Lethargy is a state of tiredness, weariness, fatigue, or lack of energy. It can be accompanied by depression, decreased motivation, or apathy. Lethargy can be a normal response to inadequate sleep, overexertion, overworking, stress, lack of exercise, improper nutrition, boredom, or a symptom of a disorder. It may also be a side-effect of medication or caused by an interaction between medications or medication(s) and alcohol. When part of a normal response, lethargy often resolves with rest, adequate sleep, decreased stress, physical exercise and good nutrition.

Very long-chain acyl-coenzyme A dehydrogenase deficiency (VLCADD) is a fatty-acid metabolism disorder which prevents the body from converting certain fats to energy, particularly during periods without food.

Those affected by this disorder have inadequate levels of an enzyme that breaks down a group of fats called very long-chain fatty acids.

Mutations in the "ACADVL" gene lead to inadequate levels of an enzyme called very long-chain acyl-coenzyme A (CoA) dehydrogenase. Without this enzyme, very long-chain fatty acids from food and fats stored in the body cannot be degraded and processed. As a result, these fatty acids are not converted into energy, which can lead to characteristic signs and symptoms of this disorder, such as lethargy and hypoglycemia. Levels of very long-chain fatty acids or partially degraded fatty acids may build up in tissues and can damage the heart, liver, and muscles, causing more serious complications.

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.

The symptoms of sedative/hypnotic toxidrome include ataxia, blurred vision, coma, confusion, delirium, deterioration of central nervous system functions, diplopia, dysesthesias, hallucinations, nystagmus, paresthesias, sedation, slurred speech, and stupor. Apnea is a potential complication. Substances that may cause this toxidrome include anticonvulsants, barbiturates, benzodiazepines, gamma-Hydroxybutyric acid, Methaqualone, and ethanol. While most sedative-hypnotics are anticonvulsant, some such as GHB and methaqualone instead lower the seizure threshold, and so can cause paradoxical seizures in overdose.

The distinction between complications of hepatitis X and symptoms of hepatitis X is often obscure. While jaundice (yellow discoloration of the skin or whites of the eyes due to an increase of bile pigments in the blood), is a symptom of hepatitis, it is also a complication. Further complications that may arise include hyperpigmentation, renal (kidney) failure, and CSF xanthochromia. Liver disease is another fatal complication of hepatitis X. This could potentially lead to abdominal pain, hepatomegaly, splenomegaly, chest pain, and an altered bowel habit.

There has been no specific drug therapy developed for hepatitis, with the exception of hepatitis C. Patients are advised to rest in the early stages of the illness, and to eat small, high-calorie, high-protein meals in order to battle anorexia. Larger meals are more easily tolerated in the morning, for patients often experience nausea later in the day. Although high-protein meals are recommended, protein intake should be reduced if signs of precoma — lethargy, confusion, and mental changes — develop.

In acute viral hepatitis, hospitalization is usually required only for patients with severe symptoms (severe nausea, vomiting, change in mental status, and PT greater than 3 seconds above normal) or complications. If the patient experiences continuous vomiting and is unable to maintain oral intake, parenteral nutrition may be required.

In order to relieve nausea and also prevent vomiting, antiemetics (diphenhydramine or prochlorperazine) may be given 30 minutes before meals. However, phenothiazines have a cholestatic effect and should be avoided. The resin cholestyramine may be given only for severe pruritus.

Hahner et al. investigated the frequency, causes and risk factors for adrenal crisis in patients with chronic adrenal insufficiency. Annane et al.'s landmark 2002 study found a very high rate of relative adrenal insufficiency among the enrolled patients with septic shock.

A 2001 study followed up on 50 patients. Of these 38% died in childhood while the rest suffered from problems with morbidity.

The prognosis is very poor. Two studies reported typical age of deaths in infancy or early childhood, with the first reporting a median age of death of 2.6 for boys and less than 1 month for girls.

It is unknown as to what causes abdominal epilepsy. While a causal relationship between seizure activity and the GI symptoms has not been proven, the GI symptoms cannot be explained by other pathophysiological mechanisms, and are seen to improve upon anticonvulsant treatment. Because the condition is so rare, no high-quality studies exist. There have been too few reported cases to identify risk factors, genetic factors, or other potential causes.

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.

Mutations in the "HADHA" gene lead to inadequate levels of an enzyme called long-chain 3-hydroxyacyl-coenzyme A (CoA) dehydrogenase, which is part of a protein complex known as mitochondrial trifunctional protein. Long-chain fatty acids from food and body fat cannot be metabolized and processed without sufficient levels of this enzyme. As a result, these fatty acids are not converted to energy, which can lead to characteristic features of this disorder, such as lethargy and hypoglycemia. Long-chain fatty acids or partially metabolized fatty acids may build up in tissues and damage the liver, heart, retina, and muscles, causing more serious complications.

