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Peripheral Neuropathy guidelines

most of neuropathy is really CIDP.

Part-1

Part-2

Table 10. Tests to Consider for Patients with Suspected Peripheral Neuropathy
Test	Indications	Interpretation
Laboratory
CBC, erythrocyte sedimentation rate	Conduct in most patients	Commonly abnormal in systemic disease. Erythroblastic anemia suggests vitamin B₁₂ or folate deficiency; erythrocyte stippling suggests lead toxicity.
Blood sugar, hemoglobin A_1C	Suspected diabetic PN Undiagnosed PN	Symptoms of neuropathy may be the first presentation of diabetes mellitus
Blood chemistry battery (e.g., SMA 20)	Conduct in most patients	Detects renal insufficiency and other metabolic disorders
Vitamin B₁₂ levels	Conduct in most patients Suspected nutritional PN	CNS and posterior-column manifestations may obscure PN; folate treatment normalizes CBC, but does not prevent progressive neurologic injury
Serum protein electrophoresis	Conduct in most patients	If a paraprotein is identified, request a bone survey and consider bone biopsy to rule out multiple myeloma or osteosclerotic myeloma.
Serum creatinine kinase (CK)	Suspected motor-neuron disease (MND)	Moderate CK elevation is often supportive of MND diagnosis [6]
Serologic testing for syphilis, HIV, Lyme disease; tuberculin skin test; antinuclear antibodies; urine tests for aminolevulinic acid, porphobilinogen; urine immunoelectrophoresis; 24-hr urine test for heavy metals (Pb, TI, As)	In selected patients with suggestive clinical indications	Yield is very low in the absence of specific clinical indications
Cerebral spinal fluid examination	May be particularly helpful in patients with predominant sensory neuropathy, with or without corticospinal findings, and in paraneoplastic neuropathies [5]	CSF protein will be elevated in >90% of patients with acute and chronic inflammatory demyelinating polyneuropathy; it is also frequently elevated in paraneoplastic sensory neuropathy [21]. Elevated total protein with <5 cells/mm³ suggest Gullain-Barré syndrome or chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).
Radiologic
MRI	Suspected nerve compression (e.g., carpal tunnel syndrome)	Used primarily to confirm peripheral-nerve entrapments/compressions or root disease
Invasive
Nerve biopsy	Considered when there is a specific diagnosis in mind or when no etiology is evident from serologic and electrodiagnostic tests	Diagnostic abnormalities present in [2]: Vasculitis Amyloidosis Sarcoidosis Leprosy Hereditary neuropathy with liability to pressure palsies Giant axonal neuropathy Metachromatic leukodystrophy Paraproteinemic neuropathy Tumor infiltration
Based on Bosch [2], Logigian [5], Barohn [6].

Table 11. Electrodiagnostic Studies: Key Measurements
Study	Key measurement	Nerves measured	Important parameters
Motor conduction	Compound muscle action potential (CMAP)	Ulnar Median Peroneal Posterior tibial	Latency Amplitude Conduction velocity F wave H reflex
Sensory conduction	Sensory-nerve action potential (SNAP)	Ulnar Median Radial Sural	Latency Amplitude
Needle electromyography	Configuration and size of individual motor unit potentials	Not relevant	Spontaneous activity Firing pattern

Table 12. Electrodiagnostic Studies: Terminology
Parameter	Definition
Amplitude	In motor-conduction studies: height in millivolts of CMAP from baseline to peak, i.e., number of muscle fibers activated by stimulus at a particular site In sensory-conduction studies: height in microvolts of SNAP from baseline to peak
CMAP	Summation of all muscle-fiber action potentials activated by motor nerve stimulation
Conduction velocity	Speed in meters per second of nerve impulse conduction
F wave	Assesses conduction along the proximal portion of the motor nerve; most commonly used in evaluating demyelinating neuropathies
Firing pattern	The number, size, and shape of motor units that initially fire and then recruit other motor units to fire, following voluntary muscle contraction
H reflex	Analogous to the ankle-jerk reflex but reflex is stimulated by a submaximal electrical current that selectively activates IA afferent sensory fibers (to cause a motor reflex)
Latency	In motor-conduction studies: time in milliseconds for conduction of a stimulus along the length of the nerve, transmission of the neurotransmitter-mediated signal across the neuromuscular junction, and depolarization of the muscle-fiber membrane In sensory-conduction studies: conduction time of the fastest-conducting fibers along a given segment
SNAP	Summation of individual action potentials of all the fibers activated
Spontaneous activity	Measures endplate muscle activity when a needle is placed near the neuromuscular junction (including spontaneous discharges - i.e., fibrillations and fasciculations - of muscle activity at rest)
CMAP, compound muscle action potential; SNAP, sensory nerve action potential.
Based on Raynor [3], Lynn and Mendell [11].

