Porth's Essentials of Pathophysiology, 4e

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Nervous System

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The pain may be persistent or intermittent. The diag- nosis depends on the mode of onset, the distribution of abnormal sensations, the quality of the pain, and other relevant medical conditions (e.g., diabetes, hypothyroid- ism, alcohol use, rash, or trauma). Injury to peripheral nerves sometimes results in pain that persists beyond the time required for the tissues to heal. Peripheral patho- logic processes (e.g., neural degeneration, neuroma formation, and generation of abnormal spontaneous neural discharges from the injured sensory neuron) and neural plasticity (i.e., changes in CNS function) are the primary working hypotheses to explain persistent neu- ropathic pain. Treatment methods include measures aimed at restor- ing or preventing further nerve damage (e.g., surgi- cal resection of a tumor causing nerve compression, improving glycemic control for diabetic patients with painful neuropathies) and interventions for the pal- liation of pain. Although many adjuvant analgesics are used for neuropathic pain, pain control often is difficult. The initial approach in seeking adequate pain control is to try these drugs in sequence and then in combination. The adjuvant analgesics can be divided into three gen- eral classes according to the pain they are used to treat: burning, tingling, or aching pain; stabbing or shoot- ing pain; and neurogenic pain. For pain that is burn- ing, tingling, or aching, tricyclic antidepressants and the α 2 -adrenergic agonist clonidine frequently are used. For the stabbing or shooting pain of neuralgias, antiseizure medications or baclofen, a drug used in the treatment of spasticity, may be used. 32 Nonpharmacologic therapies such as electrical stimulation of the peripheral or spinal nerves can be used for radiculopathies and neuralgias. As a last resort, neurolysis or neurosurgical blockade sometimes is used. Neuralgia Neuralgia is characterized by severe, brief, often repeti- tive attacks of lightninglike or throbbing pain. It occurs along the distribution of a spinal or cranial nerve and usually is precipitated by stimulation of the cutaneous region supplied by that nerve. Trigeminal Neuralgia. Trigeminal neuralgia, or tic douloureux, is one of the most common and severe neu- ralgias. It is manifested by facial tics or spasms and char- acterized by paroxysmal attacks of stabbing pain that usually are limited to the unilateral sensory distribution of one or more branches of the trigeminal cranial nerve (CN V), most often the maxillary or mandibular divi- sions. 32,33 Although intermittent, the pain often is excru- ciating and may be triggered by light touch, movement, drafts, and eating. Considerable controversy remains regarding the pathophysiology of trigeminal neuralgia, but it is thought to be related to neurovascular com- pression. It also occurs secondary to major neurological diseases such as multiple sclerosis or tumor formation. 33 Treatment of trigeminal neuralgia includes pharma- cologic and surgical modalities. Other interventions

include avoidance of precipitating factors (e.g., stimula- tion of trigger spots) and eye injury due to irritation; provision for adequate nutrition; and avoidance of social isolation. Carbamazepine, an antiseizure drug, is recognized as a first-line agent for treatment of tri- geminal neuralgia. There is also some research showing the addition of lamotrigine, an anti-convulsant medica- tion, to the treatment plan may be helpful. 33 Surgical release of vessels, dural structures, or scar tissue sur- rounding the semilunar ganglion or root in the middle cranial fossa often eliminates the symptoms. If not, per- cutaneous blocking or partial destruction of peripheral branches of the trigeminal nerve with heat, glycerol, or balloon compression may be used. Gamma knife radio- surgery, one of the newest techniques, involves imaging of the trigeminal nerve root entry zone, and radiation of the trigeminal nerve. There has also been recent interest in the use of botulinum toxin as a treatment modality. 33 Postherpetic Neuralgia. Herpes zoster (also called shingles ) is caused by the same herpes virus (varicella- zoster virus) that causes chickenpox and is thought to represent a localized recurrent infection by the varicella- zoster virus that has remained latent in the dorsal root ganglia since the initial attack of chickenpox 34 (see Chapter 46). Reactivation of viral replication is associ- ated with a decline in cellular immunity, such as occurs with aging. Thus, the probability of developing herpes zoster increases strikingly with aging, and most cases occur in the elderly. Impaired cellular immunity also increases the risk. During the acute stage of herpes zoster, the reacti- vated virus travels from the affected sensory ganglia and peripheral nerve to the skin of the corresponding derma- tomes, causing a unilateral localized vesicular eruption and hyperpathia (i.e., abnormally exaggerated subjec- tive response to pain). Persons with postherpetic neuralgia may suffer from constant pain (“burning, aching, throbbing”), intermit- tent pain (“stabbing, shooting”), and stimulus-evoked pain (allodynia). Persons with allodynia often suf- fer from excruciating pain after the slightest touch to affected skin by such things as cold wind or clothing. These subtypes of pain may interfere with sleep and basic activities of living, causing chronic fatigue, depres- sion, anorexia, weight loss, and social isolation. Early treatment of shingles with antiviral drugs such as acyclovir or valacyclovir that inhibit herpes virus deoxyribonucleic acid (DNA) replication may reduce the severity of herpes zoster. Initially, postherpetic neuralgia can be treated with a topical anesthetic agent, lidocaine– prilocaine cream or 5% lidocaine gel. A tricyclic antide- pressant medication, such as amitriptyline or desipramine, may be used for pain relief. Regional nerve blockade (i.e., stellate ganglion, epidural, local infiltration, or peripheral nerve block) has been used with limited success. A live attenuated vaccine is now available for preven- tion of herpes zoster in adults 60 years of age and older. The vaccine is not indicated for treatment of herpes zoster or postherpetic neuralgia. 35