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The acid-base balance of muscle from control and K-deficient rats was studied. From the measured buffering capacity, 8–11 mEq excess of anions or deficit of cations would be required to acidify 100 gm fat-free dry weight of muscle, 0.5 pH units. No evidence of increased organic acids, increased anionic equivalence of muscle proteins, or of decreased concentrations of weak bases which are potential cations in cell acidosis was found. This evidence, supplemented with data in the literature, fails to account for the cell acidosis reported in the literature. Reliability of the ‘chloride space’ as a measure of the extracellular phase of muscle in K deficiency has been confirmed by showing its agreement with the ‘raffinose space.’ The cell pH has then been calculated from the distribution of CO2 in muscle (indirect method) and from the pH of muscle homogenates (direct method) in control and K-deficient animals. Control and K-deficient muscle pH's are, respectively, 6.89 and 6.83 by the direct method, and 7.11 and 7.05 by the indirect method.

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T w o cases of prosopagnosia (failure to recognize faces) are presented, together with the autopsy findings. Only 7 other cases of prosopagnosia caused by pathologically verified occlusive vascular lesions have been described. All t h e patients had significant bilateral lesions of the cerebral hemispheres, at least one being in the medial-ventral occipital region. In our patients the bilateral lesions were grossly symmetrical in the distribution of the posterior cerebral arteries but with somewhat more extensive involvement on one side. In all reported cases one or both fusiform gyri were destroyed, and there were variably sized lesions in the pericalcarine structures. These findings suggest that the fusiform gyrus functions as a visual association area for the recognition of specific faces.Cohn R, Neumann MA, Wood DH: Prosopagnosia: a clinicopathological study. Ann Neurol 1: [177][178][179][180][181][182] 1977 Failure to recognize previously well-known human faces, which occurs in certain patients with cerebral lesions, was explicitly noted by Jackson [ 11, Charcot [2], and Wilbrand [3-51. Nevertheless, many present-day investigators begin their discussions of the phenomenon with the report of Hoff and Potzl[6] because these authors specifically considered it as a distinct entity. Bodamer [7] named the condition prosopagnosia. Although m o r e than 100 papers have been published o n this subject, few have included the pathological findings in the brain. However, it should be recognized that only selected localized vascular lesions allow precise correlation between behavior and pathological findings. O t h e r types of central nervous system abnormalities such as those presented by Meadows [8], which included trauma and neoplasia, may generate useful information, but their general and progressive effects preclude anatomical accuracy. Similarly, neurosurgical observations, because