Diagnosis and Neuroanatomical Correlates of Depression in Brain-Damaged Patients

Ross, Elliott D.

doi:10.1001/archpsyc.1981.01780370046005

Cited by 258 publications

(80 citation statements)

References 47 publications

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“…Several cognitive domains are predictably impaired, including frontal executive functions (problem solving, set shifting, impulse control, self-monitoring) (33,35), attention (36,37), short-term memory and learning (38)(39)(40)(41)(42)(43), speed of information processing (44,45), and speech and language functions (46)(47)(48)(49). Obviously, these are not completely independent domains, and there is typically a mixture of deficits of varying degrees across domains.…”

Section: Changes In Cognitionmentioning

confidence: 99%

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

2008

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Traumatic brain injury (TBI) is a universal public health problem. A recent review of epidemiological studies in Europe suggests an incidence of 235 hospitalized cases (including fatalities) per 100,000 population (1). In the US, the incidence is estimated at 150 per 100,000 population (2). Less data is available from other regions of the world, but TBI is acknowledged as a significant problem worldwide. Of note is that the incidence rates are calculated from hospitalized cases only, and do not include injured individuals who do not seek or have access to care. Thus, the actual incidence of injury is probably 3 to 4 fold larger than the quoted numbers. Most studies suggest that the incidence rates for TBI are greatest in the second and third decades of life, with a secondary increase in the elderly stemming from falls (2,3). Males are more likely to suffer a TBI than females (2,3).In developed countries, there has been a reduction in the mortality rates associated with TBI over the last several decades, generally attributed to improved systems of trauma care and improved motor vehicle safety design. Many individuals with mild traumatic brain injury and virtually all individuals who survive moderate and severe TBI are left with significant long-term neurobehavioral sequelae (4-6). Thus, the reduction in TBI-associated mortality rates (7) has led to a significant increase in the number of individuals with long-term neurobehavioral disorders related to TBI (8,9).Brain trauma can be caused in a number of ways, including mechanisms which penetrate the substance of the brain (e.g., projectiles) and those that do not. This paper focuses on non-penetrating injuries. Despite different contexts and instruments, the physics and biomechanics underlying damage to the brain from non-penetrating injuries have some common features. This results in certain brain regions being at greater risk for damage than others and allows for some general statements to be made about typical profiles of brain injury associated with trauma. The assessment and treatment of the neurobehavioral sequelae of TBI follow logically from an understanding of this injury profile. RELATIONSHIP OF PROFILE OF INJURY TO NEUROBEHAVIORAL SEQUELAEThere are two broad categories of forces that result in brain injury: contact (or impact) and inertial (acceleration or deceleration). Contact injuries result from the brain coming into contact with an object (which might include the skull, or some external object). Contact mechanisms often result in damage to scalp, skull, and brain surface (e.g., contusions, lacerations, hematomas) (10). Frequent sites of such injury are the anterior temporal poles, lateral and inferior temporal cortices, frontal poles, and orbital frontal cortices.Inertial injury results from rapid acceleration or deceleration of the brain that produces shear, tensile, and compression forces. These forces have maximum impact on axons and blood vessels, resulting in axonal injury, tissue tears, and intracerebral hematomas. These mechanisms also produc...

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Section: Changes In Cognitionmentioning

confidence: 99%

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

2008

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“…The results of these and other similar studies led Ross and Rush [34] to theorize that depression may be initiated by structures in the right hemisphere.…”

Section: Depression and Hemispheric Asymmetrymentioning

confidence: 68%

Brain Lateralization of Emotional Processing in Depression

Pereira¹,

Хан²

2017

Depression

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There are three major hypotheses regarding the lateralization of emotion in the brainthe right-hemisphere hypothesis (RHH), the valence hypothesis, and the approachwithdrawal hypothesis. The approach-withdrawal hypothesis, which is the most widely accepted, states that emotions that elicit approach behaviors are lateralized to the left hemisphere, while emotions that elicit withdrawal behaviors are lateralized to the right hemisphere. In line with this hypothesis, it has been found that persons with depression show left frontal hypoactivity and right frontal hyperactivity. This hemispheric asymmetry appears not to influence mood but rather emotional reactions to affective stimuli. That is, a person with such an asymmetry does not show a predominant negative mood, but rather heightened negative reactions to occurrences in the environment. The asymmetry may also be a biological marker of depression, with research evidence that it is found in remitted depressives and in infants of depressed mothers. Currently, research in this area focuses on identifying the mechanism underlying the link between the asymmetry and depression.

