Central touch disorders
Central touch disorders comprise a wide range of deficits in the tactile perception than can occur after damage to the central nervous system. They vary from deficits in the detection of a touch to complex cognitive deficits such as the inability to recognize objects through touch or the experience of having an additional body parts such as a third arm. To understand these disorders, first the neural pathways involved in tactile information processing in the central nervous system will be summarized. This is followed by an overview of the touch disorders ranging from primary-, to higher order deficits.
Pathways of tactile information processing in the Central Nervous SystemTactile information is processed within the somatosensory system. Somatosensory input is derived from a variety of receptors in the skin, muscles and joints which convey information about different elementary sensory modalities such as i) discriminative touch (pressure, vibration), ii) pain and sensitivity to hot and cold and iii) proprioception which concerns information about the position and movement of one’s own body and limbs. Two ascending systems are responsible for conveying somatosensory input to the brain. The medial lemniscal system is involved in discriminative touch and proprioception, while the anterolateral system mediates pain, thermal and some tactile information. Both systems terminate in the thalamus after which most somatosensory input is relayed to the primary somatosensory cortex (SI), located in the anterior parietal cortex.somatotopic maps of the contralateral side of the body.
Overview of Central Touch Disorders
Primary tactile disorders
Primary tactile disorders consist of an inability to discriminate elementary somatosensory aspects, including the loss of pressure sensitivity, elevated two-point discrimination, loss of vibratory sense or deficits in proprioception. Deficits in the primary somatosensory perception have been reported most often after damage to the (hand area of the) contralateral SI, the thalamus, or the subcortical somatosensory pathways. These deficits can selectively impair a somatosensory submodality while others remain functionally intact (Corkin et al. 1978). For example, some patients are able to feel temperature while they have no sense of where their limbs are when they have their eyes closed. Obviously, these primary tactile disorders can lead to problems in higher order touch disorders such as tactile object recognition. However, higher order tactile disorders can be present in the absence of primary elementary defects (Wiebers et al. 1998).
Higher order touch disorders
A higher level in the hierarchical processing is the discrimination of the tactile features of an object. Tactile features include texture, substance, size, shape, weight and the hardness of a stimulus. It appears that the extraction of these features is neuroanatomically segregated between the micro- and macrogeometrical properties of an object (Morley et al. 1983). The microgeometrical properties correspond to the surface of the object (texture, roughness or hardness) and are associated with activation in the parietal operculum (Roland et al. 1987, 1998, Binkofski et al. 1999. O’Sullivan et al. 1994). The macrogeometrical properties correspond to the length of axes of the object (size and shape) and seem to be processed predominantly by the anterior part of the intraparietal sulcus. The idea of separate processing of these features is supported by tactile feature disorders, where amorphognosia (disorders in discriminating the size or shape of an object) and ahylognosia (disorders in discrimination the texture, weight or thermal properties of objects) are dissociated disorders (Delay et al. 1935) and might have different underlying neural networks (Caselli et al. 1991, Knecht et al. 1996).
Object explorationTactile discrimination of features and recognizing an object are not passive processes and require hand movements to interact with the object. These are stereotypical hand movements that are elicited spontaneously through interaction with an object by touch (Lederman et al. 1987). The type of hand movements depends on the object characteristics. Deficits in making these hand movements at this level are called tactile apraxia, in which difficulties arise in attuning hand movements to the characteristics of an object in the presence of preserved elementary motor or sensory abilities.
Besides intact somatosensory processing at lower levels and purposeful exploratory hand movements, multiple somatosensory signals have to be combined to form a representation of an object. An example is when you try to discriminate between the key and coins in your pocket by touch. To recognize the keys, information about its thermal properties, the weight and its size and shape has to be extracted by purposeful hand movements and needs to be integrated into a coherent object representation. Subsequently, the representation of the object, in this case the key, is used to access the semantic properties (its use and function). An impairment in building the object representation despite relatively preserved primary somatosensory function is called tactile agnosia (Caselli 1997). Object identification through other modalities is usually preserved. In tactile agnosia, the level at which an abnormality in information processing occurs can vary. First, problems concerning the perception and integration of the micro- and/or macrogeometrical properties can arise. This is also referred to as tactile apperceptive agnosia (astereognosis), which can be feature specific (for instance, having difficulty in integrating texture information). Clinical reports of pure apperceptive agnosia (i.e. without somatosensory or motor deficits) are rare and are often associated with right hemispheric damage. Since the right hemisphere is associated with supra-modal spatial perception, some studies suggest that higher order tactile disorders are merely a disorder in spatial skills (Semmes 1965, Sterzi et al. 1993). Since the right hemisphere is associated with supra-modal spatial perception, some studies suggest that higher order tactile disorders are merely a disorder in spatial skills (Semmes 1965). Indeed, somatosensory deficits often co-occur with deficits in higher order spatial processing such as neglect. However, more recent studies found that tactile agnosia can exist without spatial deficits (Reed et al. 1996, Saetti et al. 1999). The second level in which an abnormality in tactile agnosia occurs concerns the tactile associative agnosia and arises when the representation of the (correctly extracted) features fail to generate the semantic knowledge of the object. Thus, patients with associative tactile agnosia can explain what an object looks like (e.g. a metal object with an irregular side in case of a key) but are not able to describe either the use nor name the object. To access semantic knowledge, input from memory storage about this object is needed (Mesulam 1998). Furthermore, it appears that prior semantic knowledge about an object improves tactile recognition performance, suggesting that top-down mechanisms are involved in tactile processing (Bohlhalter et al. 2002).
