Some elements of cholinergic crisis can be treated with antimuscarinic drugs like atropine, but the most important element, respiratory arrest, cannot. The neuromuscular junction, where the brain communicates with muscles (like the diaphragm, the main breathing muscle), works by acetylcholine activating nicotinic acetylcholine receptors and leading to muscle contraction. Atropine blocks muscarinic acetylcholine receptors (a different subtype than the nicotinic receptors at the neuromuscular junction), so atropine will not improve the muscle strength and ability to breathe in someone with cholinergic crisis. Such a patient will require mechanical ventilation support via endotracheal intubation until the crisis resolves on its own. The respiratory compromise from cholinergic crisis unfortunately has no pharmacologic solution or therapy.

As a result of cholinergic crisis, the muscles stop responding to the bombardment of ACh, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis.

This crisis may be masked by the concomitant use of atropine along with cholinesterase inhibitor in order to prevent side effects. Flaccid paralysis resulting from cholinergic crisis can be distinguished from myasthenia gravis by the use of the drug edrophonium (Tensilon), which worsens the paralysis caused by cholinergic crisis, but strengthens the muscle in the case of myasthenia gravis. (Edrophonium is an cholinesterase inhibitor hence increases the concentration of acetylcholine present).

Because the adrenergic storm overlaps with so many other similar conditions, such as hypertensive crises, stimulant intoxication or overdose, or even panic attack, and because the treatments for these overlapping conditions are largely alike, it is not necessary to obtain a differential and definitive diagnosis before initiating treatment. However, analysis of the patient's medical history, checked against the possible causes of the adrenergic storm such as those above, should be done, because some adrenergic storms can be caused by serious underlying conditions. If a patient has an adrenergic storm and all or most of the other factors are ruled out, the adrenergic storm could lead to the discovery of a pheochromocytoma, which can become malignant. However, not all cases of adrenergic storm have an identifiable cause. Like a seizure, sometimes a patient has a single one, or perhaps a few, and then does not for the rest of their life. The mechanisms of idiopathic adrenergic storm are very poorly understood.

Serotonin syndrome, in which an excess of serotonin in the synapses causes a similar crisis of hypertension and mental confusion, could be confused with an adrenergic storm. The difference is that serotonin, being a tryptamine (non-catecholamine) involved in higher brain functions, can cause dangerous hypertension and tachycardia from its effects on the sympathetic nervous system, but as there are no serotonin receptors in the heart or blood vessels there are no direct effects on the heart. Thus, the presence of arrythmia, abnormal echocardiograms, or chest pain indicates an adrenergic crisis and rules out serotonin syndrome.

If there is evidence of overdose or it is suspected, the patient should be given gastric lavage, activated charcoal, or both; this could make the difference between life and death in a close situation. It can however aggravate the patient which should be taken into account.

The first line treatments are diazepam and a non-selective beta blocker; other antihypertensive drugs may also be used. It is important to note that not all benzodiazepines and beta blockers are safe to use in an adrenergic storm; for instance, alprazolam and propranolol; alprazolam weakly agonizes dopamine receptors and causes catecholamine release while propranolol mildly promotes some catecholamine release - each worsening the condition.

Adrenergic storms are often idiopathic in nature; however if there is an underlying condition, then that must be addressed after bringing the heart rate and blood pressure down.

Familial dysautonomia is inherited in an autosomal recessive pattern, which means 2 copies of the gene in each cell are altered. If both parents are shown to be carriers by genetic testing, there is a 25% chance that the child will produce FD. Prenatal diagnosis for pregnancies at increased risk for FD by amniocentesis (for 14–17 weeks) or chorionic villus sampling (for 10–11 weeks) is possible.

Various investigations aid the diagnosis.

- ACTH (cosyntropin) stimulation test

- Cortisol level (to assess the level of glucocorticoids)

- Fasting blood sugar

- Serum potassium (to assess the level of mineralocorticoids)

- Serum sodium

Immediate treatment of drug induced OGC can be achieved with intravenous antimuscarinic benzatropine or procyclidine; which usually are effective within 5 minutes, although may take as long as 30 minutes for full effect. Further doses of procyclidine may be needed after 20 minutes. Any causative new medication should be discontinued. Also can be treated with 25 mg diphenhydramine.

