Juan Pablo Recagno Cepeda, Carlos Ballario

Changes in the internal or external environment, with a threshold sufficient to cause some modification in the organism, cause the appearance of stimuli that, in the form of impulses, are carried to the nervous centers by a very extensive set of afferent fibers that constitute the pathways of sensitivity. , and that, incorporated into the central nervous system, they will follow private courses until they reach higher structures to become aware or remain at lower levels to induce reflex reactions.

The sensitivity, that is, the impression that any stimulus produces in the body, is not always the same, and depends on the physicochemical characteristics of the stimulus and to a lesser extent on the stimulated pathways. There is a special sensitivity, that of the senses, whose stimuli are waves that specifically act on special receptors, such as sight and hearing, or are particles capable of giving sensations of taste and smell. The sensitivity that comprises the sense of touch is called general sensitivity and its sensations are not uniform, because some different forms are easily distinguished, such as superficial touch - the simple impression that produces an instantaneous stimulation on the skin, cold, heat and pain, which are modalities identifiable by any individual; All of these are grouped into what is called superficial sensitivity, because it is basically cutaneous, or exteroceptive, or protopathic or non-discriminatory. But there is another type of sensitivity, the deep, or discriminatory, or epicritic or proprioceptive, which is what allows us to capture differences in weight and size, vibrations (vibratory sense or paresthesia), and the positional sense or conscious proprioception, which reveals the position of a limb or one of its segments in space due to particular and muscular sensitivity. Furthermore, it makes it possible to recognize two separate and close points on the skin — discriminative touch — and to distinguish the quality of objects — shape and texture — by touch without the aid of sight, or stereognosia. Both types of sensitivity, perfectly differentiable in their physiological and psychological aspects,

The stimuli initiated inside the body's cavities give impulses that constitute the afference of the vegetative or autonomous system, carried in their final part by the same routes of general sensitivity; remember that the motor part of this autonomous system has its own individuality, since it is clearly separated from the central nervous system, in its ortho and para-sympathetic portions. These fibers correspond to enteroceptive or visceral sensitivity.

In other words, sensitivity can be divided into the following classes:

1. Special sensitivity
2. General sensitivity:
   • superficial
   • deep
3. Visceral sensitivity

In this chapter we will deal exclusively with general sensitivity.

Anatomy and Physiology

For a long time it was accepted that each type of sensitivity was related to certain skin formations, known as corpuscles of different names. Today it is estimated that there is no such specificity of the receptors and it is only believed that the free endings are closely related to pain and that the Pacini corpuscles are capable of being specifically stimulated by compression and deformation.

The afferent pathways, which in any case begin at the level of these formations, constitute the sensory fibers of the peripheral nerves, either exclusively, or in the superficial or cutaneous nerves, which transmit only superficial sensitivity, or more frequently mixed with the motor fibers in the mixed nerves. All the sensory fibers are the peripheral extensions of the T-node cells, the first neuron of all kinds of sensitivity, and which settle in the node of the posterior root; in cranial nerves of general sensitivity — basically, the trigeminal or V pair — the first neuron is in the semilunar or Gasser's node only

The peripheral distribution of sensitivity is perfectly known; the posterior or sensory roots exit the marrow in stages, to join the anterior or motor roots and form the spinal nerve, which is distributed in such a way that each cutaneous segment in relation to an embryological metaphor corresponds to a specific root; This metameric distribution is well schematized and today agrees with Keegan that each one reaches the posterior midline since the posterior branches of all the spinal nerves supply skin regions. Some roots, such as the thoracic ones, are arranged directly in the body, but most, at the level of the limbs, intermingle forming the plexuses that will have collaterals and will give rise to the peripheral nerves, almost always with fibers from more than one root . As a consequence of the superposition and intermingling of fibers that is thus produced, the root, plexual and peripheral distribution will be different and the anatomical knowledge will allow locating the probable alteration; however, there are schemes that facilitate clinical examination, which can also be assisted with complementary electrical diagnostic methods.

In practice, it is interesting to recognize certain milestones of the root metameric distribution to guide a better diagnosis of lesional location; thus, the shoulder corresponds to C5; the outer edge of the arm to C6 and the inner edge to C8; the areoles to D4, the navel to D9, the groins to D12-L1 and in the lower limbs the arrangement is helical, beginning in front and in such a way that L5 corresponds to the internal edge of the foot and S1 to the external one; from there, the metamers continue on the back of the limb and the last ones are related to the perineum.

