One of those related neurotoxins is neosaxitoxin (NSTX) in which the nitrogen at position 2 is not bound to a hydrogen, but to a hydroxyl group.

Even though there are slight differences between all saxitoxin-related compounds, all those saxitoxins are neurotoxins which affect the sodium channels.

One of them is sensory and motor paralysis, known as paralytic shellfish poisoning (PSP), which results from ingestion of saxitoxin and its derivatives, such as decarbamoylsaxitoxin.

Since saxitoxins and their derivatives are mainly produced by the Gonyaulax tamarensis dinoflagellate, for a long time the exact synthesis pathway was unknown.

In 2004, a study[10] on people who died from paralytic shellfish poisoning reported detected oxidation of saxitoxin into neosaxitoxin.

In a more recent study[9] on human liver samples, a metabolic pathway was proposed for saxitoxin which is shown in figure 2.

[needs update] They found that saxitoxin can be converted into neosaxitoxin in the human body, which harmonizes the earlier research.

[8] This study showed that the neuromuscular transmission in the motor axon and the muscular membrane is targeted whereas the end-plate is left unaffected.

However, what can be concluded for sure is that decarbamoylsaxitoxin is converted into other compounds in the body or has trouble reaching the sodium channels.

[14] In coastal waters, mostly in temperate and subtropical regions, dinoflagellate blooms can occur when the conditions for growth and aggregation are optimal.

[1][16] This gradually proceeds to the neck, arms, legs and toes, together with general muscular incoordination.

[1] Patients can start feeling numb, due to which it is hard to make voluntary movements.

In the final stage of the poisoning, respiratory distress and full muscular paralysis occur, usually between 2 and 12 hours after ingestion.

[1] Also alkaline and sodium-containing fluids can be used to block the effect of paralytic shellfish toxins on nerve conduction.