Neurology: A Clinician's Approach (Cambridge Medicine (Paperback)), 1st Ed.

15. Distal and generalized sensory symptoms

Overview of sensory symptoms

Pain is the sensory symptom that most frequently brings a patient to neurological attention. The first step in evaluating pain is to determine its character. Neuropathic pain has sharp, burning, or electrical qualities. Nociceptive pain, by comparison, has dull and aching qualities. While cold or freezing sensations may be due to neuropathic processes, these sensations are more often the result of vascular insufficiency. In general, pain may be divided into focal (Chapter 16) and generalized or distal-predominant (this chapter) in distribution. Because patients may report only the most prominent location of symptoms, when taking the history, you must inquire specifically about pain involving the face, scalp, trunk, back, arms, hands, groin, legs, and feet.

Numbness is the second important symptom of sensory dysfunction. When patients use the term numbness, they may mean one of several different sensations: a lack of feeling or deadness, a sensation that the affected body part is covered by something such as a glove, sock, or extra layer of skin, or a sensation that the body part is asleep. Some patients will report that they feel as if their socks are bunched up around their feet, that they are walking on sponges, or that their hands or feet are buried in cement. Be aware that some patients with limb weakness will erroneously describe numbness rather than recognizing that a motor deficit is responsible for their abnormal sensation.

Paresthesia is a sense of tingling, pins and needles, abnormal vibration, or a feeling that a body part is asleep. Some patients with paresthesia may describe it initially as pain or numbness, and an accurate description of the problem may be obtained only by specifically asking about a perception of pins and needles. Paresthesia is highly specific for neurological dysfunction.

There are several abnormal sensations that are actually due to motor dysfunction. The most common of these are cramps, twitching (fasciculations), and restlessness.

Because sensory symptoms are entirely subjective, they can be feigned or exaggerated quite easily. Important clues to factitious sensory symptoms include a large number and variety of symptoms, requests for narcotic medications or completion of disability paperwork at an initial office visit, and a lack of a plausible anatomical distribution of symptoms.

Sensory system anatomy

Pain and temperature sensations from the limbs and trunk are mediated by small-diameter nerve fibers. These fibers travel through the nerves and nerve roots, reaching their cell bodies in the dorsal root ganglia. After entering the spinal cord, pain and temperature fibers ascend one or two segments before decussating in the ventral white commissure. They ascend through the spinal cord in the spinothalamic tract, eventually reaching the ventroposterolateral nucleus of the thalamus. These fibers from the thalamus project to the insula.

Vibratory and proprioceptive sensations are mediated by large-diameter nerve fibers. These fibers also travel through the nerves and nerve roots to reach cell bodies in the dorsal root ganglia and enter the spinal cord. Within the cord, fibers from the lower extremity travel through the gracile fasciculus, while those from the upper extremity travel through the cuneate fasciculus. These fibers reach the gracile and cuneate nuclei in the medulla and decussate in the medial lemniscus. Lemniscal fibers synapse in the ventroposterolateral nucleus of the thalamus and project to the primary sensory cortex of the postcentral gyrus.

Sensory examination

Sensory examination should include tests of pinprick, vibration, position sense, and cortical modalities.

Pinprick and temperature sensation

Pinprick examination of every square inch of the skin is time-consuming and leads to a great deal of extraneous

Figure 15.1

Figure 15.1 Cutaneous sensory distributions of the nerve roots and individual nerves on the ventral surface of the body. Note in particular the T2 (axilla), T4 (areolae), and T10 (umbilicus) dermatomes. See Chapter 16Figure 16.1 for additional details on the innervation of the hand.

