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.

Signs and symptoms can include:

- hypoglycemia

- lethergy

- hepatomegaly

- muscle pain

- cardiomyopathy

Symptoms which can return over the following month include:

- Flu-like symptoms

- Fatigue

- Fever

- Abdominal pain

- Strong headaches similar to migraines

- Nausea

- Vomiting

- Diarrhea

- Lack of concentration

- Appetite loss

- Depression

- Jaundice, a yellowing of the skin or whites of the eyes

- Sharp pains in the right-upper quadrant of the abdomen

- Weight loss

The symptoms of a cholinergic toxidrome include bronchorrhea, confusion, defecation, diaphoresis, diarrhea, emesis, lacrimation, miosis, muscle fasciculations, salivation, seizures, urination, and weakness. Complications include bradycardia, hypothermia, and tachypnea. Substances that may cause this toxidrome include carbamates, mushrooms, and organophosphates.

Common mnemonics for organophosphate poisoning include the "killer B's" of bradycardia, bronchorrhea and bronchospasm because they are the leading cause of death, and SLUDGE - Salivation, Lacrimation, Urination, Diarrhea, Gastrointestinal distress, and Emesis.

An alternative mnemonic is DUMBBELLSS - Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Emesis, Lacrimation, Lethargy, Salivation and Seizures.

Typically, initial signs and symptoms of this disorder occur during infancy and include low blood sugar (hypoglycemia), lack of energy (lethargy), and muscle weakness. There is also a high risk of complications such as liver abnormalities and life-threatening heart problems. Symptoms that begin later in childhood, adolescence, or adulthood tend to be milder and usually do not involve heart problems. Episodes of very long-chain acyl-coenzyme A dehydrogenase deficiency can be triggered by periods of fasting, illness, and exercise.

It is common for babies and children with the early and childhood types of VLCADD to have episodes of illness called metabolic crises. Some of the first symptoms of a metabolic crisis are: extreme sleepiness, behavior changes, irritable mood, poor appetite.

Some of these other symptoms of VLCADD in infants may also follow: fever, nausea, diarrhea, vomiting, hypoglycemia.

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 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.

Typically, initial signs and symptoms of this disorder occur during infancy or early childhood and can include feeding difficulties, lethargy, hypoglycemia, hypotonia, liver problems, and abnormalities in the retina. Muscle pain, a breakdown of muscle tissue, and abnormalities in the nervous system that affect arms and legs (peripheral neuropathy) may occur later in childhood. There is also a risk for complications such as life-threatening heart and breathing problems, coma, and sudden unexpected death. Episodes of LCHAD deficiency can be triggered by periods of fasting or by illnesses such as viral infections.

The symptoms may not appear for several days. The main symptom is the animal has a wet tail, matted with faeces. Other signs of the disease are:

- Smell/ foul odor

- Diarrhea

- Lethargy

- Lack of appetite

- Excess sleeping

- Walking with a hunched back

- Folded ears

- Unusual temper(biting or nipping)

The most common symptom of abdominal epilepsy is abdominal pain followed by uncontrollable vomiting, usually preceded by lethargy. Symptoms also include generalized tonic-clonic seizures followed by sleep, confusion, and unresponsiveness.

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).

Characteristic symptoms are:

- Sudden penetrating pain in the legs, lower back or abdomen

- Confusion, psychosis, slurred speech

- Severe lethargy

- Convulsions

- Fever

- Hyperkalemia (elevated potassium level in the blood)

- Hypercalcemia (elevated calcium level in the blood): the cause of hypercalcemia is a combination of increased calcium input into the extracellular space and reduced calcium removal by the kidney, this last caused by decreased glomerular filtration and increased tubular calcium reabsorption. Both renal factors are secondary to volume depletion and, in fact, improve rapidly during rehydration with saline infusion.

- Hypoglycemia (reduced level of blood glucose)

- Hyponatremia (low sodium level in the blood)

- Hypotension (low blood pressure)

- Hypothyroid (low T4 level)

- Severe vomiting and diarrhea, resulting in dehydration

- Syncope (loss of consciousness and ability to stand)

The clinical manifestations of absence seizures vary significantly among patients. Impairment of consciousness is the essential symptom, and may be the only clinical symptom, but this can be combined with other manifestations. The hallmark of the absence seizures is abrupt and sudden-onset impairment of consciousness, interruption of ongoing activities, a blank stare, possibly a brief upward rotation of the eyes. If the patient is speaking, speech is slowed or interrupted; if walking, they stand transfixed; if eating, the food will stop on its way to the mouth. Usually, the patient will be unresponsive when addressed. In some cases, attacks are aborted when the patient is called. The attack lasts from a few seconds to half a minute, and evaporates as rapidly as it commenced. Absence seizures generally are not followed by a period of disorientation or lethargy (post-ictal state), in contrast to the majority of seizure disorders.

