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Nutritional Neuropathy Clinical Presentation

  • Author: Jasvinder Chawla, MD, MBA; Chief Editor: Nicholas Lorenzo, MD, MHA, CPE  more...
 
Updated: Dec 28, 2015
 

History

Peripheral neuropathies due to nutritional deficiencies have few individually characteristic signs but can be differentiated by observing other symptoms of the patient's underlying systemic disease. Neuropathies mostly affect the long fibers first, starting in the feet and progressing upward. Once they have progressed to the calf, symptoms may appear in the hands. Cyanocobalamin (vitamin B12) deficiency occasionally manifests in the upper extremities.

Alcohol neuropathy

This disease is characterized by paresthesias (decreased pain and temperature sensation in a stocking-glove distribution), pain, and weakness, especially in the feet but extending proximally to the arms, causing difficulty in climbing stairs and walking.

Autonomic symptoms are less common than those listed above, but include GI dysmotility, urinary or fecal incontinence, and abnormal sweat patterns.

The neuropathy may be seen in conjunction with Wernicke encephalopathy (ie, ophthalmoplegia, ataxia, encephalopathy) or Korsakoff syndrome (ie, amnestic dementia).

Thiamine (vitamin B1) deficiency

Dry beriberi is characterized by severe burning dysesthesias (feet more than hands), weakness and wasting (distal more than proximal), trophic changes (shiny skin, hair loss), and acrodistal sensory loss in a graded fashion typical of dying-back polyneuropathies.

Some patients do not become symptomatic, possibly because they are absorbing thiamine produced by bacteria in the large intestine. However, one half become symptomatic by 7 weeks; by 15 weeks, axonal changes start to appear histologically.

The neuropathy begins with fatigue and loss of sensation, pain, and heaviness in the legs. Then, pretibial edema develops, along with glove-and-stocking paresthesias and difficulty with tasks such as climbing stairs and standing on one leg.

If the thiamine deficiency is long standing, muscles on the dorsum of the feet atrophy and paralysis can ensue.

Difficulty with talking or swallowing may also be noted.

Niacin (vitamin B3) deficiency

Pellagra is characterized by the 3 D s, which are (1) dermatitis, ie, hyperkeratotic skin lesions, particularly on hands, feet, face, and neck (sun-exposed regions); (2) diarrhea; and (3) dementia. In addition, patients may exhibit peripheral neuropathy and other CNS signs, such as depression, excitation, seizures, insomnia, dizziness, cog-wheeling of the extremities, tremor, loss of hearing, tingling fingers, muscle tenderness, and bilateral symmetric glove-and-stocking numbness.

Polyneuropathy is not always associated with pellagra and may be related to accompanying thiamine or pyridoxine deficiency. Therefore, it should be considered an accompanying rather than guiding symptom. It is characterized by acrodistal sensory excitation, the itching and burning in the hands, feet, and trunk, and it sometimes manifests as hydromania, or the compulsion to immerse oneself in cold water.

The dysesthesias progress proximally to the knees, thighs, and hips, after which weakness in the legs becomes manifest.

Paresis is rare, but bulbopontine symptoms can ensue, with abnormalities of the cranial nerves, especially the vestibular, acoustic, and ocular nerves (where symptoms manifest as optic atrophy or amblyopia), as well as seizures.

Eventually, the initial peripheral excitation, erythema, and GI distress progress to cerebral and spinal defects.

Finally, marasmus, cachexia, macrocytic anemia, and coma develop.

Pyridoxine (vitamin B 6) deficiency or excess

This deficiency must be suspected any time a sensory polyneuropathy occurs after hyperesthesia-causalgia syndrome.

First, bilateral numbness and tingling begin in the distal feet. This proceeds proximally up the feet and legs, occasionally appearing in the fingers and hands. Then pain becomes prevalent in these areas, and symptoms can include a burning sensation in the feet.

In rare cases, patients experience loss of power in the legs, in which sensory loss is greater than motor loss; the etiology is axonal loss.

