The hallmark of encephalopathy is an altered mental state. Characteristic of the altered mental state is impairment of the cognition, attention, orientation, sleep–wake cycle and consciousness. An altered state of consciousness may range from failure of selective attention to drowsiness. Hypervigilance may be present; with or without: congnitive deficits, headache, epileptic seizures, myoclonus (involuntary twitching of a muscle or group of muscles) or asterixis ("flapping tremor" of the hand when wrist is extended).

Depending on the type and severity of encephalopathy, common neurological symptoms are loss of cognitive function, subtle personality changes, inability to concentrate. Other neurological signs may include dysarthria, hypomimia, problems with movements (they can be clumsy or slow), ataxia, tremor. Another neurological signs may include involuntary grasping and sucking motions, nystagmus (rapid, involuntary eye movement), jactitation (restless picking at things characteristic of severe infection), and respiratory abnormalities such as Cheyne-Stokes respiration (cyclic waxing and waning of tidal volume), apneustic respirations and post-hypercapnic apnea. Focal neurological deficits are less common.

Encephalopathies exhibits both neurologic and psychopathologic symptoms.

Wernicke encephalopathy (alcoholic encephalopathy) also develop Korsakoff's syndrome, characterized by amnestic-confabulatory syndrome: retrograde amnesia, anterograde amnesia, confabulations (invented memories), poor recall and disorientation.

Anti-NMDA receptor encephalitis is the most common autoimmune encephalitis. It can cause paranoid and grandiose delusions, agitation, hallucinations (visual and auditory), bizarre behavior, fear, short-term memory loss, confusion.

HIV encephalopathy develop dementia ( †).

The mildest form of hepatic encephalopathy is difficult to detect clinically, but may be demonstrated on neuropsychological testing. It is experienced as forgetfulness, mild confusion, and irritability. The first stage of hepatic encephalopathy is characterised by an inverted sleep-wake pattern (sleeping by day, being awake at night). The second stage is marked by lethargy and personality changes. The third stage is marked by worsened confusion. The fourth stage is marked by a progression to coma.

More severe forms of hepatic encephalopathy lead to a worsening level of consciousness, from lethargy to somnolence and eventually coma. In the intermediate stages, a characteristic jerking movement of the limbs is observed (asterixis, "liver flap" due to its flapping character); this disappears as the somnolence worsens. There is disorientation and amnesia, and uninhibited behaviour may occur. In the third stage, neurological examination may reveal clonus and positive Babinski sign. Coma and seizures represent the most advanced stage; cerebral oedema (swelling of the brain tissue) leads to death.

Encephalopathy often occurs together with other symptoms and signs of liver failure. These may include jaundice (yellow discolouration of the skin and the whites of the eyes), ascites (fluid accumulation in the abdominal cavity), and peripheral edema (swelling of the legs due to fluid build-up in the skin). The tendon reflexes may be exaggerated, and the plantar reflex may be abnormal, namely extending rather than flexing (Babinski's sign) in severe encephalopathy. A particular smell ("foetor hepaticus") may be detected.

Hepatic encephalopathy (HE) is an altered level of consciousness as a result of liver failure. Onset may be gradual or sudden. Other symptoms may include movement problems, changes in mood, or changes in personality. In the advanced stages it can result in a coma.

Hepatic encephalopathy can occur in those with acute or chronic liver disease. Episodes can be triggered by infections, GI bleeding, constipation, electrolyte problems, or certain medications. The underlying mechanism is believed to involve the build up of ammonia in the blood, a substance that is normally removed by the liver. The diagnosis is typically made after ruling out other potential causes. It may be supported by blood ammonia levels, an electroencephalogram, or a CT scan of the brain.

Hepatic encephalopathy is possibly reversible with treatment. This typically involves supportive care and addressing the triggers of the event. Lactulose is frequently used to decrease ammonia levels. Certain antibiotics and probiotics are other potential options. A liver transplant may improve outcomes in those with severe disease.

More than 40% of people with cirrhosis develop hepatic encephalopathy. More than half of those with cirrhosis and significant HE live less than a year. In those who are able to get a liver transplant, the risk of death is less than 30% over the subsequent five years. The condition has been described since at least 1860.

Hypertensive encephalopathy is most commonly encountered in young and middle-aged people who have hypertension. Overall, the condition is rare even among people with hypertension. Studies report that from 0.5 to 15% of people with malignant hypertension develop hypertensive encephalopathy. With the development of methods for detection and treatment of hypertension, hypertensive encephalopathy has been becoming more rare.

