Juan Pablo Recagno Cepeda, Carlos Ballario

Balance is a state of matter in which opposing forces counteract each other; in the body, it allows you to maintain certain postures and attitudes that facilitate the development of your normal activities, either in static or dynamic situations such as walking. This balance, considered by some authors as a complex sensation in higher organisms, is not really such, since there is no impression of "normal equilibrium as it occurs with other somatic sensations, it only becomes conscious when the system is excited. It would function as an element of non-equivalence, which means that it does not discharge as long as it is not stimulated or as long as the stimulations it may receive through different routes remain coordinated and congruent, within the framework of normality; when some inconsistency occurs in such inferences, the sensation of imbalance or "imbalance" would occur. Balance «depends on the brain integration of a series of afferent stimulations that act at the level

Subconscious and reaching the centers through three channels:

1. the sense of sight, which allows the spatial location of the object seen, its relationship with the subject and its relative displacements, and informs about the position and movements of the body and the space that surrounds it;
2. the general proprioceptive system, which, when capturing pressures through cutaneous and deep receptors, relates the individual to the plane of space referring to the force of gravity and the difference in the positions of the different parts of the body relative to each other and in its relation to space. All this system is essential for the correct execution of any reflex, postural or voluntary movement, and in this sense it is the proprioceptors of the neck that inform about the position of the head in relation to the rest of the body;
3. the vestibular apparatus, whose input is the most important and which functions as an accelerometer, detecting changes in the speed of movements and reporting on the position of the head and body in space, and orienting the organism in its relation to the gravity.

The cerebellum is the only predetermined system of the nervous system, capable of preparing the body to compensate for an alteration that will happen immediately; the other related centers of the neuroaxis are coordinators and facilitate the postural adjustment, of the erect position and locomotion.

All this allows the organism to coordinate its body schema with the environment, which is essential for normal operation.

When alterations occur in the afferences of any of these three basic systems, the subject will be unbalanced; In general and from now on, we can say that, when it depends on a disease of proprioception, it is usual that there are concomitant symptoms and signs of deep sensitivity and that the patient refers his discomfort to his "heavy legs"; Aggregated diplopia is frequent in visual conditions, while in vestibular lesions the disorder is frankly referred to as a problem related to the head.

Anatomy. The vestibular apparatus is formed by the membranous labyrinth, a cavitated structure lodged in the inner ear of the rock, within the bone labyrinth and separated from it by a liquid called perilymph; It is occupied by another liquid, the endolymph, whose movements — related to movement or position — cause stimulation of the sensory endings.

From the anatomical point of view it is closely related to the hearing apparatus; It is made up of the three semicircular canals, oriented in the three planes of space, whose two ends end in the utricle; one of them does it by means of an ampullary dilation, the ampoule, where a ciliated structure of specialized cells is found, the amputar crest, excitable by the displacement of the endolymph. In addition, there are two sacs: the utricle, where the semicircular canals open, and the saccule, linked together by a duct and the latter also to the snail. On one of the walls of these saccular structures there is a specialized endothelium, oriented in two different planes of space, acoustic spots or macules, formed by hair cells covered by a gelatinous mass where there are numerous and tiny calcium carbonate crystals; changes in the position of the head modify the pressure that these otoliths exert on the acoustic spots and originate impulses that reveal the position of the head in space in relation to gravity; this is an undoubtedly utricular function, and as for the saccule, its probable connection with hearing is discussed. In the aforementioned specialized structures, the distal fillets of the Scarpa ganglion bipolar cells are connected, whose central extensions form the vestibular nerve. This nerve leaves the internal auditory canal with the cochlear fibers, which carries the sense of hearing, and both form the pair or auditory IHV, which passes through the cerebellopontine angle and enters the brainstem through the bulb-protuberance groove; from there, the two branches of the VIII pair are divided in their intraxial route to end in different nuclei. The fibers of the vestibular nerve do so in four nuclei: lateral, superior, median, and descending; some fibers do not synapse at the bulbar level and end in the fastigionodular lobe of the cerebellum, from where they project to the vestibular nuclei of the bulb, a circuit that seems to be the basis of a feedback system of great physiological importance, as perhaps it is the anatomical substrate of the default role of cerebellar function. The fibers of the vestibular nerve do so in four nuclei: lateral, superior, median, and descending; some fibers do not synapse at the bulbar level and end in the fastigionodular lobe of the cerebellum, from where they project to the vestibular nuclei of the bulb, a circuit that seems to be the basis of a feedback system of great physiological importance, as perhaps it is the anatomical substrate of the default role of cerebellar function. The fibers of the vestibular nerve do so in four nuclei: lateral, superior, median, and descending; some fibers do not synapse at the bulbar level and end in the fastigionodular lobe of the cerebellum, from where they project to the vestibular nuclei of the bulb, a circuit that seems to be the basis of a feedback system of great physiological importance, as perhaps it is the anatomical substrate of the default role of cerebellar function.

