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.

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.

Encephalopathy is a difficult term because it can be used to denote either a disease or finding (i.e., an observable sign in a patient).

When referring to a finding, encephalopathy refers to permanent (or degenerative) brain injury, or a reversible one. It can be due to direct injury to the brain, or illness remote from the brain. The individual findings that cause a clinician to refer to a patient as having encephalopathy include intellectual disability, irritability, agitation, delirium, confusion, somnolence, stupor, coma and psychosis. As such, describing a patient as having a clinical picture of encephalopathy is not a very specific description.

When referring to a disease, encephalopathy refers to a wide variety of brain disorders with very different etiologies, prognoses and implications. For example, prion diseases, all of which cause transmissible spongiform encephalopathies, are invariably fatal, but other encephalopathies are reversible and can have a number of causes including nutritional deficiencies and toxins.

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.

The diagnosis is typically made clinically with magnetic resonance imaging of the brain often revealing hyperintensities on "T"-weighed imaging. Three patterns have been described: superior frontal sulcus, dominant parieto-occipital, and holohemispheric watershed.

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.

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.

The key symptom of RCVS is recurrent thunderclap headaches, which over 95% of patients experience. In two-thirds of cases, it is the only symptom. These headaches are typically bilateral, very severe and peak in intensity within a minute. They may last from minutes to days, and may be accompanied by nausea, photophobia, phonophobia or vomiting. Some patients experience only one headache, but on average there are four attacks over a period of one to four weeks. A milder, residual headache persists between severe attacks for half of patients.

1–17% of patients experience seizures. 8–43% of patients show neurologic problems, especially visual disturbances, but also hemiplegia, ataxia, dysarthria, aphasia, and numbness. These neurologic issues typically disappear within minutes or a few hours; more persistent symptoms may indicate a stroke. Posterior reversible encephalopathy syndrome is present in a small minority of patients.

This condition features the unique property that the patient's cerebral arteries can spontaneously constrict and relax back and forth over a period of time without intervention and without clinical findings. Vasospasm is common post subarachnoid hemorrhage and cerebral aneurysm, but in RCVS only 25% of patients have symptoms post subarachnoid hemorrhage.

Reversible cerebral vasoconstriction syndrome (RCVS, sometimes called Call-Fleming syndrome) is a disease characterized by a weeks-long course of thunderclap headaches, sometimes focal neurologic signs, and occasionally seizures. Symptoms are thought to arise from transient abnormalities in the blood vessels of the brain. In some cases, it may be associated with childbirth, vasoactive or illicit drug use, or complications of pregnancy.

For the vast majority of patients, all symptoms disappear on their own within three weeks. Deficits persist in a small minority of patients, with severe complications or death being very rare. Because symptoms resemble a variety of life-threatening conditions, differential diagnosis is necessary.

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.

A Posterior Circulation Infarct (POCI) is a type of cerebral infarction affecting the posterior circulation supplying one side of the brain.

Posterior Circulation Stroke Syndrome (POCS) refers to the symptoms of a patient who clinically appears to have had a posterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It can cause the following symptoms:

- Cranial nerve palsy AND contralateral motor/sensory defect

- motor or sensory defect

- Eye movement problems (e.g.nystagmus)

- Cerebellar dysfunction

- Isolated homonymous hemianopia

It has also been associated with deafness.

FIRES seizures are non-focal - there is no specified starting or stopping point - making brain surgery impossible. These seizures damage cognitive abilities of the brain such as memory or sensory abilities. This can result in learning disabilities, behavioral disorders, memory issues, sensory changes, inability to move, and death. Children continue to have seizures throughout their lives.

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

WE is characterized by the presence of a triad of symptoms;

1. Ocular disturbances (ophthalmoplegia)

2. Changes in mental state (confusion)

3. Unsteady stance and gait (ataxia)

This triad of symptoms results from a deficiency in vitamin B which is an essential coenzyme. The aforementioned changes in mental state occur in approximately 82% of patients' symptoms of which range from confusion, apathy, inability to concentrate, and a decrease in awareness of the immediate situation they are in. If left untreated, WE can lead to coma or death. In about 29% of patients, ocular disturbances consist of nystagmus and paralysis of the lateral rectus muscles or other muscles in the eye. A smaller percentage of patients experience a decrease in reaction time of the pupils to light stimuli and swelling of the optic disc which may be accompanied by retinal hemorrhage. Finally, the symptoms involving stance and gait occur in about 23% of patients and result from dysfunction in the cerebellum and vestibular system. Other symptoms that have been present in cases of WE are stupor, low blood pressure (hypotension), elevated heart rate (tachycardia), as well as hypothermia, epileptic seizures and a progressive loss of hearing.