Table 13. Electrophysiologic Findings of Axonal vs. Demyelinating Peripheral Neuropathies
Study	Axonal degeneration	Segmental demyelination
Motor-nerve conduction studies
CMAP^a amplitude	Decreased	Normal^b
Distal latency	Normal	Prolonged
Conduction velocity	Normal	Slow
Conduction block	Absent	Present
Temporal dispersion	Absent	Present
F wave	Normal	Prolonged or absent
H reflex	Normal	Prolonged or absent
Sensory-nerve conduction studies
SNAP amplitude Distal latency Conduction velocity	Decreased Normal Normal	Normal Prolonged Slow
Needle electromyography (spontaneous activity)
Fibrillations	Present	Absent
Fasciculations	Present	Absent
Recruitment
Number of motor units	Decreased	Decreased
^a Compound motor action potential. ^b Except with conduction block.
Reprinted with permission from Barohn R: Approach to peripheral neuropathy and neuronopathy. Semin Neurol. 1998;18(1):7-18.

Table 14. Categorical Classification of Selected Peripheral Neuropathies
Axonal	Demyelinating
Mononeuropathies
Diabetes	Entrapments
Generalized neuropathies
Diabetes Alcohol Carcinoma Vitamin deficiencies Toxic/metabolic neuropathies [Table 6], including heavy metals, industrial solvents and hydrocarbons, and medications Hereditary peroneal muscular atrophy Familial amyloidosis Porphyria Whipples disease Leprosy	Guillain-Barré syndrome Leprosy Hereditary peroneal muscular atrophy/Dejerine-Sottas disease Diphtheria Chronic inflammatory demyelinating polyneuropathy (CIDP) Toxic neuropathies

Table 3. Distribution of Neuropathies by Age and in General Population
Subcategory^a	Age <49	Age >50	Overall population
Mononeuropathy
	35%	50%	30%
Generalized neuropathies
Toxic/metabolic	60%	55%	69%^a
Hereditary	5%	<1%	30%^a
Malignancy	2%	10%	5%
Idiopathic	8%	5%	5%
^a Categories coexist in up to one-third of cases.

Table 4. Age-Related Changes in the Peripheral Nervous System
Type	Changes
Clinical	Decreased vibratory sense Decreased threshold response to tactile stimuli, but normal threshold response to pain No change in position sense Decreased muscle bulk and strength
Histologic	Reduction in number of nerve fibers Preferential loss of large-diameter fibers Reduction in muscle-fiber size Decline in number of motor units (distal muscles) Evidence of denervation and reinnervation with advancing age
Physiologic	Decline in motor- and sensory-nerve conduction velocity (MCV) Decreased amplitude in sensory-nerve action potential (SNAP) Increased amplitude and duration of voluntary motor units suggesting denervation and reinnervation

Table 5. Signs and Symptoms of Peripheral-Nerve Disorders
System	Positive	Negative
Motor^a	Cramps Fasciculations Myokymia (quivering) Restless legs Tightness	Weakness Fatigability Hypotonia Areflexia Deformities (pes cavus, claw hand)
Sensory (large fiber)^b	Paresthesias Tingling	Loss of vibration sense Loss of joint position sense Areflexia Sensory ataxia (positive Romberg test) Hypotonia
Sensory (small fiber)^c	Burning, jabbing pain (dysesthesias)	Loss of pain sense Loss of temperature sense
Autonomic^d	Hyperhidrosis Excess saliva	Orthostasis Erectile dysfunction Bowel and/or bladder dysfunction Anhidrosis
^a All motor fibers are large fibers. ^b Mediate vibration, proprioception, touch. ^c Mediate pain, temperature sensations. ^d All autonomic fibers are small fibers.

