Chapter Three - Numbness: A Practical Guide For Family Physicians

PHYSICIANS

Jeffrey Rosenfeld, MD, PhD
Carolinas Neuromuscular/ALS Center
Charlotte, NC

Raymond A. Martin, MD
Houston Neurology Associates
Houston, TX

David W. Bauer, MD, PhD
Memorial Family Medicine Residency Program
Houston, TX

Localizing The Problem By History And Examination

Numbness can result from either a disease process located in the central nervous system (brain or spinal cord) or the peripheral nervous system (nerve root, dorsal root ganglion, or nerve). Often, localization of the problem can be identified by the patient's history alone. Recognition of both the timing and onset of the patient's symptoms and the distribution of the patient's signs and symptoms are essential.

Localizing a patient's deficits to a specific area of the nervous system can frequently be accomplished by attention to:

• Distribution of symptoms
  • Right vs. left
  • Presence of facial involvement
  • Arm vs. leg
  • Proximal vs. distal
  • Symmetric vs. asymmetric
• Characteristics of symptoms
  • Sensory and motor
  • Painless or Painful
  • Sensory only
  • Autonomic involvement
• Temporal Features
  • Acute or Chronic
  • Static or Progressive

History: The Chief Complaint

Patient complaints of "numbness" can include a range of true sensory disturbances. "Tingling," "burning," or true loss of sensation can each be described simply as "numbness." Specific questioning, therefore, can help in identifying the etiology of the disease process, and simultaneous evaluation of the distribution of these complaints can significantly limit the differential diagnosis. Prompt recognition of these common symptoms has a major impact on appropriate treatment and ultimately can minimize long-term residual deficits for the patient.

Table 1.

Patient's Description of Sensory Loss	Likelihood of the localization
"Tingling"	Peripheral NS > Central NS
"Burning"	Peripheral NS > Central NS
"Total loss of feeling"	Central NS1 > Peripheral NS2
"Poor coordination" 3	Central NS = Peripheral NS
1Localization to the central nervous system would most commonly involve unilateral signs and symptoms except with spinal cord lesions where symptoms are usually bilateral. 2Peripheral nervous system lesions can be either multifocal or, commonly, bilateral and symmetric. Early signs in a neuropathy may involve only one extremity (usually the feet) but peripheral involvement would be much less likely with all unilateral complaints. 3Poor coordination can result from either central (cerebellar, brainstem) or peripheral (impaired proprioception, nerve, dorsal root ganglion) pathology.

The neuronal projections determine the extent and characteristics of the patient's symptoms. Individual populations of neurons are vulnerable in specific disease states. This vulnerability may arise from the effect of a disease on a specific vascular territory (i.e., stroke, vasculitis, aneurysm), a space occupying lesion (tumor, herniated disk) or an autoimmune, inflammatory attack on the nervous system. By history alone one can frequently appreciate the basics of localization (Table 1, 2).

Table 2: Distribution and selected characteristics of localizing patient complaints along the neuraxis

	Distribution	Facial Involvement	Characteristic	Pain
Brain	Unilateral	often	sensory + motor	no
Spinal Cord	Bilateral	no	sensory + motor	possible
Nerve Root	Unilateral	no	sensory + motor	yes
Nerve	Unilateral or bilateral	possible	sensory, motor, autonomic or combinations	yes
Neuromuscular junction	often bilateral	yes, but not always	motor	no
Muscle	Bilateral	rare	motor	unlikely

The distribution of lesions affecting the brain or spinal cord (central nervous system) are usually distinct from those affecting nerve root, nerve, neuromuscular junction or muscle (peripheral nervous system).

