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Traumatic brain injury

A traumatic brain injury (TBI), also known as an intracranial injury, is an injury to the brain caused by an external force. TBI can be classified based on severity ranging from mild traumatic brain injury (mTBI/concussion) to severe traumatic brain injury. TBI can also be characterized based on mechanism (closed or penetrating head injury) or other features (e.g., occurring in a specific location or over a widespread area). Head injury is a broader category that may involve damage to other structures such as the scalp and skull. TBI can result in physical, cognitive, social, emotional and behavioral symptoms, and outcomes can range from complete recovery to permanent disability or death.

Causes include falls, vehicle collisions and violence. Brain trauma occurs as a consequence of a sudden acceleration or deceleration within the cranium or by a complex combination of both movement and sudden impact. In addition to the damage caused at the moment of injury, a variety of events following the injury may result in further injury. These processes may include alterations in cerebral blood flow and pressure within the skull. Some of the imaging techniques used for diagnosis of moderate to severe TBI include computed tomography (CT) and magnetic resonance imaging (MRIs).

Prevention measures include use of seat belts and helmets, not drinking and driving, fall prevention efforts in older adults and safety measures for children. Depending on the injury, treatment required may be minimal or may include interventions such as medications, emergency surgery or surgery years later. Physical therapy, speech therapy, recreation therapy, occupational therapy and vision therapy may be employed for rehabilitation. Counseling, supported employment and community support services may also be useful.

TBI is a major cause of death and disability worldwide, especially in children and young adults. Males sustain traumatic brain injuries around twice as often as females. The 20th century saw developments in diagnosis and treatment that decreased death rates and improved outcomes.

Classification
Traumatic brain injury is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile. Brain function is temporarily or permanently impaired and structural damage may or may not be detectable with current technology.

TBI is one of two subsets of acquired brain injury (brain damage that occur after birth); the other subset is non-traumatic brain injury, which does not involve external mechanical force (examples include stroke and infection). All traumatic brain injuries are head injuries, but the latter term may also refer to injury to other parts of the head; however, the terms head injury and brain injury are often used interchangeably. Similarly, brain injuries fall under the classification of central nervous system injuries and neurotrauma. In neuropsychology research literature, in general the term "traumatic brain injury" is used to refer to non-penetrating traumatic brain injuries.

TBI is usually classified based on severity, anatomical features of the injury, and the mechanism (the causative forces). Mechanism-related classification divides TBI into closed and penetrating head injury. A closed (also called nonpenetrating, or blunt) injury occurs when the brain is not exposed. A penetrating, or open, head injury occurs when an object pierces the skull and breaches the dura mater, the outermost membrane surrounding the brain.

Severity
Brain injuries can be classified into mild, moderate, and severe categories. The Glasgow Coma Scale (GCS), the most commonly used system for classifying TBI severity, grades a person's level of consciousness on a scale of 3–15 based on verbal, motor, and eye-opening reactions to stimuli. In general, it is agreed that a TBI with a GCS of 13 or above is mild, 9–12 is moderate, and 8 or below is severe. Similar systems exist for young children; however, the GCS grading system has limited ability to predict outcomes. Because of this, other classification systems such as the one shown in the table are also used to help determine severity. A current model developed by the Department of Defense and Department of Veterans Affairs uses all three criteria of GCS after resuscitation, duration of post-traumatic amnesia (PTA), and loss of consciousness (LOC). It also has been proposed to use changes that are visible on neuroimaging, such as swelling, focal lesions, or diffuse injury as method of classification.

Pathological features

Systems also exist to classify TBI by its pathological features. Lesions can be extra-axial, (occurring within the skull but outside of the brain) or intra-axial (occurring within the brain tissue). Damage from TBI can be focal or diffuse, confined to specific areas or distributed in a more general manner, respectively; however, it is common for both types of injury to exist in a given case.

Diffuse injury manifests with little apparent damage in neuroimaging studies, but lesions can be seen with microscopy techniques post-mortem, and in the early 2000s, researchers discovered that diffusion tensor imaging (DTI), a way of processing MRI images that shows white matter tracts, was an effective tool for displaying the extent of diffuse axonal injury. Types of injuries considered diffuse include edema (swelling), concussion and diffuse axonal injury, which is widespread damage to axons including white matter tracts and projections to the cortex.

Focal injuries often produce symptoms related to the functions of the damaged area. Research shows that the most common areas to have focal lesions in non-penetrating traumatic brain injury are the orbitofrontal cortex (the lower surface of the frontal lobes) and the anterior temporal lobes, areas that are involved in social behavior, emotion regulation, olfaction, and decision-making, hence the common social/emotional and judgment deficits following moderate-severe TBI. Symptoms such as hemiparesis or aphasia can also occur when less commonly affected areas such as motor or language areas are, respectively, damaged.

One type of focal injury, cerebral laceration, occurs when the tissue is cut or torn. Such tearing is common in orbitofrontal cortex in particular, because of bony protrusions on the interior skull ridge above the eyes. In a similar injury, cerebral contusion (bruising of brain tissue), blood is mixed among tissue. In contrast, intracranial hemorrhage involves bleeding that is not mixed with tissue.

Hematomas, also focal lesions, are collections of blood in or around the brain that can result from hemorrhage. Intracerebral hemorrhage, with bleeding in the brain tissue itself, is an intra-axial lesion. Extra-axial lesions include epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intraventricular hemorrhage. Epidural hematoma involves bleeding into the area between the skull and the dura mater, the outermost of the three membranes surrounding the brain. In subdural hematoma, bleeding occurs between the dura and the arachnoid mater. Subarachnoid hemorrhage involves bleeding into the space between the arachnoid membrane and the pia mater. Intraventricular hemorrhage occurs when there is bleeding in the ventricles.

Signs and symptoms
Symptoms are dependent on the type of TBI (diffuse or focal) and the part of the brain that is affected. Unconsciousness tends to last longer for people with injuries on the left side of the brain than for those with injuries on the right. Symptoms are also dependent on the injury's severity. With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing, lightheadedness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns. Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking. Mild TBI symptoms may also be present in moderate and severe injuries.

A person with a moderate or severe TBI may have a headache that does not go away, repeated vomiting or nausea, convulsions, an inability to awaken, dilation of one or both pupils, slurred speech, aphasia (word-finding difficulties), dysarthria (muscle weakness that causes disordered speech), weakness or numbness in the limbs, loss of coordination, confusion, restlessness, or agitation. Common long-term symptoms of moderate to severe TBI are changes in appropriate social behavior, deficits in social judgment, and cognitive changes, especially problems with sustained attention, processing speed, and executive functioning. Alexithymia, a deficiency in identifying, understanding, processing, and describing emotions occurs in 60.9% of individuals with TBI. Cognitive and social deficits have long-term consequences for the daily lives of people with moderate to severe TBI, but can be improved with appropriate rehabilitation.

When the pressure within the skull (intracranial pressure, abbreviated ICP) rises too high, it can be deadly. Signs of increased ICP include decreasing level of consciousness, paralysis or weakness on one side of the body, and a blown pupil, one that fails to constrict in response to light or is slow to do so. Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP. Anisocoria, unequal pupil size, is another sign of serious TBI. Abnormal posturing, a characteristic positioning of the limbs caused by severe diffuse injury or high ICP, is an ominous sign.

Small children with moderate to severe TBI may have some of these symptoms but have difficulty communicating them. Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat, and irritability.

Causes
The most common causes of TBI in the U.S. include violence, transportation accidents, construction site mishaps, and sports. Motor bikes are major causes, increasing in significance in developing countries as other causes reduce. The estimates that between 1.6 and 3.8 million traumatic brain injuries each year are a result of sports and recreation activities in the US. In children aged two to four, falls are the most common cause of TBI, while in older children traffic accidents compete with falls for this position. TBI is the third most common injury to result from child abuse. Abuse causes 19% of cases of pediatric brain trauma, and the death rate is higher among these cases. Although men are twice as likely to have a TBI. Domestic violence is another cause of TBI, as are work-related and industrial accidents. Firearms and blast injuries from explosions are other causes of TBI, which is the leading cause of death and disability in war zones. According to Representative Bill Pascrell (Democrat, NJ), TBI is "the signature injury of the wars in Iraq and Afghanistan." There is a promising technology called activation database-guided EEG biofeedback, which has been documented to return a TBI's auditory memory ability to above the control group's performance

Physical forces
The type, direction, intensity, and duration of forces all contribute to the characteristics and severity of TBI. Forces that may contribute to TBI include angular, rotational, shear, and translational forces.

Even in the absence of an impact, significant acceleration or deceleration of the head can cause TBI; however in most cases, a combination of impact and acceleration is probably to blame. Forces involving the head striking or being struck by something, termed contact or impact loading, are the cause of most focal injuries, and movement of the brain within the skull, termed noncontact or inertial loading, usually causes diffuse injuries. The violent shaking of an infant that causes shaken baby syndrome commonly manifests as diffuse injury. In impact loading, the force sends shock waves through the skull and brain, resulting in tissue damage. Shock waves caused by penetrating injuries can also destroy tissue along the path of a projectile, compounding the damage caused by the missile itself.

Damage may occur directly under the site of impact, or it may occur on the side opposite the impact (coup and contrecoup injury, respectively). When a moving object impacts the stationary head, coup injuries are typical, while contrecoup injuries are usually produced when the moving head strikes a stationary object.

Primary and secondary injury

A large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event; rather than improving after being hospitalized, some 40% of TBI patients deteriorate. Primary brain injury (the damage that occurs at the moment of trauma when tissues and blood vessels are stretched, compressed, and torn) is not adequate to explain this deterioration; rather, it is caused by secondary injury, a complex set of cellular processes and biochemical cascades that occur in the minutes to days following the trauma. These secondary processes can dramatically worsen the damage caused by primary injury and account for the greatest number of TBI deaths occurring in hospitals.

Secondary injury events include damage to the blood–brain barrier, release of factors that cause inflammation, free radical overload, excessive release of the neurotransmitter glutamate (excitotoxicity), influx of calcium and sodium ions into neurons, and dysfunction of mitochondria. Injured axons in the brain's white matter may separate from their cell bodies as a result of secondary injury, potentially killing those neurons. Other factors in secondary injury are changes in the blood flow to the brain; ischemia (insufficient blood flow); cerebral hypoxia (insufficient oxygen in the brain); cerebral edema (swelling of the brain); and raised intracranial pressure (the pressure within the skull). Intracranial pressure may rise due to swelling or a mass effect from a lesion, such as a hemorrhage. As a result, cerebral perfusion pressure (the pressure of blood flow in the brain) is reduced; ischemia results. When the pressure within the skull rises too high, it can cause brain death or brain herniation, in which parts of the brain are squeezed by structures in the skull.

Diagnosis

Diagnosis is suspected based on lesion circumstances and clinical evidence, most prominently a neurological examination, for example checking whether the pupils constrict normally in response to light and assigning a Glasgow Coma Score. Neuroimaging helps in determining the diagnosis and prognosis and in deciding what treatments to give. DSM-5 can be utilized to diagnose TBI and its psychiatric sequelae.

The preferred radiologic test in the emergency setting is computed tomography (CT): it is quick, accurate, and widely available. Follow-up CT scans may be performed later to determine whether the injury has progressed.

Magnetic resonance imaging (MRI) can show more detail than CT, and can add information about expected outcome in the long term. It is more useful than CT for detecting injury characteristics such as diffuse axonal injury in the longer term; however, MRI is not used in the emergency setting for reasons including its relative inefficacy in detecting bleeds and fractures, its lengthy acquisition of images, the inaccessibility of the patient in the machine, and its incompatibility with metal items used in emergency care. A variant of MRI since 2012 is high-definition fiber tracking (HDFT).

Other techniques may be used to confirm a particular diagnosis. X-rays are still used for head trauma, but evidence suggests they are not useful; head injuries are either so mild that they do not need imaging or severe enough to merit the more accurate CT. Angiography may be used to detect blood vessel pathology when risk factors such as penetrating head trauma are involved. Functional imaging can measure cerebral blood flow or metabolism, inferring neuronal activity in specific regions and potentially helping to predict outcome.

Neuropsychological assessment can be performed to evaluate the long-term cognitive sequelae and to aid in the planning of the rehabilitation. Instruments range from short measures of general mental functioning to complete batteries formed of different domain-specific tests.

Prevention

Since a major cause of TBI are vehicle accidents, their prevention or the amelioration of their consequences can both reduce the incidence and gravity of TBI. In accidents, damage can be reduced by use of seat belts, child safety seats and motorcycle helmets, and presence of roll bars and airbags. Education programs exist to lower the number of crashes. In addition, changes to public policy and safety laws can be made; these include speed limits, seat belt and helmet laws, and road engineering practices.

Changes to common practices in sports have also been discussed. An increase in use of helmets could reduce the incidence of TBI. Due to the possibility that repeatedly "heading" a ball practicing soccer could cause cumulative brain injury, the idea of introducing protective headgear for players has been proposed. Improved equipment design can enhance safety; softer baseballs reduce head injury risk. Rules against dangerous types of contact, such as "spear tackling" in American football, when one player tackles another head first, may also reduce head injury rates.

Falls can be avoided by installing grab bars in bathrooms and handrails on stairways; removing tripping hazards such as throw rugs; or installing window guards and safety gates at the top and bottom of stairs around young children. Playgrounds with shock-absorbing surfaces such as mulch or sand also prevent head injuries. Child abuse prevention is another tactic; programs exist to prevent shaken baby syndrome by educating about the dangers of shaking children. Gun safety, including keeping guns unloaded and locked, is another preventative measure. Studies on the effect of laws that aim to control access to guns in the United States have been insufficient to determine their effectiveness preventing number of deaths or injuries.

Treatment
It is important to begin emergency treatment within the so-called "golden hour" following the injury. People with moderate to severe injuries are likely to receive treatment in an intensive care unit followed by a neurosurgical ward. Treatment depends on the recovery stage of the patient. In the acute stage, the primary aim is to stabilize the patient and focus on preventing further injury. This is done because the initial damage caused by trauma cannot be reversed. Rehabilitation is the main treatment for the subacute and chronic stages of recovery. International clinical guidelines have been proposed with the aim of guiding decisions in TBI treatment, as defined by an authoritative examination of current evidence.

Acute stage
Tranexamic acid within three hours of a head injury decreases the risk of death. Certain facilities are equipped to handle TBI better than others; initial measures include transporting patients to an appropriate treatment center. Both during transport and in hospital the primary concerns are ensuring proper oxygen supply, maintaining adequate blood flow to the brain, and controlling raised intracranial pressure (ICP), since high ICP deprives the brain of badly needed blood flow and can cause deadly brain herniation. Other methods to prevent damage include management of other injuries and prevention of seizures. Some data supports the use of hyperbaric oxygen therapy to improve outcomes. Further research is required to determine the effectiveness and clinical importance of positioning the head at different angles (degrees of head-of-bed elevation) while the person is being treated in intensive care.

Neuroimaging is helpful but not flawless in detecting raised ICP. A more accurate way to measure ICP is to place a catheter into a ventricle of the brain, which has the added benefit of allowing cerebrospinal fluid to drain, releasing pressure in the skull. Treatment of raised ICP may be as simple as tilting the person's bed and straightening the head to promote blood flow through the veins of the neck. Sedatives, analgesics and paralytic agents are often used. Propofol and midazolam are equally effective as sedatives.

Hypertonic saline can improve ICP by reducing the amount of cerebral water (swelling), though it is used with caution to avoid electrolyte imbalances or heart failure. Mannitol, an osmotic diuretic, appears to be as effective as hypertonic saline at reducing ICP; however, some concerns have been raised regarding some of the studies performed. Hyertonic saline is also suitable in children with severe traumatic brain injury.

Diuretics, drugs that increase urine output to reduce excessive fluid in the system, may be used to treat high intracranial pressures, but may cause hypovolemia (insufficient blood volume). Hyperventilation (larger and/or faster breaths) reduces carbon dioxide levels and causes blood vessels to constrict; this decreases blood flow to the brain and reduces ICP, but it potentially causes ischemia and is, therefore, used only in the short term. Giving corticosteroids is associated with an increased risk of death, and so their routine use is not recommended. There is no strong evidence that the following pharmaceutical interventions should be recommended to routinely treat TBI: magnesium, monoaminergic and dopamine agonists, progesterone, aminosteroids, excitatory amino acid reuptake inhibitors, beta-2 antagonists (bronchodilators), haemostatic and antifibrinolytic drugs.

Endotracheal intubation and mechanical ventilation may be used to ensure proper oxygen supply and provide a secure airway. Hypotension (low blood pressure), which has a devastating outcome in TBI, can be prevented by giving intravenous fluids to maintain a normal blood pressure. Failing to maintain blood pressure can result in inadequate blood flow to the brain. Blood pressure may be kept at an artificially high level under controlled conditions by infusion of norepinephrine or similar drugs; this helps maintain cerebral perfusion. Body temperature is carefully regulated because increased temperature raises the brain's metabolic needs, potentially depriving it of nutrients. Seizures are common. While they can be treated with benzodiazepines, these drugs are used carefully because they can depress breathing and lower blood pressure. Anti-convulsant medications have only been found to be useful for reducing the risk of an early seizure. Phenytoin and leviteracetam appear to have similar levels of effectiveness for preventing early seizures. People with TBI are more susceptible to side effects and may react adversely to some medications. During treatment monitoring continues for signs of deterioration such as a decreasing level of consciousness.

Traumatic brain injury may cause a range of serious coincidental complications that include cardiac arrhythmias and neurogenic pulmonary edema. These conditions must be adequately treated and stabilised as part of the core care. Surgery can be performed on mass lesions or to eliminate objects that have penetrated the brain. Mass lesions such as contusions or hematomas causing a significant mass effect (shift of intracranial structures) are considered emergencies and are removed surgically. For intracranial hematomas, the collected blood may be removed using suction or forceps or it may be floated off with water. Surgeons look for hemorrhaging blood vessels and seek to control bleeding. In penetrating brain injury, damaged tissue is surgically debrided, and craniotomy may be needed. Craniotomy, in which part of the skull is removed, may be needed to remove pieces of fractured skull or objects embedded in the brain. Decompressive craniectomy (DC) is performed routinely in the very short period following TBI during operations to treat hematomas; part of the skull is removed temporarily (primary DC). DC performed hours or days after TBI in order to control persistently high intracranial pressures (secondary DC), although can reduce intracranial pressure and length of stay in ICU, but have worse Glasgow Coma Scale (GCS) scores, and high chances of death, vegetative state, or severe disability when compared to those receiving standard medical therapies.