Table 6. Drugs and Toxins Causing Peripheral Neuropathy
Drug	Special features
Antibiotics
Chloramphenicol	Distal, primarily sensory neuropathy, optic neuritis during prolonged high-dose use
Dapsone	Predominantly motor neuropathy
Dideoxycytidine, dideoxyinosine, Dideoxythmidine	Painful sensory neuropathy
Ethambutol	Optic neuritis
Isoniazid	Distal axonal neuropathy, paresthesiae are prominent. Prevented by vitamin B₆
Metronidazole	Distal sensory neuropathy
Nitrofurantoin	Distal sensorimotor neuropathy; occurs in renal failure
Suramin	Distal sensorimotor and demyelinating neuropathy
Antineoplastics
Cisplatin	Sensory ataxia
Cytarabine	Sensorimotor neuropathy; rare
Misonidazole	Painful sensory neuropathy
Procarbazine	Distal paresthesias
Paclitaxel	Distal sensorimotor neuropathy
Vinca alkaloids: vincristine, vinblastine, vindesine, vinorelbine	Distal sensorimotor neuropathy
Antirheumatics
Chloroquine	Neuromyopathy
Chlochicine	Mild sensory neuropathy, myopathy
Organic gold	Demyelinating sensorimotor neuropathy
Penicillamine	Demyelinating sensorimotor neuropathy
Other pharmaceuticals
Amiodarone	Mild sensorimotor neuropathy
Disulfiram	Distal sensorimotor neuropathy
Ergots	Distal paresthesiae and dysesthesiae
FK 506	Axonal neuropathy
Hydralazine	Prevented by vitamin B₆
Nitrous oxide	Associated with myelopathy
Perhexiline	Demyelinating neuropathy
Phenytoin	Mild distal sensory loss
Procainamide	Demyelinating neuropathy; rare
Pyridoxine	Sensory ataxia
Thalidomide	Painful axonal neuropathy, primarily sensory
L-Tryptophan	Associated eosinophilia, fasciitis
Nonpharmaceutical toxic agents
Acrylamide	Excessive sweating
Allyl chloride	Distal numbness
Arsenic	Elevated hair, urine, and fingernail levels
Buckthorn	Motor neuron syndrome causing bulbar and limb paralysis
Cadmium	Sensory neuronopathy
Propionitriles (e.g., dimethylaminopropionitrile)	Urinary hesitancy, sexual dysfunction
Ethylene oxide	Associated cognitive impairment
Hexacarbons (n-hexane, methyl n-butyl ketone)	Distal axonopathy
Lead	Predominantly motor; associated anemia
Mercury	Associated central nervous system manifestations
Methyl bromide	Calf-muscle tenderness
Organophosphorus esters	Diarrhea, sweating, fasciculations
Polychlorinated biphenyls	Acne, brown-pigmented nails
Thallium	Gastrointestinal symptoms, delayed alopecia
Trichlorethylene	Facial numbness
Vacor	Acute diabetes mellitus
Based on Lynn and Mendell [11].

Table 7. Key Findings from History and Physical Examination: Pattern Recognition for Generalized Neuropathies
Pattern	Classification/possible diagnoses	Comments
Symmetric proximal and distal weakness with sensory loss	Inflammatory demyelinating polyneuropathy Guillain-Barré syndrome (GBS) Chronic inflammatory demyelinating polyneuropathy	Patient complaints include: difficulty raising arms to brush teeth and comb hair, problems climbing stairs, difficulty rising from a seated position, sensory loss, and sensory ataxia
Symmetric distal weakness with sensory loss	Metabolic disorders (e.g., amyloidosis, diabetes, Sjögrens syndrome) Drugs (amitriptyline, chloroquine, dapsone) and toxins Hereditary neuropathies (Charcot-Marie-Tooth disease, amyloidosis)	Underlying conditions may be axonal or demyelinating; therefore, laboratory investigations (e.g., fasting blood sugar, hemoglobin A_1C, vitamin B₁₂ levels, molecular genetic blood tests) are recommended based on initial suspicions
Asymmetric distal weakness with sensory loss	Vasculitis Hereditary neuropathy with predisposition to pressure palsies Infectious diseases (leprosy, Lyme, HIV) Sarcoidosis Compression and entrapment neuropathies	Vasculitis is the most common diagnosis when multiple nerves not normally subject to compression are involved. Compressive mononeuropathy, radiculopathy should be considered with single nerve/region involvement.
Asymmetric distal weakness without sensory loss	Upper-motor-neuron disease Generalized: multifocal motor neuropathy (MMP)	Bulbar findings (i.e., slurred or nasal speech, drooling, nasal regurgitation of liquids, difficulty whistling, swallowing), fasciculations,and hyperreflexia suggest upper-motor-neuron disease, and are rare with MMP
Asymmetric proximal and distal weakness with sensory loss	Polyradiculopathy Plexopathy (brachial or lumbar) Meningeal carcinomatosis or lymphomatosis	In diabetic plexopathy, pain typically precedes weakness
Symmetric sensory loss without weakness	Cryptogenic sensory polyneuropathy (CSPN) Metabolic derangements (diabetes, alcohol), drugs, toxins	CSPN is primarily observed in older adults. Diabetic and alcoholic neuropathies may present with few or no motor signs.
Asymmetric proprioceptive sensory loss without weakness	Sensory neuropathy (ganglionopathy) Paraneoplastic syndrome Sjögrens syndrome Idiopathic sensory neuropathy Drug (e.g., cisplatin and its analogues) or vitamin B₆ toxicity HIV sensory neuropathy	Primarily affects large fibers. May warrant a cancer workup.
Autonomic symptoms	Generalized - diseases affecting small fibers: e.g., acute dysautonomia, familial/ primary amyloidosis, GBS, diabetes, Chagas disease, porphyria, HIV-related autonomic neuropathy, idiopathic pandysautonomia	Typically associated with other types of neuropathy. Conduct autonomic testing (e.g., Valsalva heart rate response to pressure changes). May be an early or sole presentation of alcoholic or diabetic neuropathy.
Based on Barohn [6], Kowalske [13].

