Central touch disorders

Figure 1: The somatosensory ascending pathways responsible for conveying somatosensory input to the brain.

Central touch disorders comprise a wide range of deficits in somatosensory 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 part 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.

## Contents

* 1 Pathways of tactile information processing in the Central Nervous System
* 2 Overview of Central Touch Disorders
* 2.1 Primary somatosensory disorders
* 2.2 Higher order touch disorders
* 2.2.1 Discrimination of features
* 2.2.2 Object exploration
* 2.2.3 Object recognition
* 2.3 Body related disorders
* 2.3.1 Structural body representation disorders
* 2.3.2 Body awareness disorders
* 3 Conclusion
* 4 References

## [edit] Pathways of tactile information processing in the Central Nervous System

Tactile 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) proprioception which concerns information about the position and movement of one’s own body and limbs, iii) pain and sensitivity to hot and cold and iv) affective touch (induced by slow stroking with a soft brush) (Loken et al., 2009). 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 spinothalamic tract mediates pain, thermal and affective tactile information. The medial lemniscal two system projects contralaterally to the thalamus after which most somatosensory input is relayed to the primary somatosensory cortex (SI), located in the anterior parietal cortex.

Figure 2: . The spinothalamic system projects to the outer layers of the spinal dorsal horn from whether projections exist via a thalamic relay nucleus (VMpo) to the posterior insular cortex. The somatosensory system located in the anterior parietal cortex. From: the digital anatomist project in the department of biological structure at the University of Washington

The SI of each hemisphere contains somatotopic maps of the contralateral side of the body.

Figure 3: The representation of body parts in the somatosensory homunculus.

In these somatotopic maps, each body part is represented according to the degree of innervation density, e.g. body parts with higher receptor density occupy larger areas in SI (Penfield et al. 1950). Damage to SI is associated with primary discriminative tactile processing disorders, i.e. impairments in processing the physical, elementary characteristics of tactile stimuli. The posterior insular cortex also contains somatotopic maps for pain, temperature sensitivity and affective touch (Bjornsdotter et al., 2010). Higher order somatosensory processes involve wider more distributed networks, including the secondary somatosensory cortex (SII), the posterior parietal cortex and the anterior insula.

Figure 4: The insula is located beneath the frontal, parietal and temporal opercula and is involved in affective touch, pain and temperature sensitivity and in higher order tactile processing. From: the digital anatomist project in the department of biological structure at the University of Washington

The higher order processes range from extracting the features of an object, to the recognition of an object and to body-perception related processes. In contrast to the contralateral involvement for primary tactile information, higher order processes can be bilaterally disturbed after a unilateral lesion. For example, a right hemispheric lesion can cause problems in object recognition in the left hand as well as in the right hand. In addition, there is growing evidence for hemispheric specialization in higher order tactile processes, where right-sided brain lesions result in more severe spatial defects (Heilman et al. 2003) or impairments in body awareness (Baier and Karnath, 2008) compared to left-sided lesions. No hemispheric lateralization for primary (elementary) tactile function appears to exist.

## [edit] Overview of Central Touch Disorders

### [edit] Primary somatosensory disorders

Primary tactile disorders consist of an inability to detect elementary somatosensory aspects, including impaired sensitivity to pressure applied to the skin, elevated two-point discrimination thresholds (i.e. impaired spatial acuity), loss of vibratory sense, or deficits in proprioception. Primary tactile impairments have been reported usually after damage to the contralateral SI, the thalamus, or the subcortical ascending somatosensory pathways. These deficits can selectively affect one somatosensory submodality while others remain functionally intact (Corkin et al. 1978). For example, some patients are able to feel hot and cold while they have no sense of where their limbs are when they have their eyes closed. This is consistent with the idea that these features are processed in parallel. Obviously, primary tactile disorders can lead to problems in higher order touch disorders such as an inability to recognize objects by touch. However, higher order tactile disorders can be present in the absence of primary elementary defects (Wiebers et al. 1998).

