Too little, too late: reduced visual span and speed characterize pure alexia

Abstract

Whether normal word reading includes a stage of visual processing selectively dedicated to word or letter recognition is highly debated. Characterizing pure alexia, a seemingly selective disorder of reading, has been central to this debate. Two main theories claim either that 1) Pure alexia is caused by damage to a reading specific brain region in the left fusiform gyrus or 2) Pure alexia results from a general visual impairment that may particularly affect simultaneous processing of multiple items. We tested these competing theories in 4 patients with pure alexia using sensitive psychophysical measures and mathematical modeling. Recognition of single letters and digits in the central visual field was impaired in all patients. Visual apprehension span was also reduced for both letters and digits in all patients. The only cortical region lesioned across all 4 patients was the left fusiform gyrus, indicating that this region subserves a function broader than letter or word identification. We suggest that a seemingly pure disorder of reading can arise due to a general reduction of visual speed and span, and explain why this has a disproportionate impact on word reading while recognition of other visual stimuli are less obviously affected.

Figure 1.

Ten degree static perimetry is shown for the 3 patients with visual field defects. JT top, BA middle, and JH bottom. Left eye fields on the left.

Figure 2.

Lesion maps from all 4 pure alexic patients have been overlaid and superimposed on a canonical single-subject MRI brain scan in MNI space. The colored scale refers to the number of voxels in common across the patients, with yellow voxels being common to all 4. All axial slices containing yellow voxels are shown (total volume of 100% overlap = 32 voxels or 256 mm³). The red crosshairs converge on the peak voxel identified in a meta-analysis as being at the center of the VWFA (−44 −58 −15). L = left.

Figure 3.

Stimuli and mask used in Experiments 1 and 2.

Figure 4.

Single-word reading speeds and word length effect for all 4 pure alexic patients and controls. The patients' word length effects, as estimated by linear regression, were TJ: 212 ms per letter (r² = 0.198, F(1, 66) = 16.3, P < 0.001); JT: 176 ms/letter (r² = 0.356, F(1, 59) = 32.5, P < 0.001); BA: 201 ms/letter (r² = 0.449, F(1, 71) = 57.9, P < 0.001); JH 146 ms/letter (r² = 0.269, F(1, 68) = 25.0, P < 0.001). For comparison, NT's word length effect was 36 ms/letter for words of 3–7 letters in length (r² = 0.062, F(1,64) = 4.25, P = 0.043).

Figure 5.

Plots to show how t₀ and C_central are calculated for a normal control (C5) and a patient with pure alexia (TJ), from Experiment 1. See Table 3 for parameter estimates.

Figure 6.

Plots to show how t₀ and C_peripheral and K are calculated for a normal control (C1) and a patient with pure alexia (JH), from Experiment 2. See Table 4 for parameter estimates.