Table 2: Classification of etiologies affecting the central vs. peripheral nervous system. These conditions can result in common patient complaints of "numbness, tingling, pain or weakness"

Etiology	Central Nervous System	Peripheral Nervous System
Vascular	stroke, arterial-venous malformation, claudication	peripheral vascular disease
Structural	tumor, disk	tumor, disk
Inflammatory	infection, vasculitis	neuropathy, vasculitis, infection, myositis
Genetic	myopathy, motor neuron disease	neuropathy
Immune mediated	Multiple sclerosis, myelopathy	neuropathy, neuromuscular junction disease

Brain

A presenting symptom of numbness may be secondary to lesions of the parietal lobe or thalamus (ventral posteromedial nucleus, VPM). As described in Chapter 1, thalamic lesions produce contralateral sensory loss and numbness, which may be painful. Abrupt onset suggests stroke and often is seen with lacunar infarcts secondary to hypertension. The patient typically has sudden onset of contralateral sensory loss without other symptoms (such as weakness). The MRI examination may confirm the presence of a lacunar infarct, in the VPM thalamus or more significantly a hemorrhagic infarction usually accompanied with significant hypertension. The thalamus is more vulnerable to hemorrhage resulting from hypertension in the brain, relative to other brain regions. Control of the patient's precipitating hypertension may constitute the major treatment modality along with addressing other stroke risk factors.

Parietal lobe lesions are characterized by sensations of contralateral numbness but on examination we find loss of discriminatory sensation, possibly accompanied by neglect of that extremity. The patient may feel touch but may not localize it well and may also demonstrate extinction (see Chapter 1). Patients may feel you touch their fingertips but may not be able to identify a number that you trace on the fingertip (impaired graphesthesia). Depending upon localization within the parietal lobe or involvement of the underlying white matter, patients may also experience weakness as well as numbness. Sensory complaints should be more prominent than motor symptoms, however, both sensory and motor signs may occur in many affected regions of the brain due to interruption of fibers affecting both functions.

Spinal Cord
Lesions in the spinal cord resulting only in numbness are less common than complaints of both numbness and weakness due to the close proximity of motor and sensory neurons and their pathways in the spinal cord. This is especially true of structural (herniated disk, trauma, tumor) and ischemic lesions.

Inflammatory lesions, however, can selectively affect sensory pathways and result in profound, usually bilateral, sensory disturbance. Inflammatory disorders such as acute myelitis and multiple sclerosis can present as only sensory disturbances. The dorsal columns (fasciculus gracilis and cuneatus) as well as the spinal thalamic tract carry distinct sensory modalities through the spinal cord. Sensory disturbance characterized by selective abnormality of position sensation (proprioception) suggests a selective involvement of the large myelinated fibers found in the dorsal columns and disorders such as multiple sclerosis, vitamin deficiencies/toxicity, and tertiary syphilis should be explored further. Temperature, light touch and pain are mediated by the smaller fibers of the spinal thalamic pathway. These fibers are not usually selected affected in the spinal cord.

Nerve Root/Dorsal Root Ganglion
Dorsal (sensory) and ventral (motor) nerve roots are separate as they exit the spinal cord until their fibers combine at the level of the dorsal root ganglion. The most common nerve root pathology results from a herniated vertebral disk causing compression on the nerve roots. This usually results in pain with radiation into the affected dermatome. Due to the proximity of dorsal and ventral roots, motor involvement is also commonly detected. The hallmark of selective nerve root involvement is a pattern of unilateral symptoms limited to the distribution of that nerve root.

The involvement of multiple nerve roots suggests a process other than a structural lesion. Inflammatory (Guillian Barré, CIDP, amyloidosis, vasculitis), neoplastic (carcinomatous meningitis) or infectious (syphilis, Lyme) processes need to be considered. Often appropriate serology and a lumbar puncture is required to further resolve this differential diagnosis.

Selective involvement of the dorsal root ganglion cells causes a profound sensory disturbance. Fortunately, the differential diagnosis of a dorsal root ganglionopathy is limited and careful attention to the physical examination can identify the proper etiology.

Cis-platinum toxicity following chemotherapy can result in a significant disability due to large fiber (position sense) sensory loss. The onset can be delayed by several months and some resolution may be expected when the dose is reduced or stopped. Paraneoplastic (anti-Hu) syndrome can result in painful, asymmetric sensory loss to all modalities with normal motor function. This pathology predominantly affects women and is commonly associated with concurrent small cell carcinoma.

