Visual symptoms of Parkinson’s 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 (6). Ophthalmologic manifestations of PD can originate from motor (efferent) or sensory (afferent) dysfunction(6). This entry summarizes the ophthalmologic manifestations of PD.
The decreased levels of dopamine in the central nervous system in PD contribute to both motor and sensory symptoms (6). 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 (4). 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 (8).
Visual hallucinations can be seen in up to 40% of patients with PD (9). 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 (1). 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 (3).
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.
- Although many patients with PD experience visual symptoms, they may not report them unless specifically asked (2). Patients may report a variety of visual afferent and efferent symptoms. Compared to age-matched patients without PD, binocular horizontal diplopia at near may occur due to convergence insufficiency, impairing reading (2). The impaired ocular motor control in Parkinson disease may decompensate pre-existing phorias.
- Patients may report photosensitivity as well as reductions in visual acuity, color sensitivity, or contrast sensitivity (4, 10).
- Oscillopsia and impaired spatial perception are among the more frequent complaints made by patients, especially in the elderly (10)
- The characteristic “stare” in PD is due to decreased blink frequency. Dry eye may produce paradoxical epiphora (excessive tearing), burning, or dryness. Monocular (unilateral or bilateral) diplopia may occur in this setting (4).
- Blepharospasm and apraxia of eyelid opening are associated with the complaint that the lids involuntary spasm bilaterally or that the patient “cannot keep their eyes open” (5). 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 and Lewy Body Dementia and are of similar quality in both (2, 7). 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” (4).
- Freezing in narrow spaces, like hallways, is also a symptom of PD thought to have a basis in the visual system (4).
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, 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.
Diagnosis of Parkinson-related ophthalmologic disorders is primarily made clinically with history and physical exam as described above.
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.
- 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) (6). 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 (5).
- 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) (5).
- Blepharospasm and apraxia of eyelid opening may benefit from botulinum toxin injections (5).
- Impairments in color vision and contrast sensitivity can be corrected with levodopa (10).
- 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 (5).
- 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 (10).
- American Academy of Ophthalmology. Neuro-Ophthalmology/Orbit: Parkinson disease Practicing Ophthalmologists Learning System, 2017 - 2019 San Francisco: American Academy of Ophthalmology, 2017.
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9. Bernardin, F., Schwan, R., Lalanne, L., Ligier, F., Angioi-Duprez, K., Schwitzer, T., & Laprevote, V. (2017). The role of the retina in visual hallucinations: A review of the literature and implications for psychosis. Neuropsychologia, 99, 128-138. doi: 10.1016/j.neuropsychologia.2017.03.002
10. Savitt, J., & Mathews, M. (2018). Treatment of visual disorders in parkinson disease. Current Treatment Options in Neurology, 20(8), 1-15. doi: 10.1007/s11940-018-0519-0