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recognition of faces, objects, pictures, colors, spatial arrangements, and words The diagnosis of these states is predicated on the assumption that the failure in perception occurs in spite of intact visual acuity and adequate language and mental function When examined carefully, agnosic patients usually do not satisfy all these criteria and instead have a number of other derangements that may at least in part explain their perceptual incompetence Often there is a unisensory or polysensory disturbance, an inadequacy of memory or of naming, or an impairment of visual oculomotor or visuomanual control Anatomic studies have established that disturbances of recognition of complex forms, human faces, and spatial arrangements accompany right (nondominant) parieto-occipital lesions more often than left-sided ones Disturbances of perception of graphic symbols of objects, of color discrimination, and naming in short, all of the lexical aspects of recognition are virtually always associated with left parieto-occipital lesions Variations in the clinical effects of such lesions are dependent not only on their location and size but also on the particular tests used to elicit these effects and whether they involve learning, recognition, and recall But there have been many critics of the concept of agnosia as a higher-order perceptual disturbance that can be clearly separated from loss of elementary sensation Such a division is said to perpetuate an archaic view of sensory reception in the brain as consisting of two separable functional attributes: elementary sensation and perception Bay, for example, claimed that careful testing of patients with visual agnosia always brings to light some degree of diminished vision in combination with general defects such as confusion and mental deterioration Others (Geschwind; Sperry and colleagues) have emphasized that the visual agnosias depend on disconnections of the visual receptive zones of the brain from the language areas of the left hemisphere, the learning and memory zones of the temporal lobes, the suprasensory zones of the parietal lobes, and the motor regions Hecaen, Gassel, and McCarthy and Warrington have presented the evidence for and against these points of view, the rst of which argues for a diminution of sensory function and the second, for a genuine disconnection The reported cases of visual agnosia emphasize the complexity of the perceptive process and the inadequacy of our knowledge of the physiology of the several receptive zones of the occipital lobes The fact that in some cases there are impairments of primary sensation that can be elicited by careful testing of visual function using tachistoscopic stimuli, visual adaptation, perception of pattern, icker-fusion, etc cannot be disputed However, even when present, such abnormalities would not fully explain the loss of discrimination and the inability to visualize or imagine the form and color of objects, their spatial arrangements, and their names Failure of a sensation to activate these visual memories must involve a higher-order disturbance of cerebral function in the heteromodal association areas Here sensory and motor functions are always integrated, the latter being essential for proper scanning and exploring by the sense organs And to reduce the agnosias to a series of disconnections between the striate and parastriate cortex and other parts of the brain, although an interesting approach, leads to an overly simpli ed mechanistic view of cerebral activity, which probably will not be sustained as more knowledge of cerebral physiology is acquired There is still a great need for the study of cases in which sensation and perception have been tested in detail and the anatomy of the lesion, in its stable end stage, has been carefully determined.

The effects of disease of the occipital lobes may be summarized as follows: I Effects of unilateral disease, either right or left A Contralateral (congruent) homonymous hemianopia, which may be central (splitting the macula) or peripheral; also homonymous hemiachromatopsia B Elementary (unformed) hallucinations usually due to irritative lesions II Effects of left occipital disease A Right homonymous hemianopia B If deep white matter or splenium of corpus callosum is involved, alexia and color-naming defect C Visual object agnosia III Effects of right occipital disease A Left homonymous hemianopia B With more extensive lesions, visual illusions (metamorphopsias) and hallucinations (more frequent with rightsided than left-sided lesions) C Loss of topographic memory and visual orientation IV Bilateral occipital disease A Cortical blindness (pupils reactive) B Anton syndrome (visual anosognosia, denial of cortical blindness) C Loss of perception of color (achromatopsia) D Prosopagnosia (temporo-occipital), simultanagnosia (parieto-occipital) E Balint syndrome (parieto-occipital)

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There are a number of motor, sensory, re ex, autonomic, and trophic symptoms and signs that are more or less typical of peripheral nerve disease Grouping them into syndromes based on their temporal and topographic features has proved to be of value in clinical diagnosis The topographic patterns are detailed further on under Approach to the Patient with Peripheral Neuropathy Here the primary symptoms of peripheral nerve disease are described Impairment of Motor Function Persistent impairment of motor function over days, weeks, or months in a topographic pattern that implicates peripheral nerves, signi es either segmental demyelination, axonal interruption, or destruction of motor neurons The degree of weakness is proportional to the number of axons or motor neurons affected, although pain and kinesthetic loss may add to the functional impairment Polyneuropathies are generally marked by a symmetric distribution of the weakness or paralysis In cases of diffuse axonal damage, the muscles of the feet and legs are affected earlier and more severely than those of the hands and forearms In milder forms of axonal disease, only the feet and lower legs are involved Truncal and cranial muscles are usually the last to yield, and then only in severe cases This represents the length dependent pattern of axonal degeneration The nutritional, metabolic, and toxic neuropathies assume the more common, predominantly distal, axonal pattern The pathologic changes in such cases begin in the far distal parts of the largest and longest nerves and advance along the affected bers toward their nerve cell bodies (dying-back neuropathy, distal axonopathy ) The typical distally predominant pattern is not generally found in the acute and chronic demyelinating in ammatory neuropathies, where the multifocal nature of lesions and blockage of electrical conduction leads to weakness of proximal limb and facial muscles before or at the same time as distal parts are affected Another exception to the pattern of distally predominant weakness is porphyria, an axonal process in which there may be mainly proximal weakness Another characteristic pattern of neuropathic weakness is one in which all the muscles of the limbs, trunk, and neck are involved,.