Abnormal heart rhythms and asystole are possible complications of hypermagnesemia related to the heart. Magnesium acts as a physiologic calcium blocker, which results in electrical conduction abnormalities within the heart.

Clinical consequences related to serum concentration:

- 4.0 mEq/l decreased reflexes

- >5.0 mEq/l Prolonged atrioventricular conduction

- >10.0 mEq/l Complete heart block

- >13.0 mEq/l Cardiac arrest

Note that the therapeutic range for the prevention of the pre-eclampsic uterine contractions is: 4.0-7.0 mEq/L. As per Lu and Nightingale, serum Mg concentrations associated with maternal toxicity (also neonate depression - hypotonia and low Apgar scores) are:

- 7.0-10.0 mEq/L - loss of patellar reflex

- 10.0-13.0 mEq/L - respiratory depression

- 15.0-25.0 mEq/L - altered atrioventricular conduction and (further) complete heart block

- >25.0 mEq/L - cardiac arrest

Hypermagnesemia is an electrolyte disturbance in which there is a high level of magnesium in the blood. It is defined as a level greater than 1.1 mmol/L. Symptoms include weakness, confusion, decreased breathing rate, and cardiac arrest.

Hypermagnesemia can occur in kidney failure and those who are given magnesium salts or who take drugs that contain magnesium (e.g. some antacids and laxatives). It is usually concurrent with other electrolyte disturbances such as a low blood calcium and/or high blood potassium level. Specific electrocardiogram (ECG) changes may be present.

Treatment when levels are very high include calcium chloride, intravenous normal saline with furosemide, and hemodialysis.

Hypermagnesemia occurs rarely because the kidney is very effective in excreting excess magnesium.

As most cases of FHH are asymptomatic and benign, the diagnosis of FHH is less likely to be made.

Typically, diagnosis is made in the pursuit of uncovering the etiology of hypercalcemia.

Calcium levels are often in the high normal range or slightly elevated.

Commonly, the parathyroid hormone level is checked and may be slightly elevated or also on the high normal end.

Normally, high calcium should cause low PTH and so this level of PTH is inappropriately high due to the decreased sensitivity of the parathyroid to calcium.

This may be mistaken for primary hyperparathyroidism.

However, evaluation of urine calcium level will reveal a low level of urine calcium.

This too is inappropriate as high serum calcium should result in high urine calcium.

If urine calcium is not checked, this may lead to parathyroidectomy for presumed primary hyperparathyroidism.

Additionally as the name implies, there may be a family history of benign hypercalcemia.

Ultimately, diagnosis of familial hypocalciuric hypercalcemia is made — as the name implies — by the combination of low urine calcium and high serum calcium.

Most cases of familial hypocalciuric hypercalcemia are asymptomatic. Laboratory signs of FHH include:

- Hypercalcemia

- Hypocalciuria ( Ca excretion rate < 0.02 mmol/L)

- Hypermagnesemia

- High normal to mildly elevated parathyroid hormone

Neuromuscular junction disease is a medical condition where the normal conduction through the neuromuscular junction fails to function correctly.

Metabolic diseases are usually a result of abnormal functioning of one of the metabolic processes required for regular production and utilization of energy in a cell. This can occur by damaging or disabling an important enzyme, or when a feedback system is abnormally functioning. Toxic diseases are a result of a form of poison that effects neuromuscular junction functioning. Most commonly animal venom or poison, or other toxic substances are the origin of the problem.

Neuromuscular junction diseases in this category include snake venom poisoning, botulism, arthropod poisoning, organophosphates and hypermagnesemia.(reference 13) Organophosphates are present in many insecticides and herbicides. They are also the basis of many nerve gases.(reference 27) Hypermagnesmia is a condition where the balance of magnesium in the body is unstable and concentrations are higher than normal baseline values.(reference 28)

Other causes may include:

- Anticonvulsant pharmaceutical drugs, such as topiramate, sultiame, and acetazolamide

- Anxiety and/or panic disorder

- Benzodiazepine withdrawal syndrome

- Beta alanine

- Carpal tunnel syndrome

- Cerebral amyloid angiopathy

- Chiari malformation

- Coeliac disease (celiac disease)

