peripheral neuropathy victor f. politi, m.d., medical director, st. anthonys school of allied health...
TRANSCRIPT
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Peripheral Neuropathy
Victor F. Politi, M.D., Medical Director, St. Anthony’s School of Allied Health
Professions, Physician Assistant Program
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Introduction
• Peripheral neuropathy describes damage to the peripheral nervous system.
• More than 100 types of peripheral neuropathy have been identified, each with its own characteristic set of symptoms, pattern of development, and prognosis.
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• Impaired function and symptoms depend on the type of nerves– motor, sensory, or autonomic
• that are damaged.
Introduction
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• Motor nerves – control movements of all muscles under conscious
control, such as those used for walking, grasping things, or talking.
• Sensory nerves – transmit information about sensory experiences, such
as the feeling of a light touch or the pain resulting from a cut.
• Autonomic nerves – regulate biological activities that people do not control
consciously, such as breathing, digesting food, and heart and gland functions.
Introduction
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• Although some neuropathies may affect all three types of nerves, others primarily affect one or two types. – Therefore, terms such as
• predominately motor neuropathy• predominately sensory neuropathy• sensory-motor neuropathy• autonomic neuropathy
– are often used to describe a patient's condition.
Introduction
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• Because every peripheral nerve has a highly specialized function in a specific part of the body, a wide array of symptoms can occur when nerves are damaged.
• Some people may experience temporary numbness, tingling, and pricking sensations (paresthesia), sensitivity to touch, or muscle weakness.
Introduction
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• Others may suffer more extreme symptoms, including burning pain (especially at night), muscle wasting, paralysis, or organ or gland dysfunction.
Introduction
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• People may become unable to digest food easily, maintain safe levels of blood pressure, sweat normally, or experience normal sexual function.
• In the most extreme cases, breathing may become difficult or organ failure may occur.
Introduction
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• Some forms of neuropathy involve damage to only one nerve and are called mononeuropathies.
• More often though, multiple nerves affecting all limbs are affected-called polyneuropathy.
Introduction
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• Occasionally, two or more isolated nerves in separate areas of the body are affected-called mononeuritis multiplex.
Introduction
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• In acute neuropathies, such as Guillain-Barré syndrome, symptoms appear suddenly, progress rapidly, and resolve slowly as damaged nerves heal.
• In chronic forms, symptoms begin subtly and progress slowly.
Introduction
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• Some people may have periods of relief followed by relapse.
• Others may reach a plateau stage where symptoms stay the same for many months or years.
Introduction
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• Some chronic neuropathies worsen over time, but very few forms prove fatal unless complicated by other diseases.
• Occasionally the neuropathy is a symptom of another disorder.
Introduction
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• In the most common forms of polyneuropathy, the nerve fibers most distant from the brain and the spinal cord malfunction first.
• Pain and other symptoms often appear symmetrically, for example, in both feet followed by a gradual progression up both legs.
Introduction
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Introduction
• Next, the fingers, hands, and arms may become affected, and symptoms can progress into the central part of the body.
• Many people with diabetic neuropathy experience this pattern of ascending nerve damage.
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Anatomy
• The body’s nervous system is made up of two parts. – The central nervous system (CNS) – The peripheral nervous system (PNS)
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Anatomy
• The peripheral nerves include:– cranial nerves
• (with the exception of the second)
– spinal nerve roots – dorsal root ganglia – peripheral nerve trunks and their terminal
branches – peripheral autonomic nervous system
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Diagnostic Approach
• The differential diagnosis of peripheral neuropathy is significantly narrowed by a focused clinical assessment that addresses several key issues –
– Does the patient actually have a neuropathy? – What is the pattern of involvement?– Is the neuropathy focal, multifocal or symmetric? – If the neuropathy is symmetric, is it proximal or distal?
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• Does the patient actually have a neuropathy? – Causes of generalized weakness include motor
neuron disease, disorders of the neuromuscular junction and myopathy.
– Peripheral neuropathy can also be mimicked by myelopathy, syringomyelia or dorsal column disorders, such as tabes dorsalis.