Nerve
Sensory disturbances caused by neuropathy are common. More commonly, however, neuropathy presents with both motor and sensory symptoms reflecting the involvement of both fiber types in the nerve. An etiology for a predominantly sensory neuropathy can be focused by recognition of some discriminating features of the patient's sensory complaints at presentation. Small fiber sensation includes light touch, pain and temperature while large fiber sensation includes position sensation (proprioception) and partial vibratory sensation. Pain and/or autonomic complaints can also limit the evaluation of possible etiologies and work-up. The list of possible etiologies resulting in sensory neuropathy is long and it is not necessary to evaluate every patient for all possible causes. Table 4 lists both common and uncommon causes of sensory predominant neuropathy.

Along with the recognition of distinguishing features of the patient's sensory disturbance, identification of significant features of the past history and family history is essential. Diabetes, alcohol abuse, chronic use of medication or vitamins, and history of similar sensory problems in the family are significant clues to identifying a proper etiology. In this country, and in many European countries, diabetes is the most common cause of neuropathy while leprosy remains the most common etiology worldwide.

Table 4

	Etiology
Primary Characteristic	Toxic	Immune	Metabolic	Inherited	Other
Pain	Alcohol Metals: thallium, arsenic, Meds: cis-platinum, disulfiram, nitrofurantoin, taxol	Guillian Barré syndrome, HIV, Sjogren's, Vasculitis, Cryoglobulinemia	Diabetes, Vitamin related	Fabry's disease (a-galactosidase), Hereditary Sensory Neuropathy, Amyloidosis, Porphyria
Large & Small Fiber	Metals: thallium, mercury, Drugs: thalidomide, taxol, metroniadazole, phenytoin	Paraneoplastic (anti-Hu), Anti-MAG, anti-sulfatide, Sjogren's, Cryoglobulinemia	Diabetes	Hereditary Sensory Neuropathy (AR)
Large Fiber & Ataxia	Vitamin related, Cis-platinum, Taxol	Miller Fischer variant of Gillian Barre syndrome, CIDP1, Anti-MAG syndrome2, GALOP syndrome3		Friedreichs ataxia, Sensory ataxic neuropathy, Ataxia telangectasia	Syphilis-tabes dorsalis
Small Fibers Mostly	Chronic Metronidazole, or misoniadazole	HIV-Associated	Diabetes, Hypertriglyceridemia	Amyloidosis Hereditary Sensory Neuropathy, Tangier's Disease, Fabry's disease	Leprosy, 1º biliary , cirrhosis
Autonomic Symptoms		Guillian Barré, Paraneoplastic (anti-Hu)	Diabetes	Amyloidosis, Porphyria	MNGIE4,#Chronic , Renal or hepatic disease

¹Chronic Inflammatory Demyelinating Polyneuropathy; ²Syndrome of Gait disorder, Autoantibody, Late age, Organomegly, Polyneuropathy; ³Syndrome of detectable antibodies directed against Myelin Associated Glycoproteins; 4A mitochondrial etiology: Myopathy and external ophthalmoplegia, Neuropathy, Gastro- Intestinal, Encephalopathy

History of the Present Illness

Onset

Slow progressive course. Slow progressive numbness or sensory disturbance is most commonly described as distal numbness or tingling in the toes. This usually progresses proximallyinto the feet and then up the legs [distal to proximal progression or "dying back" pattern]. The most distal segments of the nerve are most dependent upon axonal transport for delivery of vital proteins and neurotransmitters. Interruption of axonal transport, or any lesion affecting the function and viability of the nerve along its course will be recognized by the patient as symptoms occurring referred in the most distal aspects of the affected nerve. Recognizing a dying back process, i.e., a slow progressive distal to proximal progression (usually symmetric) would strongly implicate neuropathy in the differential diagnosis. Sensory complaints due to radiculopathy can also evolve slowly, however they are frequently characterized by pain in the affected root distribution, which is exacerbated by activity. Sensory complaints from a radiculopathy or neuropathy can be episodic, especially earlier in their course.

Sensory disturbances from pathology in the brain or spinal cord usually evolves more acutely. Ischemia or inflammatory disease in the central nervous system also evolves rapidly over several days. Numbness or paresthesias due to multiple sclerosis are examples of such a process.

