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Loss of Somatic Sensation Selzer 2-16.qxd 05/09/2005 15:09 Page 231 16 Loss of somatic sensation Leeanne Carey Evidence of behavioral recovery of somatic sensations such as Kandel, Schwartz and Jessell (Gardner and following peripheral and central nervous system Martin, 2000). Further, neuroimaging studies are lesions challenges therapists to not only understand complementing and extending information gained the nature and extent of the change, but the condi- from animal and lesion studies in humans (Schnitzler tions under which the recovery can be maximized and et al., 2000). the mechanisms underlying. This challenge requires Two features of the structure and function of the input from basic sciences and rehabilitation fields. system have particular implication for understanding Integration of these fields will provide direction for the nature of impairment and neurorehabilitation. the development and testing of scientific-based inter- First is the high degree of specificity in the organiza- ventions designed to maximize recovery by driving tion and processing of information. Specialized and shaping neural reorganization. sensory receptors, modality-specific line of commu- The focus of this chapter will be on loss of somatic nication (Gardner and Martin, 2000), specific colum- sensations, treatments currently available to address nar organization and sub-modality-specific neurons this problem, and the potential application of theo- in primary (SI) and secondary (SII) somatosensory ries of perceptual learning and neural plasticity. areas (Mountcastle, 1997) support this specificity. More detail will be given to therapies following cen- Second, the opportunity for convergence of somato- tral nervous system (CNS) lesions, with particular sensory information within the CNS (Mesulam, reference to stroke. Comparisons will also be made 1998), as well as the presence of distributed sensory in relation to loss following peripheral nervous system networks and multiple somatotopic representation (PNS) lesions. (Gardner and Kandel, 2000), impact on the scope for neural plastic changes and rehabilitation outcome. 16.1 Nature of impairment and functional implications of loss Loss of somatic sensation following interruption to central and peripheral Definition and processing within the nervous systems somatosensory system Loss of somatic sensations can be sustained due to Somatosensory function is the ability to interpret damage at various levels of the sensory system, for bodily sensation (Puce, 2003). Sensory systems are example from receptors to peripheral nerves, spinal organized to receive, process and transmit informa- cord, brainstem and cerebral cortex. This may result tion obtained from the periphery to the cerebral from disease or trauma associated with a wide range cortex. Within the somatosensory system submodal- of conditions (see Section E Disease-specific ities of touch, proprioception, temperature sense, Neurorehabilitation Systems of Volume II). Somato- pain and itch are identified. (Gardner and Martin, sensory impairment may be in the form of anesthe- 2000). Detailed description of the system involved sia (total loss of one or more sensory submodalities in sensory processing is provided in seminal texts in the region), hyposensitivity (reduced ability to 231 Selzer 2-16.qxd 05/09/2005 15:09 Page 232 232 Leeanne Carey perceive sensations, including poor localization, of an object without crushing or dropping it, using discrimination and integration), or hypersensitivity cutlery, fastening buttons, writing and walking on (non-noxious stimuli become irritating, for exam- uneven ground become difficult and often frustrat- ple dyesthesia, paraesthesia or causalgia). Clinical ing (Carey, 1995). The important role of sensation in description of loss should include identification of motor function is particularly evident in: control of body part and submodalities affected as well as the pinch grip (Johansson and Westling, 1984); ability to level of processing impairment, for example detec- sustain and adapt appropriate force without vis- tion, discrimination and integration of information ion (Jeannerod et al., 1984); object manipulation across submodalities. (Johansson, 1996); combining component parts of There are differences in the nature of the loss fol- movement such as transport and grasp (Gentilucci lowing peripheral and CNS lesions. For example, et al., 1997); discrimination of surfaces at end of hand- injury to the PNS involves well-defined loss of spe- held objects (Chan and Turvey, 1991); restraint of cific modalities that can be mapped relative to the moving objects (Johansson et al., 1992); and adjust- nerve distribution or receptor location. In compari- ment to sensory conflict conditions such, as a son, loss following CNS lesions