The vestibular nuclei also include proprioceptive afferent fibers, especially from the neck, in addition to those already reported in the cerebellum, and fibers of higher levels and origin in the same brain stem, predominantly from the posterior longitudinal band. The fibers originating in the vestibular system have multiple destinations; some, undoubtedly important, will reach the cortex in areas not yet well established, but which appear to be in the superior and posterior parietal or temporal region near the cortical center of hearing; others are linked to the hypothalamus and the vegetative nuclei of the brain stem, causing the intense autonomic reactions typical of vestibular injury, others more reach the limbic system, which explains the particular feeling of displeasure that characterizes the symptoms of these symptoms. Many are incorporated into the longitudinal band, connecting with the oculomotor nuclei, a relationship that is very important both clinically and experimentally. Finally, some go to the cerebellum and others descend to the medulla by the vestiouloespinal bundles that end in the Rexed anterior layers of the gray antlers.

Symptomatology

Before describing it in detail, it is convenient to specify two facts of practical interest:

1. the anatomical proximity, in the middle ear, of the vestibular system with the hearing organ, which makes the concomitance of symptoms frequent and which always requires a complete study of hearing against any disorder attributable to balance;
2. the particular characteristic that the compensation and habituation phenomena adopt in the vestibular system, which although they are a general peculiarity of organisms and especially of the nervous system, is of considerable interest in this case as it explains the relatively rapid disappearance of the symptoms despite the persistent injury persisting; It is a complex phenomenon, which requires, in the vestibular system, a central participation and the indemnity of the cerebellum.

The fundamental symptoms of the vestibular system are vertigo, which is the sensation of movement of the surrounding environment or of itself (objective or subjective vertigo, respectively), and which is produced by a compromise of the semicircular canals; and the drive or sensation of being pushed to one side, of utricular cause. Usually together, they have greater intensity the more peripheral the injury to the vestibular pathway, but they present in compromised pathways at any level.

Vertigo is divided, in turn, into peripheral and central.

Peripheral vertigo.

