Peripheral neuropathy is the most common neurological disorder in peo- ple with HIV infection. It can be a ma- jor source of pain and discomfort and a limiting. Peripheral neuropathy is a general term for any disorder affecting the Signs of peripheral neuropathy also include sensory, motor and autonomic components. Peripheral neuropathy is a common neurological problem. Because the presentation of neuropathy is variable and the causes are disparate, a logical and.
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PDF | Peripheral neuropathy has a variety of systemic, metabolic, and toxic causes. The most common treatable causes include diabetes. Peripheral Neuropathy: A Practical Approach to. Diagnosis and Symptom ahcd/macawebsrilni.ga Accessed May. ABSTRACT. Purpose of Review: This article provides a clinical approach to peripheral neuropathy based on anatomic localization and diagnostic testing.
Whether these differences extend to the clinical setting has not been adequately explored, although the results reported here do suggest potential differences as well as the need for further evaluating pain perceptions in multicultural populations, including sensations related to neuropathic pain such as pDPN.
The robustness of these results was demonstrated by additional analyses that adjusted for demographic and socioeconomic factors, since age, education level, and income may be potential confounding factors that contribute to pain perceptions or HCP interactions. These additional analyses suggest that regardless of socioeconomic status, ethnicity is a general factor in how symptoms associated with pDPN are manifested or perceived.
While it is well-recognized that diabetes disproportionally affects African-Americans and Hispanics [ 18 ], to our knowledge this is the first study to suggest that these populations may also have a high prevalence of pDPN symptoms in such a young age group, but a more rigorous epidemiologic study would be needed to corroborate these observations.
The overall similarity across ethnicities for time since a diabetes diagnosis further suggests that duration of diabetes is unlikely to meaningfully impact the observed results and their clinical implications. The differences in symptoms and severity were paralleled by the impact of pain on daily activities on the WPAI:SHP reported by the three populations; the least impairment was consistently reported by Hispanics, and this was significant for Activity impairment vs both other populations, and for Presenteeism vs Caucasians.
It should again be noted that the WPAI:SHP responses on work productivity were obtained only from employed respondents, while the activity impairment question was answered by all respondents and was limited to activities other than employment. These observations on the WPAI:SHP are consistent with a recent review suggesting lower rates of activity limitation among Hispanics with pain relative to other cultural groups despite greater pain sensitivity [ 15 ].
Among those employed, presenteeism was three times that of absenteeism in all cultural groups, suggesting that this was the primary driver of work impairment, as has been previously reported among patients with chronic pain conditions [ 5 ]. Despite the presence of these symptoms and pain of moderate or severe severity in substantial proportions of African-Americans and Hispanics, fewer of these patients reported receiving a pDPN diagnosis than Caucasians.
This lower rate of diagnosis may potentially be due, at least in part, to the observations related to interactions of these populations with their HCPs: Fewer African-American and Hispanic patients reported discussing their pain symptoms with their HCP, and there was consistently less comfort with their HCPs in these groups.
These interactions with HCPs are consistent with the disparities in healthcare resource availability and use that have been reported among minority populations and that contribute to the challenge of diagnosis and management of these patients [ 19 ].
In particular, Hispanics have reported language and cultural barriers such as the unavailability of Spanish-speaking healthcare providers or interpreters [ 15 , 20 ].
While these language and cultural barriers may in part account for the lower comfort level of Hispanics with their HCPs in the current study, it should also be noted that African-Americans reported a similarly hard time communicating with their HCPs as Hispanics did.
Limitations As with any survey dependent upon respondents, an important limitation is potential selection bias, since patients who agreed to participate may have characteristics and perceptions different from those who refused. A related limitation is that the patient-level data on diagnosis, pain, and symptoms were based on self-report and, as such, may be subject to misunderstanding or misinterpretation of the questions that may result, at least in part, from cultural differences across the populations.
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Phenytoin Dilantin. Procainamide Pronestyl. Vincristine Oncovin. Vitamin B 6 excess. Genetic testing.
