Changes in connectivity after visual cortical brain damage underlie altered visual function

Abstract

The full extent of the brain's ability to compensate for damage or changed experience is yet to be established. One question particularly important for evaluating and understanding rehabilitation following brain damage is whether recovery involves new and aberrant neural connections or whether any change in function is due to the functional recruitment of existing pathways, or both. Blindsight, a condition in which subjects with complete destruction of part of striate cortex (V1) retain extensive visual capacities within the clinically blind field, is an excellent example of altered visual function. Since the main pathway to the visual cortex is destroyed, the spared or recovered visual ability must arise from either an existing alternative pathway, or the formation of a new pathway. Using diffusion-weighted MRI, we show that both controls and blindsight subject GY, whose left V1 is destroyed, show an ipsilateral pathway between LGN (lateral geniculate nucleus) and human motion area MT+/V5 (bypassing V1). However, in addition, GY shows two major features absent in controls: (i) a contralateral pathway from right LGN to left MT+/V5, (ii) a substantial cortico-cortical connection between MT+/V5 bilaterally. Both observations are consistent with previous functional MRI data from GY showing enhanced ipsilateral activation in MT+/V5. There is also evidence for a pathway in GY from left LGN to right MT+/V5, although the lesion makes its quantification difficult. This suggests that employing alternative brain regions for processing of information following cortical damage in childhood may strengthen or establish specific connections.

Cortico-subcortical visual, somatosensory, and motor activations for perceiving dynamic whole-body emotional expressions with and without striate cortex (V1)

“…In fact, after V1 damage, cortically blind patients retain a limited visual ability for movement discrimination (4, 6-9), akin to what has been previously observed in animals with V1 destruction (10,11). This spared ability to process simple movement is probably based on the extrageniculostriate connections that motion-sensitive human middle temporal/V5 complex (hMT/V5) has with subcortical structures like the lateral geniculate nucleus (LGN) or pulvinar nucleus of the thalamus (Pulv), as shown in humans and primates (12)(13)(14). However, compared with the perception of single moving dots or simple patches, perception of biological movement in healthy observers seems to recruit more temporal areas along the ventral visual stream, like the superior temporal sulcus (STS) (15, 16) and the fusiform gyrus (FG) (17), as well as subcortical and cortical areas related to visuomotor integration and action preparation, like the superior colliculus (SC), amygdala (Amg), and somatosensory, premotor, and motor areas (17,18).…”

From affective blindsight to emotional consciousness

“…Recently, tractography techniques such as diffusor tensor imaging (DTI) have been used to document anatomical connections between structures implicated in blindsight (Bridge et al, 2008;Leh, Johansen-Berg, & Ptito, 2006) and in affective blindsight , as well as to document post-lesion anatomical plasticity and structural reorganization of fiber connections following lesions to the visual cortex.…”

“…The study involved patient GY, a patient with blindness in his right visual field following a lesion to his left V1 and well-documented blindsight (for a detailed description of the patient see : Baseler, Morland, & Wandell, 1999;Bridge, Thomas, Jbabdi, & Cowey, 2008;Goebel, Muckli, Zanella, Singer, & Stoerig, 2001;. In May 1997 GY came to our lab in Tilburg, accompanied by Larry Weiskrantz, to give us the opportunity to test some of Paul Bertelson's ideas about the automaticity of ventriloquism and to participate in ongoing studies on the role of visual awareness in audiovisual speech perception.…”

“…In fact, GY suffered a lesion strictly confined to his left V1 as a consequence of a traumatic brain injury during a traffic accident that occurred very early in his life, when he was only 7 years old (Barbur, Ruddock, & Waterfield, 1980;de Gelder et al, 2005;Morris et al, 2001;Sahraie et al, 1997). Thus, it has been proposed, and later on verified with different neuroimaging methods, that considerable post-lesion and experience-dependent plasticity has taken place in GY's brain (Bridge et al, 2008;Tamietto et al, 2012). Although we will discuss the neural underpinnings of affective blindsight in a dedicated section below, it has become increasingly clear that affective blindsight is not such a rare phenomenon, for it has been reported in more than 20 different patients studied by at least five independent research teams in several different countries (Anders et al, 2004(Anders et al, , 2009Bertini et al, 2013;Cecere et al, 2014;de Gelder & Hadjikhani, 2006;de Gelder et al, 1999de Gelder et al, , 2002de Gelder et al, , 2005de Gelder et al, , 2014Hamm et al, 2003;Heywood & Kentridge, 2000;Morris et al, 2001;Pegna et al, 2005;Rossion et al, 2000;Tamietto & de Gelder, 2008;Tamietto et al, 2009Tamietto et al, , 2012Van den Stock et al, 2011).…”

Modulation of cortical excitability can speed up blindsight but not improve it

“…But these phosphenes occurred only when TMS was applied over MT/V5 of both hemispheres or over MT/V5 on the left and V1 on the right. Their existence almost certainly reflects the abnormal hypertrophic connexions between MT/V5 of the blind hemisphere and the normal hemispheres and/or the enhanced connexions between the pulvinar, superior colliculus and amygdala, with their subsequent connexions with cortex, in GY's blind hemisphere as revealed by diffusion tensor imaging (Bridge et al, 2008;Tamietto et al, 2012).…”