia), warmth, emotions, or the mere idea of pain ( Sympsychalgia ). There is neuropathic pain. There are usually also disorders of blood circulation and skin tropism (= nutritional/growth status of the skin). The spread of pain is independent of the innervation area (= supply area of a nerve ), and may also occur on the mutual limbs ( alloparalgia ). In the chronic stage, repeated blocks ( anesthesia) of the affected nerve with long-acting local anesthetics (= local anesthetics ) are helpful; continuous blocks with a catheter (= implanted thin plastic tube) are optimal. The latter measure should only be carried out on an inpatient basis ( pain clinic ).
2: Neuropathic pain is also present in polyneuropathy. This is caused by metabolic (= metabolism-related) disorders or damage.
In practice, alcoholic and diabetic genesis dominate, accounting for a third of cases each ( Neundörfer 1988 ). In unclear cases, exotoxic (= poisons supplied from outside) causes caused by medications (Vinca alkaloids, nitrofurantoin, etc.) and commercial poisons should be considered, as well as endotoxic (= poisons that arise in the body itself) (porphyria, uremia) and Possibly infectious causes ( Lyme disease, Ehrlichiosis after a tick bite or tick bite ) are in question. The patients complain of constant burning pain in the area supplied by peripheral ( = more superficial) nerves, paresthesia (= abnormal sensations), hyperesthesia (= increased sensitivity to touch stimuli) and hyperpathia (= hypersensitivity to all local stimuli with an increased stimulus threshold), and tenderness of nerves and
muscles as well as possibly via motor (= muscle function-related) irritation phenomena ( cram pi ) ( Gerstenbrand et Rumpl 1988). Sock or glove-shaped sensitivity disorders ( = sensitivity disorders) are characteristic.
Neuropathic pain caused by polyneuropathy is primarily treated causally, i.e. according to the cause: in the case of diabetes mellitus, optimization of sugar control, in the case of toxic (= caused by poisons) polyneuropathy, avoidance of “nerve poisons” such as alcohol.
Symptomatic therapy (= focused on the signs of the disease): Thioctic acid (alpha-lipoic acid) leads to a reactivation of the multienzyme complex and possibly to the binding of diabetic ketones. Neurotropic vitamins (= “nerve vitamins”): The more or less high-dose administration of neurotropic vitamins is common practice in polyneuropathies. Unfortunately, this therapeutic measure rarely leads to improvement. Analgesics (= painkillers ): Poly-neuropathic pain is usually difficult to influence favorably with painkillers. An effect from centrally acting analgesics (= painkillers that act in the spinal cord/brain) is most likely to be expected. For this reason, it is not possible to recommend a safe, effective medication. Neuropathic pain responds best to so-called anti-epileptic drugs (= remedies for epilepsy, but also helpful for this pain ). Today, the first choice is gabapentin or pregabalin, and the second choice is carbamazepine. A combination of metamizole and quinine is said to provide relatively reliable pain relief. A mixture of uridine and disodium salts (Keltican) can be tried.
Repeated nerve blocks: Repeated blocking (anesthesia) of the corresponding nerve pathways with a long-acting local anesthetic (e.g. bupivacaine) has proven very effective for nerve pain. In addition to the (desired) inhibition of pain conduction, there is also a blockage of vegetative (sympathetic) fiber parts, which results in a very significant increase in blood flow in the corresponding tissue area, which sustainably counteracts any inflammatory /degenerative process. In this sense, this treatment, for example in polyneuropathy, is not only symptomatic but almost curative (= aimed at the cause).
