Ariel Scheinermann, אריאל שיינרמןon 26 February 1928) is an Israeli statesman and retired general, who served as Israel’s 11th Prime Minister. He has been in a permanent vegetative statesince suffering a stroke on 4 January 2006. In 2013, tests showed "robust activity" in his brain in response to pictures of his family and recordings of his son's voice.[1]Sharon was a commander in the Israeli Army from its inception in 1948. As a paratrooper and then an officer, he participated prominently in the 1948 War of Independence, becoming a platoon commander in the Alexandroni Brigadeand taking part in many battles, including Operation Ben Nun Alef. He was an instrumental figure in the creation of Unit 101, the Retribution operations, the1956 Suez War, the Six-Day War of 1967, the War of Attrition and the Yom-Kippur War of 1973. As Minister of Defense, he directed the 1982 Lebanon War.
During his military career, he was considered the greatest field commander in Israel's history, and one of the country's greatest ever military strategists.[2]After his assault of the Sinai in the Six-Day War and his encirclement of the Egyptian Third Army in the Yom Kippur War, the Israeli public nicknamed him "The King of Israel" and "The Lion of God".[2]
After retiring from the army, Sharon joined the Likud party, and served in a number of ministerial posts in Likud-led governments in 1977–92 and 1996–99. He became the leader of the Likud in 2000, and served as Israel’s Prime Minister from 2001 to 2006. In 1983 the commission established by the Israeli Government found that as Minister of Defense during the 1982 Lebanon WarSharon bore "personal responsibility" for the massacre by Lebanese militias of Palestinian civilians in the refugee camps of Sabra and Shatila, for his having disregarded the prospect of acts of bloodshed by the Phalangists against the population of the refugee camps, and not having prevented their entry.[3] The Kahan Commission recommended Sharon's removal as Defense Minister, and Sharon did resign after initially refusing to do so. In the 1970s, 1980s, and 1990s, Sharon championed construction of Israeli settlements in the West Bank and Gaza Strip. However, as Prime Minister, in 2004–5 Sharon orchestrated Israel's unilateral disengagement from the Gaza Strip. Facing stiff opposition to this policy within the Likud, in November 2005 he left Likud to form a new Kadima party. His stroke occurred a few months before he had been expected to win a new election on what Matt Rees and Rafi Eitan have described as "clearing Israel out of most of the West Bank", in a planned unilateral withdrawal.[4][5]
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Tbilisi State University, Georgia, where Sharon's father was studying agronomy and his mother had just started her fourth year of medical studies. AsBolshevik forces advanced towards independent Georgia, his parents emigrated to the British Mandate of Palestine, fleeing the pogroms associated with the Russian Civil War.
The family arrived in the Third Aliyah and settled in a Kfar Malal, a socialist,secular community where, despite being Mapai supporters, they were known to be contrarians against the prevailing community consensus:
The Scheinermans' eventual ostracism... followed the 1933 Arlozorovmurder when Dvora and Shmuel refused to endorse the Labor movement's anti-Revisionist calumny and participate in Bolshevic-style public revilement rallies, then the order of the day. Retribution was quick to come. They were expelled from the local health-fund clinic and village synagogue. The cooperative's truck wouldn't make deliveries to their farm nor collect produce.[6]
----------------Causes of vegetated state;
*Person experiencing vegetated state are not on life-support. Not experiencing coma.
Brain is awake-controls heart-body is alive.
Yet, one is unable to gain use of one's body.
Head injury is present in ancient myths that may date back before recorded history.[137] Skulls found in battleground graves with holes drilled over fracture lines suggest that trepanation may have been used to treat TBI in ancient times.[138] Ancient Mesopotamians knew of head injury and some of its effects, including seizures, paralysis, and loss of sight, hearing or speech.[139] The Edwin Smith Papyrus, written around 1650–1550 BC, describes various head injuries and symptoms and classifies them based on their presentation and tractability.[140] Ancient Greek physicians including Hippocrates understood the brain to be the center of thought, probably due to their experience with head trauma.[141]
Medieval and Renaissance surgeons continued the practice of trepanation for head injury.[141] In the Middle Ages, physicians further described head injury symptoms and the term concussion became more widespread.[142] Concussion symptoms were first described systematically in the 16th century by Berengario da Carpi.[141]
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.[138]
In the 19th century it was noted that TBI is related to the development of psychosis.[143] At that time a debate arose around whether post-concussion syndrome was due to a disturbance of the brain tissue or psychological factors.[142] The debate continues today.
Phineas Gage carrying the rod that caused his TBI
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.[24][26][27][36][37][41][144][145]
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.[93][146] 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.[137] Facilities dedicated to TBI rehabilitation were probably first established during World War I.[137] 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.[147] 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.[148]
In the 1970s, awareness of TBI as a public health problem grew,[149] and a great deal of progress has been made since then in brain trauma research,[93] such as the discovery of primary and secondary brain injury.[138] 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.[93] Research since the early 1990s has improved TBI survival;[138] that decade was known as the "Decade of the Brain" for advances made in brain research.[150]
Research
No medication to halt the progression of secondary injury exists,[55] but the variety of pathological events presents opportunities to find treatments that interfere with the damage processes.[2] Neuroprotection, methods to halt or mitigate secondary injury, have been the subject of great interest for their ability to limit the damage that follows TBI. However, clinical trials to test agents that could halt these cellular mechanisms have met largely with failure.[2] For example, interest existed in hypothermia, cooling the injured brain to limit TBI damage, but clinical trials showed that it is not useful in the treatment of TBI.[93] 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.[93] 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.[93] Recent research has gone into monitoring brain metabolism for ischaemia, in particular the parameters of glucose, glycerol, and glutamate through microdialysis[citation needed].
Developments in technologies may provide doctors with valuable medical information. For example, work has been done to design a device to monitor oxygenation that could be attached to a probe placed into the brain—such probes are currently used to monitor ICP.[93] 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.[151]
Hyperbaric oxygen therapy (HBO) has been evaluated as an adjunctive treatment following TBI, concluding a Cochrane review stating that its use could not be justified.[152] HBO for TBI has remained controversial as studies have looked for improvement mechanisms,[153][154][155] and further evidence shows that it may have potential as a treatment.[156][157]
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.[2] Brain function is temporarily or permanently impaired and structural damage may or may not be detectable with current technology.[3]
All traumatic brain injuries are head injuries, but the latter term may also refer to injury to other parts of the head.[6][7][8] However, the terms head injury and brain injury are often used interchangeably.[9] Similarly, brain injuries fall under the classification ofcentral nervous system injuries[10] and neurotrauma.[11] 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).[12]Mechanism-related classification divides TBI into closed and penetrating head injury.[2] A closed (also called nonpenetrating, or blunt)[6] injury occurs when the brain is not exposed.[7] A penetrating, or open, head injury occurs when an object pierces the skull and breaches the dura mater, the outermost membrane surrounding the brain.[7]
Unconsciousness tends to last longer for people with injuries on the left side of the brain than for those with injuries on the right.[7]
Other symptoms of mild TBI include headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing,[35]lightheadedness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns.[34] Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking.[34]
ex. West German Prez Lubke (only compassionate humanitarian to have lent a helping
hand to Assasinated South Korean Prez Park seeking financial loan to rebuild war-destructed-country
occupied by 'lying-deceitful' Pro-Jap American Military not lifting a finger to rebuild
Korea it occupied); Prez Lubke showed following symptoms leading to his resignation and his death.
(Those who remember his compassionate aide to war-destructed-Korea will remember him as a Hero;
it is unfortunate that the very Germans, whom Prez Lubke credited when he lent a helping hand to
Korea, 'joke' and 'discredit' his 'disability' leading to his tragic death. It is sinful that
each display of compassion and moral ethics Prez
Lubke and 11th Israel Prime
Minister Ariel Scheinermann
displayed follows in 'disabling conditions' that
debilitate and kill. Human being must have the
courage to know when to 'stop' as well as when
to say 'enough is enough'.