Chronic stage

Once medically stable, people may be transferred to a subacute rehabilitation unit of the medical center or to an independent rehabilitation hospital. Rehabilitation aims to improve independent functioning at home and in society, and to help adapt to disabilities. Rehabilitation has demonstrated its general effectiveness when conducted by a team of health professionals who specialize in head trauma. As for any person with neurologic deficits, a multidisciplinary approach is key to optimizing outcome. Physiatrists or neurologists are likely to be the key medical staff involved, but depending on the person, doctors of other medical specialties may also be helpful. Allied health professions such as physiotherapy, speech and language therapy, cognitive rehabilitation therapy, and occupational therapy will be essential to assess function and design the rehabilitation activities for each person. Treatment of neuropsychiatric symptoms such as emotional distress and clinical depression may involve mental health professionals such as therapists, psychologists, and psychiatrists, while neuropsychologists can help to evaluate and manage cognitive deficits. Social workers, rehabilitation support personnel, nutritionists, therapeutic recreationists, and pharmacists are also important members of the TBI rehabilitation team. After discharge from the inpatient rehabilitation treatment unit, care may be given on an outpatient basis. Community-based rehabilitation will be required for a high proportion of people, including vocational rehabilitation; this supportive employment matches job demands to the worker's abilities. People with TBI who cannot live independently or with family may require care in supported living facilities such as group homes. Respite care, including day centers and leisure facilities for disabled people, offers time off for caregivers, and activities for people with TBI.

Pharmacological treatment can help to manage psychiatric or behavioral problems. Medication is also used to control post-traumatic epilepsy; however the preventive use of anti-epileptics is not recommended. In those cases where the person is bedridden due to a reduction of consciousness, has to remain in a wheelchair because of mobility problems, or has any other problem heavily impacting self-caring capacities, caregiving and nursing are critical. The most effective research documented intervention approach is the activation database guided EEG biofeedback approach, which has shown significant improvements in memory abilities of the TBI subject that are far superior than traditional approaches (strategies, computers, medication intervention). Gains of 2.61 standard deviations have been documented. The TBI's auditory memory ability was superior to the control group after the treatment.

Effect on the gait pattern
In patients who have developed paralysis of the legs in the form of spastic hemiplegia or diplegia as a result of the traumatic brain injury, various gait patterns can be observed, the exact extent of which can only be described with the help of complex gait analysis systems. In order to facilitate interdisciplinary communication in the interdisciplinary team between those affected, doctors, physiotherapists and orthotists, a simple description of the gait pattern is useful. J. Rodda and H. K. Graham already described in 2001 how gait patterns of CP patients can be more easily recognized and defined gait types which they compared in a classification. They also described that gait patterns can vary with age. Building on this, the Amsterdam Gait Classification was developed at the free university in Amsterdam, the VU medisch centrum. A special feature of this classification is that it makes different gait patterns very recognizable and can be used in patients in whom only one leg and both legs are affected. The Amsterdam Gait Classification was developed for viewing patients with cerebral palsy; however, it can be used just as well in patients with traumatic brain injuries. According to the Amsterdam Gait Classification, five gait types are described. To assess the gait pattern, the patient is viewed visually or via a video recording from the side of the leg to be assessed. At the point in time at which the leg to be viewed is in mid stance and the leg not to be viewed is in mid swing, the knee angle and the contact of the foot with the ground are assessed on the one hand.

Classification of the gait pattern according to the Amsterdam Gait Classification: In gait type 1, the knee angle is normal and the foot contact is complete. In gait type 2, the knee angle is hyperextended and the foot contact is complete. In gait type 3, the knee angle is hyperextended and foot contact is incomplete (only on the forefoot). In gait type 4, the knee angle is bent and foot contact is incomplete (only on the forefoot). With gait type 5, which is also known as crouch gait, the knee angle is bent and the foot contact is complete.

Orthotics
To improve the gait pattern, orthotics can be included in the therapy concept. An Orthosis can support physiotherapeutic treatment in setting the right motor impulses in order to create new cerebral connections. The orthosis must meet the requirements of the medical prescription. In addition, the orthosis must be designed by the orthotist in such a way that it achieves the effectiveness of the necessary levers, matching the gait pattern, in order to support the proprioceptive approaches of physiotherapy. The orthotic concepts of the treatment are based on the concepts for the patients with cerebral palsy. The characteristics of the stiffness of the orthosis shells and the adjustable dynamics in the ankle joint are important elements of the orthosis to be considered.

The orthotic concepts of the treatment are based on the concepts for the patients with cerebral palsy. Due to these requirements, the development of orthoses has changed significantly in recent years, especially since around 2010. At about the same time, care concepts were developed that deal intensively with the orthotic treatment of the lower extremities in cerebral palsy. Modern materials and new functional elements enable the rigidity to be specifically adapted to the requirements that fits to the gait pattern of the patient. The adjustment of the stiffness has a decisive influence on the gait pattern and on the energy cost of walking. It is of great advantage if the stiffness of the orthosis can be adjusted separately from one another via resistances of the two functional elements in the two directions of movement, dorsiflexion and plantar flexion.

Prognosis
Prognosis worsens with the severity of injury. Most TBIs are mild and do not cause permanent or long-term disability; however, all severity levels of TBI have the potential to cause significant, long-lasting disability. Permanent disability is thought to occur in 10% of mild injuries, 66% of moderate injuries, and 100% of severe injuries. Most mild TBI is completely resolved within three weeks. Almost all people with mild TBI are able to live independently and return to the jobs they had before the injury, although a small portion have mild cognitive and social impairments. Over 90% of people with moderate TBI are able to live independently, although some require assistance in areas such as physical abilities, employment, and financial managing. Most people with severe closed head injury either die or recover enough to live independently; middle ground is less common. Coma, as it is closely related to severity, is a strong predictor of poor outcome.

Prognosis differs depending on the severity and location of the lesion, and access to immediate, specialised acute management. Subarachnoid hemorrhage approximately doubles mortality. Subdural hematoma is associated with worse outcome and increased mortality, while people with epidural hematoma are expected to have a good outcome if they receive surgery quickly. Diffuse axonal injury may be associated with coma when severe, and poor outcome. Following the acute stage, prognosis is strongly influenced by the patient's involvement in activity that promote recovery, which for most patients requires access to a specialised, intensive rehabilitation service. The Functional Independence Measure is a way to track progress and degree of independence throughout rehabilitation.

Medical complications are associated with a bad prognosis. Examples of such complications include: hypotension (low blood pressure), hypoxia (low blood oxygen saturation), lower cerebral perfusion pressures, and longer times spent with high intracranial pressures. Patient characteristics also influence prognosis. Examples of factors thought to worsen it include: abuse of substances such as illicit drugs and alcohol and age over sixty or under two years (in children, younger age at time of injury may be associated with a slower recovery of some abilities). Other influences that may affect recovery include pre-injury intellectual ability, coping strategies, personality traits, family environment, social support systems and financial circumstances.

Life satisfaction has been known to decrease for individuals with TBI immediately following the trauma, but evidence has shown that life roles, age, and depressive symptoms influence the trajectory of life satisfaction as time passes. Many people with traumatic brain injuries have poor physical fitness following their acute injury and this may result with difficulties in day-to-day activities and increased levels of fatigue.

Complications

Improvement of neurological function usually occurs for two or more years after the trauma. For many years it was believed that recovery was fastest during the first six months, but there is no evidence to support this. It may be related to services commonly being withdrawn after this period, rather than any physiological limitation to further progress. Children recover better in the immediate time frame and improve for longer periods.

Complications are distinct medical problems that may arise as a result of the TBI. The results of traumatic brain injury vary widely in type and duration; they include physical, cognitive, emotional, and behavioral complications. TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death, persistent vegetative state (in which patients are unable to achieve a state of alertness to interact with their surroundings), and minimally conscious state (in which patients show minimal signs of being aware of self or environment). Lying still for long periods can cause complications including pressure sores, pneumonia or other infections, progressive multiple organ failure, and deep venous thrombosis, which can cause pulmonary embolism. Infections that can follow skull fractures and penetrating injuries include meningitis and abscesses. Complications involving the blood vessels include vasospasm, in which vessels constrict and restrict blood flow, the formation of aneurysms, in which the side of a vessel weakens and balloons out, and stroke.

Movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), spasticity (muscle contractions are overactive), myoclonus (shock-like contractions of muscles), and loss of movement range and control (in particular with a loss of movement repertoire). The risk of post-traumatic seizures increases with severity of trauma and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. 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). People may lose or experience altered vision, hearing, or smell.

Hormonal disturbances may occur secondary to hypopituitarism, occurring immediately or years after injury in 10 to 15% of TBI patients. Development of diabetes insipidus or an electrolyte abnormality acutely after injury indicate need for endocrinologic work up. Signs and symptoms of hypopituitarism may develop and be screened for in adults with moderate TBI and in mild TBI with imaging abnormalities. Children with moderate to severe head injury may also develop hypopituitarism. Screening should take place 3 to 6 months, and 12 months after injury, but problems may occur more remotely.

Cognitive deficits that can follow TBI include impaired attention; disrupted insight, judgement, and thought; reduced processing speed; distractibility; and deficits in executive functions such as abstract reasoning, planning, problem-solving, and multitasking. Memory loss, the most common cognitive impairment among head-injured people, occurs in 20–79% of people with closed head trauma, depending on severity. People who have had TBI may also have difficulty with understanding or producing spoken or written language, or with more subtle aspects of communication such as body language. Post-concussion syndrome, a set of lasting symptoms experienced after mild TBI, can include physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression. Multiple TBIs may have a cumulative effect. A young person who receives a second concussion before symptoms from another one have healed may be at risk for developing a very rare but deadly condition called second-impact syndrome, in which the brain swells catastrophically after even a mild blow, with debilitating or deadly results. About one in five career boxers is affected by chronic traumatic brain injury (CTBI), which causes cognitive, behavioral, and physical impairments. Dementia pugilistica, the severe form of CTBI, affects primarily career boxers years after a boxing career. It commonly manifests as dementia, memory problems, and parkinsonism (tremors and lack of coordination).