3: Chronic neuropathic pain is also present in the so-called postherpetic neuralgia ( zoster neuralgia ), triggered by nerve damage or disorder as a result of a viral infection. This was preceded by herpes zoster disease, a neurodermal (= nerve and skin) infectious disease. The pathogen is the herpes varicella virus. The name Zoster comes from Greek and means “belt” corresponding to the belt-shaped spread of skin on the trunk of the body. For this reason, the disease is also known as shingles. Herpes zoster predominantly affects the nerve segments of the lower thoracic spine, and more rarely the facial or head area ( herpes zoster ophthalmicus, zoster oticus ). Herpes zoster disease begins with burning, itching nerve pain in the area of the affected nerve segments and is accompanied by sensory disorders. Just touching the skin in the affected area causes severe nerve pain (so-called allodynia ). A few days later, skin symptoms such as red spots, pustules, and papules appear. These so-called rashes usually heal after 2 – 4 weeks and the pain usually disappears again. If the neuropathic pain outlasts the skin symptoms of herpes zoster, usually after 4-6 weeks, then the disease has progressed to herpes zoster neuralgia (( postherpetic neuralgia (PZN)). The character of the pain in postherpetic neuralgia is described inconsistently by patients: persistent deep pressing or burning, shooting like lightning, stabbing, and burning. In some cases, there is also allodynia ( = pain triggered by non-painful stimuli, e.g. clothing).
Treatment is difficult and should therefore be left to an experienced pain therapist. Permanent pain, also in the form of nerve pain, practically always requires a combination of different therapeutic methods:
- Information about the disease
- Drug treatment (including analgesics(= painkillers ), pain-relieving psychotropic drugs, also as infusions, individually tested)
- Therapeutic local anesthesia ( = treatment with a local anesthetic) in the form of infiltrations and nerve blocks, possibly blocks near the spinal cord, also continuously with a catheter
- Physiotherapy (physical therapy and other applications) for loss of function
- Acupuncture (pain acupuncture )
- TENS therapy (pain-relieving electrical currents delivered from a small portable device)
- Psychological therapy procedures(especially relaxation procedures and pain management training )
- Possibly physiotherapy (physical therapy and applications) in the event of loss of function
4: Neuropathic pain can also arise from a nerve severance, for example in the context of amputations (due to surgery or an accident); it is then referred to as phantom pain (= sensation of pain in a part of the body that is no longer there). Phantom pain usually occurs immediately after amputation. However, we repeatedly see cases in which phantom pain only appears after years, and in exceptional cases even after decades. The information on pain periodicity and pain quality does not reveal a consistent pattern. When asked about the quality of pain, terms such as “burning”, “cutting” and “like being pinched” dominate. An attack-like course of pain is predominantly reported, with the pain attacks lasting minutes to days. In almost all patients with phantom pain, there is climatic pain modulation
(= change in the pain condition) .
In the case of amputations in the leg area, symptoms requiring treatment later also arise in the contralateral ( =opposite ) joints and the spinal column, due to unphysiological (= unnatural) long-term stress. Seizure-like, shooting neuropathic pain should be treated with anticonvulsants (e.g. carbamazepine, gabapentin, pregabalin) (= medication for the seizure disorder, but also effective for this pain). Now and then a treatment attempt with baclofen (= muscle relaxant) is successful. Pain-relieving antidepressants (= remedies for depression, but also helpful for neuropathic pain ) have proven to be very supportive (rarely sufficient as the only therapy). We prefer maprotiline and doxepin.
Therapeutic local anesthesia ( = treatment with a local anesthetic ) in the form of frequently repeated nerve and conduction anesthesia is often very helpful.
5: Furthermore, neuropathic pain can arise from central (= the spinal cord/brain) disorders or damage, for example as a result of paraplegia. Little is known about the mechanism of pain development after spinal cord injury. According to Thoden (1987), 50% of all patients with injury-related cross-sectional lesions
complain of disturbing sensations below the injury site. At least 27% suffer from nerve pain, primarily in the leg area. In some cases, cramp-like, visceral (= affecting the viscera ) nerve pain in the abdominal area also occurs. Pain can also emanate from the injured segment itself, which is often due to instability. This instability can be corrected surgically. The pain condition after a complete spinal cord injury is also known as deafferentation pain.
