It is very important for family members and health care professionals to be aware of natural movements also known as Lazarus sign or Lazarus reflex that can occur on a brain-dead person whose organs have been kept functioning by life support. The living cells that can cause these movements are not living cells from the brain or brain stem, these cells come from the spinal cord. Sometimes these body movements can cause false hope for the family members.

A brain-dead individual has no clinical evidence of brain function upon physical examination. This includes no response to pain and no cranial nerve reflexes. Reflexes include pupillary response (fixed pupils), oculocephalic reflex, corneal reflex, no response to the caloric reflex test, and no spontaneous respirations.

It is important to distinguish between brain death and states that may be difficult to differentiate from brain death, (such as barbiturate overdose, alcohol intoxication, sedative overdose, hypothermia, hypoglycemia, coma, and chronic vegetative states). Some comatose patients can recover to pre-coma or near pre-coma level of functioning, and some patients with severe irreversible neurological dysfunction will nonetheless retain some lower brain functions, such as spontaneous respiration, despite the losses of both cortex and brain stem functionality. Such is the case with anencephaly.

Note that brain electrical activity can stop completely, or drop to such a low level as to be undetectable with most equipment. An EEG will therefore be flat, though this is sometimes also observed during deep anesthesia or cardiac arrest. Although in the United States a flat EEG test is not required to certify death, it is considered to have confirmatory value. In the UK it is not considered to be of value because any continuing activity it might reveal in parts of the brain above the brain stem is held to be irrelevant to the diagnosis of death on the Code of Practice criteria.

The diagnosis of brain death needs to be rigorous, in order to be certain that the condition is irreversible. Legal criteria vary, but in general they require neurological examinations by two independent physicians. The exams must show complete and irreversible absence of brain function (brain stem function in UK), and may include two isoelectric (flat-line) EEGs 24 hours apart (less in other countries where it is accepted that if the cause of the dysfunction is a clear physical trauma there is no need to wait that long to establish irreversibility). The patient should have a normal temperature and be free of drugs that can suppress brain activity if the diagnosis is to be made on EEG criteria.

Also, a radionuclide cerebral blood flow scan that shows complete absence of intracranial blood flow must be considered with other exams – temporary swelling of the brain, particularly within the first 72 hours, can lead to a false positive test on a patient that may recover with more time.

CT angiography is neither required nor sufficient test to make the diagnosis.

Brain death is the complete loss of brain function (including involuntary activity necessary to sustain life). It differs from persistent vegetative state, in which the person is alive and some autonomic functions remain.

Brain death is used as an indicator of legal death in many jurisdictions, but it is defined inconsistently. Various parts of the brain may keep functioning when others do not anymore, and the term "brain death" has been used to refer to various combinations. For example, although a major medical dictionary says that "brain death" is synonymous with "cerebral death" (death of the cerebrum), the US National Library of Medicine Medical Subject Headings (MeSH) system defines brain death as including the brainstem. The distinctions can be important because, for example, in someone with a dead cerebrum but a living brainstem, the heartbeat and ventilation can continue unaided, whereas in whole-brain death (which includes brain stem death), only life support equipment would keep those functions going. Patients classified as brain-dead can have their organs surgically removed for organ donation.

In the UK, the formal rules for the diagnosis of brainstem death have undergone only minor modifications since they were first published in 1976. The most recent revision of the UK's Department of Health Code of Practice governing use of that procedure for the diagnosis of death reaffirms the preconditions for its consideration. These are:

1. There should be no doubt that the patient’s condition – deeply comatose, unresponsive and requiring artificial ventilation—is due to irreversible brain damage of known cause.

2. There should be no evidence that this state is due to depressant drugs.

3. Primary hypothermia as the cause of unconsciousness must have been excluded, and

4. Potentially reversible circulatory, metabolic and endocrine disturbances likewise.

5. Potentially reversible causes of apnoea (dependence on the ventilator), such as muscle relaxants and cervical cord injury, must be excluded.

With these pre-conditions satisfied, the definitive criteria are:

1. Fixed pupils which do not respond to sharp changes in the intensity of incident light.

2. No corneal reflex.

3. Absent oculovestibular reflexes – no eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric reflex test).

4. No response to supraorbital pressure.

5. No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation.

6. No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and diffusion oxygenation during the disconnection (so the brainstem respiratory centre is not challenged by the ultimate, anoxic, drive stimulus). This test—the apnoea test—is dangerous – and may prove lethal.

Two doctors, of specified status and experience, are required to act together to diagnose death on these criteria and the tests must be repeated after “a short period of time ... to allow return of the patient’s arterial blood gases and baseline parameters to the pre-test state”. These criteria for the diagnosis of death are not applicable to infants below the age of two months.