and sometimes misleading information. There are several strategies that improve both the diagnostic yield and efficiency of this portion of the sensory examination. First, take a thorough history in order to gain a sense of the likely distribution of sensory deficits. The examination of a patient with a probable length-dependent polyneuropathy requires a different strategy from the examination of a patient with a mononeuropathy or monoradiculopathy. It is often quite helpful to ask the patient to trace the area of cutaneous sensory loss before initiating the sensory examination. When testing pinprick, begin by examining a completely normal area to establish that the patient can perceive the sharp sensation of a pinprick accurately. Next, test an area that is possibly abnormal based on the information gained from the history, and march the pin from the abnormal area back into the normal area. For example, in a patient with a length-dependent polyneuropathy, begin distally at the toes to see whether the patient can detect the pinprick, and then march the pin proximally, determining where the patient first perceives the sensation properly. More subtle deficits require a different technique. In a patient with mild sensory abnormalities, it is helpful to use one body part as a control and compare it with the possibly abnormal part. For example, when testing a patient with a possible right L5 radiculopathy, poke the dorsum of the left foot with the pin and tell them that this sensation is 100%. Next, poke the dorsum of the right foot and ask the patient to assign a percentage to the strength of this sensation. When examining pinprick for the purposes of a screening examination, establish that sensation is preserved by testing two or three pinpricks in each dermatome and nerve distribution (Figure 15.1).

Because pinprick and temperature perception are both mediated by small-diameter nerve fibers, examining temperature usually does not add much new information to the neurological examination. False-positive results with testing of cold sensation are frequent in patients with cold extremities. In addition, it may be difficult to find standardized cold and warm stimuli. Despite these limitations, if pinprick sensation is entirely preserved and there is a high index of suspicion for small-diameter nerve fiber dysfunction, testing perception of warmth and coldness may help to disclose an important deficit. Temperature testing is also useful for patients who do not tolerate or cannot accurately report the results of the pinprick examination.

Vibratory and joint position perception

Examine vibratory sensation with a 128 Hz tuning fork. Absence of vibratory perception at the great toe is clearly abnormal. If the patient cannot appreciate vibration at the great toe, move the tuning fork to the medial or lateral malleolus, to the knee, and then to the sternum until they feel the vibration. The normal duration of tuning fork perception is not clearly defined. Some neurologists use the criterion that both patient and doctor should feel the vibratory perception for the same length of time. Others use cut-offs such as 12 or 14 seconds of vibratory perception at the great toe. My idiosyncratic (and unvalidated) technique involves striking the tuning fork vigorously so that its heads hit each other, then placing the base of the tuning fork on the interphalangeal joint of the great toe. Using this technique, the expected number of seconds of vibratory perception at the great toe may be computed by subtracting the first digit of the patient’s age from 16. For example, a 49-year-old patient should have 12 seconds of vibratory perception at the great toe.

Joint position examination generally offers little more information beyond what is obtained by testing vibratory perception. To test joint position, instruct the patient to close their eyes and tell them that you will move their great toe either upward or downward. Grasp the toe by the sides (not by the top and bottom) and move it by no more than 5 mm. Normal subjects should be able to detect this movement reliably.

Cortical sensory modalities

The most commonly tested cortical sensory modalities are graphesthesia, stereognosis, and two-point discrimination. These higher-order sensory functions are considered functions of the contralateral parietal lobe. Bear in mind that these modalities may only be tested when the patient has otherwise-preserved gross touch and pinprick sensation. Test graphesthesia by instructing the patient to close their eyes and then asking them to interpret a number that you trace on their palm. Trace at least five different numbers (2, 3, 6, 7, and 8 seem to be the most straightforward ones to interpret) on one palm, and compare the results to the other palm. Test stereognosis by asking the patient to distinguish between three different-sized coins placed in each hand. Most patients can do this easily. Finally, test two-point discrimination by placing the tips of a caliper against the patient’s skin. Determine whether they can discriminate between one point and two points separated by 5–10 mm. Abnormal graphesthesia, stereognosis, and two-point discrimination point to dysfunction in the contralateral parietal lobe, but should not be judged too strictly, as false-positive test results are common.