The central extensions of the T ganglion cells form the posterior root of the spinal nerves and follow different paths in their ascent towards the centers, according to the kind of sensitivity they lead.

The various types of superficial sensitivity, carried by the thinner fibers, enter through the outermost part of the root and enter the spinal cord, where they divide into a descending and an ascending branch that participate in the formation of the dorsolateral or Lissauer, located in the part adjacent and external to the posterior body. The ascending fiber goes up some segments - plus the fibers of tactile sensitivity - and enters the posterior horn where it connects with neurons located in the striated Rexed layers, where the second neuron of the pathway sits; the axons of this second neuron are directed forward and inward to intersect with those on the other side in the gray commissure and bend upward as they reach the outside of the anterolateral cord and form the ventral spinothalamic bundles (of superficial tactile sensitivity) and dorsal (of thermoalgesic sensitivity), with pain fibers located at the most posterior part. Backwards, these bundles do not extend beyond the insertion of the dentate ligament in the medulla —a repair of great surgical significance— and are systematized in such a way that the fibers that come from the highest levels are placed inside the most inferior, which are then closer to the medullary surface. with the pain fibers located in the most posterior part. Backwards, these bundles do not extend beyond the insertion of the dentate ligament in the medulla —a repair of great surgical significance— and are systematized in such a way that the fibers that come from the highest levels are placed inside the most inferior, which are then closer to the medullary surface. with the pain fibers located in the most posterior part. Backwards, these bundles do not extend beyond the insertion of the dentate ligament in the medulla —a repair of great surgical significance— and are systematized in such a way that the fibers that come from the highest levels are placed inside the most inferior, which are then closer to the medullary surface.

In the medulla oblongata, the spinothalamic bundle retains its lateral position and is separated from the Reil band by the bulbar olive; In the lower part of the protuberance it will be attached to the outermost portion of the tape to continue together through the midbrain and end in the posterolateral ventral nucleus of the optic thalamus, seat of the third neuron of all the fibers of sensitivity.

The path of painful sensitivity deserves a separate comment, given that, due to its clinical significance, a series of studies of great interest have revealed important aspects of its physiology.

Pain is a defense of the organism against any eventuality that threatens its integrity. Two types of pain can be recognized: a fast or instantaneous pain, well localized, born in the most superficial layers of the skin as a result of something that crosses them; and another slower, more diffuse and that extends over time. The fibers that transmit both types of pain are different; rapid pain is carried by fine myelin fibers (A delta) and the other by myelin fibers (C). Both are the thinnest of the sensory fibers and after their station in the posterior root ganglion they reach the posterior horn, the Rolando's gelatinous substance, where they make multiple synapses with intercalary cell fibers and with collaterals of the thicker fibers of the posterior cord; and it is not known whether directly or not,

The complexity of all these connections is evident, but the real thing is that they exert, among other effects, a very important inhibitory component on this second neuron; and this effect seems to be the physiological support of the satisfactory results obtained by electrical stimulation of the nerve trunks or the posterior cord for pain relief. Likewise, it is believed that this type of sensitivity ascends by two differentiable pathways: 1) the neospinothalamic beam, which is the one described, and 2) the multisynaptic paleoespinotaamic beam, which would transmit slow pain and make numerous stations at the medullary and brainstem level, and it would end in the intralaminar nucleus of the thalamus; from there its connections would be multiple, towards the frontal and temporal lobes, the limbic gyrus and the hypothalamus,

Other important data derived from pharmacological investigations; studying morphine, it was concluded that there were cells capable of incorporating this drug into its membrane, and that pain would be calmed by this mechanism; then drugs that antagonized this effect were found, such as naloxone. Subsequently, substances were discovered in the body — endorphins and enkephalins, globally — that repeated the morphinic effect. The different areas of the brain and trunk were studied by biochemical methods and the accumulation of these substances in regions similar to those related to morphine and also linked to nuclei that, electrically stimulated, brought analgesia, was verified. It was then postulated that said substances would be or function as neurotransmitters and that, Located in some nuclei of the periaqueductal gray matter, the central raphe and the reticular area, they would descend through the reticulospinal or corticospinal pathways to the second-order neurons of the posterior horn and would cause an inhibitory effect on pain. These facts, mentioned very briefly, reveal the complexity of the pain problem.

