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Eye movement disorder without double vision
Last reviewed: 04.07.2025
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If the eye movement disorder is not accompanied by double vision, then this suggests a supranuclear nature of the lesion, i.e. gaze disorders. During clinical examination, paralysis is detected only in concomitant eye movements, the same movement deficit is detected in both eyes, the eyeballs remain parallel with the direction of gaze preserved. If there is strabismus without double vision, then one of the other two disorders is present: concomitant strabismus or internuclear ophthalmoplegia. Let us consider these three situations in sequence.
A. Concomitant paralysis.
Concomitant paralysis (impaired eye movements without divergence along the axis) is always caused by damage to the supranuclear centers.
- I. Paresis (paralysis) of sideways gaze.
- Damage to the brainstem gaze center (stroke, tumors, multiple sclerosis, intoxication).
- Damage to the frontal cortical gaze center in field 8, the patient “looks at the lesion” (strokes, tumors, atrophic processes, trauma).
- II. Paresis (paralysis) of upward gaze (as well as downward gaze) differs from peripheral paralysis of the external eye muscles by the presence of Bell's phenomenon, the phenomenon of "doll's eyes".
- Brain stem tumor.
- Non-communicating hydrocephalus.
- Progressive supranuclear palsy.
- Whipple's disease.
- Wilson-Konovalov disease.
- Huntington's chorea.
- Progressive multifocal leukoencephalopathy in malignant neoplasms.
B. Other gaze disorders:
- Ocular dysmetria (the eyes oscillate on a fixed object, which is observed in diseases of the cerebellum).
- Congenital ocular apraxia (Cogan syndrome)
- Oculogyric crises
- Psychogenic gaze deviations
C. Concomitant strabismus
D. Internuclear ophthalmoplegia (vascular lesion of the brainstem, multiple sclerosis, tumor, rarely - other causes)
A. Concomitant paralysis.
I. Paralysis of gaze to the side.
Impaired eye movements without divergence in the axis are known as concomitant palsies. They are always caused by damage to the supranuclear gaze centers in the brainstem or cortex. Nystagmus in gaze paresis is often accompanied by other disorders. Differentiation from progressive ocular muscular dystrophy (a slowly progressing disease, often accompanied by ptosis, dysfunction of the pharyngeal muscles) with complete paralysis of all eye movements in parallel axes is rarely difficult. Concomitant palsies may be caused by:
Lesions of the brainstem gaze center ("nucleus para-abducens") in the caudal part of the pons. Lesions in this area result in the inability to look at the affected side.
Causes: vascular (often in elderly patients, sudden onset, always accompanied by other disorders), tumors, multiple sclerosis, intoxication (eg, carbamazepine).
Damage to the frontal cortical gaze center in field 8. When it is irritated, there is a deviation of the eyes and head to the opposite side, which sometimes develops into an epileptic adversive seizure. Damage to this area leads to a deviation of the gaze and head to the side of the lesion, since the activity of the opposite field 8 predominates (concomitant deviation); "the patient looks at the lesion." A few days after the onset of the lesion, the patient is able to look straight ahead, but there is still restlessness of the eyeballs when trying to look in the opposite direction. With time, even this function is restored. But the nystagmus observed during gaze paresis remains, with a fast component to the opposite side. Tracking eye movements are preserved.
Causes of damage to the frontal gaze center include strokes, tumors (often accompanied by symptoms of irritation, sometimes by mental disorders of the frontal type); atrophic processes (in elderly patients, accompanied by dementia and other cortical disorders, in particular, neuropsychological); trauma (indication in the anamnesis, sometimes external injuries, skull fractures, subjective symptoms of concussion, blood in the cerebrospinal fluid, rarely other neurological disorders).
Bilateral horizontal gaze palsy (a rare neurological phenomenon) has been described in multiple sclerosis, pontine infarction, pontine hemorrhage, metastases, cerebellar abscess, and as a congenital disorder.
II. Paresis (paralysis) of upward gaze (as well as downward)
Paresis of upward gaze (Parinaud's syndrome, when accompanied by a convergence disorder), as well as downward gaze, indicates a lesion in the tegmentum of the rostral parts of the midbrain. However, it should be noted that many patients, especially elderly patients, in severe condition or stupor, experience restlessness of the eyeballs when looking upward. True vertical gaze palsy can be recognized (and differentiated from peripheral paralysis of the external eye muscles) by the presence of the following signs:
Bell's phenomenon. The examiner passively lifts the upper eyelid when the patient attempts to forcefully close the eyes; a reflex upward rotation of the eyeball is detected. The phenomenon of "doll's eyes". When the patient fixes his gaze on an object located directly in front of the eyes, the examiner bends the patient's head forward. In this case, the patient's gaze remains fixed on the object due to upward rotation of the gaze (despite paresis of voluntary upward gaze).
