The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure.Methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation, has long-lasting behavioral consequences that appear in adulthood and, in some cases, may not appear until aging. Prefrontal cortex or dopamine neurotransmission could be especially sensitive to even subtle gestational methylmercury exposure and suggests that public health assessments of methylmercury based on intellectual performance may underestimate the impact of methylmercury in public health. Ethylmercury is a breakdown product of the antibacteriological agent ethylmercurithiosalicylate, which has been used as a topical antiseptic and a vaccine preservative (further discussed under Thiomersal below). Its characteristics have not been studied as extensively as those of methylmercury. It is cleared from the blood much more rapidly, with a half-life of seven to ten days, and it is metabolized much more quickly than methylmercury. It is presumed not to have methylmercurys ability to cross the blood–brain barrier via a transporter, but instead relies on simple diffusion to enter the brain. Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate. These compounds were used in indoor latex paints for their antimildew properties, but were removed in 1990 because of cases of toxicity. Inorganic mercury compounds
Mercury occurs as salts such as mercuric chloride (HgCl2) and mercurous chloride (Hg2Cl2), the latter also known as calomel. Because they are more soluble in water, mercuric salts are usually more acutely toxic than mercurous salts.
If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a seizure may result from the bloods inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense.The autonomic nervous systems physiological state (see below) leading to loss of consciousness may persist for several minutes, so

If patients try to sit or stand when they wake up, they may pass out again
The person may be nauseated, pale, and sweaty for several minutes or hours

Causes
Reflex syncope occurs in response to a trigger due to dysfunction of the heart rate and blood pressure regulating mechanism. When heart rate slows or blood pressure drops, the resulting lack of blood to the brain causes fainting. Vasovagal
Typical triggers include:

Prolonged standing
Emotional stress
Pain
The sight of blood
Fear of needles
Time varying magnetic field (i.e. transcranial magnetic stimulation)

Situational
After or during urination (micturition syncope)
Straining, such as to have a bowel movement
Coughing
Swallowing
Lifting a heavy weight

Carotid sinus
Pressing upon a certain spot in the neck. This may happen when wearing a tight collar, shaving, or turning the head. Pathophysiology
Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes.