New-Onset Visual Snow Syndrome Following Prescription of Bupropion in a Patient With Macular Degeneration and Geographic Atrophy

Visual snow syndrome (VSS) is a perceptual disorder characterized by continuous visual disturbances often described as resembling television “static.” Patients experiencing VSS also often report palinopsia, photophobia, and entoptic phenomena such as floaters or blue field “sprites.” Increasing evidence suggests that VSS is a distinct neurological entity rather than a subtype of migraine with aura or Charles Bonnet syndrome. Neuroimaging studies have demonstrated hypermetabolism in the lingual gyrus and altered thalamocortical connectivity in affected patients, implicating cortical dysrhythmia and impaired visual processing inhibition as potential mechanisms.^1–3 This report describes the case of a patient who developed VSS following exposure to bupropion, a commonly prescribed antidepressant, and tracks their clinical course through to resolution of symptoms following withdrawal of bupropion.

Case Report

A patient in their 60s with advanced macular degeneration complicated by bilateral geographic atrophy presented with new-onset visual disturbances shortly after initiation of bupropion for depression. Their medical history included major depressive disorder, hypertension, hypothyroidism, nephrolithiasis, gastroesophageal reflux disease, and breast cancer in remission. Additional medications included venlafaxine, levothyroxine, amlodipine, and pantoprazole, which were all tolerated with no adverse effects. They had no history of migraine, seizure disorder, traumatic brain injury, or substance use. There was no family history of psychiatric or migraine disorders.

The patient developed a major depressive episode after functional decline related to progressive central vision loss. They endorsed low mood, anhedonia, amotivation, early morning awakening, and loss of appetite, with no psychotic symptoms or suicidal ideation. Outpatient psychiatric evaluation led to the initiation of bupropion ER 150 mg daily for depressive symptoms in the context of an incomplete response to venlafaxine 262.5 mg daily and psychotherapy. The initial response to bupropion ER 150 mg daily was positive, and this was well tolerated, so the dose was increased to 300 mg daily to enhance therapeutic response.

Within 10 days of starting the 300-mg dose of bupropion, the patient reported continuous flickering of tiny dots across their entire visual field, described as “like static on an old television.” The disturbance was binocular, persistent, and unaffected by light level. The patient also developed mild photophobia and afterimages consistent with palinopsia. Symptoms were distressing, interfering with amplified reading, ambulation, and sleep. There were no additional visual or focal neurological symptoms, and there were no changes in mental status.

Urgent ophthalmology follow-up confirmed stable bilateral geographic atrophy with no new choroidal neovascularization or acute retinal changes. Optical coherence tomography (OCT) was unchanged from baseline. The patient’s symptoms were not felt to be consistent with progression of macular degeneration, Charles Bonnet syndrome, or ocular migraine.

Bupropion was tapered and discontinued after 3 weeks due to the suspected adverse effect. VSS symptoms improved dramatically as the dose was tapered to 150 mg daily and ceased 3–4 days after bupropion was discontinued. Baseline visual impairment persisted, but the patient reported no persistent VSS symptoms and has been stable from an ophthalmic perspective for approximately 2 months since the discontinuation of bupropion, and the psychiatric symptoms have stabilized as well.

Discussion

This case describes the novel onset of VSS in temporal association with initiation of bupropion in a patient with macular degeneration with geographic atrophy. Several considerations highlight its clinical and scientific significance.

Although antidepressant-associated hallucinations and perceptual changes are described in the literature, this appears to be only the second report of persistent VSS following bupropion exposure.^4–6 The close temporal relationship between drug initiation and symptom onset, in addition to the resolution of symptoms with drug discontinuation, suggests a possible triggering role for dopaminergic modulation.

Functional imaging of VSS has demonstrated hyperexcitability of the visual association cortex, particularly the lingual gyrus, and abnormal thalamocortical processing.^1–3 Bupropion enhances synaptic dopamine and norepinephrine, which may alter visual cortical excitability. In patients with reduced retinal input due to macular degeneration with geographic atrophy, cortical processing may be further destabilized, unmasking latent susceptibility to VSS.

Differential Diagnosis

The persistent static-like phenomenon was inconsistent with the following:

• Progression of macular degeneration: OCT and fundus imaging–confirmed stability.
• Charles Bonnet syndrome: Typically involves complex formed hallucinations rather than uniform static.⁷
• Migraine aura: Absent episodic course, headache association, stereotypical aura, or transient symptoms.⁸
• Medication-induced hallucinosis: Bupropion has been associated with complex hallucinations, but the continuous, grainy disturbance was distinct.⁹
• Temporal lobe epilepsy: No history of seizures, no alteration in mental status, and no stereotypies.

Thus, medication-induced VSS was the most consistent diagnosis.

Clinical Implications

This case underscores several points for clinical practice:

• Providers should consider VSS in the differential diagnosis of new visual disturbances during antidepressant treatment, especially with dopaminergic medications and with a stereotypical phenomenological presentation.
• Patients with retinal disease may be particularly vulnerable to drug-induced dysregulation of cortical visual processing.
• Once established, offending agents should be discontinued to avoid persistent symptoms due to possible enduring neuroplastic changes.

Causality cannot be established from a single case. However, the temporal relationship, absence of prior history, resolution with drug discontinuation, and ophthalmologic stability support a probable association. Additional pharmacovigilance and mechanistic studies are warranted.

Article Information

Published Online: June 18, 2026. https://doi.org/10.4088/PCC.25cr04169
© 2026 Physicians Postgraduate Press, Inc.
Prim Care Companion CNS Disord 2026;28(3):25cr04169
Submitted: December 18, 2025; accepted February 22, 2026.
To Cite: Volle DC. New-onset visual snow syndrome following prescription of bupropion in a patient with macular degeneration and geographic atrophy. Prim Care Companion CNS Disord 2026;28(3):25cr04169.
Author Affiliation: Department of Psychiatry, Geisel School of Medicine at Dartmouth, Dartmouth Health, Lebanon, New Hampshire.
Corresponding Author: Dax C. Volle, MD, 1 Medical Center Dr – 5D Psychiatry, Lebanon, New Hampshire 03766 ([email protected]).
Financial Disclosure: None.
Funding/Support: None.
Patient Consent: Consent was received from the patient to publish the case report, and information has been de-identified to protect anonymity.