Diffuse axonal injury

Imajo, Takeshi; Roessman, U.

doi:10.1097/00000433-198409000-00005

Cited by 21 publications

(11 citation statements)

References 0 publications

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“…Similar conclusions were advanced in an Australian study (McLean, 1995). Falls, assaults, and pedestrian incidents applying dynamic forces to the head and producing severe head injuries are reported (Adams et al, 1984, Imajo, 1996Imajo et al, 1987;Imajo and Kazee, 1992;Imajo and Roessman, 1984;Strich, 1961). While not specific to motor vehicle crashes, these literatures reinforce the present findings regarding the role of head contact loading.…”

Section: Discussionsupporting

confidence: 89%

Severe-to-fatal head injuries in motor vehicle impacts

Yoganandan

Baisden

Maiman

et al. 2010

Accident Analysis & Prevention

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Section: Discussionsupporting

confidence: 89%

Severe-to-fatal head injuries in motor vehicle impacts

Yoganandan

Baisden

Maiman

et al. 2010

Accident Analysis & Prevention

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“…This possibility appears to be supported by the presence of large numbers of intensely fluorescent enlargements in the VAChT-ir nerve bundles of estrogen-treated animals. These structures resemble the retraction balls observed in axons after trauma (Imajo and Roessman 1984;Emery et al 1987;Toupalik et al 2000), as well as the swollen varicosities observed in adrenergic (Lincoln et al 1984), vasoactive intestinal polypeptide-immunoreactive (Belai et al 1985), and calcitonin gene-related peptide-immunoreactive (Belai and Burnstock 1987) enteric nerve fibers of streptozotocin-induced diabetic rats. In line with this idea, it is possible that swollen or detached axons could account for the increased diameter of nerve fibers observed in estrogen-treated animals.…”

Section: Discussionmentioning

confidence: 61%

Effects of Infantile/Prepubertal Chronic Estrogen Treatment and Chemical Sympathectomy with Guanethidine on Developing Cholinergic Nerves of the Rat Uterus

Richeri

Viettro

Chávez-Genaro

et al. 2002

J Histochem Cytochem.

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(TC) S U M M A R Y The innervation of the uterus is remarkable in that it exhibits physiological changes in response to altered levels in the circulating levels of sex hormones. Previous studies by our group showed that chronic administration of estrogen to rats during the infantile/prepubertal period provoked, at 28 days of age, an almost complete loss of norepinephrine-labeled sympathetic nerves, similar to that observed in late pregnancy. It is not known, however, whether early exposure to estrogen affects uterine cholinergic nerves. Similarly, it is not known to what extent development and estrogen-induced responses in the uterine cholinergic innervation are affected by the absence of sympathetic nerves. To address this question, in this study we analyzed the effects of infantile/prepubertal chronic estrogen treatment, chronic chemical sympathectomy with guanethidine, and combined sympathectomy and chronic estrogen treatment on developing cholinergic nerves of the rat uterus. Cholinergic nerves were visualized using a combination of acetylcholinesterase histochemistry and the immunohistochemical demonstration of the vesicular acetylcholine transporter (VAChT). After chronic estrogen treatment, a well-developed plexus of cholinergic nerves was observed in the uterus. Quantitative studies showed that chronic exposure to estrogen induced contrasting responses in uterine cholinergic nerves, increasing the density of large and medium-sized nerve bundles and reducing the intercept density of fine fibers providing myometrial and perivascular innervation. Estrogen-induced changes in the uterine cholinergic innervation did not appear to result from the absence/impairment of sympathetic nerves, because sympathectomy did not mimic the effects produced by estrogen. Estrogen-induced responses in parasympathetic nerves are discussed, considering the direct effects of estrogen on neurons and on changes in neuron-target interactions.

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“…Liver disease also has been suggested as a contributing factor, either through associated reduction of blood flow or as a manifestation of hepatic encephalopathy. Widespread axonal damage, observed pathologically (Imajo and Kazee, 1992) or inferred from proton magnetic resonance spectroscopy (Cecil et al, 1998;Friedman et al, 1998), also has been associated with head injury. Because malnutrition, liver disease, and head injury are frequent concomitants of chronic alcoholic use, these and other factors should be considered in addition to alcoholism itself in future DTI studies as factors that contribute to white matter abnormalities.…”

Section: Discussionmentioning

confidence: 99%