Generally, a person who is unable to voluntarily open the eyes, does not have a sleep-wake cycle, is unresponsive in spite of strong tactile (painful) or verbal stimuli, and who generally scores between 3 and 8 on the Glasgow Coma Scale is considered in a coma. Coma may have developed in humans as a response to injury to allow the body to pause bodily actions and heal the most immediate injuries before waking. It therefore could be a compensatory state in which the body's expenditure of energy is not superfluous. The severity and mode of onset of coma depends on the underlying cause. For instance, severe hypoglycemia (low blood sugar) or hypercapnia (increased carbon dioxide levels in the blood) initially cause mild agitation and confusion, but progress to obtundation, stupor, and finally, complete unconsciousness. In contrast, coma resulting from a severe traumatic brain injury or subarachnoid hemorrhage can be instantaneous. The mode of onset may therefore be indicative of the underlying cause.

In the initial assessment of coma, it is common to gauge the level of consciousness by spontaneously exhibited actions, response to vocal stimuli ("Can you hear me?"), and painful stimuli; this is known as the AVPU (alert, vocal stimuli, painful stimuli, unresponsive) scale. More elaborate scales, such as the Glasgow Coma Scale, quantify an individual's reactions such as eye opening, movement and verbal response on a scale; Glasgow Coma Scale (GCS) is an indication of the extent of brain injury varying from 3 (indicating severe brain injury and death) to a maximum of 15 (indicating mild or no brain injury).

In those with deep unconsciousness, there is a risk of asphyxiation as the control over the muscles in the face and throat is diminished. As a result, those presenting to a hospital with coma are typically assessed for this risk ("airway management"). If the risk of asphyxiation is deemed high, doctors may use various devices (such as an oropharyngeal airway, nasopharyngeal airway or endotracheal tube) to safeguard the airway.

Cerebral hypoxia can be caused by any event that severely interferes with the brain's ability to receive or process oxygen. This event may be internal or external to the body. Mild and moderate forms of cerebral hypoxia may be caused by various diseases that interfere with breathing and blood oxygenation. Severe asthma and various sorts of anemia can cause some degree of diffuse cerebral hypoxia. Other causes include status epilepticus, work in nitrogen-rich environments, ascent from a deep-water dive, flying at high altitudes in an unpressurized cabin without supplemental oxygen, and intense exercise at high altitudes prior to acclimatization.

Severe cerebral hypoxia and anoxia is usually caused by traumatic events such as choking, drowning, strangulation, smoke inhalation, drug overdoses, crushing of the trachea, status asthmaticus, and shock. It is also recreationally self-induced in the fainting game and in erotic asphyxiation.

- Transient ischemic attack (TIA), is often referred to as a "mini-stroke". The American Heart Association and American Stroke Association (AHA/ASA) refined the definition of transient ischemic attack. TIA is now defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. The symptoms of a TIA can resolve within a few minutes, unlike a stroke. TIAs share the same underlying etiology as strokes; a disruption of cerebral blood flow. TIAs and strokes present with the same symptoms such as contralateral paralysis (opposite side of body from affected brain hemisphere), or sudden weakness or numbness. A TIA may cause sudden dimming or loss of vision, aphasia, slurred speech, and mental confusion. The symptoms of a TIA typically resolve within 24 hours, unlike a stroke. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke.

- Silent stroke is a stroke which does not have any outward symptoms, and the patient is typically unaware they have suffered a stroke. Despite its lack of identifiable symptoms, a silent stroke still causes brain damage and places the patient at increased risk for a major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as fMRI. The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with hypertension and current cigarette smoking being predisposing factors.

The brain requires approximately 3.3 ml of oxygen per 100 g of brain tissue per minute. Initially the body responds to lowered blood oxygen by redirecting blood to the brain and increasing cerebral blood flow. Blood flow may increase up to twice the normal flow but no more. If the increased blood flow is sufficient to supply the brain's oxygen needs then no symptoms will result.