To treat neuropathic pain caused by paraplegia (= paralysis of the legs ), continuous epidural ( = near the spinal cord) blockade with a catheter (= thin plastic tube) can be helpful. However, the catheter must be implanted above the damaged segment. In the case of tetraplegia ( = paralysis of the legs and arms ), continuous epidural blockade above the damaged segment requires a strict indication (= weighing up the benefits and risks) because of the increased risk. Medications that can be tried include carbamazepine or gabapentin or pregabalin (= drug against epilepsy, but also effective for neuropathic pain), baclofen, and pain-relieving antidepressants as well as neuroleptics (= drug that affects the psyche). Baclofen works best against unpleasant spasticity. If the side effects become too severe when administered orally (= tablets), administration near the spinal cord using an implanted pump (or port) can be considered. The second choice is Sirdalud.
Treatment
Neuropathic pain is also the so-called thalamic pain. This is a so-called central pain syndrome (= affecting the brain), triggered by disorders or damage in pain-controlling areas of the central nervous system ( thalamus ). The main cause is a stroke ( apoplexy ). Affected patients usually complain of severe nerve pain in the focal side of the body ( hemialgesia ). The constant burning pain can intensify like an attack. In some cases, there is allodynia ( = pain triggered by stimuli that are not in themselves painful). Hyperpathy (= delayed stimulus-response, the pain persists beyond the stimulus period with an overall increased stimulus threshold) almost always occurs. The neurological examination reveals hemiparesis (= hemiparesis ) with usually a good tendency to regression. Motor disorders (= affecting muscle strength) (chorea (= so-called Vitus dance), athetosis (= posture, tone and movement disorders) ) occur, as does the so-called thalamus hand according to Poeck (the fingers are bent at the base joint and in The interphalangeal joints (= middle joints) are overstretched, they show restlessness in movement; the misalignment corrects itself when the hand is placed on a firm surface) and ataxia that is usually mild (= functional disorder of the movement sequences). Detection of the underlying disorder or damage is possible using computer tomography, angiography (= vascular visualization with X-rays), and magnetic resonance imaging.
Treating this pain is a major challenge even for the experienced pain therapist.
So-called antiepileptic drugs (actually remedies for epilepsy, but also helpful for polyneuropathy) can be tried. Today, the first choice is gabapentin or pregabalin, and the second choice is carbamazepine. Phenytoin is also said to relieve pain ( Cantor 1972). In some cases we also saw a beneficial effect of baclofen (= a muscle relaxant that works in the spinal cord/brain). Otherwise, the only option is often to prescribe opiates.
In some cases, considerable success can be achieved with therapeutic local anesthesia ( = treatment with a local anesthetic ). After testing using diagnostic blocks (anesthesia), repeated brachial plexus, femoral nerve, and/or sciatic nerve blocks are carried out in the extremity area ( = arms and legs ); they are often only continuous in the long term with a catheter (= implanted thin plastic tube) successfully. If the face is involved, repeated blockages of the affected trigeminal branches are possible. Given “ central pain ” (= pain that arises in the spinal cord/brain), carrying out nerve blocks admittedly seems paradoxical ( = contradictory). However, we have found that in around 40-50% of affected patients, this therapy works and leads to pain relief. It is possible that the central lesion (= disorder/damage) partially causes a peripheral (= more superficial, not present in the brain or spinal cord) pain syndrome, perhaps by neurobiological mechanisms of perception (= sensation, perception) through the efferent sympathetic system (= excitations directed away in the involuntary nervous system) can be activated to a greater or lesser extent. The reports by Loh et al. also support the involvement of the sympathetic system. (1980) and Nathan (1980), according to which pain in the arm and/or leg following a disorder/damage to the central nervous system (= spinal cord and brain) can be eliminated or alleviated by sympathetic blockades. Since the nerve trunks (especially the brachial plexus (= nerve plexus of the arm) ) also carry vegetative, sympathetic fibers, such an effect can be postulated.