Another class of object recognition disorder is tactile aphasia (anomia), where the patient is unable to name the object when perceived by touch. Interestingly, the patient is capable of naming the object when it is perceived through another modality. In addition, patients can pantomime the use of a tactile presented object or are able to categorize objects by their meaning, indicating that the semantic knowledge of the object is accessible. Whether the semantic knowledge of the object is completely intact remains controversial but it is clear that semantic problems do not fully account for the problems in naming the object. Thus, a patient with tactile aphasia would be able to successfully discriminate his key from the coins in his pocket. He is capable to describe that this is the object for opening his front door, although he is unable to come up with the word ‘key’. When he can see the key (other modality), he immediately is able to name it.
The somatosensory system is not only capable of recognizing objects, but primarily provides a representation of the body. Disorders in bodily experience after damage to the central nervous system have been widely reported. In the next section an overview of these deficits is given.
Information about the position of the different parts of our body relatively to each other is based on an integration of visual, vestibular, proprioceptive and tactile input. Some authors have proposed that multiple representations of our body exist and a common distinction is that between body image and body schema (Gallagher 2005, Paillard 1999). The body image represents a conscious ‘perceptual identification of body features’. It may be more visually based and is influenced by stored knowledge about the body structure and semantics. The body schema is related to the position of body parts in space and is mainly based on tactile input combined with proprioceptive information. In contrast to the body image, information about the body schema is continuously updated as our body moves or changes. The cerebral basis of the body schema is still unclear, though a central role for the superior part of the posterior parietal cortex has frequently been suggested (Dijkerman 2007). Disorders in the body representations may include features of both types. In the next two paragraphs, we will describe a few examples from the huge variety of disorders that exists.
Body representation disorders
Disorders of body representations can affect the entire body or only specific body parts. An example of the latter is finger agnosia, in which a person is unable to identify their fingers, despite a preserved ability to use them. Finger agnosia is the most common of all body representation disorders and is most often present in the middle three fingers of both hands (Frederiks 1985). Another body representation disorder concerns left- right disorientation where an ability to identify the right and the left side of one’s body is disturbed while other spatial concepts (for example, up –down or front - back) and left – right identification of other objects and other persons, are preserved (Denes, 1989). Left-right disorientation and finger agnosia often occur after lesions to the (left) inferior parietal lobe. Together with dyscalculia and dysgraphia they constitute Gerstmann’s syndrome (Gerstmann 1942). Another example of a body representation disorder is autotopagnosia in which a person is not capable to localise their own body parts, where in heterotopagnosia problems arise in localising somebody else’s body parts. These disorders are also associated with left posterior parietal lesions.
Body awareness disorders
For disorders concerning body awareness, a distinction can be made between awareness with respect to a deficit, and awareness toward one’s owns body. In the first category, a prominent example is anosognosia, where there is a lack of awareness of any physical (or cognitive) deficit. In case of denial, patients reject the idea of physical impairment, where patients with a lack of insight admit the existence of their deficit but underestimate the severity and the implications of their physical impairment (anosodiaphoria). In the second class, several disorders with respect to body awareness occur. In asomatognosia, patients feel that parts of their body are ‘missing’ or have disappeared from corporal awareness. For example, the loss of awareness of one body-half (which may or may not be paralyzed). Another disorder related to disturbances in body ownership is somatoparaphrenia where patients deny the ownership of a paralysed hand, arm or foot. This is not limited to a denial or lack of awareness, because there is an active, though unaware, denial involved, where patients might give alternative interpretation to explain their affected functions, for example by believing that the affected limb belongs to someone else, that is an animal or that it is part of a rotting corpse. Also, a reverse interpretation is possible, meaning that patients may identify the body parts of another person as their own (Garcin et al. 1938, Gerstmann 1942). Although the duration of symptoms of asomatognosia and somatoparaphrenia can range from minutes to months, presenting evidence which contradicts the delusion only temporarily reduces the denial, after which the asomatognosia or somatoparaphrenia returns. Misoplegia is a more severe form of somatoparaphrenia and is defined as a hatred for the affected limb, with offensive behaviours toward the limb as a result. Disorders associated with deficits in the ownership are often observed after extensive right hemispheric lesions, where premotor, parietal and posterior insular damage are particularly implicated (for review see Vallar et al. 2009).Problems concerning the ownership of limbs and can also be present when the particular limb is not a physical part of the body to any further extent, as in the case of phantom limb phenomenon. This can be defined as “the persistent experience of the postural and motor aspects of a limb after its physical loss” (Brugger 2006). The phantom limb phenomenon occurs in approximately 95% of patients who undergo amputation of a limb (Melzack 1990)
Neuropsychological disorders of body awareness after brain damage occur relatively infrequently and recover over time. As a consequence, in depth research of the underlying neural mechanisms are sparse. However, these disorders are of great interest as they can provide insight into the mechanisms underlying bodily awareness, body ownership and self-other distinctions.
Central touch disorders can occur on multiple levels ranging from primary somatosensory perception disorders (e.g. a deficit in two-point discrimination) to higher order disorders (e.g. shape detection, object recognition or body related disorders). These disorders can be present in absence of other deficits, although it is more common that they influence, and are influenced by other tactile and/or cognitive deficiencies. Compared to visual disorders, touch disorders receive less attention both in research as well as in clinical practice and their presence can therefore be underestimated.
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