TBI may cause emotional, social, or behavioral problems and changes in personality. These may include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, problems with social judgment, and impaired conversational skills. TBI appears to predispose survivors to psychiatric disorders including obsessive compulsive disorder, substance abuse, dysthymia, clinical depression, bipolar disorder, and anxiety disorders. In patients who have depression after TBI, suicidal ideation is not uncommon; the suicide rate among these persons is increased 2- to 3-fold. Social and behavioral symptoms that can follow TBI include disinhibition, inability to control anger, impulsiveness, lack of initiative, inappropriate sexual activity, asociality and social withdrawal, and changes in personality.

TBI also has a substantial impact on the functioning of family systems Caregiving family members and TBI survivors often significantly alter their familial roles and responsibilities following injury, creating significant change and strain on a family system. Typical challenges identified by families recovering from TBI include: frustration and impatience with one another, loss of former lives and relationships, difficulty setting reasonable goals, inability to effectively solve problems as a family, increased level of stress and household tension, changes in emotional dynamics, and overwhelming desire to return to pre-injury status. In addition, families may exhibit less effective functioning in areas including coping, problem solving and communication. Psychoeducation and counseling models have been demonstrated to be effective in minimizing family disruption.

Epidemiology

TBI is a leading cause of death and disability around the globe and presents a major worldwide social, economic, and health problem. It is the number one cause of coma, it plays the leading role in disability due to trauma, and is the leading cause of brain damage in children and young adults. In Europe it is responsible for more years of disability than any other cause. It also plays a significant role in half of trauma deaths.

Findings on the frequency of each level of severity vary based on the definitions and methods used in studies. A World Health Organization study estimated that between 70 and 90% of head injuries that receive treatment are mild, and a US study found that moderate and severe injuries each account for 10% of TBIs, with the rest mild.

The incidence of TBI varies by age, gender, region and other factors. Findings of incidence and prevalence in epidemiological studies vary based on such factors as which grades of severity are included, whether deaths are included, whether the study is restricted to hospitalized people, and the study's location. The annual incidence of mild TBI is difficult to determine but may be 100–600 people per 100,000.

Mortality
In the US, the case fatality rate is estimated to be 21% by 30 days after TBI. A study on Iraq War soldiers found that severe TBI carries a mortality of 30–50%. Deaths have declined due to improved treatments and systems for managing trauma in societies wealthy enough to provide modern emergency and neurosurgical services. The fraction of those who die after being hospitalized with TBI fell from almost half in the 1970s to about a quarter at the beginning of the 21st century. This decline in mortality has led to a concomitant increase in the number of people living with disabilities that result from TBI.

Biological, clinical, and demographic factors contribute to the likelihood that an injury will be fatal. In addition, outcome depends heavily on the cause of head injury. In the US, patients with fall-related TBIs have an 89% survival rate, while only 9% of patients with firearm-related TBIs survive. In the US, firearms are the most common cause of fatal TBI, followed by vehicle accidents and then falls. Of deaths from firearms, 75% are considered to be suicides.

The incidence of TBI is increasing globally, due largely to an increase in motor vehicle use in low- and middle-income countries. In developing countries, automobile use has increased faster than safety infrastructure could be introduced. In contrast, vehicle safety laws have decreased rates of TBI in high-income countries, which have seen decreases in traffic-related TBI since the 1970s. Each year in the United States, about two million people have a TBI, approximately 675,000 injuries are seen in the emergency department, and about 500,000 patients are hospitalized. The yearly incidence of TBI is estimated at 180–250 per 100,000 people in the US, 281 per 100,000 in France, 361 per 100,000 in South Africa, 322 per 100,000 in Australia, and 430 per 100,000 in England. In the European Union the yearly aggregate incidence of TBI hospitalizations and fatalities is estimated at 235 per 100,000.

Demographics
TBI is present in 85% of traumatically injured children, either alone or with other injuries. The greatest number of TBIs occur in people aged 15–24. Because TBI is more common in young people, its costs to society are high due to the loss of productive years to death and disability. The age groups most at risk for TBI are children ages five to nine and adults over age 80, and the highest rates of death and hospitalization due to TBI are in people over age 65. The incidence of fall-related TBI in First-World countries is increasing as the population ages; thus the median age of people with head injuries has increased.

Regardless of age, TBI rates are higher in males. Men have twice as many TBIs as women do and have a fourfold risk of fatal head injury, and males account for two thirds of childhood and adolescent head trauma; however, when matched for severity of injury, women appear to fare more poorly than men.

Socioeconomic status also appears to affect TBI rates; people with lower levels of education and employment and lower socioeconomic status are at greater risk. Approximately half of those incarcerated in prisons and jails in the United States have had TBIs.

History

Head injury is present in ancient myths that may date back before recorded history. Skulls found in battleground graves with holes drilled over fracture lines suggest that trepanation may have been used to treat TBI in ancient times. Ancient Mesopotamians knew of head injury and some of its effects, including seizures, paralysis, and loss of sight, hearing or speech. The Edwin Smith Papyrus, written around 1650–1550 BC, describes various head injuries and symptoms and classifies them based on their presentation and tractability. Ancient Greek physicians including Hippocrates understood the brain to be the center of thought, probably due to their experience observing the effects of head trauma.

Medieval and Renaissance surgeons continued the practice of trepanation for head injury. In the Middle Ages, physicians further described head injury symptoms and the term concussion became more widespread. Concussion symptoms were first described systematically in the 16th century by Berengario da Carpi.

It was first suggested in the 18th century that intracranial pressure rather than skull damage was the cause of pathology after TBI. This hypothesis was confirmed around the end of the 19th century, and opening the skull to relieve pressure was then proposed as a treatment.

In the 19th century it was noted that TBI is related to the development of psychosis. At that time a debate arose around whether post-concussion syndrome was due to a disturbance of the brain tissue or psychological factors. The debate continues today.

Perhaps the first reported case of personality change after brain injury is that of Phineas Gage, who survived an accident in which a large iron rod was driven through his head, destroying one or both of his frontal lobes; numerous cases of personality change after brain injury have been reported since.

The 20th century saw the advancement of technologies that improved treatment and diagnosis such as the development of imaging tools including CT and MRI, and, in the 21st century, diffusion tensor imaging (DTI). The introduction of intracranial pressure monitoring in the 1950s has been credited with beginning the "modern era" of head injury. Until the 20th century, the mortality rate of TBI was high and rehabilitation was uncommon; improvements in care made during World War I reduced the death rate and made rehabilitation possible. Facilities dedicated to TBI rehabilitation were probably first established during World War I. Explosives used in World War I caused many blast injuries; the large number of TBIs that resulted allowed researchers to learn about localization of brain functions. Blast-related injuries are now common problems in returning veterans from Iraq & Afghanistan; research shows that the symptoms of such TBIs are largely the same as those of TBIs involving a physical blow to the head.

In the 1970s, awareness of TBI as a public health problem grew, and a great deal of progress has been made since then in brain trauma research, such as the discovery of primary and secondary brain injury. The 1990s saw the development and dissemination of standardized guidelines for treatment of TBI, with protocols for a range of issues such as drugs and management of intracranial pressure. Research since the early 1990s has improved TBI survival; that decade was known as the "Decade of the Brain" for advances made in brain research.

Diagnosis
Quantitative EEG and EEG, which has no specific patterns in TBI is used in research settings to differentiate between mild TBI and no TBI.

Medications
No medication is approved to halt the progression of the initial injury to secondary injury. The variety of pathological events presents opportunities to find treatments that interfere with the damage processes. Although neuroprotection methods to decrease secondary injury have been the subject of interest follows TBI, trials to test agents that could halt these cellular mechanisms have met largely with failure. For example, interest existed in cooling the injured brain; however, a 2020 Cochrane review did not find enough evidence to see if it was useful or not. Maintaining a normal temperature in the immediate period after a TBI appeared useful. One review found a lower than normal temperature was useful in adults but not children. While two other reviews found it did not appear to be useful.

Further research is necessary to determine if the vasoconstrictor indomethacin (indometacin) can be used to treat increased pressure in the skull following a TBI. In addition, drugs such as NMDA receptor antagonists to halt neurochemical cascades such as excitotoxicity showed promise in animal trials but failed in clinical trials. These failures could be due to factors including faults in the trials' design or in the insufficiency of a single agent to prevent the array of injury processes involved in secondary injury. Other topics of research have included investigations into mannitol, dexamethasone, progesterone, xenon, barbiturates, magnesium (no strong evidence), calcium channel blockers, PPAR-γ agonists,  curcuminoids, ethanol, NMDA antagonists, caffeine.

Procedures
In addition to traditional imaging modalities, there are several devices that help to monitor brain injury and facilitate research. Microdialysis allows ongoing sampling of extracellular fluid for analysis of metabolites that might indicate ischemia or brain metabolism, such as glucose, glycerol, and glutamate. Intraparenchymal brain tissue oxygen monitoring systems (either Licox or Neurovent-PTO) are used routinely in neurointensive care in the US. A non invasive model called CerOx is in development.