One week after the removal of vitamin B6 from the diet, levels of xanthurenic acid increase and levels of pyridoxine decrease in the urine. At 3 weeks, EEG abnormalities manifest, and tonic-clonic seizures refractory to anticonvulsants may follow.

The 4 main symptoms and signs are as follows:

  • Cutaneous mucosal symptoms - Glossitis, conjunctivitis, cheilosis
  • CNS symptoms - Lethargy, decreased level of consciousness, anorexia, vomiting, seizures
  • Ascending sensory polyneuropathy
  • Anemia - Lymphopenia with eosinophilia

Neuropathy due to toxicity occurs 1 month to 3 years after the individual starts excessive consumption.

Cyanocobalamin (vitamin B12) deficiency

About 80% of all cases are due to pernicious anemia, and another 10% are due to achlorhydria. Exposure to nitrous oxide can suddenly precipitate the deficiency, which should be considered in any patient who develops postoperative paresthesias.

The disease predominantly affects the spinal cord; therefore, separating the painful sensory and sensorimotor paresthesias of the peripheral neuropathy from the symptoms of spinal cord involvement is difficult.

Presentations vary greatly among patients.

The symmetric glove-and-stocking paresthesias, or tingling in the distal aspect of the toes, numbness, coldness, a pins-and-needles feeling, and occasional feelings of swelling or constriction, are slowly progressive and insidious. Symptoms progress up the legs, occasionally affect the fingers, and culminate in weakness and spasticity.

In late stages, manifestations include moderate muscular wasting, optic atrophy, sphincter dysfunction, and mental disturbances. Examples of these disturbances are mild dementia (which is often the first symptom and clinically indistinguishable from other dementias), disorientation, depression, psychosis, and persecutory delusions.

The hematologic manifestation of anemia, if present, can cause weakness, light-headedness, vertigo, tinnitus, palpitations, angina, heart failure, cardiomegaly, pallor, tachycardia, and hepatosplenomegaly.

GI symptoms include a sore, beefy red tongue and anorexia.

If left untreated, the gait becomes ataxic, followed by paraplegia with spasticity and contractures.

The subacute combined degeneration that develops results in a severe myelopathy, involving posterior columns and lateral corticospinal tracts, with other manifestations including optic (retrobulbar) neuropathy[16] , sensorimotor polyneuropathy, and dementia.

Pantothenic acid deficiency

This manifests as painful burning paresthesias in the feet, ataxia, and hyperreflexia, followed by weakness, fatigue, apathy, and psychiatric disturbances 5-8 weeks later.

Alpha-tocopherol (vitamin E) deficiency

This syndrome resembles Friedreich ataxia. Symptoms include hyporeflexia progressing to areflexia, decreased proprioception and vibration sense with preserved pain and temperature senses, distal muscular weakness progressing to ataxia, dysphagia, and cardiac problems, and nyctalopia (night blindness). Nystagmus, ophthalmoplegia, and blindness, and dementia follow.

Symptoms vary with etiology. Patients with isolated vitamin E deficiency syndrome tend to present without the hyporeflexia, and deficiency from abetalipoproteinemia manifests as increased eye problems, in contrast with deficiency from cholestatic disease, which tends to spare the eye but causes increased psychiatric and behavioral problems.

Folate deficiency

The symptoms of folate deficiency are indistinguishable from those of cobalamin (vitamin B12) deficiency, though the dementia tends to be more prominent.

Hypophosphatemia

Invariably found in patients on total parenteral nutrition, this deficiency causes tingling paresthesias in the tongue, fingers, and toes but can progress to severe weakness and areflexia, sensory loss, and cranial neuropathies.

It can resemble Guillain-Barré syndrome.

Patients may have gluten sensitivity.

Neurologic manifestations can include ataxia, myoclonus, myopathy, myelopathy, dementia, and a peripheral neuropathy that can include sensorimotor axonal neuropathy, axonal motor and mononeuropathy multiplex.