– Hysterical symptoms can sometimes mimic a neuropathy.
Diagnostic Approach
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• Is the neuropathy focal, multifocal or symmetric?
– Focal neuropathies include common compressive neuropathies such as carpal tunnel syndrome, ulnar neuropathy at the elbow or peroneal neuropathy at the fibular head
– A multifocal neuropathy suggests a mononeuritis multiplex that may be caused, for example, by vasculitis or diabetes
Diagnostic Approach
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• If the neuropathy is symmetric, is it proximal or distal? – Most toxic and metabolic neuropathies present as a
distal symmetric or dying-back process.– Proximal sensory neuropathies are rare and include
porphyria.– Predominantly motor neuropathies are often proximal
and include acquired inflammatory neuropathies such as Guillain-Barré syndrome.
• An exception is lead neuropathy, which initially affects motor fibers in radial and peroneal distributions.
Diagnostic Approach
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Distal Symmetric Sensorimotor Polyneuropathies
• Infectious diseases – Acquired immunodeficiency
syndrome – Lyme disease
• Sarcoidosis • Toxic neuropathy
– Acrylamide – Carbon disulfide – Dichlorophenoxyacetic acid – Ethylene oxide – Hexacarbons – Carbon monoxide – Organophosphorus esters – Glue sniffing
• Metal neuropathy – Chronic arsenic
intoxication – Mercury – Gold – Thallium
• Medications (see next slide)
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Medications Causing Neuropathies
• Axonal Vincristine (Oncovin, Vincosar PFS) Paclitaxel (Taxol) Nitrous oxide Colchicine (Probenecid, Col-Probenecid) Isoniazid (Laniazid) Hydralazine (Apresoline) Metronidazole (Flagyl) Pyridoxine (Nestrex, Beesix) Didanosine (Videx) Lithium Alfa interferon (Roferon-A, Intron A, Alferon N) Dapsone
• Axonal - continued..Phenytoin (Dilantin) Cimetidine (Tagamet) Disulfiram (Antabuse) Chloroquine (Aralen) Ethambutol (Myambutol) Amitriptyline (Elavil, Endep)
• Demyelinating Amiodarone (Cordarone) Chloroquine Suramin (Fourneau 309, Bayer 205, Germanin) Gold
• Neuronopathy Thalidomide (Synovir) Cisplatin (Platinol) Pyridoxine
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Proximal Symmetric Motor Polyneuropathies
– Guillain-Barré syndrome– Chronic inflammatory demyelinating polyradiculoneuropathy – Diabetes mellitus – Porphyria – Osteosclerotic myeloma– Waldenstrom's macroglobulinemia – Monoclonal gammopathy of undetermined significance– Acute arsenic polyneuropathy – Lymphoma – Diphtheria – HIV/AIDS – Lyme disease– Hypothyroidism– Vincristine (Oncovin, Vincosar PFS) toxicity
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• Neuropathies can be categorized according to the fiber type that is primarily involved.
• Most toxic and metabolic neuropathies are initially sensory and later may involve the motor fibers.
Diagnostic Approach
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• Pure sensory neuropathies can result from drug toxicity (e.g., thalidomide, cisplatin [Platinol]), paraneoplastic syndromes or nutritional deficiencies.
• Primarily motor neuropathies include Guillain-Barré syndrome.
Diagnostic Approach
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• Alcoholism and diabetes can both cause small-fiber, painful neuropathies
Diagnostic Approach
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• Autonomic involvement occurs in many small-fiber neuropathies but can also occur in Guillain-Barré syndrome and is sometimes life-threatening.
Diagnostic Approach
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• It is important to distinguish whether the neuropathy is axonal, demyelinating, or both.
• This differentiation is best achieved using nerve conduction studies (NCS) and electromyography (EMG).
Diagnostic Approach
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• Diabetes, HIV infection and alcoholism can cause several patterns of neuropathy.
• They most commonly cause a distal, symmetric axonal sensorimotor neuropathy.
• The second most common presentation in these conditions is a small-fiber, painful neuropathy.
