Severity Of Brain Lesions Research Articles

Effect of mannitol treatment on soman‐induced brain and heart lesions in the rat

AbstractThe effect of intravenous mannitol on soman‐induced neuropathology and cardio‐myopathy was studied in rats. Soman, an organophosphorus agent, irreversibly inhibits total body acetylcholinesterase and induces a cholinototoxic syndrome in rats which results in the development of sezures, brain damage, and degenerative cardiomyopathy. The severity of the cardiomyopathy parallels the severity of the neuropathology. When mannitol at a dose of 1.5 g/kg was administered at the onset of sezures and followed by a second dose 5 h later, there was a significant increase in 24 h survival. Moreover, the severity of brain lesions was reduced in the piriform cortex, thalamus, amygdala, and the caudate putamen. The same treatment schedule also provided almost complete protection against the concomitant development of degenerative cardiomyopathy. The finding that the mannitol treatments reduced both the severity of the neuropathology and the degenerative cardiomyopathy reinforces the concept of a possible central neurogenic mechanism for the development of the cardiomyopathy. These results suggest that mannitol may be useful to reduce the severity of sezure‐related neuropathology and to provide additional protection to other vital organs which may be secondarily susceptible to neurogenically mediatd pathologic change, such as the heart in rats which develop cardiomyopathy following soman‐induced seizures. © 1993 wiley‐Liss, Inc.

Limits of brain tolerance to daily increments in serum sodium in chronically hyponatraemic rats treated with hypertonic saline or urea: advantages of urea

1. At present there is no consensus about the optimal management of hyponatraemia to prevent demyelinating brain lesions. We have evaluated in a large series of rats (n = 136) the protective role of urea for the brain in the treatment of severe chronic hyponatraemia. Urea (group I, n = 51) was compared with hypertonic saline in boluses (group II, n = 46) and with hypertonic saline in divided doses (group III, n = 39). Treatment was administered intraperitoneally over 48 h. The severity of brain lesions was assessed by histological scoring. 2. For 95% of the injured animals treated with hypertonic saline, brain lesions appeared for an absolute increment in serum Na+ concentration (delta SNa+) of 20 mmol day-1 l-1. Above this limit neurological injuries gradually worsened, and beyond a transition zone (delta SNa+ greater than or equal to 20 less than or equal to 23 mmol day-1 l-1) 89% (group III) to 100% (group II) of the animals were injured. This limit can be reached rapidly, as attested by the comparable severity of brain lesions observed in group II (mean delta SNa+ 1 h after a bolus injection, 19 mmol/l) and in group III (mean delta SNa+ 1 h after an injection, 2 mmol/l), both groups achieving similar daily delta SNa+. 3. A correction above the threshold of 20 mmol day-1 l-1 is as toxic during the first 24 h as during the second day of the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenesis of scrapie is faster when infection is intraspinal instead of intracerebral

Previous studies of mice infected peripherally with 139A scrapie showed that scrapie agent initially replicates outside the CNS and that invasion of the CNS occurs several weeks later by neural spread of infection along visceral autonomic fibres to the mid-thoracic cord, and thence to brain. Direct intracerebral infection of brain bypasses the need for extraneural replication and gives shorter incubation periods than peripheral routes. However, it was also found that the duration of the scrapie replication phase in brain, before clinical disease develops, is actually shorter with peripheral routes than with the intracerebral route. We have now investigated this surprising observation using the intraspinal route to reproduce just the neural phase of scrapie pathogenesis seen after peripheral infection. In studies of three strains of scrapie (263K, 139A and ME7) in either hamsters or mice, we have fulfilled the prediction that incubation periods should be shorter after intraspinal infection than after intracerebral infection. Detailed studies of 139A scrapie showed that the shorter incubation period by the intraspinal route could be accounted for by the shorter duration of the scrapie replication phase in brain before clinical disease developed. As a consequence, the severity of the vacuolar lesions in brain at the clinical stage of all three scrapie models was less after intraspinal infection than after intracerebral infection but the severities of vacuolation after intraspinal and intraperitoneal infection were remarkably similar. We speculate that (a) the site of injection (or of invasion) of the central nervous system determines which neural pathways become accessible for the spread of scrapie infection, and that (b) the duration of the neural phase of scrapie pathogenesis is related to the complexity of the pathways between the site of invasion and the clinical target areas in which, it is suggested, scrapie must replicate for disease to develop.

Changes in serum and cerebrospinal fluid enzyme activity after head injury.

We studied simultaneously in serum (S) and CSF (L) the enzyme activities of GOT, GPT, LDH, ICDH, MDH, ALD, and CPK in 28 patients with head injuries divided into three groups according to the severity of the trauma. We found a correlation between severity of brain lesion and enzyme activity. The best correlation was found for SGOT, SCPK, LGOT, LLDH, LMDH and LCPK. We do not believe that enzyme activity is of prognostic value. We think that further studies should be made of the specific isoenzymes of the Central Nervous System.

Impairment in visual recognition of geometric figures in patients with circumscribed retrorolandic brain lesions

Twenty patients with left-sided and 21 patients with right-sided circumscribed retrorolandic brain lesion were given Gottschaldt's Test, Benton's Visual Retention Test and several tests for pertinent control variables. Analyses of variance demonstrated, that aphasic patients were inferior to left-sided patients without aphasia. There was no difference in the performance of aphasic and right brain damaged patients. Visou-spatial disturbance was associated with lesions of either hemisphere. The impairment of the aphasic patients was not due to language disturbance per se, nor to severity of brain lesion. Rather, presence of aphasia indicated a locus of lesion critical for the performances tested.

The recognition of simple and complex realistic figures in patients with unilateral brain lesion.

Forty-one patients with unilateral retro-rolandic brain lesion were examined by means of three experimental tests requiring the recognition of complex realistic figures. In addition, all patients were given two tests for the recogniion of common objects and simple realistic line drawings. A set of control variables included tests for elementary visual functions, non-verbal intelligence and aphasia. Furtheron, the influence of side and hemispheric locus as well as severity of brain lesion was examined.