Copper deficiency (usually following bariatric surgery) is commonly associated with myelopathy and spastic gait. Other features can include peripheral neuropathy, myeloneuropathy, optic neuropathy[17] , CNS demyelination, myopathy, myelo-opticoneuropathy, and motor neuron disease. Clinically and radiologically it can appear similar to B12 deficiency.[2]

Bariatric surgery

History is generally sufficient to establish the diagnosis. Three distinctive patterns are most common: sensory polyneuropathy, mononeuropathies, and radiculoplexopathy.

Sensory neuropathies tend to present with symmetrical numbness, burning, sharp pain, and tingling. Some also have distal motor weakness, commonly foot drop. Cramping, autonomic and bulbar symptoms, and involvement of trunk nerves may also occur.

Mononeuropathies are usually asymmetric and have been described in the radial, sensory radial, ulnar, greater occipital, and fibular nerves, as well as carpal tunnel syndrome, and meralgia paresthetica. The last 2 are the most common, and the carpal tunnel syndrome is usually symmetrical.

Radiculoplexopathies affect the cervical and lumbosacral regions, and are usually unilateral, causing pain and numbness followed by limb weakness but usually no autonomic or bulbar symptoms.

Multifactorial disease

This paresthesia-causalgia syndrome (ie, acrodynia or burning-foot syndrome) escalates from a mild paresthesia to painful burning and freezing sensations in the feet, prominent at night, relieved with exercise. This disease may mask sensory deficits, especially those on the soles of the feet.

Tobacco-alcohol amblyopia is a slowly progressive symmetrical visual field loss often described as a central haze or cloud. There is no pain, photopsia, or other positive symptoms, but loss of color vision (especially red) is more profound than the loss of visual acuity. It presents clinically as a characteristic retrobulbar optic neuropathy with slow evolution and a classical cecocentral scotoma with an appearance of "champagne cork" and red-green dyschromatopsia.[18]

Less common is mild-to-moderate unilateral or bilateral hearing loss with tinnitus or vertigo.

Hoarseness and other laryngeal symptoms are equally rare.

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Physical

Several physical findings can provide clues to the etiology of the nutritional neuropathy.

  • Mouth: Glossitis suggests cyanocobalamin (vitamin B 12 ) deficiency; glossitis and cheilosis suggest pyridoxine (vitamin B 6 ) deficiency; gingivitis, stomatitis, and glossitis, niacin (vitamin B 3 ) deficiency. See the image below.
    Pernicious anemia. Characteristic lemon-yellow–tin Pernicious anemia. Characteristic lemon-yellow–tinged pallor with raw-beef tongue lacking filiform papillae. Used with permission from Forbes and Jackson.
  • Skin: Nasolabial seborrhea suggests pyridoxine (vitamin B 6 ) deficiency; pellagrous skin rash, niacin (vitamin B 3 ) deficiency; and hyperpigmentation, cobalamin (vitamin B 12 ) deficiency.
  • Cardiovascular: CHF suggests thiamine (vitamin B 1 ) deficiency.
  • Hematologic: Megaloblastic anemia suggests a cobalamin (vitamin B 12 ) or folate deficiency. Hypochromic anemia is usually iron deficiency but also can represent a pyridoxine vitamin (B 6 ) deficiency.

Findings in specific syndromes include the following:

  • Alcohol neuropathy
    • This is characterized by decreased pain and temperature sensation in a stocking-glove distribution, distal muscle weakness and atrophy (legs worse than arms) with stasis pigmentation and plantar ulcerations, wrist and foot drop, hyporeflexia with absent Achilles reflex, and antalgic gait.
    • The skin may be dry and scaly with rhinophyma (alcohol nose).
    • Hepatomegaly, jaundice, or ascites may result from concurrent liver dysfunction.
    • Alcohol neuropathy frequently is associated with entrapment or pressure neuropathies, particularly ulnar and peroneal, which may be superimposed on the polyneuropathy.
    • Charcot joints and Wernicke-Korsakoff syndrome may also be present.
  • Thiamine (vitamin B 1 ) deficiency (beriberi)
    • About 70% of patients have a polyneuropathy; of those, 20% have only motor involvement; 50%, motor-sensory involvement; and 30%, only sensory involvement.
    • It is both subchronic and chronic; presentation includes paresthesias and numbness, fasciculations and cramps, followed by dorsiflexor weakness with a stepping gait. Finally, bilateral lower-extremity paraplegia develops.
    • In about 30% of patients, the neuropathy spreads to the proximal muscles of the pelvic girdle, to the trunk, and to the upper extremities.
    • The patellar and Achilles tendon reflexes are decreased.
    • Cranial nerve manifestations include retrobulbar optic neuropathy, hoarseness, dysphagia, and tachycardia from vagal involvement and even bilateral facial paralysis in some cases.
    • In rare cases, an acute paraplegic form results in anorexia and vomiting. In a day or two, rapidly progressive paralysis ascends from legs to arms and shoulder girdle. Death from cardiac insufficiency follows within 2 days.
  • Niacin (vitamin B 3 ) deficiency
    • Patients present with decreased proprioception and vibratory sense, weakness in legs with some fasciculations and cramping, Babinski reflexes equivocal or positive.
    • Paresis is rare, deep tendon reflexes are decreased in 10-20% but increased in most.
    • Simultaneous psychiatric disorders, extrapyramidal symptoms, cranial nerve dysfunctions, and seizures ultimately result.
  • Pyridoxine (vitamin B 6 ) deficiency
    • The presentation includes seborrheic dermatitis, cheilosis, glossitis, nausea, vomiting, weakness, and dizziness.
    • Neurologic examination shows decreased proprioception and vibration sense with spared pain and temperature sensations; normal strength; decreased or absent Achilles reflex and decreased patellar reflex.
    • Ataxia, if present, is sensory.
  • Pyridoxine toxicity
    • Pyridoxine toxicity can also cause a neuropathy.
    • Acute high-dose (180 g) intoxication causes a sensory neuronopathy. Clinical manifestations include diffuse paresthesias, proximal and distal sensory loss, sensory ataxia, and autonomic dysfunction. Recovery tends to be poor.
    • Long-term low dosages (0.2-10 g/d) cause a milder distal sensory neuropathy, which presents with distal paresthesias and numbness.
    • Recovery is usually good after pyridoxine is stopped.
  • Folate deficiency: Patients present with subacute combined degeneration, sensorimotor polyneuropathy, and dementia.
  • Cyanocobalamin (vitamin B 12 ) deficiency: The presentation includes a number of neurologic findings.
    • Corticospinal tract abnormalities include spasticity. About 50% of patients lack an Achilles reflex, some have no patellar reflex, some have a bilateral positive Babinski sign, and hyperreflexia is rare.
    • Posterior column abnormalities - Decreased vibration, temperature, and proprioception senses (lower extremities); sensory ataxia; positive Romberg sign in later stages
    • Peripheral neuropathy - Moderately severe to severe, with muscular atrophy and weakness in later stages
    • Behavioral and personality changes, particularly depression
  • Nutritional amblyopia: Patients present with decreased visual acuity and sometimes bilateral field defects with central or cecocentral scotomas. Early on, the optic discs show no change or papillitis on funduscopic examination. Later, the discs become pallid. Pain is not a symptom; its presence should prompt the consideration of other diagnoses. See the image below.
    Ischemic retinopathy caused by severe megaloblasti Ischemic retinopathy caused by severe megaloblastic anemia.
  • Nutritional sensorineural deafness: The presentation includes mild-to-moderate unilateral or bilateral hearing loss.
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Causes

See the list below:

  • Thiamine (vitamin B 1) deficiency
    • Malabsorption from pyloric stenosis, gastroenterostomy, ulcerative colitis, dysentery, steatorrhea, gastritis, pancreatitis, or prolonged diarrhea
    • Leigh disease (subacute necrotizing encephalomyelopathy)
    • Thiamine-responsive acidosis
    • Abnormal pyruvate dehydrogenase
    • Decreased dietary intake as in alcohol dependence
    • Nothing by mouth (NPO) status when patients receive intravenous fluids without thiamine supplementation
    • Hyperemesis of pregnancy
    • Acute postgastric reduction surgery[19]
    • Dialysis
    • Refeeding syndrome
    • Chastek paralysis from ingestion of raw fish containing thiaminidases
    • Infection with Bacillus thiaminolyticus
  • Niacin (vitamin B 3) deficiency
    • Inadequate intake (eaters of a predominantly maize diet, pregnant or lactating women whose requirements have increased, those who are alcohol dependent and have poor nutrition)
    • Hartnup disease
    • Malabsorption syndromes
  • Pyridoxine (vitamin B 6) deficiency
    • Deficient infant formula
    • Deficient intake (usually due to preferential ethanol ingestion)
    • Increased metabolic demands as in pregnancy, febrile states, and after abdominal surgery
    • Malabsorption
    • Medications, such as isoniazid (the most likely etiology), hydralazine, cycloserine, penicillamine, desoxypyridoxine, and oral contraceptives
    • Rare genetic disorders, such as pyridoxine dependency, which is evident within a few days of birth
  • Cyanocobalamin (vitamin B 12) deficiency
    • Pernicious anemia
    • Gastrectomy or gastric mucosa atrophy
    • Chronic pancreatitis (40% manifest deficiency, as cyanocobalamin binds proteins other than intrinsic factor that are not being broken down by pancreatic proteases)
    • Distal ileal disease (inflammatory bowel syndrome or neoplasm)
    • Infections (eg, tropical sprue, regional enteritis, Diphyllobothrium latum tapeworm, blind-loop syndrome)
    • Congenital malabsorption (Imerslund-Grãbeck disease)
  • Pantothenic acid: A primary deficiency almost never occurs; therefore, symptoms must be presumed to be from secondary deficiency
  • Alpha-tocopherol (vitamin E)
    • Malabsorption syndromes, such as (1) Crohn disease, (2) Bassen-Kornzweig disease (abetalipoproteinemia), (3) pancreatic dysfunction (cystic fibrosis), (4) vitamin E transporter deficiency, and (5) chronic cholestatic hepatobiliary disease (eg, idiopathic neonatal hepatitis, familial cholestatic syndromes, intrahepatic bile duct disease, extrahepatic biliary atresia)
    • Short-bowel syndrome
    • Total parenteral nutrition
    • Other malabsorption syndromes
  • Folic acid deficiency
    • Poor intake (eg, alcohol dependence, pregnancy)
    • Malabsorption syndromes
    • Medications (particularly phenytoin)
  • Bariatric surgery
    • The most frequent deficiencies appear to be iron, B1, folate, vitamin D, and calcium.
    • Delayed (>2 years after surgery) deficiency of copper has also been reported.
  • Nutritional optic neuropathy [16]
  • Tobacco and alcohol
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Contributor Information and Disclosures
Author

Jasvinder Chawla, MD, MBA Chief of Neurology, Hines Veterans Affairs Hospital; Professor of Neurology, Loyola University Medical Center

Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Glenn Lopate, MD Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University School of Medicine; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital

Glenn Lopate, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American Academy of Neurology

Disclosure: Nothing to disclose.

Additional Contributors

Milind J Kothari, DO Professor, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Penn State Milton S Hershey Medical Center

Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Lawrence D Recht, MD Professor of Neurology and Neurosurgery, Department of Neurology and Clinical Neurosciences, Stanford University Medical School

Lawrence D Recht, MD is a member of the following medical societies: American Academy of Neurology, American Association for Cancer Research, American Neurological Association, and Society for Neuroscience

Disclosure: Nothing to disclose.

R Andrew Sewell, MD Associate Research Scientist in Psychiatry and Mental Illness Research, Education,Veterans Affairs Connecticut Health Care System, Yale University School of Medicine

R Andrew Sewell, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, American Pain Society, and American Psychiatric Association

Disclosure: Nothing to disclose.

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Pernicious anemia. Characteristic lemon-yellow–tinged pallor with raw-beef tongue lacking filiform papillae. Used with permission from Forbes and Jackson.
Ischemic retinopathy caused by severe megaloblastic anemia.
 
 
 
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