Peripheral Neuropathy: Differential Diagnosis and Management
Type 1. Type 2. Metachromatic leukodystrophy. Neuropathy with liability to pressure palsies. Refsum disease. Arsenic causes sensorimotor neuropathy. Gold may cause some demyelination. When a patient presents with symptoms of distal numbness, tingling and pain, or weakness, the first step is to determine whether the symptoms are the result of peripheral neuropathy or of a lesion in the CNS, and whether a single nerve root, multiple nerve roots, or a peripheral nerve plexus is involved.
CNS lesions may be associated with other features, such as speech difficulty, double vision, ataxia, cranial nerve involvement, or, in cases of myelopathy, impairment of bowel and bladder functions.
Deep tendon reflexes are usually brisk, and muscle tone is spastic. Lesions of the peripheral nerve roots are typically asymmetric, follow a dermatomal pattern of sensory symptoms, and may have associated neck and low back pain. Lesions of the plexus are asymmetric with sensorimotor involvement of multiple nerves in one extremity.
A Hz tuning fork should be used to test the vibratory sensations in extremities. Loss of sensation including vibration, proprioception, temperature, and pinprick sensations in distal extremities suggests peripheral neuropathy, as does a distal-to-proximal gradient of reflex elicitation. Once the lesion has been localized to peripheral nerves, the next step is to find the etiology and exclude potentially treatable causes, such as acquired toxic, nutritional, inflammatory, or immune-mediated demyelinating disorders.
The neuropathies must be further characterized by onset and chronicity of symptoms, the pattern and extent of involvement, and the type of nerve fibers involved i. Over time, the numbness may extend proximally, and mild distal muscle weakness and atrophy may occur. In disorders that cause acute peripheral neuropathy, such as those produced by toxic exposures, patients may present with similar but more fulminant symptoms, and pain predominates; symptoms also typically have a faster progression.
In other disorders, such as acute inflammatory demyelinating disorder i. The presence of neuropathic symptoms, decreased ankle reflexes, and decreased distal sensations, regardless of distal muscle weakness and atrophy, makes the diagnosis of peripheral neuropathy likely.
Some causes of peripheral neuropathy are characterized by mononeuropathy, some involve multiple nerves, and others have autonomic dysfunction or pain prominence Table 2. Multifocal motor neuropathy. Vasculitic syndromes. Acquired immunodeficiency syndrome.
Conditions causing neuropathy with autonomic features. The evaluation of a patient with peripheral neuropathy starts with simple blood tests, including a complete blood count, comprehensive metabolic profile, and measurement of erythrocyte sedimentation rate and fasting blood glucose, vitamin B 12 , and thyroid-stimulating hormone levels 5 Figure 1. Additional tests, if clinically indicated, may include a paraneoplastic panel to evaluate for occult malignancy; antimyelin-associated glycoprotein antibodies to evaluate for sensorimotor neuropathies; antiganglioside antibodies; cryoglobulins; cerebrospinal fluid CSF analysis to evaluate for chronic inflammatory demyelinating neuropathy; antisulfatide antibodies to evaluate for auto-immune polyneuropathy; and genetic testing if hereditary peripheral neuropathy is suspected Table 3.
Approach to the patient with peripheral neuropathy.
If indicated by clinical suspicion. Tests are listed in the approximate frequency of the potential underlying disorder. Electrodiagnostic studies are recommended if the diagnosis remains unclear after initial diagnostic testing and a careful history and physical examination.
Nerve conduction studies assess the shape, amplitude, latency, and conduction velocity of an electrical signal conducted over the tested nerve.
Axonal loss leads to lower amplitudes, and demyelination causes prolonged latency and slow conduction velocity. EMG can detect active axonal damage, as evidenced by the presence of spontaneous muscle fiber activity at rest resulting from the absence of neuro-regulation denervation. The motor unit action potential on voluntary muscle contraction also is assessed. In neuropathic conditions, reinnervation changes are recorded, the details of which are beyond the scope of this article.
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Electrodiagnostic studies can help determine whether the neuropathy is the result of damage to the axons axonal neuropathy or the myelin demyelinating neuropathy , or both mixed. Normal nerve conduction studies and needle EMG significantly decrease the likelihood of peripheral neuropathy, whereas abnormal nerve conduction findings confirm the diagnosis. A potential limitation of electrodiagnostic studies is that they are able to test only the large, myelinated nerve fibers. This limits their sensitivity in detecting neuropathies of the small nerve fibers i.
In these cases, a specialized test directed at autonomic functions, and other non-electrodiagnostic tests e.
Nerve biopsy should be considered when the diagnosis remains uncertain after laboratory and electrodiagnostic testing, or when confirmation of the diagnosis is needed before initiating aggressive treatment e. Sural and superficial peroneal nerves are preferred for biopsy. When all investigations fail to identify a cause and electrodiagnostic studies show axonal-type symmetric peripheral neuropathy, idiopathic peripheral neuropathy is the presumptive diagnosis.
Epidermal skin biopsy can be performed in patients with burning, numbness, and pain, and in whom small, unmyelinated nerve fibers are suspected to be the cause.
Small nerve fiber damage may constitute the earliest stages of some peripheral neuropathies and cannot be detected by electrodiagnostic studies. Treatment of peripheral neuropathy has two goals: The former is usually achieved by eliminating offending agents, such as toxins or medications; correcting a nutritional deficiency; or treating the underlying disease e. Acute inflammatory neuropathies require more urgent and aggressive management with intravenous immunoglobulin 9 or plasmaphereis.
Mechanical ventilation should be considered in patients whose forced vital capacity is less than 20 mL per kg or is reduced by more than 30 percent of baseline, or if maximal inspiratory pressure is less than 30 cm of water.
It is important to help patients control troublesome symptoms of peripheral neuropathy, such as severe numbness and pain, as well as to alleviate disability resulting from weakness. A second opinion regarding the patient's diagnosis and management also should be considered before initiating long-term opioid therapy. Already a member or subscriber? Log in. Reprints are not available from the authors. Epidemiology of peripheral neuropathy.
J Neurol Neurosurg Psychiatry. Hughes RA. Peripheral neuropathy. The prevalence, severity, and impact of painful diabetic peripheral neuropathy in type 2 diabetes. Diabetes Care. Distal symmetric polyneuropathy: Clinical evaluation and investigation of neuropathy.
Winer JB. Chronic inflammatory polyradiculoneuropathy. Mayo Clin Proc. Lewis RA. Chronic inflammatory demyelinating polyneuropathy. Neurol Clin. Cochrane Database Syst Rev. Arch Neurol. Consequences of neuropathic pain: Am J Manag Care. Anticonvulsant drugs for management of pain: Symptomatic treatment of peripheral diabetic neuropathy with carbamazepine Tegretol: Ollat H, Cesaro P.
Pharmacology of neuropathic pain. Clin Neuropharmacol. Pharmacologic treatment of pain in polyneuropathy. Neuropathic pain: Mendell JR, Sahenk Z. Clinical practice.
Peripheral Neuropathy: Differential Diagnosis and Management
Painful sensory neuropathy. N Engl J Med.
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Peripheral Neuropathy: Differential Diagnosis and Management
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Peripheral Neuropathy: C 5 Electrodiagnostic studies are recommended if symptoms persist and if the diagnosis remains unclear after initial diagnostic testing and a careful history and physical examination. C 4 , 5 Options for symptomatic treatment of peripheral neuropathy include antiseizure medications, tricyclic antidepressants, and topical medications.
Table 1. Table 2.Initial blood tests should include a complete blood count, comprehensive metabolic profile, and measurement of erythrocyte sedimentation rate and fasting blood glucose, vitamin B 12 , and thyroid-stimulating hormone levels; specialized tests should be ordered if clinically indicated. Diabetes Care. Email Alerts Don't miss a single issue. Peripheral nerves serve different motor, sensory, and autonomic functions.
In other disorders, such as acute inflammatory demyelinating disorder i. Ollat H, Cesaro P. Since these diseases can have a multitude of etiologies and concomitant disorders, virtually all medical specialties come into contact with polyneuropathy patients.
Normal nerve conduction studies and needle EMG significantly decrease the likelihood of peripheral neuropathy, whereas abnormal nerve conduction findings confirm the diagnosis.