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Vertigo and dizziness are not unique disease entities. Sometimes vertigo is attributed to vestibular disorders, while dizziness is not ( Neuhäuser and Lempert 2004 ). There is, however, no general agreement, and visual stimuli can cause vertigo (e.g., height vertigo or optokinetic vection), just as central vestibular or otolith disorders can cause dizziness. The two terms cover a number of multisensory and sensorimotor syndromes of various aetiologies and pathogeneses, which can be elucidated only within an interdisciplinary approach. After headache, vertigo and dizziness are among the most frequent presenting symptoms, not only in neurology. According to a survey of over 30,000 persons, the prevalence of vertigo as a function of age is around 17%; it rises to 39% in those over 80 years of age ( Davis and Moorjani 2003 ). Whether caused by physiological stimulation (motion sickness, height vertigo) or a lesion (unilateral labyrinthine failure, central vestibular pathway lesions), the resulting vertigo syndrome characteristically exhibits similar signs and symptoms despite the different pathomechanisms—dizziness/vertigo, nausea, nystagmus and ataxia (Figure 1.1). Disorders of perception (dizziness/vertigo), gaze stabilisation (nystagmus), postural control (falling tendency, ataxia) and the vegetative system (nausea) are related to the main functions of the vestibular system, which are located in different sites in the brain.

Three forms of peripheral vestibular disorders, each with its typical symptoms and clinical signs, can be differentiated: Bilateral peripheral loss of vestibular function (bilateral vestibulopathy) . The main symptoms are oscillopsia during head movements (failure of the vestibulo-ocular reflex) and instability of gait and posture. The latter two symptoms increase in darkness and on uneven ground (due to reduced or absent visual or somatosensory information). Acute/subacute unilateral failure of vestibular function (labyrinth and/or vestibular nerve), which causes a vestibular tonus imbalance. Main symptoms are rotatory vertigo (for a few days or weeks), nausea, oscillopsia and a tendency to fall in a certain direction. Inadequate paroxysmal stimulation of the peripheral vestibular system of the labyrinth (e.g., during benign paroxysmal positioning vertigo) or of the vestibular nerve (e.g., during vestibular paroxysmia due to ectopic discharges). The main symptoms are attacks of rotatory or postural vertigo.

Central vestibular forms of vertigo are caused by lesions along the vestibular pathways, which extend from the vestibular nuclei in the medulla oblongata to the ocular motor nuclei and integration centres in the rostral midbrain, and to the vestibulocerebellum, the thalamus, and multisensory vestibular cortex areas in the temporoparietal cortex ( Brandt and Dieterich 1995 ). These forms of vertigo are often clearly defined clinical syndromes of various aetiologies, with typical ocular motor, perceptual and postural manifestations that permit precise (topographical) localization. The analysis of nystagmus can also be helpful for localising the lesion site ( Büttner et al. 1995 ). This section discusses such typical findings in detail. Depending on the size of the lesion, central vestibular syndromes can occur in isolation or as part of a complex infratentorial syndrome. Additional symptoms of supranuclear or nuclear ocular motor disorders and/or other neurological brainstem deficits can also occur (e.g., Wallenberg’s syndrome with ocular tilt reaction, as well as Horner’s syndrome, sensory deficits, ataxia, dysarthria and dysphagia).

After head and neck pain, vertigo/dizziness is the most frequent complication of a head trauma or a whiplash injury. If a petrous bone fracture is not seen radiologically, and since it is not possible to clinically confirm a brainstem concussion, the first questions to ask are the following: Is this dizziness organic or psychogenic? What is the underlying mechanism of the dizziness (peripheral, central vestibular or cervical)?

Somatoform disorders play a causal or contributory role in a large portion of patients presenting with complex forms of dizziness. In the course of their illness, even after several years, about 70% of these patients with complex somatoform dizziness still show symptoms and are more impaired in their professional and daily activities than those with organic forms of dizziness ( Furman and Jacob 1997 ; Yardley and Redfern 2001 ; Eckhardt-Henn et al. 2003 ). The most frequent underlying psychiatric disorders are anxiety and depression as well as dissociative somatoform (ICD-10:F45) disorders.

Dizziness occurs less often as a major symptom in childhood than in adulthood. Most forms of dizziness and vestibular syndromes of adulthood, however, can also appear in childhood. For this reason we will limit ourselves in this chapter to the essential features of an indicative patient history. Episodic vertigo syndromes can manifest in childhood as an equivalent of migraine, an epileptic aura, or in the presence of perilymph fistulas; they seldom occur in the context of a familial episodic ataxia. Sustained rotatory vertigo can be the sequela of vestibular neuritis, a labyrinthitis or brain concussion. Benign paroxysmal positioning vertigo in children is also often caused by trauma. Oscillopsia during head movements and balance disorders that worsen in darkness are typical for bilateral vestibulopathy, which can develop in children after a case of bacterial meningitis, for example, or be caused by ototoxic antibiotics. Moreover, labyrinthine malformations may also cause congenital bilateral vestibulopathy (Table 6.1). The treatment of these various forms of vertigo corresponds to that in adults; however, a paediatrician should be closely consulted.