### [edit] Higher order touch disorders

#### [edit] Discrimination of features

A next hierarchical level in the somatosensory processing of stimuli, is the discrimination of haptic features. The term haptic is used here to show that it involves more than just passive tactile input, but a combination of tactile and proprioceptive information gained through active exploratory hand movements (see below under Object exploration). Haptic features include texture, substance, size, shape, weight and the hardness of a stimulus. Evidence from studies with healthy participants suggests that haptic object feature discrimination can be designated into two categories, i.e. pertaining to the micro- and macrogeometrical properties of an object (Morley et al. 1983). Texture, density or thermal properties are regarded as the microgeometrical aspects, whereas size and shape are regarded as macrogeometrical properties. Evidence for this segregation stems also from reports of selective dissociated impairments within tactile feature discrimination (Delay, 1935). That is, hylognosia is an impairment that is characterized by the inability to discriminate texture, density or the thermal properties of an object (microgeometrical). Conversely, suffering from morphognosia means that the patient has an inability to discriminate the size of shape of an object (macrogeometrical). Is has been found that discriminating microgeometrical properties of an object is associated with activation in the parietal operculum (Roland et al. 1987, 1998, Binkofski et al. 1999., O'Sullivan et al. 1994), whereas the anterior part of the intraparietal sulcus is predominantly associated with processing macrogeometrical properties, suggesting that these two functions are segregated on a neuroanatomical level as well (Caselli et al. 1991, Knecht et al. 1996, Homke, 2009). However, other reports have disputed the theory of two separate feature processing disorders. It has been argued that impairments in perceiving macrogeomatrical properties of an object is a consequence of impaired spatial abilities. For example, perceiving the size or shape of an object requires for an analysis of the direction and extension of the movement, the sense of limb position in space and tactile localisation (Saetti, 1998). However, some reported patients with morhphognosia showed no spatial deficits in other (visual) modalities (Reed et al. 1996) or only mild spatial deficits (Delay, 1935).

#### [edit] Object exploration

Discrimination of features and recognizing an object through touch is not a passive process and requires 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 we want to extract. 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. Tactile apraxia is usually associated with damage to superior posterior parietal areas (Binkofski et al., 2002).

Figure 5: Difficulty in attuning hand movements to the characteristics of object in a case of tactile apraxia. From: Binkofski et al. 2001

Not surprisingly, difficulties in the exploration of an object can lead to problems in object recognition (Valenza et al., 2002), although this is not obligatory (Caselli, 1991). In the case of problems in object recognition, different causes can underlie this deficit. In the next paragraph, the haptic recognition of objects and their associated disorders are discussed.

#### [edit] Object recognition

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 grasp your keys from your pocket. This requires purposeful hand movements to search for the expected object features, for example a flat, hard, cool object with a circular shape on one end and ridges on that other end. The information then needs to be integrated into a coherent representation of an object. Subsequently, the semantic properties (its use and function) are retrieved. A deficit in building the object representation or in accessing the semantic properties of the object is called 'tactile agnosia' (Delay, 1935, Heeanen and David, 1945, Caselli, 1991, Endo et al., 1992; Reed and, Caselli 1994, Reed et al. 1996, Caselli 1997). In tactile agnosia, primary somatosensory processing as well as object recognition through other modalities are usually preserved. The level at which an abnormality in information processing occurs in tactile agnosia can vary. First, the integration of the micro- and/or macrogeometrical properties into a coherent representation of the object can be impaired, which is called tactile apperceptive agnosia or astereognosis. These patients are unable to draw the object they have explored through touch. Clinical reports of apperceptive agnosia without primary somatosensory or motor deficits are rare and are often linked to right hemispheric damage. Since the right hemisphere is associated with spatial perception, some authors have suggested that higher order tactile disorders are merely a consequence of impairments in spatial skills (Semmes 1965, Sterzi et al. 1993). Indeed, somatosensory impairments often occur together with deficits in higher order spatial processing such as neglect. More recent studies, however, reported that tactile agnosia can exist without spatial deficits (Reed et al. 1996, Saetti et al. 1999). The second type of haptic object recognition deficit is tactile associative agnosia and occurs when a representation of object is achieved (i.e.. the patient can make a drawing of the object), but when access to semantic knowledge of the object is is lost, therefore preventing recognition. Recently, a case of pure associative agnosia of the left hand has been described (Veronelli et al. 2014). A right haemorrhagic lesion limited to the post-central and supra-marginal gyri resulted in an inability to recognize objects in only the left hand, with a preserved tactile discrimination or visuo-tactile matching of objects. Thus, patients with associative tactile agnosia can describe the object (e.g. a metal object with an irregular side in case of a key) but are not able to indicate either the use nor name the object. To access this semantic knowledge, input from memory storage about this object is needed (Mesulam 1998). Furthermore, 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 haptic 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. Although not many case studies on tactile aphasia have been described, there is evidence that tactile aphasia and tactile agnosia are different on symptomatology as well as the neuroanatomical substrate (Endo et al. 1992).

