Nystagmus

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Classification according to ICD-10
H55 Nystagmus and other abnormal eye movements
ICD-10 online (WHO version 2019)

Nystagmus (from ancient Greek νυσταγμός nystagmos 'drowsiness', to νυστάζειν nystazein 'nod', 'slumber') denotes the uncontrollable, rhythmic movements of an organ , usually the eyes ( ocular nystagmus ), so that nystagmus is usually understood as an eye tension . It occurs physiologically or pathologically , e.g. B. as a typical symptom of vertigo . Basically, a pathological nystagmus is differentiated into a "jerk nystagmus", which has a slow initial and a quick return movement, and a "pendulum nystagmus" without any discernible speed differences in the back and forth movement. With frequency and amplitude , the frequency and the magnitude of the deflection also be described. The direction of impact and characteristics can vary depending on the current viewing direction. The most common are horizontal beat patterns, but vertical and rotatory shapes are also found.

Physiological nystagmus

Optokinetic nystagmus

The physiological nystagmus is used to keep the image projected through the lens so constant on the retina that perception is possible. Movements of the observed object as well as proper movements of the eye, head and the entire organism in space lead to movements of the light stimulus on the retina. If the angular speed of these light reflections becomes too great (> 5 ° / s), the image can no longer be perceived clearly. In eyes with a retina, such as in humans, it is also useful to always keep the focus in the area of ​​sharpest vision ( fovea centralis ) (see also eye movement ). An example of physiological nystagmus is optokinetic nystagmus , which occurs when objects of perception move continuously relative to the retina, for example when looking from a moving train.

Pathological nystagmus

A nystagmus, on the other hand, can also be of pathological origin and in this case belongs to the group of supranuclear eye movement disorders . In this case, the eye twitch occurs at rest; However, provocation movements may be necessary beforehand to trigger them. Above all, certain disorders in eye control in diseases in the brain stem and cerebellum or in the vestibular system , but also certain drugs such as ecstasy trigger nystagmus. In these cases it is an expression of a miscoordination between two important physiological senses: the sense of balance and sight.

The pathological nystagmus can be divided into a peripheral and a central nystagmus. Peripheral nystagmus occurs when the organ of equilibrium ( vestibular organ ) or the vestibulocochlear nerve (8th cranial nerve) is damaged . In the event of an acute failure of the equilibrium organ on one side, one can observe the sudden failure nystagmus that then lasts for several days. Another form of peripheral nystagmus occurs, for example, in benign paroxysmal positional vertigo . Here the eye movements can only be triggered by a few minutes and by certain head movements. The central nystagmus, on the other hand, is the result of damage to the brain .

Pathological forms of nystagmus are also often found in young children. An ophthalmological examination, if possible with a strabologist in the orthoptic department of a practice or eye clinic, is always indicated, since nystagmus can be a sign of the presence of albinism or other eye diseases. It is often part of the congenital squint syndrome .

Depending on the form and extent of the nystagmus, the result is a differently pronounced reduction in visual acuity up to a severe visual impairment .

Nystagmus can also be associated with syndromes such as B. the Karsch-Neugebauer syndrome occur.

to form

A distinction is made between jerk nystagmus, which has a faster phase in the direction of impact, and the rarer pendulum nystagmus, which is characterized by a constant frequency and the lack of a clear direction of impact. In most cases, horizontal eye tremors occur, but vertical and rotational forms also exist.

Gaze retention

Direction-dependent forms of nystagmus are known which are based on the fact that an innervation impulse cannot be kept at a constant level. Depending on the cause and extent, one differentiates:

  • End position nystagmus (low level, only occurs beyond a 35 ° turn and is not yet rated as pathological)
  • Direction of gaze nystagmus (medium severity, already occurs with deviations below 35 °)
  • Gaze paretic nystagmus (severe expression with back drift in the slow phase to the middle).

Eye retention problems are not to be confused with eye paralysis , in which the innervation impulse necessary for rapid eye movements is already disturbed. The causes vary and range from drug triggers (e.g. anti-epileptic drugs or sedatives ) to damage to the brain stem or cerebellum.

Fixation nystagmus

In contrast to vestibular spontaneous nystagmus, fixation nystagmus is not slowed down by visual stimuli, but continues to beat unhindered, in some cases even intensified.