It is due to a lesion of the first neuron and is usually acute, of great intensity, with a sudden onset and regressive evolution. It is, as Brain says, a conscious perception of disordered orientation of the body in space, a hallucination of movement; the subject has the impression that things rotate around her, usually to a certain side, in an acceleratory movement; but this sensation of movement may not only be rotational, but also horizontal, vertical, oblique; or when the eyes are closed, it seems that the body turns, falls or is lifted or pushed or lowered, as if it were in an elevator; and all referring to the head, which the patient recognizes as the truly affected body segment. In a violent attack, you can fall to the ground, without losing consciousness. This painting, undoubtedly dramatic, it forces the patient to remain in strict rest (since any mobilization of the head worsens it), with the eyes closed and in a position in which the discomfort is less, almost always in lateral decubitus with the affected ear down. There is always a clear vegetative component, with nausea, vomiting, paleness and perspiration, and a clear psychic aggregate with displeasure and frank anguish. The patient refuses to be mobilized for the examination, which, when it can be carried out, will reveal an intense peripheral-type nystagmus towards the opposite side, deviation of the indexes and inability to stand up with falls towards the affected side. There are usually various types of hearing components: ringing, hearing loss, deafness. This sudden, variable intensity picture tends to improve rapidly, for the compensation phenomena are established early; By 48 hours the discomfort has clearly decreased and by the week — and sometimes before — the individual may start to wander, complaining of some dizzying sensation when moving his head; after a month, the patient only presents some discomforts, which he basically refers to as imbalance, insecurity and drive to one side; can manifest oscilopsia »which is the sensation of movements of things when walking or when moving the head; all discomforts that tend to disappear. the patient only presents some discomforts that he basically refers to as imbalance, insecurity and drive to one side; can manifest oscilopsia »which is the sensation of movements of things when walking or when moving the head; all discomforts that tend to disappear. the patient only presents some discomforts that he basically refers to as imbalance, insecurity and drive to one side; can manifest oscilopsia »which is the sensation of movements of things when walking or when moving the head; all discomforts that tend to disappear.

Central vertigo.

It is due to an injury to the vestibular pathways within the neuroaxis and has characteristics similar to those indicated for cases of peripheral vertigo in frank regression, namely: discreet dizzying sensation, which here does not improve when closing the eyes or worsens when moving the head; insidious onset, irregular intensity and prolonged duration, without acoustic aggregates and sometimes with symptoms or signs of the brainstem and a component of dislike very different from the anxiety of the acute episode. There is also, and perhaps as the most important symptom, a feeling of imbalance, with some drive to one side, which brings an annoying insecurity to the patient.

The differentiation between a regressing peripheral vertigo and a central vertigo can be difficult and that is why the anamnesis is essential to determine the acute antecedent, which, with functional tests, will confirm the diagnosis.

Central vertigo, the fundamental characteristic of which is imbalance with some added sensation of movement, is frequently described as dizziness. This term is very indefinite and is used as an explanation for many very different symptoms; hence the importance of practicing a detailed anamnesis to pin down, define, and classify the true meaning of the discomfort afflicted.

The sickness can be defined as sensation that causes some discomfort or distress vaguely, and although among them can involve vertigo, especially the central, actually it comprises discomfort such as empty head, sensation of floating in the air, instability , mental or visual clouding, fleeting loss of consciousness, dizziness, etc. Before a patient who complains of dizziness, it will be necessary to determine:

1. if it is central vertigo, as has been described, with its component of imbalance and slight movement, and in which functional tests will confirm the diagnosis, although in highly compensated conditions, the examinations may be normal;
2. if the patient makes a mistake, because he ignores the meaning of the term, and gives that name to an episode with well-defined clinical characteristics, such as a small epileptic illness, a temporary absence, syncope, etc .;
3. if the instability that it refers to is due to a true ataxia, as in deep sensitivity injuries, to paresis due to motor weakness, or to an anteroposterior drive typical of extrapyramidal symptoms;
4. if we are in the presence of nonspecific dizziness, diffuse sensations where instability predominates and in which functional tests are normal: these cases are usually vascular, as in anemia, postural hypotension, vertebrobasilar insufficiency;
5. if they are psychically caused, easily reproducible by hyperventilation, although we must remember that the unpleasant nature of the imbalance and its connection with the limbic structures, always provoke psychic reactions of anxiety and worry.

To end this chapter, we are going to define and clarify the most important sign of vestibular disorders, nystagmus, consisting of repetitive and involuntary eye movement. They are divided into:

1. Vestibular or spring nystagmus, that they have a slow phase towards the injured deficit side, dependent on the vestibular apparatus (and that needs occipital compensation); and a rapid correction phase, attributed to reticular formation. It is horizontal, rotary or oblique and of fixed direction, that is, it always appears or predominantly towards the same side, preserving its characteristics; the vertical nystagmus is always of a techtal origin. Peripheral stimulation tests will clarify some of its characteristics and it is essential to perform them to determine if a nystagmus is of central or peripheral origin. In peripheral nystagmus, quantitative alterations will be observed in the tests * (especially unilateral hypo or areflexia), while in the central ones, basically qualitative modifications will be detected:
2. Gazing nystagmus, which are not seen in the primary position but are seen in the lateral positions (and even in the vertical ones); They beat in the direction of the gaze and can be: a) of toxic origin, bilateral and symmetrical; b) cerebellar, which are better perceived towards the injured side and with atypical characters that simulate central vestibular nystagmus; and c) paretic, related to the lesion of the lateral, wide, irregular and predominant or exclusive centers of lateral gaze towards the parenchymal side.
3. Ocular nystagmus or definition, which are pendular , that is, with their two equal phases; they are seen in congenital, occupational cases, in the nutans spasm, in postoperative, etc.

Etiology of dizziness and vertigo

Vertigos can be classified into two large groups, peripheral and central, whose characters we have already mentioned; There are also some entities whose link with the vestibular system is not very clear but whose symptoms deserve to be considered.

Peripheral vertigo

They are produced by lesions of the first neuron or at the level of its peripheral receptors.

Headphones. They are fundamentally acute and have a very clear beginning, and include the following tables:

1. Infectious processes of the ear. These are those that directly or secondarily compromise the labyrinth and cause vertigo; the symptoms are usually subacute and there is a clear signology of the causal process. In some infectious or viral diseases — parotitis, for example — there may be occasional dizziness, which is attributed to toxic involvement of the labyrinth.
   
   
2. Méniére's disease.It consists of episodes of not long duration - from minutes to hours, up to 24 hours of violent vertigo, almost always preceded by deafness and intense pain in the affected ear with a sensation of cephalic and auditory fullness, although it can rarely happen without prodromes. During the attack there is all the leafy symptoms of acute vertigo and sometimes the abruptness of the beginning makes the subject fall without loss of consciousness; recovery is rapid, and a slight instability of movement persists for a relatively short time. Its fundamental characteristic is that it repeats with unpredictable variable intervals, and its spontaneous and definitive disappearance has been seen in a few cases. Cochlear function study reveals progressive perceptual hearing loss with recruitment, which demonstrates the commitment of the organ of Corti; Vestibular tests also reveal a net hypoexcitability with great variability in subsequent examinations. The condition is progressive, leads to deafness, becomes bilateral in 15% of cases — sometimes it is so at the outset — and is due to idiopathic dropsy of the labyrinth whose pathophysiology is not yet fully elucidated.
   
   
3. PseudoMéniere. There are recurrent vertigo tables with aspects similar to those of Méniére's disease, but where there are no abnormalities in the complementary studies. Sometimes a benign positional vertigo is added, a term whose use has become too widespread and which is applied indiscriminately against any vertigo with an unclear cause; However, it is interesting to note that some of these pictures have ended up agreeing to a true Méniére disease.
   
   
4. Vestibular neuronitis. It is a picture of intense vertigo without a cochlear component * that tends to improve in a relatively short time, from days to weeks; the cure is final, but sometimes relapses are found. In the vestibular tests there is a deficit of variable degree and the inexcitability of the labyrinth affected in the galvanic test occurs, as pathognomonic data. It is usually seen after infections of the rhinopharynx or upper respiratory tract and, as it can appear epidemic, it has been called epidemic neuronitis and previously acute labyrinthitis. It is believed to be due to a scarpa ganglion injury.
   
   
5. Vestibular death or sudden vestibular areflexia. It constitutes the best example of intense peripheral vertigo and the one used for its classic description. It is of vascular origin due to the occlusion of the arteries of the internal ear, the internal auditory or its branches; if the arterial trunk is affected, it is accompanied by definitive deafness, but if the injury is more limited, there may be cochlear indemnity together with definitive vestibular inexcitability; evolution, anyway, is towards improvement, by compensation mechanisms.
   
   
6. Benign positional paroxysmal vertigo.Any vertigo, at some point in its evolution, can appear exclusively when changing the position of the head. However, this picture is seen in middle-aged people, without an acute history and especially at bedtime or upon standing up; it lasts less than a minute and can be reproduced by repeating the movements that provoke it, there are regulated techniques for this purpose; it is exhaustible, that is, it is increasingly difficult to obtain, it has a latency of around 20 sec. and it coincides with a rotating nystagmus that changes direction according to the position of the head. It is a benign condition with a tendency to cure, but which can become chronic. The responses to caloric stimulation are almost always normal. This picture has been described as a consequence of otological processes, trauma, cervical injuries, of psychic problems. It must be differentiated from a similar picture of central origin, due to organic lesions of the brain stem, where the nystagmus appears immediately, without latency, is not exhaustible (that is, it persists as long as the head position is maintained) and has the appearance of central type.
   
   
7. Lesions of the cerebellopontine angle.Acoustic neurinoma is the most frequent (80% of cases), but it can be caused by aneurysms, cysts, other tumors, etc. Injury to the VÍÍI par causes progressive hearing loss of the neural type without recruitment that leads to deafness in a variable time, which can reach 20 years; and it also produces a vestibular lesion, which rarely brings net vertigo, but which in half of the cases is accompanied by instability, especially in position changes; there is continuous, variable type nystagmus thought to be due more than compression of the nerve itself to compression of neighboring structures. The study found the hitherto frequently inadvertent cochlear involvement (80%) and the total hypo or inexcitability of the labyrinth on the affected side (95%). Later other location symptoms will be added, very typical. In a small percentage of cases, the tumor is bilateral, almost always due to Recklinghausen's neurofibromatosis. When some of the data described are not verified in the order and quality expected, consideration should be given to the possibility that it is a different process from the neurinoma.

Vertigo and dizziness of central origin

They are produced by alterations in the central connections of the vestibular system. They will be commented according to whether the alteration is located in the following sectors:

1. Brain stem. They are the typical central vertigos already described, which are often accompanied by an added symptomatology that facilitates the diagnosis, such as Parinaud syndrome, intemuclear ophthalmoplegia, lateral gaze paralysis, etc. Multiple sclerosis may have them as the only symptom for a period of time; therefore, its inexplicable persistence in young people should make the disease suspicious and investigate it. Tumors can occur, with headaches and vomiting that are not coincident, but previous, and sometimes positional, with the characteristics of central vertigo already mentioned. Vascular injuries will be referred separately.
   
   
2. Cerebellum. It is doubted that there is a true cerebellar vertigo, since injuries with great ataxia are not accompanied by this symptom. When it appears, it is believed to be due to compromise at a distance, although some attribute it to alterations in the flocculonodular lobe. Its characteristics have already been pointed out.
   
   
3. Brain.Subcortical lesions do not give it, although they can produce pulses in the anteroposterior direction. In the cortex, injury to the undetermined areas of the vestibular system — parietal and posterior temporal — can give focal epilepsy with an intense and rotatory vertiginous aura; when the picture is not completed with a seizure, which is what defines the diagnosis, it should be suspected in cases of recurrent paroxysmal vertigo without cause or relation to movements, since they sometimes appear at rest; the electroencephalogram is usually abnormal and the labyrinth functional tests are normal. In exceptional cases, very intense vertigo can be accompanied by unconsciousness and even convulsions; it would be a vestibulogenic reflex sensory epilepsy,
   
   
4. Marrow. Arguably, they will be discussed when talking about cervical vertigo.

Other tables linked to vertigo

1. Vertigo of vascular origin. It is common that various circulatory processes are sometimes manifested by dizziness, such as hypotension from any cause, Stokes-Adams syndrome, aortic stenosis, etc. But here we will refer to the cerebral vascular processes:
   1. Due to global cerebral circulatory failure. It is seen in young people with orthostatic hypotension or in old people with arteriosclerosis due to poor vascular adjustment; Above all, there is instability and blurred or blurred vision, more than true vertigo.
   2. Due to vertebrobasilar insufficiency. Very common, due to vascular abnormalities in young people or arteriosclerosis in adults. They are recurring pictures of vertigos when changing position or when looking up, periodic and intermittent; they usually present other types of trunk disorders, especially diplopia, but sometimes drop attacks, hemianesiesias, hemianopsias, etc. Functional tests are normal
   3. Due to vascular infarction. Of great importance in Wallenberg syndrome, due to obstruction of the posteroinferior cerebellar artery, the vertebral artery or another branch related to the area. The vestibular nuclei are affected and among many important signs the picture begins with an acute vertigo of peripheral aspect, but that on functional examination is disharmonic, since the nystagmus does not beat in the expected plane.
   4. Due to cervical injury. It is discussed later.
2. Cervical vertigo. Disputable and uncommon, three mechanisms are accepted: a) of vascular origin, due to compression of the vertebral artery by osteophytes during movements or an exaggerated turn of the head in travel, which compresses the vertebral at the level of its passage between the axis and the atlas; b) by pure spondylosis, which would bring an imbalance in the cervical tonic affections; c) Barré Liéou syndrome, debatable, due to cervical arthropathies that would injure the sympathetic cervix, causing secondary circulatory disorders.
3. Traumatic vertigo. They can be immediate, due to trauma to the labyrinth in longitudinal fractures of the rock (transverse fractures more often cause vestibular death), or late, forming part of the much-questioned post-traumatic syndrome. In general, it was caused by benign positional vertigo, which is sometimes accompanied by alterations in functional tests, indicating a possible organic cause.
4. Vertigo and migraine. They can coincide, either with vertigo as an aura of an attack or replacing headache. In these cases it is necessary to carry out a good questioning, because sometimes vertigo alternates with headache, but in others it appears exclusively; In addition to the antecedents, the diagnosis should be considered when faced with periodic vertigo that passes without sequelae of instability, with negative tests and that improves with specific treatment.
5. Medicated vertigo. Certain ototoxic drugs. like salicylates and quinine, they affect hearing and balance interchangeably; but others have a predilection for one of the devices, such as streptomycin, kanamycin, gentamicin, etc. Almost always, and except for a very early and timely suspension of treatment, hearing recovery is poor, but the balance is compensated, even if functional inexcitability is maintained.
6. Psychogenic vertigo. Vertigo can be a symptom of neurosis or another more serious mental disorder. In such cases the description of the symptoms is very unclear and it can be deduced that the patient's complaint does not refer to a true vestibular disorder; On the other hand, it has been proven that anxiety states can condition the appearance of a true positional vertigo. And we must remember that all vertigo has a considerable affective component and that, before classifying vertigo as psychogenic, studies must be exhausted, which will show normal results with great exaggeration of subjective reactions and sometimes reproduction of symptoms with hyperventilation.
7. Vertigo eye. Uncommon, it is usually seen at the beginning of diplopia due to alteration in the perception of both visual fields.
8. Motion sickness or motion sickness.It is the feeling of discomfort with dizziness, nausea and often vomiting, which occurs in some subjects subjected to prolonged and iterative movements of their body, in relation to gravity, as occurs in air, boat, train or car travel. It seems to be due to a discrepancy between the impulses received from the different inputs of the vestibular system; in a ship, for example, the constant excitement of the labyrinth by the continuous movement of the ship is not matched by the visual sensation of stillness provided by the environment in which the subject remains (the cabin or the saloons); therefore, the improvement of the painting is checked when the subject goes out on deck and visually checks the movement of the horizon. Well controlled experiments have shown that, for its production,

The vertigo of height and that produced when looking at moving objects from a fixed place, such as trains or cars, would have the same presumed causal mechanism: a discordance in the inferences of the vestibular non-equivalence system.