The fibers of deep sensitivity are thicker than the previous ones and, after forming the innermost part of the posterior root, they enter directly into the posterior cord, collateralize cells of the posterior horn, as we have already seen, and then ascend; as fibers from more proximal regions enter, they are placed more externally with respect to the previous ones; In addition, from the mid-dorsal level a longitudinal groove appears, without clinical significance, that divides the cord into two bundles, one external, Burdach and the other internal or Gol !. The fibers end in the second-order cells, in two nuclei, of Goli and Burdach, which occupy almost the entire height of the bulb. Their axons cross at the midline and ascend behind the pyramidal path, forming the middle Reil ribbon;

The sensitivity of the face is conveyed by the trigeminal or V pair; a few sensory fibers from cranial nerves VII and IX terminate in the central trigeminal nuclei. This nerve, which is divided into three peripheral branches, has its primary neuron in Gasser's ganglion, located on the upper face of the rock; the axons of its cells form the trigeminal sensory root that enters the trunk in the medial part of the protuberance, outside the thinnest motor branch of the same nerve, which supplies the chewing muscles. These fibers enter the protuberance and some end their journey in the trigeminal main nucleus, while fibers related to superficial sensitivity bend downward and form the trigeminal descending root, close to the bulbar surface below the restiform bodies and extending to the C4 level in the medulla. In its internal part there is a cellular formation, the nucleus of the descending root, which continues upwards similar structures of the posterior horn (gelatinous substance). There the fibers of the first neuron of superficial sensitivity end with a particular arrangement, since those corresponding to the innervation of the highest parts of the face and painful sensitivity end more inferiorly in the nucleus, from where the axons of the second neuron to form the trigeminal ventral and dorsal secondary bundles that, after a fairly complicated journey, will join the Reil ribbon to end in the posteromedial ventral nucleus of the thalamus. These fibers make numerous connections at the level of the brain stem, the basis of the numerous reflexes related to the face. It is also interesting to note that the fibers of the deep sensitivity of the face end, not in Gasser's ganglion, but in the trigeminal mesencephalic nucleus, which has ganglion-like cells and seems a structure that has not migrated in the corresponding embryological period ; its axons end in the main trigeminal nucleus, from where the path continues as described. that it has ganglion type cells and looks like a structure that has not migrated in the corresponding embryological period; its axons end in the main trigeminal nucleus, from where the path continues as described. that it has ganglion type cells and looks like a structure that has not migrated in the corresponding embryological period; its axons end in the main trigeminal nucleus, from where the path continues as described.

The axons of the third neuron, located in the thalamus, are directed towards the cerebral cortex by means of the thalamic projection that ends: 1) in Brodmann's areas 1, 2 and 3, the primary somatosensory zone, behind Rolando's groove and with a somatotopic organization similar to the motor region, with the lower parts of the body projecting to the upper part of the gyrus, and even on the internal face of the hemisphere; and the face in the lower part; 2) in a secondary somatosensory zone located at the bottom of the upper lip of Silvio's fissure and with a specific location, in which the anterior part of the region corresponds to the upper body and 3) the upper parietal lobe, areas 5 and Brodmann's 7, without somatotopic organization.

Studies have shown that stimuli related to sensory discrimination reach the primary zone and that higher-level integrative processes are established in the parietal region; It seems proven that the most elemental sensitivities, such as pain, can be raised at the subcortical level if the thalamus is intact, and that the most highly discriminatory functions require cortical integrity. To end this topic, we must remember that all the cortical regions emit an important efferent projection destined to the sensitive nuclei of all levels, which would serve to regulate and modulate the quality of the primary sensation.

Sensory disturbances

Alterations in sensitivity can be subjective or objective. Of the former, the most significant is pain, which has deserved a special chapter in this book due to its medical importance and physiological interest. Another frequent discomfort is an unpleasant sensation that is perceived in the areas of distribution of the nerves, almost always distally, such as tingling or pricks that the patient recognizes as similar to those experienced after local anesthesia, especially dental; They are paresthesias, which when they acquire a frankly unpleasant character are called disesiestas, although in reality both terms are synonyms. There may be a burning sensation, which in causalgias has very special aspects, and may be spontaneous or caused by tactile stimulation.