Brainstem death is a clinical syndrome defined by the absence of reflexes with pathways through the brainstem—the “stalk” of the brain, which connects the spinal cord to the mid-brain, cerebellum and cerebral hemispheres—in a deeply comatose, ventilator-dependent patient.

Identification of this state carries a very grave prognosis for survival; cessation of heartbeat often occurs within a few days although it may continue for weeks or even months if intensive support is maintained.

In the United Kingdom, the formal diagnosis of brainstem death by the procedure laid down in the official Code of Practice permits the diagnosis and certification of death on the premise that a person is dead when consciousness and the ability to breathe are permanently lost, regardless of continuing life in the body and parts of the brain, and that death of the brainstem alone is sufficient to produce this state.

This concept of brainstem death is also accepted as grounds for pronouncing death for legal purposes in India and Trinidad & Tobago. Elsewhere in the world the concept upon which the certification of death on neurological grounds is based is that of permanent cessation of all function in all parts of the brain—whole brain death—with which the reductionist United Kingdom concept should not be confused. The United States' President's Council on Bioethics made it clear, in its White Paper of December 2008, that the United Kingdom concept and clinical criteria are not considered sufficient for the diagnosis of death in the United States of America.

In medicine, cerebral softening (encephalomalacia) is a localized softening of the brain substance, due to hemorrhage or inflammation. Three varieties, distinguished by their color and representing different stages of the morbid process, are known respectively as red, yellow, and white softening.

Ischemia: A decreased or restriction of circulating blood flow to a region of the brain which deprives neurons of the necessary substrates (primarily glucose); represents 80% of all strokes. A thrombus or embolus plugs an artery so there is a reduction or cessation of blood flow. This hypoxia or anoxia leads to neuronal injury, which is known as a stroke. The death of neurons leads to a so-called softening of the cerebrum in the affected area.

Hemorrhage: Intracerebral hemorrhage occurs in deep penetrating vessels and disrupts the connecting pathways, causing a localized pressure injury and in turn injury to brain tissue in the affected area. Hemorrhaging can occur in instances of embolic ischemia, in which the previously obstructed region spontaneously restores blood flow. This is known as a hemorrhagic infarction and a resulting red infarct occurs, which points to a type of cerebral softening known as red softening.

Exsanguination is the process of blood loss, to a degree sufficient to cause death. One does not have to lose all of one's blood to cause death. Depending upon the age, health, and fitness level of the individual, people can die from losing half to two-thirds of their blood; a loss of roughly one-third of the blood volume is considered very serious. Even a single deep cut can warrant suturing and hospitalization, especially if trauma, a vein or artery, or another comorbidity is involved. It is most commonly known as "bleeding to death" or colloquially as "bleeding out". The word itself originated from Latin: "ex" ("out of") and "sanguis" ("blood").

Like coma, chronic coma results mostly from cortical or white-matter damage after neuronal or axonal injury, or from focal brainstem lesions.Usually the metabolism in the grey matter decreases to 50-70% of the normal range. The patient lacks awareness and arousal. The patient lies with eyes closed and is not aware of self or surroundings. Stimulation cannot produce spontaneous periods of wakefulness and eye-opening, unlike patients in vegetative state. In medicine, a coma (from the Greek κῶμα koma, meaning deep sleep) is a state of unconsciousness, lasting more than six hours in which a person cannot be awakened, fails to respond normally to painful stimuli, light, sound, lacks a normal sleep-wake cycle and does not initiate voluntary actions. Although, according to the Glasgow Coma Scale, a person with confusion is considered to be in the mildest coma. But cerebral metabolism has been shown to correlate poorly with the level of consciousness in patients with mild to severe injury within the first month after traumatic brain injury (TBI).

A person in a state of coma is described as comatose. In general patients surviving a coma recover gradually within 2–4 weeks. But recovery to full awareness and arousal is not always possible. Some patients do not progress further than vegetative state or minimally conscious state and sometimes this also results in prolonged stages before further recovery to complete consciousness.

Although a coma patient may appear to be awake, they are unable to consciously feel, speak, hear, or move. For a patient to maintain consciousness, two important neurological components must function impeccably. The first is the cerebral cortex which is the gray matter covering the outer layer of the brain. The other is a structure located in the brainstem, called reticular activating system (RAS or ARAS). Injury to either or both of these components is sufficient to cause a patient to experience a coma.

