Neuropathic Pain

The Peripheral Neuropathy Solution

Dr. Labrum Peripheral Neuropathy Solution

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In contrast, neuropathic pain is believed to be associated with sustained activity at a site of aberrant somatosensory processing in the peripheral or central nervous system resulting from neural injury or irritation. Typically, neuropathic pain persists long after the precipitating event.

Neuropathic pain is clinically diverse. Patients may describe unfamiliar burning, electric shock-like or shooting dysesthesias, which may be spontaneous or evoked by movement. Examination may reveal allodynia, hypal-gesia or hyperalgesia, hypesthesia or hyperesthesia, or hyperpathia. There may be other focal neurological deficits, including weakness or autonomic changes, such as swelling or vasomotor instability. Trophic changes in the form of alterations of skin, subcutaneous tissues, hair, and nails may also occur. However, neuropathic pain is not always dysesthetic. The neurological deficit may be very subtle, thus the diagnosis is not always straightforward.

Neuropathic pain may result from a variety of central and peripheral mechanisms that can interact in complex ways. The observation that some patients with neuropathic pain have disorders that appear to be primarily sustained by processes within the central nervous system (e.g., pain precipitated by stroke) and others by peripheral processes (e.g., a painful peripheral neuroma) allows an extended classification based on inferred pathophysiol-ogy. Neuropathic pain syndromes are usually refractory to traditional analgesics. "Adjuvant" analgesics are often prescribed, such as anticonvulsants or antidepressants. Chronic narcotic usage has been especially controversial;

however, it is now clear that a significant proportion of neuropathic pain patients with diverse diagnoses do indeed respond to systemic or intrathecal narcotics.

2.2.1 Deafferentation Pain

The response characteristics of central neurons in the pain pathway may change if the peripheral input is partially or completely damaged. This is known as ''central sensitization'' and is essentially the result of abnormal signal amplification, such that nonnoxious stimuli can now trigger pain. The neural pathways that lead to the sensation of pain have not been clearly delineated. The mechanistic substrate is thought to involve both functional and structural changes at the cellular level and is poorly understood. Examples of specific central deafferentation syndromes include central pain, pain associated with plexus avulsion injuries, spinal cord injuries, post-her-petic neuralgia, and phantom pain.

''Central pain'' generically includes a large number of deafferentation pain syndromes that can occur after injury to the central nervous system. These include thalamic pain, post-stroke pain, pain caused by multiple sclerosis, parkinsonism, and syringomyelia. Phantom pain is the neuropathic pain that may occur after the amputation of any body part (limb, breast, tooth).

Certain of these syndromes can be successfully treated by ablative procedures (paradoxically accentuating the deafferentation), notably plexus avulsion, and some spinal cord injury (SCI) pain syndromes by dorsal root entry zone ablation (DREZ procedure).

2.2.2 Sympathetically Maintained Pain

Sympathetically maintained pain (SMP) is a subtype of neuropathic pain that appears to be sustained by release of norepinephrine caused by efferent activity in the sympathetic nervous system. There is controversy concerning the mechanisms involved, which pain syndromes may be included in this category, and even whether such an entity truly exists. Furthermore, there has been considerable confusion between the diagnosis of SMP and complex regional pain syndrome (CRPS). Sympathetically maintained pain may also simultaneously exist with sympathetically independent pain.

Both peripheral and central mechanisms have been implicated in the generation of SMP. Campbell considers SMP to be a complication of a neuropathic pain trigger, rather than an entity in itself [3]. Sympathetically maintained pain may be diagnosed by way of a sympathetic ganglion block or by intravenous administration of the a-adrenergic antagonist, phentol-amine. These tests may also give an indication of whether pharmacological sympatholysis or surgical sympathectomy is likely to palliate the pain syndrome.

Complex regional pain syndrome is a term adopted by the IASP to refer to disorders that have the clinical characteristics of reflex sympathetic dystrophy (RSD), (CRPS type I) or causalgia (CRPS type II). Patients with CRPS are assumed to have neuropathic pain that may or may not have an SMP component. Similarly, a patient with SMP may or may not meet the criteria for CRPS. Thus, although there is a clear association between CRPS and SMP, they are considered to be independent entities.

