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The woman who saw the light
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:
- drug toxicity
- migraine headache
- thyroid ophthalmopathy
- arteriovenous malformations
- seizures
- psychiatric disorders.
Digoxin, cocaine, paclitaxel, and clomiphene may have ocular side effects, including photopsia. The first symptoms of digitalis toxicity often are visual and include photopsia, yellow or green discoloration of the visual field, halos, and the appearance of frost over objects.5 Signs of cocaine intoxication can include visual hallucinations such as photopsia, shadows, moving objects, and insects crawling and co-occurring euphoria, hypervigilance, impaired judgment, and autonomic changes such as tachycardia, pupillary dilation, hypertension, and nausea.6 High-dose paclitaxel infusion has been reported to cause photopsia.7 Clomiphene can cause flickering lights and shimmering that persists after discontinuing the medication.8
Migraine with aura, which includes photopsia 39% of the time,9 often involves an expanding central visual disturbance or scotoma, and usually is confined to 1 visual field but may involve both. The aura typically lasts 10 to 20 minutes and often is followed by headache. Patients often report a history of episodic stereotyped auras and headache. Ocular examination is normal.
Ophthalmic migraine, also known as ocular or retinal migraine, is thought to be caused by transient vasospasm of the choroidal or retinal arteries and can be precipitated by postural changes, exercise, and oral contraceptives. It manifests as a gradual visual disturbance in a mosaic scotomata pattern that enlarges, producing total unilateral visual loss lasting from minutes to an hour, and—misleadingly—can be associated with minimal or no headache. Ocular examination is normal, and a personal or family history of migraine confirms the diagnosis.
Seizure activity in the occipital cortex and adjacent association areas can produce static light and stars. In a prospective study of 18 patients with occipital epilepsy, visual seizures lasted from a few seconds to 3 minutes—although rarely 20 to 150 minutes—and occurred in multiple clusters a day or week.10 All but 2 patients had secondary generalized tonic-clonic convulsions. Occipital seizures often are misdiagnosed as the visual aura of migraine, particularly when elementary visual hallucinations are followed by post-ictal headache and vomiting.11 Lights with a color or a spherical shape suggest occipital epilepsy. Consider ordering an electroencephalogram (EEG) if the clinical diagnosis is unclear.
EXAMINATION: No obvious cause
During a mental status exam, Ms. G is pleasant, cooperative, alert, and oriented to person, place, and time. Her speech is fluent, her affect is full, and she describes her mood as a “sensitive, overwhelmed state.” Her thoughts occasionally are tangential, and she perseverates on guilty, embarrassed, and paranoid thoughts. She has auditory hallucinations and experiences photopsia during the interview, but denies other visual hallucinations. She shows no deficits in attention, concentration, memory, language, calculations, visuospatial abilities, or general fund of knowledge.
Her physical exam shows pupils that are equal, round, and reactive to light with normal extraocular movements, intact visual fields, 20/20 visual acuity in both eyes with glasses, and sharp optic disc margins with no retinal abnormalities apparent on funduscopic exam. The rest of her physical and neurologic exam is normal. Her complete blood count, electrolytes, kidney, liver function tests, urinalysis, and serum toxicology screens are normal. She has no history of immunodeficiency.
An MRI performed a year earlier showed mild diffuse congestion of a left maxillary sinus but no other intracranial abnormalities, and a waking EEG with sphenoidal electrodes was normal.