Acute or subacute onset with rapid progression (Table 5). Rapidly progressive sensory complaints, usually accompanied by weakness are compatible with localization to either the brain spinal cord, nerve root or nerve. In general, ischemic injury is most commonly implicated in sudden onset of sensory symptoms. As mentioned above, inflammatory disorders can evolve rapidly over several days and also can affect any area of the neuraxis.

In the brain, acute onset of significant sensory symptoms is usually accompanied by either weakness and/or encephalopathy. Common etiologies include: stroke, multiple sclerosis, cancer (lymphoma, metastasis), and infection. In the nerve root, acute sensory symptoms are most commonly due to compression from a disk or trauma as discussed above. In the nerve, the differential diagnosis of potential etiologies is longer but equally critical. Acute inflammatory demyelinating neuropathy (Guillian-Barré syndrome) often requires prompt attention to maintain life support and initiate treatment. Arsenic, thallium, tick paralysis and porphyria may also result in rapidly progressive disability for the patient warranting emergent treatment.

Table 5: Considerations of differential diagnosis for neuropathy in patients with sensory complaints using the onset and progression as criteria.

	ACUTE (Days)	CHRONIC (Weeks - Months)
Immune	Guillain-Barré & variants, Vasculitis	Chronic demyelinating neuropathy
Toxins	Botulism, Buckthorn, Diphtheria; Tick; Arsenic; Organophosphates; Thallium; Vacor	Heavy Metals , Environmental Chemicals
Drugs (see Table 6)	Captopril (few case reports); Gangliosides; Gold; Nitrofurantoin; Suramin; Zimeldine	Chemotherapeutic Agents
Metabolic	Porphyria	Porphyria, Diabetes
Nutritional		Vitamin toxicity or deficiency
Hereditary		Hereditary motor and sensory neuropathy (HMSN), hereditary sensory neuropathy (HSN)

Family History
Family history is most helpful in identifying the etiology of neuropathy. Localization to the brain or spinal cord can be aided by identification of similar disease in the family, however, the symptoms are usually not limited to sensory complaints or numbness.

Identification of genetic lesions resulting in inherited neuropathy has significantly increased our understanding of normal biology of nerve, myelin and their interaction. The hereditary motor and sensory neuropathies (HMSN, Charcot-Marie-Tooth neuropathies) comprise a group of disorders with overlapping clinical characteristics but distinct pathology. Some of these disorders can be identified by currently available commercial laboratory tests (see below). Inherited disorders affecting only sensation (hereditary sensory neuropathy, HSN) are more rare and may involve either small fiber sensory loss (pain and temperature) or loss of larger sensory fibers (proprioception, vibration). Distinguishing the type of sensory loss on examination, therefore, can limit the differential diagnosis and an accurate family history can lend further support for a diagnosis even prior to definitive genetic testing when available. Genetic markers screening for these disorders have not been established for general clinical use at this time and the diagnosis is made based on the clinical observations and family history.

Occupational Exposure
Incidental exposure to agents, which are toxic to nerve, may be easily missed on a routine history and review of systems. Contact with solvents, glues, fertilizer, oils and lubricants can result in a neuropathy indistinguishable from other causes of idiopathic or hereditary etiology. Table 6 includes a summary of several categories of neurotoxic exposure leading to neuropathy.

Table 6: Selected agents found in various industrial applications associated with neuropathy affecting sensation.

Solvents, Glues & Lacquers	n-hexane allylchloride	Hexacarbons	Trichloroethylene(TCE)
Pesticides	methylbromide	Organophosphates	Thallium
Oils/ Lubricants	Spanish"toxic" oil	Triorthocresylphosphate (TOCP)
Disinfectants	ethyleneoxide
Miscellaneous	carbon disulfide, acrylamide	DMAPN	Polychlorinatedbiphenyls (PCBs)

Medications
Inadvertent or iatrogenic injury to nerve caused by medications or vitamins is likely not fully recognized in a routine history and physical evaluation. Over-the-counter oral preparations can result in a profound sensory predominant neuropathy even when taken at therapeutic doses. Patients who have neuropathy not associated with or caused by a medication may still be vulnerable to exacerbation of their symptoms by taking these neuropathic agents and should be advised to avoid these preparations (Table 7).

