An Animal Model for Delirium

Trzepacz, Paula T.; Leavitt, M. L.; Ciongoli, K.

doi:10.1016/s0033-3182(92)71945-8

Cited by 50 publications

(27 citation statements)

References 27 publications

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“…Han and colleagues [98] proposed that patients with greater anticholinergic activity owing to medication side effects may be at greater risk for delirium. Case studies reported that when the administration of anticholinergic agents was discontinued, symptoms of delirium ceased [99]; however, evidence also suggests that perturbations in the cholinergic system may occur independent of medication effects [100], and some investigators [101] have begun to question the relevance of anticholinergic activity in cognitive functioning.…”

Section: The Cholinergic Hypothesismentioning

confidence: 99%

Pathophysiology of Delirium in the Intensive Care Unit

Gunther

Morandi

Ely

2008

Critical Care Clinics

156

101

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Section: The Cholinergic Hypothesismentioning

confidence: 99%

Pathophysiology of Delirium in the Intensive Care Unit

Gunther

Morandi

Ely

2008

Critical Care Clinics

156

101

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“…E a deficiência central colinérgica é, freqüentemente, presumida como o principal mecanismo fisiopatológico no delirium (Lipowski, 1990). Esta teoria é apoiada pela associação entre delirium e drogas, como atropina (Granacher et al, 1976), delirium e toxinas anticolinérgicas, como a Datuea sauveolens (trombeta de anjo), uma planta encontrada ao longo da costa do Golfo do México (Hall et al, 1977), a ocorrência de manifestações características do delirium, incluindo alterações no EEG com a administração de substâncias anticolinérgicas em animais (Trzepacz et al, 1992) e humanos (Itil e Fink, 1966,) e a reversão do delirium com drogas colinérgicas (Lipowski, 1990).…”

Section: Hipótese Dos Neurotransmissores O Sistema Colinérgicounclassified

Mecanismos fisiopatológicos do delirium

Santos¹

2005

Rev. psiquiatr. clín.

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ResumoO delirium é uma das síndromes mais fascinantes na medicina, apesar de pobremente compreendida. Apesar de sua ocorrência freqüente e de haver crescente informação sobre o diagnóstico, fenomenologia, epidemiologia e etiologias, estudos sobre os mecanismos que mediam a fisiopatologia são, freqüentemente, ausentes. O desenvolvimento de sofisticadas metodologias de imagem cerebral tem permitido ir além das considerações diagnósticas e investigar a neurobiologia dos sintomas específicos observados no delirium. Esses avanços na neuropsiquiatria e na neuroimagem têm revelado diferenças entre as regiões cerebrais, incluindo os hemisférios. O delirium é uma síndrome que pode ocorrer como o resultado de múltipla e complexa interação entre sistemas de neurotransmissores e processos patológicos. Os neurotransmissores, acetilcolina e serotonina, podem ter participação importante no delirium devido a condições clínicas comuns, bem como no delirium pós-cirúrgico. Outros neurotransmissores (dopamina e GABA) e fatores neurobiológicos tais como citocinas, hormônios e radicais livres precisarão de mais estudos para definir as suas participações na gênese do delirium. Futuros estudos, centralizados na fisiopatologia do delirium, poderão levar a melhores estratégias de prevenção e tratamento.Palavras-chave: Delirium, estado confusional, transtorno mental orgânico, fisiopatologia. AbstractDelirium is one of the most fascinating and poorly understood syndromes in medicine. Despite its frequent occurrence and growing information on diagnosis, phenomenology, epidemiology, and aetiologies, studies on mediating pathophysiological mechanisms in delirium are largely lacking. The emergence of sophisticated brain imaging methodologies has made it possible to move beyond diagnostic consideration and investigate the neurobiology of specific symptom clusters observed in delirium. Advances in neuropsychiatry and neuroimaging have revealed differences between brain regions, including the hemispheres. Delirium is a syndrome that may occur as the result of multiple complex interacting neurotransmitter systems and pathologic processes. The

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“…Though a number of neurotransmitter systems has been suggested as playing a role in delirium, the predominant hypothesis for which there is the most evidence involves underactivity of the cholinergic system [14]. The Ach hypothesis is probably not separable from DA because these two neurotransmitters interact closely with each other in the brain, often reciprocally.…”

Section: Neurochemistry and The Neuroanatomy Of Deliriummentioning

confidence: 99%

“…The Ach hypothesis is probably not separable from DA because these two neurotransmitters interact closely with each other in the brain, often reciprocally. Insufficient Ach is implicated in many causes of delirium -metabolic, pharmacological, and structural -and cholinergic agents reverse delirium [14]. DA excess also can cause delirium, including from dopaminergic medications, cocaine intoxication and ECT [3,15].…”

Section: Neurochemistry and The Neuroanatomy Of Deliriummentioning

confidence: 99%

Update on the Neuropathogenesis of Delirium

Trzepacz¹

1999

Dement Geriatr Cogn Disord

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175

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Delirium has been considered a syndrome of generalized dysfunction of higher cortical functions due to its breadth of symptoms and associated diffuse slowing on electroencephalogram. Advances in neuropsychiatry have revealed differences between brain regions, including the hemispheres, which may underlie the constellation of symptoms among different psychiatric disorders. For example, different neural pathways are involved in major depression and obsessive-compulsive disorder, including lateralization to one or the other hemisphere. In this article the author proposes that delirium, too, involves particular neural pathways and that lateralization to the right may be relevant. Structural and functional neuroimaging reports and recent neuropsychological studies support this lateralization. Prefrontal cortices, anterior and right thalamus, and right basilar mesial temporoparietal cortex may play a significant role in subserving delirium symptoms and may be the ‘final common pathway’ for delirium from a variety of etiologies. The final common pathway may be responsible for certain ‘core symptoms’ (disorientation, cognitive deficits, sleep-wake cycle disturbance, disorganized thinking, and language abnormalities), while other symptoms (delusions, hallucinations, illusions, and affective lability) may occur depending on the etiology causing delirium. An imbalance in the cholinergic and dopaminergic neurotransmitter systems is most commonly implicated in causing delirium, and could both account for delirium symptoms and be consistent with the neuroanatomical pathways being implicated.

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An Animal Model for Delirium

Cited by 50 publications

References 27 publications

Pathophysiology of Delirium in the Intensive Care Unit

Pathophysiology of Delirium in the Intensive Care Unit

Mecanismos fisiopatológicos do delirium

Update on the Neuropathogenesis of Delirium

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