Table 8. Assessment of Muscle-Group Weakness
Symptoms	Likely source of weakness
Slurred/nasal speech Drooling Nasal regurgitation of liquids Difficulty whistling, smiling Difficulty swallowing, weight loss	Bulbar muscles
Diplopia Ptosis	Extraocular muscles
Trouble reaching Difficulty holding razor, comb, hair dryer Difficulty placing things in high cabinets	Proximal upper-extremity muscles
Difficulty opening jars, doors, using keys, silverware Trouble buttoning clothing	Distal upper-extremity muscles
Trouble rising from chairs, sofas Trouble getting out of car, bath, or off toilet Difficulty climbing stairs	Proximal lower-extremity muscles
Tripping Sprained ankles	Distal lower-extremity muscles

Table 9. Principal Motor Innervation of Peripheral Nerves: Localizing Muscle Weakness
Nerves	Muscles	Action
Axillary	Deltoid	Shoulder abduction
Musculocutaneous	Biceps, brachialis	Flexion of elbow
Median	Flexor carpi radialis	Radial flexion of wrist
	Flexor digitorum sublimis	Flexion of middle phalanges (digiti II-V)
	Flexor digitorum profundus (lateral half)	Flexion of distal phalanges (digiti II, III)
	Pronator teres, pronator quadratus	Pronation of forearm
	Abductor pollicis brevis	Abduction of thumb
	Opponens pollicis brevis	Opposition of thumb
	Flexor pollicis longus	Flexion of distal phalanx of thumb
	Flexor pollicis brevis	Flexion of proximal phalanx of thumb
Ulnar	Flexor carpi ulnaris	Ulnar flexion of wrist
	Flexor digitorum profundus (medial half)	Flexion of distal phalanges (digiti IV, V)
	Abductor digiti minimi	Abduction of digiti V
	All other intrinsics of hand	Finger abduction/adduction
Radial	Triceps	Extension at elbow
	Brachioradialis	Flexion of forearm
	Extensor carpi radialis/ulnaris	Extension at wrist with radial/ulnar deviation
	Supinator	Supination of forearm
	Extensor pollicis brevis	Extension of thumb (proximal)
	Extensor pollicis longus	Extension of thumb (distal)
	Extensor indicis proprius	Extension of index (proximal)
	Extensor digiti V proprius	Extension of little finger (proximal)
	Extensor digiti communis	Extension of digits (II-V, proximal)
Femoral	Iliopsoas	Flexion of thigh at hip
Femoral	Quadriceps	Extension of leg at knee
Obturator	Adductor longus, adductor brevis, adductor magnus	Adduction of thigh at hip
Superior gluteal	Gluteus medius, gluteus minimus, gluteus maximus	Abduction of thigh at hip
Sciatic	Biceps femoris, semitendinosus, semimembranosus	Flexion of leg at knee
Sciatic branches: fibular (deep)	Tibialis anterior	Dorsiflexion of foot
	Extensor digitorum longus	Extension of toes
	Extensor hallucis longus	Extension of great toe
Sciatic branches: fibular (superficial)	Peroneus	Everts foot
Tibial	Gastrocnemius, soleus	Plantar flexion of foot
	Flexor digitorum longus	Flexion of distal phalanges (II-IV)
	Flexor hallucis longus	Flexion of distal phalanges (I)
	Flexor digitorum brevis	Flexion of middle phalanges (II-V)
	Flexor hallucis brevis	Flexion of middle phalanges (I)
Pudendal	Perineal and sphincters	Closure of sphincters, contraction of pelvic floor
From Ronthal [14].

