Biomedical subjects
Publications and source records attributed to N G Henriksson.
The eye tracking test is today a well established part of clinical otoneurological examination. In the present paper some applications of the test in evaluating of the level of lesion within the vestibular system are reviewed.
During recent decades a vast amount of literature concerning horizontal optokinetic nystagmus has emerged, regarding which--and especially as regards our own work--this report is intended to consider the clinical value of optokinetic nystagmus.
Optokinetic nystagmus (OKN) was studied in ten patients with vestibular neuritis, and in seventeen patients with unilateral and thirteen patients with bilateral infratentorial lesions and compared with OKN in fifty healthy subjects. Mean and maximum slow phase velocity of OKN was calculated as well as the asymmetry of responses. The efficiency of the different variables in OKN, in discriminating between different lesion sites, was tested in a linear discriminant function analysis. Slow phase velocity of OKN could satisfactorily separate patients with infratentorial lesions from healthy subjects or subjects with vestibular neuritis. Asymmetry of OKN did not contribute further to the correct diagnosis.
The effects of TTS-scopolamine, dimenhydrinate, lidocaine, and tocainide on motion sickness and vertigo and on caloric and postrotatory nystagmus were evaluated in healthy volunteers. TTS-scopolamine was administered transdermally (delivering approximately 10 micrograms X h-1 scopolamine base) and 100 mg dimenhydrinate orally. Lidocaine and tocainide were administered intravenously (average plasma concentration of lidocaine 6 mol X L-1 and of tocainide 20 mol X L-1). TTS-scopolamine and dimenhydrinate significantly reduced vertigo induced by calorization of the ears, nausea provoked with Coriolis maneuvre, and nystagmus in caloric and rotatory tests. During treatment with lidocaine and tocainide no alleviation of vertigo and nausea was observed. Caloric nystagmus was reduced but rotation induced nystagmus was virtually unchanged. Presumably the motion sickness drugs act at the brain stem where TTS-scopolamine and dimenhydrinate have their target cells in the vestibular nuclei. Furthermore, the alleviation of motion sickness was linked to a decline of nystagmus. Lidocaine and tocainide, the action of which in vertigo and nausea in patients is proposed to be on the vestibular end organs and the supratentorial brain structures, consistently failed to alleviate motion sickness.
The number of saccades, vestibular gain and visual suppression as a function of smooth pursuit gain were determined in 10 cerebellar cases. Visual suppression increased and the number of saccades decreased with increasing smooth pursuit gain while a high vestibular gain was found in most cases but without relation to the gain of smooth pursuit. An eye-motor model is presented according to which all findings could be related to a disturbance of proper cerebellar processing of optic impulses and of impulses to the vestibular nuclei in the paramedian reticular formation.
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Mean peak velocity and accuracy of vertical saccades were measured in 15 patients with disorders in the brain stem and in 12 normal subjects. (1) In the normal group up-directed saccades were faster than down-directed and the velocity of the saccade was not dependent on the age of the subject. Up-saccades were faster whether electro-oculography or photo-electro-oculography were used. (2) In patients with brain stem disorders the velocity of vertical saccades did not significantly differ from the saccadic velocity in the normal group. This is in contrast to what was found in horizontal saccades, where a reduced velocity was characteristic.
The maximum velocity gain of smooth pursuit and optokinetic, vestibular, and optovestibular slow phases was examined in 15 patients with pontine, 10 with medullary, 10 with cerebellar, and 5 with combined cerebello-brain stem disorders. Marked dissociations were observed between smooth pursuit and optokinetic slow phases, especially in medullary disease. A cerebellar deficit enhanced slow phase velocity gain during rotation in darkness, whereas the corresponding gain during rotation in light was normal.
The accuracy and velocity of voluntary saccades together with the velocity of fact phases of nystagmus were studied in 26 patients belonging to 4 groups with defined neurological disorders. Patients with speech disorders of the dyspraxia type, indicating the lesion in the left frontal cortex, showed a pronounced decrease in saccadic accuracy in combination with normal saccadic and quick phase velocity. Patients with pontine disorders showed a significant decrease in the peak velocity of saccades and quick phases of nystagmus while the accuracy of the saccades ranged from normal to severely disturbed. Patients with acute meningo-encephalitis showed increases in peak velocity of saccades and of quick phases of nystagmus and the accuracy was somewhat reduced. Patients with a labyrinthine disease showed normal velocity of saccades and of quick phases as well as normal accuracy of saccades.
Eye movements in 30 patients with brain-stem lesions were evaluated with electro-oculography, and the findings were analyzed with regard to the site of the lesion in the brain stem. Eye velocities generally were reduced more severely in pontine than in medullary lesions. In medullary lesions, there even was a slight enhancement of the velocities in the fast component of optokinetic and postrotatory nystagmus. In contrast to the slow-phase velocity of OKN, which often was preserved in medullary lesions, the smooth-pursuit velocity was reduced in lesions at all levels in the brian stem. This indicates that these two types of visually induced eye movements use different mechanisms.
In patients consulting otologists for vertigo a functional source can be expected in 50% of the patients and more frequently among young females than among older male subjects. Functional vertigo is frequently perceived as a turning sensation inside the head, functional dizziness frequently as a rocking sensation of the whole body, while patients with vertigo of somatic origin frequently seem to complain of a spinning sensation outside the head. The duration pattern of functional vertigo is frequently of a fluctuating or continuous type, while in the nonfunctional subjects it is of 2-5 hr. duration. In patients with vertigo of functional origin eye-closure tends to release rather than inhibit nystagmus.
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A conception of the mechanism for initiating symptoms in Ménière's disease has been forwarded. According to this conception production of endolymph may vary also in normals. The hydrops in Ménière cases is brought about by a relative insufficiency in endolymphatic draining routes and the hydrops presents itself only at peak endolymph production periods. The attacks of vertigo are brought about at the distension of the sacs as well as of the regaining of normal shape of the sacs. The mechanism causing the vertigo could be an effect of mechanical push-and-pull effect on the sensory epithelium of the cristae. The early low-tone hearing loss and the persistant normal caloric reactivity also in advanced Méière cases may be due to simple physical laws : distensions of sacs with equal walls will more easily be brought about in wider than narrow compartments.
The theoretical point of departure here was the assumption that a psychogenic vertigo patient displaces affect, or experience of anxiety to one of dizziness, the dizziness serving as an anxiety equivalent. This is seen to imply a change in the locus of experience from the me to the not-me sphere. "Percept-genetic" techniques and a spiral after-effect measurement were used to compare 23 patients with presumed psychogenic vertigo with a control group matched in sex, age, education and occupation. Results of the percept-genetic techniques showed the patients to display stronger signs of affect anxiety than subjects in the control group. Also two main subgroups of patients were differentiated with the help of the descriptive instruments, one group with signs of a primitive-hysteroid mode of functioning, the other with signs of an obsessive-compulsive mode. For both subgroups the suggested displacement mechanism seemed to be functioning. Its apparent effect differed, however, for the two subgroups: in the "primitive-hysteroid" group the displacement mechanism was more effective. The "obsessive-compulsive" group showed stronger signs of affect anxiety, dizziness here being better characterized as a concomitant than as an equivalent of anxiety. Results of a follow-up two years after the investigation also showed a poorer development of symptoms within the "obsessive-compulsive" group.
A vertigo perceived as a spinning sensation outside the head indicates a somatic vestibular disturbance including a Ménièr's disease. A turning sensation inside the head indicates a functional or vascular disorder while a sensation of unsteadiness often as if being slowly rocked indicates a functional disorder.
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