The authors’ observations
Evaluation of patients with photopsia includes taking a history and performing an eye examination including visual acuity testing, visual field testing, and funduscopic examination. The appearance, location, and duration of photopsia may help narrow the differential diagnosis and identify emergent cases (Table 1 and Table 2). Seizure activity associated with flashing lights suggests occipital epilepsy. A history of hypertension, diabetes, or polymyalgia rheumatica points to vascular causes, and hyperthyroidism suggests that flashing lights may be phosphenes of Graves’ disease. Myopia or eye trauma could indicate vitreous traction. Prescription medications and illicit drug use may point to a toxic etiology.12
Table 1
Diagnoses suggested by photopsia phenomena
| Feature | Suggested diagnosis |
|---|---|
| Appearance | |
| Twinkling lights with grey spots | Emboli |
| Zigzag lines | Occipital epilepsy |
| White flashes | Vitreous traction on the retina |
| Flickering lights and shimmering | Clomiphene use |
| Temporally located flashes of light, floaters, or blurred vision that is worse in dim illumination | Posterior vitreous detachment and retinal tearing |
| Location | |
| Temporal | Migraine or retinal pathology |
| Central | Occipital lesion or embolus |
| Monocular | Retinal pathology |
| Binocular | Cerebral cause |
| Duration | |
| Lightning quick | Vitreous detachment |
| Lasts up to 30 minutes | Migraine or occipital epilepsy |
Table 2
Photopsia differential diagnosis: Look for co-occurring symptoms
| Co-occurring symptoms | Suggests |
|---|---|
| Seizure activity associated with flashing lights | Occipital epilepsy |
| Yellow or green discoloration to the visual field, halos, and appearance of frost over objects | Digitalis toxicity |
| Shadows, moving objects, and insects crawling with co-occurring euphoria, hypervigilance, impaired judgment, and autonomic changes such as tachycardia, pupillary dilation, hypertension, and nausea | Cocaine intoxication |
| Floaters, or a ‘curtain’ or ‘shadow’ moving over the visual field, which may be accompanied by central or peripheral vision loss | Retinal detachment |
| Bilateral blurred vision, ataxia, vertigo, dysarthria, or drop attacks | Vertebrobasilar artery insufficiency |
OUTCOME: Diagnosis of exclusion
Ms. G’s visual disturbance resembles vitreous detachment or classic migraine; however, the onset is not sudden, her funduscopic exam is normal, and she has no discrete episodes with concomitant headache. Ms. G’s improvement with topiramate is inconsistent with an ophthalmic origin because such photopsia should not improve with medication. It is consistent with recurrent seizures or status epilepticus of the occipital cortex; however, she did not experience multiple discrete episodes a day or generalized seizures experienced by most occipital seizure patients, and her EEG and clinical history are not consistent with seizures. Because we cannot rule out occipital lobe epilepsy, we refer Ms. G for repeat EEG and routine ophthalmologic exam, both of which are normal.
Perceptual disturbances are common in schizoaffective disorder and schizophrenia,13-15 which we consider the most likely etiology of Ms. G’s photopsia, given her normal neurologic and ophthalmologic examinations. We switch her from aripiprazole to ziprasidone, 40 mg/d, discontinue phentermine, and taper and discontinue oxcarbazepine.
Related resources
- Ophthalmology Web. www.ophthalmologyweb.com.
- Aleman A, Larøi F. Hallucinations: the science of idiosyncratic perception. Washington, DC: American Psychological Association; 2008.
Drug Brand Names
- Aripiprazole • Abilify
- Clomiphene • Clomid, Serophene
- Digoxin • Lanoxin
- Nizatidine • Axid
- Olanzapine • Zyprexa
- Oxcarbazepine • Trileptal
- Paclitaxel • Onxol, Taxol
- Phentermine • Adipex-P, Inoamin
- Sertraline • Zoloft
- Topiramate • Topamax
- Ziprasidone • Geodon
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Jaspers K. General psychopathology. Manchester, United Kingdom: Manchester University Press; 1962.
2. Manford M, Andermann F. Complex visual hallucinations. Clinical and neurobiological insights. Brain. 1998;121:1819-1840.
3. Amos JF. Differential diagnosis of common etiologies of photopsia. J Am Optom Assoc. 1999;70(8):485-504.
4. Biousse V, Touboul PJ, D’Anglejan-Chatillon J, et al. Ophthalmologic manifestations of internal carotid artery dissection. Am J Ophthalmol. 1998;126(4):565-577.
5. Butler VP, Jr, Odel JG, Rath E, et al. Digitalis-induced visual disturbances with therapeutic serum digitalis concentrations. Ann Intern Med. 1995;123(9):676-680.
6. Mitchell J, Vierkant AD. Delusions and hallucinations of cocaine abusers and paranoid schizophrenics: a comparative study. J Psychol. 1991;125(3):301-310.
