JNNP

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER


[Advanced]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this link to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Add article to my folders
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by HANNA, M. G
Right arrow Articles by KULLMANN, D. M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by HANNA, M. G
Right arrow Articles by KULLMANN, D. M
J Neurol Neurosurg Psychiatry 1998;65:427-431 ( October )

Editorial

Ion channels and neurological disease: DNA based diagnosis is now possible, and ion channels may be important in common paroxysmal disorders

The first 150 words of the full text of this article appear below.

Ion channels are large transmembrane proteins which are essential for the normal function of all eukaryotic cells.1 They are especially important in excitable cells because they determine the membrane potential, both at rest and during firing, and also play a critical part in neurotransmitter release. Ion channels may be broadly classified into voltage gated and ligand gated, although many voltage gated channels are also affected by intracellular messengers.1 It is well recognised that autoimmune attack of the nicotinic acetylcholine receptor underlies acquired myasthenia gravis. Research over the past few years has, however, established that genetic defects in both ligand and voltage gated ion channels also cause some inherited neurological disorders.2-5 Collectively, these immunological and genetic conditions have become known as the neurological channelopathies. The genetic channelopathies are listed in tables 1 and 2.

Table Removed (Available Only in the Full Text)


Table Removed (Available Only in the Full Text)

The genetic advances have increased our understanding of the molecular pathogenesis of several relatively rare muscle . . . [Full text of this article]


This article has been cited by other articles:


Home page
 BrainHome page
E. M. Valente, S. D. Spacey, G. M. Wali, K. P. Bhatia, P. H. Dixon, N. W. Wood, and M. B. Davis
A second paroxysmal kinesigenic choreoathetosis locus (EKD2) mapping on 16q13-q22.1 indicates a family of genes which give rise to paroxysmal disorders on human chromosome 16
Brain, October 1, 2000; 123(10): 2040 - 2045.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
S. F. Berkovic
Paroxysmal movement disorders and epilepsy: Links across the channel
Neurology, July 25, 2000; 55(2): 169 - 170.
[Full Text] [PDF]

Home page
 QJMHome page
G. Emilien, M. Ponchon, C. Caldas, O. Isacson, and J.-M. Maloteaux
Impact of genomics on drug discovery and clinical medicine
QJM, July 1, 2000; 93(7): 391 - 423.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurol. Neurosurg. PsychiatryHome page
A C PEREIRA, W J LOO, M BAMFORD, and S J WROE
Use of lamotrigine to treat paroxysmal kinesigenic choreoathetosis
J. Neurol. Neurosurg. Psychiatry, June 1, 2000; 68(6): 796a - 797.
[Full Text]

Home page
 J. Neurol. Neurosurg. PsychiatryHome page
N P Davies, L H Eunson, R P Gregory, K R Mills, P J Morrison, and M G Hanna
Clinical, electrophysiological, and molecular genetic studies in a new family with paramyotonia congenita
J. Neurol. Neurosurg. Psychiatry, April 1, 2000; 68(4): 504 - 507.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
Terms and conditions relating to subscriptions purchased online  ¦  Website terms and conditions  ¦  Privacy policy
Copyright © 1998 by the BMJ Publishing Group Ltd.