- Complex regional pain syndrome

- Decompression sickness

- Dehydration

- Dextromethorphan (recreational use)

- Fabry disease

- Erythromelalgia

- Fibromyalgia

- Fluoroquinolone toxicity

- Guillain–Barré syndrome (GBS)

- Heavy metals

- Herpes zoster

- Hydroxy alpha sanshool, a component of Sichuan peppers

- Hyperglycemia (high blood sugar)

- Hyperkalemia

- Hyperventilation

- Hypoglycemia (low blood sugar)

- Hypocalcemia, and in turn:

- Hypermagnesemia, a condition in which hypocalcemia itself is typically observed as a secondary symptom

- Hypomagnesemia, often as a result of long term proton-pump inhibitor use

- Hypothyroidism

- Immunodeficiency, such as chronic inflammatory demyelinating polyneuropathy (CIDP)

- Intravenous administering of strong pharmaceutical drugs acting on the central nervous system (CNS), mainly opioids, opiates, narcotics; especially in non-medical use (drug abuse)

- Ketorolac

- Lidocaine poisoning

- Lomotil

- Lupus erythematosus

- Lyme disease

- Menopause

- Mercury poisoning

- Migraines

- Multiple sclerosis

- Nitrous oxide, long-term exposure

- Obdormition

- Pyrethrum and pyrethroid (pesticide)

- Rabies

- Radiation poisoning

- Sarcoidosis

- Scorpion stings

- Spinal disc herniation or injury

- Spinal stenosis

- Stinging nettles

- Syringomyelia

- Transverse myelitis

- Vitamin B deficiency

- Vitamin B deficiency

- Withdrawal from certain selective serotonin reuptake inhibitors (or serotonin-specific reuptake inhibitors) (SSRIs), such as paroxetine or serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine

Acroparesthesia is severe pain in the extremities, and may be caused by Fabry disease, a type of sphingolipidosis.

It can also be a sign of hypocalcemia.

Brief hallucinations are not uncommon in those without any psychiatric disease. Causes or triggers include:

- Falling asleep and waking: hypnagogic and hypnopompic hallucinations, which are entirely normal

- Bereavement, in which hallucinations of a deceased loved one are common

- Severe sleep deprivation

- Sensory deprivation and sensory impairment

- Caffeine intoxication

- An extremely stressful event

Cycloid psychosis is a psychosis that progresses from normal to full-blown, usually between a few hours to days, not related to drug intake or brain injury. The cycloid psychosis has a long history in European psychiatry diagnosis. The term "cycloid psychosis" was first used by Karl Kleist 1926. Despite the significant clinical relevance, this diagnosis is neglected both in literature as in nosology. The cycloid psychosis has attracted much interest in the international literature of the past 50 years, but the number of scientific studies have greatly decreased over the past 15 years, possibly partly explained by the misconception that the diagnosis has been included incorporated in current diagnostic classification systems. The cycloid psychosis is therefore only partially described in the diagnostic classification systems used. "polymorph acute psychotic disorder", with or without schizophrenic symptoms. (F23.0 ICD 10). Cycloid psychosis is nevertheless its own specific disease that is distinct from both the manic-depressive disorder, and from schizophrenia, and this despite the fact that the cycloid psychosis can include both bipolar (basic mood shifts) as well as schizophrenic symptoms. The disease is an acute, usually self-limiting, functionally psychotic state, with a very diverse clinical picture that almost consistently is characterized by the existence of some degree of confusion or distressing perplexity, but above all, of the multifaceted and diverse expressions the disease takes. The main features of the disease is thus that the onset is acute, the multifaceted picture of symptoms and typically reverses to a normal state and that the long-term prognosis is good. In addition, diagnostic criteria include at least four of the following symptoms:

- Confusion

- Mood-incongruent delusions

- Hallucinations

- Pan-anxiety, a severe anxiety not bound to particular situations or circumstances

- Happiness or ecstasy of high degree

- Motility disturbances of akinetic or hyperkinetic type

- Concern with death

- Mood swings to some degree, but less than what is needed for diagnosis of an affective disorder

Cycloid psychosis occurs in people of generally 15–50 years of age.