The somatosensory system is not only important for recognizing external stimuli such as objects, but primarily provides information and a conscious experience about the body of the observer. A wide range of disorders in bodily experience after damage to the central nervous system has been reported. In the next section an overview of these deficits is given.

### [edit] Body related disorders

Information about our body is based on an integration of visual, vestibular, proprioceptive and tactile input. Several authors have proposed that different representations of our body exist and a common distinction is that between body image and body schema (Gallagher 2005, Paillard 1999; but see de Vignemont 2010 for a critical appraisal of this idea). 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 as well as by bottom-up incoming sensory input. In contrast, the body schema codes the position of body parts in space for the guidance of action and is mainly based on tactile input combined with proprioceptive information. 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 & de Haan, 2007). Disorders in the body representations may include features of both types. An alternative organization with respect to the role of the somatosensory system to body representations is proposed by Longo et al. (2010). They described different levels of processing with somatosensation being the lowest (linked to a primary somatosensory processing in SI). Somatoperception concerns the process leading to bodily perception especially related to achieving perceptual constancy. Finally, somatorepresentation refers to more cognitive processes that result in building semantic, configural and emotional knowledge and attitudes about the body. Both somatoperception and somatorepresentation seem to be linked more to the concept of body image rather than the action related body schema. In the next two paragraphs, we will describe a few examples from the huge variety of disorders that exists and we will link them to some of the more cognitive concepts described above.

#### [edit] Structural body representation disorders

Structural body representation concerns the knowledge about the arrangement and form of body parts, crucial to form a sense of body awareness. In "autotopagnosia", patients are unable to point to their own body parts on a visual scheme (Poeck and Orgass, 1971; Semenza and Goodglass, 1985), whereas in heterotopagnosia problems arise in pointing to somebody else’s body parts. These disorders have been associated with middle-temporal or parietal lesions of the dominant hemisphere (Schwoebel and Coslett, 2005). Structural body representation disorders not necessarily affect the whole body, but can be selectively impaired for the fingers, in the case of "finger agnosia" in which patients are unable to identify the fingers despite a preserved ability to use them (Gerstman, 1940, Kinsbourne and Warrington, 1962). It usually affects the middle three fingers of both hands (Frederiks 1985). Although finger agnosia was initially regarded as a form of autotopagnosia (Gerstmann, 1940), the disorders appeared to be dissociated (De Renzi and Scotti, 1970, Goldeberg, 2000). Finger gnosis has been repeatedly associated with bilateral parietal activation (Rusconi, 2005). The bilateral parietal lobe has been repeatedly associated with finger gnosis. A recent study on the neuroanatomical correlates of finger gnosis specified that left anteromedial parietal lobule plays an important role in finger identification. (Rusconi et al. 2014). Finger agnosia can be considered to be a body image deficit, as tactile input to individual fingers can be used correctly to guide movements (Anema et al., 2008). Traditionally, finger agnosia was not regarded a unitary phenomenon, but has been described a part of a cluster of impairments, known as the Gerstmann syndrome. Gerstmann syndrome is characterized by four core symptoms, i.e. finger agnosia, dyscalculia, dysgraphia and left-right orientation. The latter is also regarded as a body representation disorder and concerns the impairment in the identification of the left and right side of one’s own, but also someone else’s body. In addition to deficits in structural and spatial aspects of body representation, disturbances in body size perception have also been reported. Macrosomatognosia refers to the perception of a body part being larger than it’s actual size, while in microsomatognosia patients experience their body (part) as being smaller (Frederiks, 1985). These deficits have been associated with a range of paroxysmal disorders such migraine or seizures and often occur temporarily (Rode et al., 2012). They also have been reported for the affected hand in patients with complex regional pain syndrome. Moreover, the perception of a smaller or larger body part can also be induced in healthy participants through proprioceptive illusions (de Vignemont, Ehrsson, & Haggard, 2005) or through temporary peripheral proprioceptive deafferentation, which results in the affected body part feeling larger (Gandevia & Phegan, 1999). Damage to the central nervous also can affect body size perception. Macrosomatognosia is reported more frequently than microsomatognosia and is usually associated with parietal lesions (Frederiks, 1985). However, it has also been reported after a frontal lesion (Weijers, Rietveld, Meijer, & de Leeuw, 2013) or in Parkinson’s patients (Sandyk, 1998).

