Restless Legs and CMT article

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Journal of Neurology Neurosurgery and Psychiatry 2002;72:555

© 2002 Journal of Neurology Neurosurgery and Psychiatry

CORRESPONDENCE

Restless legs syndrome and peripheral neuropathy

F Gemignani and A Marbini

Institute of Neurology, University of Parma, via del Quartiere 4,

I-43100 Parma, Italy

Correspondence to;

Dr F Gemignani;

gemignan@...

Keywords: restless legs syndrome; peripheral neuropathy

The Editorial by Chaudhuri et al1 opportunely reviews various aspects of

restless legs syndrome (RLS), but it is disappointing that RLS

associated with peripheral neuropathies is poorly treated. A few types

of peripheral neuropathy associated with RLS are mentioned in table 1

(sensory neuropathy, Charcot-Marie-Tooth disease type 2), but are not

discussed or referenced.2,3 The occurrence of RLS in association with

peripheral neuropathy may be more frequent than usually thought. Rutkove

et al4 reported a 5.2% prevalence of RLS in miscellaneous peripheral

neuropathies, but we found RLS in 20 out of 70 consecutive patients

(28.6%) with various forms

of peripheral neuropathy.5 Definite types of peripheral neuropathy, such

as cryoglobulinaemic neuropathy, CMT2, diabetic neuropathy, and amyloid

neuropathy, are especially prone to develop RLS, often as an early

manifestation.6 A significant association of RLS with positive sensory

symptoms of peripheral neuropathy has been found,3,6 suggesting that a

disorder of the sensory inputs may be involved in the pathogenesis.

Small fibre involvement could be the crucial factor for neuropathy to

develop RLS, as small fibre neuropathy has been often demonstrated in

association with the disease, by means of quantitative sensory testing7

or skin biopsy with

quantification of intraepidermal nerve fibres.2

Restless legs syndrome deserves consideration as a frequent, treatable,

and probably

underrecognised condition. Its prevalence in the general population may

range between 5% and 15%.1

It is unclear how much of this percentage can be attributed to

peripheral neuropathy; however it is suggested that as many as 45% of

patients with RLS might have subclinical sensory neuropathies, and it

seems that patients can be stratified based on the age of onset, which

tends to be later in neuropathy associated RLS.2 On the other hand,

patients with common forms of neuropathy, such as diabetic and

cryoglobulinaemic neuropathy, are known often to have RLS, further

contributing to the population of " peripheral " RLS.

Pathogenetic hypotheses on RLS should deal with the paradox of a

condition associated with either peripheral or central dysfunction.

According to current views, the disease might be caused by dopaminergic

dysfunction with loss of supraspinal inhibition and enhanced

excitability of propriospinal mechanisms,1 possibly including generators

involved in locomotor patterns. Spinal structures involved in RLS,

besides being released by dopaminergic dysfunction, might be activated

by abnormal sensory nerve inputs associated with peripheral nerve

damage2,3,6; in particular, changes in small fibres may trigger

mechanisms of rewiring in the dorsal horn, as experimentally

demonstrated after small fibre injury.8

As suggested by Polydefkis et al,2 RLS associated with peripheral

neuropathy may require a different therapeutic approach, using

neuropathic pain medications rather than dopaminergic therapy. In our

experience, gabapentin, trazodone, and amitryptiline were anecdotally

effective.3,6

REFERENCES

1.Chaudhuri KR, Appiah-Kubi LS, Trenkwalder C. Restless legs syndrome.

J Neurol

Neurosurg Psychiatry 2001;71:143–6.[Full Text]

2.Polydefkis M, RP, Hauer P, et al. Subclinical sensory

neuropathy in late-onset

restless legs syndrome. Neurology 2000;55:1115–21.[Abstract/Full

Text]

3.Gemignani F, Marbini A, Di Giovanni G, et al. Charcot-Marie-Tooth

disease type 2 with

restless legs syndrome. Neurology 1999;52:1064–6[Abstract/Full Text]

4.Rutkove SB, Matheson JK, Logigian EL. Restless legs syndrome in

patients with

polyneuropathy. Muscle Nerve 1996;19:670–2.[Medline]

5.Melli G, Marbini A, Grosso R, et al. Restless legs syndrome in

peripheral neuropathy

[abstract]. J Peripher Nerv Syst 2001;6:52.

6.Gemignani F, Marbini A, Di Giovanni G, et al. Cryoglobulinaemic

neuropathy manifesting

with restless legs syndrome. J Neurol Sci 1997;152:218–23.[Medline]

7.Iannaccone S, Zucconi M, Marchettini P, et al. Evidence of

peripheral axonal neuropathy

in primary restless legs syndrome. Mov Disord 1995;10:2–9.[Medline]

8.Mannion RJ, Doubell TP, Coggeshall RE, et al. Collateral sprouting

of uninjured primary

afferent A fibers into the superficial dorsal horn of the adult rat

spinal cord after topical

capsaicin treatment to the sciatic nerve. J Neurosci

1996;16:5189–95.[Abstract/Full Text]