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Motion Sickness
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 2, doi.org, Abstract
Motion sickness is induced during passive locomotion in vehicles and is generated either by unfamihar bodily accelerations, to which the person has therefore not adapted, or by intersensory mismatch involving conflicting vestibular and visual stimuli (Dichgans and Brandt 1973, 1978; Benson 1977; Reason 1978; Brandt and Daroff 1980). According to the “mismatch theory”; (see also p. 3), spatial orientation and perception of movement are disturbed by a conflict between stimuli when the multisensory motion signals do not correspond to the expected pattern of sensory signals established from earlier experience with active locomotion. This may give rise to unpleasant illusions of movement with consequences of posture and the control of vehicles (Dichgans and Brandt 1978; Leibowitz et al. 1982) and to motion sickness as a result of summation. Thus, motion sickness is not a superfluous epiphenomenon of vestibular stimulation but — in a teleological sense — it represents a meaningful warning signal to withdraw the body from unusual stimulus situations which cannot be integrated with adequate dynamic spatial orientation. The first known reports on seasickness originate from Hippocrates. The major symptom of nausea is derived from the Greek word “naus” for ship. The general term “motion sickness” was coined by Irwin (1881). It stresses the phenomenological similarity of air-, sea-, car-, and space-sickness despite their different modes of provocation.
Benign Paroxysmal Positioning Vertigo (BPPV)
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 1, doi.org, Abstract
Benign paroxysmal positional vertigo (preferably described as positioning vertigo) was initially described by Bárány in 1921, and the term was coined by Dix and Hallpike (1952). In this condition brief attacks of rotational vertigo and concomitant positioning rotary-linear nystagmus are precipitated by rapid head extension and by lateral head tilt towards the affected ear (Fig. 11.1). Cupulolithiasis of the posterior semicircular canal is responsible (Schuknecht 1969), and the condition is the most common cause of vertigo in the elderly. Spontaneous recovery is common, but there is also a high effective form of mechanical therapy which involves the use of positioning manoeuvres applied serially (Brandt and Daroff 1980).
Somatosensory Vertigo
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 3, doi.org, Abstract
Cervical vertigo is unlike other vertigo syndromes, and has given rise to violent controversy. Neck afferents not only assist the coordination of eye, head and body, but also affect spatial orientation and control of posture. This implies that stimulation of, or lesions in, these structures could produce cervical vertigo. In fact, unilateral local anaesthesia of the upper dorsal cervical roots induces ataxia and nystagmus in animals, and ataxia without nystagmus in man. Cervical vertigo, if it exists outside these experimental conditions, is obviously characterised by ataxia and unsteadiness of gait rather than by a clear rotational or linear vertigo.
Upbeat Nystagmus/Vertigo Syndrome
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
Upbeat nystagmus in the primary position of gaze with concomitant oscillopsia and postural instability is a pendant of downbeat nystagmus, and most probably reflects an imbalance of vertical vestibulo-ocular reflex tone. It has the same causes and involves central eye-head coordination in the pitch plane as mediated by pathways from the vertical semicircular canals and the otoliths. Since the manifestations are typically modulated by otolithic input arising from static head tilt (Fig. 8.1), upbeat nystagmus is also a kind of positional nystagmus (see central positional nystagmus, p. 165) in a broader sense. Two separate intra-axial brainstem lesions in the tegmentum of the pontomesencephalic and the pontomedullary junction near the perihypoglossal nuclei (Fig. B.l, Fig. 8.2) are likely to be responsible for this syndrome (Fisher et al. 1983), but there is insufficient evidence to show whether the cerebellar vermis is involved. Differential diagnosis includes gaze-evoked nystagmus, acquired pendular nystagmus, spasmus nutans, and rare forms of vertical congenital nystagmus. In coma it should not be confused with reversed ocular bobbing.
Central Positional Vertigo
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
When the position of the head is brought to an off-vertical, lateral or head-hanging position a change in graviceptive (otholithic?) input occurs. This change is the precipitating factor for central positional vertigo. The most probable explanation for this response is a vestibular tone imbalance with directional positional nystagmus and rotational/linear vertigo caused by disinhibition of the vestibular reflexes on perception, eye, head, and body position (Brandt 1990). Thus, it is not (as one might speculate) the dislocation of the brain and intracerebral structures that depend on head position which causes the manifestations.