Length-dependent polyneuropathy

Polyneuropathy is a pathological process that, by definition, involves all the nerves in the body. It is exceedingly rare, however, for all the nerves to be clinically involved at disease onset, or indeed at any point during the course of the disorder. Polyneuropathy is most often a length-dependent process and symptoms develop in a slowly progressive, somewhat stereotyped fashion. The classic initial complaints of polyneuropathy are numbness, tingling, and pain, which begin in the toes and spread more proximally over months to years. When symptoms reach the knees, nerves of equivalent length in the fingertips and hands become involved. By the time the elbows are involved, symptoms are present in the midline of the trunk. In patients with severe neuropathy, only small patches of sensation over the vertex of the head and along the spine are preserved. Symptoms usually do not progress to this extent, and many patients have symptoms confined to the feet and distal legs for many years.

Most patients with polyneuropathy have mostly or exclusively sensory symptoms at onset. Motor symptoms may be minor and go unnoticed by patients. Imbalance, however, is often a problem at presentation (Chapter 18). To elicit a history of balance problems, ask the patient whether they feel as if they are going to fall when they close their eyes in the shower or whether it is difficult for them to keep their balance if they get up at night to use the bathroom.

Several abnormal physical examination findings may help to confirm the localization of length- dependent polyneuropathy. Careful visual inspection may disclose wasting of the intrinsic muscles of the feet, clawing of the toes with high arches and wasting of the distal legs suggestive of Charcot–Marie–Tooth disease. Bear in mind, however, that any distal-predominant polyneuropathy may cause muscle wasting. The most obvious muscle in which wasting may be detected is the extensor digitorum brevis, a small spherical muscle that is palpable over the proximal dorsolateral foot. Another sign of polyneuropathy that may be detected with simple visual inspection is reduced hair growth over the distal legs. Patients with early polyneuropathy usually have little weakness, but when it is present, it is subtle and involves toe extension and flexion. Deep-tendon reflexes may be lost or reduced. On sensory examination, patients with polyneuropathy have a combination of pinprick and vibratory loss. The term “stocking and glove” sensory loss is often used to refer to involvement of the distal before the proximal extremities. The last examination technique that is often helpful in assessing for large-fiber involvement in polyneuropathy is testing for a Romberg sign, described further in Chapter 18.

Non-length-dependent polyneuropathy

Although length-dependent sensorimotor polyneuropathy accounts for the majority of polyneuropathies in clinical practice, you will miss many diagnoses if you consider only this variety. Polyneuropathies with predominantly motor manifestations include chronic inflammatory demyelinating polyneuropathy (Chapter 10) and multifocal motor neuropathy with conduction block (Chapter 11). Rapidly progressive polyneuropathies are discussed in Chapter 12. Some uncommon causes of polyneuropathy such as Tangier disease, lead toxicity, and porphyria may produce predominantly proximal rather than distal symptoms. Neuropathies associated with prominent ataxia include vitamin E deficiency, Sjögren’s syndrome, and certain variants of Charcot–Marie–Tooth disease.

Evaluation of polyneuropathy

Laboratory screening

Polyneuropathy is caused by a wide variety of medical disorders. In the absence of a relevant past medical history or clear clinical clues to the presence of one of these underlying disorders, a screening battery should consist of a restricted number of high-yield tests (Table 15.1).

Electromyography and nerve conduction studies

The purposes of electromyography (EMG) and nerve conduction studies (NCS) are to confirm the presence of a polyneuropathy, to determine its severity, and to