Brain death is the irreversible end of all brain activity, and function (including involuntary activity necessary to sustain life). The main cause is total necrosis of the cerebral neurons following loss of brain oxygenation. After brain death the patient lacks any sense of awareness; sleep-wake cycles or behavior, and typically look as if they are dead or are in a deep sleep-state or coma. Although visually similar to a comatose state such as persistent vegetative state, the two should not be confused. Criteria for brain death differ from country to country. However, the clinical assessments are the same and require the loss of all brainstem reflexes and the demonstration of continuing apnea in a persistently comatose patient (< 4 weeks).

Functional imaging using PET or CT scans, typically show a hollow skull phenomenon. This confirms the absence of neuronal function in the whole brain.

Patients classified as brain dead are legally dead and can qualify as organ donors, in which their organs are surgically removed and prepared for a particular recipient.

Brain death is one of the deciding factors when pronouncing a trauma patient as dead. Determining function and presence of necrosis after trauma to the whole brain or brain-stem may be used to determine brain death, and is used in many states in the US.

Exsanguination is a relatively uncommon cause of death in human beings. Traumatic injury can cause exsanguination if bleeding is not promptly controlled, and is the most common cause of death in military combat. Non-combat causes can include gunshot or stab wounds; motor vehicle crash injuries; suicide by severing arteries, typically those in the wrists; and partial or total limb amputation, such as via accidental contact with a circular or chain saw, or becoming entangled in operating machinery.

Patients can also develop catastrophic internal hemorrhages, such as from a bleeding peptic ulcer, postpartum bleeding or splenic hemorrhage, which can cause exsanguination without any external signs of distress. Another cause of exsanguination in the medical field is that of aneurysms. If a dissecting aortic aneurysm ruptures through the adventitia, massive hemorrhage and exsanguination can result in a matter of minutes.

Blunt force trauma to the liver, kidneys, and spleen can cause severe internal bleeding as well, though the abdominal cavity usually becomes visibly darkened as if bruised. Similarly, trauma to the lungs can cause bleeding out, though without medical attention, blood can fill the lungs causing the effect of drowning, or in the pleura causing suffocation, well before exsanguination would occur. In addition, serious trauma can cause tearing of major blood vessels without external trauma indicative of the damage.

Alcoholics and others with liver disease can also suffer from exsanguination. Thin-walled, normally low pressure dilated veins just below the lower esophageal mucosa called esophageal varices can become enlarged in conditions with portal hypertension. These may begin to bleed, which with the high pressure in the portal system can be fatal. The often causative impaired liver function also reduces the availability of clotting factors (many of which are made in the liver), making any rupture in vessels more likely to cause a fatal loss of blood.

Epidural hematoma is when bleeding occurs between the tough outer membrane covering the brain and the skull. Often there is loss of consciousness following a head injury, a brief regaining of consciousness, and then loss of consciousness again. Other symptoms may include headache, confusion, vomiting, and an inability to move parts of the body. Complications may include seizures.

The cause is typically head injury that results in a break of the temporal bone and bleeding from the middle meningeal artery. Occasionally it can occur as a result of a bleeding disorder or blood vessel malformation. Diagnosis is typically by a CT scan or MRI. When this condition occurs in the spine it is known as a spinal epidural hematoma.

Treatment in generally by urgent surgery in the form of a craniotomy or burr hole. Without treatment death typically results. The condition occurs in one to four percent of head injuries. Typically it occurs in young adults. Males are more often affected than females.

Epidural, subdural, and subarachnoid hemorrhages are extra-axial bleeds, occurring outside of the brain tissue, while intra-axial hemorrhages, including intraparenchymal and intraventricular hemorrhages, occur within it.

Epidural hematomas may present with a lucid period immediately following the trauma and a delay before symptoms become evident. After the epidural hematoma begins collecting, it starts to compress intracranial structures which may impinge on the CN III. This can be seen in the physical exam as a fixed and dilated pupil on the side of the injury. The eye will be positioned down and out, due to unopposed CN IV and CN VI innervation.

Other manifestations will include weakness of the extremities on the opposite side as the lesion (except in rare cases), due to compression of the crossed pyramid pathways, and a loss of visual field opposite to the side of the lesion, due to compression of the posterior cerebral artery on the side of the lesion.

The most feared event that takes place is tonsillar herniation which could result in respiratory arrest since the medullary structures are compromised. The trigeminal nerve (CN V) may be involved late in the process as the pons becomes compressed, but this is not a significant clinical presentation, since by that time the patient may already be dead. In the case of epidural hematoma in the posterior cranial fossa, the herniation is tonsillar and causes the Cushing's triad: hypertension, bradycardia, and irregular respiration.