Vestibular Neuritis
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 1, doi.org, Abstract
Acute unilateral (idiopathic) vestibular paralysis, also known as vestibular neuritis, is the second commonest cause of vertigo. It was first described by Ruttin in 1909 and later by Nylen (1924). The term “vestibular neuronitis” coined by Hallpike (1949) and Dix and Hallpike (1952) should be replaced by “vestibular neuritis” because the neuron itself cannot become inflamed.
Vertigo Due To Barotrauma
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
This vertigo is associated with exposure to alterations in ambient pressure, either an increase (diving) or a decrease (flying). The atmosphere exerts an absolute pressure of 760 mm Hg at sea level, the standard one atmosphere absolute (1 ATA) pressure. Changes of pressure in water increase linearly with increasing depth: one atmosphere is added for each 33 ft. This increased pressure is balanced by breathing air delivered at the new ambient pressure and by equalising the pressure in all gas-containing body cavities to ambient (Farmer and Thomas 1976; Margulies 1987). The volume of gas varies inversely with ambient pressure and this pressure–volume relationship mostly causes the barotrauma. The likelihood of damage to the Eustachian tube and middle and inner ear increases as the rate of change of external pressure increases, because it is in these areas that large pressure differentials are produced.
Downbeat Nystagmus/Vertigo Syndrome
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
Downbeat nystagmus in the primary gaze position, or more particularly on lateral gaze, is often accompanied by oscillopsia and postural instability. This is a clearly defined and often permanent association of symptoms, which is almost entirely specific to structural lesions of the paramedian craniocervical junction (Cogan 1968). It involves eye-head coordination in the pitch plane, mediated by pathways from the vertical semicircular canals and the otoliths. This is not a pure oculomotor disorder, but a central vestibular disorder that affects perception and balance. Differential diagnoses include gaze-evoked nystagmus, acquired pendular nystagmus, spasmus nutans and rare vertical forms of congenital nystagmus; in coma, downbeat nystagmus should not be confused with ocular bobbing. Downbeat nystagmus differs from these other conditions in that it is a spontaneous jerk nystagmus which is activated by lateral gaze, and is not suppressed by fixation.
Hyperviscosity Syndrome and Vertigo
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
Pathological hyperviscosity of the blood may be associated with polycythaemia, hypergammaglobulinaemia, or Waldenström’s macroglobulinaemia. The clinical hyperviscosity syndrome includes nonspecific symptoms such as headache, visual disturbances, hearing loss and vertigo; it can cause cerebral infarctions and heart or renal failure (Baer et al. 1985, Fahey et al. 1965; Preston et al. 1978).
Familial Periodic Ataxia/Vertigo
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
Parker in 1946 was the first to describe a syndrome of periodic ataxia in 11 patients, which was familial in four and a manifestation of multiple sclerosis in the remainder. This was before periodic attacks of dysarthria and ataxia (p. 130) were recognised as characteristic paroxysms caused by demyelinated pathways within pontine and brachium conjunctivum structures in multiple sclerosis (Andermann et al. 1959; Harrison and McGill 1969; Osterman and Westerberg 1975).
Drugs and Vertigo
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
The list of drugs which may have adverse effects on hearing or balance is impressive. It includes anaesthetic agents, anticonvulsants, antidepressants, analgesics, antidiabetic agents, antihypertensive agents, anti-inflammatory drugs, contraceptives, cytotoxic agents, cardiovascular drugs, sedatives, and tranquilhsers (Table 21.1; Ballantyne and Ajodhia 1984). There is no common syndrome or mechanism of drug vertigo. The spectrum covers all kinds of side effects. Beta-blockers may induce bradycardia with unspecific drowsiness or dizziness (Cruickshank 1981). More severe side effects include hypoglycaemia (Harrill 1951; Currier 1970), positional alcohol nystagmus/vertigo (p. 154), cerebellar ataxia and oculomotor dysfunction in acute diphenylhydantoine intoxication (Nozue et al. 1973), and bilateral vestibular loss with oscillopsia and unsteadiness of gait due to gentamicin toxicity (Ramsden and Ackrill 1982). Drug induced patterns of pathological eye movements include positional, downbeat, and gaze-evoked nystagmus and preferably reflect transient flocculus dysfunction (Esser and Brandt 1983).