Research is also planned to clarify factors correlated to outcome in TBI and to determine in which cases it is best to perform CT scans and surgical procedures.

Hyperbaric oxygen therapy (HBO) has been evaluated as an add on treatment following TBI. The findings of a 2012 Cochrane systematic review does not justify the routine use of hyperbaric oxygen therapy to treat people recovering from a traumatic brain injury. This review also reported that only a small number of randomized controlled trials had been conducted at the time of the review, many of which had methodological problems and poor reporting. HBO for TBI is controversial with further evidence required to determine if it has a role.

Psychological
Further research is required to determine the effectiveness of non-pharmacological treatment approaches for treating depression in children/adolescents and adults with TBI.

As of 2010, the use of predictive visual tracking measurement to identify mild traumatic brain injury was being studied. In visual tracking tests, a head-mounted display unit with eye-tracking capability shows an object moving in a regular pattern. People without brain injury are able to track the moving object with smooth pursuit eye movements and correct trajectory. The test requires both attention and working memory which are difficult functions for people with mild traumatic brain injury. The question being studied, is whether results for people with brain injury will show visual-tracking gaze errors relative to the moving target.

Monitoring pressure
Pressure reactivity index is used to correlate intracranial pressure with arterial blood pressure to give information about the state of cerebral perfusion, thus guiding treatment and prevent excessively high or low blood flow to the brain. However, such method of monitoring intracranial pressure of equal or less than 20 mmHg is no better than imaging and clinical examination that monitor the neurological status of the brain in prolonging the survival, preserving the mental or functional status of the subject.

Sensory processing
In animal models of TBI, sensory processing has been widely studied to show systematic defects arise and are slowly but likely only partially recovered. It is especially characterised by an initial period of decreased activity in upper cortical layers. This period of decreased activity has also been characterised as by specific timing effects in the patterns of cortical activity in these upper layers in response to regular sensory stimuli.

Cited texts

The original version of this article contained text from the NINDS public domain pages on TBI

title: Traumatic brain injury


text: Talk:New Moon Shine

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Talk:New Moon Shine


text:
Talk:Hourglass (James Taylor album)

Fair use rationale for Image:James Taylor - Hourglass.jpg
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BetacommandBot (talk) 23:49, 13 February 2008 (UTC)

title: Talk:Hourglass (James Taylor album)


text:
Talk:Greatest Hits Volume 2 (James Taylor album)

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text:
Talk:October Road (album)

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BetacommandBot (talk) 23:50, 13 February 2008 (UTC)

title: Talk:October Road (album)


text: Talk:The Best of James Taylor

title: Talk:The Best of James Taylor


text: Talk:Heads & Tales (album)

title: Talk:Heads & Tales (album)


text: Talk:Sniper and Other Love Songs

title: Talk:Sniper and Other Love Songs


text:
Talk:Short Stories (Harry Chapin album)

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BetacommandBot (talk) 23:50, 13 February 2008 (UTC)

title: Talk:Short Stories (Harry Chapin album)


text: Talk:Verities & Balderdash

title: Talk:Verities & Balderdash


text: Talk:Portrait Gallery (album)

title: Talk:Portrait Gallery (album)


text:
Typographical error

A typographical error (often shortened to typo), also called a misprint, is a mistake (such as a spelling or transposition error) made in the typing of printed or electronic material. Historically, this referred to mistakes in manual typesetting. Technically, the term includes errors due to mechanical failure or slips of the hand or finger, but excludes errors of ignorance, such as spelling errors, or changing and misuse of words such as "than" and "then". Before the arrival of printing, the copyist's mistake or scribal error was the equivalent for manuscripts. Most typos involve simple duplication, omission, transposition, or substitution of a small number of characters.

"Fat finger" typing (especially in the financial sector) is a slang term referring to an unwanted secondary action when typing. When a finger is bigger than the touch zone, with touchscreens or keyboards, there can be inaccuracy and one may hit two keys in a single keystroke. An example is buckled instead of bucked, due to the "L" key being next to the "K" key on the QWERTY keyboard, the most common keyboard for Latin-script alphabets.

Typesetting
Historically, the process of converting a manuscript to a printed document required a typesetter to copy the text and print a first "galley proof" (familiarly, "a proof"). It may contain typographical errors ("printer's errors"), as a result of human error during typesetting. Traditionally, a proofreader compares the manuscript with the corresponding typeset portion, and then marks any errors (sometimes called "line edits") using standard proofreaders' marks.

Typing
When using a typewriter without correction tape, typos were commonly struck out with another character such as a strikethrough. This saved the typist the trouble of retyping the entire page to eliminate the error, but as evidence of the typo remained, it was not aesthetically pleasing. Correction fluid was invented to hide the original mark and allow the typist to correct the error almost invisibly. Word processing software all but eliminated the need for this solution.

Social media
In computer forums, sometimes "^H" (a visual representation of the ASCII backspace character) was used to "erase" intentional typos: "Be nice to this fool^H^H^H^Hgentleman, he's visiting from corporate HQ."

In instant messaging, users often send messages in haste and only afterward notice the typo. It is common practice to correct the typo by sending a subsequent message in which an asterisk (*) is placed before (or after) the correct word.

Textual analysis
In formal prose, it is sometimes necessary to quote text containing typos or other doubtful words. In such cases, the author will write "[sic]" to indicate that an error was in the original quoted source rather than in the transcription.

Scribal errors
Scribal errors received a lot of attention in the context of textual criticism. Many of these mistakes are not specific to manuscripts and can be referred to as typos. Some classifications include homeoteleuton and homeoarchy (skipping a line due to the similarity of the ending or beginning), haplography (copying once what appeared twice), dittography (copying twice what appeared once), contamination (introduction of extraneous elements), metathesis (reversing the order of some elements), unwitting mistranscription of similar elements, mistaking similar looking letters, the substitution of homophones, fission and fusion (joining or separating words).

Biblical errors
The Wicked Bible omits the word "not" in the commandment, "thou shalt not commit adultery".

The Judas Bible is a copy of the second folio edition of the authorized version, printed by Robert Barker, printer to James VI and I, in 1613, and given to the church for the use of the Mayor of Totnes. This edition is known as the Judas Bible because in Matthew 26:36 "Judas" appears instead of "Jesus". In this copy, the mistake is corrected with a slip of paper pasted over the misprint.

"Intentional" typos
Certain typos, or kinds of typos, have acquired widespread notoriety and are occasionally used deliberately for humorous purposes. For instance, the British newspaper The Guardian is sometimes referred to as The Grauniad due to its reputation for frequent typesetting errors in the era before computer typesetting. This usage began as a running joke in the satirical magazine Private Eye. The magazine continues to refer to The Guardian by this name.

Typos are common on social media, and some—such as "teh", "pwned", and "zomg"—have become in-jokes among Internet groups and subcultures. P0rn is not a typo but an example of obfuscation, where people make a word harder for filtering software to understand while retaining its meaning to human readers.

In mapping, it was common practice to include deliberate errors so that copyright theft could be identified.

Typosquatting
Typosquatting is a form of cybersquatting that relies on typographical errors made by users of the Internet. Typically, the cybersquatter will register a likely typo of a frequently-accessed website address in the hope of receiving traffic when internet users mistype that address into a web browser. Deliberately introducing typos into a web page, or into its metadata, can also draw unwitting visitors when they enter these typos in Internet search engines.

An example of this is  instead of   which could potentially be harmful to the user.

Typos in online auctions
Since the emergence and popularization of online auction sites such as eBay, misspelled auction searches have quickly become lucrative for people searching for deals. The concept on which these searches are based is that, if an individual posts an auction and misspells its description and/or title, regular searches will not find this auction. However, a search that includes misspelled alterations of the original search term in such a way as to create misspellings, transpositions, omissions, double strikes, and wrong key errors would find most misspelled auctions. The resulting effect is that there are far fewer bids than there would be under normal circumstances, allowing the searcher to obtain the item for less. A series of third-party websites have sprung up allowing people to find these items.

Atomic typos
Another kind of typo—informally called an "atomic typo"—is a typo that happens to result in a correctly spelled word that is different from the intended one. Since it is spelled correctly, a simple spellchecker cannot find the mistake. The term was used at least as early as 1995 by Robert Terry.

A few illustrative examples include: and many more. For any of these, the converse is also true.
 * "now" instead of "not",
 * "unclear" instead of "nuclear"
 * "you" instead of "your"
 * "Sudan" instead of "sedan" (leading to a diplomatic incident in 2005 between Sudan and the United States regarding a nuclear test code-named Sedan)
 * instead of "United States"
 * "the" instead of "they"

title: Typographical error


text: Talk:Greatest Stories Live

title: Talk:Greatest Stories Live


text: Talk:On the Road to Kingdom Come

title: Talk:On the Road to Kingdom Come


text:
Talk:MG Rover Group

Sales figures
Would you really say it was helpful to include Septembers sales figures? I would suggest if you want to include sales figures you give the full statistics (ie year to date %'s, market share, sales for both marques, which country those sales figures are for etc) and over a longer period than a single month. I don't believe I've seen sales figures quoted other than in broad terms in articles on other manufacturers.

