Three Months of Chronic Ethanol Administration and the Behavioral Outcome of Rats After Lateral Fluid Percussion Brain Injury

Masse, James; Billings, B J; Dhillon, Harabhajan S.; Mace, Derek; Hicks, Ramona; Barron, Susan; Kraemer, Phillip J.; Dendle, Peter; Prasad, Renuka M.

doi:10.1089/neu.2000.17.421

Cited by 9 publications

(4 citation statements)

References 30 publications

(63 reference statements)

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“…Additionally, behavioral abnormalities similar to those found in humans with Type C HE were observed in these rats, including drowsiness, decreased wakefulness and attentiveness, and impaired grooming and exploratory behavior. While animals with Type C HE were behaviorally defective, no evidence of severe distress, such as intense pain, muscular spasms, fainting, or breathing difficulties, was observed, consistent with features associated with Type C HE in humans, as well as with observations by other investigators in experimental animals [49][50][51]56,57,[59][60][61]. These findings strongly suggest that young/aged male rats are more prone to develop TAA-induced Type C HE as compared to adult males or young or aged females.…”

Section: Effect Of Taa On the Motor And Cognitive Functionssupporting

confidence: 87%

Age and Sex in the Development of Hepatic Encephalopathy: Role of Alcohol

Tong,

Hussain,

Shamaladevi

et al. 2024

Biology

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Hepatic encephalopathy (HE) is a neurological condition linked to liver failure. Acute HE (Type A) occurs with acute liver failure, while chronic HE (Type C) is tied to cirrhosis and portal hypertension. HE treatments lag due to gaps in understanding its development by gender and age. We studied how sex and age impact HE and its severity with combined liver toxins. Our findings indicate that drug-induced (thioacetamide, TAA) brain edema was more severe in aged males than in young males or young/aged female rats. However, adding alcohol (ethanol, EtOH) worsens TAA’s brain edema in both young and aged females, with females experiencing a more severe effect than males. These patterns also apply to Type A HE induced by azoxymethane (AZO) in mice. Similarly, TAA-induced behavioral deficits in Type C HE were milder in young and aged females than in males. Conversely, EtOH and TAA in young/aged males led to severe brain edema and fatality without noticeable behavioral changes. TAA metabolism was slower in aged males than in young or middle-aged rats. When TAA-treated aged male rats received EtOH, there was a slow and sustained plasma level of thioacetamide sulfoxide (TASO). This suggests that with EtOH, TAA-induced HE is more severe in aged males. TAA metabolism was similar in young, middle-aged, and aged female rats. However, with EtOH, young and aged females experience more severe drug-induced HE as compared to middle-aged adult rats. These findings strongly suggest that gender and age play a role in the severity of HE development and that the presence of one or more liver toxins may aggravate the severity of the disease progression.

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Section: Effect Of Taa On the Motor And Cognitive Functionssupporting

confidence: 87%

Age and Sex in the Development of Hepatic Encephalopathy: Role of Alcohol

Tong,

Hussain,

Shamaladevi

et al. 2024

Biology

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“…There is some evidence to suggest that a dosedependent relationship may exist, with higher BAL being associated with lower post-injury cognitive functioning (Tate et al, 1999). There is also evidence from recent animal studies that suggests that at lower or moderate doses, alcohol may have a neuroprotective effect (Janis et al, 1998;Kelly et al, 1997aKelly et al, ,b, 2000 or limited effect (Masse et al, 2000;Taylor et al, 2002) on cognitive functioning and structural changes following TBI. Clearly this is an important area for further investigation.…”

Section: Interactive Effects Of Alcohol and Tbi Hypothesismentioning

confidence: 99%

Alcohol Abuse and Traumatic Brain Injury: Quantitative Magnetic Resonance Imaging and Neuropsychological Outcome

Wilde

Bigler

Gandhi

et al. 2004

Journal of Neurotrauma

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Prior or concurrent alcohol use at the time of traumatic brain injury (TBI) was examined in terms of post-injury atrophic changes measured by quantitative analysis of magnetic resonance imaging (MRI) and neuropsychological outcome. Two groups of TBI subjects were examined: those with a clinically significant blood alcohol level (BAL) present at the time of injury (TBI + BAL) and those without a significant BAL (TBI-only). To explore the potential impact of both acute and chronic alcohol use, subjects in both groups were further clustered into one of four subgroups (NONE, MILD, MODERATE or HEAVY) based upon available information regarding their pre-injury alcohol use. One-way analysis of covariance (ANCOVA) and multiple analysis of covariance (MANCOVA) were used with subject grouping as the main factor. Age, injury severity as measured by Glasgow Coma Scale (GCS) score, years of education, total intracranial volume (TICV), and the number of days post-injury were included as covariates where appropriate. Increased general atrophy was observed in patients with (a) a positive BAL and/or (b) a history of moderate to heavy pre-injury alcohol use. In addition, performance on neuropsychological outcome variables (WAIS-R and WMS-R Index scores) was generally worse in the subgroups of patients with positive BAL and a history of preinjury alcohol use, as compared to the other TBI groups though not statistically significant. Implications of alcohol use, at the time of brain injury, are discussed.

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“…19,42,43 Animal studies have suggested that at lower or moderate doses, alcohol may have a neuroprotective effect, 5,44 -46 although others have contended that the effect on cognitive performance and structural changes after head injury may be limited. 47,48 Our findings suggest that a mortality benefit because of the presence of alcohol may exist. The possible rationales for this result are not yet well defined.…”

Section: Discussionmentioning

confidence: 67%