Epidural bleeding is rapid because it is usually from arteries, which are high pressure. Epidural bleeds from arteries can grow until they reach their peak size at six to eight hours post injury, spilling from 25 to 75 cubic centimeters of blood into the intracranial space. As the hematoma expands, it strips the dura from the inside of the skull, causing an intense headache. Epidural bleeds can become large and raise intracranial pressure, causing the brain to shift, lose blood supply, or be crushed against the skull. Larger hematomas cause more damage. Epidural bleeds can quickly expand and compress the brain stem, causing unconsciousness, abnormal posturing, and abnormal pupil responses to light.

As of 2007, fewer than 500 Yakut individuals have been infected with VE. Viliuisk Encephalomyelitis is classified as a progressive neurological disorder that ultimately ends in the death of the infected individual. The disease has three distinguishable phases: The acute form, the progressive form, and the chronic form.

The acute form is the most rapid and most violent of all the stages. It begins with the characteristic rigidity of the muscles, accompanied by slurred speech, severe headaches, and exaggeration of cold-like symptoms. Patients usually die within weeks of the initial symptoms. Routine post-mortem examinations yield: severe inflammation of the brain lining, clusters of dead cells and tissue, and largely increased amounts of macrophages and lymphocytes.

The progressive form is the most common case. Patients initially experience acute-like symptoms which are not as severe, and subside within a few weeks. Following the sub-acute phase, the patients experience a few mild symptoms including some behavioral changes, incoordination, and difficulty in speech. Eventually the disease developed fully and those infected were stricken with the characteristic symptoms of rigidity, slurred speech, and deterioration of cognitive functions. Ultimately, brain function depreciates rapidly resulting in death.

Many patients who undergo the chronic form claim never to have had an acute attack. These patients endure varying measures of impairment and suffer mental deterioration for the remainder of their lives. Usually they live to be very old and succumb to other diseases.

In almost all cases there are changes characteristic of VE. Early onset shows an increased number of lymphocytes and increased protein concentration — which reduces over many years. These factors help neurologists determine the form of VE based on progression. The trademark changes in the brain include: thickened inflamed meninges, necrotic cortical lesions, increased number of lymphocytes, and neuronal death.

Viliuisk Encephalomyelitis (VE) is a fatal progressive neurological disorder found only in the Sakha (Iakut/Yakut) population of central Siberia. About 15 new cases are reported each year. VE is a very rare disease and little research has been conducted. The causative agents, origin of the disease, and involved candidate genes are currently unknown, but much research has been done in pursuit of the answers.

Those inflicted with the disease survive for a period of only a few months to several years. VE follows three main courses of infection: an acute form, a sub-acute form subsiding into a progressive form, and a chronic form. Initially, the infected patients experience symptoms such as: severe headaches, delirium, lethargy, meningism, bradykinesia, and incoordination. A small percentage of patients die during the acute phase as result of a severe coma. In all cases the disease is fatal.

Lazarus syndrome, (the Lazarus heart) also known as autoresuscitation after failed cardiopulmonary resuscitation, is the spontaneous return of circulation after failed attempts at resuscitation. Its occurrence has been noted in medical literature at least 38 times since 1982. It takes its name from Lazarus who, as described in the New Testament of The Bible, was raised from the dead by Jesus.

Occurrences of the syndrome are extremely rare and the causes are not well understood. One hypothesis for the phenomenon is that a chief factor (though not the only one) is the buildup of pressure in the chest as a result of cardiopulmonary resuscitation (CPR). The relaxation of pressure after resuscitation efforts have ended is thought to allow the heart to expand, triggering the heart's electrical impulses and restarting the heartbeat. Other possible factors are hyperkalemia or high doses of epinephrine.

The National Institute of Neurological Disorders and Stroke (NINDS) describes the presentation of this condition as follows: "A baby born with anencephaly is usually blind, deaf, unaware of its surroundings and unable to feel pain. Although some individuals with anencephaly may be born with a main brain stem, the lack of a functioning cerebrum permanently rules out the possibility of ever gaining awareness of their surroundings. Reflex actions such as breathing and responses to sound or touch may occur."

Anencephaly is the absence of a major portion of the brain, skull, and scalp that occurs during embryonic development. It is a cephalic disorder that results from a neural tube defect that occurs when the rostral (head) end of the neural tube fails to close, usually between the 23rd and 26th day following conception. Strictly speaking, the Greek term translates as "no in-head" (that is, totally lacking the inside part of the head, i.e. the brain), but it is accepted that children born with this disorder usually only lack a telencephalon, the largest part of the brain consisting mainly of the cerebral hemispheres, including the neocortex, which is responsible for cognition. The remaining structure is usually covered only by a thin layer of membrane—skin, bone, meninges, etc. are all lacking. With very few exceptions, infants with this disorder do not survive longer than a few hours or possibly days after their birth.