Causes of progressive vertical ophthalmoplegia may include:
Brainstem tumor (a common cause, also manifested by other oculomotor disorders, convergence palsy, other neurological disorders, including symptoms of midbrain damage, headache, manifestations of increased intracranial pressure, and in pinealoma also precocious puberty).
Non-communicating hydrocephalus (symptoms of increased intracranial pressure are noted; in children, the head size increases).
Progressive supranuclear palsy syndrome
Steele-Richardson-Olydevsky syndrome (observed in elderly patients, accompanied by akinetic parkinsonian syndrome, dementia, and rarely total external ophthalmoplegia).
Whipple's disease (uveitis, dementia, gastrointestinal disorders).
Wilson-Konovalov disease.
Huntington's chorea.
Progressive multifocal leukoencephalopathy in malignant diseases.
B. Other gaze disorders
Other gaze disorders (which partly manifest themselves as reading difficulties) should also be briefly mentioned:
Ocular dysmetria, in which the eyes oscillate on a fixed object. This disorder is found in diseases of the cerebellum.
Congenital ocular apraxia or Cogan's syndrome. To shift the gaze to another object, the patient must turn the head further, beyond the fixed object. When the eyes are fixed on the object again from the position with excessive head rotation, the head turns back to the correct direction. This process leads to bizarre head movements (which must be differentiated from tics), as well as difficulties in reading and writing (need to be differentiated from congenital alexia).
Oculogyric crises are involuntary deviation of the eyes to one side, or more often upward. Previously, they were observed in postencephalitic parkinsonism, being an early symptom of this disease (indications in the anamnesis of the disease with high temperature, other extrapyramidal symptoms; which helps differentiate from hysteria). Currently, the most common cause is iatrogenic (side effect of neuroleptics).
Psychogenic gaze deviations.
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C. Concomitant strabismus
Concomitant strabismus has the following characteristics: It is observed from childhood.
Often accompanied by decreased visual acuity (amblyopia). When examining eye movements, strabismus is noted, one eye does not participate in certain directions of movement.
When examining eye movements separately, when one eye is closed, the movements of the other eye are carried out in full.
The non-focusing eye (covered by the examiner) deviates to one side (consensus divergent or convergent strabismus). This phenomenon may alternate in both eyes (consensus alternating strabismus; e.g., divergent), and may be detected by the eye-covering test. Strabismus is also a consequence of a congenital or early acquired disorder of the balance (equilibrium) of the eye muscles, is usually accompanied by a decrease in visual acuity in one eye, and has no specific neurological significance.
D. Internuclear ophthalmoplegia
Internuclear ophthalmoplegia causes disturbance of the ocular axes without diplopia. Lesion of the medial longitudinal fasciculi between the brainstem gaze center and the oculomotor nuclei interrupts lateral gaze impulses from the brainstem center and the homolateral abducens nucleus to the orally located third nerve nuclei, which control the internal rectus muscle of the opposite eye. The abducted eye moves easily laterally. The adducted eye does not cross the midline. However, convergence is preserved on both sides, since impulses to both eyes from the rostrally located convergence center (Perlia nucleus) allow the "paretic" eye to move together with the "nonparetic" eye.
Complete internuclear ophthalmoplegia is rare, but many patients with partial internuclear ophthalmoplegia present with slow saccades of the adducted eye only.
The cause of internuclear ophthalmoplegia is usually a vascular lesion of the brainstem; multiple sclerosis or a tumor. Very rarely, non-diplopia is the result of other causes - for example, as part of giant cell arteritis syndrome.
Diagnostic studies for internuclear ophthalmoplegia
- General and biochemical blood analysis,
- MRI or CT,
- Evoked potentials of different modalities
- Examination of cerebrospinal fluid, fundus, consultation with an ophthalmologist.
Global gaze palsy is the inability to voluntarily move the gaze in any direction (total ophthalmoplegia). Global gaze palsy in isolation is rare; it is usually accompanied by symptoms of involvement of adjacent structures.
Main causes: oculomotor apraxia; Guillain-Barré syndrome; myasthenia; thyroid ophthalmopathy (especially when combined with myasthenia); chronic progressive external ophthalmoplegia syndromes; Wilson-Konovalov disease; pituitary apoplexy; botulism; tetanus; progressive supranuclear palsy; anticonvulsant intoxication; Wernicke's encephalopathy; acute bilateral pontine or mesodiencephalon lesions, abetalipoproteinemia, HIV encephalopathy, Alzheimer's disease, adrenoleukodystrophy, corticobasal degeneration, Fahr disease, Gaucher disease, Leigh disease, neuroleptic malignant syndrome, neurosyphilis, paraneplastic syndrome, Whipple disease
To clarify the diagnosis, MRI, myasthenic tests, and EMG are used. Botulism must be excluded.