Format

Send to

Choose Destination
See comment in PubMed Commons below
Curr Opin Neurol. 2007 Dec;20(6):719-25.

Neurologic complications of chemotherapy agents.

Author information

1
Division of Hematology-Oncology, Department of Medicine, University of Virginia Health System, Charlottesville, Virginia 22908-0432, USA.

Abstract

PURPOSE OF REVIEW:

To review neurologic complications of common and recently developed chemotherapeutic agents, as well as recent research regarding 'chemobrain'.

RECENT FINDINGS:

Bortezomib, a new anticancer agent, has a propensity toward causing a largely sensory and reversible peripheral neuropathy. Infusion of magnesium and calcium pre and post-oxaliplatin infusion reduces neuropathy but may interfere with clinical response to oxaliplatin. No other measures currently reduce the incidence or severity of neuropathy related to platinum compounds, taxanes, or thalidomide. Chemobrain, cognitive decline attributed to chemotherapy, has garnered research interest. Prevalence and epidemiology of chemobrain are poorly understood. Potential underlying mechanisms are under investigation in animal models and include effects on long-term potentiation and cerebral blood flow. Blood-brain barrier permeability, efficiency of cellular efflux pumps, DNA damage, telomere shortening, alteration of cytokine regulation, defects in neural repair, and oxidative stress may play roles in the effects of chemotherapy on central nervous system function.

SUMMARY:

Data on prevention and treatment of chemotherapy-induced peripheral neuropathy are limited. Calcium and magnesium infusions for oxaliplatin administration have the most scientific support and are widely used in practice but may interfere with the clinical efficacy of oxaliplatin. Some novel agents, particularly bortezomib, have significant risk of chemotherapy-induced peripheral neuropathy. Animal models are beginning to reveal the mechanisms underlying the impact of individual chemotherapeutic drugs on cognition.

PMID:
17992096
DOI:
10.1097/WCO.0b013e3282f1a06e
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wolters Kluwer
    Loading ...
    Support Center