Table 15.1 Screening panel for common causes of polyneuropathy

Table 15.1

distinguish between axonal and demyelinating pathologies. Although localization of sensory complaints to the peripheral nerves is often quite straightforward, diagnostic mimics including lumbosacral polyradiculopathy, cervical myelopathy, and psychogenic disorders make EMG and NCS helpful in confusing cases. While neuropathy severity is often obvious from clinical history and examination, electrodiagnostic studies may offer insight into disease severity, which becomes important when determining appropriate treatment. Distinguishing between axonal and demyelinating pathologies is perhaps the most important role of EMG and NCS. Axonal polyneuropathies are characterized by decreased response amplitudes with normal or mildly reduced conduction velocities, whereas demyelinating polyneuropathies are characterized by relatively preserved response amplitudes and severe slowing of conduction velocities. The distinction between these two types of nerve pathology is important, as demyelinating polyneuropathies often respond to immunomodulatory therapy, while axonal polyneuropathies do not. Use of EMG and NCS should be judicious, as their sensitivities and specificities are both limited. Because NCS assess only large-diameter nerve fibers, they are frequently normal when pain is the only symptom, as pain is mediated by small-diameter nerve fibers. Although many electrodiagnostic studies offer little in the way of additional diagnostic information for polyneuropathy, the following factors always prompt me to order EMG and NCS:

• asymmetric symptom onset

• proximal symptom onset

• rapid symptom progression

• patient age < 50

• foot deformities suggestive of inherited neuropathy

• prominent motor signs

• suspected demyelinating polyneuropathy

Nerve biopsy

Sural nerve biopsy may offer additional diagnostic information for several different and uncommon etiologies of polyneuropathy including vasculitis, amyloidosis, tuberculosis, and sarcoidosis. In most cases, nerve biopsy shows nonspecific axon loss, a finding that offers little diagnostic information beyond what is provided by the clinical examination and electrodiagnostic studies. Skin-nerve biopsy may help to confirm the diagnosis of a small-fiber neuropathy, but rarely offers specific information that helps in patient management.

Etiologies of polyneuropathy

A detailed discussion of the vast number of causes of polyneuropathy can fill a multivolume textbook.1 The following is a summary of some of the most common and important causes of polyneuropathy.

Diabetes mellitus

Diabetes mellitus is the most common cause of polyneuropathy in the USA. It may take many forms, including a length-dependent sensorimotor polyneuropathy, a painful small-fiber polyneuropathy, diabetic thoracic radiculopathy (Chapter 17), diabetic amyotrophy (Chapter 16), mononeuropathy multiplex (Chapter 11), or a syndrome that resembles chronic inflammatory demyelinating polyneuropathy (Chapter 10). Although elevated blood hemoglobin A1cpercentages are often used to diagnose diabetic neuropathy, oral glucose-tolerance testing is more sensitive.2 Because diabetes is so common, it is important not to wear blinders by assuming that diabetes is the only source of neuropathy in a diabetic patient: always conduct a thorough evaluation to exclude other reversible causes. Treating diabetic polyneuropathy is somewhat unsatisfying. Tight glycemic control may arrest its progression, but reverses symptoms only rarely. Strict euglycemia may lead to the unfortunate consequence of “insulin neuritis” in which symptoms worsen as blood sugar comes under better control. In most cases, agents for neuropathic pain are the mainstay of therapy. Treatment with α-lipoic acid (600 mg qd–tid) may help in some cases.3 One additional critical aspect of diabetic neuropathy care is prevention of foot ulcers with properly fitting shoes, careful daily foot examinations, and periodic podiatric assessments.

Vitamin B12 deficiency

Vitamin B12 deficiency may affect the brain, optic nerves, spinal cord, and peripheral nerves. In a small percentage of patients, the peripheral nerves are affected in isolation. Because the spinal cord is involved in up to 90% of cases, B12 deficiency is discussed further in Chapter 17.4

Monoclonal gammopathy

Monoclonal proteins are circulating immunoglobulins formed from a single clone of plasma cells. They are especially common in the older population, and their association with multiple myeloma is well known. Monoclonal proteins may produce neuropathy by cross-reacting with peripheral nerve antigens, but in other cases the precise mechanism of neuropathy secondary to monoclonal gammopathy is not entirely clear.5 Neuropathies associated with monoclonal gammopathies include:

• length-dependent axonal polyneuropathy in patients with monoclonal gammopathy of undetermined significance (MGUS)

• axonal neuropathy associated with multiple myeloma

• POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, skin changes), a severe demyelinating polyneuropathy associated with multiple myeloma

