Protracted post-traumatic encephalopathy

Jellinger, K. A.; Seitelberger, F

doi:10.1016/0022-510x(70)90091-2

Cited by 63 publications

(7 citation statements)

References 41 publications

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“…These secondary brainstem hemorrhages are thought to result from stretching/tearing of upper brainstem penetrating arteries during sudden downward transtentorial herniation 30, 102, 109, 110 . Focal brainstem infarcts may also occur via the same mechanism 30, 102, 111 .…”

Section: Imaging Findings Of Traumatic Brain Injuriesmentioning

confidence: 99%

Imaging Evaluation of Acute Traumatic Brain Injury

Mutch

Talbott

Gean

2016

Neurosurgery Clinics of North America

122

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SYNOPSIS Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Imaging plays an important role in the evaluation, diagnosis, and triage of patients with TBI. Recent studies suggest that it will also help predict patient outcomes. TBI consists of multiple pathoanatomical entities. Here we review the current state of TBI imaging including its indications, benefits and limitations of the modalities, imaging protocols, and imaging findings for each these pathoanatomic entities. We also briefly survey advanced imaging techniques, which include a number of promising areas of TBI research.

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Section: Imaging Findings Of Traumatic Brain Injuriesmentioning

confidence: 99%

Imaging Evaluation of Acute Traumatic Brain Injury

Mutch

Talbott

Gean

2016

Neurosurgery Clinics of North America

122

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“…It is likely that the dentate nucleus and its hilus were primarily damaged simultaneously at the time when the rostral brain stem lesion occurred. It is apparent that this lesion was due neither to compression of the superior cerebellar artery nor to herniation (Lindenberg, 1955;Jellinger & Seitelberger, 1970).…”

Section: Discussionmentioning

confidence: 96%

“…In the present case, white matter lesions were localized rather than diffuse in distribution. This could have been related to the fact that there was no evidence of severe secondary brain damage (Lindenberg, 1955;Jellinger & Seitelberger, 1970;Adams & Graham, 1976;Graham, Adams & Doyle, 1978).…”

Section: Discussionmentioning

confidence: 99%

“…There is no doubt that the lesions in the corpus callosum, in the anterior commissure and in the left dorsolateral quadrant of the rostral brain stem were a typical form of primary axonal injury (Lindenberg, et a/., 1952;Strich, 1956;Peerless & Rewcastle, 1967;Adams et a/., 1977;Zimmerman, Bilaniuk & Genneralli, 1978;Adams et al, 1982a). It is likely that the dentate nucleus and its hilus were primarily damaged simultaneously at the time when the rostral brain stem lesion occurred.…”

Section: Discussionmentioning

confidence: 99%

“…White matter lesions are one of the most important pathological features of non-missile head injury. Secondary brain changes, such as hypoxia, oedema and intracranial lesion expansion can cause diffuse change in the white matter (Lindenberg, 1955;Jellinger & Seitelberger, 1970). However, a body of opinion has grown to suggest that white matter lesions are due to actual tearing of the axons at the time of the accident (Strich, 1956;Nevin, 1967;Oppenheimer, 1968;Peerless & Rewcastle, 1969;Adams et al, 1977).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Non‐missile head injury: report of a patient surviving for 6 years

Mizutani¹,

Hayakawa²,

Takizawa³

et al. 1990

Neuropathology Appl Neurobio

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A female patient with non-missile head injury is described. She showed slight improvement in her level of consciousness, and survived for 6 1/2 years after injury. At autopsy, the white matter lesions were localized rather than diffuse in distribution. In addition to lesions in the corpus callosum, anterior commissure and dorsolateral quadrant of the rostral brain stem, those in the parasagittal cerebral white matter, and in the hilus of the dentate nucleus and superior cerebellar peduncle were considered to be due to primary axonal injury. A cavity in the frontal white matter was remarkable in that there was no evidence to indicate expansion of the lesion due to haemorrhage. These features suggested that the injurious physical forces had acted parallel to the direction of the axons.

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