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Clinicopathologic features of folate-deficiency neuropathy.
Neurology. 2015 Mar 10; 84(10):1026-33.Neur

Abstract

OBJECTIVE

The clinical significance and characteristics of neuropathy caused by folate deficiency remain to be established.

METHODS

We examined the clinicopathologic features of 18 consecutive patients with neuropathy caused by folate deficiency who presented with low serum folate levels but normal blood thiamine and serum cobalamin levels in the absence of chronic alcoholism.

RESULTS

Symptoms were relatively uniform, characterized by slowly progressive polyneuropathy with predominant involvement of the lower extremities, with a tendency to manifest as sensory rather than motor neuropathy and predominant deep rather than superficial sensory loss. The electrophysiologic features were consistent with axonal neuropathy. The histopathologic features of sural nerve biopsy specimens indicated large fiber-predominant axonal loss without segmental demyelination. Although macrocytosis was found in 7 patients, only 3 patients exhibited hemoglobin levels less than 10 g/dL. During the same study period, we found 12 patients who had low blood thiamine levels but normal serum folate and cobalamin levels without chronic alcoholism. Compared with patients who had thiamine-deficiency neuropathy, patients with a folate deficiency showed significantly slower progression (p < 0.01), a tendency to manifest sensory neuropathy (p < 0.05), predominant deep sensory loss (p < 0.01), and preservation of biceps tendon reflexes (p < 0.05).

CONCLUSIONS

Folate-deficiency neuropathy was characterized by a slowly progressive and sensory-dominant pattern, which was different from thiamine-deficiency neuropathy (i.e., beriberi neuropathy). This study demonstrates the importance of folate deficiency in the differential diagnosis of neuropathy, particularly in countries where folic acid fortification has not yet been practiced.

Authors+Show Affiliations

From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan. koike-haruki@med.nagoya-u.ac.jp sobueg@med.nagoya-u.ac.jp.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan.From the Department of Neurology (H.K., M.T., K.O., R.H., Y.K., M.I., M.K., G.S.), Nagoya University Graduate School of Medicine; and Department of Neurology and Stroke Medicine (H.D., F.T.), Yokohama City University Graduate School of Medicine, Japan. koike-haruki@med.nagoya-u.ac.jp sobueg@med.nagoya-u.ac.jp.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25663227

Citation

Koike, Haruki, et al. "Clinicopathologic Features of Folate-deficiency Neuropathy." Neurology, vol. 84, no. 10, 2015, pp. 1026-33.
Koike H, Takahashi M, Ohyama K, et al. Clinicopathologic features of folate-deficiency neuropathy. Neurology. 2015;84(10):1026-33.
Koike, H., Takahashi, M., Ohyama, K., Hashimoto, R., Kawagashira, Y., Iijima, M., Katsuno, M., Doi, H., Tanaka, F., & Sobue, G. (2015). Clinicopathologic features of folate-deficiency neuropathy. Neurology, 84(10), 1026-33. https://doi.org/10.1212/WNL.0000000000001343
Koike H, et al. Clinicopathologic Features of Folate-deficiency Neuropathy. Neurology. 2015 Mar 10;84(10):1026-33. PubMed PMID: 25663227.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Clinicopathologic features of folate-deficiency neuropathy. AU - Koike,Haruki, AU - Takahashi,Mie, AU - Ohyama,Ken, AU - Hashimoto,Rina, AU - Kawagashira,Yuichi, AU - Iijima,Masahiro, AU - Katsuno,Masahisa, AU - Doi,Hiroshi, AU - Tanaka,Fumiaki, AU - Sobue,Gen, Y1 - 2015/02/06/ PY - 2015/2/10/entrez PY - 2015/2/11/pubmed PY - 2015/5/15/medline SP - 1026 EP - 33 JF - Neurology JO - Neurology VL - 84 IS - 10 N2 - OBJECTIVE: The clinical significance and characteristics of neuropathy caused by folate deficiency remain to be established. METHODS: We examined the clinicopathologic features of 18 consecutive patients with neuropathy caused by folate deficiency who presented with low serum folate levels but normal blood thiamine and serum cobalamin levels in the absence of chronic alcoholism. RESULTS: Symptoms were relatively uniform, characterized by slowly progressive polyneuropathy with predominant involvement of the lower extremities, with a tendency to manifest as sensory rather than motor neuropathy and predominant deep rather than superficial sensory loss. The electrophysiologic features were consistent with axonal neuropathy. The histopathologic features of sural nerve biopsy specimens indicated large fiber-predominant axonal loss without segmental demyelination. Although macrocytosis was found in 7 patients, only 3 patients exhibited hemoglobin levels less than 10 g/dL. During the same study period, we found 12 patients who had low blood thiamine levels but normal serum folate and cobalamin levels without chronic alcoholism. Compared with patients who had thiamine-deficiency neuropathy, patients with a folate deficiency showed significantly slower progression (p < 0.01), a tendency to manifest sensory neuropathy (p < 0.05), predominant deep sensory loss (p < 0.01), and preservation of biceps tendon reflexes (p < 0.05). CONCLUSIONS: Folate-deficiency neuropathy was characterized by a slowly progressive and sensory-dominant pattern, which was different from thiamine-deficiency neuropathy (i.e., beriberi neuropathy). This study demonstrates the importance of folate deficiency in the differential diagnosis of neuropathy, particularly in countries where folic acid fortification has not yet been practiced. SN - 1526-632X UR - https://www.unboundmedicine.com/medline/citation/25663227/Clinicopathologic_features_of_folate_deficiency_neuropathy_ L2 - http://www.neurology.org/cgi/pmidlookup?view=long&amp;pmid=25663227 DB - PRIME DP - Unbound Medicine ER -