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.

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.

Criteria for diagnosis of abdominal epilepsy includes frequent periodic abdominal symptoms, an abnormal electroencephalogram (EEG) and significant improvement of gastrointestinal symptoms after taking anti-seizure medication. Medical testing for diagnosis can be completed using MRI scans of the brain, CT scans and ultrasounds of the abdomen, endoscopy of the gastrointestinal tract, and blood tests.

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 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.

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

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.

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.

Besides the clinical picture, fasting VIP plasma level may confirm the diagnosis, and CT scan and somatostatin receptor scintigraphy are used to localise the tumor, which is usually metastatic at presentation.

Tests include:

- Blood chemistry tests (basic or comprehensive metabolic panel)

- CT scan of the abdomen

- MRI of the abdomen

- Stool examination for cause of diarrhea and electrolyte levels

- Vasoactive intestinal peptide (VIP) level in the blood

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.

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.

Pyruvate dehydrogenase deficiency can be diagnosed via the following methods:

- Blood test (Lactate and pyruvate levels)

- Urine analysis

- Magnetic resonance spectroscopy

- MRI

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).

The differential diagnosis of pyruvate dehydrogenase deficiency can consist of either D-Lactic acidosis or abnormalities associated with gluconeogenesis.

Metabolic disorder screening can be done in newborns via the following methods:

- Blood test

- Skin test

- Hearing test

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."

Congenital lactic acidosis can be suspected based on blood or cerebrospinal fluid tests showing high levels of lactate; the underlying genetic mutation can only be diagnosed with genetic testing.

The primary diagnostic test for absence seizures is EEG. However, brain scans such as by an MRI can help rule out other diseases, such as a stroke or a brain tumor.

During electroencephalography, hyperventilation can be used to provoke these seizures. Ambulatory EEG monitoring over 24 hours can quantify the number of seizures per day and their most likely times of occurrence.

Absence seizures are brief (usually less than 20 seconds) generalized epileptic seizures of sudden onset and termination. When someone experiences an absence seizure they are often unaware of their episode. Those most susceptible to this are children, and the first episode usually occurs between 4–12 years old. It is very rare that someone older will experience their first absence seizure. Episodes of absence seizures can often be mistaken for inattentiveness when misdiagnosed, and can occur 50-100 times a day. They can be so difficult to detect that some people may go months or years before being given a proper diagnosis. There are no known before or after effects of absence seizures.

Absence seizures have two essential components:

- Clinical - the impairment of consciousness (absence)

- Electroencephalography - an (EEG) shows generalized spike-and-slow wave discharges

Absence seizures are broadly divided into typical and atypical types:

- Typical absence seizures usually occur in the context of idiopathic generalised epilepsies and an EEG shows fast >2.5 Hz generalised spike-wave discharges. The prefix "typical" is to differentiate them from atypical absences rather than to characterise them as "classical" or characteristic of any particular syndrome.

- Atypical absence seizures:

- Occur only in the context of mainly severe symptomatic or cryptogenic epilepsies of children with learning difficulties who also suffer from frequent seizures of other types, such as atonic, tonic and myoclonic.

- Onset and termination is not so abrupt and changes in tone are more pronounced.

- Ictal - EEG is of slow (less than 2.5 Hz) spike and slow wave. The discharge is heterogeneous, often asymmetrical and may include irregular spike and slow wave complexes, fast and other paroxysmal activity. Background interictal EEG is usually abnormal.

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.

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.

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

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.)

The prognosis for gliomatosis cerebri is generally poor. Surgery is not practical considering the extent of the disease, standard chemotherapy (nitrosourea) has been unsuccessful, and while brain irradiation can stabilize or improve neurologic function in some patients, its impact on survival has yet to be proven.

In 2014, Weill Cornell Brain and Spine Center launched an international registry for Gliomatosis Cerebri, where tissue samples can be stored for genomic study.

As one of the urea cycle disorders, citrullinemia type I needs to be distinguished from the others: carbamyl phosphate synthetase deficiency, argininosuccinic acid lyase deficiency, ornithine transcarbamylase deficiency, arginase deficiency, and N-Acetylglutamate synthase deficiency. Other diseases that may appear similar to CTLN1 include the organic acidemias and citrullinemia type II. To diagnose CTLN1, a blood test for citrulline and ammonia levels can indicate the correct diagnosis; high levels of both are indicative of this disorder. Newborns are routinely screened for CTLN1 at birth. A genetic test is the only definitive way to diagnose it.

While the progression of dysfunction is variable, it is regarded as a serious complication and untreated can progress to a fatal outcome. Diagnosis is made by neurologists who carefully rule out alternative diagnoses. This routinely requires a careful neurological examination, brain scans (MRI or CT scan) and a lumbar puncture to evaluate the cerebrospinal fluid. No single test is available to confirm the diagnosis, but the constellation of history, laboratory findings and examination can reliably establish the diagnosis when performed by experienced clinicians. The amount of virus in the brain does not correlate well with the degree of dementia, suggesting that secondary mechanisms are also important in the manifestation of ADC.