Information is processed within the S-I cortex in vertical arrays of neurons called columns. The neurons within a cortical column receive sensory inputs from the same receptor class and share overlapping receptive fields on the skin. The columns are arranged topographically such that sacral segments are represented medially, lumbar and thoracic segments centrally, cervical segments more laterally and the trigeminal representation at the most lateral boundary. The internal representation of the body in the human brain is essential for maintaining self-awareness and for controlling movement. This somatotopic map is referred to as a homunculus because it provides a distorted image of the body surface.
Each part of the body is represented in the brain in proportion to its relative importance to sensory perception, as measured by its innervation density rather than its surface area. Thus the homunculus exaggerates the hand, foot, and mouth, and compresses more proximal body parts. There are approximately 100 times more cortical neurons per square centimeter of skin that sense touch on the tips of the fingers than sense touch on the back. Therefore, it is not surprising that deficits in touch sensation following injury to the cortex are more pronounced in these magnified areas of the body.
Plasticity of somatotopic maps
Although all brains in a given species share a common somatotopic arrangement of columns, the details of the map characterize each individual and are determined largely by experience. The importance of these maps for constructing one’s body image is demonstrated most dramatically in human amputees. These individuals often experience phantom sensations of touch on their missing limbs, long after they know that the limb is gone forever. Although the neurons in the brain that previously represented the missing limb are deprived of their normal inputs, most of them do not die. They continue to function but are apparently activated by receptors that innervate neighboring portions of the body. For example, neurons representing an amputated arm eventually receive inputs from touch receptors on the face or on the limb stump and acquire new receptive fields on these regions.
However, the gentle touch of these body parts evokes phantom sensations that are referred to as the missing limb, because the patient has many years of experience that correlate firing in that portion of the cortex with touch on a particular region of the hand. We do not understand fully why the hand becomes permanently imprinted on these neurons, even though the patient is fully cognizant that the missing arm is no longer a part of the body.
Not only can the maps in the brain be altered by depriving certain areas of their normal input, but they can also be changed by increasing the sensory input. We do this when we learn, and we learn by practice, repeating a task over and over. Repetitive activation of a pathway strengthens those synapses, making it easier to pass information forward. The alteration of the sensory maps by experience is highly specific to the stimulated pathway. For example, functional magnetic resonance imaging (fMRI) studies of professional violinists demonstrate an unusually large representation of the fingers placed on the strings of their instruments, and on the fingertips of the bowing hand. The long hours of practice have impressed themselves on the brain.
Deficits in the sense of touch caused by damage to the brain
An intact cerebral cortex deprived of its normal sensory innervation still preserves its representation of the entire body. However, when specific regions of the parietal cortex are damaged by stroke, head injury, or disease, deficits in tactile sensation occur. These sensory abnormalities are localized to the regions of the body that innervate the injured cortex. The losses in the sense of touch are so specific that they are widely used by neurologists to diagnose cortical malfunction. Lesions to the S-I cortex in humans result in a loss of touch sensation on the contralateral side of the body. The severity of the deficit depends on the extent of cortical tissue that is damaged.
Although some sensations of touch are eventually restored, the ability to discriminate shape and textures is disrupted permanently. Experimental lesions in animals provide even clearer insights into the sensory functions of specific cytoarchitectonic fields. Lesions confined to area 3b produce the severest sensory deficits, as the tactile input to the cortex is almost completely severed. Ablation of area 1 results in deficits in texture discrimination, whereas lesions in area 2 impair stereognosis (the ability to discriminate the size and shape of objects).
Lesions to the higher somatosensory cortical areas result in deficits consistent with their sensory properties. In these higher cortical areas, the sense of touch flows seamlessly into the act of touching. Although the patient can detect and localize touch in the lesioned area, complex cognitive or sensorimotor functions of touch are abnormal. Lesions to the S-II cortex result in deficits in both stereognosis and texture discrimination, but hand movements are relatively normal. By contrast, lesions in the posterior parietal cortex disrupt normal hand motor behavior.
Reaching movements are inaccurate, the wrist cannot be oriented properly to place an object in a narrow space, and visually guided preshaping of the fingers for grasp is disrupted. Disruption of active touch is perhaps the most striking deficit observed following lesions to the parietal cortex. Hand movements are clumsy and poorly coordinated, the fingers are difficult to control, and the patient is often unable to manipulate or explore novel objects without visual guidance. Faced with this motor deficit, patients refrain from touching objects in the environment, further depriving the remaining tissue of sensory stimulation.
The neurobiological processes that underlie sensations of touch are initiated by mechanoreceptors that transform the physical deformation of the skin into electrical signals proportional to the applied forces. The information is conveyed to the central nervous system by the peripheral nerves as a pulse code of action potentials. Topographically organized ascending anatomical pathways transmit tactile information to the cerebral cortex where it is analyzed by the conscious mind to perceive the specific object that is touched. Tactile sensations may be altered by experience or by lesions in somatosensory areas of the brain.