Table 7: Selected medications, which are associated with a sensory or a sensory predominant neuropathy. These medications should also be avoided in patients with other etiologies

chloramphenicol	metronidazole	phenytoin	Nitrofurantoin
cis-platinum	nitrous oxide	pyridoxine	taxol
ethambutol	nucleosides	thalidomide
glutethemide	[didianoside (ddI)	dapsone
hydralazine	dideoxycytosine (ddC)	disulfram
isoniazid	stavudine (d4T)]	disulfram

Evaluating Changes In Sensation

Examination

The clinical signs. Few signs in the neurological examination are as localizing and sensitive as the deep tendon reflexes (DTRs). Intact DTRs require both an afferent (sensory) component to carry input from the muscle tendon to the spinal cord and an efferent (motor) component to produce a muscle twitch during a reflex. Furthermore, the motor neurons are affected by descending cortical-spinal inputs that effect the reflex arc. Nerve impulse conduction throughout this entire afferent/efferent loop is, therefore, vulnerable to injury, which could exaggerate, diminish or obliterate the corresponding reflex.

Pathology in the central nervous system is characterized by pathologically brisk reflexes and extensor plantar reflexes (abnormal Babinski sign). In addition, increased tone and spasticity are consistent features. By contrast, with pathology in the peripheral nervous system diminished or absent reflexes are seen along with atrophy and reduced muscle tone. Asymmetric or absent reflexes should generate clinical suspicion for a neuropathy or radiculopathy.

In a sensory (or sensory predominant) neuropathy the type of sensory loss can localize the process to small, large or both small and large, axons as discussed above. The primary modalities of sensory loss which should be evaluated include those listed below.

Table 8: Sensory modalities which should be included on a through examination and their anatomic correlates.

Modality	Fiber type (Periphery)	Tract (Central)
Light touch	small fiber	Spinothalamic
Temperature	small fiber	Spinothalamic
Pinprick	small fiber	Spinothalamic
Two-point discrimination	small fiber	Spinothalamic (parietal)
Proprioception	large fiber	Dorsal columns
Vibration	both small and large fiber

The nature of the sensory examination relies on a patient's subjective report and is therefore prone to additional variability. Differences between patient perceptions and their ability to relate subtle differences in pinprick or temperature can make this the most challenging part of the physical examination. In general, absolute differences in sensation are not as important for localization or diagnosis as are the relative differences in perceived sensation. The most useful information from the sensory examination results, therefore, from the distribution of the deficit (symmetric vs. asymmetric) and the quality of the sensory loss.

Sensory loss and neuropathy associated with systemic disease. Clinical signs on the general examination can be essential clues to the etiology of sensory loss (Table 9). Systemic diseases commonly involve multiple organ systems. The nervous system is frequently implicated due to its widespread distribution, long projections and unique metabolic demands. Autoimmune, inflammatory, metabolic, and neoplastic disease are among the categories of systemic illness, which can involve the peripheral nerve resulting in numbness, paresthesia, and/or weakness. Careful attention to key clinical signs on general examination can result in the underlying disease as well as the etiology for the neuropathy.

Table 9.

Clinical Sign	May suggest:
Rash	Lupus
Funduscopic examination	Diabetes, Vasculitis
Adenopathy	Infection, Cancer
Weight loss	Diabetes, Cancer, Endocrinopathy
Bony or Cutaneous abnormalities	Inherited neuropathy, Endocrinopathy
Organomegly	"POEMS" syndrome1

¹Syndrome of: Polyneuropathy: sensory & motor Organomegaly: liver; spleen; lymph nodes Endocrinopathy or Edema: diabetes; hypothyroid; gynecomastia M-protein: Usually IgG or IgA Skin changes: hypertrichosis; hyperpigmentation; clubbed fingers; white nails

Evaluation: Work-Up
The primary goal in identifying a proper localization is to identify treatable etiologies of the underlying process. Each localization along the neuraxis mentioned above (brain–spinal cord–nerve root–nerve) has treatable conditions associated with it. Evaluation should include serologic and radiographic evaluation where appropriate to identify overt contributing conditions and proper referral to a neurologist for assistance in further resolution of the differential diagnosis and treatment plan.

