Aspects of the quantitative analysis of neurons in the cerebral cortex

Skoglund, Thomas; Pascher, R.; Berthold, C.‐H.

doi:10.1016/s0165-0270(96)00119-7

Cited by 43 publications

(19 citation statements)

References 27 publications

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“…Many studies have concluded that neuronal loss is responsible, but measurements in those reports relied on semiquantitative or qualitative assessments (DeFelipe et al, 1993(DeFelipe et al, , 1994Spreafico et al, 1998;DeFelipe, 1999). As noted by others, potential bias can be introduced into such studies because the analysis requires assumptions about the size, shape, and orientation of neurons as well as the volume of the tissue (West and Gundersen, 1990;Skoglund et al, 1996;Morrison and Hof, 1997;West, 1999). In the present study, we used design-based stereology without such assumptions to address the question of whether there is a detectable loss of neurons in the neocortex of TLE patients.…”

Section: Discussionmentioning

confidence: 99%

Neuronal Hypertrophy in the Neocortex of Patients with Temporal Lobe Epilepsy

et al. 2001

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The underlying cause of neocortical involvement in temporal lobe epilepsy (TLE) remains a fundamental and unanswered question. Magnetic resonance imaging has shown a significant loss in temporal lobe volume, and it has been proposed that neocortical circuits are disturbed functionally because neurons are lost. The present study used design-based stereology to estimate the volume and cell number of Brodmann's area 38, a region commonly resected in anterior temporal lobectomy. Studies were conducted on the neocortex of patients with or without hippocampal sclerosis (HS). Results provide the surprising finding that TLE patients have significant atrophy of neocortical gray matter but no loss of neurons. Neurons are also significantly larger, dendritic trees appear sparser, and spine density is noticeably reduced in TLE specimens compared with controls. The increase in neuronal density we found in TLE patients is therefore attributable to large neurons occupying a much smaller volume than in normal brain. Neurons in the underlying white matter are also increased in size but, in contrast to other reports, are not significantly elevated in number or density. Neuronal hypertrophy affects HS and non-HS brains similarly. The reduction in neuropil and its associated elements therefore appears to be a primary feature of TLE, which is not secondary to cell loss. In both gray and white matter, neuronal hypertrophy means more perikaryal surface area is exposed for synaptic contacts and emerges as a hallmark of this disease. Key words: temporal lobe epilepsy; stereology; Brodmann's area 38; ectopia; cortical atrophy; neuronal hypertrophy; hippocampal sclerosisHippocampal sclerosis (HS) is the most frequently encountered pathologic abnormality in intractable epilepsy. There is however increasing evidence of more widespread temporal lobe pathology in HS patients (Nakasato et al., 1992;Sisodiya et al., 1995) and prevalent temporal lobe hypometabolism in patients with temporal lobe epilepsy (TLE) (Rausch et al., 1994). Moreover, magnetic resonance imaging (MRI) studies show a reduction in temporal lobe volume both ipsilateral and contralateral to the seizure focus (Lee et al., 1995Marsh et al., 1997). Volume reduction is also independent of the presence of HS (Sisodiya et al., 1997), which indicates that it underlies a broader spectrum than mesial temporal disease alone.Pathologic studies of TLE neocortex are dominated by those focused on readily detectable lesions and gross developmental abnormalities (Choi and Matthias, 1987;Haines et al., 1991;Raymond et al., 1995). There are far fewer investigations of subtle morphological abnormalities in the neocortex than in the hippocampus (Mathern et al., 1995), even though such studies might be expected to answer basic questions about epileptogenic activity originating outside the hippocampus and gross volume reductions in the temporal lobe.A common view of cortical pathology in TLE is that of neuronal loss. This notion is based on reports of reduced numbers of inhibitory neurons (DeFelip...

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Section: Discussionmentioning

confidence: 99%

Neuronal Hypertrophy in the Neocortex of Patients with Temporal Lobe Epilepsy

et al. 2001

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“…This presents a problem however, as the histological preparation of neural tissue is known to introduce a number of morphological anomalies. Tissue perfusion, removal, staining, and dehydration can lead to artificial tissue shrinkage, nicks in surface brain areas, and changes in tissue shape and location (Garman, 1990;Overgaard and Meden, 2000;Sadowski et al, 1995;Simmons and Swanson, 2009;Skoglund et al, 1996). It is possible that any cortical thinning, movement, volume, or density loss observed after stroke in the adult rat could be exaggerated by histological preparation.…”

Section: Introductionmentioning

confidence: 99%

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

et al. 2010

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“…Comparable visualizations have been published by Skoglund et al (1993Skoglund et al ( , 1996 and Schmolke (1996). Additionally, Schmolke has determined dendrites and axons beneath cellular profiles in the cerebral cortex and visualized these data in an integrative view.…”

Section: Resultsmentioning

confidence: 99%

Videomicroscopy, image processing, and analysis of whole histologic sections of the human brain

Schmitt¹,

Eggers²,

Modersitzki³

2005

Microsc. Res. Tech.

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Serial histologic sections of a whole human brain may have extensions of up to 130 x 130 mm within the coronal plane around the temporal lobe. To date, however, technology has not provided a bright field microscope that is able to shift the object holder continuously in the x- and y-direction over such distances and still possess the same optical capabilities as comparable devices. We developed a new light microscope to continuously quantify such sections. We also developed the computing environment for controlling the device and for analyzing the data produced. In principle, we are now able to quantify each neuron of a human brain. The data ultimately will provide the most detailed structural information about the human brain ascertained thus far. Such detailed information of the spatial distribution of neurons is essential to develop realistic models for simulation of large-scale neuronal networks and to investigate the significance of neuronal arrangements with respect to neuronal signal processing in the CNS. After preprocessing of the data produced by the new microscope, we are able to detect lamination patterns in the spatial distribution of gravity centers of cells. Furthermore, morphological features like size of the projection area and mean staining intensity are visualized as a particle process. The particle process presents the sizes and staining intensity of perikaryons and allows a distinction of gray matter and white matter. These results provide evidence that the system works correctly and can be applied to a systematic analysis of a larger sequence of serial histologic sections. The objective of this study is to introduce the very large section analyzing microscope (VLSAM) and to present the initial data produced by the system. Moreover, we will discuss workload and future developments of the parallel image analysis system that are associated with the microscope.

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Aspects of the quantitative analysis of neurons in the cerebral cortex

Cited by 43 publications

References 27 publications

Neuronal Hypertrophy in the Neocortex of Patients with Temporal Lobe Epilepsy

Neuronal Hypertrophy in the Neocortex of Patients with Temporal Lobe Epilepsy

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

Videomicroscopy, image processing, and analysis of whole histologic sections of the human brain

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