1. Absence with impairment of consciousness only as per the above description.

2. Absence with mild clonic components. Here the onset of the attack is indistinguishable from the above, but clonic components may occur in the eyelids, at the corner of the mouth, or in other muscle groups which may vary in severity from almost imperceptible movements to generalised myoclonic jerks. Objects held in the hand may be dropped.

3. Absence with atonic components. Here there may be a diminution in tone of muscles subserving posture as well as in the limbs leading to dropping of the head, occasionally slumping of the trunk, dropping of the arms, and relaxation of the grip. Rarely tone is sufficiently diminished to cause this person to fall.

4. Absence with tonic components. Here during the attack tonic muscular contraction may occur, leading to increase in muscle tone which may affect the extensor muscles or the flexor muscles symmetrically or asymmetrically. If the patient is standing, the head may be drawn backward and the trunk may arch. This may lead to retropulsion, which may cause eyelids to twitch rapidly, eyes may jerk upwards or the patients head may rock back and forth slowly, as if nodding. The head may tonically draw to one or another side.

5. Absence with automatisms. Purposeful or quasipurposeful movements occurring in the absence of awareness during an absence attack are frequent and may range from lip licking and swallowing to clothes fumbling or aimless walking. If spoken to, the patient may grunt, and when touched or tickled may rub the site. Automatisms are quite elaborate and may consist of combinations of the above described movements or may be so simple as to be missed by casual observation.

6. Absence with autonomic components. These may be pallor, and less frequently flushing, sweating, dilatation of pupils and incontinence of urine.

Mixed forms of absence frequently occur.

These seizures can happen a few times a day or in some cases hundreds of times a day, to the point that the person cannot concentrate in school or in other situations requiring sustained, concentrated attention.

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".

Abdominal epilepsy, also known as autonomic epilepsy, is a rare condition most frequently found in children, consisting of gastrointestinal (GI) disturbances caused by epileptiform seizure activity.

It has been described as a type of temporal lobe epilepsy. Responsiveness to anticonvulsants can aid in the diagnosis.

Most published medical literature dealing with abdominal epilepsy is in the form of individual case reports. A 2005 review article found a total of 36 cases described in the medical literature.

It typically presents as a severe encephalopathy with myoclonic seizures, is rapidly progressive and eventually results in respiratory arrest.Standard evaluation for inborn errors of metabolism and other causes of this presentation does not reveal any abnormality (no acidosis, no hypoglycaemia, or hyperammonaemia and no other organ affected). Pronounced and sustained hiccups in an encephalopathic infant have been described as a typical observation in non-ketotic hyperglycinaemia.

There are several different forms of glycine encephalopathy, which can be distinguished by the age of onset, as well as the types and severity of symptoms. All forms of glycine encephalopathy present with only neurological symptoms, including mental retardation (IQ scores below 20 are common), hypotonia, apneic seizures, and brain malformations.

With the classical, or neonatal presentation of glycine encephalopathy, the infant is born after an unremarkable pregnancy, but presents with lethargy, hypotonia, apneic seizures and myoclonic jerks, which can progress to apnea requiring artificial ventilation, and often death. Apneic patients can regain spontaneous respiration in their second to third week of life. After recovery from the initial episode, patients have intractable seizures and profound mental retardation, remaining developmentally delayed. Some mothers comment retrospectively that they noticed fetal rhythmic "hiccuping" episodes during pregnancy, most likely reflecting seizure episodes in utero. Patients with the infantile form of glycine encephalopathy do not show lethargy and coma in the neonatal period, but often have a history of hypotonia. They often have seizures, which can range in severity and responsiveness to treatment, and they are typically developmentally delayed. Glycine encephalopathy can also present as a milder form with episodic seizures, ataxia, movement disorders, and gaze palsy during febrile illness. These patients are also developmentally delayed, to varying degrees. In the later onset form, patients typically have normal intellectual function, but present with spastic diplegia and optic atrophy.