Perilymph Fistulas
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
The perilymph space surrounds the endolymph-filled membranous labyrinth, both being encapsuled by the bony labyrinth. Perilymph fistulas may lead to episodic vertigo and sensorineural hearing loss owing to a pathological elasticity of the otic capsule, usually at the oval and round windows. This elasticity permits abnormal transfer of ambient pressure changes to maculae and cupulae receptors. The typical history is that of an “otolithic ataxia”, or a semicircular canal type of vertigo and/or a sudden hearing loss resulting from barotrauma (flying, diving; p. 197), trauma to the head, to the ear (e.g., post-surgery) or from strenuous activity, especially lifting of heavy weights (excessive valsalva manoeuvre). In some patients perilymph fistulas manifest with sound-induced vestibular symptoms, which are called the Tullio phenomenon (p. 62), either of the semicircular canal or otolith type.
Miscellaneous Vestibular Nerve and Labyrinthine Disorders
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
Unilateral vestibular loss can be produced by conditions other than the common disorders mentioned in previous chapters. These other conditions can conveniently be classified under the following headings: inflammatory, vascular, tumour, trauma (see traumatic vertigo; p. 189) toxic and congenital.
Menière’s Disease
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
This syndrome was first described by Menière in 1861. It is characterised by fluctuating hearing loss, tinnitus and prolonged but gradually decreasing attacks of vertigo and nystagmus which may last for some hours. Endolymphatic hydrops and periodic ruptures in the membranes separating endolymph from perilymph give rise to intermediate potassium palsy of vestibular nerve fibres (Dohlman 1976). This striking triad made Menière’s disease the most popular but certainly the most frequently over-diagnosed vertigo syndrome. It is the fourth commonest cause of vertigo (Table 24.3) and chiefly affects those aged between 30 and 50 years, with irregular frequency of attacks and a tendency to bilateral involvement. Spontaneous improvement can occur a few years, or even a decade, after the onset of the condition.
Vertigo and/or Tinnitus associated with Neurovascular Compression “Vestibular Paroxysmia” (“Disabling Positional Vertigo”)
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
Neurovascular cross-compression of the root entry zone of the fifth, seventh, and ninth cranial nerves can cause local demyelination and axonal hyperactivity (e.g., by transversally spreading ephaptic activation) with the accompanying distressing symptoms of trigeminal neuralgia, hemifacial spasm and glossopharyngeal neuralgia. Compressing vessels which had made indentations on the relevant nerve have been found surgically, and the efficacy of microvascular decompression as a successful treatment of these symptoms is well established (Janetta 1982).
Positional Nystagmus/Vertigo with Specific Gravity Differential Between Cupula and Endolymph (Buoyancy Hypothesis)
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
Transient positional nystagmus has been repeatedly described following the ingestion of water-soluble molecules with differing specific gravities, such as alcohol or heavy water. The semicircular canals selectively transduce angular velocity and acceleration, and under normal circumstances are insensitive to gravitational orientation and linear acceleration. A major reason for this lack of sensitivity is that the cupula and endolymph have the same specific gravity (the sensory haircells are embedded in the cupula which is housed in the ampulla of the canals). The neutral buoyancy of the cupula in the endolymph prevents any out-of-balance forces when linear accelerations are apphed. If a considerable specific gravity differential occurs between cupula and endolymph then the semicircular canals should become sensitive to changes in head position within the gravitational field, resulting in positional rotatory vertigo and nystagmus. The direction of nystagmus and vertigo should be dependent on the particular head position (according to the different planes of the horizontal and vertical semicircular canals) and on whether the specific gravity of the cupula is greater or less than that of the endolymph. Thus, nystagmus should be direction-changing with either head position right lateral or left lateral, beating towards the undermost ear with the cupula lighter than endolymph and beating towards the uppermost ear with the cupula heavier than endolymph.