Genetic testing is performed on a small sample of blood from the tested individual. The DNA is examined with a designed probe specific to the known mutations. The accuracy of the test is above 99%. Dr. Anat Blumenfeld of the Hadasah Medical center in Jerusalem identified chromosome number 9 as the responsible chromosome.

Adrenal crisis is triggered by physiological stress (such as trauma). Activities that have an elevated risk of trauma are best avoided. Treatment must be given within two hours of trauma and consequently it is advisable to carry injectable hydrocortisone in remote areas.

Rabbit syndrome is a rare form of extrapyramidal side effect of antipsychotic drugs in which tremors occur at a rate of approximately 5 Hz. Rabbit syndrome is characterized by involuntary, fine, rhythmic motions of the mouth along a vertical plane, without involvement of the tongue. It is usually seen after years of pharmacotherapy, and is more prominent with high potency drugs like haloperidol, fluphenazine, and pimozide. There is also a low incidence with thioridazine, clozapine, olanzapine, aripiprazole, and low doses of risperidone.

Rabbit syndrome can be treated with anticholinergic drugs. It generally disappears within a few days of treatment but may re-emerge after anticholinergic treatment is stopped. Another treatment strategy is to switch the patient to an atypical antipsychotic with high anti-cholinergic properties.

If the diagnosis is suspected, serology can be performed:

- One test is for antibodies against the acetylcholine receptor; the test has a reasonable sensitivity of 80–96%, but in ocular myasthenia, the sensitivity falls to 50%.

- A proportion of the patients without antibodies against the acetylcholine receptor have antibodies against the MuSK protein.

- In specific situations, testing is performed for Lambert-Eaton syndrome.

Treatment of AIGA almost always consists of steroid pulse therapy or high-dose oral steroids and is not consistently effective. Much remains unclear regarding the reasons for recurrent anhidrosis.

Diagnosis is typically made upon patient history, although EEG recordings can be confirmatory if they occur during attacks.

When diagnosed with MG, a person is assessed for his or her neurological status and the level of illness is established. This is usually done using the accepted Myasthenia Gravis Foundation of America Clinical Classification scale, which is:

Breeds that began in the Pacific Rim, among them Akitas and Shiba Inus, tend to have higher potassium values in laboratory test, and elevated levels are not abnormal. Dogs who do not have hypoadrenocorticism have normal values on ACTH tests.

A toxidrome (a portmanteau of "toxic" and "syndrome") is a syndrome caused by a dangerous level of toxins in the body. The term was coined in 1970 by Mofenson and Greensher. It is often the consequence of a drug overdose. Common symptoms include dizziness, disorientation, nausea, vomiting, and oscillopsia. A toxidrome may indicate a medical emergency requiring treatment at a poison control center. Aside from poisoning, a systemic infection may also lead to a toxidrome. "Classic" toxidromes are presented below, but they are often variable or obscured by the co-ingestion of multiple drugs.

Dogs with infected with the whipworm "Trichuris trichiura" can exhibit low sodium and high potassium values, as is seen in hypoadrenocorticism; however, their ACTH values are normal.

The symptoms of an anticholinergic toxidrome include blurred vision, coma, decreased bowel sounds, delirium, dry skin, fever, flushing, hallucinations, ileus, memory loss, mydriasis (dilated pupils), myoclonus, psychosis, seizures, and urinary retention. Complications include hypertension, hyperthermia, and tachycardia. Substances that may cause this toxidrome include the four "anti"s of antihistamines, antipsychotics, antidepressants, and antiparkinsonian drugs as well as atropine, benztropine, datura, and scopolamine.

Due to the characteristic appearance and behavior of patients with this toxidrome, they are colloquially described as "Blind as a bat, mad as a hatter, red as a beet, hot as Hades (or hot as a hare), dry as a bone, the bowel and bladder lose their tone, and the heart runs alone."

