On average, symptoms begin 3-4 hours after consumption, but can begin anywhere from several minutes to 18 hours afterward. Symptoms typically include neurologic and gastrointestinal issues including:
nauseavomiting
diarrhea
numbness and tingling in the lips, mouth, face, and extremitiesThe latter has been described as “nerves being on fire” or “ants crawling and biting all over”.Other less common symptoms can include:
ataxia
loss of coordination
limb paralysis
reversal of hot and cold sensations
slurred speech
headache
pupil dilation
generalized fatiguePatients may be thought to be disoriented or intoxicated. Rarely, patients may experience respiratory distress requiring ventilatory support. Despite this seemingly severe constellation of symptoms, there have been no documented deaths due to NSP. NSP can present similar to other disorders such as:
common food poisoning
seafood allergy
paralytic shellfish poisoning
ciguatera fish poisoning
pesticide poisoning
alcohol intoxication
certain psychiatric disorders.Due to the extensive list of disorders with similar symptoms, a detailed food history is necessary to make the diagnosis. Management and treatment
Treatment for NSP is mostly supportive with monitoring and symptom management. Intravenous fluids and observation of respiratory function are the mainstay of treatment along with pain control. Activated charcoal can be given if the patient presents within four hours of consumption to decontaminate the gastrointestinal tract. Currently, there is no specific antidote for brevetoxins, however there may be a role for mannitol (the primary treatment for ciguatoxin, a dinoflagellate-produced toxin found in some species of fish) or brevatal, a natural antagonist of brevetoxin produced by K. brevis. Though public health policy differs by state, measures are taken to prevent shellfish poisoning outbreaks.
Barbiturate dependence develops with regular use of barbiturates. This in turn may lead to a need for increasing doses of the drug to get the original desired pharmacological or therapeutic effect. Barbiturate use can lead to both addiction and physical dependence, and as such they have a high potential for excess or non-medical use, however, it does not affect all users. Management of barbiturate dependence involves considering the affected persons age, comorbidity and the pharmacological pathways of barbiturates.Psychological addiction to barbiturates can develop quickly. The patients will then have a strong desire to take any barbiturate-like drug. The chronic use of barbiturates leads to moderate degradation of the personality with narrowing of interests, passivity and loss of volition. The somatic signs include hypomimia, problems articulating, weakening of reflexes, and ataxia.The GABAA receptor, one of barbiturates main sites of action, is thought to play a pivotal role in the development of tolerance to and dependence on barbiturates, as well as the euphoric "high" that results from their use. The mechanism by which barbiturate tolerance develops is believed to be different from that of ethanol or benzodiazepines, even though these drugs have been shown to exhibit cross-tolerance with each other and poly drug administration of barbiturates and alcohol used to be common. The management of a physical dependence on barbiturates is stabilisation on the long-acting barbiturate phenobarbital followed by a  gradual titration down of dose. People who use barbiturates tend to prefer rapid-acting barbiturates (amobarbital, pentobarbital, secobarbital) rather than long-acting barbiturates (barbital, phenobarbital).