Abstract
LES is an autoimmune disorder of the neuromuscular junction in which autoantibodies directed against voltage-dependent Ca2+ channels block nerve-evoked Ca2+ entry at the motor nerve terminal. The pathogenic IgG is likely to produce a similar inhibitory effect on the Ca2+ channel function in other cholinergic synapses of the autonomic nervous system. This pathophysiology is sufficient to account for the distinctive clinical, immunologic, and electrophysiologic manifestations in patients with LES. Etiology of this disease is uncertain but in view of its frequent association with small cell lung cancer, this specific type of neoplasm may be implicated in the initiation of auto-immune response. Recent studies indeed support the possibility that the antigenic stimulus in the neoplastic form of LES may arise from voltage-dependent Ca2+ channels found in the lung cancer cells.
| Original language | English |
|---|---|
| Pages (from-to) | 35-41 |
| Number of pages | 7 |
| Journal | Seminars in Neurology |
| Volume | 10 |
| Issue number | 1 |
| State | Published - 1990 |
Fingerprint
ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
Cite this
Lambert-eaton syndrome. / Pascuzzi, Robert; Kim, Y. I.
In: Seminars in Neurology, Vol. 10, No. 1, 1990, p. 35-41.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Lambert-eaton syndrome
AU - Pascuzzi, Robert
AU - Kim, Y. I.
PY - 1990
Y1 - 1990
N2 - LES is an autoimmune disorder of the neuromuscular junction in which autoantibodies directed against voltage-dependent Ca2+ channels block nerve-evoked Ca2+ entry at the motor nerve terminal. The pathogenic IgG is likely to produce a similar inhibitory effect on the Ca2+ channel function in other cholinergic synapses of the autonomic nervous system. This pathophysiology is sufficient to account for the distinctive clinical, immunologic, and electrophysiologic manifestations in patients with LES. Etiology of this disease is uncertain but in view of its frequent association with small cell lung cancer, this specific type of neoplasm may be implicated in the initiation of auto-immune response. Recent studies indeed support the possibility that the antigenic stimulus in the neoplastic form of LES may arise from voltage-dependent Ca2+ channels found in the lung cancer cells.
AB - LES is an autoimmune disorder of the neuromuscular junction in which autoantibodies directed against voltage-dependent Ca2+ channels block nerve-evoked Ca2+ entry at the motor nerve terminal. The pathogenic IgG is likely to produce a similar inhibitory effect on the Ca2+ channel function in other cholinergic synapses of the autonomic nervous system. This pathophysiology is sufficient to account for the distinctive clinical, immunologic, and electrophysiologic manifestations in patients with LES. Etiology of this disease is uncertain but in view of its frequent association with small cell lung cancer, this specific type of neoplasm may be implicated in the initiation of auto-immune response. Recent studies indeed support the possibility that the antigenic stimulus in the neoplastic form of LES may arise from voltage-dependent Ca2+ channels found in the lung cancer cells.
UR - http://www.scopus.com/inward/record.url?scp=0025160901&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025160901&partnerID=8YFLogxK
M3 - Article
C2 - 2189179
AN - SCOPUS:0025160901
VL - 10
SP - 35
EP - 41
JO - Seminars in Neurology
JF - Seminars in Neurology
SN - 0271-8235
IS - 1
ER -