Diagnostic Approach
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History
• The temporal course of a neuropathy varies, based on the etiology.
– With trauma or ischemic infarction, the onset will be acute, with the most severe symptoms at onset.
– Inflammatory and some metabolic neuropathies have a subacute course extending over days to weeks.
– A chronic course over weeks to months is the hallmark of most toxic and metabolic neuropathies.
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History
• A chronic, slowly progressive neuropathy over many years occurs with most hereditary neuropathies or with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).
• Neuropathies with a relapsing and remitting course include Guillain-Barré syndrome.
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• Ischemic neuropathies often have pain as a prominent feature.
• Small-fiber neuropathies often present with burning pain, lightning-like or lancinating pain, aching, or uncomfortable paresthesias (dysesthesias).
History
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• Dying-back (distal symmetric axonal) neuropathies initially involve the tips of the toes and progress proximally in a stocking-glove distribution.
History
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• Peripheral neuropathy can present as restless leg syndrome.
• Proximal involvement may result in difficulty climbing stairs, getting out of a chair, lifting and swallowing, and in dysarthria.
History
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• The clinical assessment should include:– careful past medical history, looking for
systemic diseases that can be associated with neuropathy, such as diabetes or hypothyroidism.
History
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• Many medications can cause a peripheral neuropathy, typically a distal symmetric axonal sensorimotor neuropathy.
• Detailed inquiries about drug and alcohol use, as well as exposure to heavy metals and solvents, should be pursued.
History
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• All patients should be questioned regarding – HIV risk factors– foreign travel (leprosy)– diet (nutrition)– vitamin use (especially B6) – possibility of a tick bite (Lyme disease)
History
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• The review of systems may provide clues regarding other organ involvement and the presence of an underlying malignancy.
History
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Differential Diagnosis of Neuropathies by Clinical
Course Acute onset (within days)
Subacute onset (weeks to months)
Chronic course/ insidious onset
Relapsing/ remitting course
Guillain-Barré syndrome
Maintained exposure to toxic agents/medications
Hereditary motor sensory neuropathies
Guillain-Barré syndrome
Acute intermittent porphyria
Persisting nutritional deficiency
Dominantly inherited sensory neuropathy
CIDP
Critical illness polyneuropathy
Abnormal metabolic state
CIDP HIV/AIDS
Diphtheric neuropathy
Paraneoplastic syndrome
Toxic
Thallium toxicity CIDP Porphyria
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Physical Examination
• A cranial nerve examination can provide evidence of mononeuropathies or proximal involvement.
• Funduscopic examination may show abnormalities such as optic pallor, which can be present in leukodystrophies and vitamin B12 deficiency.
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• Direct strength testing of muscles enervated by cranial nerves V, VII, IX/X, XI and XII is important, as mild bilateral weakness can be missed by observation only.
Physical Examination
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• The motor examination includes a search for fasciculations or cramps, or loss of muscle bulk.
• Tone is normal or reduced.
Physical Examination
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• The pattern of weakness helps narrow the diagnosis: symmetric or asymmetric, distal or proximal, and confined to a particular nerve, plexus or root level.
Physical Examination
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• Deep tendon reflexes are reduced or absent.
• A bilateral foot drop may result in a steppage gait in which the patient must lift the knees very high in order to clear the toes.
• Proximal weakness results in an inability to squat or to rise unassisted from a chair.
Physical Examination
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• The general physical examination can provide evidence of orthostatic hypotension without a compensatory rise in heart rate when autonomic fibers are involved.
Physical Examination
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• Respiratory rate and vital capacity should be evaluated in Guillain-Barré syndrome to assess for respiratory compromise.
• The presence of lymphadenopathy, hepatomegaly or splenomegaly, and skin lesions may provide evidence of systemic disease.
Physical Examination
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• Pale transverse bands in the nail beds, parallel to the lunula (Mees' lines), suggest arsenic poisoning.
Physical Examination
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Laboratory Evaluation
• EMG and nerve conduction studies (NCS) are often the most useful initial laboratory studies in the evaluation of a patient with peripheral neuropathy
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• They can confirm the presence of a neuropathy and provide information as to the type of fibers involved (motor, sensory, or both), the pathophysiology (axonal loss versus demyelination) and a symmetric versus asymmetric or multifocal pattern of involvement.