7. Seidman AD, Barrett S, Canezo S. Photopsia during 3-hour paclitaxel administration at doses > or = 250 mg/m2. J Clin Oncol. 1994;12(8):1741-1742.
8. Purvin VA. Visual disturbance secondary to clomiphene citrate. Arch Ophthalmol. 1995;113(4):482-484.
9. Queiroz LP, Rapoport AM, Weeks RE, et al. Characteristics of migraine visual aura. Headache. 1997;37(3):137-141.
10. Panayiotopoulos CP. Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. Epileptic Disord. 1999;1(4):205-216.
11. Walker MC, Smith SJ, Sisodiya SM, et al. Case of simple partial status epilepticus in occipital lobe epilepsy misdiagnosed as migraine: clinical, electrophysiological, and magnetic resonance imaging characteristics. Epilepsia. 1995;36(12):1233-1236.
12. Lichter M. Flashing lights—a warning. The Canadian Journal of Diagnosis. 2002;19:31-35.
13. Parnas J, Handest P, Saebye D, et al. Anomalies of subjective experience in schizophrenia and psychotic bipolar illness. Acta Psychiatr Scand. 2003;108(2):126-133.
14. Phillipson OT, Harris JP. Perceptual changes in schizophrenia: a questionnaire survey. Psychol Med. 1985;15(4):859-866.
15. Cutting J, Dunne F. Subjective experience of schizophrenia. Schizophr Bull. 1989;15(2):217-231.
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:
- drug toxicity
- migraine headache
- thyroid ophthalmopathy
- arteriovenous malformations
- seizures
- psychiatric disorders.
Digoxin, cocaine, paclitaxel, and clomiphene may have ocular side effects, including photopsia. The first symptoms of digitalis toxicity often are visual and include photopsia, yellow or green discoloration of the visual field, halos, and the appearance of frost over objects.5 Signs of cocaine intoxication can include visual hallucinations such as photopsia, shadows, moving objects, and insects crawling and co-occurring euphoria, hypervigilance, impaired judgment, and autonomic changes such as tachycardia, pupillary dilation, hypertension, and nausea.6 High-dose paclitaxel infusion has been reported to cause photopsia.7 Clomiphene can cause flickering lights and shimmering that persists after discontinuing the medication.8
Migraine with aura, which includes photopsia 39% of the time,9 often involves an expanding central visual disturbance or scotoma, and usually is confined to 1 visual field but may involve both. The aura typically lasts 10 to 20 minutes and often is followed by headache. Patients often report a history of episodic stereotyped auras and headache. Ocular examination is normal.
Ophthalmic migraine, also known as ocular or retinal migraine, is thought to be caused by transient vasospasm of the choroidal or retinal arteries and can be precipitated by postural changes, exercise, and oral contraceptives. It manifests as a gradual visual disturbance in a mosaic scotomata pattern that enlarges, producing total unilateral visual loss lasting from minutes to an hour, and—misleadingly—can be associated with minimal or no headache. Ocular examination is normal, and a personal or family history of migraine confirms the diagnosis.
Seizure activity in the occipital cortex and adjacent association areas can produce static light and stars. In a prospective study of 18 patients with occipital epilepsy, visual seizures lasted from a few seconds to 3 minutes—although rarely 20 to 150 minutes—and occurred in multiple clusters a day or week.10 All but 2 patients had secondary generalized tonic-clonic convulsions. Occipital seizures often are misdiagnosed as the visual aura of migraine, particularly when elementary visual hallucinations are followed by post-ictal headache and vomiting.11 Lights with a color or a spherical shape suggest occipital epilepsy. Consider ordering an electroencephalogram (EEG) if the clinical diagnosis is unclear.
EXAMINATION: No obvious cause
During a mental status exam, Ms. G is pleasant, cooperative, alert, and oriented to person, place, and time. Her speech is fluent, her affect is full, and she describes her mood as a “sensitive, overwhelmed state.” Her thoughts occasionally are tangential, and she perseverates on guilty, embarrassed, and paranoid thoughts. She has auditory hallucinations and experiences photopsia during the interview, but denies other visual hallucinations. She shows no deficits in attention, concentration, memory, language, calculations, visuospatial abilities, or general fund of knowledge.
