Acquired Nystagmus

As mentioned in the article Nystagmus in Childhood, the acquired form comprises different types of nystagmus that can begin at any age and are mainly related to systemic and neurological disorders.

Bi-foveal fixation, the vestibular-ocular system, and the integrity of the visual pathways make it possible to maintain a stable image and avoid the rhythmic and oscillatory movements typical of nystagmus.

In acquired pathological conditions or in inflammatory pictures, this fixation stability may be lost and thus nystagmus occurs.

Acquired nystagmus often manifests with vertigo, oscillopsia, postural instability, and sometimes nausea.

The Vestibular System is closely linked to the oculomotor system and an imbalance in the inputs to the vestibular centers can generate nystagmus.

Vestibular Nystagmus can be subdivided into Central and Peripheral.

Central Vestibular Nystagmus

It is caused by a lesion of the central vestibular connections. The symptoms are generally less pronounced and of longer duration than the peripheral form. Vestibulo-ocular movements are frequently altered and may be bi-directional in which case neuroradiological investigations are always indicated.

Peripheral Vestibular Nystagmus

Vestibular diseases can cause nystagmus due to the interconnection between the vestibular system and the oculomotor nuclei. It is generally horizontal, rotary, and with tremors that beat towards the healthy side. The amplitude of the shocks increases if the gaze is directed to the other side.

It may increase by changing head position or vigorously shaking the head (head-shaking nystagmus).

The initial assessment of nystagmus is performed with the patient supine with an unfocused gaze (+30 diopter lenses or Frenzel lenses can be used to avoid fixation of the gaze). The patient is then slowly rotated to the left lateral position and then to the right; the direction and duration of nystagmus and any development of vertigo are observed.

Nystagmus occurs when the head is turned towards the affected ear, for example in paroxysmal positional vertigo.

The plane according to which the nystagmus “beats” depends on many factors and mainly on the affected district and, in labyrinthine alterations, the affected semicircular canal. In labyrinthine alterations, the nystagmus will therefore almost always be horizontal.

When describing the direction of nystagmus we always indicate that of the rapid phase, which in the case of vestibular syndromes beats towards the hyperfunctioning side.

Vestibular Nystagmus typically has an acute onset and is characterized by annoying tinnitus, vertigo, oscillopsia, and sometimes nausea.

The most common causes include:

• Labyrinthitis
• Neuritis
• Meniere’s syndrome
• Toxins
• Benign paroxysmal positional vertigo
• Vascular ischemia

Pendular Nystagmus

Acquired Pendular Nystagmus (APN) is an oscillatory eye movement in which the two opposite slow phases have similar waveforms.

APN commonly occurs in Multiple Sclerosis (MS) and causes a visual impairment related to the presence of oscillopsia.

It is frequently seen following demyelinating lesions of the brainstem or following unilateral visual impairment.

It is characterized by pendular movements with a mixed trajectory, unlike congenital pendular where oscillations are mostly horizontal.

It is often associated with Internuclear Ophthalmoplegia or Skew Deviation.

Previous studies have shown that symptomatic therapy with gabapentin or memantine can reduce the amplitude or frequency of nystagmus, but there is not enough scientific evidence.

Other studies with intravenous administration of Ioscin 0-4 mg

(Scopolamine) have abolished nystagmus fluctuations in MS patients (also certified using electro-oculography). Nystagmus reappeared approximately 15 minutes after the injection of the drug. The long-term therapeutic application of hyoscine is still under investigation.

Saccadic intrusions

Oscillatory movements that may interfere with fixation stability and have no rhythmicity. They are usually secondary to brainstem damage, cerebellar pathology, or in progressive supranuclear palsy.

Therapy and Treatment of Nystagmus

The goals of treatment are to reduce the amplitude and frequency of nystagmus and to correct and possibly improve vestibular disorders that can cause an involuntary eye movement called nystagmus, as there is a connection between the vestibular system and the oculomotor nuclei.

In the case of acquired forms, unlike congenital and childhood forms, medical therapy aims at resolving the cause of nystagmus, whether it is related to vestibular or neurological alterations.

Several rare syndromes are associated with nystagmus and as such should be treated in collaboration with a neurologist, ophthalmologist, and orthoptist if they are associated with binocular vision disorders or torticollis.

Biblography

1. American Journal of Case Reports, Pharmacological and Behavioral Strategies to Improve Vision in Acquired Pendular Nystagmus, 2022.07.03, Hassen Kerkeni, Dominik Brügger, Georgios Mantokoudis, Mathias Abegg, David S. Zee
2. Journal of Neurology, Neurosurgery, and Psychiatry 1982;45:431-439, Acquired pendular nystagmus: its characteristics, localizing value and pathophysiology, MA Gresty, JJ Ell, LJ Findley