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Patients with optic neuritis (ON) undergo cortical and subcortical neuroplasticity as revealed by functional magnetic resonance imaging (fMRI). However, the effect of the heterogeneity of scotomas has not been adequately addressed previously. We introduce a new method of modelling scotomas in fMRI, to reveal a clearer pattern of neuroplasticity, across a mixed patient population. A longitudinal fMRI-study of visual function in 19 ON patients examined at four timepoints between presentation and 6 months was performed. Four different models were compared. The first model included the four different examination timepoints as separate explanatory variables without adjustment for visual field defects. The second model also included covariates reflecting subject-specific deviations in visual field defect from the average group value of the Humphrey mean deviation (HMD) at each examination timepoint. In the third and fourth models the four examination timepoints were not modelled explicitly, but entered vicariously through the associated changes in the HMD for each subject that marked their individual recovery. The results show that the third and fourth models were more sensitive to geniculate and visual cortical neuroplasticity during recovery. Moreover, inferences from the fourth model can be extended to the general population of patients recovering from ON. In conclusion, we present a method of accommodating subject-specific differences between patients with acute ON by inclusion of an HMD-index. This method is sensitive to the processes of neuroplasticity whilst the generalisation of inferences makes the method suitable for future studies of treatment.

Optic neuritis (ON) is the first clinical manifestation in approximately 20% of patients with multiple sclerosis (MS). The inflammation and demyelination of the optic nerve are characterized by symptomatic visual impairment and retrobulbar pain, and associated with decreased visual acuity, decreased colour and contrast sensitivity, delayed visual evoked potentials and visual field defects. Spontaneous recovery of vision typically occurs within weeks or months after onset, depending on the resolution of inflammation, remyelination, restoration of conduction in axons which persist demyelinated and neuronal plasticity in the cortical and subcortical visual pathways. To assess where recovery takes place along the visual pathway, visual activation was studied in the lateral geniculate nucleus (LGN), the main thalamic relay nucleus in the visual pathway and in three areas of the visual cortex: the lateral occipital complexes (LOC), V1 and V2. We conducted a longitudinal functional magnetic resonance imaging (fMRI) study of regions of interest (ROI) of activation in LGN and visual cortex in 19 patients with acute ON at onset, 3 and 6 months from presentation. With fMRI we measured the activation in the ROIs and compared activation during monocular stimulation of the affected and unaffected eye. In the acute phase the activation of LGN during visual stimulation of the affected eye was significantly reduced (P < 0.01) compared to the unaffected eye. This difference in LGN activation between the affected and unaffected eye diminished during recovery, and after 180 days the difference was no longer significant (P = 0.59). The decreased difference during recovery was mainly due to an increase in the fMRI signal when stimulating the affected eye, but included a component of a decreasing fMRI signal from LGN when stimulating the unaffected eye. In LOC, V1 and V2 activation during visual stimulation of the affected eye in the acute phase was significantly reduced (P < 0.01) compared to the unaffected eye, and during recovery the difference diminished with no significant differences left after 180 days. As the pattern of activation in LOC, V1 and V2 resembled the development in LGN we found no evidence of additional cortical adaptive changes. The reduced activation of the LGN to stimulation of the unaffected eye is interpreted as a shift away from early compensatory changes established in the acute phase in LGN and may indicate very early plasticity of the visual pathways.

Illusory motion can be generated by successively flashing a stationary visual stimulus in two spatial locations separated by several degrees of visual angle. In appropriate conditions, the apparent motion is indistinguishable from real motion: The observer experiences a luminous object traversing a continuous path from one stimulus location to the other through intervening positions where no physical stimuli exist. The phenomenon has been extensively investigated for nearly a century but little is known about its neurophysiological foundation. Here we present images of activations in the primary visual cortex in response to real and apparent motion. The images show that during apparent motion, a path connecting the cortical representations of the stimulus locations is filled in by activation. The activation along the path of apparent motion is similar to the activation found when a stimulus is presented in real motion between the two locations.

It has previously been demonstrated that sleeping and sedated young children respond with a paradoxical decrease in the blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) signal in the rostro-medial occipital visual cortex during visual stimulation. It is unresolved whether this negative BOLD response pattern is of developmental neurobiological origin particular to a given age or to a general effect of sleep or sedative drugs. To further elucidate this issue, we used fMRI and positron emission tomography (PET) to study the brain activation pattern during visual stimulation in spontaneously sleeping adult volunteers. In five sleeping volunteers fMRI studies confirmed a robust signal decrease during stimulation in the rostro-medial occipital cortex. A similar relative decrease at the same location was found during visual stimulation and polysomnographically verified slow-wave sleep in a separate group of six subjects using H215O PET measures of the regional cerebral blood flow (rCBF). This decrease was more rostro-dorsal compared to the relative rCBF increase along the calcarine sulcus found during visual stimulation in the awake state. This study reconfirms the previously described paradoxical stimulation-correlated negative BOLD signal change in the rostro-medial occipital cortex, expanding this response mode to an age spectrum ranging from the newborn to the adult. Further, the use of complementary brain mapping techniques suggests that this decrease was secondary to a relative rCBF decrease. Possible mechanisms for the paradoxical response pattern during sleep include an active inhibition of the visual cortex or a disruption of an energy-consuming process. [Copyright &y& Elsevier]