Table 7. Key Findings from History and Physical Examination: Pattern Recognition for Generalized Neuropathies
Pattern	Classification/possible diagnoses	Comments
Symmetric proximal and distal weakness with sensory loss	Inflammatory demyelinating polyneuropathy Guillain-Barré syndrome (GBS) Chronic inflammatory demyelinating polyneuropathy	Patient complaints include: difficulty raising arms to brush teeth and comb hair, problems climbing stairs, difficulty rising from a seated position, sensory loss, and sensory ataxia
Symmetric distal weakness with sensory loss	Metabolic disorders (e.g., amyloidosis, diabetes, Sjögrens syndrome) Drugs (amitriptyline, chloroquine, dapsone) and toxins Hereditary neuropathies (Charcot-Marie-Tooth disease, amyloidosis)	Underlying conditions may be axonal or demyelinating; therefore, laboratory investigations (e.g., fasting blood sugar, hemoglobin A_1C, vitamin B₁₂ levels, molecular genetic blood tests) are recommended based on initial suspicions
Asymmetric distal weakness with sensory loss	Vasculitis Hereditary neuropathy with predisposition to pressure palsies Infectious diseases (leprosy, Lyme, HIV) Sarcoidosis Compression and entrapment neuropathies	Vasculitis is the most common diagnosis when multiple nerves not normally subject to compression are involved. Compressive mononeuropathy, radiculopathy should be considered with single nerve/region involvement.
Asymmetric distal weakness without sensory loss	Upper-motor-neuron disease Generalized: multifocal motor neuropathy (MMP)	Bulbar findings (i.e., slurred or nasal speech, drooling, nasal regurgitation of liquids, difficulty whistling, swallowing), fasciculations,and hyperreflexia suggest upper-motor-neuron disease, and are rare with MMP
Asymmetric proximal and distal weakness with sensory loss	Polyradiculopathy Plexopathy (brachial or lumbar) Meningeal carcinomatosis or lymphomatosis	In diabetic plexopathy, pain typically precedes weakness
Symmetric sensory loss without weakness	Cryptogenic sensory polyneuropathy (CSPN) Metabolic derangements (diabetes, alcohol), drugs, toxins	CSPN is primarily observed in older adults. Diabetic and alcoholic neuropathies may present with few or no motor signs.
Asymmetric proprioceptive sensory loss without weakness	Sensory neuropathy (ganglionopathy) Paraneoplastic syndrome Sjögrens syndrome Idiopathic sensory neuropathy Drug (e.g., cisplatin and its analogues) or vitamin B₆ toxicity HIV sensory neuropathy	Primarily affects large fibers. May warrant a cancer workup.
Autonomic symptoms	Generalized - diseases affecting small fibers: e.g., acute dysautonomia, familial/ primary amyloidosis, GBS, diabetes, Chagas disease, porphyria, HIV-related autonomic neuropathy, idiopathic pandysautonomia	Typically associated with other types of neuropathy. Conduct autonomic testing (e.g., Valsalva heart rate response to pressure changes). May be an early or sole presentation of alcoholic or diabetic neuropathy.
Based on Barohn [6], Kowalske [13].

Table 16. Management of Neuropathic Pain
Symptom	Treatment
Mild neuropathic pain	Simple non-narcotic analgesics such as nonsteroidal anti-inflammatory agents or tramadol hydrochloride up to 50 mg PO t.i.d. may be helpful for all types of pain
Diffuse, poorly localized pain	Amitriptyline, 10-150 mg/day, in gradually increasing dosages (contraindicated in heart block, urinary tract obstruction, or narrow-angle glaucoma) If orthostatic hypotension is problematic: Other tricyclic depressants, including nortriptyline
Sharp, well-localized pain	Carbamazepine: initial dose, 100 mg b.i.d.; gradually increasing to 400-1,200 mg/day as tolerated If carbamazepine is not tolerated: Phenytoin, in gradually increasing doses beginning with 300 mg/day Gabapentin, beginning with 100-300 mg/day and titrating up to 600 mg t.i.d. or more Capsaicin, 0.075% topical ointment, applied q.i.d. For both diffuse and sharp pains: Mexiletine, up to 10 mg/kg/day
Lancinating pains	Clonazepam, 0.5-10.0 mg/day
Nocturnal leg pain, cramping	Clonidine, 0.1-0.5 mg q.h.s., quinine sulfate 200-400mg at bedtime
b.i.d., twice daily; q.h.s., before bedtime; q.i.d., 4 times a day; PO, orally; t.i.d., 3 times a day.
Modified from Lynn and Mendell [11].