Chemobrain

I have many patients who complain about lack of concentration and short-term memory issues. The idea of “chemobrain” or “chemofog” has been around at least 10 years . It is a difficult area to research methodologically: What are the deficits? How do you measure them? How do you quantify detriment? How do you adjust for other factors? How do you assess baseline cognitive function? etc. Dr. Mark Noble and colleagues documented delayed damage and cell death of oligodendrocytes in the brains of rodents who received 5-FU chemotherapy. Results of study give evidence of explicit cell damage, presumably as a direct result of chemotherapy. Oligodendrocytes are a key component in the production of myelin and this could be a link to diminished cognitive function. This is certainly hypothesis generating and warrants further investigation.

We know that chemotherapy causes peripheral neuropathies. We know, in the era of high-dose chemotherapy before stem-cell rescue in breast cancer, that high-dose chemotherapy rarely causes acute neuronal death in the dorsal root ganglion, so called neuronopathy. We also know that chemotherapy, more commonly, causes a length-dependent peripheral neuropathy: an axonopathy. With this recent evidence of oligodendrocyte death, I suggest this may be further evidence of chemotherapy-induced neuropathy. It certainly highlights the need to continue to flesh out the pathophysiology behind the common complaint of “chemobrain.”