Migraine and Vertigo
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
The incidence of vertigo in association with migraine has been reported to range between 50% and 70%, if one includes under the heading of vertigo sensations of dizziness, light-headedness and unsteadiness (Selby and Lance 1960; Kayan 1984). This surprisingly high incidence rate does not, however, reflect the clinical importance of vertigo in relation to other more characteristic and distressing symptoms of the disorder, since only one-third to one-half of these patients describe “true vertigo” which, after Kayan and Hood (1984), appears to be either the major symptom or a severe complication of migraine in only 5% of cases. In order to diagnose and treat this minority of migraine sufferers effectively, it is most important to know that vertigo attacks (with nystagmus and postural imbalance) may occur without accompanying headache (Table 15.1) in children (benign paroxysmal vertigo of childhood), adolescents (basilar artery migraine), and adults (benign recurrent vertigo). It is most important to obtain a thorough personal and family history to explore any association of vertigo attacks with headache or other typical features of migraine.
Miscellaneous Central Vestibular Disorders
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
Small Cerebellar Infarctions. Such lesions in the territory of either the anterior inferior cerebellar artery (AICA) or the posterior inferior cerebellar artery (PICA) have been repeatedly reported to mimic unilateral peripheral labyrinthine disorder, mostly with a similarly benign course (Duncan et al. 1975; Guiang and Ellington 1977; Rubinstein et al. 1980; Samson et al. 1981; Kömpf 1986). The areas covered by these arteries and the anatomy of the collaterals are both variable, so it is sometimes difficult to decide which artery is responsible for clinical signs or infarcted areas seen on CT scans or MRI. When the PICA is hypoplastic, the AICA takes over the territory usually supplied by the lateral branch of the PICA (Amarenco and Hauw 1989). All reports are entitled “cerebellar infarctions causing vertigo”, which is correct on the basis of the imaging data and concurrent clinical signs, but it is more likely that the vertigo itself results from pontomedullary brainstem ischaemia near the vestibular nuclei. The AICA supplies the rostral part of the vestibular nuclei, the middle cerebellar peduncle, the flocculus and the neighbouring lobules of the cerebellum. The PICA supplies the caudal part of the vestibular nuclei and the dorsal medullary territory, the uvular and the nodulus (Amarenco and Hauw 1989). Occlusion of the PICA causes the typical Wallenberg’s syndrome.
Vertigo in Childhood
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 0, doi.org, Abstract
In the paediatric and adolescent age group, vertigo is less common than in adults, but because of the variety of presentations and underlying causes it is a diagnostic challenge (Beddoe 1977; Blayney and Colman 1984; Brandt and Büchele 1984; Balkany and Finkel 1986; Britton and Block 1988).
Head and Neck Injury
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 1, doi.org, Abstract
There are several types of post-traumatic vertigo (Table E.l), and the pathogeneses are controversial (Friedman et al. 1945, Tuohimaa 1978). It seems that what Friedman et al. wrote in 1945 about this subject is still valid: “In a discussion of dizziness per se following trauma, or as a part of the post-traumatic syndrome, there are many opinions as to what are the important factors in the evaluation of dizziness. In general there are three schools of thought — one group who consider dizziness, as well as the other symptoms of the post-traumatic syndrome, to be of psychogenic origin; another group who report it to be exclusively of physiogenic origin; and others who emphasize the importance of both types of factors”.
Visual Vertigo
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 1, doi.org, Abstract
Vision contributes significantly to spatial orientation, self-motion perception, and postural balance. Therefore, either unusual stimulation or sensory dysfunction may cause distressing vertigo and disequilibrium, such as height vertigo or “visual ataxia” associated with the sudden onset of an extraocular eye muscle paresis.