 

Central Nervous System
As discussed above, sensory loss or numbness localized to the central nervous system most commonly is associated with stroke or inflammatory disease.

Proper evaluation of a patient with a suspected stroke, primarily involving sensation, should include screening for the commonly accepted risk factors (HTN, diabetes, cholesterol, tobacco use, arrhythmia). In addition, an MRI scan of the brain with gadolinium contrast is usually indicated as this can illustrate the extent of the current lesion and reflect prior, perhaps subclinical, lesions.

Ischemic or inflammatory disease localized to the spinal cord by both a gadolinium enhanced MRI scan and a lumbar puncture. The presence of elevated protein and an increased number of white blood cells in the cerebrospinal fluid is consistent with inflammation (myelitis). A specific etiology for an inflammatory lesion in the spinal cord is often more elusive. Specific viral pathogens such as varicella, HTLV-1, and HIV have been identified. Multiple sclerosis is a clinical diagnosis requiring multiple signs and symptoms at more than one point in time.

Table 10. Initial screening evaluation for suspected localization of sensory loss.

Localization	Lab tests	Radiology	Other
Brain	Hb-A1c, lipid profile, ESR, ANA, CBC, electrolytes, RPR	MRI with contrast Transcranial doppler, Carotid doppler	EKG, ECHO, possible Holter
Spinal cord	Routine lab screen evaluating underlying illness, B12	MRI with contrast	LP with opening pressure, protein, chemistry and cytology
Nerve Root	Not usually indicated	CT or MRI of the suspected area. Myelogram may be indicated	Nerve conduction and electromyography including F and H wave evaluation
Nerve	Hb-A1c , ESR, ANA, CBC, electrolytes, RPR, SPEP, immunofixation, B12 As indicated: ANCA, cryoglobulins	Not usually indicated	Nerve conduction and electromyography Possible nerve & muscle biopsy as indicated

Electrodiagnosis (Table 11)

The evaluation of electrical impulses along affected nerves (nerve conduction studies) and within affected muscles (electromyography) often provides an essential aspect to the work-up, localizing nerve/muscle pathology and etiology. These tests are highly dependent upon multiple variables impacting the technical quality of the study. Consequently it is important to have confidence in the referral as interpretation of the data can be markedly affected by these technical issues.

Nerve conduction studies are especially helpful in identifying treatable causes of neuropathy by revealing evidence of demyelination. Impaired speed of conduction or a complete block of conduction over a defined segment are compatible with demyelinating neuropathy. Conversely, a reduced amplitude of the conducted response is characteristic of an axonal neuropathy. It is important to note that axonal loss can either result from a primary pathologic process or secondary to demyelination. Ultimately, the goal of the nerve conduction study is to determine whether a treatable process is present. This goal is usually realized by noting pathology that is selective or focal (i.e., nerve compression, radiculopathy) or compatible with demyelination.

Table 11: Summary of common patterns found on nerve conduction studies in various areas of neuromuscular pathology

Result	Axonal neuropathy	Demyelinating neuropathy	Radiculopathy	Myopathy
Reduced amplitude	Common	Possible secondary change	Not common and only in motor nerves affected by the root	Possibly due to reduced impulse in the disease muscle not disease in the nerve
Slow conduction velocity	Not common	Common. Also look for focal conduction block	Not commonly found	Not found
Prolonged distal latency	Possible	More common	Not expected	Not usually found
Sensory nerves	Can be affected	Can be affected	Not found	Not Found

Psychological Considerations
A number of the conditions described above may be associated with psychological and behavioral complications. In some cases the condition itself produces psychological changes (e.g., stroke). In other cases the effects of the condition may precipitate those changes (e.g., depression over loss of independence). Studies have found an incidence of depression after stroke as high as 60%, and the risk of suicide is increased for patients with conditions such as stroke or multiple sclerosis Occasionally our treatment interventions may be associated with adverse psychological effects.