#### [edit] Body awareness disorders

Disorders in body awareness can arise at different levels. First, being aware of a physical deficit such as a paralysis can be disturbed. Different gradations exist, patients with anosognosia for hemiplegia reject the idea of physical impairment, while other patients admit the existence of their deficit but underestimate the severity and the implications of their physical impairment (anosodiaphoria). Anosognosia can exist for both motor and somatosensory impairments. The first is related to lesions to the posterior insula (Karnath et al., 2005), the second is a consequence of lesions to the basal ganglia (i.e. putamen) (Pia et al., 2014). Anosognosia for hemiplegia is relatively common with 18% of the first-ever stroke patients and 32% of the right hemisphere stroke patients suffering from this disorder (Appelros et al., 2002; Vocat et al., 2010). A second group of disorders concerns impairments in awareness about (part) of the body itself. Patients with asomatognosia experience that a body part is ‘missing’ or has 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 in which patients suffer from asomatognosia plus extensive delusions, misidentifications, and confabulations regarding the limb. For example, patients might give an alternative explanation for the limb disownership, 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. A reverse interpretation has been observed as well, with patients identifying body parts of another person as their own (Garcin et al. 1938, Gerstmann 1942). Different theories on the etiology of asomatognosia and somatoparaphrenia exist, also because patients often suffer from other neuropsychological impairments. Therefore, hemispatial neglect, hemianesthesia, prioprioceptive and attentional impairments have been commonly associated with asomatognosia and somatoparaphrenia (Feinberg et al. 2010, Gandola et al. 2012, Vallar & Ronchi. 2009). Furthermore, it has been suggested that multisensory integration and building a spatial representation of the body is hampered (Vallar & Ronchi. 2009). Interestingly, these problems are only present for a first-person perspective, but diminishes when a patients views him or herself in the mirror (Fotopoulou et al. 2011). The duration of symptoms of asomatognosia and somatoparaphrenia varies from minutes to months. Interestingly, providing evidence to the patient that contradicts the delusion only temporarily reduces the denial, after which the asomatognosia or somatoparaphrenia returns. Misoplegia is a more affective form of body awareness disorder and can be defined as a hatred for the affected limb, with offensive behaviours toward the limb as a result. With respect to the underlying neural substrate, disorders of body awareness and ownership are often a consequence of large right hemispheric lesions, involving premotor, parietal and posterior insular areas (for review see Vallar & Ronchi, 2009). In addition, cases have been described in which somatoparaphrenic symptoms were induced through vestibular stimulation suggesting that body awareness disorders might be a consequence of functional rather that structural deficits (Ronchi et al. 2013).

Problems concerning body ownership and awareness can also occur when a limb is no longer a physical part of the body, 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). Phantom limb experiences a present in approximately 95% of patients who undergo amputation of a limb (Melzack 1990).

Figure 6: An example of the phantom limb phenomenon. A patient experiences a phantom hand but no forearm after amputation. From: Wright Halligan and Kew, Wellcome SciArt Project 1997

A similar phenomenon (i.e. experience of a limb that is not physically present) can also occur after brain damage, but is less frequently observed. This is referred to as supernumerary phantom limb (SPL), and is defined as “the awareness of having an "extra limb" in addition to the regular set of two arms and two legs.” Multimodal experience of the extra limb has been reported including tactile (feel objects with their phantom arm), visual (visually perceive their phantom limb) and motor components (generate action). Neural representations of this extra limb have been reported in the brain areas that represent these modalities, particularly in the left hemisphere (Khateb 2009), although the phenomenon has been described after right-sided lesions as well (Miyazawa 2004). Except for anosognosia, disorders of body awareness after brain damage appear to occur relatively infrequently, although it’s prevalence so far has not been well-documented. They also tend to recover over time. These disorders are nevertheless of great interest as they can further our understanding of the functional and neural mechanisms underlying bodily awareness, body ownership and self-other distinctions.

## [edit] Conclusion

Central touch disorders can occur on multiple levels ranging from primary somatosensory perception disorders (e.g. a deficit in spatial acuity) 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. Nevertheless, they are linked to limitations in functional independence and therefore deserve more attention.

## [edit] References

* Anema, H A et al. (2008). Differences in finger localisation performance in patients with finger agnosia. Neuroreport 19: 1429-1433.

* Appelros, P; Karlsson, G M; Seiger, A and Nydevik, I (2002). Neglect and anosognosia after first-ever stroke: Incidence and relationship to disability. Journal of Rehabilitation Medicine 34: 215-220.

* Binkofski, F et al. (1999) A parieto-premotor network for object manipulation: Evidence from neuroimaging. Experimental Brain Research 128: 210-213.

* Binkofski, F; Kunesch, E; Classen, J; Seitz, R J and Freund, H J (2001). Tactile apraxia. Brain 124: 132-144.

* Bohlhalter, S; Fretz, C and Weder, B (2002). Hierarchical versus parallel processing in tactile object recognition: A behavioural-neuroanatomical study of aperceptive tactile agnosia. Brain 125: 2537-2548.

* Björnsdotter, M; Morrison, I and Olausson, H (2010). Feeling good: On the role of C fiber mediated touch in interoception. Experimental Brain Research 207: 149-155.

* Brugger, P (2006). From phantom limb to phantom body: varieties of extracorporeal awareness. In: G Knoblich, I M Thornton, M Grosjean and M Shiffrar (Eds.), Human Body Perception from the Inside Out (pp. 171-210). New York: Oxford University Press.

* Caselli, R J (1991). Rediscovering tactile agnosia (review). Mayo Clinical Proceedings 66: 129-142.

* Caselli, R J (1997). Tactile agnosia and disorders of tactile perception. In: T E Feinberg and M J Farah (Eds.), Behavioral Neurology and Neuropsychology (pp. 277-288). New York: McGraw-Hill.

* Corkin, S (1978). The role of different cerebral structures in somesthetic perception. In: E C Carterette and M P Friedman (Eds.), Handbook of Perception, Vol. 6B (pp. 105-155). New York: Academic press.

* Delay, J P (1935). Les Astereognosies: Pathologie du Toucher. Paris: Masson.

* Denes, G (1989). Disorders of body awareness and body knowledge. In: F Boller and J Grafman (Eds.), Handbook of Neuropsychology, Vol. 2 (pp. 207-225). Amsterdam: Elsevier Science Publishers.

* De Renzi, E and Scotti, G (1970). Autotopagnosia: fiction or reality? Report of a case. Archives of Neurology 23: 221-227.

* De Vignemont, F; Ehrsson, H H and Haggard, P (2005). Bodily illusions modulate tactile perception. Current Biology 15: 1286-1290.