Fever, headache, and neurological problems, while classic, only occur in 20% of people with brain abscess.

The famous triad of fever, headache and focal neurologic findings are highly suggestive of brain abscess. These symptoms are caused by a combination of increased intracranial pressure due to a space-occupying lesion (headache, vomiting, confusion, coma), infection (fever, fatigue etc.) and focal neurologic brain tissue damage (hemiparesis, aphasia etc.).

The most frequent presenting symptoms are headache, drowsiness, confusion, seizures, hemiparesis or speech difficulties together with fever with a rapidly progressive course. Headache is characteristically worse at night and in the morning, as the intracranial pressure naturally increases when in the supine position. This elevation similarly stimulates the medullary vomiting center and area postrema, leading to morning vomiting.

Other symptoms and findings depend largely on the specific location of the abscess in the brain. An abscess in the cerebellum, for instance, may cause additional complaints as a result of brain stem compression and hydrocephalus. Neurological examination may reveal a stiff neck in occasional cases (erroneously suggesting meningitis).

Cavitations are an area of dead bone caused by a dearth of blood flow to that part of the bone. A cavitation is a hole in the blood vessel that cannot be visually detected with the naked eye. Jawbone cavitations, also called neuralgia-inducing cavitational osteonecrosis (NICO) if they are associated with pain, are extraction sites in the jaw that have not healed.

Symptoms include: rigid body, rigid limbs, limbs staying in same position when moved (waxy flexibility), no response, loss of muscle control, and slowing down of bodily functions, such as breathing.

Dogs with canine cognitive dysfunction may exhibit many symptoms associated senile behavior and dementia. Dogs will often find themselves confused in familiar places of the home, spending long periods of time in one area of the home, not responding to calls or commands, and experiencing abnormal sleeping patterns. Although some of these symptoms may be attributed to old age itself, when they are exhibited together, there is a higher likelihood of CCD.

Headaches as a result of raised intracranial pressure can be an early symptom of brain cancer. However, isolated headache without other symptoms is rarer, and other symptoms often occur before headaches become common. Certain warning signs for headache exist which make it more likely to be associated with brain cancer. These are as defined by the American Academy of Neurology: "abnormal neurological examination, headache worsened by Valsalva maneuver, headache causing awakening from sleep, new headache in the older population, progressively worsening headache, atypical headache features, or patients who do not fulfill the strict definition of migraine".

The brain is divided into 4 lobes and each lobe or area has its own function. A tumor in any of these lobes may affect the area's performance. The location of the tumor is often linked to the symptoms experienced but each person may experience something different.

- Frontal lobe tumors may contribute to poor reasoning, inappropriate social behavior, personality changes, poor planning, lower inhibition, and decreased production of speech (Broca's area).

- Temporal lobe: Tumors in this lobe may contribute to poor memory, loss of hearing, difficulty in language comprehension (Wernicke's area).

- Parietal lobe: Tumors here may result in poor interpretation of languages, decreased sense of touch and pain, and poor spatial and visual perception.

- Occipital lobe: Damage to this lobe may result in poor or loss of vision.

- Cerebellum: Tumors in this area may cause poor balance, muscle movement, and posture.

- Brain stem: Tumors on this can affect blood pressure, swallowing, and heartbeat.

Catalepsy (from Greek "κατάληψις" "seizing/grasping") is a nervous condition characterized by muscular rigidity and fixity of posture regardless of external stimuli, as well as decreased sensitivity to pain.

In order to properly diagnose CCD in dogs, there is a list of symptoms that when observed together, show signs of the disease.

- Disorientation – loss of ability to navigate the house or remember where specific places are (i.e. furniture, corners of rooms)

- Interaction changes – decreased interest in social interaction (i.e. petting, grooming, playing)

- Sleep/wake cycle Changes – restlessness throughout the night, sleeping during the day

- Housebreaking issues – defecating indoors, not signaling to go outside

- Physical activity level – decreased interest in being outside, decreased responses to stimuli (e.g. sounds around home, people)

Any medical causes for these symptoms must be ruled out. Medical diagnoses that may contribute to these symptoms include thyroid disorders, Cushing's disease, diabetes, kidney disease, musculoskeletal disease, cancer, liver problems, and sensory loss. Also, behavioral problems in dogs may be factors that influence these symptoms (i.e. lack of housetraining, lack of social interaction, separation anxiety, phobias, aggression and compulsive disorders).