such as stroke can rough surface (Wing et al., 1997). Moreover, the result in very different patterns of deficit, from com- affected limb may not be used spontaneously, plete hemianaesthesia of multiple modalities to despite adequate movement abilities. This may dissociated loss of sub-modality specificity in a par- contribute to a learned non-use of the limb and ticular body location (see Carey, 1995 for review). further deterioration of motor function after stroke Loss of discriminative sensibilities is most charac- (Dannenbaum and Dykes, 1988). These activity teristic (Bassetti et al., 1993; Carey, 1995; Kim and limitations impact on life roles, social communica- Choi-Kwon, 1996), thresholds for primary sensory tion, safety and participation in personal and domes- qualities (e.g., touch) are often indefinable (Head tic activities of daily living as well as sexual and and Holmes, 1911–1912), qualitative alterations, leisure activities (Carey, 1995). response variability (Carey, 1995) and dissociated The personal and functional implications of sen- sensory loss (Roland, 1987; Bassetti et al., 1993) are sory loss are highlighted in the words of a client who observed, and hypersensitivity may be present ini- experienced sensory loss after stroke: “… my right tially or develop over time (Holmgren et al., 1990). side cannot discriminate rough, smooth, rigid or Typically the loss is contralateral to the injury, malleable, sharp or blunt, heavy or light. It cannot although ipsilateral deficits are also reported (Carey, tell whether that which touches it as hand or tennis 1995; Kim and Choi-Kwon, 1996). The early and racket…it is frustratingly difficult to control or feel chronic pattern of deficit may be influenced by the relaxed about any right-sided movement … . How site of lesion, relative sparing and redundancy within does one trust a foot that “feels” as though it has no the distributed sensory system and neural plastic real connection with the earth? It is difficult to pick changes that may occur with recovery. up or hold a pair of glasses or a sheet of paper when one’s right hand/fingers feel uncontrollably strong and very big and clumsy, capable of crushing objects Functional implications of loss with one’s grip yet incapable of letting go or throw- Impairment of body sensations poses a significant ing off even the lightest objects (e.g. a tissue). … loss in its own right and has a negative impact on better to feel something-however bizarre-than effective exploration of the environment, personal nothing.” safety, motor function, and quality of life (Rothwell Loss of somatic sensations also negatively impacts et al., 1982; Carey, 1995). Everyday tasks such as on rehabilitative and functional outcomes, as indi- searching for a coin in a pocket, feeling if a plate is cated in a review of stroke outcome studies (Carey, clean when washing dishes, maintaining the grip 1995). It has a cumulative impact on functional Selzer 2-16.qxd 05/09/2005 15:09 Page 233 Loss of somatic sensation 233 deficits beyond severity of motor deficits alone “normal”, “impaired” or “absent” (Wade, 1992), have (Patel et al., 2000) and negatively impacts on reac- variable reliability (Winward et al., 1999), no defined quisition of skilled movements of the upper limb criterion of abnormality, and are often insensitive or (Kusoffsky et al., 1982; Jeannerod et al., 1984), pos- inaccurate (Carey et al., 2002c). Kim and Choi-Kwon tural control and ambulation (Reding and Potes, found that discriminative sensation remained in 1988). The importance of the sensory system as an only 3 of 25 stroke patients who were reported as early indicator of motor recovery after stroke has having no sensory impairment on the basis of con- been suggested in neuroimaging (Weiller, 1998) and ventional sensory tests (Kim and Choi-Kwon, 1996). clinical (Kusoffsky et al., 1982) studies. It has been Over the past decade new measures have been suggested that sensory reorganization may precede developed for use post-stroke. Clinical test batteries motor reorganization and may, in fact, trigger the developed are the Nottingham Sensory Assessment latter (Weiller, 1998). (NSA) (Lincoln et al., 1991; Lincoln et al., 1998) and the Rivermead Assessment of Somatosensory Performance (RASP) (Winward et al., 2002). The RASP is standardized, uses seven quantifiable sub- 16.2 Assessment of somatic sensation tests of touch and proprioceptive discrimination and includes three new instruments, the neurome- Guidelines for the selection of ter, neurotemp and two-point neurodiscriminator. measures for use in clinical settings Intra and inter-rater reliability are high (r ϭ 0.92). The directive to follow evidence-based practice The NSA employs methods consistent with clinical demands that clinicians employ quantitative
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