What causes ‘chemobrain’? It’s time for neuroscientists to find out

  • Cancer patient resting (Dreamstime/TNS) Dreamstime/TNS

Los Angeles Times
Wednesday, June 13, 2018

At some point in their treatment for cancer, somewhere between 17 percent and 75 percent of patients with malignancies that don’t affect the central nervous system report the sensation that a mental fog has set in.

For months or years after their hair has grown back, the exhaustion has lifted and the medical appointments taper off, the “new normal” for these patients includes problems with concentration, word-finding, short-term memory and multitasking.

Their doctors nod their heads knowingly: It’s “chemobrain,” they report.

Among the nation’s roughly 15.5 million cancer survivors, the ranks of those who’ve experienced mental fog after cancer treatment are probably increasing as detection and therapies improve, survival rates rise and lives are extended.

But when it comes to cancer’s cognitive aftermath, the medical profession’s expertise ends. Why chemobrain happens, how long it will linger, and what deficits it actually causes — and especially whether it could be treated, or even prevented — are questions for which oncologists have no answers.

But they want them. And three specialists from the National Cancer Institute have issued an appeal to neuroscientists for help.

Writing this week in the journal Trends in Neurosciences, Horowitz and two fellow researchers at the institute drafted a road map toward a better understanding of the condition officially known as cancer-related cognitive impairment, which was first described by breast cancer survivors.

Until now, experts have tried to characterize the phenomenon using standard batteries of neuropsychological tests. The tests gauge problems in a variety of cognitive “domains,” including attention, processing speed, visuospatial skill and several different kinds of memory.

Those clinical measures were typically devised to diagnose or assess the injury wrought by severe brain diseases such as Alzheimer’s, traumatic brain injury or stroke. They are unlikely to detect, measure or explain the often subtle impairments that, for many cancer survivors, make it hard to return to a mentally demanding job or lay plans for the future.

That problem is evident in the wide-ranging estimates of how many patients are affected by chemobrain. That the latest prevalence figures stretch from 17 percent to 75 percent of cancer patients suggests that existing tests are missing their mark.

Chemobrain sufferers often complain of a mix of impairments across several domains. And, to make matters more complicated, patients with different cancers, or who have been treated with different therapies, lodge different mixes of complaints.

Gaining a better understand of chemobrain’s causes and consequences will require “embracing theories and methods of experimental neuroscience,” the researchers wrote.

That would include thoroughly examining some of the theories researchers have had about chemobrain’s origins.

Among them is the possibility that cancer, and/or its treatment, somehow knocks the immune system off balance and unleashes a toxic flood of inflammatory agents upon the central nervous system. Researchers have also speculated that chemotherapy may inflame the brain and scramble DNA there, or that it acts to accelerate the aging process or disable normal repair mechanisms. Another theory is that chemotherapies designed to kill certain cells are breaching the blood-brain barrier and attacking neurons directly.