Cortical lesion

Emerick, A. J., Neafsey, E. J., Schwab, M. E. and Kartje, G. L. Functional reorganization of the motor cortex in adult rats after cortical lesion and treatment with monoclonal antibody IN-1. /. Neurosci. 23 4826-4830, 2003. 

Renal 26 (edema of the convoluted tubules, slightly advanced focal cortical lesions, glomerular degeneration)... 

L., Paskevitch, P.A., and Domesick, V.B. (1983) Changes in cortical and subcortical levels of monoamines and their metabolites following unilateral ventrolateral cortical lesions in the rat. Brain Res, 271 279-288. 

Kennard C, Lawden M, Morland AB and Ruddock KH 1995 Colour identification and colour constancy are impaired in a patient with incomplete achromatopsia associated with prestriate cortical lesions. Proceedings of the Royal Society of London B 260, 169-175. 

Maysinger, D., Filipovic-Grdc, J., and Cuello, A. C. (1993). Effects of coencapsulated NGF and GM1 in rats with cortical lesions. NeuroReport 4, 971 -974. 

Detection of Cortical Lesions Is Dependent on Choice of Slice Thickness in Patients with Multiple Sclerosis... 

The author examined comatose patients with suspected cortical ischemia with DWI who had suffered from cerebral hypoxia often after cardiac arrest (Lovblad et al. 2004). A further evaluation of an expanded series of these patients is presented in Table 16.1 26 patients with lesions attributed to hypoxia that resumes the clinical signs of all patients. This series confirms the initial observation that DWI was superior to T2-weighted MRI regarding the prediction of lesion extent. Table 16.2 presents the patterns and localizationof findings. The DWI lesions were localized in the typical watershed regions in 7 of 26 (27%) (Fig. 16.8). The cortical lesions were unilateral in one patient (4%). Basal ganglia involvement was found in 10 of 26 patients (38%), and there was also white matter involvement in 9 of 26 patients (35%) (Figs. 16.8 and 16.9). Additional infratentorial lesions were found in 3 of 19 patients (35%) (Fig. 16.8). 

Additional studies of striatal DA loss in the marmoset also show that this fails to impair extra-dimensional shift performance as affected by prefrontal cortical lesions (Collins et al., 2000). However, the striatal DA loss does produce an impairment in shifting between stimulus dimensions when the requirement is to shift back towards a previously irrelevant dimension, which is possibly relevant to impaired performance of human patients with Parkinson s disease of shifting between two well-established task sets (Cools et al., 2001). 

Acute or chronic cerebral injury may cause effects in remote areas of brain (Meyer et at 1993), so-called diaschisis, by reducing neuronal inputs and metabolic activity in the contralateral cerebellum and ipsilateral internal capsule, thalamus and basal ganglia after cortical lesions in the ipsilateral cortex following internal capsule and thalamic lesions and in the contralateral hemisphere. The functional consequences of diaschisis are not clear (Bowler et at 1995). 

Sabin M, Bowen WD, Donoghue JP. 1992. Location of nicotinic and muscarinic cholinergic and mu-opiate receptors in rat cerebral neocortex Evidence from thalamic and cortical lesions. Brain Res 579 135-147. 

Ortega F, Hennequet L, Sarria R, Streit P, Grandes P (1995) Changes in the pattern of glutaraate-like immunoreactivity in rat superior colliculus following retinal and visual cortical lesions. Neuroscience 67 125-134. 

FGF-1 expression seems to follow a different time course, supporting the notion that its functions in the lesioned brain are distinct from those of FGF-2. Following cortical cavity lesioning, FGF-1 (quantified by ELISA) first became detectable in the cortical lesion fluid 10 days after surgery, and its level increased further until 30 days (Ishikawa et al., 1991b). In contrast, NGF levels increased much more rapidly, with a peak 16 h after lesioning. It is unclear how these data can be reconciled with a study reporting a rapid and drastic increase of FGF-1 in a cortical cavity within 1 h after after trauma (Nieto-Sampedro et al., 1988). 

Butterley, W. S., Bender, M. B., Pollack, N., and Kahn, R. L. (1956) Unilateral spa-cial-agnosia in patentiants with cortical lesions. Brain 78, 68-99. 

O Neil, R. D., Grunewald, R. A., Fillenz, M., and Albery, W. J., 1983, The effect of unilateral cortical lesions on the circadian changes in rat striatal ascorbate and homovanillic acid levels measured in vivo using voltammetry, Neurosci. Lett. 42 105-110. 

A more direct means of assessing performance at low luminance was undertaken in this laboratoiy, It was based on the substantial literature in neuropsychology indicating that cortical lesions in primates in those areas subserving vision (area 17) impaired or eliminated the ability of macaque monkeys to discriminate geometric forms. An apparatus was designed to test this abil-... 

Tallantyre EC, Morgan PS, Dixon JE, et al. (2009) 7-Tesla MRI Improves the Detection of Cortical Lesions in Multiple Sclerosis. Neurology. 72 A269-A269. 

An ECM protein, laminin, which participates in neuronal development and survival, can be immobilised on the backbone of the HA hydrogel, and this has been proven by Hou and co-workers [21]. In this case, the gel still possesses the mechanical properties and rheological behaviour similar to brain tissue. After being implanted into a cortical lesion it promotes neurite extension and angiogenesis into the porous scaffold, and simultaneously inhibits glial scar formation. 

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