HISTORY: Visual disturbances
Ms. G, age 30, has schizoaffective disorder and presents with worsening auditory hallucinations, paranoid delusions, and thought broadcasting and insertion, which is suspected to be related to a change from olanzapine to aripiprazole. She complains of visual disturbances—a hallucination of flashing lights—that she describes as occurring “all the time, like salt-and-pepper dancing, and sometimes splotches.” Her visual symptoms are worse when she closes her eyes and in dimly lit environments, but occur in daylight as well. Her vision is otherwise unimpaired.
The visual disturbances started with Ms. G’s first psychotic break at age 23 and have persisted continuously. She reports that at first, the spots were more intense, like an incessant strobe light. These symptoms are aggravated by sleep deprivation and anger and improve only with topiramate, 100 mg/d, which was prescribed a year earlier after a neurologic consultation but discontinued because of cognitive side effects.
Ms. G also complains of dull, aching, continuous headaches in the center of her forehead, which do not wake her, are not worse in the morning, and do not vary with the intensity of her visual symptoms. The headaches are incorporated into her system of delusions; she believes they “drain the electricity from her head” and make her feel better. She denies a history of migraines. Ms. G has a history of experiencing well-formed visual hallucinations, such as the devil, but has not had them for several years.
She had 5 to 10 episodes over the last 2 years that she describes as seizures—“an earthquake, a huge whooshing noise,” accompanied by heart palpitations that occur with stress, in public, in bright lights, or whenever she feels vulnerable. These episodes are not associated with loss of consciousness, incontinence, amnesia, or post-ictal confusion and she can stop them with relaxation techniques such as deep breathing and reminding herself to calm down. The last episode was 2 months ago and seemed unrelated to her visual phenomena. She also complains of occasional paresthesias in her extremities but denies dizziness, presyncope, or blurry or double vision.
Ms. G is obese and has no history of head injury or birth defects. Her family history is negative for epilepsy; however, her mother has bipolar disorder and father has schizophrenia. Her medications are phentermine, 37.5 mg/d for short-term management of obesity, oxcarbazepine, 600 mg/d for supposed partial seizures, sertraline, 100 mg/d for depression, aripiprazole, 10 mg/d, and nizatidine, 150 mg/d, for gastroesophageal reflux disease. She does not use alcohol, cigarettes, or illicit drugs. Ms. G obtained a master’s degree in health communications and works as a research assistant at a local medical school.
The authors’ observations
Visual hallucinations are not distortions of reality but original false perceptions that co-occur with real perceptions.1 They vary from simple, elemental hallucinations involving flashes of light or geometric figures to more complex elaborations such as seeing crawling insects or a flock of angels.2 Hallucinations can originate anywhere in the visual system from the lens to the visual cortex and can be vascular, toxic, electrophysiologic, structural, or neurochemical manifestations of neurologic, psychiatric, or ophthalmologic disorders. Depending on the hallucination’s etiology, treatment varies from emergent ophthalmologic examination and retinal surgery to antipsychotic therapy to simple observation. Photopsia is a perception of flashing lights, and its etiology varies; causes can be categorized as emergent or nonemergent.
Emergent causes of photopsia typically have a sudden onset, often can be diagnosed from associated symptoms or medical history, and must be recognized quickly to prevent permanent vision loss. Posterior vitreous detachment and retinal tearing can manifest as flashes of light, floaters, or blurred vision in the peripheral visual field that are worse in dim illumination and localizable by the patient. Retinal detachment can cause photopsia, floaters, or a “curtain” or “shadow” moving over the visual field, which may be accompanied by central or peripheral vision loss.3 Severe myopia is a risk factor for retinal detachment.
New-onset photopsia can suggest cytomegaloviral retinitis in an immune-compromised patient, and ocular-vascular crisis in a patient with sickle cell disease. New-onset or recurrent photopsia with bilateral blurred vision, ataxia, vertigo, dysarthria, or drop attacks may be caused by vertebrobasilar artery insufficiency (VBAI). Photopsia has been reported as the presenting symptom in carotid artery dissection.4 Photopsia correlated with eye movement implicates the retina or optic nerve. All of these etiologies except for VBAI should be referred to an ophthalmologist for indirect ophthalmoscopy and evaluation.
Nonemergent causes of photopsia include: