Visual symptoms of Parkinson’s disease

From EyeWiki
Original article contributed by: Stacy V. Smith, MD, Grecia Rico
All contributors: Stacy V. Smith, MD
Assigned editor: Andrew G. Lee
Review: Assigned status Not reviewed by Stacy V. Smith, MD on October 30, 2015.

Parkinson disease (PD) is a progressive neurodegenerative disorder characterized by multiple clinical features associated with decreased levels of dopamine.

Disease Entity


PD is a progressive and degenerative disease of the central nervous system presenting with a diverse variety of clinical features. Ophthalmologic manifestations of PD can originate from a motor or a sensory dysfunction.


The decreased levels of dopamine in the central nervous system contribute to both motor and sensory symptoms. In the eye, dopamine is a neurotransmitter present in amacrine cells in the retina and it is thought to regulate the activity among ganglion cells, bipolar cells and photoreceptors.



A history of PD or parkinsonian symptoms should lead the clinician to consider the many possible ophthalmic disorders that could occur as part of the disease syndrome. An individual patient may have one or multiple Parkinson-related disorders.

Physical examination

Physical exam findings will vary depending on the patient’s presentation. Some patients may have a normal ophthalmologic exam, either due to symptoms arising from higher cortical areas or the transient nature of some symptoms.


General exam signs include bradykinesia, resting tremor, cogwheel rigidity, and a stooped, festinating gate.

Ophthalmologic signs may include impaired convergence (i.e. convergence insufficiency), decreased blinking frequency, dry eye, punctate epithelial erosions, blepharitis, blepharospasm, and apraxia of eyelid opening.

Corneal epithelial erosions, dry eyes, and lacrimal gland dysfunction may be worsened by apraxia of eyelid opening, decreased blink rate, and reduced tear secretion.


Patients may report a variety of symptoms. Binocular horizontal diplopia at near may occur in convergence insufficiency. The impaired ocular motor control in Parkinson disease may decompensate pre-existing phorias.

Dry eye may produce paradoxical epiphora (excessive tearing), burning, or dryness. Monocular (unilateral or bilateral) diplopia may occur in this setting.

Blepharospasm and apraxia of eyelid opening are associated with the complaint that they “cannot keep their eyes open.” Apraxia of eyelid opening often can be overcome by opening the eye mechanically with the fingers, but blepharospasm may resist opening in this manner until the spasm subsides.

Visual hallucinations may occur in PD.

Clinical diagnosis

Diagnosis of Parkinson-related ophthalmologic disorders is primarily made clinically with history and physical exam as described above.


General treatment

Support care and conventional therapy of the underlying dopaminergic disorder is the main treatment. If the patient is already being treated with dopamine replacement it can result beneficial to re-evaluate treatment adherence and assure correct dosage.

Medical therapy

Symptomatic treatment of the individual complaints is the primary ophthalmologic approach.

Patients with PD need individual and separate sets of glasses (as opposed to bifocal or progressive lenses) for reading, the computer, and distance. The bradykinesia is manifest in the eye movements as well, leading to difficulty in transitioning between the different lens areas. In addition, their PD postural changes (e.g., chin down) may position their gaze through the upper segment of the bifocal lens. This may increase the risk of falls because they are unable to focus at distance to see the floor and may not be able to avoid obstacles in their path. Prisms may be added to reading glasses to help with convergence insufficiency.

The dry eye and blepharitis can be treated with topical tears and ointments, topical anti-inflammatory drops, ocular lubricants, oral fish oil, oral medications (e.g., doxycycline) and lid hygiene (e.g., lid scrubs).

Blepharospasm and apraxia of eyelid opening can be treated with botulinum toxin injections.

Visual hallucinations may be related to the underlying disease or the medications. Consider working with the patient’s neurologist to adjust the dopaminergic medication, if possible. Atypical antipsychotics such as quetiapine or cholinesterase inhibitors such as rivastigmine may help control the symptoms.

Additional Resources


1.- Almer, Zina, Kathyrn S. Klein, Laura Marsh, Melissa Gerstenhaber, and Michael X. Repka. "Ocular Motor and Sensory Function in Parkinson's Disease." Ophthalmology: 178-82. Print.

2.- Straughan, S., Collerton, D., & Bruce, V. (2015). Visual Priming and Visual Hallucinations in Parkinson's Disease. Evidence for Normal Top-Down Processes. Journal of Geriatric Psychiatry and Neurology.

3.-Biousse, V., Skibell, B., Watts, R., Loupe, D., Drews-Botsch, C., & Newman, N. (2004). Ophthalmologic features of Parkinson's disease. Neurology, 177-180.

4.- L.A. Hunt, A.A. Sadun, C.J. Bassi. Review of the visual system in Parkinson's disease. Optom Vis Sci, 72 (1994), pp. 92–99