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“…Lipsey et al 54 encontraram associação estatisticamente significativa para a não supressão na DPAVC e episódio depressivo maior. Também a presença de sintomas vegetativos como distúrbios do humor, sono e apetite foram relacionados a não supressão 56 . Ao mesmo tempo, outros estudos não confirmaram esses achados.…”

Section: Eixo Hipotálamo-hipófise-adrenal (Hha)unclassified

Depressão pós-AVC: aspectos psicológicos, neuropsicológicos, eixo HHA, correlato neuroanatômico e tratamento

Terroni

Mattos

Sobreiro³

et al. 2009

Rev. psiquiatr. clín.

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ResumoContexto: A depressão pós-AVC (DPAVC) possui uma prevalência elevada. Apesar disso, ela é pouco detectada e tratada. Muitos fatores de risco e repercussões negativas na recuperação dos pacientes estão associados à DPAVC. Objetivo: Revisar alguns aspectos da DPAVC como: qualidade de vida, prejuízos cognitivos, eixo HHA, localização do AVC e tratamento. Métodos: Pesquisa dos últimos 10 anos da base de dados MedLine/PubMed usando as palavraschave post-stroke depression, stroke, quality of life, hypercortisolism, cogntitive dysfunction e treatment. Resultados: A prevalência de DPAVC é de 23% a 60%. Há poucos estudos sobre a incidência de DPAVC. A DPAVC está associada a pior prognóstico e evolução, agravo das disfunções cognitivas e redução da qualidade de vida. O hipercortisolismo está associado à DPAVC que ocorre tardiamente ao AVC. AVC em gânglios da base, região frontal esquerda e estruturas do circuito prefrontosubcortical está relacionado à frequência e à gravidade da DPAVC. Conclusões: É necessário melhoria na metodologia dos estudos para maior esclarecimento sobre a fisiopatologia da incidência da DPAVC. Programas objetivando o aumento das taxas de detecção dos pacientes deprimidos se fazem necessários inclusive para a redução dos impactos negativos na recuperação desses pacientes.Terroni LMN, et al. / Rev Psiq Clín. 2009;36(3):100-8 Palavras-chave: depressão pós-AVC, acidente vascular cerebral, qualidade de vida, disfunção cognitiva, hipercortisolismo, tratamento. AbstractBackground: The prevalence of post-stroke depression (PSD) is elevated. Some risk factors and poor outcome have been associated with PSD. The treatment of PSD reduced the negative impact in patients recovery. Appart from these data the PSD has been under diagnosed and under treated. Objective: Review some aspects such as quality of life, cognitive dysfunction, hypercortisolism, stroke localization and treatment of PSD. Methods: MedLine/PubMed database search using the terms post-stroke depression, stroke, quality of life, hypercortisolism, cognitive dysfunction and treatment, published in MedLine in the last 10 years. Results: PSD has a high rate of prevalence, from 23% to 60%. Few incidence rates are investigated. PSD is associated with poor outcome, increase of cognitive dysfunction and reduced quality of life. The hypercortisolism seems to be associated with PSD in the latter period of stroke. Stroke in the left frontal region, basal ganglia and some structures of prefrontosubcortical circuits have been related with

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Diagnosis and Neuroanatomical Correlates of Depression in Brain-Damaged Patients

Cited by 258 publications

References 47 publications

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

Brain Lateralization of Emotional Processing in Depression

Depressão pós-AVC: aspectos psicológicos, neuropsicológicos, eixo HHA, correlato neuroanatômico e tratamento

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