Her physical exam shows pupils that are equal, round, and reactive to light with normal extraocular movements, intact visual fields, 20/20 visual acuity in both eyes with glasses, and sharp optic disc margins with no retinal abnormalities apparent on funduscopic exam. The rest of her physical and neurologic exam is normal. Her complete blood count, electrolytes, kidney, liver function tests, urinalysis, and serum toxicology screens are normal. She has no history of immunodeficiency.
An MRI performed a year earlier showed mild diffuse congestion of a left maxillary sinus but no other intracranial abnormalities, and a waking EEG with sphenoidal electrodes was normal.
The authors’ observations
Evaluation of patients with photopsia includes taking a history and performing an eye examination including visual acuity testing, visual field testing, and funduscopic examination. The appearance, location, and duration of photopsia may help narrow the differential diagnosis and identify emergent cases (Table 1 and Table 2). Seizure activity associated with flashing lights suggests occipital epilepsy. A history of hypertension, diabetes, or polymyalgia rheumatica points to vascular causes, and hyperthyroidism suggests that flashing lights may be phosphenes of Graves’ disease. Myopia or eye trauma could indicate vitreous traction. Prescription medications and illicit drug use may point to a toxic etiology.12
Table 1
Diagnoses suggested by photopsia phenomena
| Feature | Suggested diagnosis |
|---|---|
| Appearance | |
| Twinkling lights with grey spots | Emboli |
| Zigzag lines | Occipital epilepsy |
| White flashes | Vitreous traction on the retina |
| Flickering lights and shimmering | Clomiphene use |
| Temporally located flashes of light, floaters, or blurred vision that is worse in dim illumination | Posterior vitreous detachment and retinal tearing |
| Location | |
| Temporal | Migraine or retinal pathology |
| Central | Occipital lesion or embolus |
| Monocular | Retinal pathology |
| Binocular | Cerebral cause |
| Duration | |
| Lightning quick | Vitreous detachment |
| Lasts up to 30 minutes | Migraine or occipital epilepsy |
Table 2
Photopsia differential diagnosis: Look for co-occurring symptoms
| Co-occurring symptoms | Suggests |
|---|---|
| Seizure activity associated with flashing lights | Occipital epilepsy |
| Yellow or green discoloration to the visual field, halos, and appearance of frost over objects | Digitalis toxicity |
| Shadows, moving objects, and insects crawling with co-occurring euphoria, hypervigilance, impaired judgment, and autonomic changes such as tachycardia, pupillary dilation, hypertension, and nausea | Cocaine intoxication |
| Floaters, or a ‘curtain’ or ‘shadow’ moving over the visual field, which may be accompanied by central or peripheral vision loss | Retinal detachment |
| Bilateral blurred vision, ataxia, vertigo, dysarthria, or drop attacks | Vertebrobasilar artery insufficiency |
OUTCOME: Diagnosis of exclusion
Ms. G’s visual disturbance resembles vitreous detachment or classic migraine; however, the onset is not sudden, her funduscopic exam is normal, and she has no discrete episodes with concomitant headache. Ms. G’s improvement with topiramate is inconsistent with an ophthalmic origin because such photopsia should not improve with medication. It is consistent with recurrent seizures or status epilepticus of the occipital cortex; however, she did not experience multiple discrete episodes a day or generalized seizures experienced by most occipital seizure patients, and her EEG and clinical history are not consistent with seizures. Because we cannot rule out occipital lobe epilepsy, we refer Ms. G for repeat EEG and routine ophthalmologic exam, both of which are normal.
Perceptual disturbances are common in schizoaffective disorder and schizophrenia,13-15 which we consider the most likely etiology of Ms. G’s photopsia, given her normal neurologic and ophthalmologic examinations. We switch her from aripiprazole to ziprasidone, 40 mg/d, discontinue phentermine, and taper and discontinue oxcarbazepine.
Related resources
- Ophthalmology Web. www.ophthalmologyweb.com.
- Aleman A, Larøi F. Hallucinations: the science of idiosyncratic perception. Washington, DC: American Psychological Association; 2008.