Symptoms of hypertensive encephalopathy typically start to occur 12–48 hours after a sudden and sustained increase in blood pressure. The first manifestation of these symptoms is a severe headache. Headache occurs in greater than 75% of patients. The patient becomes restless. Alterations in consciousness may follow several hours later, which include impaired judgement and memory, confusion, somnolence and stupor. If the condition is not treated, these neurological symptoms may worsen and ultimately turn into a coma. Other symptoms may include increased irritability, vomiting, diplopia, seizures, twitching and myoclonus of the limbs. Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness) are common. They occur in 4 out of 11 cases (Jellinek et al. 1964). Hemiparesis, intracerebral hemorrhage, aphasia may also occur, but they are less common.

Neonatal encephalopathy (NE), also known as neonatal hypoxic-ischemic encephalopathy (neonatal HIE or NHIE), is defined by signs and symptoms of abnormal neurological function in the first few days of life in an infant born at term. In this condition there is difficulty initiating and maintaining respirations, a subnormal level of consciousness, and associated depression of tone, reflexes, and possibly seizures. Encephalopathy is a nonspecific response of the brain to injury which may occur via multiple methods, but is commonly caused by birth asphyxia.

In neonates born at or beyond 35 weeks, neonatal encephalopathy may present itself as the following symptoms:

- Reduced level of consciousness

- Seizures (which peak at 48 hours)

- Difficulty initiating and maintaining respiration

- Depression of tone and reflexes

This illness has a minimum incubation period of 7 months with a maximum of 12 months. This disease results in mortality of adult animals.

Clinical signs of TME include the characteristic behavioural changes such as confusion, loss of cleanliness, and aimless circling. An affected animal shows signs of weight loss, might develop matted fur, hindquarter ataxia, and its tail arched over its back. Seizures may very rarely occur. Near-death stages include the animal showing signs of drowsiness and unresponsiveness.

Currently, no tests are available to detect signs of this illness in live animals. However, veterinary pathologists can confirm this illness by microscopic examination of the brain tissue in animals suspected to have died of this disease, where they expect to detect areas of distinct sponge-like formations, or by the identification of the prion protein in these tissue samples.

The classic triad of symptoms found in Wernicke's encephalopathy is:

- ophthalmoplegia (later expanded to other eye movement abnormalities, most commonly affecting the lateral rectus or any eye sign. Lateral nystagmus is most commonly seen although lateral rectus palsy, usually bilateral, may be seen).

- ataxia (later expanded to imbalance or any cerebellar signs)

- confusion (later expanded to other mental changes. Has 82% incidence in diagnosis cases)

However, in actuality, only a small percentage of patients experience all three symptoms, and the full triad occurs more frequently among those who have overused alcohol.

Also a much more diverse range of symptoms has been found in patients with this condition, including:

- pupillary changes, retinal hemorrhage, papilledema, impaired vision and hearing, vision loss

- hearing loss,

- fatigability, apathy, irritability, drowsiness, psycho and/or motor slowing

- dysphagia, blush, sleep apnea, epilepsy and stupor

- lactic acidosis

- memory impairment, amnesia, depression, psychosis

- hypothermia, polyneuropathy, hyperhidrosis.

Although hypothermia is usually diagnosed with a body temperature of 35 °C / 95° Fahrenheit, or less, incipient cooling caused by deregulation in the CNS needs to be monitored because it can promote the development of an infection. The patient may report feeling cold, followed by mild chills, cold skin, moderate pallor, tachycardia, hypertension, tremor or piloerection. External warming techniques are advised to prevent hypothermia.

Among the frequently altered functions are the cardio circulatory. There may be tachycardia, dyspnea, chest pain, orthostatic hypotension, changes in heart rate and blood pressure. The lack of thiamine sometimes affects other major energy consumers, the myocardium, and also patients may have developed cardiomegaly. Heart failure with lactic acidosis syndrome has been observed. Cardiac abnormalities are an aspect of the WE, which was not included in the traditional approach, and are not classified as a separate disease.

Infections have been pointed out as one of the most frequent triggers of death in WE. Furthermore, infections are usually present in pediatric cases.

In the last stage others symptoms may occur: hyperthermia, increased muscle tone, spastic paralysis, choreic dyskinesias and coma.

Because of the frequent involvement of heart, eyes and peripheral nervous system, several authors prefer to call it Wernicke disease rather than simply encephalopathy.

Early symptoms are nonspecific, and it has been stated that WE may present nonspecific findings. In Wernicke Korsakoff’s syndrome some single symptoms are present in about one-third.

Depending on the location of the brain lesion different symptoms are more frequent:

- Brainstem tegmentum. - Ocular: pupillary changes. Extraocular muscle palsy; gaze palsy: nystagmus.

- Hypothalamus. Medulla: dorsal nuc. of vagus. - Autonomic dysfunct.: temperature; cardiocirculatory; respiratory.

- Medulla: vestibular region. Cerebellum. - Ataxia.

- Dorsomedial nuc. of thalamus. Mammillary bodies. - Amnestic syndrome for recent memory.

