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Optic Pathway (optic + pathway)
Selected AbstractsCognitive visual dysfunctions in preterm children with periventricular leukomalaciaDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 12 2009ELISA FAZZI MD PHD Aim, Cognitive visual dysfunctions (CVDs) reflect an impairment of the capacity to process visual information. The question of whether CVDs might be classifiable according to the nature and distribution of the underlying brain damage is an intriguing one in child neuropsychology. Method, We studied 22 children born preterm (12 males, 10 females; mean age at examination 8y, range 6,15y; mean gestational age 30wks, range 28,36wks) with periventricular leukomalacia, spastic diplegia, normal intelligence (mean Full-scale IQ 84; mean Verbal IQ 97; mean Performance IQ 74), and normal visual acuity, focusing on higher visual functions. Brain magnetic resonance images (MRI) were analysed to establish the presence of lesions along the primary optic pathway, in the occipitoparietal and occipitotemporal regions. Results, Most children displayed an uneven cognitive profile, with deficits in visual object recognition, visual imagery, visual,spatial skills, and visual memory, and sparing of visual associative abilities, non-verbal intelligence, and face and letter recognition. Conventional brain MRI did not document major alterations of parietal and temporal white matter, or cortical alteration of areas involved in visual associative functions. Interpretation, We suggest a widespread involvement of higher visual processing systems, involving both the ventral and dorsal streams, in preterm children with periventricular leukomalacia. The lack of major alterations on conventional MRI does not exclude the possibility of malfunctioning of higher visual processing systems, expressing itself through discrete CVDs. Possible mechanisms underlying these neuropsychological deficits are discussed. [source] Tenascin-R and axon growth-promoting molecules are up-regulated in the regenerating visual pathway of the lizard (Gallotia galloti)DEVELOPMENTAL NEUROBIOLOGY, Issue 7 2008Dirk M. Lang Abstract It is currently unclear whether retinal ganglion cell (RGC) axon regeneration depends on down-regulation of axon growth-inhibitory proteins, and to what extent outgrowth-promoting substrates contribute to RGC axon regeneration in reptiles. We performed an immunohistochemical study of the regulation of the axon growth-inhibiting extracellular matrix molecules tenascin-R and chondroitin sulphate proteoglycan (CSPG), the axon outgrowth-promoting extracellular matrix proteins fibronectin and laminin, and the axonal tenascin-R receptor protein F3/contactin during RGC axon regeneration in the lizard, Gallotia galloti. Tenascin-R and CSPG were expressed in an extracellular matrix-, oligodendrocyte/myelin- and neuron-associated pattern and up-regulated in the regenerating optic pathway. The expression pattern of tenascin-R was not indicative of a role in channeling or restriction of re-growing RGC axons. Up-regulation of fibronectin, laminin, and F3/contactin occurred in spatiotemporal patterns corresponding to tenascin-R expression. Moreover, we analyzed the influence of substrates containing tenascin-R, fibronectin, and laminin on outgrowth of regenerating lizard RGC axons. In vitro regeneration of RGC axons was not inhibited by tenascin-R, and further improved on mixed substrates containing tenascin-R together with fibronectin or laminin. These results indicate that RGC axon regeneration in Gallotia galloti does not require down-regulation of tenascin-R or CSPG. Presence of tenascin-R is insufficient to prevent RGC axon growth, and concomitant up-regulation of axon growth-promoting molecules like fibronectin and laminin may override the effects of neurite growth inhibitors on RGC axon regeneration. Up-regulation of contactin in RGCs suggests that tenascin-R may have an instructive function during axon regeneration in the lizard optic pathway. © 2008 Wiley Periodicals, Inc. Develop Neurobiol, 2008 [source] Effects of oestrogen replacement therapy on pattern reversal visual evoked potentialsEUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2000H. Yilmaz As a result of a regression in the ovarian functions, oestrogen level in circulation during the menopause drops to 1/50 of its value in the normal reproductive cycle. Excitatory oestrogen increases the sensitivity of the central nervous system to catecholamines by changing the opening frequency of voltage-related L-type calcium channels and augmenting the effect of glutamate; in addition it inhibits the formation of gamma-amino butyric acid (GABA) by the inhibition of glutamate decarboxylase enzyme. It is argued that oestrogen increases transmission in the optic pathways and that oestrogen is responsible for the shorter latency values and higher amplitudes of visual evoked potentials in women. We recorded the monocular pattern reversal visual evoked potentials (PRVEP) of both eyes of 54 post-menopausal women before treatment and of 30 of them after replacement therapy with Tibolon, and of 24 women receiving placebo treatment. The explicit values of P100 latency of right and left eyes before treatment were 98.8 ± 3.5 and 99.0 ± 3.3 ms, respectively. The explicit values of P100 latency of right and left eyes after placebo treatment were 98.6 ± 3.7 and 98.8 ± 4.0, respectively. The explicit values of P100 latency of right and left eyes after replacement treatment were 94.6 ± 3.7 and 94.8 ± 4.0, respectively. We found a statistically significant decrease in the mean PRVEP latencies and a statistically significant increase in mean amplitudes after replacement treatment (P < 0.001) compared with those before treatment and those after placebo treatment. We attributed the changes in PRVEP values after replacement treatment to the action of Tibolon, which acted as a natural sex steroid and speeded the visual transmission time via the widespread receptors in the central nervous system. It is concluded that PRVEP is an objective electrophysiological assessment method in evaluating the efficiency of hormone replacement therapy in post-menopausal women. [source] Neurofibromatosis type 1-associated unusual pleomorphic astrocytoma displaying continual malignant progressionPATHOLOGY INTERNATIONAL, Issue 7 2001Hideaki Yokoo Patients with neurofibromatosis type 1 (NF1) often have gliomas as a complication, most of which are benign pilocytic astrocytomas which have arisen in optic pathways. In the present case, a 17-year-old girl (at death) with stigmata of NF1, initially had a bulky tumor mass in the left thalamus, developing into the lateral ventricle, at 13 years of age. Partially resected tissue samples showed pleomorphic astrocytoma with abundant xanthoma cells and degenerative structures such as Rosenthal fibers (RF) and eosinophilic granular bodies. Fine eosinophilic granules identical to RF, both immunophenotypically and ultrastructurally, were also seen. The residual tumor was subtotally resected 6 months later, and the tumor histology was essentially similar as before, accompanying the regenerative structures; this was believed to be a good prognostic indicator. However, several anaplastic features such as mitosis, necrosis and vascular proliferation appeared even in areas rich in the regenerative structures. After a 2-year, disease-free interval, multiple tumor relapse occurred in June 1997. Partially resected tumor tissues were composed of monotonous small anaplastic cells with prominent proliferative activity. Surprisingly, the tumor cells had retained eosinophilic granules within the cell bodies. Postoperative chemotherapy with procarbazine, MCNU and vincristine (PCV) suppressed the residual tumor dramatically, but the regrowing tumor finally became uncontrollable, leading to the patient's death. TP53 mutation was not detected, while p27 immunopositivity was constantly high during malignant progression, suggesting acquisition of proliferative activity to overcome p53 and p27 inhibitory functions. A review of previously published reports failed to reveal any cases of this type. [source] | ||||||||||