Trichur R. Vidyasagar

Dyslexia: a deficit in visuo-spatial attention, not in phonological processing

Developmental dyslexia affects up to 10 per cent of the population and it is important to understand its causes. It is widely assumed that phonological deficits, that is, deficits in how words are sounded out, cause the reading difficulties in dyslexia. However, there is emerging evidence that phonological problems and the reading impairment both arise from poor visual (i.e., orthographic) coding. We argue that attentional mechanisms controlled by the dorsal visual stream help in serial scanning of letters and any deficits in this process will cause a cascade of effects, including impairments in visual processing of graphemes, their translation into phonemes and the development of phonemic awareness. This view of dyslexia localizes the core deficit within the visual system and paves the way for new strategies for early diagnosis and treatment.

Neural Mechanisms of Visual Attention: How Top-Down Feedback Highlights Relevant Locations

Attention helps us process potentially important objects by selectively increasing the activity of sensory neurons that represent the relevant locations and features of our environment. This selection process requires top-down feedback about what is important in our environment. We investigated how parietal cortical output influences neural activity in early sensory areas. Neural recordings were made simultaneously from the posterior parietal cortex and an earlier area in the visual pathway, the medial temporal area, of macaques performing a visual matching task. When the monkey selectively attended to a location, the timing of activities in the two regions became synchronized, with the parietal cortex leading the medial temporal area. Parietal neurons may thus selectively increase activity in earlier sensory areas to enable focused spatial attention.

A neuronal model of attentional spotlight: parietal guiding the temporal

Recent studies have reported an attentional feedback that highlights neural responses as early along the visual pathway as the primary visual cortex. Such filtering would help in reducing informational overload and in performing serial visual search by directing attention to individual locations in the visual field. The magnocellular (M) and parvocellular (P) subdivisions are two of the major parallel pathways in primate vision that originate in the retina and carry distinctly different types of information. The M pathway, characterized by its high sensitivity to movement and to low contrast stimuli, forms the predominant visual input into the dorsal, parietal stream in the neocortex. The P inputs, characterized by their colour selectivity and higher spatial resolution, are channeled mainly into the ventral, temporal stream. It is proposed that the attentional spotlight originates in the dorsal stream and helps in serially searching the field for conjunction of the relevant target features in the temporal stream, effectively performing a gating function on all visual inputs. This model predicts that a defect limited to the magnocellular or the dorsal pathway can lead to widespread deficits in cognitive abilities, including those functions that are largely based on parvocellular information. For example, the model provides a neural mechanism linking a peripheral defect in the magnocellular pathway to the reading disabilities in dyslexia. Even though there has been strong evidence for a magnocellular deficit in dyslexia, the paradox has been that the cognitive disability seems to be related to P pathway function. The scheme proposed here shows how M input may be vital for controlling sequential attention during reading.

The responses of cells in macaque lateral geniculate nucleus to sinusoidal gratings.

Responses of cells in the parvocellular (p.c.l.) and magnocellular (m.c.l.) layers of the macaque lateral geniculate nucleus to sine‐wave gratings were studied. Both p.c.l. and m.c.l. cells responded best at a temporal frequency (drift rate) of 10‐20 Hz. P.c.l. cells responded at temporal frequencies lower than 1 Hz; m.c.l. cells did not. With coloured‐ or white‐black luminance‐modulated gratings, responses of m.c.l. cells were weaker at low than at medium spatial frequencies. With coloured gratings, p.c.l. cell responses were not attenuated at low spatial frequencies. With white gratings a few p.c.l. cells did show such attenuation. Optimal responses from p.c.l. cells were obtained with coloured gratings; white gratings evoked weaker responses. With a grating of a colour causing suppression of a p.c.l. cells activity, the modulation of firing was much less than with a grating of a colour excitatory for the cell. M.c.l. on‐ and off‐centre cells responded equally well to moving gratings. The ability of p.c.l. cells to resolve fine gratings was dependent on cell type as well as on the colour of grating used. The ability of m.c.l. cells to resolve fine gratings was comparable to that of p.c.l. cells. The contrast sensitivity of m.c.l. cells was much higher than that of p.c.l. cells. This may account for their ability to resolve fine gratings, despite their larger centre size. In comparison with luminance‐modulated gratings, chromatically modulated gratings could evoke larger or smaller responses, depending on p.c.l. cell type and the colours in the grating. M.c.l. cells responded poorly or not at all.

Impaired Visual Search in Dyslexia Relates to the Role of the Magnocellular Pathway in Attention

We tested the hypothesis that in a cluttered visual scene, the magnocellular (M) pathway is crucial for focusing attention serially on the objects in the field. Since developmental dyslexia is commonly associated with an M pathway deficit, we compared reading impaired children and age-matched normal readers in a search task that required the detection of a target defined by the conjunction of two features, namely form and colour, that are processed by the parvocellular dominated ventral neocortical stream. The dyslexic groups performance was significantly poorer than the controls when there were a large number of distractor items. The scheme of selective attention proposed from these results provides a neural mechanism that underlies reading and explains the pathophysiology of dyslexia.