* De Vignemont, F (2010). Body schema and body image--Pros and cons. Neuropsychologia 48: 669-680.

* Dijkerman, H C and de Haan, E H (2007). Somatosensory processing subserving perception and action. Behavioral and Brain Sciences 30: 189-201.

* Gandola, M et al. (2012). An anatomical account of somatoparaphrenia. Cortex 48: 1165-1178.

* Feinberg, T E; Venneri, A; Simone, A M; Fan, Y and Northoff, G. The neuroanatomy of asomatognosia and somatoparaphrenia. Journal of Neurology, Neurosurgery, and Psychiatry 81: 276-281.

* Frederiks, J A M (1985). Disorders of the body schema. In: F J Vinken and G W Bruyn (Eds.), Handbook of Clinical Neurology 4: 207-240. Amsterdam, North Holland.

* Fotopoulou, A et al. (2011). Mirror-view reverses somatoparaphrenia: Dissociation between first- and third-person perspectives on body ownership. Neuropsychologia 49: 3946-3955.

* Gallagher, S (2005). How the Body Shapes the Mind. Oxford: Oxford University Press.

* Gandevia, S C and Phegan, C M (1999). Perceptual distortions of the human body image produced by local anaesthesia, pain and cutaneous stimulation. Journal of Physiology 514: 609-616.

* Garcin, R; Varay, A and Hadji-Dimo (1938). Document pour servir à l’étude des troubles du schéma corporel (sur quelques phénomènes moteurs, gnosiques et quelques troubles de l’utilisation des membres du côté gauche au cours d’un syndrome temporo-pariétal par tumeur, envisagés dans leurs rapports avec l’anosognosie et les troubles du schéma corporel). Revue Neurologique, Paris 69: 498-510.

* Gerstmann, J (1942). Problem of imperception of disease and of impaired body territories with organic lesions. Archives of Neurology and Psychiatry 48: 890-913.

* Heilman, K (2003). Clinical Neuropsychology, 4th ed. USA: Oxford University Press.

* Homke, L et al. (2009). Analysis of lesions in patients with unilateral tactile agnosia using cytoarchitectonic probabilistic maps. Human Brain Mapping 30: 1444-1456.

* Karnath, H O; Baier, B and Nagele, T (2005). Awareness of the functioning of one’s own limbs mediated by the insular cortex? Journal of Neuroscience 25: 7134-7138.

* Kinsbourne, M and Warrington, E K (1962). A study of finger agnosia. Brain 85: 47-66.

* Khateb, A (2009). Seeing the phantom: a functional magnetic resonance imaging study of a supernumerary phantom limb. Annals of Neurology 65: 698-705.

* Knecht, S; Kunesch, E and Schnitzler, A (1996). Parallel and serial processing of haptic information in man: Effects of parietal lesions on sensorimotor hand function. Neuropsychologia 37: 669-687.

* Lederman, S J and Klatzky, R L (1987). Hand movements: A window into haptic object recognition. Cognitive Psychology 19: 342-368.

* Loken, L S; Wessberg, J; Morrison, I; McGlone, F and Olausson, H (2009). Coding of pleasant touch by unmyelinated afferents in humans. Nature Neuroscience 12: 547-548.

* Longo, M R; Azañón, E and Haggard, P (2010). More than skin deep: Body representation beyond primary somatosensory cortex. Neuropsychologia 48: 655-668.

* Melzack, R (1990). Phantom limbs and the concept of a neuromatrix. Trends in Neuroscience 13: 88-92.

* Mesulam, M (1998). From sensation to cognition. Brain 121: 1013-1152.

* Miyazawa, N; Hayashi, M; Komiya, K and Akiyama, I (2004). Supernumerary phantom limbs associated with left hemisphere stroke: Case report and review of the literature. Neurosurgery 54: 228-231.

* Morley, J W; Goodwin, A W and Darian-Smith, I (1983). Tactile discrimination of gratings. Experimental Brain Research 49: 291-299.

