Mechanism of Neurological Injury:  Three independent sets of information have been used to discuss a plausible mechanism for neurological impairment observed in humans exposed to contaminated air.  The first set includes clinical observations on humans exposed to water-damaged environments.   The second entails animal experiments demonstrating neurological injury from mycotoxins instilled into the olfactory mucosa.  The third set of data involves clinical and pathology of brain injury to children and young adults exposed to the polluted air of Mexico City.

    A.  Clinical findings in patients exposed to water-damaged buildings. Both central and peripheral neuropathy have been reported in individuals chronically exposed to damp indoor environments (Gray et al., 2003; Campbell et al., 2003; 2004; Crago et al., 2003; Kilburn, 2003, 2004, 2009; Kilburn et al, 2009; Rea et al., 2003; Gordon and Cantor, 2004; Gordon et al 2004, 2006).  Briefly, exposed individuals develop peripheral neuropathy with autoantibodies directed against several neural antigens (Campbell et al., 2004).   Toxic encephalopathy involves multiple symptoms, including loss of balance, recent memory decline, headaches, lightheadedness, spaciness/disorientation, insomnia, loss of coordination (Gray et al., 2003; Rea et al., 200, 2009; Kilburn 2003, 2004).  Exposed individuals had alterations in QEEG involving the frontal cortex and other regions of the brains (Crago et al., 2003) coupled with neurocognitive decline (Crago et al., 2003; Gordon and Cantor, 2004, 2006; Kilburn 2003, 2004) as well as significant changes in various neurological measurements (declines in simple reaction and choice reaction times, increased body sway with eyes open and closed, increased latency of blink reflex, and decreased grip strength, among others (Kilburn 2003, 2004).  The probable explanation of the causative mechanism comes from both animal models and humans exposed to air pollution.
     Recently, Empting (2009) published his clinical observations on mold patients  suffering from chronic fungal sinusitis (CFS) with neurological complaints referred to his office by Donald (2009).  Trained in Psychiatry and Neurology he has begun to defining systems of a syndrome or cluster of signs/symptoms occurring in individuals with neurological disorders following exposure to microbes (molds and bacteria) in damp indoor spaces.  His goal is to delineate these mold and mycotoxin-induced signs and symptoms from classic neurologic disorders.  The patients he has seen fall into categories which will be described below:
      1.  Local and Focal Pain Syndrome: (a) Migraine and atypical facial pain result from inflammation of the sinuses irritation to the trigeminal nerve branches as they pass through the walls of the sinuses.  Alleviation of the inflammatory condition allows management of the migraines.  The migraines occur in patients with or without a history of migraines and/or headaches;  (b) Pharyngitis and glossopharyngeal neuralgia.  This condition results from post nasal drainage from inflamed sinuses leading to irritation of throat and are nociceptive pain generators.  The inflammation irritates the innervations of the throat resulting in neuropathic pain.  Once started the condition is more easily instigated by levels of stimulation.; c) Local head and neck myalgias: The inflammatory, nociceptive and migraine pain in the head and throat can feed into cranial nerve and upper cervical root pain pathways and myofascial pain loops.  Secondarily this can involve increased muscle tone,  spasm and local trigger points can develop independent facial, temporal, suboccipital and cervical myofascial pain syndromes.
     2.  Inflammation induction of distant and diffuse pain.  According to Dr. Empting, any inflammatory process in the body, including CFS, can induce myalgias and arthralgias.  Inflammatory cytokines and circulating immune complexes can reach any joint, muscle or connective tissue in body via the circulatory system.  Once instigated, these conditions can be self-perpetuating with continuing and/or additional exposure to the offending environment.
      3.  Unusual Neuropathic Focal Pain.  Single or multiple peripheral nerves can occasionally become painfully involved leading to peripheral neuropathy.  Dorsa root ganglia involvement (e.g. Bilateral L1, L2, L3)  may rarely be involved.

       4.  Disorder Movements:  These involve tremors, jerking movements, spastic dysphonia, tic-like motions and idiopathic paroxysmal unique involuntary movements.  The movements are similar, but not stereotypical of, well-defined neurologic signs such as chorea, hemiballismus, Parkinson’s tremor, myoclonic jerks, etc.  Other neurologic features such as strength, reflexes and sensation are almost always normal.  The patient can exert come voluntary control of these movements, which is typical of an impaired rather than a damaged motor nervous system.

       5.  Balance and Ataxia:  Imbalance and gait ataxia are observed more commonly than cerebellar findings.  Balance relies on multiple sensory inputs (e.g. visual, proprioception, vestibular). The pyramidal motor system, and multiple extrapyramidal and cerebellar modulating systems. Having so many sites susceptible to attack makes imbalance a common symptom

       6.  Diffuse Neuropsychiatric Syndromes:  A common label affixed to this condition is “Brain Fog.”  These individuals have varying degrees of altered mental states, usually with attention, blunted executive function and faulty short-term memory.  These condition can wax and wane (exposure vs re-exposure).