Brain fog is one of the most devastating effects of mold-related neurological injury.
It is a syndrome caused by a range of medical problems, as well as more mundane stressors such as sleep deprivation. The symptoms of brain fog include difficulty concentrating, confusion, slowed thinking, poor decision making, forgetfulness, and mental fatigue.
Chronic medical problems such as long COVID, chronic Lyme, and chronic fatigue syndrome feature brain fog. In fact, chronic fatigue syndrome is so intertwined with brain inflammation that the condition is commonly combined with the term myalgic encephalomyelitis—ME/CFS—to denote the essential role of central nervous system inflammation.
Toxic Encephalopathy — A Poisoned Brain
As with ME/CFS, mold-induced brain fog is caused by immunological, metabolic, and neurological effects on the brain. One limitation of a ME/CFS diagnosis alone is it does not point toward the cause of injury, just toward the symptom complex.
By contrast, toxic encephalopathy is a diagnostic categorization that connects harmful environmental exposures, as well as metabolic problems, with brain injury. Breathing in biological pollutants, such as toxic mold and bacteria, causes toxic encephalopathy from injury mechanisms that include brain inflammation and suppressed mitochondrial function.
The diagnostic criteria of toxic encephalopathy can be made after documentation of:
- a sufficiently intense or prolonged exposure to the neurotoxin,
- a neurological syndrome appropriate for the putative neurotoxins,
- evolution of symptoms and sings over a compatible temporal course,
- and exclusion of other neurological disorders that may account for a similar syndrome.
A Moldy Brain
Toxic encephalopathy can arise respiratory exposure to water-damaged buildings. The indoor biological pollutants are inflammatory and toxic to the brain. Toxic encephalopathy has multiple other environmental and occupational causes including from exposures to heavy metals, organic solvents, and noxious gasses.
The symptom profile may depend in part on the type of environmental exposure. Multiple studies have described the impairments of mold-exposure to be like those observed in mild traumatic brain injury.
In one study, subjects described “moderate” to “severe” psychological problems including acute stress, adjustment disorder, and post-traumatic stress. In addition, the subjects exhibited impaired functioning in a range of basic mental abilities such as memory.
Another study found mold-exposed subjects to perform below the 10th percentile in cognitive measures. The worst deficits were in visual processing, verbal learning, and psychomotor speed–the time it takes to process and act on new information.
Of Mice and Mold — Proving the Mechanism of Action
Neuroscientist Cheryl Harding uses research on mice to study the effects of mold exposure on the brain. In one study, Harding exposed mice to toxicStachybotrys spores or Stachybotrysspores with the toxins chemically removed.
With three respiratory exposures per week for six weeks, both groups of mice exhibited evidence of brain inflammation, damage to brain cells, and worsened memory. Some of the mice exhibited behavior indicative of anxiety and pain sensitivity.
On assessment of the brain tissue, Harding found a type of inflammatory injury known as innate immune activation. This type of inflammation occurred in both treatment groups, proving that the Stachybotrys fragments alone—even without toxins—injured the immune system which, in turn, would spread inflammation to the brain.
The brain tissue specimens of the hippocampus, a key structure for memory, showed an increase in microglial cell activation, a brain immune cell that releases cytokines into the central nervous system. Harding theorized that this form of brain inflammation explained the mice sickness behavior including pain, fatigue, and social withdrawal.
The inflammatory character of mold fragments, the neuroscientist noted, was predictable:
“This is not surprising given that there are at least nineteen pattern recognition receptors that recognize carbohydrates in fungal cell walls or RNA/DNA and activate immune responses.”