Objectively, one can find decreases in sensitivity, which are globally known as hypoesthesias, or anesthesia when sensitivity is abolished; If it refers to pain, it refers to hypoalgesia or analgesia. Although there are other specific names for the alterations of the other types of superficial and deep sensitivity, in practice it is preferred to clarify the type of modified sensitivity, without using the technical term, with the exception of the abolition of stereognosia, which is called astereognosia. . Extinction of the stimulus, which is actually a sign and not a symptom, is of great locator value in parietal lesions. When there is an increase in sensitivity, there is talk of hyperesthesia and when any stimulus causes a painful sensation, there is said to be hyperpathy.

Sensory syndromes

The diversity of the types of sensitivity, the specificity of its pathways and the length of its path make it feasible that at any level of the nervous system, sensory changes can be verified with particular characteristics that contribute to the localization diagnosis. We will describe the different syndromes that are recognized according to the level of the injury.

1. Peripherals:
   1. When an exclusively sensitive peripheral nerve is injured, therefore a decrease or abolition of sensitivity occurs in its distribution area; the tactile one will be more extensively affected than the painful one, by the greater superposition of the fibers of the latter one. In the compression processes, the tactile fibers suffer more intense and early than the painful ones, contrary to what happens in local anesthesia, where there may be a total analgesia with maintenance of touch. In these cases, deep sensitivity,which runs through the mixed deep nerves, is unchanged.
   2. When the lesion is of a mixed nerve, the aforementioned disorders are compounded by the motor components of that nerve, with a practically constant peripheral distribution, and alterations in deep sensitivity.
   3. In multiple lesions of the peripheral nerves, the individual alterations of each of the affected nerves are added together.
   4. In polyneuropathies, the process takes most of the peripheral nerves bilaterally and symmetrically, with alterations that predominate at the distal level, because the longest fibers are the most exposed to the different noxes; There is usually pain and the sensory alteration takes the form of glove or stocking anesthesia with imprecise upper limits. The motor component is almost constant, with the exception of purely sensitive polyneuropathies, which are less frequent and will be discussed in a separate chapter.
   5. In multiple mononeuropathies, two or more peripheral nerves are affected, distant from each other and with the semiological characters referred to in each one.
2. Plexuals: The disorders are practically always mixed, sensitive and motor and appear multiple lesions of peripheral nerves; but due to the intermingling of the fibers and the emergence of plexus collaterals, they can be differentiated by means of a careful clinical examination, supported by solid anatomical knowledge and aided by comparative distribution schemes of roots, plexuses and nerves and by electrical study.
3. Root: The posterior roots may be individually injured by some limited process, the best example of which is a herniated disc, and their involvement is revealed by hypoesthesia reduced to only part of its metameric distribution, both tactile and painful; There is usually radicular pain, with exacerbations with exertions such as coughing and sneezing, and motor involvement that is revealed by weakness, areflexia and atrophy. If several roots are affected, the disorders of each add up.
4. Medulars: There are numerous syndromes, due to the complexity of the spinal systematization.
   1. Complete sección: They are fundamentally traumatic cases or, by exception, terminal in the evolution of chronic spinal compression. There is a sensitive level, corresponding to the height of the lesion and from that limit downwards a disappearance of all types of sensitivity; At the level of the lesion, some differences between the types of sensitivity are described, but in practice they lack true clinical significance. Naturally, there is paraplegia and sphincter disorders.
   2. Incomplete section: The persistence of some form of sensitivity below the lesion will depend on the lesion anatomy; but the important thing is to know that, in progressive pictures, when the tumor is extramedullary, the sensitivity is lost in an ascending direction until reaching the lesional height, because the marrow is compressed from the outside and the spinothalamic bundles have their systematized fibers, with the lowest on the surface. If the tumor is intramedullary, intrinsic to the medulla, the process is reversed and the sensory alteration begins at the level of the lesion and gradually descends. Almost constant motor components and pain are added to these pictures, which in the extramedullary ones is frankly of the root type and indicates the height of the lesion.