Psychogenic Vertigo
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 3, doi.org, Abstract
The sensation of vertigo, a subjective complaint, is sometimes defined as a hallucination of movement or an illusion. Since evaluation of hallucinations and illusions is an essential part of psychiatric practice, such definitions place vertigo at the doorstep of clinical psychiatry (Trimble 1984). Vertigo is a frequent symptom of psychiatric illness, in particular in anxiety, depression, and personahty disorders, but less frequent in psychosis. However, to complicate matters, because of its incapacitating nature vestibular dysfunction frequently causes psychiatric illness. This may bias the diagnosis of organic vertigo syndromes by a considerable neurotic overlay e.g. in patients with Menière’s disease. Alternatively, a transient labyrinthine dysfunction, e.g. in vestibular neuritis, may initiate development of neurosis in which anxiety, panic attacks and depression are most common, and which typically preserves subjective vertigo and postural imbalance although the peripheral lesion is already either recovered or centrally compensated. In the latter case there is a history of an initial rotational vertigo, lateropulsion and nausea (with the objective clinical signs of horizontal rotatory nystagmus and unilateral hyporesponsiveness to caloric irrigation) which is followed by a more indefinite chronic dizziness with subjective postural imbalance or spells of vertigo during active body movements, associated with anxiety and change in behaviour (see Phobic Postural Vertigo, p. 292). Obsessional subjects are more likely to proceed from organic to psychiatric disease, and the obvious presence of an obsessional personality will support the diagnosis of this condition.
Introduction
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 3, doi.org, Abstract
Vertigo is an unpleasant distortion of static gravitational orientation, or an erroneous perception of motion of either the sufferer or the environment. It is not a well-defined disease entity, but rather may be the outcome of many pathological or normal processes. It is best described as a multisensory syndrome which is induced either by stimulation of the intact sensory systems by motion, or by pathological dysfunction. Different treatments are appropriate for different types of vertigo, and may include drug therapy, physical therapy (exercises), surgery and psychotherapy.
Ocular Tilt Reaction
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 1, doi.org, Abstract
Ocular tilt reaction (OTR) is a central vestibular disorder involving the vertical vestibulo-ocular reflex in the roll plane. OTR also represents a fundamental pattern of coordinated eye-head roll motion. It is based upon both utricular and vertical canal input, and is mediated by the graviceptive pathways from the labyrinths via pontomedullary vestibular nuclei to the rostral midbrain tegmentum. It consists of lateral head tilt, skew deviation of the eyes (hypotropia of the undermost eye) and cyclorotation (clockwise with head tilt left; counterclockwise with head tilt right; see Figs 9.1, 9.2, 9.3). It was first clearly delineated by Westheimer and Blair (1975a, b) during electrical stimulation of the rostral midbrain tegmentum in the region of the interstitial nucleus of Cajal of the monkey. Only a few cases of paroxysmal OTR have been reported: in multiple sclerosis (Rabinovitch et al. 1977), in a brainstem abscess in the region of the zona incerta (Hedges and Hoyt 1982), and as an otolithic Tullio phenomenon (Brandt et al. 1978; see p. 63). Tonic OTR is not rare, and occurs in upper brainstem lesions (Brandt and Dieterich 1988; Halmagyi et al. 1990), in lateral medullary lesions, especially in Wallenberg’s syndrome (Brandt and Dieterich 1987), as well as in cases of otolithic dysfunction (Halmagyi et al. 1979).
Vestibular Epilepsy
Brandt T.
Springer Nature
Clinical Medicine and the Nervous System, 1991, цитирований: 1, doi.org, Abstract
Vestibular epilepsy is a cortical vertigo syndrome secondary to focal discharges from either the temporal lobe or the parietal association cortex (Foerster 1936; Penfield and Jasper 1954; Schneider et al. 1968), both of which receive bilateral vestibular projections from the ipsilateral thalamus. Results of electrical stimulation in man have shown that the intraparietal sulcus (Foerster 1936) and the posterior part of the superior temporal gyrus (Penfield and Jasper, 1954) form part of the vestibular cortex, and experiments in monkeys have similarly identified the posterior caudal part of the postcentral gyrus (Fredrickson et al. 1966). Fig. 6.1 gives a schematic representation of the vestibular cortex areas. An acute unilateral functional deficit of the vestibular cortex (for example, in medial cerebral artery infarction) does not usually manifest with vertigo, unlike lesions in the vestibular area of the brainstem. It is not the functional loss but the focal discharge that causes central vertigo. This has been repeatedly demonstrated by stimulation experiments. Electrical stimulation of the human thalamus during stereotactic neurosurgical procedures induced sensations of movement in space, most frequently described as horizontal or vertical rotation or sensations of falling or rising (Hawrylyshyn et al. 1978). These sensations were similar to those induced by stimulation of the vestibular cortex (Foerster 1936; Penfield and Jasper 1954).
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