• anti-MAG (myelin-associated glycoprotein) neuropathy, a demyelinating polyneuropathy characterized electrophysiologically by markedly prolonged distal motor latencies

• amyloidosis, a multisystem disorder that usually produces an exquisitely painful neuropathy with prominent autonomic dysfunction

In order to ensure the highest yield for detecting monoclonal gammopathy in patients with neuropathy, request not only serum protein electrophoresis, but also immunofixation and 24-hour urine collection for protein electrophoresis.6 Patients with MGUS should undergo evaluation for multiple myeloma including skeletal survey, calcium level measurement, and hematologic referral. Neuropathy secondary to MGUS, multiple myeloma, and amyloidosis may respond to immunosuppressive and chemotherapeutic regimens, which should be designed in conjunction with a hematologist.


Vasculitic neuropathies are discussed further in Chapter 11. Although mononeuropathy multiplex is the most widely known type of vasculitic neuropathy, many patients with vasculitis have length-dependent polyneuropathies or simultaneous overlapping patterns with features of both length-dependent polyneuropathy and mononeuropathy multiplex.


Polyneuropathy secondary to chronic heavy ethanol use (i.e. four to six drinks a day for many years) is most likely secondary to a combination of direct toxic effects from the ethanol and nutritional deficiencies. Discontinuing ethanol consumption and ensuring adequate nutrition may result in modest symptom improvement.

Charcot–Marie–Tooth disease

Charcot–Marie–Tooth (CMT) disease is the most common inherited polyneuropathy. Wasting, weakness, and areflexia in the lower extremities usually begin in childhood or adolescence. As the disease progresses, patients develop joint deformities. The most common variety is CMT1A, an autosomal-dominant inherited demyelinating polyneuropathy caused by duplication of the PMP-22 gene. There is a wide variety of other phenotypes of CMT disease, each associated with a distinct mutation.7 CMT2 is perhaps the most important among the other types of CMT disease in adults, as it causes a length-dependent axonal polyneuropathy, which may mimic more common causes of polyneuropathy. CMT2 is usually distinguished from other axonal polyneuropathies by the presence of severe or predominantly motor symptoms or a family history of neuropathy.8 The mainstay of treatment for CMT disease is referral to orthopedists and podiatrists for correction of foot deformities. Unfortunately, there is no specific cure for the neuropathy.


Approximately 50% of patients with HIV, usually those with advanced disease, develop a length-dependent polyneuropathy, often with prominent pain.9 HIV may also cause a variety of other peripheral nerve problems including chronic inflammatory demyelinating polyradiculoneuropathy and mononeuropathy multiplex. Highly active anti-retroviral therapy and pain control are the mainstays of treatment.

Table 15.2 Medications that may produce polyneuropathy

Table 15.2

Thyroid dysfunction

Thyroid dysfunction is an important cause of neuropathy because it is reversible. Neuropathy usually takes a length-dependent form, and occurs more commonly in patients with hypothyroidism than in those with hyperthyroidism.10Because thyroid dysfunction is identified so readily by primary care physicians, new diagnoses of neuropathy related to thyroid disease are actually uncommon in neurological practice.

Medication-induced neuropathies

A variety of medications may lead to polyneuropathy (Table 15.2).


After extensive screening, many patients with polyneuropathy still lack an identifiable cause. Patients with idiopathic polyneuropathy tend to have mild, slowly progressive disease and do not tend to become disabled. While there is no specific treatment to reverse idiopathic polyneuropathy, patients do respond to agents for neuropathic pain.

Treatment of neuropathic symptoms

Sensory symptoms fall into two classes: positive symptoms in which there is an emergence of abnormal sensation, such as pain or paresthesias, and negative symptoms in which sensorimotor function is attenuated or lost, such as numbness or weakness. Broadly speaking, medications are available to mask positive symptoms,

Table 15.3 Medications used to treat neuropathic pain

Table 15.3

a Preferred initial agent

b Should be reserved for patients with refractory symptoms

but unless a reversible cause is identified, there are few treatments for negative neuropathic symptoms. A wide variety of agents is available to treat neuropathic pain and paresthesias (Table 15.3). Because these medications all work by reducing the firing of neural impulses in both the peripheral and central nervous systems, all but the topically applied agents may lead to sedation.

Other causes of distal sensory symptoms

Spine disease

Both lumbosacral polyradiculopathy and cervical myelopathy may produce lower-extremity symptoms that mimic length-dependent polyneuropathy. Compression of the L5 and S1 nerve roots may lead to pain, numbness, and tingling in the feet unaccompanied by back pain. Examination usually shows signs of asymmetry that help to make the distinction, but, in some cases, NCS and needle EMG are required to make the diagnosis. Cervical myelopathy may also produce distal paresthesias and numbness, and should be considered when the hands are more involved than the feet, when pain is absent, or when hyperreflexia and spasticity are present on examination. Both medical and surgical causes of cervical myelopathy may produce a pseudopolyneuropathic presentation. Further evaluation of patients with cervical myelopathy is discussed in Chapter 17.

Plantar fasciitis

Inflammation of the plantar fascia is a source of foot pain that may mimic polyneuropathy when it is bilateral. Wear and tear damage to the plantar fascia is common in obese people and in runners, and leads to pain that is most severe with the first steps in the morning. Pain is most often centered at the medial calcaneus, but may involve the entirety of the sole. On physical examination, the pain of plantar fasciitis may be reproduced by dorsiflexing the toes and palpating the plantar fascia. Treat plantar fasciitis with nonsteroidal anti-inflammatory medications, gentle physical therapy, and, in refractory cases, local steroid injections. Although patients should avoid activities that precipitate pain, it is usually impractical for patients to comply with instructions to stay off of their feet.

Tarsal tunnel syndrome

The tarsal tunnel is formed by connective tissue posterior to the medial malleolus. The tibial nerve passes through the tarsal tunnel in order to reach and innervate the sole. Compression of the tibial nerve within the tarsal tunnel may therefore lead to pain and paresthesias in the bottom of the foot. Tarsal tunnel syndrome could be considered the lower-extremity analog of carpal tunnel syndrome (Chapter 16), but it is actually quite uncommon and occurs almost always in the setting of ankle trauma rather than as a gradual-onset process secondary to overuse. Polyneuropathy and plantar fasciitis are more likely explanations for symptoms in patients referred for tarsal tunnel syndrome. Signs on examination include numbness in the sole of the foot and paresthesias reproduced by percussing the tibial nerve just posterior to the medial malleolus. Be aware that sensation over the sole is frequently decreased due simply to the thickness of the overlying skin rather than to any specific neuropathology, so pinprick examination must be interpreted cautiously. Electrodiagnostic studies show slowing of tibial NCS across the ankle, but are frequently challenging and uninformative in patients with tarsal tunnel syndrome, particularly in patients with underlying polyneuropathy. Surgical release of the tibial nerve at the tarsal tunnel is curative, although seldom performed due to the rarity of the condition.

Morton’s neuroma

Morton’s neuroma is a benign tumor of the plantar nerve. Patients characteristically develop pain and paresthesias in the plantar surfaces of two adjacent toes (e.g. lateral half of digit three and medial half of digit four), which worsen with pressure and wearing shoes. Symptoms may be reproduced by applying pressure directly to the plantar nerve. Morton’s neuroma should be evaluated and treated by an orthopedist or podiatrist.


Cramps are characterized by a squeezing pain, which occurs most commonly in the calves and feet and has a tendency to be worse at night. They are discussed in greater detail in Chapter 14.