--Pseud 14:15, Oct 11, 2004 (UTC)
 * I put them in to show the downturn in sales in just one year - perhaps that should be written more explicitly. I don't know any breakdown of those stats, unfortunately, so I can't add any more details to the numbers. violet/riga (t) 18:31, 11 Oct 2004 (UTC)

Changing owners
I changed the amount Rover was sold to the Tower group by BMW to £1 (as opposed to £10) cos it's well-known that it was a pound and it's stated on a BBC News page: http://news.bbc.co.uk/1/hi/uk_politics/4294709.stm. Dunno where the £10 figure came from but there's my explanation, although if you have proof that it is indeed £10, feel free to change it back and post up your link to prove it. --Smoothy 13:45, April 4, 2005 (BST)

OK... now visited the same page above and BBC News have changed it to £10, so changed it on article, especially as this link (http://news.bbc.co.uk/1/hi/business/4423181.stm) says £10 also. Very weird! --Smoothy 11:50, April 8, 2005 (BST)

The End
It seems the end for MG Rover has come. A funny thing is well not so funny but more of a coincidence is that the Longbridge factory was set up 100 years ago exactly. Not to this day but to this year. Wierd don't you think. (Erebus555 13:32, 8 Apr 2005 (UTC))

"Wierd" spelling? —Preceding unsigned comment added by Nitramrekcap (talk • contribs) 19:42, 4 June 2008 (UTC)

Hope
There is news circulating around the net that when MG Rover liquidates, Sir Richard Branson might acquire some of the assets, even possibly intangibles like the brand name itself. Branson intends to build Europe's first entirely hybrid car maker. There is still hope at least for the name of the company, the jobs on the other hand, well that's another story.

 * What evidence is there of Sir Richard Branson's interest in acquisition? This is news to me. I have heard Sir Richard suggesting the hybrid route may be an option, but that's far from saying that he has expressed an interest in acquiring some of the assets. Google News reveals an opinion piece by Sir Richard, but no reports. Stombs 13:05, May 4, 2005 (UTC)

Rapid Tense Shifting
The article, especially the opening paragraph, seems to shift between tenses faster than a midge going for a person's exposed arms. Can we decide whether to keep the whole thing in past tense or present? I'm going to put it generally into past tense, but if you disagree feel free to change it back.

Branson
See [1]. Andy Mabbett 21:48, 16 Jun 2005 (UTC)

Ownership and Year: 1986 Qvale
Statement: 1986 Qvale (date of first car - company was in existence longer) ... this lacks some facts. The Qvale Mangusta was launched back 1996 (back in 1986 the engine and drivetrain didn't exist so De Tomaso couldn't have designed the car by then) and put into the market in 2000. Qvale as car manufacturer was founded 2000 while Qvale (the importer) was founded 1947 in the USA. According to my sources the brand name Qvale still belongs to Qvale and wasn't sold to MG Rover. See also Qvale--NicolasCH 07:34, 18 October 2005 (UTC)

Nanjings intentions
I'm a student at the Technology Innovation Centre in Birmingham, it's part of the University of Central England group. Before MGR stopped trading we were one of their major research and development facilities, in this area.

Subsequently, Nanjing have unsurprisingly commited themselves to continue using us as an R&D facility. I say unsurprising because the reasons are that the province of Nanjing has universities that are twinned with UCE, and many of their students are put on placements here. So a lot of the engineering and design knowledge they're gaining is through us.

Their intentions as far as Longbridge is concerned are not quite clear even after the latest announcemnets. The MGTF (or whatever it may be called) will go ahead - but only for a few reasons.

-No one in China understands the car. Of course 2-seater roadsters are not a big seller in the Chinese market, and they see little point in producing it there. The main reason for producing it here is because there's a ready market for it and there's literally only one rival, the MX5.

-The profit made on the MG-TF is 15% - This was what it was designed to do from the outset. The typical profit of a normal car is only 6%, so it is worth producing to the end of its life possibly in 3 years time, in order to make the extra cash.

-Quality Control in China, as far as cars are concerned is terrible and their engineering knowledge is based on use of other companies technologies, so they need the help of the engineers we have in this country to help them develop their products.

Once they have the knowledge on building cars such as this, and once they have developed their engineering know-how, Longbridge is likely to close for good. Chinese labour is cheap, and as in all other areas of industry in China, quality control will improve quickly. I would like to be proved wrong, but it is the most likely scenario.

Austin-Healey
I've read articles that says Nanjin only owns the Austin name, not the Healey or Austin-Healey name. It appears that the Healey family retained ownership of the Healey name (and recently sold it to HFI Automotive). Anyone else have alternative references?

http://www.namedevelopment.com/blog/archives/2006/02/product_naming_24.html

For now I will remove Austin-Healey as a brand owned by MG Rover Group or now Nanjing.

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External links modified
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Carsalesbase.com
There's a discussion of the source carsalesbase.com at Reliable sources/Noticeboard. --Dennis Bratland (talk) 01:17, 19 March 2017 (UTC)

Last domestically owned in Britain
What about Aston Martin? Wolf O'Donnel (talk) 02:19, 18 June 2021 (UTC)

title: Talk:MG Rover Group


text: Talk:Dance Band on the Titanic

title: Talk:Dance Band on the Titanic


text: Talk:Living Room Suite

title: Talk:Living Room Suite


text:
Talk:Legends of the Lost and Found

Cover?
Is that the correct album cover? I remember the album cover having a spaceship on it. I think the image in the article might be the back cover? Doc Sigma (wait, what?)  18:50, 17 April 2007 (UTC)

Correct
The image shown in the article is in fact the back cover. It even says show in the picture caption. —Preceding unsigned comment added by 4RM0 (talk • contribs) 07:04, 23 March 2008 (UTC)

title: Talk:Legends of the Lost and Found


text:
Talk:Sequel (album)

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title: Talk:Sequel (album)


text:
Lobkowicz family

The House of Lobkowicz (Lobkovicové in modern Czech, sg. z Lobkovic; Lobkowitz in German) is an important Bohemian noble family that dates back to the 14th century and is one of the oldest noble families of the region. Over the centuries, the family expanded their possessions through marriage with the most powerful families of the region, which resulted in gaining vast territories all across central Europe. Due to that, the family was also incorporated into the German, Austrian and Belgian nobility.

History
The first Lobkowiczs were members of the gentry of north-eastern Bohemia in the late 14th century. On 3 August 1459 they were granted the title of Freiherr. In the 17th century, members of the family were awarded with the title of Prince, which was granted to them on 17 October 1623 by Ferdinand II, Holy Roman Emperor. The family's Imperial immediacy over Princely county of Störnstein was mediatized to Bavaria in 1807. As such, the House of Lobkowicz belong to the small group of families that constitute the and is one of the mediatised houses.

Princes of Lobkowicz

 * Zdenko Adalbert, 1st Prince 1624–1628 (1568–1628)
 * Wenzel Eusebius, 2nd Prince 1628–1677 (1609–1677)
 * Ferdinand August, 3rd Prince 1677–1715 (1655–1715)
 * Philipp Hyazinth, 4th Prince 1715–1737 (1680–1737)
 * Wenzel Ferdinand, 5th Prince 1737–1739 (1723–1739)
 * Ferdinand, 6th Prince 1739–1784 (1724–1784)
 * Joseph Franz Maximilian, 7th Prince 1784–1816 (1772–1816)
 * Ferdinand Joseph, 8th Prince 1816–1868 (1797–1868)
 * Moritz, 9th Prince 1868–1903 (1831–1903)
 * Ferdinand, 10th Prince 1903–1938 (1858–1938)
 * Prince Ferdinand, renounced his succession rights 1920
 * Prince Johann of Lobkowicz (1799–1878)
 * Prince Franz Eugen of Lobkowicz (1839–1898)
 * Jaroslav, 11th Prince 1938–1953 (1877–1953)
 * Friedrich, 12th Prince 1953–1954 (1907–1954)
 * Jaroslav, 13th Prince 1953–1985 (1910–1985)
 * Jaroslav, 14th Prince 1985–present (b. 1942)
 * Vladimir, Hereditary Prince of Lobkowicz (b. 1972)
 * Prince Jaroslav of Lobkowicz (b. 2012)
 * Prince Jaroslav of Lobkowicz (b. 1974)
 * Prince Philippe of Lobkowicz (b. 1978)
 * Prince Frederich of Lobkowicz (b. 2006)
 * Prince Casimir of Lobkowicz (b. 2009)
 * Prince Rudolf of Lobkowicz (b. 2011)