However, if blood flow cannot be increased or if doubled blood flow does not correct the problem, symptoms of cerebral hypoxia will begin to appear. Mild symptoms include difficulties with complex learning tasks and reductions in short-term memory. If oxygen deprivation continues, cognitive disturbances, and decreased motor control will result. The skin may also appear bluish (cyanosis) and heart rate increases. Continued oxygen deprivation results in fainting, long-term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death.

Objective measurements of the severity of cerebral hypoxia depend on the cause. Blood oxygen saturation may be used for hypoxic hypoxia, but is generally meaningless in other forms of hypoxia. In hypoxic hypoxia 95–100% saturation is considered normal; 91–94% is considered mild and 86–90% moderate. Anything below 86% is considered severe.

It should be noted that cerebral hypoxia refers to oxygen levels in brain tissue, not blood. Blood oxygenation will usually appear normal in cases of hypemic, ischemic, and hystoxic cerebral hypoxia. Even in hypoxic hypoxia blood measures are only an approximate guide; the oxygen level in the brain tissue will depend on how the body deals with the reduced oxygen content of the blood.

A persistent vegetative state (PVS) is a disorder of consciousness in which patients with severe brain damage are in a state of partial arousal rather than true awareness. After four weeks in a vegetative state (VS), the patient is classified as in a persistent vegetative state. This diagnosis is classified as a "permanent vegetative state" some months (3 in the US and 6 in the UK) after a non-traumatic brain injury or one year after a traumatic injury. Nowadays, more doctors and neuroscientists prefer to call the state of consciousness an "unresponsive wakefulness syndrome", primarily because of ethical questions about whether a patient can be called "vegetative" or not.

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.

The symptoms of an opiate toxidrome include the classic triad of coma, pinpoint pupils, and respiratory depression as well as altered mental states, shock, pulmonary edema and unresponsiveness. Complications include bradycardia, hypotension, and hypothermia. Substances that may cause this toxidrome are opioids.

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.

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.

The vegetative state is a chronic or long-term condition. This condition differs from a coma: a coma is a state that lacks both awareness and wakefulness. Patients in a vegetative state may have awoken from a coma, but still have not regained awareness. In the vegetative state patients can open their eyelids occasionally and demonstrate sleep-wake cycles, but completely lack cognitive function. The vegetative state is also called a "coma vigil". The chances of regaining awareness diminish considerably as the time spent in the vegetative state increases.

Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault, gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed.

Symptoms include nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centers in the pons and medulla oblongata.

People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. It is usually mild enough to reverse by eating or drinking carbohydrates, but blood glucose occasionally can fall fast enough and low enough to produce unconsciousness before hypoglycemia can be recognized and reversed. Hypoglycemia can be severe enough to cause unconsciousness during sleep. Predisposing factors can include eating less than usual or prolonged exercise earlier in the day. Some people with diabetes can lose their ability to recognize the symptoms of early hypoglycemia.

Unconsciousness due to hypoglycemia can occur within 20 minutes to an hour after early symptoms and is not usually preceded by other illness or symptoms. Twitching or convulsions may occur. A person unconscious from hypoglycemia is usually pale, has a rapid heart beat, and is soaked in sweat: all signs of the adrenaline response to hypoglycemia. The individual is not usually dehydrated and breathing is normal or shallow. Their blood sugar level, measured by a glucose meter or laboratory measurement at the time of discovery, is usually low but not always severely, and in some cases may have already risen from the nadir that triggered the unconsciousness.

Unconsciousness due to hypoglycemia is treated by raising the blood glucose with intravenous glucose or injected glucagon.

Diabetic ketoacidosis (DKA), if it progresses and worsens without treatment, can eventually cause unconsciousness, from a combination of a very high blood sugar level, dehydration and shock, and exhaustion. Coma only occurs at an advanced stage, usually after 36 hours or more of worsening vomiting and hyperventilation.

In the early to middle stages of ketoacidosis, patients are typically flushed and breathing rapidly and deeply, but visible dehydration, pale appearance from diminished perfusion, shallower breathing, and a fast heart rate are often present when coma is reached. However these features are variable and not always as described.

If the patient is known to have diabetes, the diagnosis of DKA is usually suspected from the appearance and a history of 1–2 days of vomiting. The diagnosis is confirmed when the usual blood chemistries in the emergency department reveal a high blood sugar level and severe metabolic acidosis.

Treatment of DKA consists of isotonic fluids to rapidly stabilize the circulation, continued intravenous saline with potassium and other electrolytes to replace deficits, insulin to reverse the ketoacidosis, and careful monitoring for complications.

In locked-in syndrome the patient has awareness, sleep-wake cycles, and meaningful behavior (viz., eye-movement), but is isolated due to quadriplegia and pseudobulbar palsy, resulting from the disruption of corticospinal and corticobulbar pathways. Locked-in syndrome is a condition in which a patient is aware and awake but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eyes. Eye or eyelid movements are the main method of communication. Total locked-in syndrome is a version of locked-in syndrome where the eyes are paralyzed as well.

The symptoms include many of the symptoms associated with milder degrees of hypoglycemia, especially the adrenergic symptoms, but do not progress to objective impairment of brain function, seizures, coma, or brain damage.

- Shakiness

- Sense of weakness

- Altered or depressed mood

- Confusion

- Fatigue

- Anxiety

- Paleness

- Perspiration

- Increased pulse or respiratory rate

- Hunger

Central nervous system depression or CNS depression refers to physiological depression of the central nervous system that can result in decreased rate of breathing, decreased heart rate, and loss of consciousness possibly leading to coma or death. CNS depression is specifically the result of inhibited brain activity.

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.

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.

Idiopathic postprandial syndrome, colloquially but incorrectly known by some as hypoglycemia, describes a collection of clinical signs and symptoms similar to medical hypoglycemia but without the demonstrably low blood glucose levels which characterise said condition.

People with this condition suffer from recurrent episodes of altered mood and cognitive efficiency, often accompanied by weakness and adrenergic symptoms such as shakiness. The episodes typically occur a few hours after a meal, rather than after many hours of fasting. The principal treatments recommended are extra small meals or snacks and avoidance of excessive simple sugars.

Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain.

Signs and symptoms of hyponatremia include nausea and vomiting, headache, short-term memory loss, confusion, lethargy, fatigue, loss of appetite, irritability, muscle weakness, spasms or cramps, seizures, and decreased consciousness or coma. The presence and severity of signs and symptoms are related to the level of salt in the blood, with lower levels of plasma sodium associated with more severe symptoms. However, emerging data suggest that mild hyponatremia (plasma sodium levels at 131–135 mmol/L) is associated with numerous complications or subtle, presently unrecognized symptoms (for example, increased falls, altered posture and gait, reduced attention).

Neurological symptoms typically occur with very low levels of plasma sodium (usually <115 mmol/L). When sodium levels in the blood become very low, water enters the brain cells and causes them to swell. This results in increased pressure in the skull and causes "hyponatremic encephalopathy". As pressure increases in the skull, herniation of the brain can occur, which is a squeezing of the brain across the internal structures of the skull. This can lead to headache, nausea, vomiting, confusion, seizures, brain stem compression and respiratory arrest, and non-cardiogenic accumulation of fluid in the lungs. This is usually fatal if not immediately treated.

Symptom severity depends on how fast and how severe the drop in blood salt level. A gradual drop, even to very low levels, may be tolerated well if it occurs over several days or weeks, because of neuronal adaptation. The presence of underlying neurological disease such as a seizure disorder or non-neurological metabolic abnormalities, also affects the severity of neurologic symptoms.

Chronic hyponatremia can lead to such complications as neurological impairments. These neurological impairments most often affect gait (walking) and attention, and can lead to increased reaction time and falls. Hyponatremia, by interfering with bone metabolism, has been linked with a doubled risk of osteoporosis and an increased risk of bone fracture.

CNS depression is generally caused by the use of depressant drugs such as ethanol, opioids, barbiturates, benzodiazepines, general anesthetics, and anticonvulsants such as pregabalin used to treat epilepsy.