Restless legs syndrome

Restless legs syndrome (RLS) is a syndrome of unclear etiology characterized by a sensation of discomfort in the lower extremities that occurs at rest, particularly in the early evening when relaxing or while trying to fall asleep. Patients with RLS describe abnormal crawling, itching, or pulling below the knees, and feel that they need to move their legs or walk around in order to get relief. There is often a family history of RLS, and women tend to be affected more often than men. The diagnosis is easily established from the clinical history alone. Although a variety of medical conditions may be associated with RLS, iron-deficiency anemia is the most common identifiable cause. Patients with ferritin levels <50 µg/l should be treated with iron supplementation.11 Caffeine and nicotine exacerbate RLS and should be avoided before bedtime. Dopamine agonists such as pramipexole (initiated at 0.125 mg qd, increased by 0.125 mg qd every 2–3 days up to 0.75 mg qd as needed) or ropinirole (0.25 mg qd, increased by 0.25 mg qd every 2–3 days up to 2 mg qd as needed) given approximately 2 hours prior to anticipated symptom onset are the first-line treatments for RLS. In patients who do not benefit from one of the dopamine agonists, gabapentin (100–600 mg before bedtime) is usually the next choice. Other medications that may be effective for RLS include levodopa, benzodiazepines, carbamazepine, diphenhydramine, and even low doses of mild narcotics. Dopamine agonists and levodopa are associated with the augmentation phenomenon, in which symptoms appear progressively earlier and earlier in the day. For patients with augmentation, problems only worsen when agents such as pramipexole or ropinirole are administered in anticipation of symptoms. Replacing dopaminergic agents with nondopaminergic ones is the most effective strategy for treating this problem.

Raynaud’s phenomenon

Raynaud’s phenomenon is a very common condition caused by low blood flow to the tips of the fingers and toes. It is diagnosed when the skin of the tips of the digits undergo a biphasic color change (at least two of pallor, erythema, and cyanosis).12 Although these color changes are the defining features of Raynaud’s phenomenon, patients may be referred for evaluation of neuropathy when the most prominent complaints are tingling, burning pain, or numbness. The first step in treating Raynaud’s phenomenon is to counsel the patient to avoid the cold as much as possible or to wear gloves or socks when exposed to the cold. Obviously, most patients have tried these techniques before consulting with a neurologist. The rationale for using calcium-channel blockers (e.g. nifedipine 30–180 mg qd) and topical nitroglycerin is that they presumably produce vasodilation. Unfortunately, these agents provide only marginal symptom relief.

Generalized pain disorders

Patients with generalized, whole-body pain are often referred for evaluation of possible neuropathy, but rarely have a neurological disorder. The conditions that result in generalized body pain are usually psychiatric or rheumatological in origin. Psychiatric conditions that may produce whole-body pain include depression, anxiety, adjustment disorders, malingering, and conversion disorders. The difficult task in treating these patients is to help them to recognize the psychiatric component of their illnes, to not feel insulted by the diagnosis, and to facilitate contact with a physician who will be better suited to treat their problems.


Although not a neurological disease, many patients with fibromyalgia end up being evaluated by neurologists. This disease of uncertain etiology affects mostly younger and middle-aged women and is characterized by aching pain involving the neck, mid-back, lower back, arms, legs, and chest wall. Patients with fibromyalgia may also describe burning, tingling, and lancinating pains. Weakness is a subjective complaint, although none is demonstrable on examination. Neurocognitive symptoms include forgetfulness, impaired concentration, and fatigue. Research diagnostic criteria include the presence of chronic widespread pain and tenderness to palpation of 11 of 18 specific points.13 By the time a patient with fibromyalgia is referred to a neurologist, an extensive battery of tests to exclude other diagnoses is usually available for interpretation. These should include complete blood count, erythrocyte sedimentation rate, thyroid function tests, and creatine kinase levels. Treatment of fibromyalgia is frequently challenging. A straightforward discussion of the diagnosis reduces accumulation of disability, whereas evasiveness and unnecessary protracted evaluations do more harm than good.14 Patients with fibromyalgia may show a modest response to antidepressants. Nonsteroidal anti-inflammatory drugs are usually not effective and narcotics should be avoided. Encourage patients to pursue alternative therapies, as conventional medical treatment is frequently disappointing. In some cases, referral to a rheumatologist (preferably one with an interest in the condition) may be helpful.


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