Mamillary lesion are characteristic-small petechial hemorrhages are found.

- Diffuse cerebral dysfunction.- Altered cognition: global confusional state.

- Brainstem: periaqueductal gray.- Reduction of consciousness

- Hypothalamic lesions may also affect the immune system, which is known in alcohol abusers, causing dysplasias and infections.

Typical symptoms of PRES, listed according to prevalence, include: altered mental status (encephalopathy), seizure, and headache. Less commonly there may be visual disturbances, focal neurologic signs, and status epilepticus.

Hypertensive encephalopathy (HE) is general brain dysfunction due to significantly high blood pressure. Symptoms may include headache, vomiting, trouble with balance, and confusion. Onset is generally sudden. Complications can include seizures, posterior reversible encephalopathy syndrome, and bleeding in the back of the eye.

In hypertensive encephalopathy, generally the blood pressure is greater than 200/130 mmHg. Occasionally it can occur at a BP as low as 160/100 mmHg. This can occur in kidney failure, those who rapidly stop blood pressure medication, pheochromocytoma, and people on a monoamine oxidase inhibitor (MAOI) who eats foods with tyramine. When it occurs in pregnancy it is known as eclampsia. The diagnosis requires ruling out other possible causes.

The condition is generally treated with medications to relatively rapidly lower the blood pressure. This may be done with labetalol or sodium nitroprusside given by injection into a vein. In those who are pregnant, magnesium sulfate may be used. Other treatments may include anti seizure medications.

Hypertensive encephalopathy is uncommon. It is believed to occur more often in those without easy access to health care. The term was first used by Oppenheimer and Fishberg in 1928. It is classified as a type of hypertensive emergency.

The signs of sepsis are non-specific and include:

- Body temperature changes

- Breathing problems

- Diarrhea

- Low blood sugar (hypoglycemia)

- Reduced movements

- Reduced sucking

- Seizures

- Bradycardia

- Swollen belly area

- Vomiting

- Yellow skin and whites of the eyes (jaundice)

A heart rate above 160 can also be an indicator of sepsis, this tachycardia can present up to 24 hours before the onset of other signs.

Toxic encephalopathy is often irreversible. If the source of the problem is treated by removing the toxic chemical from the system, further damage can be prevented, but prolonged exposure to toxic chemicals can quickly destroy the brain. Long term studies have demonstrated residual cognitive impairment (primarily attention and information-processing impairment resulting in dysfunction in working memory) up to 10 years following cessation of exposure. Severe cases of toxic encephalopathy can be life-threatening.

Several factors appear to play a role in the pathogenesis of PRES, including medications that suppress the function of the immune system (immunosuppressive medications), kidney failure, eclampsia, severe high blood pressure, systemic lupus erythematosus, and postpartum haemorrhage.

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.

"Encephalopathy" is a general term describing brain malfunctions and "toxic" asserts that the malfunction is caused by toxins on the brain. The most prominent characteristic of toxic encephalopathy is an altered mental status. Acute intoxication is a reversible symptom of exposure to many synthetic chemical neurotoxicants. Acute intoxication symptoms include lightheadedness, dizziness, headache and nausea, and regular cumulative exposure to these toxic solvents over a number of years puts the individual at high risk for developing toxic encephalopathy. Chronic exposure to low levels of neurotoxic chemicals can also cause reversible changes in mood and affect which resolve with cessation of exposure. Acute and chronic toxic encephalopathy on the other hand, are persistent changes in neurological function that typically occur with exposure to higher concentrations and longer durations respectively. The symptoms of acute and chronic toxic encephalopathy do not resolve with cessation of exposure and can include memory loss, small personality changes/increased irritability, insidious onset of concentration difficulties, involuntary movements (parkinsonism), fatigue, seizures, arm strength problems, and depression. Neurobehavioral effects of occupational exposure to organic solvents exists among painters. The condition may also be referred to as substance-induced persistent dementia.

Magnetic Resonance Imaging (MRI) analyses have also demonstrated increased rates of dopamine synthesis in the putamen, reduced anterior and total corpus callosum volume, demyelination in the parietal white matter, basal ganglia, and thalamus, as well as atypical activation of frontal areas of the brain due to neural compensation. A thorough and standard diagnostic process is paramount with toxic encephalopathy, including a careful occupational history, medical history, and standardized imaging/neurobehavioral testing.

Transmissible mink encephalopathy (TME) is a rare sporadic disease that affects the central nervous system of ranch-raised mink. It is classified as a transmissible spongiform encephalopathy, believed to be caused by proteins called prions. This disease is only known to affect adult mink.