Depression may decrease a patient's ability and willingness to take part in needed therapy, thus resulting in prolonged or increased disability. Caregivers of patients with some of the chronic conditions described in this chapter are also often affected. Many of these patients require intense and ongoing efforts by family members, which can lead to depression and anxiety among these caregivers. Physicians must be attentive and proactive in searching for this co-morbidity, both in the patient and in the family members.

Community Resources
As noted in the section on weakness, ongoing needs will vary tremendously from patient to patient. The effects of neuropathy, stroke or multiple sclerosis will span the range from incapacitation to minimal impact. Physical therapy, occupational therapy, and speech therapy can be provided in various settings, including the acute care hospital, extended care facilities, and the home. In the case of stroke, education can play a valuable role in reducing the likelihood of reoccurrence through lifestyle changes (e.g., lowering of cholesterol, management of blood pressure, smoking cessation). Education may also be valuable to the multiple sclerosis patient in terms of management of symptoms and avoidance of exacerbation triggers (e.g., avoidance of overheating). Often, patient education regarding the site and nature of pathology can be a powerful tool to helping a patient cope with progressive disability. This may be especially true in distinguishing demyelinating, axonal and inherited neuropathy.

National organizations for specific conditions offer a number of services, including literature directed to the lay audience, lists of local support groups, and treatment advances. Some of those for the conditions discussed in this chapter include:

The Neuropathy Association
60 East 42nd Street
New York, NY 10165
(800) 247-6968, 212-692-0662
info@neuropathy.org
Regularly published informative newsletter is also available.

Charcot Marie-Tooth Association
800-606-CMTA

Sjogren's Syndrome Foundation
516-933-6365
Patient Support Group

Guillain-Barré Syndrome Foundation International
P.O. Box 262
Wynnewood, PA 19096
(610) 667-0131
Website
gbint@ix.netcom.com

The National Multiple Sclerosis Society
733 Third Avenue
New York, NY 10017
(800) 344-4867
info@nmss.org

National Stroke Association
96 Inverness Drive East, Suite I
Englewood, Colorado, 80112-5112
(800) 787-6537

American Heart Association
National Center
7272 Greenville Avenue
Dallas, Texas 75231
(800) 242-8721

Review article on multiple sclerosis from American Family Physician

Review article on Guillain-Barré Syndrome from American Family Physician

Questions

1. All of the following statements are true except:
   
   1. brain lesions usually cause unilateral numbness without associated pain
   2. spinal cord lesions usually cause bilateral sensory loss
   3. nerve root lesions usually are associated with sensory loss or symptoms and pain.
   4. myopathies are commonly associated with severe pain
2. A brain lesion that may be associated with painful sensory loss is located in the:
   1. thalamus
   2. frontal lobe
   3. motor cortex
   4. parietal lobe
3. Motor and sensory symptoms in a multiple nerve root distribution can be seen:
   1. carcinomatous meningitis
   2. Guillain-Barré syndrome
   3. Lyme disease
   4. diabetes mellitus
   5. all of the above
4. The most common pathology to affect a single nerve root is:
   1. diabetic radiculopathy
   2. Guillain-Barré Syndrome
   3. herniated intervertebral disc
   4. disc space infection
5. Neuropathy in Charcot-Marie-Tooth disease is:
   1. due to nutritional deficiency
   2. secondary to benzene exposure
   3. a genetically determined degenerative disorder.
   4. reversible in most cases
6. Chronic nitrofurantoin use can cause peripheral neuropathy. True or False?
7. Slowly progressive numbness, beginning slowly in the feet and moving proximally may >be secondary to the "dying-back" phenomenon characteristic of multiple sclerosis. True or False?
8. Absent reflexes may be seen with:
   1. neuropathy
   2. radiculopathy
   3. myelopathy
   4. A and B
   5. none of the above
9. (True or False) Nerve conduction studies are sensitive in detecting areas of demyelination on peripheral nerves that result in slowing of nerve conduction velocities. True or False?
10. Electromyography is useful in distinguishing a neuropathic process from a myopathic process. True or False?

Answers

1. D
2. A
3. E
4. C
5. C
6. True
7. False
8. D
9. True
10. True