....Cowards stop 'Courageous Leaders' via
'disabling the very Courageous Leaders' they'd
never be themselves'... Cowards will be
miserably haunted by their hatred and
cowardly deceitful tactics that'll engulf
them to eternal misery.... Enjoy your hell, cowards!
"Victory to the Courageous Leaders!"
Hero will live eternally...
as a Legend... never forgotten...
... always thanked.
...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.[34] 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.[27][36][37][38][39] Alexithymia, a deficiency in identifying, understanding, processing, and describing emotions occurs in 60.9% of individuals with TBI.[40] 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.[39][41][42][43]
Brain trauma can occur as a consequence of a focal impact upon the head, by a sudden acceleration/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, brain trauma causes secondary injury, a variety of events that take place in the minutes and days following the injury. These processes, which include alterations in cerebral blood flow and thepressure within the skull, contribute substantially to the damage from the initial injury.
When the pressure within the skull (intracranial pressure, abbreviated ICP) rises too high, it can be deadly.[44] 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.[44] Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP.[3] Anisocoria, unequal pupil size, is another sign of serious TBI.[32] Abnormal posturing, a characteristic positioning of the limbs caused by severe diffuse injury or high ICP, is an ominous sign.[3]
Small children with moderate to severe TBI may have some of these symptoms but have difficulty communicating them.[45]Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat,[45] and irritability.[3]
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.[49] TBI is the third most common injury to result from child abuse.[50] Abuse causes 19% of cases of pediatric brain trauma, and the death rate is higher among these cases.[51] Domestic violence is another cause of TBI,[52] as are work-related and industrial accidents.[53] Firearms[7] and blast injuries from explosions[54] are other causes of TBI, which is the leading cause of death and disability in war zones.[55] According to Representative Bill Pascrell (Democrat, NJ), TBI is "the signature injury of the wars in Iraq and Afghanistan."[56] 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[57] [58]
The type, direction, intensity, and duration of forces all contribute to the characteristics and severity TBI.[2] Forces that may contribute to TBI include angular, rotational, shear, and translational forces.[30]
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.[30] 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, termednoncontact or inertial loading, usually causes diffuse injuries.[12] The violent shaking of an infant that causes shaken baby syndrome commonly manifests as diffuse injury.[60] In impact loading, the force sends shock waves through the skull and brain, resulting in tissue damage.[30] Shock waves caused bypenetrating injuries can also destroy tissue along the path of a projectile, compounding the damage caused by the missile itself.[15]
Damage may occur directly under the site of impact, or it may occur on the side opposite the impact (coup and contrecoup injury, respectively).[59] When a moving object impacts the stationary head, coup injuries are typical,[61] while contrecoup injuries are usually produced when the moving head strikes a stationary object.[62]
A large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event;[63] rather than improving after being hospitalized, some 40% of TBI patients deteriorate.[64] 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.[65] These secondary processes can dramatically worsen the damage caused by primary injury[55] and account for the greatest number of TBI deaths occurring in hospitals.[32]
Secondary injury events include damage to the blood–brain barrier, release of factors that cause inflammation, free radical overload, excessive release of theneurotransmitter glutamate (excitotoxicity), influx of calcium and sodium ions into neurons, and dysfunction of mitochondria.[55] Injured axons in the brain'swhite matter may separate from their cell bodies as a result of secondary injury,[55] 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).[66] Intracranial pressure may rise due to swelling or a mass effect from a lesion, such as a hemorrhage.[44]As a result, cerebral perfusion pressure (the pressure of blood flow in the brain) is reduced; ischemia results.[32][67] When the pressure within the skull rises too high, it can cause brain death or herniation, in which parts of the brain are squeezed by structures in the skull.[44] A particularly weak part of the skull that is vulnerable to damage causing extradural haematoma is the pterion, deep in which lies the middle meningeal artery which is easily damaged in fractures of thepterion. Since the pterion is so weak this type of injury can easily occur and can be secondary due to trauma to other parts of the skull where the impact forces spreads to the pterion.