Laboratory Evaluation
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• The limitations of EMG/NCS should be taken into account when interpreting the findings. – There is no reliable means of studying proximal
sensory nerves. – NCS results can be normal in patients with small-fiber
neuropathies– Lower extremity sensory responses can be absent in
normal elderly patients.
• EMG/NCS are not substitutes for a good clinical examination.
Laboratory Evaluation
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• Subsequent studies should be tailored to the most likely diagnostic possibilities, and to the acuteness and severity of the neuropathy.
• With an acute progressive neuropathy, a neurologic consultation early in the course of the evaluation is essential.
• Further evaluation of these patients includes EMG/NCS, lumbar puncture, chest radiograph, electrocardiogram and determination of forced vital capacity.
Laboratory Evaluation
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• The most common presentation is that of a distal symmetric sensorimotor neuropathy.
• Initial evaluation should include:– fasting serum glucose, glycosylated hemoglobin,
blood urea nitrogen, creatinine, complete blood cell count, erythrocyte sedimentation rate, urinalysis, vitamin B12 and thyrotropin stimulating hormone levels.
– Neurologic assessment may be warranted if the initial evaluation does not produce a diagnosis.
Laboratory Evaluation
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• CSF is useful in evaluation of myelinopathies and polyradiculopathies.
• An elevated total protein level with < 5 wbc(albuminocytologic dissociation) is present in acquired inflammatory neuropathy (e.g., Guillain-Barré syndrome, CIDP).
Laboratory Evaluation
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• Other studies useful in specific clinical contexts are:– cytology (lymphoma) – special studies
• such as Lyme polymerase chain reaction and cytomegalovirus branched chain DNA (polyradiculopathy or mononeuritis multiplex in AIDS).
Laboratory Evaluation
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• Nerve biopsy is only helpful in very specific cases to diagnose vasculitis, leprosy, amyloid neuropathy, leukodystrophies, sarcoidosis and, occasionally, CIDP.
Laboratory Evaluation
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• It can be difficult to document a small-fiber neuropathy because the only abnormalities on neurologic examination may be loss of pinprick and temperature sensation in a distal distribution.
Laboratory Evaluation
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• EMG/NCS may be normal.
• Autonomic studies are only helpful if the autonomic fibers are involved.
• As a result, small-fiber neuropathy remains a primarily clinical diagnosis.
Laboratory Evaluation
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• The evaluation should include the most likely causes (i.e., diabetes, alcoholism, AIDS).
• If these studies are normal, a neurologic consultation is recommended.
Laboratory Evaluation
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Treatment
• The goal of treatment is to manage the underlying condition causing the neuropathy and repair damage, as well as provide symptom relief.
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Treatment
• Controlling a chronic condition may not eliminate the neuropathy, but it can play a key role in managing it.
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Treatment
• Neuropathic pain is often difficult to control.
• Medications :– OTC analgesics . – antiepileptic drugs, including gabapentin, phenytoin,
and carbamazepine– some classes of antidepressants, including tricyclics
such as amitriptyline. – Mexiletine– local anesthetics such as lidocaine or topical patches
containing lidocaine – Codeine/oxycodone
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• Mechanical aids can help reduce pain and lessen the impact of physical disability.
– Hand or foot braces can compensate for muscle weakness or alleviate nerve compression.
– Orthopedic shoes can improve gait disturbances and help prevent foot injuries in people with a loss of pain sensation.
• If breathing becomes severely impaired, mechanical ventilation can provide essential life support.
Treatment
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• Surgical intervention often can provide immediate relief from mononeuropathies caused by compression or entrapment injuries.
– Repair of a slipped disk can reduce pressure on nerves where they emerge from the spinal cord; the removal of benign or malignant tumors can also alleviate damaging pressure on nerves.
– Nerve entrapment often can be corrected by the surgical release of ligaments or tendons.
Treatment
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Questions ???