Death of the central neuron: An electron microscopic study of thalamic retrograde degeneration following cortical ablation

Matthews, Murray A.

doi:10.1007/bf01104030

Cited by 106 publications

(28 citation statements)

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“…Thalamic neuronal death is detectable from 4 to 7 days after cortical lesion in mice and rats 5,20 and is delayed, appearing from 1 to 7 months after cortical lesion, in rabbits. 21 In a transient MCAO model in rats neuronal death in the thalamus was not detectable before 7 days, whereas a primary astrocytic and microglial reaction appeared already 3 days after the insult. 22 In our model we detected extensive neuronal death and glial reactivity, both events causing localized edema in the VPL and VPM nuclei 3 weeks after the ischemic insult.…”

Section: Discussionmentioning

confidence: 99%

MRI Detection of Secondary Damage After Stroke

Justicia

Hoehn

2008

Stroke

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Background and Purpose-Iron plays a central role in many metabolic processes. Under certain pathological situations it accumulates, producing negative effects such as increasing damage by oxidative stress. The present study examined long-term iron accumulation in a stroke model with secondary degeneration, using MRI and histological techniques. Methods-Male Wistar rats (nϭ22) were subjected to 60 minutes MCA occlusion. MR images (T2-and T2*-weighted)were obtained weekly between weeks 1 and 7 after reperfusion, and at weeks 10, 14, 20, and 24. Histological iron detection and immunohistochemical examination for different markers (NeuN, GFAP, OX-42, HO-1, and APP) were performed at the 3 survival time points (3, 7, and 24 weeks). Results-Infarcts affecting MCA territory were evident on T2-weighted imaging, and all animals showed deficits on behavioral tests. In the thalamus, T2 hyperintensity was detected 3 weeks after stroke, and disappeared around week 7 when T2*-weighted images showed a marked hypointensity in that area. Histology revealed neuronal loss in the thalamus, accompanied by strong microglial reactivity and microglial HO-1 expression. APP deposits were detected in the thalamus from week 3 on and persisted until week 24. Iron storage was detected in microglia at week 3, in the parenchyma at week 7, and around APP deposits at week 24. Conclusions-T2*-weighted MRI allows the detection of secondary damage in the thalamus after MCAO. Iron accumulation in the thalamus is mediated by HO-1 expression in reactive microglia.

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Section: Discussionmentioning

confidence: 99%

MRI Detection of Secondary Damage After Stroke

Justicia

Hoehn

2008

Stroke

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“…In the thalamus, 45 Ca accumulation was limited to the ventral posterior nucleus, which has fiber con nections in anatomic proximity to the postcentral gyrus of the cerebral cortex. Damage in this area may be due to retrograde degeneration resulting from thalamocortical fiber damage caused by the ischemic insult to the postcentral gyrus (Matthews, 1973;Fujie et al, 1990;Nagasawa and Kogure, 1990;Iizuka et al, 1990). In this study, we fo und a direct-proportion relationship between damaged tween the two correlation coefficients shows 15 that the probability of the distribution of the plotted values for calcium accumulation in the thalamus and cortex is greater than that seen in ... E the striatum and cortex (Z = 1.9834; P < 0.05).…”

Section: Discussionmentioning

confidence: 99%

Calcium Accumulation following Middle Cerebral Artery Occlusion in Stroke-Prone Spontaneously Hypertensive Rats