Congenital nystagmus

Congenital nystagmus usually only occurs from the 2nd to 3rd month of life and can in some cases intensify drastically in the following weeks. Visual gifts are often hardly recognizable. The assessment is based on the following characteristics:

  • the tremor is not slowed down by fixation , but rather intensified
  • the stroke shape is pathological
  • the striking plane is mostly horizontal, also when looking up or down
  • the intensity (frequency and amplitude) changes with the viewing direction
  • There is often (relative) nystagmus calming in the vicinity
  • the optokinetic nystagmus is clearly disturbed.

In addition, a scientific study showed a significantly higher prevalence of astigmatism > 1.25 D in people with congenital nystagmus than in normal people, at around 85% .

Ocular nystagmus

Ocular nystagmus is caused by disturbances in the visual system which do not allow normal fixation behavior. Possible here are for. B. organic causes such as lens opacities or aniridia .

Laten-type nystagmus

A Latenstyp nystagmus or "nystagmus from Latenstyp" (formerly latent nystagmus and nystagmus latens ) is characterized in that its impact direction has at fixation with the right eye to the right, but with the fixation with the left eye to the left. By covering one eye, it is often intensified or only then becomes conspicuously visible. Although a "latent nystagmus" or "nystagmus latens" has the same features in the impact direction, but is offset in most cases and is only visible when the binocular vision ( binocular vision ) is interrupted.

Acquired fixation nystagmus

This form of nystagmus is common in multiple sclerosis and is very similar to congenital nystagmus. Cerebral circulatory disorders and angiomas can also be a trigger. In leprosy , too, nystagmus was a symptom that was already known in the Middle Ages.

Spasm nutans

Nutans spasm is a form of nystagmus that occurs sometime in the first year of life and spontaneously disappears after a period of about one to two years. The reasons for this are not yet known. Often the nutans spasm has a much higher frequency than a congenital nystagmus. The expression in the right and left eye is also often different. In addition, the optokinetic response works, which calls into question a classification as fixation nystagmus .

Compensation mechanisms

Relative calming of a nystagmus is possible in some cases by means of compensation mechanisms, for example when looking up close ( convergence , accommodation ) or by adopting a forced head position , for example by turning the head often in the opposite direction of the stroke. The direction of view in which the nystagmus is calmest and thus the visual acuity is highest is called the neutral zone . A frequent compensation mechanism for spasm nutans is what is known as head nodding , a head wobbling , the frequency of which, however, is usually well below that of nystagmus.

Relationships with early childhood squint

While patients with congenital nystagmus rarely a squint have (strabismus), almost always found in a nystagmus from Latenstyp also an early childhood strabismus, usually in the form of a pronounced inner squint. One attempt to explain this correlation used to be that the squint was viewed as an attempt to calm the nystagmus, which is why the term nystagmus blocking syndrome was found. However, since the causal relationships between nystagmus and strabismus have not yet been fully explored, the term congenital squint syndrome is preferred .

therapy

Treatment options depend on the type, cause and extent of the nystagmus and its compensation mechanisms (if any). The primary aim will be to improve visual acuity and  to shift the neutral zone into the field of vision in use - ideally into the primary position . Possibilities for this exist in the adaptation of prism lenses , but usually by performing one or more eye muscle operations , which also aim to significantly reduce any existing head posture. If a convergence movement is used for the relative calming of the nystagmus, this can also be implemented surgically in some cases if a usable binocular vision is available.

A drug treatment with gabapentin or memantine has shown positive results in smaller studies.

Diagnosis

In order to describe a nystagmus more precisely, so-called Frenzel glasses are used during the examination by the ophthalmologist , ear, nose and throat specialist or neurologist . Using electronystagmography (ENG), the eye movement and thus the nystagmus can be recorded and evaluated. Another apparatus-based examination method is video oculography.

documentation

There is a diagram for the graphic documentation of findings of a nystagmus, from which the type of nystagmus can be seen immediately. Different arrow symbols are used to represent the amplitude, frequency and direction of impact. These are entered in a basic scheme for the respective viewing directions or primary and secondary positions. If there is jerk nystagmus, the arrowhead is drawn in the direction of the stroke, if there is pendulum nystagmus, the arrow is provided with two arrowheads.

