Visual Symptoms of Parkinson’s Disease

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Article initiated by:

Ayman Okla Suleiman, MD, Grecia Rico, Stacy V. Smith, MD, Michael Apolinario

All contributors:

Bayan Al Othman, MD, Randy Igbinoba, MD, MPH, MBA, Dan Gudgel, Stacy V. Smith, MD, Aroucha Vickers, DO, Claudia Prospero Ponce, MD, Ashwini Kini, MD

Assigned editor:

Claudia Prospero Ponce, MD

Review:

Assigned status Up to Date

 by Claudia Prospero Ponce, MD on May 29, 2024.

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Contributing Editors:	add

Disease Entity

For an audio summary of this entity visit AAO: https://www.aao.org/audio/ocular-disease-in-older-population-parkinson39s. [1]

For further information for patients and family members caring for patients with PD, other links to visit: https://www.parkinson.org/Understanding-Parkinsons/Symptoms/Non-Movement-Symptoms/Vision-Changes and https://www.apdaparkinson.org/what-is-parkinsons/symptoms/eye-vision-issues/

Disease

Parkinson disease (PD) is a progressive, neurodegenerative disease of the central nervous system, particularly the basal ganglia and dopaminergic pathways, presenting with a variety of clinical features. Ophthalmologic manifestations of PD can originate from motor (efferent) or sensory (afferent) dysfunction. Recent studies at Mayo showed that some of the ocular findings can actually herald the progression, or even diagnose, Parkinsons disease, such as rapid eye movement sleeping disorder, stereopsis, smooth pursuits, saccades, impaired contrast sensitivity and color vision, in addition to the very well known decreased blinking rate

This entry summarizes the ophthalmologic manifestations of PD.

Pathophysiology

The decreased levels of dopamine in the central nervous system in PD 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. Reduced levels of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) have also been shown to be associated with visual hallucinations in PD, and is believed to be a result of impaired signaling to the visual cortex.

Visual hallucinations can be seen in up to 40% of patients with PD. The pathophysiology of visual hallucinations in PD is not well described, but some hypotheses include dysfunction in the visual association cortex, “dream overflow” from the pontogeniculo-occipital regulating system, or deficiencies in the visual afferent system including retinal nerve fiber layer (RNFL) thinning. There is some evidence suggesting that hallucinations are possibly due to errors in “bottom-up processing” of data from the retina and less likely from “top-down processing” involving memory and imagination.

Diagnosis

History

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

Symptoms

Although many patients with PD experience visual symptoms, they may not report them unless specifically asked. Patients may report a variety of visual afferent and efferent symptoms. Compared to age-matched patients without PD:

• Binocular horizontal diplopia, mostly at near, and may occur due to convergence insufficiency, impairing reading. The impaired ocular motor control in Parkinson disease may also decompensate pre-existing phorias.
• Monocular diplopia, uni or bilateral, secondary to ocular surface disease (see below)

• Photosensitivity
• Subjective reductions in visual quality, such as visual acuity, color sensitivity, or contrast sensitivity
• Oscillopsia
• Impaired spatial perception

• Decreased blinking rate, the characteristic “stare” in PD is common and may cause Dry eyes that could produce paradoxical epiphora (excessive tearing), burning, or dryness. The dryness of the ocular surface may cause Monocular (unilateral or bilateral) diplopia.

• Apraxia of eyelid opening, where patient can close the eyes voluntarily but can Not open them back. This can be overcome by opening the eye mechanically with the fingers
• Blepharospasm, lids involuntary spasm bilaterally and patients may complain that they “cannot keep their eyes open”.

• Visual hallucinations, may occur in PD and Lewy Body Dementia and are of similar quality in both. Compared to patients without PD, the hallucinations in PD tend to be complex (formed, definite figures) instead of simple (patterns, or abstract forms like flashes of light or dots). Hallucinations can also include the sensation of a “passing shadow”. These hallucinations may be a narcolepsy-like REM sleep disorder during daytime with characteristics of: vision of human figures, animals, faces or "scenery of great beauty"

• Freezing in narrow spaces, like hallways, is also a symptom of PD thought to have a basis in the visual system.

Over the last decade studies have shown that patients with Age Related Macular Degeneration (AMD) are at a higher risk to develop PD than those who do not have AMD, but a causation effect has not been identified.

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.

Signs

• General exam signs include bradykinesia, resting tremor, cogwheel rigidity, postural instability, and a stooped, festinating gait.

• 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.

Clinical diagnosis

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

Management

General treatment

Supportive 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 might benefit from individual and separate sets of glasses (as opposed to bifocal or progressive lenses) for different distances (e.g., reading, the computer, and distance). The bradykinesia of PD is manifest in the eye movements as well, leading to difficulty in transitioning between the different lens areas, so bifocals and progressive lenses may be difficult to use in PD. 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.

• 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 may benefit from botulinum toxin injections.
• Impairments in color vision and contrast sensitivity can be corrected with levodopa.

• Visual hallucinations may be related to the underlying disease or to medications. Consider working with the patient’s neurologist to adjust dopaminergic medications, if possible. Atypical antipsychotics such as quetiapine or cholinesterase inhibitors such as rivastigmine may help control these symptoms. Attention to the patient's adequate sleep cycle may prove beneficial to reduce hallucinations.
• Patients that experience exacerbation of visual symptoms as antiparkinson drug doses wane should receive more frequent doses, switch to longer acting medications, or be treated with an additional medication that augments the efficacy of their original medication.

Additional Resources

• American Parkinson's Disease Association: Eye Problems in Parkinson’s Disease.