Drug Brand Names
- Aripiprazole • Abilify
- Clomiphene • Clomid, Serophene
- Digoxin • Lanoxin
- Nizatidine • Axid
- Olanzapine • Zyprexa
- Oxcarbazepine • Trileptal
- Paclitaxel • Onxol, Taxol
- Phentermine • Adipex-P, Inoamin
- Sertraline • Zoloft
- Topiramate • Topamax
- Ziprasidone • Geodon
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
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:
- drug toxicity
- migraine headache
- thyroid ophthalmopathy
- arteriovenous malformations
- seizures
- psychiatric disorders.
Digoxin, cocaine, paclitaxel, and clomiphene may have ocular side effects, including photopsia. The first symptoms of digitalis toxicity often are visual and include photopsia, yellow or green discoloration of the visual field, halos, and the appearance of frost over objects.5 Signs of cocaine intoxication can include visual hallucinations such as photopsia, shadows, moving objects, and insects crawling and co-occurring euphoria, hypervigilance, impaired judgment, and autonomic changes such as tachycardia, pupillary dilation, hypertension, and nausea.6 High-dose paclitaxel infusion has been reported to cause photopsia.7 Clomiphene can cause flickering lights and shimmering that persists after discontinuing the medication.8
Migraine with aura, which includes photopsia 39% of the time,9 often involves an expanding central visual disturbance or scotoma, and usually is confined to 1 visual field but may involve both. The aura typically lasts 10 to 20 minutes and often is followed by headache. Patients often report a history of episodic stereotyped auras and headache. Ocular examination is normal.
Ophthalmic migraine, also known as ocular or retinal migraine, is thought to be caused by transient vasospasm of the choroidal or retinal arteries and can be precipitated by postural changes, exercise, and oral contraceptives. It manifests as a gradual visual disturbance in a mosaic scotomata pattern that enlarges, producing total unilateral visual loss lasting from minutes to an hour, and—misleadingly—can be associated with minimal or no headache. Ocular examination is normal, and a personal or family history of migraine confirms the diagnosis.
Seizure activity in the occipital cortex and adjacent association areas can produce static light and stars. In a prospective study of 18 patients with occipital epilepsy, visual seizures lasted from a few seconds to 3 minutes—although rarely 20 to 150 minutes—and occurred in multiple clusters a day or week.10 All but 2 patients had secondary generalized tonic-clonic convulsions. Occipital seizures often are misdiagnosed as the visual aura of migraine, particularly when elementary visual hallucinations are followed by post-ictal headache and vomiting.11 Lights with a color or a spherical shape suggest occipital epilepsy. Consider ordering an electroencephalogram (EEG) if the clinical diagnosis is unclear.
EXAMINATION: No obvious cause
During a mental status exam, Ms. G is pleasant, cooperative, alert, and oriented to person, place, and time. Her speech is fluent, her affect is full, and she describes her mood as a “sensitive, overwhelmed state.” Her thoughts occasionally are tangential, and she perseverates on guilty, embarrassed, and paranoid thoughts. She has auditory hallucinations and experiences photopsia during the interview, but denies other visual hallucinations. She shows no deficits in attention, concentration, memory, language, calculations, visuospatial abilities, or general fund of knowledge.
Her physical exam shows pupils that are equal, round, and reactive to light with normal extraocular movements, intact visual fields, 20/20 visual acuity in both eyes with glasses, and sharp optic disc margins with no retinal abnormalities apparent on funduscopic exam. The rest of her physical and neurologic exam is normal. Her complete blood count, electrolytes, kidney, liver function tests, urinalysis, and serum toxicology screens are normal. She has no history of immunodeficiency.
An MRI performed a year earlier showed mild diffuse congestion of a left maxillary sinus but no other intracranial abnormalities, and a waking EEG with sphenoidal electrodes was normal.
