Finally, there is a distinction between astereognosis and tactile agnosia. Some authors (e.g., Caselli) have defined tactile agnosia as a strictly unilateral disorder, right or left, in which the impairment of tactile object recognition is unencumbered by a disturbance of the primary sensory modalities. Such a disorder would be designated by others as a form of astereognosis (see above). In our view, tactile agnosia is a disturbance in which a one-sided lesion lying posterior to the postcentral gyrus of the dominant parietal lobe results in an inability to recognize an object by touch in both hands. According to this view, tactile agnosia is a disorder of apperception of stimuli and of translating them into symbols, akin to the defect in naming parts of the body, visualizing a plan or a route, or understanding the meaning of the printed or spoken word (visual or auditory verbal agnosia). These and other agnosias are discussed in Chap. 21.
Interruption of a Single Peripheral Nerve
The region of sensory loss after complete transection of a sensory or mixed nerve corresponds to the distribution of the cutaneous fibers that derive from the nerve. This is the basis of the sensory map shown in Fig. 8-1. This can be contrasted with the patterns of sensory loss due to section of nerve roots, depicted by the dermatomal map (see Fig. 8-3), which is highly predictable but has less distinctive boundaries. Of course, section of a mixed nerve weakens the muscles that it innervates and the full syndrome can be identified by the combination of these features.
If a large area of skin is involved, the sensory defect characteristically consists of a central portion in which all forms of cutaneous sensation are lost, surrounded by a zone of partial loss, which becomes less marked as one proceeds from the center to the periphery. Following experimental cutting of a nerve, the area of cutaneous sensory loss is less than its anatomic distribution because of overlap from adjacent nerves. After a period of time, the area of tactile loss is greater than that for analgesia because collateral growth from adjacent fibers is more rapid for small free nerve ending subserving pain than it is for fibers for touch. Moreover, there is greater overlap of adjacent pain sensory fields. Along the margin of the hypesthetic zone, the skin becomes excessively sensitive (hyperesthetic); light contact may be felt as smarting and mildly painful. According to Weddell, the dysesthesias are attributable to the greater sensitivity of collateral regenerating fibers that have made their way from surrounding healthy pain fibers into the denervated region. With section of purely cutaneous nerves, perceptions of deep pressure and passive movement remain intact because these modalities are mediated by nerve fibers from subcutaneous structures and joints.