Testing by spin

The examination is usually carried out on a swivel chair. This results in a slow horizontal eye movement against the direction of rotation, followed by rapid return movements in the direction of rotation in order to image a new object, as described above, on the fovea centralis . The vestibular nystagmus (also vestibulo-ocular reflex ) thus runs with the direction of rotation. By braking the rotating chair there is, however, (due to the inertia of the endolymph in the semicircular canals ) to a postrotary, the original direction of rotation opposite nystagmus: For a right turn it is therefore initially at a right nystagmus with the completion of turning in a left-nystagmus transforms. Like the caloric nystagmus described below, this nystagmus can also be observed in healthy people if the Frenzel glasses have deprived them of the possibility of fixation.

Vestibular compensatory movements are therefore a result of rapid, short-term turning movements of the head, while optokinetic nystagmus is triggered by sustained, slow head movements. The vestibular and optokinetic systems thus form an ideal complement to each other for image stabilization.

Thermal test

The caloric nystagmus is triggered by stimulating the vestibular organ by introducing cold (22-27 ° C) or warm (40-45 ° C) water into the external auditory canal. This changes the discharge rate of the vestibular organ, which is interpreted by the brain as a rotation. The so-called vestibulo-ocular reflex (VOR) creates a jerk nystagmus - with warm irrigation towards the irrigated ear, with cold irrigation towards the opposite side. Motto: "Hot - homolateral, cold - contralateral".

Until a few years ago it was assumed that the temperature differences induced an endolymph flow. In fact, in experiments with the exclusion of gravity in space, caloric nystagmus continued to occur, which means that another, previously unknown cause must cause this reaction.

differentiation

Nystagmus should not be confused with microsaccades , local adaptation , ocular tremor or blepharospasm . Refer to the article eye movement and superior oblique myokymia .

See also

literature

  • Herbert Kaufmann (Ed.): Strabismus . 4th fundamentally revised and expanded edition, with Heimo Steffen. Georg Thieme Verlag, Stuttgart / New York 2012, ISBN 3-13-129724-7 .
  • Theodor Axenfeld (founder), Hans Pau (ed.): Textbook and atlas of ophthalmology. 12th, completely revised edition. With the collaboration of R. Sachsenweger u. a. Gustav Fischer Verlag, Stuttgart a. a. 1980, ISBN 3-437-00255-4 .

Web links

Wiktionary: Nystagmus  - explanations of meanings, word origins, synonyms, translations

Individual evidence

  1. EC Campos, M. Fresina, E. Bendo, S. Belli, P. Versura: Astigmatism in congenital nystagmus. Clinical study. In: Clinical monthly sheets for ophthalmology. Volume 223, No. 7, 2006, pp. 615-619, ISSN  0023-2165 , doi: 10.1055 / s-2006-926852 .
  2. T. Shery, FA Proudlock, N. Sarvananthan, RJ McLean, I. Gottlob: The effects of gabapentin and memantine in acquired and congenital nystagmus: a retrospective study. In: The British Journal Of Ophthalmology. Volume 90, No. 7, 2006, pp. 839-843. ISSN  0007-1161 , PMID 16556621 , doi: 10.1136 / bjo.2005.086322 .
  3. Michaela Starck, Holger Albrecht, Walter Pöllmann, Marianne Dieterich, Andreas Straube: Acquired pendular nystagmus in multiple sclerosis: an examiner-blind cross-over treatment study of memantine and gabapentin. In: Journal of Neurology. Volume 257, No. 3, Mar 2010, pp. 322-327. ISSN  0340-5354 PMID 19756822 , doi: 10.1007 / s00415-009-5309-x .
  4. Rudolf Sachsenweger (Ed.): Neuroophthalmology. 3rd, revised edition. Thieme, Stuttgart a. a. 1983, ISBN 3-13-531003-5 , p. 217.
  5. H. Scherer, U. Brandt, AH Clarke, U. Merbold, Parker R: European vestibular experiments on the Spacelab-1 mission: 3. Caloric nystagmus in microgravity. In: Exp Brain Res. 64 (2), 1986, pp. 255-263.