The authors’ observations
Evaluation of patients with photopsia includes taking a history and performing an eye examination including visual acuity testing, visual field testing, and funduscopic examination. The appearance, location, and duration of photopsia may help narrow the differential diagnosis and identify emergent cases (Table 1 and Table 2). Seizure activity associated with flashing lights suggests occipital epilepsy. A history of hypertension, diabetes, or polymyalgia rheumatica points to vascular causes, and hyperthyroidism suggests that flashing lights may be phosphenes of Graves’ disease. Myopia or eye trauma could indicate vitreous traction. Prescription medications and illicit drug use may point to a toxic etiology.12
Table 1
Diagnoses suggested by photopsia phenomena
| Feature | Suggested diagnosis |
|---|---|
| Appearance | |
| Twinkling lights with grey spots | Emboli |
| Zigzag lines | Occipital epilepsy |
| White flashes | Vitreous traction on the retina |
| Flickering lights and shimmering | Clomiphene use |
| Temporally located flashes of light, floaters, or blurred vision that is worse in dim illumination | Posterior vitreous detachment and retinal tearing |
| Location | |
| Temporal | Migraine or retinal pathology |
| Central | Occipital lesion or embolus |
| Monocular | Retinal pathology |
| Binocular | Cerebral cause |
| Duration | |
| Lightning quick | Vitreous detachment |
| Lasts up to 30 minutes | Migraine or occipital epilepsy |
Table 2
Photopsia differential diagnosis: Look for co-occurring symptoms
| Co-occurring symptoms | Suggests |
|---|---|
| Seizure activity associated with flashing lights | Occipital epilepsy |
| Yellow or green discoloration to the visual field, halos, and appearance of frost over objects | Digitalis toxicity |
| Shadows, moving objects, and insects crawling with co-occurring euphoria, hypervigilance, impaired judgment, and autonomic changes such as tachycardia, pupillary dilation, hypertension, and nausea | Cocaine intoxication |
| Floaters, or a ‘curtain’ or ‘shadow’ moving over the visual field, which may be accompanied by central or peripheral vision loss | Retinal detachment |
| Bilateral blurred vision, ataxia, vertigo, dysarthria, or drop attacks | Vertebrobasilar artery insufficiency |
OUTCOME: Diagnosis of exclusion
Ms. G’s visual disturbance resembles vitreous detachment or classic migraine; however, the onset is not sudden, her funduscopic exam is normal, and she has no discrete episodes with concomitant headache. Ms. G’s improvement with topiramate is inconsistent with an ophthalmic origin because such photopsia should not improve with medication. It is consistent with recurrent seizures or status epilepticus of the occipital cortex; however, she did not experience multiple discrete episodes a day or generalized seizures experienced by most occipital seizure patients, and her EEG and clinical history are not consistent with seizures. Because we cannot rule out occipital lobe epilepsy, we refer Ms. G for repeat EEG and routine ophthalmologic exam, both of which are normal.
Perceptual disturbances are common in schizoaffective disorder and schizophrenia,13-15 which we consider the most likely etiology of Ms. G’s photopsia, given her normal neurologic and ophthalmologic examinations. We switch her from aripiprazole to ziprasidone, 40 mg/d, discontinue phentermine, and taper and discontinue oxcarbazepine.
Related resources
- Ophthalmology Web. www.ophthalmologyweb.com.
- Aleman A, Larøi F. Hallucinations: the science of idiosyncratic perception. Washington, DC: American Psychological Association; 2008.
Drug Brand Names
- Aripiprazole • Abilify
- Clomiphene • Clomid, Serophene
- Digoxin • Lanoxin
- Nizatidine • Axid
- Olanzapine • Zyprexa
- Oxcarbazepine • Trileptal
- Paclitaxel • Onxol, Taxol
- Phentermine • Adipex-P, Inoamin
- Sertraline • Zoloft
- Topiramate • Topamax
- Ziprasidone • Geodon
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Jaspers K. General psychopathology. Manchester, United Kingdom: Manchester University Press; 1962.
2. Manford M, Andermann F. Complex visual hallucinations. Clinical and neurobiological insights. Brain. 1998;121:1819-1840.
3. Amos JF. Differential diagnosis of common etiologies of photopsia. J Am Optom Assoc. 1999;70(8):485-504.
4. Biousse V, Touboul PJ, D’Anglejan-Chatillon J, et al. Ophthalmologic manifestations of internal carotid artery dissection. Am J Ophthalmol. 1998;126(4):565-577.