Absence seizures are one of several kinds of seizures. These seizures are sometimes referred to as petit mal seizures (from the French for "little illness", a term dating from the late 18th century). Absence seizures are characterized by a brief loss and return of consciousness, generally not followed by a period of lethargy (i.e. without a notable postictal state).

Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD).

Wet-tail is a disease in the animal's intestines caused by the bacteria, "Lawsonia intracellularis". Wet-tail is a stress related illness—such stress can be caused by a variety of factors, including:

- Too much handling

- Change in environment

- Change in diet

- Extremely unclean caging

- Being away from mother and/or siblings

- Illness or death of a pair-bond or mate

Like other forms of epilepsy, abdominal epilepsy is treated with anticonvulsant drugs, such as phenytoin. Since no controlled studies exist, however, other drugs may be equally effective.

Taravana is a disease often found among Polynesian island natives who habitually dive deep without breathing apparatus many times in close succession, usually for food or pearls. These free-divers may make 40 to 60 dives a day, each of 30 or 40 metres (100 to 140 feet).

Taravana seems to be decompression sickness. The usual symptoms are vertigo, nausea, lethargy, paralysis and death. The word "taravana" is Tuamotu Polynesian for "to fall crazily".

Taravana is also used to describe someone who is "crazy because of the sea".

Recovery is most likely if it is spotted within the first 24–48 hours, and you should seek veterinary advice—a vet may choose to give the animal drugs.

The sick animal should be kept in a cage by itself so that others do not catch the disease—wet tail can be very contagious so sanitize all objects the animal has come in contact with (wheel, food dish, huts, etc.).

If the animal doesn't want to eat, then dry, unflavored oats can be hand fed, which can also help with the diarrhea. The animal should only be fed dry foods, any foods with a high water content should be avoided.

If the animal has an unclean or matted rear-end, this should not be remedied using a bath in water—instead a q-tip (cotton bud) or cotton ball can be used to very gently clean the animal's rear end to avoid discomfort or rashes.

If the animal is not drinking, hydration can be aided by scruffing (i.e. very gently holding the rodent by the extra skin on the back of the neck) the animal so that they open their mouth; then in small, short intervals, water can be provided with a 1 ml syringe. It is very important that this is done slowly, to avoid getting water down the animal's wind pipe. Unflavored pedialyte can be purchased from a grocery store and can be very helpful with wet tail. If feeding is also an issue, a suggested aide is to feed extremely small amounts of no garlic, no onion, no added sugar mashed baby food, and administered using the same scruffing method, and again at a very slow pace.

Enterotoxemia is a condition induced by the absoption of large volumes of toxins produced by "Clostridum perfringens" from the intestines. There are several strains of "C.perfringens" (Type B, Type C & Type D) that may lead to the development of this gastrointestinal condition.

Less than 20 patients with MGA type I have been reported in the literature (Mol Genet Metab. 2011 Nov;104(3):410-3. Epub 2011 Jul 26.)

A form of enterotoxemia caused by an infection of Type B "C. perfringens", affecting lambs whom are less than 3 weeks old. Lambs often die before displaying clinical signs, nonetheless common behaviours of lambs with this condition include, cessation of nursing, lethargy, and recumbency. Diarrhea is typical as well, death usually occurs within a few days.

These syndromes are childhood absence epilepsy, epilepsy with myoclonic absences, juvenile absence epilepsy and juvenile myoclonic epilepsy. Other proposed syndromes are Jeavons syndrome (eyelid myoclonia with absences), and genetic generalised epilepsy with phantom absences.

These types of seizures are also known to occur to patients suffering with porphyria and can be triggered by stress or other porphyrin-inducing factors.

This condition is sometimes mistaken for Reye syndrome, a severe disorder that develops in children while they appear to be recovering from viral infections such as chicken pox or flu. Most cases of Reye syndrome are associated with the use of aspirin during these viral infections.

Mutations in the "HADH" gene lead to inadequate levels of an enzyme called 3-hydroxyacyl-coenzyme A dehydrogenase. Medium-chain and short-chain fatty acids cannot be metabolized and processed properly without sufficient levels of this enzyme. As a result, these fatty acids are not converted to energy, which can lead to characteristic features of this disorder, such as lethargy and hypoglycemia. Medium-chain and short-chain fatty acids or partially metabolized fatty acids may build up in tissues and damage the liver, heart, and muscles, causing more serious complications.

This condition is inherited in an autosomal recessive pattern, which means two copies of the gene in each cell are altered. Most often, the parents of an individual with an autosomal recessive disorder each carry one copy of the altered gene but do not show signs and symptoms of the disorder.