Notable family members

 * Mikuláš Chudý ("the Poor") z Újezda (c. 1378–1435) was a poor squire from the village of Újezd in Bohemia. After studying at the Charles University in Prague, he became a scribe in Kutná Hora. King Wenceslaus IV rewarded him for his services with the title to the village of Lobkovice (after which he began styling himself Nicholas of Lobkowicz), and he became the supreme scribe of the Bohemian kingdom in 1417. At the king's command, he captured several castles belonging to rebellious nobles; he was allowed to keep one, Hasištejn Castle, as a hereditary possession.
 * Nicholas Hasištejnský z Lobkowicz (died 1462). The elder son of Nicholas of Lobkowicz, he inherited Hasištejn Castle. He and his brother Jan were raised to the status of free lords by Emperor Frederick III in 1459. Twenty years later, they were awarded Czech lordly status as well.
 * Jan Popel z Lobkowicz (died 1470) was the younger son of Nicholas of Lobkowicz. He inherited Hluboká Castle and the village of Lobkovice from his father's estate. Along with his elder brother Nicholas, he was ennobled in 1459.
 * Jan Hasištejnský z Lobkovic (1450–1517) was a diplomat who traveled on ambassadorial missions to Luxembourg in 1477 and Rome in 1487. King Vladislaus II entrusted him with negotiating his marriage to Mary of Burgundy, but the match ultimately never occurred. Much like his younger brother Bohuslav, the so-called “Czech Ulysses,” Jan journeyed to the Holy Land, later writing a book about his experiences (Pilgrimage to the Holy Grave in Jerusalem, 1505). He helped develop a Franciscan monastery in Kadaň, and is buried there.
 * His brother Bohuslav Hasištejnský z Lobkovic (1461–1510) was a poet, essayist, and philosopher. He was well known for his prose, letters, and verses, including a satire on life in Bohemia. An extensive traveler who studied in Bologna and Ferrara and who voyaged to Egypt and the Holy Land, Bohuslav was elected Bishop of Olomouc but never held that office, as the pope refused to appoint him. He collected more than 650 books, primarily humanist and classical texts—an astonishing number for the era in which he lived. Roughly two thirds of his collection remains in the Lobkowicz Library, including more than 400 of the 750 incunabula belonging to the library.
 * Krystof Popel the Younger of Lobkowicz (1549–1609) was the Chief Steward of Bohemia during the reign of Emperor Rudolf II. Kryštof was a close friend of Hans von Aachen, the celebrated court painter. Known for his diplomatic and linguistic skills, he was often tasked with welcoming foreign visitors—including Persians, Turks, and Russians—to the Emperor's court, and was responsible for peace negotiations with the Polish king Sigismund.
 * Jiří Popel z Lobkowicz (c. 1551–1607 or 1613) was a devout Catholic nobleman who founded a Jesuit college in Chomutov and reestablished a monastery in Kadaň after it had been abolished due to connections with Lutheranism. Influential at the Imperial Court, in 1585 he became the Court Administrator, the second-highest office in Bohemia. However, he soon fell out of favor with Emperor Rudolf II, who blamed him and the other councillors for his brother Maximilian's defeat at the Battle of Byczyna and subsequent imprisonment. In 1593, he and his brother Ladislav Popel z Lobkowicz led an unsuccessful revolt against Rudolf II among the nobility. The two brothers fled Prague and were sentenced to death in absentia; Jiří was captured, but the Emperor lessened his sentence to life imprisonment and loss of property. He remained in prison for the rest of his life; the date of his death is unknown, but the years most frequently cited are 1607 and 1613.
 * Vilém mladší Popel z Lobkovic (c. 1575–1647). On 15 June 1587, he inherited the lordship of Horšovský Týn, which his father, John the Younger, had purchased in 1546. He was a royal councillor, and a court justice from 1628 to 1634. Being a Protestant, he was dispossessed in favour of the Catholic Lobkowicz line after the Battle of White Mountain in 1620.
 * Zdeněk Vojtěch Popel z Lobkovic (1568–1628), 1st Prince Lobkowicz, was Chancellor to the Czech Kingdom under Emperors Rudolf II, Matthias, and Ferdinand II. Zdeněk Vojtěch was a major political figure in both Bohemia and the larger Habsburg empire. He and his wife Polyxena Pernštejn (1566–1642), the daughter of a Chancellor to the Czech Kingdom and an influential Spanish noblewoman, were leaders of the “Spanish” (i.e. Catholic) bloc at court, opposed to the Protestant factions. When the Emperor's Catholic ministers were hurled from the windows of Prague Castle in the famous Defenestration of Prague in 1618, they took refuge in the nearby Lobkowicz Palace. The incident also signalled a turning point in the fortunes of the Lobkowicz family: although their property was confiscated by rebellious Protestants in 1618, the Catholic victory at the Battle of White Mountain in 1620 resulted in the restoration of their property and ensured that the family, as Catholic nobles, would continue to be highly influential. That same year, King Philip III of Spain awarded Zdeněk Vojtěch the Order of the Golden Fleece, the highest order of European chivalry. In 1624, Ferdinand II granted him the title of Imperial Prince, and he became the first hereditary Prince Lobkowicz.
 * Polyxena Pernštejn (1566–1642), 1st Princess Lobkowicz, was the daughter of Vratislav of Pernštejn (1530–1582), Chancellor of the Czech Kingdom, and Maria Maximiliana Manrique de Lara y Mendoza (1538–1608), an influential Spanish noblewoman. In 1587, she became the fourth wife of William of Rosenberg (1535–1592), High Treasurer and High Burgrave of Bohemia and the wealthiest man in the country. After William's death, she married Zdeněk Vojtěch of Lobkowicz, Chancellor of the Czech Kingdom and later 1st Prince Lobkowicz. As all of William's marriages had been childless, Polyxena's marriage to Zdeněk Vojtěch brought considerable wealth and property into the Lobkowicz family. Polyxena and her husband were highly influential at the Imperial Habsburg court, where they spearheaded Catholic opposition to Protestant factions. After the Defenestration of Prague in 1618, the Emperor's Catholic ministers took refuge in the Lobkowicz Palace. A later painting shows a romanticized version of the incident, with Polyxena barring the door of the palace against a Protestant mob while the battered ministers cower behind her—while another version of events claims that Polyxena concealed the ministers under her skirts. The defeat of the Protestants at the Battle of White Mountain in 1620 ensured that the Lobkowicz family would continue to play a major role in Bohemian and Imperial politics.
 * Kateřina Benigna Popelovna Lobkowicz (1594–1653), wife of Vilém mladší Popel z Lobkowicz, helped establish Loreta as a significant pilgrimage destination in Prague. She financed the construction of the site, which was designed by Italian architect Giovanni Orsi and built between 1626 and 1631.
 * Anna Magdalene (1606–1668), Baroness Popel von Lobkowicz, was the daughter of William the Younger Popel of Lobkowicz, Lord of Horšovský Týn. She married Julius Henry, Imperial Field Marshal and future Duke of Saxe-Lauenburg, in 1632. Of their six children, two survived infancy. The youngest, Julius Francis (1641–1689), was the last Ascanian duke of Saxe-Lauenburg.
 * Juan Caramuel y Lobkowitz (1606–1682) was a Spanish Catholic philosopher, mathematician, architect and architectural theorist, ecclesiastic, and writer, believed to be a grandson of the eldest daughter of Jan Popel z Lobkowicz (c. 1527–1590). After a precocious childhood, he entered the Cistercian Order and was later awarded a doctorate of theology by the University of Leuven. His titles and positions included Philip IV of Spain's envoy to the court of Emperor Ferdinand III; Abbot of Melrose, Scotland; Abbot-Superior of the Benedictines of Vienna; Grand Vicar to the Archbishop of Prague; Bishop of Satrianum; Bishop of Campagna; and, at his death, Bishop of Vigevano. His intellectual pursuits were no less illustrious: he published 262 works on subjects from poetry to astronomy to asceticism, was one of the earliest scholars to write on probability, and designed the façade of the Vigevano Cathedral. When the Swedes attacked Prague in 1648, he armed and led a band of ecclesiastics to serve in defense of the city, and the emperor rewarded him for his bravery with a collar of gold.
 * Václav Eusebius František (1609–1677), 2nd Prince Lobkowicz, was the only child of Zdeněk Vojtěch and Polyxena Pernštejn, and became one of the most influential European statesmen of the 17th century. He raised his own regiment to fight in the Thirty Years' War and held high offices at the Habsburg court, advising Emperors Ferdinand III and Leopold I in his capacity as President of the Imperial War Cabinet (from 1652) and President of the Imperial Privy Council (from 1669). He had a close connection with the Infanta Margarita Teresa of Spain, Leopold I's young wife. The Lobkowicz Collections’ portrait of the Infanta (attributed to Velázquez) was presumably acquired during Leopold's reign. He also transformed his family's properties, overseeing the remodeling of the Lobkowicz Palace in Prague by Italian Baroque artists and the reconstruction of Roudnice Castle from a ruin to the family seat, and purchasing the ducal estate of Sagan in Silesia from Ferdinand III in 1646.
 * František Vilém (1616–1670), the fourth son of Vilém mladší Popel z Lobkowicz, served as a councillor to Emperors Ferdinand III and Leopold I between 1647 and 1659. He was rewarded with the title of Highest Hunter in the Kingdom of Bohemia, a hereditary honor.
 * Ferdinand August (1655–1715), 3rd Prince Lobkowicz, was a painting connoisseur whose additions to the Lobkowicz Collections include Veronese's David with the Head of Goliath, Rubens's Hygieia and the Sacred Serpent, Pieter Brueghel the Younger’s Village in Winter and Jan Brueghel the Elder’s St. Martin Dividing His Cloak. In addition to his own acquisitions, his wives also brought paintings as their dowries. The first, Claudia Franziska von Nassau Hadamar, brought with her portraits from the house of Nassau as well as a series of amateur portraits painted by her mother. The second, Maria Anna von Baden, brought a variety of Northern paintings, including Lucas Cranach the Elder's The Virgin and Child with Saints Barbara and Catherine of Alexandria and Cranach the Younger's Jesus and the Woman Taken in Adultery. Ferdinand August was also the first Prince Lobkowicz to systematically collect musical scores, and was an accomplished lutenist.
 * Wenzel Ferdinand (1656–1697), Count of Bílina. As well as being Count of Bílina, a Bohemian town famous for its healing mineral water, Wenzel Ferdinand was an Imperial councillor and chamberlain. He served as an envoy to Bavaria, France, Spain, England, and the Netherlands. While in the Netherlands, he commissioned a Delft service from Lambertus Cleffius – the earliest and largest Delft service still in existence.
 * Philip Hyacinth (1680–1734), 4th Prince Lobkowicz, was a patron of the arts who collected musical scores on several journeys to England. The composer Sylvius Leopold Weiss, one of the finest lutenists of his day, taught music to both Philip Hyacinth and his second wife Anna Maria Wilhelmina von Althan, and dedicated several works to the princess.
 * Eleonore, Princess Lobkowicz (1682–1741) was the daughter of Ferdinand August, 3rd Prince Lobkowicz. At the beginning of the 18th century, she had the mineral spring at Bílina cleaned, leading to the town becoming a well-known spa. In 1701 she married Adam Franz Eusebius, hereditary Prince von Schwarzenberg, whom Emperor Charles VI killed in a hunting accident in 1732. Subsequently, the Emperor took her son Joseph Adam to his court in Vienna, and she was paid a baronial maintenance of 5,000 gulden.
 * Eleonora Carolina (1685–1720), Countess of Bílina. The daughter and sole heir of Count Wenzel Ferdinand, she married her distant cousin Philip Hyacinth, 4th Prince Lobkowicz.
 * Johann Georg Christian, Prince of Lobkowicz (1686–1755). A field marshal of the Imperial forces, Georg Christian was the fourth son of Ferdinand August, 3rd Prince Lobkowicz. He commanded the Lobkowicz regiment founded during the Thirty Years' War by Václav Eusebius, 2nd Prince Lobkowicz, and was commander-in-chief of the Habsburg armies in Italy. The Lobkowicz Collections holds portraits of eighteen officers that served in the Lobkowicz regiment under his command.
 * Ferdinand Philip (1724–1784), 6th Prince Lobkowicz. After Frederick the Great of Prussia invaded Silesia during the War of the Austrian Succession, Ferdinand Philip supported Frederick over Empress Maria Theresa of Austria in order to protect his huge and highly profitable Silesian estate, originally acquired by Václav Eusebius, 2nd Prince Lobkowicz. It was probably for this reason that he was one of only two reigning princes of Lobkowicz not to be awarded the Order of the Golden Fleece, the highest Austrian order of chivalry. Wishing to avoid the war in Silesia and Bohemia but unwelcome at the Habsburg court in Vienna, Ferdinand Philip spent much of the 18th century in England, accompanied by Christoph Willibald Gluck, whom he had employed in the Lobkowicz Palace orchestra. He returned to Bohemia with two of Canaletto's finest paintings of London. His shrewd protection of his Silesian estate paid off: after his death, it was sold to the Duke of Courland for the incredible (at the time) sum of one million gulden.
 * Joseph František Maximilian (1772–1816), 7th Prince Lobkowicz, was a patron of Joseph Haydn and Ludwig van Beethoven. Despite the previous Prince of Lobkowicz's lack of support for Maria Theresa, Joseph František Maximilian remained on good terms with the Habsburgs: Emperor Joseph II granted him the title of Duke of Roudnice in 1786, and to celebrate the coronation of Emperor Leopold II as King of Bohemia in 1791 he commissioned a reconstruction of the Lobkowicz Palace's exterior, giving it the appearance that it retains to this day. A talented singer, violinist, and violoncellist, Joseph František Maximilian was a noted patron of the arts: he was a founding member of the Society of the Friends of Music in Vienna, a member of the Society for the Promotion of Musical Culture in Bohemia, and a director of the Court Theatre of Vienna. He made his greatest impact on the musical world as a patron of Beethoven, who dedicated several major works to him, including the 3rd (Eroica), 5th, and 6th (Pastoral) symphonies.
 * Ferdinand Joseph Johann Nepomuk (1797–1868), 8th Prince Lobkowicz. A notable industrialist as well as a patron of the arts, he was a particular benefactor of the geologist and paleontologist August Emanuel von Reuss. In 1835 he established one of the largest sugar factories in Bohemia, in the town of Bílina. He served as a member of parliament in Bohemia from 1860 to 1863.
 * Karl Johann Josef of Lobkowicz (1815–1879). After having been head of government from 1852 to 1856, he served as a privy councillor in 1857. He was a stadholder in Lower Austria, Moravia, and Tyrol and Vorarlberg in the late 1850s and early 1860s.
 * Moric (1831–1903), 9th Prince Lobkowicz. He served as an Imperial Privy Councilor beginning in 1890.
 * Georg Christian, Prince of Lobkowicz (1835–1908) was a political leader among the conservative Bohemian nobility. Georg Christian was a member of the Bohemian Diet from 1865 to 1872 and 1883 to 1907, presiding over it twice as Land Marshal of Bohemia. He served as deputy in the Austrian Parliament from 1879 to 1883 and became a hereditary member of the Austrian House of Lords in 1883.
 * Ferdinand Zdenko Maria (1858–1938), 10th Prince Lobkowicz. In 1907, he was appointed chamberlain to Archduke Charles, later Charles I of Austria, the last ruler of the Austro-Hungarian Empire.
 * Wilhelmina(1863–1945) was the daughter of Moric, 9th Prince Lobkowicz. She sponsored a religious institution for widowed and unmarried noblewomen, The Order of the Sisters of God's Love, in Nelahozeves Castle. She was the last Lobkowicz to live in the castle, and is buried in the Nelahozeves village cemetery.
 * Ferdinand Lobkowicz (1885–1953), known as "the Evangelist". He was the eldest son of Ferdinand Zdenko Maria, 10th Prince Lobkowicz, but renounced his inheritance rights in 1920. His younger brother Maximilian inherited the family's properties instead.
 * Maximilian Lobkowicz (1888–1967). Despite the government's decision to redistribute inherited property and abolish the use of noble titles, Maximilian provided crucial support to the newly formed, democratic Czechoslovakia as a lawyer and diplomat, campaigning abroad for international recognition of the young republic. In the 1930s he mustered diplomatic support for opposition to the German annexation of the Sudetenland, and during World War II he served as ambassador to Great Britain for the Czechoslovakian government in exile. In 1945 he and his family regained the property that had been confiscated by the Nazis, only to see it seized again in 1948 by the Communist government. At the same time, Maximilian and his family were forced into exile.
 * Georg Christian of Lobkowicz (1907–1932), a racing driver who died after a crash at the 1932 Avusrennen, a motor race held at the AVUS circuit.
 * Princess Edward Joseph de Lobkowicz (1903–1976) was an American golfer and real estate broker who married Prince Edward Joseph de Lobkowicz.
 * Edouard de Lobkowicz (1926–2010) was an investment banker, an ambassador of the Sovereign Military Order of Malta, and the husband of Princess Marie-Françoise of Bourbon-Parma.
 * Bedřich (Frederick) Lobkowicz (1932–1998), physicist at University of Rochester.
 * Stéphane de Lobkowicz, his wife Barbara d'Ursel de Lobkowicz and their daughter Ariane de Lobkowicz-d'Ursel have served in the Brussels Parliament.