5. Butler VP, Jr, Odel JG, Rath E, et al. Digitalis-induced visual disturbances with therapeutic serum digitalis concentrations. Ann Intern Med. 1995;123(9):676-680.
6. Mitchell J, Vierkant AD. Delusions and hallucinations of cocaine abusers and paranoid schizophrenics: a comparative study. J Psychol. 1991;125(3):301-310.
7. Seidman AD, Barrett S, Canezo S. Photopsia during 3-hour paclitaxel administration at doses > or = 250 mg/m2. J Clin Oncol. 1994;12(8):1741-1742.
8. Purvin VA. Visual disturbance secondary to clomiphene citrate. Arch Ophthalmol. 1995;113(4):482-484.
9. Queiroz LP, Rapoport AM, Weeks RE, et al. Characteristics of migraine visual aura. Headache. 1997;37(3):137-141.
10. Panayiotopoulos CP. Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. Epileptic Disord. 1999;1(4):205-216.
11. Walker MC, Smith SJ, Sisodiya SM, et al. Case of simple partial status epilepticus in occipital lobe epilepsy misdiagnosed as migraine: clinical, electrophysiological, and magnetic resonance imaging characteristics. Epilepsia. 1995;36(12):1233-1236.
12. Lichter M. Flashing lights—a warning. The Canadian Journal of Diagnosis. 2002;19:31-35.
13. Parnas J, Handest P, Saebye D, et al. Anomalies of subjective experience in schizophrenia and psychotic bipolar illness. Acta Psychiatr Scand. 2003;108(2):126-133.
14. Phillipson OT, Harris JP. Perceptual changes in schizophrenia: a questionnaire survey. Psychol Med. 1985;15(4):859-866.
15. Cutting J, Dunne F. Subjective experience of schizophrenia. Schizophr Bull. 1989;15(2):217-231.
1. Jaspers K. General psychopathology. Manchester, United Kingdom: Manchester University Press; 1962.
2. Manford M, Andermann F. Complex visual hallucinations. Clinical and neurobiological insights. Brain. 1998;121:1819-1840.
3. Amos JF. Differential diagnosis of common etiologies of photopsia. J Am Optom Assoc. 1999;70(8):485-504.
4. Biousse V, Touboul PJ, D’Anglejan-Chatillon J, et al. Ophthalmologic manifestations of internal carotid artery dissection. Am J Ophthalmol. 1998;126(4):565-577.
5. Butler VP, Jr, Odel JG, Rath E, et al. Digitalis-induced visual disturbances with therapeutic serum digitalis concentrations. Ann Intern Med. 1995;123(9):676-680.
6. Mitchell J, Vierkant AD. Delusions and hallucinations of cocaine abusers and paranoid schizophrenics: a comparative study. J Psychol. 1991;125(3):301-310.
7. Seidman AD, Barrett S, Canezo S. Photopsia during 3-hour paclitaxel administration at doses > or = 250 mg/m2. J Clin Oncol. 1994;12(8):1741-1742.
8. Purvin VA. Visual disturbance secondary to clomiphene citrate. Arch Ophthalmol. 1995;113(4):482-484.
9. Queiroz LP, Rapoport AM, Weeks RE, et al. Characteristics of migraine visual aura. Headache. 1997;37(3):137-141.
10. Panayiotopoulos CP. Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. Epileptic Disord. 1999;1(4):205-216.
11. Walker MC, Smith SJ, Sisodiya SM, et al. Case of simple partial status epilepticus in occipital lobe epilepsy misdiagnosed as migraine: clinical, electrophysiological, and magnetic resonance imaging characteristics. Epilepsia. 1995;36(12):1233-1236.
12. Lichter M. Flashing lights—a warning. The Canadian Journal of Diagnosis. 2002;19:31-35.
13. Parnas J, Handest P, Saebye D, et al. Anomalies of subjective experience in schizophrenia and psychotic bipolar illness. Acta Psychiatr Scand. 2003;108(2):126-133.
14. Phillipson OT, Harris JP. Perceptual changes in schizophrenia: a questionnaire survey. Psychol Med. 1985;15(4):859-866.
15. Cutting J, Dunne F. Subjective experience of schizophrenia. Schizophr Bull. 1989;15(2):217-231.