Influence of alcohol intake on the course and consequences of spinal cord injury

Kiwerski, J; Krasuski, Marek

doi:10.1097/00004356-199209000-00008

Cited by 10 publications

(6 citation statements)

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“…High risk activities, such as alcohol intoxication, have contributed to SCI etiology, 23,25 and as much as 35% to 40% of persons with SCI may have sustained their injury as a direct result of alcohol involvement. 18,26,27 Overall, post-injury alcohol consumption decreased after SCI onset, confirming hypothesis 2. The decrease in alcohol use, particularly heavy drinking, is consistent with research on both SCI and TBI.…”

Section: Discussionsupporting

confidence: 66%

Changes in alcohol use after the onset of spinal cord injury

Davis

Cao

Krause

2017

The Journal of Spinal Cord Medicine

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Section: Discussionsupporting

confidence: 66%

Changes in alcohol use after the onset of spinal cord injury

Davis

Cao

Krause

2017

The Journal of Spinal Cord Medicine

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“…Another obvious condition associated with liver damage is alcoholism. Notably, alcohol is a factor in a large proportion of SCIs (Heinemann et al ., 1988; Kiwerski and Krasuski, 1992) and individuals with history of alcohol abuse have poorer outcomes from injury (Hawkins and Heinemann, 1998; Elliott et al ., 2002). SCI in this population again would occur on a background of hepatic inflammation and pathology.…”

Section: Discussionmentioning

confidence: 99%

Liver inflammation before spinal cord injury worsens neuropathology, hepatic injury, metabolic syndrome and locomotor deficits

Goodus

Carson

Sauerbeck

et al. 2020

Preprint

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Liver inflammation can enhance acute leukocyte recruitment to sites of central nervous system (CNS) injury. The consequences of hepatic inflammation on recovery after injury, however, are unknown. Here, we hypothesize that liver inflammation at the time of spinal cord injury (SCI) will exacerbate spinal cord pathology and impair recovery. Rats receiving SCI with concomitant liver inflammation had worse intraspinal pathology and greater locomotor deficits than rats with baseline liver inflammation. Hepatic inflammation also potentiated SCI-induced non-alcoholic steatohepatitis (NASH), endotoxemia, insulin resistance and adiposity. Circulating and cerebrospinal levels of Fetuin-A were higher in SCI rats with liver inflammation. When microinjected into intact spinal cords, Fetuin-A caused robust macrophage activation, iron accumulation and neuron loss. These studies verify that outcomes from CNS injury are worse if the liver is concomitantly inflamed and implicate Fetuin-A as a potential neuropathological mediator. These novel data suggest hepatic inflammation is a potential clinical target for improving recovery from SCI.

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“…Alcohol may have both neuroprotective and neurotoxic effects in the context of acute TBI (Kelly, 1995). However, both animal (Halt, Swanson, & Faden, 1992) and human studies (Kiwerski & Krauski, 1992) suggest that alcohol intoxication may be associated with more severe SCI and higher rates of cervical SCI (Garrison et al, 2004). Preinjury alcohol problems.…”

Section: Effects Of Alcohol-related Factors On Outcomementioning

confidence: 99%