1. Brain injury: Epidemiology and pathophysiology

Greenwald, Brian D.; Burnett, Derek M.; Miller, Michelle

doi:10.1053/ampr.2003.50052

Cited by 72 publications

(64 citation statements)

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“…A score of 13 -15 is considered mild, 9 -12 moderate and # 8 severe TBI (23). Clinical severity of TBI is also defined by duration of loss of consciousness (LOC), loss of memory for events immediately before or after the accident (post-traumatic amnesia) and identified intracranial lesion (11,24). Radiological findings by computed tomography (CT) may be helpful in TBI severity evaluation, and the most used radiological scale is the Marshall's classification (25).…”

Section: Definition Epidemiology and Classifications Of Tbimentioning

confidence: 99%

“…Secondary injury develops in the hours or days following the initial insult and may lead to further damage and a worse neurological outcome. In fact, as a result of the primary injury brain edema and circulatory disturbance occur, and hypoxia due to increased intracranial pressure results in secondary brain injury (24,27). Inflammatory mediators (cytokines, free radicals, amino acids and nitric oxide) and excitatory amino acids (such as N-methyl-D-aspartate) appear to be implicated in secondary brain injury development (24,27,28).…”

Section: Pathophysiology Of Tbimentioning

confidence: 99%

“…In fact, as a result of the primary injury brain edema and circulatory disturbance occur, and hypoxia due to increased intracranial pressure results in secondary brain injury (24,27). Inflammatory mediators (cytokines, free radicals, amino acids and nitric oxide) and excitatory amino acids (such as N-methyl-D-aspartate) appear to be implicated in secondary brain injury development (24,27,28). Cytokines -in particular interleukin-6 -which stimulate vasopressin secretion, may also be involved in the pathogenesis of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) after TBI (29).…”

Section: Pathophysiology Of Tbimentioning

confidence: 99%

“…in motor vehicle collisions) can induce shearing injury of the axons, with disruption of the white matter and widespread damage, most likely vasogenic. Shearing injury is most often seen in midline structures of the brain and may represent a possible mechanism of hypothalamicpituitary dysfunction in TBI (24). Skull fractures observed in TBI may be associated with hematoma, cranial nerve damage and severe brain injury (28).…”

Section: Pathophysiology Of Tbimentioning

confidence: 99%

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Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

185

152

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Traumatic brain injury (TBI) is one of the main causes of death and disability in young adults, with consequences ranging from physical disabilities to long-term cognitive, behavioural, psychological and social defects. Post-traumatic hypopituitarism (PTHP) was recognized more than 80 years ago, but it was thought to be a rare occurrence. Recently, clinical evidence has demonstrated that TBI may frequently cause hypothalamic -pituitary dysfunction, probably contributing to a delayed or hampered recovery from TBI. Changes in pituitary hormone secretion may be observed during the acute phase post-TBI, representing part of the acute adaptive response to the injury. Moreover, diminished pituitary hormone secretion, caused by damage to the pituitary and/or hypothalamus, may occur at any time after TBI. PTHP is observed in about 40% of patients with a history of TBI, presenting as an isolated deficiency in most cases, and more rarely as complete pituitary failure. The most common alterations appear to be gonadotropin and somatotropin deficiency, followed by corticotropin and thyrotropin deficiency. Hyper-or hypoprolactinemia may also be present. Diabetes insipidus may be frequent in the early, acute phase post-TBI, but it is rarely permanent. Severity of TBI seems to be an important risk factor for developing PTHP; however, PTHP can also manifest after mild TBI. Accurate evaluation and long-term follow-up of all TBI patients are necessary in order to detect the occurrence of PTHP, regardless of clinical evidence for pituitary dysfunction. In order to improve outcome and quality of life of TBI patients, an adequate replacement therapy is of paramount importance.European Journal of Endocrinology 152 679-691

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Section: Definition Epidemiology and Classifications Of Tbimentioning

confidence: 99%

Section: Pathophysiology Of Tbimentioning

confidence: 99%

Section: Pathophysiology Of Tbimentioning

confidence: 99%

Section: Pathophysiology Of Tbimentioning

confidence: 99%

See 2 more Smart Citations

Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

185

152

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“…Najčešći mehanizmi povređivanja su saobraćajne nesreće, padovi i nasilje. 1 Usled razvoja medicine povećan je nivo preživljavanja žrtava teških nesreća. Pored ošećenja ekstremiteta, najčešće se javljaju povrede glave.…”

Section: Uvodunclassified

Vocational rehabilitation models after traumatic brain injury

Odović¹,

Eminović²,

Rapaić³

et al. 2012

PONS

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APSTRAKTCilj ovog rada je identifikacija glavnih modela profesionalne rehabilitacije nakon traumatske povrede mozga koji su opisani u literaturi, opis njihovih karakteristika i identifikacija sličnosti i razlika među tim modelima. Traumatska povreda mozga može da prouzrokuje niz fizičkih, kognitivnih, emocionalnih i bihejvioralnih efekata, a ishod može da varira od potpunog oporavka do trajnog invaliditeta ili smrti. Zbog svoje kompleksnosti rehabilitacija osoba nakon traumatske povrede mozga podrazumeva kontinuiranu brigu od akutne faze do ponovne integracije u duštvenu zajednicu. Rehabilitacija se može podeliti na ranu rehabilitaciju kao i medicinsku i profesionalnu rehabilitaciju. Tokom poslednje tri decenije razvijeni su različiti tipovi programa rehabilitacije nakon traumatske povrede mozga, a to su: tradicionalni dnevni program, holistički, podržano zapošljavanje, rezidentalni i bihejvioralni. Na osnovu pretraživanja baze podataka Medline pregledana je novija literatura o rehabilitaciji nakon traumatske povrede mozga koja se odnosi na savremene koncepte profesionalne rehabilitacije kao strategije za brži i uspešniji povratak na posao. Kao dva glavna modela profesionalne rehabilitacije nakon traumatske povrede mozga izdvojeni su holistički program rehabilitacije i program podržanog zapošljavanja. S obzirom da proces profesionalne rehabilitacije prolazi kroz određene faze tako je poređenje ovih modela izvršeno prema tri globalne oblasti: izbor za ulazak u program i procena sposobnosti, intervencije u periodu pred zapošljavanje i podrška, intervencije u periodu posle zapošljavanja i podrška.KLJUČNE REČI: povrede mozga; rehabilitacija, vokalna; holističko zdravlje; evaluacija radnog kapaciteta; zapošljavanje, stimulisano. ABSTRACTThe aim of this study is identification main models of vocational rehabilitation after traumatic brain injury as described in the literature, describe its characteristic and identifying similarities and differences between these models. Traumatic brain injury can cause a series of physical, cognitive, emotional and behavioral effects, and the outcome can vary from complete recovery to permanent disability or death. Because of its complexity rehabilitation of persons after traumatic brain injury involves the continuous care from the acute phase to the reentry into community. Rehabilitation can be divided into early rehabilitation and medical and vocational rehabilitation. Different types of rehabilitation after traumatic brain injury have developed over the past three decades, and these are: the traditional outpatient program, holistic, supported employment, residential, and behavioral. Recent literature on rehabilitation after traumatic brain injury regarding to the modern vocational rehabilitation concept as a strategy for rapid and successful return to work was reviewed by research Medline database. Holistic rehabilitation program and supported employment program were found as two main models of vocational rehabilitation after traumatic brain injury

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