Damage to intracranial optic pathways in fatal closed head injury in man

Perunovic, Branko; Quilty, Robert D.; Athanasiou, Athanasios E.; Love, Seth

doi:10.1016/s0022-510x(01)00463-4

Cited by 12 publications

(7 citation statements)

References 38 publications

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“…In this context, Ding and associates (2008) suggested that motor and visual deficits after diffuse TAI could lead to cognitive, learning, and motor abnormalities. Axonal damage in the visual system has been observed in clinical cases of severe focal and diffuse TBI (Perunovic et al, 2001;Sabates et al, 1991); however, due to the complexity of injury and intensive care treatment, the primary visual impairment is grossly underdiagnosed in a large number of severe TBI patients (Mahmutyaziciog lu and Ogawa, 2005). Further studies are required to elucidate other mechanisms of axonal damage that may trigger immune cell activation and infiltration into the optic tracts following TAI.…”

mentioning

confidence: 99%

Post-Traumatic Hypoxia Exacerbates Brain Tissue Damage: Analysis of Axonal Injury and Glial Responses

Hellewell

Yan

Agyapomaa

et al. 2010

Journal of Neurotrauma

120

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Traumatic brain injury (TBI) resulting in poor neurological outcome is predominantly associated with diffuse brain damage and secondary hypoxic insults. Post-traumatic hypoxia is known to exacerbate primary brain injury; however, the underlying pathological mechanisms require further elucidation. Using a rat model of diffuse traumatic axonal injury (TAI) followed by a post-traumatic hypoxic insult, we characterized axonal pathology, macrophage/microglia accumulation, and astrocyte responses over 14 days. Rats underwent TAI alone, TAI followed by 30 min of hypoxia (TAI + Hx), hypoxia alone, or sham-operation (n = 6/group). Systemic hypoxia was induced by ventilating rats with 12% oxygen in nitrogen, resulting in a ∼ 50% reduction in arterial blood oxygen saturation. Brains were assessed for axonal damage, macrophage/microglia accumulation, and astrocyte activation at 1, 7, and 14 days post-treatment. Immunohistochemistry with axonal damage markers (β-amyloid precursor protein [β-APP] and neurofilament) showed strong positive staining in TAI + Hx rats, which was most prominent in the corpus callosum (retraction bulbs 69.8 ± 18.67; swollen axons 14.2 ± 5.25), and brainstem (retraction bulbs 294 ± 118.3; swollen axons 50.3 ± 20.45) at 1 day post-injury. Extensive microglia/macrophage accumulation detected with the CD68 antibody was maximal at 14 days post-injury in the corpus callosum (macrophages 157.5 ± 55.48; microglia 72.71 ± 20.75), and coincided with regions of axonal damage. Astrocytosis assessed with glial fibrillary acidic protein (GFAP) antibody was also abundant in the corpus callosum and maximal at 14 days, with a trend toward an increase in TAI + Hx animals (18.99 ± 2.45 versus 13.56 ± 0.81; p = 0.0617). This study demonstrates for the first time that a hypoxic insult following TAI perpetuates axonal pathology and cellular inflammation, which may account for the poor neurological outcomes seen in TBI patients who experience post-traumatic hypoxia.

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mentioning

confidence: 99%

Post-Traumatic Hypoxia Exacerbates Brain Tissue Damage: Analysis of Axonal Injury and Glial Responses

Hellewell

Yan

Agyapomaa

et al. 2010

Journal of Neurotrauma

120

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“…This diagnosis can be obtained through a careful palpation of the eyeball and, if possible, a fundoscopy. In doubtful diagnostic cases, it is important to perform CT of the skull and orbit [18].…”

Section: Retrobulbar Hemorrhage (Rbr)mentioning

confidence: 99%

Pathophysiological mechanisms of blindness in facial trauma: A review

Ribeiro¹,

Reis²,

Ramalho

et al. 2013

OJST

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Blindness is a serious complication that can occur after facial trauma and may represent the loss of one of the most useful senses in the human relationship with the world—the sight. This study aims to review the pathophysiology of blindness related to facial trauma in order to identify the mechanisms by which it develops and to recognize the signs and symptoms required to establish proper diagnosis and treatment. Blindness following facial trauma may occur due to mechanisms that involve injury to the eyeball, optic nerve and eyelids. The leading causes of blindness resulting from facial trauma, and which may be altered by medical interference, are related to retrobulbar hemorrhage and traumatic optic neuropathy, which require extremely rapid diagnosis and can be accomplished with the resources available in most trauma-based emergency services. The authors conclude that loss of vision tends to be irreversible in direct eyeball and optic nerve lesions, but can be prevented in retrobulbar hemorrhage and traumatic optic neuropathy. Eyeball and, especially, sight accuracy evaluation should be included in the initial care of trauma patients, so that the lesions that might lead to loss of vision are diagnosed and treated early.

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“…In an autopsy study of 45 patients with fatal TBI, 53% of patients had histologic evidence of optic tract injury. 5 In experimentally induced TBI in cats, axonal swelling was identified in the optic tracts by day 2 post-injury. 6 The above studies suggest that large calibre optic tract axons are highly susceptible to the shear and tensile forces of brain trauma.…”

Section: G M Rogers Et Almentioning

confidence: 99%

“…6 The above studies suggest that large calibre optic tract axons are highly susceptible to the shear and tensile forces of brain trauma. 5,6 Several mechanisms of injury have been proposed to explain post-traumatic visual field defects, including direct mechanical disruption, thrombosis of the vascular supply with infarction, or axonal shear injury. We propose focal optic tract hemorrhage as the mechanism of our patient's injury.…”

Section: G M Rogers Et Almentioning

confidence: 99%