Neonatal sepsis is a type of neonatal infection and specifically refers to the presence in a newborn baby of a bacterial blood stream infection (BSI) (such as meningitis, pneumonia, pyelonephritis, or gastroenteritis) in the setting of fever. Older textbooks may refer to neonatal sepsis as "sepsis neonatorum". Criteria with regards to hemodynamic compromise or respiratory failure are not useful clinically because these symptoms often do not arise in neonates until death is imminent and unpreventable. Neonatal sepsis is divided into two categories: early-onset sepsis (EOS) and late-onset sepsis (LOS). EOS refers to sepsis presenting in the first 7 days of life (although some refer to EOS as within the first 72 hours of life), with LOS referring to presentation of sepsis after 7 days (or 72 hours, depending on the system used). neonatal sepsis is the single most important cause of neonatal death in hospital as well as community in developing country.

It is difficult to clinically exclude sepsis in newborns less than 90 days old that have fever (defined as a temperature > 38 °C (100.4 °F). Except in the case of obvious acute viral bronchiolitis, the current practice in newborns less than 30 days old is to perform a complete workup including complete blood count with differential, blood culture, urinalysis, urine culture, and cerebrospinal fluid (CSF) studies and CSF culture, admit the newborn to the hospital, and treat empirically for serious bacterial infection for at least 48 hours until cultures are demonstrated to show no growth. Attempts have been made to see whether it is possible to risk stratify newborns in order to decide if a newborn can be safely monitored at home without treatment despite having a fever. One such attempt is the Rochester criteria.

MRI: medial temporal lobe signal change bilateral hippocampal lesions, with signals that were hypointense in IR sequences and hyperintense in FLAIR.

Coagulopathy is another cardinal feature of ALF. The liver has the central role in the synthesis of almost all coagulation factors and some inhibitors of coagulation and fibrinolysis. Hepatocellular necrosis leads to impaired synthesis of many coagulation factors and their inhibitors. The former produces a prolongation in prothrombin time which is widely used to monitor the severity of hepatic injury. There is significant platelet dysfunction (with both quantitative and qualitative platelet defects). Progressive thrombocytopenia with the loss of larger and more active platelets is almost universal. Thrombocytopenia with or without DIC increases risk of intracerebral bleeding.

In ALF, hepatic encephalopathy leads to cerebral edema, coma, brain herniation, and eventually death. Detection of encephalopathy is central to the diagnosis of ALF. It may vary from subtle deficit in higher brain function (e.g. mood, concentration in grade I) to deep coma (grade IV). Patients presenting as acute and hyperacute liver failure are at greater risk of developing cerebral oedema and grade IV encephalopathy. The pathogenesis remains unclear, but is likely to be a consequence of several phenomena. There is a buildup of toxic substances like ammonia, mercaptan, benzodiazepines, serotonin and tryptophan in the brain. This affects neurotransmitter level and neuroreceptor activation. Autoregulation of cerebral blood flow is impaired, and is associated with anaerobic glycolysis and oxidative stress. Neuronal cell astrocytes are susceptible to these changes, and they swell up, resulting in increased intracranial pressure. Inflammatory mediators also play important role.

Unfortunately, signs of elevated intracranial pressure, such as papilledema and loss of pupillary reflexes, are not reliable, and occur late in the disease process. CT imaging of the brain is also unhelpful in detecting early cerebral oedema, but is often performed to rule out intra-cerebral bleeding. Invasive intracranial pressure monitoring via subdural route is often recommended; however, the risk of complications must be weighed against the possible benefit (1% fatal haemorrhage). The aim is to maintain intracranial pressures below 25 mm Hg, and cerebral perfusion pressures above 50 mm Hg.

Based on syndrome with focal or diffuse neurological dysfunction associated with fever. Inflammatory lesion in MRI and CSF pleocytosis. EEG signs of encephalitis.

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.

Waterhouse-Friderichsen Syndrome can be caused by a number of different organisms (see below). When caused by Neisseria meningitidis, WFS is considered the most severe form of meningococcal sepsis. The onset of the illness is nonspecific with fever, rigors, vomiting, and headache. Soon a rash appears; first macular, not much different from the rose spots of typhoid, and rapidly becoming petechial and purpuric with a dusky gray color. Low blood pressure (hypotension) develops and rapidly leads to septic shock. The cyanosis of extremities can be extreme and the patient is very prostrated or comatose. In this form of meningococcal disease, meningitis generally does not occur. Low levels of blood glucose and sodium, high levels of potassium in the blood, and the ACTH stimulation test demonstrate the acute adrenal failure. Leukocytosis need not be extreme and in fact leukopenia may be seen and it is a very poor prognostic sign. C-reactive protein levels can be elevated or almost normal. Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of disseminated intravascular coagulation (DIC). Acidosis and acute kidney failure can be seen as in any severe sepsis. Meningococci can be readily cultured from blood or cerebrospinal fluid, and can sometimes be seen in smears of cutaneous lesions. Difficulty swallowing, atrophy of the tongue, and cracks at the corners of the mouth are also characteristic features.