   3. Medullary hemisection or Brown-Séquard syndrome: Its most typical form is seen in stab wounds, but a similar picture is recognized in some unilateral injuries at some point in their evolution; it consists of the abolition of deep sensitivity on the homolateral side —where there is also direct hemiparesis— and preservation of thermoalgesic sensitivity on that side and frank decrease on the opposite side, since the pathways have crossed under the lesion; the touch is preserved, because in its different forms it passes through the anterolateral and posterior cords.
   4. Posterior cordonal syndrome: Due to degenerative causes, often of a vitamin deficiency origin, the posterior cords are injured and therefore deep sensitivity, especially the vibratory and positional sense, has been abolished; thermoalgesic sensitivity is preserved. The tabétic syndrome, of lutic etiology, due to injury to the innermost part of the posterior roots, is similar, but it adds other disorders derived from its etiology, although some other diseases, such as diabetes, can simulate it. In these pictures there is also hypotonia and areflexia.
   5. Anterior cordonal or anterior spinal artery síndrome:  It is due to obstructions of this artery or to compressions of the anterior part of the medulla, and consists of the abolition of thermoalgesic sensitivity with preservation of the deep; There is almost always paraplegia, because the motor bundles are supplied by this artery. It is important to keep this table in mind in cervical trauma, since it indicates the existence of an acute herniated disc and constitutes an urgent surgical indication.
   6. Commissural, medullary gray or syringomyelic syndrome: It is produced by syringomyelia, a degenerative process that consists of cavitation of the central part of the medulla (sometimes settling in the bulb: syringobulbia) and which is sometimes simulated by hematomyelia or an intramedullary tumor. Due to the section of the fibers that intersect at the level of the gray commissure and that will form the spinothalamic bundles, there is a suspended anesthesia at the level of the lesion —especially cervical—, of thermoalgesic sensitivity and with indemnity of deep sensitivity; when cavitation increases it can compress neighboring regions, giving atrophy or paresis.
5. Trunk: In this location, the sensory disturbances are dissociated by exception - since from the low protuberance level, the Reil tape carries all types of sensitivity - and they are added to the vast symptomatology of cranial nerves. motor, extrapyramidal and cerebellar bundles, which cause a large number of syndromes with very different names and different clinical significance. Due to its frequency, we will remember Wallenberg syndrome, due to vascular injury, which is characterized by anesthesia of the ipsilateral side of the face and crossed hemianesthesia, due to injuries to the trigeminal and spinotaiic pathways, respectively. Very rare cases of dissociation between superficial and deep sensitivity in low bulbar lesions are described, when both modalities are separated by the bulbar olive.
6. Thalamic: They obey an injury, almost always vascular, of the posterolateral nucleus, where all sensitivities end; there is hypoesthesia or anesthesia for all sensitivities on the other side of the body that, when it improves, almost always causes the classic spontaneous thalamic pain, which increases with stimuli, is burning and is related to the patient's emotional state. The complete Déjérine-Roussy syndrome is made up of. a) contralateral sensory deficit; b) contralateral hemiparesis, often fleeting; c) hemiataxia and homolateral choreoathetosic movements; d) Claudio Bernard-Horner syndrome; e) perspiration disorders; f) psychic disorders, and often contralateral hemianopsia
7. Cortical:  Due to parietal lobe injury, there is alteration of deep sensitivity and especially of the most discriminating functions, astereognosia being observed on the contralateral side, with greater preservation of superficial sensitivity. There may be coincident signs of cortical arousal, such as tactile hallucinations and epilepsy with a sensory aura; the history may be changeable and on examination it is possible to find very localized lesions that make interpretation difficult. There is almost always a fairly incongruous lower quadrant hemianopia and there is the phenomenon of extinction of the stimulus.
   Differences between both lobes are described, apart from and in addition to the typical alexia due to injury to the angular gyrus on the dominant side. On the non-dominant side there is an altered perception of the opposite side, without recognition of the position of the body and its parts in space, and denial of everything that is on the opposite side and of the deficit itself, even if a complete hemiplegia is added. This picture, known as anosognosia, could exist on the dominant side, but the concomitant aphasia prevents its recognition. However, on the dominant side, Gerstmann syndrome is described, where there is agraphia, acalculia, inability to distinguish between both sides of the body, and lack of recognition of the fingers and toes; apraxia can be added and it would be a true agnosia with ignorance of many symbols.
8. Psychogens: They are usually not directly referred to or linked to paresis; In the examination, modifications unrelated to any known pattern can be found, and anesthesia in a stocking or glove is common, with the characteristic that they make very clear edges, unlike organic processes.