The family today
Today, there are four main branches of the Lobkowicz family: of Roudnice, Křimice, Dolní Beřkovice and Mělník.

Notable Lobkowiczs of today include:
 * Mikuláš Lobkowicz (b. 1931), philosopher, rector of the Ludwig Maximilian University of Munich, president of the Catholic University of Eichstätt-Ingolstadt.
 * Jaroslav Lobkowicz (b. 1942), MP 1998–2006 and 2010–present, head of the Křimice branch of the family.
 * František Václav Lobkowicz (1948–2022), O.Praem., Bishop of Ostrava-Opava.
 * Jiří Lobkowicz (b. 1956), businessman and politician, head of the Mělník branch of the family.
 * William Lobkowicz (b. 1961), current heir and manager of most of the Lobkowicz lands in the Czech Republic, including the Lobkowicz Palace, Nelahozeves, Roudnice, and Střekov Castle.
 * Prince Edouard-Xavier de Lobkowicz (1960–1984), son of Prince Edouard de Lobkowicz and Princess Marie-Françoise of Bourbon-Parma, murder victim
 * Prince Charles-Henri de Lobkowicz (b. 1964), son of Prince Edouard de Lobkowicz and Princess Marie-Françoise of Bourbon-Parma, proprietor of the château de Boszt in Besson, heir to the Manoir d'Ujezd in Goderville, and to the château de Lignières.
 * Princess Marie Gabrielle de Lobkowicz (born 1967), French nun
 * Michal Lobkowicz (b. 1964), MP 1992–2002, Minister of Defence of the Czech Republic in 1998.
 * Princess Edouard de Lobkowicz (born 1928), French humanist and wife of Edouard de Lobkowicz.

Properties of the family
After the Velvet Revolution of 1989, a number of castles and estates were restored to different branches of the family. These estates included the Lobkowicz Palace in Prague Castle (now a museum with a famous art collection), Nelahozeves Castle (also a museum), Roudnice Castle, Střekov Castle, Mělník Castle, Bílina Castle, Křimice Castle, Dolní Beřkovice Castle (inherited by the Thurn und Taxis family), Jezeří Castle (sold by the family), Vysoký Chlumec Castle (sold by the family), Hasištejn Castle, Chomutov Castle, Líčkov Castle, Felixburk, Neustadt an der Waldnaab, Horšovský Týn Castle, and Zbiroh.

title: Lobkowicz family


text:
Talk:Eagles Live

Possible Frey-Henley feud
The article says "Eagles Live was mixed by Glenn Frey and Don Henley on opposite coasts, as the two decided they could not stand to be in the same state, let alone the same studio". Is that hinting to a possible feud between Frey and Henley? I never knew of anything of that sort. ICE77 (talk) 07:29, 26 January 2016 (UTC)

title: Talk:Eagles Live