Interestingly, about 19% of patients have none of the symptoms in the classic triad at first diagnosis of WE; however, usually one or more of the symptoms develops later as the disease progresses.

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.

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.

Ohtahara syndrome is rare and the earliest-appearing age-related epileptic encephalopathy, with seizure onset occurring within the first three months of life, and often in the first ten days. Many, but not all, cases of OS evolve into other seizure disorders, namely West syndrome and Lennox-Gastaut syndrome.

The primary outward manifestation of OS is seizures, usually presenting as tonic seizures (a generalized seizure involving a sudden stiffening of the limbs). Other seizure types that may occur include partial seizures, clusters of infantile spasms, and, rarely, myoclonic seizures. In addition to seizures, children with OS exhibit profound mental and physical retardation.

Clinically, OS is characterized by a "burst suppression" pattern on an EEG. This pattern involves high voltage spike wave discharge followed by little brain wave activity.

It is named for the Japanese neurologist Shunsuke Ohtahara (1930–2013), who identified it in 1976.

Most symptoms of people with post-viral cerebellar ataxia deal to a large extent with the movement of the body. Some common symptoms that are seen are clumsy body movements and eye movements, difficulty walking, nausea, vomiting, and headaches.

Peripheral Territory Lesions

1. Contralateral homonymous hemianopsia

2. cortical blindness with bilateral involvement of the occipital lobe branches

3. visual agnosia

4. prosopagnosia

5. dyslexia, Anomic aphasia, color naming and discrimination problems

6. memory defect

7. topographic disorientation

Central Territory Lesions

1. central post-stroke (thalamic) pain: spontaneous pain, dysesthesias and sensory impairments

2. involuntary movements: chorea, intention tremor, hemiballismus

3. contralateral hemiplegia

4. Weber’s syndrome: occulomotor nerve palsy

5. Bálint's syndrome: loss of voluntary eye movements optic ataxia, asimultagnosia (inability to understand visual objects)

Ohtahara syndrome (OS), also known as early infantile epileptic encephalopathy with burst-suppression (EIEE), is a progressive epileptic encephalopathy. The syndrome is outwardly characterized by tonic spasms and partial seizures, and receives its more elaborate name from the pattern of burst activity on an electroencephalogram (EEG). It is an extremely debilitating progressive neurological disorder, involving intractable seizures and severe mental retardation. No single cause has been identified, although in many cases structural brain damage is present.

Posterior cerebral artery syndrome is a condition whereby the blood supply from the posterior cerebral artery (PCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the occipital lobe, the inferomedial temporal lobe, a large portion of the thalamus, and the upper brainstem and midbrain.

This event restricts the flow of blood to the brain in a near-immediate fashion. The blood hammer is analogous to the water hammer in hydrology and it consists of a sudden increase of the upstream blood pressure in a blood vessel when the bloodstream is abruptly blocked by vessel obstruction. Complete understanding of the relationship between mechanical parameters in vascular occlusions is a critical issue, which can play an important role in the future diagnosis, understanding and treatment of vascular diseases.

Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with PCA syndrome. Blockages of the proximal portion of the vessel produce only minor deficits due to the collateral blood flow from the opposite hemisphere via the posterior communicating artery. In contrast, distal occlusions result in more serious complications. Visual deficits, such as agnosia, prosopagnosia or cortical blindness (with bilateral infarcts) may be a product of ischemic damage to occipital lobe. Occlusions of the branches of the PCA that supply the thalamus can result in central post-stroke pain and lesions to the subthalamic branches can produce “a wide variety of deficits”.

Left posterior cerebral artery syndrome presents alexia without agraphia; the lesion is in the splenium of the corpus callosum.

Differential diagnosis may include:

- Opsoclonus-myoclonus-ataxia syndrome

- Miller-Fisher syndrome

- Meningoencephalitis

- Cerebral abscess

- Tumor

- Hydrocephalus

- Inner-ear Disease

- Acute Vestibulitis

- Acute Labyrinthitis

Reported neurological symptoms include difficulty sleeping, decrease in intellectual capacity, dizziness, altered visual perceptive abilities, affected psychomotor skills, forgetfulness, and disorientation. The mechanism behind these symptoms beyond solvent molecules crossing the blood-brain barrier is currently unknown. Neurological signs include impaired vibratory sensation at extremities and an inability to maintain steady motion, a possible effect from psychomotor damage in the brain. Other symptoms that have been seen range from fatigue, decreased strength, and unusual gait. One study found that there was a correlation between decreased red blood cell count and level of solvent exposure, but not enough data has been found to support any blood tests to screen for CSE.