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Neuronal involvement in cisplatin neuropathy: prospective clinical and neurophysiological studies

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Krarup-Hansen, A ; Helweg-Larsen, Susanne Elisabeth ; Schmalbruch, H ; Rørth, M ; Krarup, C. / Neuronal involvement in cisplatin neuropathy : prospective clinical and neurophysiological studies. In: Brain. 2007 ; Vol. 130, No. Pt 4. pp. 1076-88.

Bibtex

@article{bfc2d35542c1416f89557dcc0a45d086,
title = "Neuronal involvement in cisplatin neuropathy: prospective clinical and neurophysiological studies",
abstract = "Although it is well known that cisplatin causes a sensory neuropathy, the primary site of involvement is not established. The clinical symptoms localized in a stocking-glove distribution may be explained by a length dependent neuronopathy or by a distal axonopathy. To study whether the whole neuron or the distal axon was primarily affected, we have carried out serial clinical and electrophysiological studies in 16 males with testicular cancer before or early and late during and after treatment with cisplatin, etoposide and bleomycin at limited (400 mg/m2 cisplatin) doses. At cumulative doses of cisplatin higher than 300 mg/m2 the patients lost distal tendon and H-reflexes and displayed reduced vibration sense in the feet and the fingers. The amplitudes of sensory nerve action potentials (SNAP) from the fingers innervated by the median nerve and the dorsolateral side of the foot innervated by the sural nerve were 50-60% reduced, whereas no definite changes occurred at lower doses. The SNAP conduction velocities were reduced by 10-15% at cumulative doses of 400-700 mg/m2 consistent with loss of large myelinated fibres. SNAPs from primarily Pacinian corpuscles in digit 3 and the dorsolateral side of the foot evoked by a tactile probe showed similar changes to those observed in SNAPs evoked by electrical stimulation. At these doses, somatosensory evoked potentials (SEPs) from the tibial nerve had increased latencies of peripheral, spinal and central responses suggesting loss of central processes of large dorsal root ganglion cells. Motor conduction studies, autonomic function and warm and cold temperature sensation remained unchanged at all doses of cisplatin treatment. The results of these studies are consistent with degeneration of large sensory neurons whereas there was no evidence of distal axonal degeneration even at the lowest toxic doses of cisplatin.",
keywords = "Action Potentials, Adult, Antineoplastic Agents, Bleomycin, Carcinoma, Embryonal, Cisplatin, Etoposide, Evoked Potentials, Somatosensory, Humans, Longitudinal Studies, Male, Middle Aged, Neural Conduction, Neurons, Afferent, Peripheral Nervous System Diseases, Prospective Studies, Reflex, Seminoma, Sensation Disorders, Sensory Thresholds, Testicular Neoplasms, Touch",
author = "A Krarup-Hansen and Helweg-Larsen, {Susanne Elisabeth} and H Schmalbruch and M R{\o}rth and C Krarup",
year = "2007",
doi = "10.1093/brain/awl356",
language = "English",
volume = "130",
pages = "1076--88",
journal = "Brain",
issn = "0006-8950",
publisher = "Oxford University Press",
number = "Pt 4",

}

RIS

TY - JOUR

T1 - Neuronal involvement in cisplatin neuropathy

T2 - prospective clinical and neurophysiological studies

AU - Krarup-Hansen, A

AU - Helweg-Larsen, Susanne Elisabeth

AU - Schmalbruch, H

AU - Rørth, M

AU - Krarup, C

PY - 2007

Y1 - 2007

N2 - Although it is well known that cisplatin causes a sensory neuropathy, the primary site of involvement is not established. The clinical symptoms localized in a stocking-glove distribution may be explained by a length dependent neuronopathy or by a distal axonopathy. To study whether the whole neuron or the distal axon was primarily affected, we have carried out serial clinical and electrophysiological studies in 16 males with testicular cancer before or early and late during and after treatment with cisplatin, etoposide and bleomycin at limited (400 mg/m2 cisplatin) doses. At cumulative doses of cisplatin higher than 300 mg/m2 the patients lost distal tendon and H-reflexes and displayed reduced vibration sense in the feet and the fingers. The amplitudes of sensory nerve action potentials (SNAP) from the fingers innervated by the median nerve and the dorsolateral side of the foot innervated by the sural nerve were 50-60% reduced, whereas no definite changes occurred at lower doses. The SNAP conduction velocities were reduced by 10-15% at cumulative doses of 400-700 mg/m2 consistent with loss of large myelinated fibres. SNAPs from primarily Pacinian corpuscles in digit 3 and the dorsolateral side of the foot evoked by a tactile probe showed similar changes to those observed in SNAPs evoked by electrical stimulation. At these doses, somatosensory evoked potentials (SEPs) from the tibial nerve had increased latencies of peripheral, spinal and central responses suggesting loss of central processes of large dorsal root ganglion cells. Motor conduction studies, autonomic function and warm and cold temperature sensation remained unchanged at all doses of cisplatin treatment. The results of these studies are consistent with degeneration of large sensory neurons whereas there was no evidence of distal axonal degeneration even at the lowest toxic doses of cisplatin.

AB - Although it is well known that cisplatin causes a sensory neuropathy, the primary site of involvement is not established. The clinical symptoms localized in a stocking-glove distribution may be explained by a length dependent neuronopathy or by a distal axonopathy. To study whether the whole neuron or the distal axon was primarily affected, we have carried out serial clinical and electrophysiological studies in 16 males with testicular cancer before or early and late during and after treatment with cisplatin, etoposide and bleomycin at limited (400 mg/m2 cisplatin) doses. At cumulative doses of cisplatin higher than 300 mg/m2 the patients lost distal tendon and H-reflexes and displayed reduced vibration sense in the feet and the fingers. The amplitudes of sensory nerve action potentials (SNAP) from the fingers innervated by the median nerve and the dorsolateral side of the foot innervated by the sural nerve were 50-60% reduced, whereas no definite changes occurred at lower doses. The SNAP conduction velocities were reduced by 10-15% at cumulative doses of 400-700 mg/m2 consistent with loss of large myelinated fibres. SNAPs from primarily Pacinian corpuscles in digit 3 and the dorsolateral side of the foot evoked by a tactile probe showed similar changes to those observed in SNAPs evoked by electrical stimulation. At these doses, somatosensory evoked potentials (SEPs) from the tibial nerve had increased latencies of peripheral, spinal and central responses suggesting loss of central processes of large dorsal root ganglion cells. Motor conduction studies, autonomic function and warm and cold temperature sensation remained unchanged at all doses of cisplatin treatment. The results of these studies are consistent with degeneration of large sensory neurons whereas there was no evidence of distal axonal degeneration even at the lowest toxic doses of cisplatin.

KW - Action Potentials

KW - Adult

KW - Antineoplastic Agents

KW - Bleomycin

KW - Carcinoma, Embryonal

KW - Cisplatin

KW - Etoposide

KW - Evoked Potentials, Somatosensory

KW - Humans

KW - Longitudinal Studies

KW - Male

KW - Middle Aged

KW - Neural Conduction

KW - Neurons, Afferent

KW - Peripheral Nervous System Diseases

KW - Prospective Studies

KW - Reflex

KW - Seminoma

KW - Sensation Disorders

KW - Sensory Thresholds

KW - Testicular Neoplasms

KW - Touch

U2 - 10.1093/brain/awl356

DO - 10.1093/brain/awl356

M3 - Journal article

C2 - 17301082

VL - 130

SP - 1076

EP - 1088

JO - Brain

JF - Brain

SN - 0006-8950

IS - Pt 4

ER -

ID: 36747306