Transient neonatal hyperglycinemia has been described in a very small number of cases. Initially, these patients present with the same symptoms and laboratory results that are seen in the classical presentation. However, levels of glycine in plasma and cerebrospinal fluid typically normalize within eight weeks, and in five of six cases there were no neurological issues detected at follow-up times up to thirteen years. A single patient was severely retarded at nine months. The suspected cause of transient neonatal hyperglicinemia is attributed to low activity of the glycine cleavage system in the immature brain and liver of the neonate.

Adrenal crisis (also known as Addisonian crisis and acute adrenal insufficiency) is a medical emergency and potentially life-threatening situation requiring immediate emergency treatment. It is a constellation of symptoms that indicate severe adrenal insufficiency caused by insufficient levels of the hormone cortisol. This may be the result of either previously undiagnosed or untreated Addison's disease, a disease process suddenly affecting adrenal function (such as bleeding from the adrenal glands in Waterhouse-Friderichsen syndrome), suddenly stopping intake of glucocorticoids or an intercurrent problem (e.g. infection, trauma, in fact any form of physical or mental stress) in someone known to have Addison's disease or congenital adrenal hyperplasia (CAH).

Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency, often shortened to LCHAD deficiency, is a rare autosomal recessive fatty acid oxidation disorder that prevents the body from converting certain fats into energy. This can become life-threatening, particularly during periods of fasting.

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.

A form of enterotoxemia caused by Type B or Type C "C.perfringens." Calves less than 1 month of old are affected. The symptoms include, diarrhea, abdominal discomfort, convulsions, and opisthotonos. Death may occur within a few days but recovery from this form is possible.

The major clinical features are prolonged watery diarrhea (fasting stool volume > 750 to 1000 mL/day) and symptoms of hypokalemia and dehydration.

Half of the patients have relatively constant diarrhea while the rest have alternating periods of severe and moderate diarrhea.

One third have diarrhea < 1yr before diagnosis, but in 25%, diarrhea is present for 5 yr or more before diagnosis.

Lethargy, muscle weakness, nausea, vomiting and crampy abdominal pain are frequent symptoms.

Hypokalemia and impaired glucose tolerance occur in < 50% of patients. Achlorhydria is also a feature.

During attacks of diarrhea, flushing similar to the carcinoid syndrome occur rarely.

PDCD is generally presented in one of two forms. The metabolic form appears as lactic acidosis. The neurological form of PDCD contributes to hypotonia, poor feeding, lethargy and structural abnormalities in the brain. Patients may develop seizures and/or neuropathological spasms. These presentations of the disease usually progress to mental retardation, microcephaly, blindness and spasticity.

Females with residual pyruvate dehydrogenase activity will have no uncontrollable systemic lactic acidosis and few, if any, neurological symptoms. Conversely, females with little to no enzyme activity will have major structural brain abnormalities and atrophy. Males with mutations that abolish, or almost abolish, enzyme activity presumably die in utero because brain cells are not able to generate enough ATP to be functionally viable. It is expected that most cases will be of mild severity and have a clinical presentation involving lactic acidosis.

Prenatal onset may present with non-specific signs such as low Apgar scores and small for gestational age. Metabolic disturbances may also be considered with poor feeding and lethargy out of proportion to a mild viral illness, and especially after bacterial infection has been ruled out. PDH activity may be enhanced by exercise, phenylbutyrate and dichloroacetate.

The clinical presentation of congenital PDH deficiency is typically characterized by heterogenous neurological features that usually appear within the first year of life. In addition, patients usually show severe hyperventillation due to profound metabolic acidosis mostly related to lactic acidosis. Metabolic acidosis in these patients is usually refractory to correction with bicarbonate.

Wet-tail or proliferative ileitis, is a disease of hamsters. It is precipitated by stress. Even with treatment, the animal can die within 48–72 hours. Baby hamsters are much more likely to get the disease than older hamsters. It commonly is found when the hamster is being weaned at about four weeks of age.

Typically, initial signs and symptoms of this disorder occur during infancy or early childhood and can include poor appetite, vomiting, diarrhea, lethargy, hypoglycemia, hypotonia, liver problems, and abnormally high levels of hyperinsulinism. Insulin controls the amount of sugar that moves from the blood into cells for conversion to energy. Individuals with 3-hydroxyacyl-coenzyme A dehydrogenase deficiency are also at risk for complications such as seizures, life-threatening heart and breathing problems, coma, and sudden unexpected death.

Problems related to 3-hydroxyacyl-coenzyme A dehydrogenase deficiency can be triggered by periods of fasting or by illnesses such as viral infections. This disorder is sometimes mistaken for Reye syndrome, a severe disorder that may develop 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.