Acta neuropathologica
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Acta neuropathologica · Oct 2004
Comparative StudyThe perineurium modifies the effects of phenol and glycerol in rat sciatic nerve.
Endoneurial cell response and type of nerve fibre damage were studied after perineural injections of 7% phenol-aqua and pure glycerol. Our previous studies have shown that phenol and glycerol induce different types of nerve fibre degeneration after intraneural injections: phenol dissolves axons and Schwann cells inside the basal lamina tubes but glycerol breaks them down into cellular flakes. The current study investigated whether the difference in type of endoneurial damage also appears after perineural application and how the perineurium affects the effect of these neurolytic agents. ⋯ The present study shows that the effects of extraneurally applied neurolytic agents phenol and glycerol are modified by the perineurium. Phenol readily penetrates the perineurium, but glycerol causes only subperineurial damage. The type of damage is rather similar to regular Wallerian degeneration in both groups and the endoneurial effects differ from those seen after intraneural injections.
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Acta neuropathologica · May 2004
Comparative StudyThe beneficial effect of mild hypothermia in a rat model of repeated thromboembolic insults.
The post-thrombotic brain has recently been reported to have an enhanced vulnerability to a second embolic insult. Although postischemic hypothermia is neuroprotective in global and focal ischemia models, the effect of mild hypothermia on outcome after thromboembolic insults has not been evaluated. This study therefore determined whether brain hypothermia (33 degrees C) was neuroprotective against repeated thromboembolic insults. ⋯ These data demonstrate that mild hypothermia is protective in a thromboembolic stroke model. In addition, post-thrombotic hypothermia decreases the histopathological vulnerability of the post-thrombotic brain to secondary embolic insults. These findings may be important in the prevention of stroke in patients at risk.
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Acta neuropathologica · Apr 2004
Comparative StudyAmyloid beta peptide 1-42 highly correlates with capillary cerebral amyloid angiopathy and Alzheimer disease pathology.
Recent studies reported both positive [Thal et al. (2003) J Neuropathol Exp Neurol 62:1287-1301] and negative [Tian et al. (2003) Neurosci Lett 352:137-140] correlations between cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD) pathology. We have recently shown high correlations between neuritic AD pathology and amyloid beta peptide (Abeta) deposits in the capillary/pericapillary compartment (CapCAA) with only low correlations to general CAA (non-capillary). We have now studied the relationship between CapCAA and AD pathology with respect to the distribution of Abeta40 and 42 in the frontal cortex of 100 human postmortem brains from both male and female, demented and non-demented patients (mean age +/- SD 84.3 +/- 9.3 years). ⋯ These data indicate that CapCAA is characterized by Abeta42 deposits in pericapillary spaces or in the glia limitans. A low correlation between CAA and CapCAA, but high correlations between morphological AD criteria and CapCAA suggest different pathomechanisms for both types of CAA, and a close relation between CapCAA and AD pathology (both neuritic and plaque type). These data support the concept of a neuronal origin of Abeta via drainage from interstitial fluid from the central nervous system along basement membranes to capillaries.
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Acta neuropathologica · Feb 2004
Comparative StudyOnly cerebral capillary amyloid angiopathy correlates with Alzheimer pathology--a pilot study.
Data on the relationship between cerebral amyloid angiopathy (CAA) ("congophilic angiopathy") and Alzheimer's disease (AD) pathology are conflicting. In the present study, CAA and capillary CAA (CapCAA) ("dyshoric angiopathy") were examined in the frontal cortex of 100 human brains obtained at autopsy from both male and female, demented and non-demented patients (mean age +/- SD 84.3+/-9.3 years); 50 brains with high (mean 5.0) and 50 with low (mean 2.4) Braak stages. CAA was assessed according to the method of Olichney et al. [25]; CapCAA was grouped into four grades by counting the affected capillaries in 10 high power fields. ⋯ The presence and severity of CAA and CapCAA showed only low correlation, suggesting a different pathogenesis of these types of lesion. Since CapCAA represents insoluble amyloid peptide (Abeta) deposits in and around capillaries, its correlation with neuritic AD pathology supports the concept of neuronal origin of Abeta via drainage from interstitial fluid from the central nervous system to capillary walls. Studies to answer the question whether CapCAA represents an epiphenomenon or an indicator of a pathogenic association between tau cytopathology and Abeta deposition in capillaries are in progress.
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Acta neuropathologica · Sep 2003
Comparative StudyThe effect of combined neurolytic blocking agent 5% phenol-glycerol in rat sciatic nerve.
Combined 5% phenol-glycerol has been used to treat cancer pain or spasticity and as sympathetic blocks. The major clinical problems have been the unpredictable effects on pain and on the duration of the blocks. Previously we have shown that intraneurally injected phenol induces haemorrhagic necrosis as well as dissolving of the nerve fibres. ⋯ An invasion of macrophages into the endoneurium occurred within 1 week after the intraneural and perineural injections and the number of endoneurial macrophages remained high for up to 6 months. The present study shows that glycerol added to phenol diminishes the necrotizing effect of phenol after an intraneural injection. Combined phenol-glycerol-induced nerve injury is reversible and the axons regenerate but residual morphological changes can be observed even after 6 months.