The overwhelming majority of reported AIGA patients are Japanese, but whether AIGA is truly rare in whites or has been simply underreported by Western physicians remains unclear.

AIGA is most prevalent among young men. In a 64 case review of the literature 58 reported cases were males and 6 female, with a mean age of onset at 28 ± 11 years. Cholinergic urticaria or sharp pain over the entire body induced by elevated body temperature was reported in 32 cases (50%). Of 28 cases tested, 12 (43%) displayed elevated serum IgE levels. Skin biopsy was performed in 53 cases, with normal findings in 20 cases (38%), and cellular infiltrates in sweat glands or ducts in 23 cases (43%).

Drugs that can trigger an oculogyric crisis include neuroleptics (such as haloperidol, chlorpromazine, fluphenazine, olanzapine), carbamazepine, chloroquine, cisplatin, diazoxide, levodopa, lithium, metoclopramide, lurasidone, domperidone, nifedipine, pemoline, phencyclidine ("PCP"), reserpine, and cetirizine, an antihistamine. High-potency neuroleptics are probably the most common cause in the clinical setting.

Other causes can include postencephalitic Parkinson's, Tourette's syndrome, multiple sclerosis, neurosyphilis, head trauma, bilateral thalamic infarction, lesions of the fourth ventricle, cystic glioma of the third ventricle, herpes encephalitis, kernicterus and juvenile Parkinson's.

The prognosis is typically good when medical care is provided and patients adequately treated are unlikely to have any long-term sequelae. However, severely affected patients with prolonged seizures or respiratory failure may have ongoing impairments secondary to the hypoxia. It has been stated that if a patient survives nicotine poisoning during the first 4 hours, they usually recover completely. At least at "normal" levels, as nicotine in the human body is broken down, it has an approximate biological half-life of 1–2 hours. Cotinine is an active metabolite of nicotine that remains in the blood for 18–20 hours, making it easier to analyze due to its longer half-life.

Increased nicotine or cotinine (the nicotine metabolite) is detected in urine or blood, or serum nicotine concentrations increase.

A number of measurements exist to assess exposure and early biological effects for organophosphate poisoning. Measurements of OP metabolites in both the blood and urine can be used to determine if a person has been exposed to organophosphates. Specifically in the blood, metabolites of cholinesterases, such as butyrylcholinesterase (BuChE) activity in plasma, neuropathy target esterase (NTE) in lymphocytes, and of acetylcholinesterase (AChE) activity in red blood cells. Due to both AChE and BuChE being the main targets of organophosphates, their measurement is widely used as an indication of an exposure to an OP. The main restriction on this type of diagnosis is that depending on the OP the degree to which either AChE or BuChE are inhibited differs; therefore, measure of metabolites in blood and urine do not specify for a certain OP. However, for fast initial screening, determining AChE and BuChE activity in the blood are the most widely used procedures for confirming a diagnosis of OP poisoning. The most widely used portable testing device is the Test-mate ChE field test, which can be used to determine levels of Red Blood Cells (RBC), AChE and plasma (pseudo) cholinesterase (PChE) in the blood in about four minutes. This test has been shown to be just as effective as a regular laboratory test and because of this, the portable ChE field test is frequently used by people who work with pesticides on a daily basis.

There are two lines of treatment for Pisa syndrome. The first line entails discontinuation or reduction in dose of the antipsychotic drug(s). The second line of treatment is an anticholinergic medication. A pharmacological therapy for Pisa syndrome caused by prolonged use of antipsychotic drugs has not been established yet.

Anticholinergic drugs have been reported to be extremely effective in 40% of the patients with the Pisa syndrome. Patients with Pisa syndrome that is resistant to anticholinergic drugs is mostly resolved by the reduction of the administration of the antipsychotic drugs as previously mentioned. While the specific pathology underlying idiopathic Pisa syndrome is unknown, the administration of anticholinergic drugs has provided resolution in known cases.