Orientation sensitivity of cat LGN neurones with and without inputs from visual cortical areas 17 and 18

SummaryOrientation sensitivity was tested, using moving bars as stimuli, in 136 LGN cells in normal cats and 82 LGN cells in cats with areas 17 and 18 lesioned.The responses of most neurones showed some dependence on the orientation of the line stimulus. The orientation bias was more pronounced for long, narrow bars moving at rather slow velocities. Length-response curves revealed less end-inhibition along the optimum orientation than along the nonoptimum orientation. Thirty-two percent of the cells in the normal cats and 50% in the lesioned animals responded best to orientations within 10 ° of the vertical or horizontal. The oblique orientations were represented poorly in the lesioned group. Thus the corticogeniculate feedback may serve to confer a more uniform distribution of orientation preferences on the LGN.It is suggested that the orientation biases of LGN neurones may play a role in building orientation-selective cells in the visual cortex. Further, the preferences for horizontal and vertical orientations in the LGN may explain the preferences for these orientations reported for visual cortical cells.

Multiple mechanisms underlying the orientation selectivity of visual cortical neurones.

For over three decades, the mechanism of orientation selectivity of visual cortical neurones has been hotly debated. While intracortical inhibition has been implicated as playing a vital role, it has been difficult to observe it clearly. On the basis of recent findings, we propose a model in which the visual cortex brings together a number of different mechanisms for generating orientation-selective responses. Orientation biases in the thalamo-cortical input fibres provide an initial weak selectivity either directly in the excitatory input or by acting via cortical interneurones. This weak selectivity of postsynaptic potentials is then amplified by voltage-sensitive conductances of the cell membrane and excitatory and inhibitory intracortical circuitry, resulting in the sharp tuning seen in the spike discharges of visual cortical cells.

Membrane properties and spike generation in rat visual cortical cells during reversible cooling

We studied the effects of reversible cooling between 35 and 7 °C on membrane properties and spike generation of cells in slices of rat visual cortex. Cooling led to a depolarization of the neurones and an increase of the input resistance, thus bringing the cells closer to spiking threshold. Excitability, measured with intracellular current steps, increased with cooling. Synaptic stimuli were most efficient in producing spikes at room temperature, but strong stimulation could evoke spikes even below 10 °C. Spike width and total area increased with cooling, and spike amplitude was maximal between 12 and 20 °C. Repetitive firing was enhanced in some cells by cooling to 20–25 °C, but was always suppressed at lower temperatures. With cooling, passive potassium conductance decreased and the voltage‐gated potassium current had a higher activation threshold and lower amplitude. At the same time, neither passive sodium conductance nor the activation threshold of voltage‐dependent sodium channels changed. Therefore changing the temperature modifies the ratio between potassium and sodium conductances, and thus alters basic membrane properties. Data from two cells recorded in slices of cat visual cortex suggest a similar temperature dependence of the membrane properties of neocortical neurones to that described above in the rat. These results provide a framework for comparison of the data recorded at different temperatures, but also show the limitations of extending the conclusions drawn from in vitro data obtained at room temperature to physiological temperatures. Further, when cooling is used as an inactivation tool in vivo, it should be taken into account that the mechanism of inactivation is a depolarization block. Only a region cooled below 10 °C is reliably silenced, but it is always surrounded by a domain of hyperexcitable cells.

Gating of neuronal responses in macaque primary visual cortex by an attentional spotlight

NEURONAL responses were recorded from the striate cortex of monkeys trained to perform visual discrimination at locations in the visual field to which their attention was drawn. A subset of neurons showed vigorous responses to visual stimuli for trials in which the monkey was directing its attention to the respective receptive field location. In trials where attention is directed elsewhere, responses to the same stimuli were significantly reduced. In some cells the early response component was not modulated by attention, but later components were affected by the locus of attention. The results suggest the operation of a feedback in the paradigm that spotlights a topographically restricted area of V1 for further processing at higher levels.

Synaptic Transmission in the Neocortex during Reversible Cooling

We studied the effects of reversible cooling on synaptic transmission in slices of rat visual cortex. Cooling had marked monotonic effects on the temporal properties of synaptic transmission. It increased the latency of excitatory postsynaptic potentials and prolonged their time-course. Effects were non-monotonic on other properties, such as amplitude of excitatory postsynaptic potentials and generation of spikes. The amplitude of excitatory postsynaptic potentials increased, decreased, or remain unchanged while cooling down to about 20 degrees C, but thereafter it declined gradually in all cells studied. The effect of moderate cooling on spike generation was increased excitability, most probably due to the ease with which a depolarized membrane potential could be brought to spike threshold by a sufficiently strong excitatory postsynaptic potential. Stimuli that were subthreshold above 30 degrees C could readily generate spikes at room temperature. Only at well below 10 degrees C could action potentials be completely suppressed. Paired-pulse facilitation was less at lower temperatures, indicating that synaptic dynamics are different at room temperature as compared with physiological temperatures. These results have important implications for extrapolating in vitro data obtained at room temperatures to higher temperatures. The data also emphasize that inactivation by cooling might be a useful tool for studying interactions between brain regions, but the data recorded within the cooled area do not allow reliable conclusions to be drawn about neural operations at normal temperatures.