2.2.3 Peripheral Nerve Pain

Both central and peripheral mechanisms contribute to neuropathic pain, and CNS changes can be demonstrated secondary to peripheral nerve pathology; however, a predominant peripheral generator may be implicated for certain entities. Peripheral nerve disease is associated with loss of function (motor, sensory, or both) and is typically nonpainful. Certain neuropathic diseases however, characteristically are associated with pain. Most painful polyneu-ropathies are axonopathies. These may be associated with diabetes or with nutritional deficiencies of thiamine, niacin, pyridoxine, or others. For the most part these have little neurosurgical relevance. Painful mononeuropa-thies are thought to be always associated with a peripheral nerve injury.

Lancinating neuralgias. Dysesthetic pain associated with lancinating neuralgias is typically short-lived and shock-like. An attack may consist of a single 'shock' or several runs of variable duration. Occasionally this is associated with a more constant background burning pain or dull ache in the same distribution. Pain may be spontaneous or triggered by benign sensory or motor stimuli in the receptive field of the affected nerve. Patients may experience pain-free periods of days, weeks, or months and will usually initially respond well to an anticonvulsant such as carbamazepine or gabapentin.

Most commonly affected are the trigeminal, glossopharyngeal, vagal (superior laryngeal branch), and geniculate nerves. One inferred mechanism involves compression of these nerves by a tortuous vascular loop, such that decompression is curative or significantly palliative.

For intercostal neuralgia and ilioinguinal neuralgia, a nerve injury is usually implicated. The mechanism responsible for occipital neuralgia remains essentially unknown. Invasive therapies often afford significant palliation. Decompression and electrical stimulation are preferred over ablative procedures, such as rhizotomy or ganglionectomy.

Nerve compression. "Entrapment neuropathy'' implies compression of a nerve in a specific location as determined by local anatomy (bony or fibrous tunnel), changes in tissue consistency (metabolic disease), trauma (accidental or occupational), or congenital anatomical variations. The neuropathy is thought to occur as a result of decreased neural blood supply.

A diagnosis of nerve compression or entrapment should be entertained whenever no other pathological lesion is found in a patient with chronic pain. Often the pain will follow a classic distribution associated with a specific nerve, but occasionally pain is referred and may involve an entire limb. Pain tends to be a constant deep "nerve" ache. It may vary according to position or movement. Typically, the severity of the pain is disproportionate to the relatively trivial extent of any neurological impairment; however, care must be taken not to miss a subtle neurological deficit, as this is often a key to the diagnosis. Local tenderness is often accompanied by a Tinel's sign over the point of compression, thought to represent ectopic excitability of the nerve in response to the slowing of axonal transport.

Electrodiagnostic tests are useful adjuncts to the clinical syndrome. Treatment is by surgical decompression.

Peripheral nerve trauma. The normal reaction to any peripheral nerve injury involving axonotmesis (disruption of axonal continuity) or worse, involves some degree of neuroma formation. Neuroma formation cannot be prevented. Neuromas are bulb shaped and consist of scar tissue intermingled with neuronal elements. Fortunately only a minority of neuromas are painful, and this seems to occur when the neuroma is easily or repeatedly traumatized in a subcutaneous position or near a joint. However, when they are painful, they may be exquisitely allodynic. A Tinel's sign over the neuroma is characteristic. There is an accompanying neurological deficit associated with the dysfunctional nerve.

Infiltrating around the neuroma with local anaesthetic in the outpatient clinic gives a good indication as to the utility of surgery for any individual case. The goal at operation is to remove the neuroma and implant the cut nerve deep within muscle or bone, away from scar tissue or a joint. If the neuroma is in-continuity and some crucial motor function remains, the situation is more problematic. External neurolysis is probably the best initial option before considering excision of the neuroma with grafting.

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