PMC

The supranuclear centers for controlling eye movements. These allow exact topographical determination: lesions in the region of the interstitial nucleus of Cajal (INC) lead to a vertical gaze-holding defect, lesions in the region of the rostral interstitial nucleus of the the medial longitudinal fasciculus (rilMF) leads to impairments of vertical saccades, lesions of the paramedian pontine reticular formation (PPRF) result in impairments of the horizontal saccades, lesions of the nucleus prepositus hypoglossi (NPH) are characterized by a horizontal gaze-holding defect (adapted from [, ]).

Defects of the medial longitudinal fasciculus (MLF) with the result of an impairment of the VI to III projection (between abducent nucleus and oculomotor nerve via abducent interneurons) (pathway shown in red) as the cause of internuclear ophthalmoplegia (INO). This leads to a lack of or defective signal transmission to the oculomotor nucleus, resulting in impaired adduction (this, not the dissociated nystagmus, is pathognomonic for INO). The side of the impaired adduction corresponds to the side of the INO and the defective MLF. The direct projection from the abducent nucleus via motoneurons to the rectal lateral eye muscle is not impaired.

Clinical examination of eye position and eye movements with an examination flashlight. The advantage of this examination is that the images reflected on the retina can be observed and ocular misalignments therefore identified. It is important that the examiner looks at the retinal images from the direction of the light and that the patient is instructed to fixate his/her gaze on the target object. Gaze-evoked nystagmus to all sides is usually caused by medication (such as antiepileptic drugs, benzodiazepines) or intoxication (for example, alcohol). Downbeat nystagmus increases when looking sideways and when looking downwards.

Clinical examination of saccades. Spontaneous saccades that are triggered by visual or acoustic stimuli should be studied first. Then the patient should be asked to switch his/her gaze between two horizontal and two vertical targets. The velocity and accuracy of the saccades should be observed, and whether they are conjugate. In healthy subjects, the target will be reached immediately or will be made by one correctional saccade. Generally slower accades, which are usually accompanied by hypometric saccades, occur in neurodegenerative disorders, for example. Slowed horizontal saccades are usually observed in pontine brainstem lesions and slowed vertical saccades in midbrain lesions. Hypermetric saccades, which are recognized by a corrective saccade back to the target, are found in cerebellar lesions. The pathognomonic sign of internuclear ophthalmoplegia is a slowed adducent saccade ipsilaterally to the defect of the medial longitudinal fasciculus.

Clinical examination using Frenzel’s spectacles. The lenses, which are illuminated from within and contain enlargement lenses (+16 diopters) prevent gaze fixation, which may suppress peripheral vestibular spontaneous nystagmus, for example. On the other hand, they make it easier to study the patient’s eye movements. When Frenzel’s spectacles are used to examine a patient, attention should be paid to possible spontaneous nystagmus, gaze-evoked nystagmus, head-shaking nystagmus (to this end, the patient should be asked to turn his/her head quickly from right to left and back, about 20 times; subsequently the eye movements should be studied), positional nystagmus and hyperventilation induced nystagmus. Pay attention to positioning nystagmus which indicates a muscle tonus imbalance of the vestibulo-ocular reflex; if this originates from a peripheral vestibular lesion—such as occurs, for example, in vestibular neuritis—then the nystagmus can be typically suppressed by visual fixation. Head-shaking nystagmus indicates a latent asymmetry of the so-called velocity storage; this may be due to peripheral or central vestibular functional disorders.