Drug overdose is often caused by combining two or more depressant drugs, although overdose is certainly possible by consuming a large dose of one depressant drug. CNS depression can also be caused by the accidental or intentional inhalation or ingestion of certain volatile chemicals such as Butanone (contained in Plastic Cement) or Isopropyl Alcohol. Other causes of CNS depression are metabolic disturbances such as hypoglycaemia.

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.

TBI patients may have sensory problems, especially problems with vision; they may not be able to register what they are seeing or may be slow to recognize objects. Also, TBI patients often have difficulty with hand–eye coordination, causing them to seem clumsy or unsteady. Other sensory deficits include problems with hearing, smell, taste, or touch. Tinnitus, a ringing or roaring in the ears, may occur. A person with damage to the part of the brain that processes taste or smell may perceive a persistent bitter taste or noxious smell. Damage to the part of the brain that controls the sense of touch may cause a TBI patient to develop persistent skin tingling, itching, or pain. These conditions are rare and difficult to treat.

Pain, especially headache, is a common complication following a TBI. Being unconscious and lying still for long periods can cause blood clots to form (deep venous thrombosis), which can cause pulmonary embolism. Other serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores, pneumonia or other infections, and progressive multiple organ failure.

The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. As many as 50% of people with penetrating head injuries will develop seizures. People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma) though seizures can appear a decade or more after the initial injury and the common seizure type may also change over time. Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients within the first week of injury only and after that only if the seizures persist.

Neurostorms may occur after a severe TBI. The lower the Glasgow Coma Score (GCS), the higher the chance of Neurostorming. Neurostorms occur when the patient's Autonomic Nervous System (ANS), Central Nervous System (CNS), Sympathetic Nervous System (SNS), and ParaSympathetic Nervous System (PSNS) become severely compromised https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology . This in turn can create the following potential life-threatening symptoms: increased IntraCranial Pressure (ICP), tachycardia, tremors, seizures, fevers, increased blood pressure, increased Cerebral Spinal Fluid (CSF), and diaphoresis https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology. A variety of medication may be used to help decrease or control Neurostorm episodes https://www.brainline.org/story/neurostorm-century-part-3-3-new-way-life.

Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease, a chronic and progressive disorder, may develop years after TBI as a result of damage to the basal ganglia. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

Skull fractures can tear the meninges, the membranes that cover the brain, leading to leaks of cerebrospinal fluid (CSF). A tear between the dura and the arachnoid membranes, called a CSF fistula, can cause CSF to leak out of the subarachnoid space into the subdural space; this is called a subdural hygroma. CSF can also leak from the nose and the ear. These tears can also allow bacteria into the cavity, potentially causing infections such as meningitis. Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space. Infections within the intracranial cavity are a dangerous complication of TBI. They may occur outside of the dura mater, below the dura, below the arachnoid (meningitis), or within the brain itself (abscess). Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries. Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue.

Injuries to the base of the skull can damage nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

- Paralysis of facial muscles

- Damage to the nerves responsible for eye movements, which can cause double vision

- Damage to the nerves that provide sense of smell

- Loss of vision

- Loss of facial sensation

- Swallowing problems

Hydrocephalus, post-traumatic ventricular enlargement, occurs when CSF accumulates in the brain, resulting in dilation of the cerebral ventricles and an increase in ICP. This condition can develop during the acute stage of TBI or may not appear until later. Generally it occurs within the first year of the injury and is characterized by worsening neurological outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.

Any damage to the head or brain usually results in some damage to the vascular system, which provides blood to the cells of the brain. The body can repair small blood vessels, but damage to larger ones can result in serious complications. Damage to one of the major arteries leading to the brain can cause a stroke, either through bleeding from the artery or through the formation of a blood clot at the site of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular complications include vasospasm, in which blood vessels constrict and restrict blood flow, and the formation of aneurysms, in which the side of a blood vessel weakens and balloons out.

Fluid and hormonal imbalances can also complicate treatment. Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone and hypothyroidism.

Another common problem is spasticity. In this situation, certain muscles of the body are tight or hypertonic because they cannot fully relax.