* O'Sullivan, B T; Roland, P E and Kawashima, R (1994). A PET study of somatosensory discrimination in man. Microgeometry versus macrogeometry. European Journal of Neuroscience 6: 137-148.

* Paillard, J (1999). Body schema and body image - A double dissociation in deafferented patients. In: G N Gantchev, S Mori and J Massion (Eds.), Motor Control, Today and Tomorrow (pp. 197-214). Sofia: Akademicno Izdatelstvo.

* Penfield, W (1950). The Cerebral Cortex of Man. New York: McMillan.

* Peltz, E; Seifert, F; Lanz, S; Müller, R and Maihöfner, C (2011). Impaired hand size estimation in CRPS. Journal of Pain 12: 1095-1101.

* Pia, L et al. (2014). Anosognosia for hemianaesthesia: A voxel-based lesion-symptom mapping study. Cortex 61: 158-166.

* Poeck, K and Orgass, B (1971). The concept of the body schema: A critical review and some experimental results. Cortex 7: 254-277.

* Reed, C L; Caselli, R J and Farah, M J (1996). Tactile agnosia. Underlying impairment and implications for normal tactile object recognition. Brain 119: 875-888.

* Rode, G et al. (2012). Facial macrosomatognosia and pain in a case of Wallenberg’s syndrome: Selective effects of vestibular and transcutaneous stimulations. Neuropsychologia 50: 245-253.

* Roland, P E and Mortensen, E (1987). Somatosensory detection of microgeometry, macrogeometry and kinesthesia in man. Brain Research 434: 1-42.

* Roland, P E; O'Sullivan, B and Kawashima, R (1998). Shape and roughness activate different somatosensory areas in the human brain. Proceedings of the National Academy of Sciences of the United States of America 95: 3295-3300.

* Ronchi, R et al. (2013). Remission of anosognosia for right hemiplegia and neglect after caloric vestibular stimulation. Restorative Neurology and Neuroscience 31: 19-24.

* Rusconi, E et al. (2014). Neural correlates of finger gnosis. The Journal of Neuroscience 34: 9012-9023.

* Saetti, M C and De Renzi, E (1999). Tactile morphagnosia secondary to spatial deficit. Neuropsychologia 37: 1087-1100.

* Sandyk, R (1998). Reversal of a body image disorder (macrosomatognosia) in Parkinson’s disease by treatment with AC pulsed electromagnetic fields. International The Journal of Neuroscience 93: 43-54.

* Semenza, C and Goodglass, H (1985). Localization of body parts in brain injured subjects. Neuropsychologia 23: 161-175.

* Semmes, J (1965). A non-tactual factor in astereognosis. Neuropsychologia 3: 295-315.

* Sterzi, R et al. (1993). Hemianopia, hemianaesthesia, and hemiplegia after left and right hemisphere damage: A hemispheric difference. Journal of Neurology, Neurosurgery, and Psychiatry 56: 308-310.

* Valenza, N et al. (2001). Dissociated active and passive tactile shape recognition: A case study of pure tactile apraxia. Brain 124: 2287-2298.

* Vallar, G and Ronchi, R (2009). Somatoparaphrenia: A body delusion. A review of the neuropsychological literature. Experimental Brain Research 192: 533-551.

* Veronelli, L; Ginex, V; Dinacci, D; Cappa, S F and Corbo, M (2014). Pure associative tactile agnosia for the left hand: Clinical and anatomo-functional correlations. Cortex 58: 206-216.

* Vocat, R; Staub, F; Stroppini, T and Vuilleumier, P (2010). Anosognosia for hemiplegia: a clinical-anatomical prospective study. Brain 33: 3578-3597.

* Weijers, N R; Rietveld, A; Meijer, F J and de Leeuw, F E (2013). Macrosomatognosia in frontal lobe infarct--A case report. Journal of Neurology 260: 925-926.

* Wiebers, D O et al. (1998). The sensory examination. In: Mayo Clinic Examinations in Neurology, 7th ed. (pp. 255-274). St Louis, MO: Mosby.