Shirotani

Shima

Iwata

et al. 1994

J Cereb Blood Flow Metab

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Summary: Delayed neuronal damage in the ischemic re gion of the rat brain following middle cerebral artery (MCA) occlusion in stroke-prone spontaneously hyper tensive rats was studied. The distribution of neuronal damage was determined by 45Ca autoradiography. Accu mulation of45Ca was observed in the corpus callosum and ipsilateral cerebral cortex immediately following MCA occlusion. After 3 days of occlusion, 45Ca had accumu lated in the ipsilateral pyramidal tract, the ventral poste rior nucleus of the thalamus, and the lateral portion of the striatum. Significant accumulation of 45Ca was observed in the same areas after 7 and 14 days of occlusion. Next the effect of MK-SOI on accumulation of 45Ca after MCA occlusion was examined using the same technique. MK SOl (0.5-10 mg/kg i.v.) or saline was administered 15 min Occlusion of the rat middle cerebral artery (MCA) is a widely used model of focal cerebral ischemia. In most models, ischemia results in dam age to the cortex and the lateral part of the striatum (Tamura et aI., 1981; Bederson et aI., 1986; Naga sawa and Kogure, 1989). It has been demonstrated that distal occlusion to the striate branches of the MCA resulted in a reproducible focal infarction in stroke-prone spontaneously hypertensive rats, but not in normotensive rats (Coyle, 1982;Coyle and Jokelainen, 1983). The infarct produced by this pro cedure was limited to the ipsilateral cerebral cortex and did not extend to the basal ganglia. A rise in the intracellular calcium concentration has been postu lated to initiate or represent a "final common path- Received February 18, 1993; final revision received February 8, 1994; accepted February 8, 1994.Address correspondence and reprint requests to Dr. Toshiki Shirotani, Department of Neurosurgery, National Defense Med ical College, 3-2, Namiki, Tokorozawa, Saitama 359, Japan.Abbreviations used: MCA, middle cerebral artery; NMDA, N-methyl-D-aspartate. 831before MCA occlusion, and volumes of accumulation of 45Ca were calculated 1 week after ischemic insults. MK SOl significantly reduced 45Ca uptake in the cortex, stri atum, and thalamus. Furthermore, there was a strong sta tistical correlation between the volume of accumulation of 45Ca in the cortex and that in the thalamus (r = 0.S974; p < 0.001; n = 25). We speculate that delayed neuronal damage in the corpus callosum, ipsilateral pyramidal tract, and thalamus may be caused by secondary neuronal degeneration. However, neuronal damage in the striatum, a segment not supplied by the MCA, may be related to excessive release of glutamate.

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“…14 Using electron microscopy, Matthews 13 reported thalamic retrograde degeneration following cortical ablation in rabbits. In that study, unequivocal signs of retrograde alteration became evident within the affected thalamic nuclei by the second postoperative day, progressing to the disappearance of many perikaryal profiles within the first 7-10 days.…”

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confidence: 99%

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.

Tamura

Tahira

Nagashima

et al. 1991

Stroke

116

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We investigated shrinkage of the ipsilateral thalamus following infarction in the territory of the middle cerebral artery in 33 patients who were admitted £2 days after the stroke and who were followed by computed tomography for >1 year with no recurrences. The thalamic area was measured on the computed tomograms, and the ratio of the ipsilateral area to the contralateral area was calculated. All values were compared with values from the initial computed tomogram taken <2 days after the stroke. The values of the ratio on follow-up computed tomograms decreased gradually in 15 patients. In these cases, the area of the ipsilateral thalamus was significantly reduced after 1 year (/xO.Ol) and marked atrophy was observed. These results demonstrate the significance of remote changes over a long period of time after focal cerebral infarction. (Stroke 1991^22:615-618) I t has been widely believed that neuronal alterations following cerebral ischemia progress rapidly. 1 Therefore, the main issue of neuropathologic studies after cerebral ischemia has been acute neuronal changes in the ischemic area. In 1982, Kirino 2 found a strikingly slow process of neuronal change in the hippocampal CA1 subfield following brief cerebral ischemia, which he called "delayed neuronal death." Since then, delayed neuropathologic changes following cerebral ischemia have attracted widespread attention. These changes are also found in the area exposed to ischemia.The aim of this study was to analyze neuropathologic changes in a distant, nonischemic area after focal cerebral ischemia. We particularly focused on delayed neuropathologic changes of the ipsilateral thalamus following infarction in the territory of the middle cerebral artery (MCA). Subjects and MethodsA total of 109 patients with cerebral infarction were admitted to our clinic from 1985 through 1989.From the Department of Neurosurgery, Teikyo University School of Medicine, Tokyo, Japan.Supported in part by a grant-in-aid for scientific research from the Ministry of Education, Science and Culture of Japan and by a research grant for cardiovascular diseases from the Ministry of Health and Welfare.Address for correspondence: Akira Tamura, MD, Department of Neurosurgery, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173, Japan.Received November 7, 1990; accepted January 31, 1991. From among these patients, we selected 33 who 1) were admitted <,2 days after the first attack of stroke, 2) had a single low-density area on an initial or follow-up computed tomogram (CT film) in the MCA territory, 3) were followed by symmetrical CT at the level of the thalamus for > 1 year, and 4) developed no symptomatic or asymptomatic recurrence of stroke on CT. In these patients, the area of the thalamus on each side was randomly measured with a computerized digitizer on the CT films at the level of the thalamus according to a CT atlas 3 1, 3, and 6 months and 1 and 2 years after the stroke. The CT films were taken in parallel planes at an angle of 15° to the infraorbitomeatal lin...

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Death of the central neuron: An electron microscopic study of thalamic retrograde degeneration following cortical ablation

Cited by 106 publications

References 63 publications

MRI Detection of Secondary Damage After Stroke

MRI Detection of Secondary Damage After Stroke

Calcium Accumulation following Middle Cerebral Artery Occlusion in Stroke-Prone Spontaneously Hypertensive Rats

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.

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