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.[15] Neuroimaging helps in determining the diagnosis and prognosis and in deciding what treatments to give.[68]
The preferred radiologic test in the emergency setting is computed tomography(CT): it is quick, accurate, and widely available.[69] Followup CT scans may be performed later to determine whether the injury has progressed.[2]
Magnetic resonance imaging (MRI) can show more detail than CT, and can add information about expected outcome in the long term.[15] It is more useful than CT for detecting injury characteristics such as diffuse axonal injury in the longer term.[2] 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.[15]
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.[69] Angiography may be used to detect blood vessel pathology when risk factors such as penetrating head trauma are involved.[2] Functional imaging can measure cerebral blood flow or metabolism, inferring neuronal activity in specific regions and potentially helping to predict outcome.[70] Electroencephalography and transcranial doppler may also be used. The most sensitive physical measure to date is the quantitative EEG which has documented an 80% to 100% ability in discriminating between normals and traumatic brain injured subjects.[71] [72]
Neuropsychological assessment can be performed to evaluate the long-term cognitive sequelae and to aid in the planning of the rehabilitation.[68] Instruments range from short measures of general mental functioning to complete batteries formed of different domain-specific tests.
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.[48]Playgrounds with shock-absorbing surfaces such as mulch or sand also prevent head injuries.[48] Child abuse prevention is another tactic; programs exist to prevent shaken baby syndrome by educating about the dangers of shaking children.[51]Gun safety, including keeping guns unloaded and locked, is another preventative measure.[76] 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.[77]
Recent clinical and laboratory research by neurosurgeon Julian Bailes, M.D., and his colleagues from West Virginia University, has resulted in papers showing that dietary supplementation with omega-3 DHA offers protection against the biochemical brain damage that occurs after a traumatic injury.[78] Rats given DHA prior to induced brain injuries suffered smaller increases in two key markers for brain damage (APP and caspase-3), as compared with rats given no DHA.[79]“The potential for DHA to provide prophylactic benefit to the brain against traumatic injury appears promising and requires further investigation. The essential concept of daily dietary supplementation with DHA, so that those at significant risk may be preloaded to provide protection against the acute effects of TBI, has tremendous public health implications.”[80]
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.[104] 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).[111] People may lose or experience altered vision, hearing, or smell.[3]
Hormonal disturbances may occur secondary to hypopituitarism, occurring immediately or years after injury in 10 to 15% of TBI patients. Development ofdiabetes 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.[112]
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.[113] Memory loss, the most common cognitive impairment among head-injured people, occurs in 20–79% of people with closed head trauma, depending on severity.[114] People who have suffered TBI may also have difficulty with understanding or producing spoken or written language, or with more subtle aspects of communication such as body language.[82] 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.[3]Multiple TBIs may have a cumulative effect.[110] 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.[115] 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).[116]
TBI may cause emotional, social, or behavioral problems and changes in personality.[117][118][119][120] These may include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, problems with social judgment, and impaired conversational skills.[117][120][121] TBI appears to predispose survivors to psychiatric disorders includingobsessive compulsive disorder, substance abuse, dysthymia, clinical depression, bipolar disorder, and anxiety disorders.[122] In patients who have depression after TBI, suicidal ideation is not uncommon; the suicide rate among these persons is increased 2- to 3-fold.[123] Social and behavioral symptoms that can follow TBI include disinhibition, inability to control anger, impulsiveness, lack of initiative, inappropriate sexual activity, poor social judgment, and changes in personality.[117][119][120][124]
TBI also has a substantial impact on the functioning of family systems[125] 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 [126]
