nerve may lead to an altered perception of motion. Because of the disparity in neuronal transmission, a pendulum, for example, may appear to trace an elliptical path instead of its true single-plane oscillation (Pulfrich phenomenon).

Cortical Origin

Because perception is a cortical phenomenon, it is not surprising that cortical pathology may be responsible for visual illusions. In addition to altering the perceived shape and position of an object, cortical abnormalities may change the perception of motion. Cortical pathology may cause loss of color vision or multiplicity of images. Cortical pathology may be located in the primary visual cortex (V1) or the associative areas (V2, V3, and V4) (see Chapter 1). Disorders of visual perception, such as micropsia, macropsia, teleopsia (objects appearing too distant), and pelopsia (objects appearing too close) are common with parietal lobe abnormalities.

The Patient With Hallucinations

Hallucinations consist of perception unrelated to active stimuli. Like illusions, hallucinations may originate anywhere along the visual pathway but most commonly do so within the globe or cortex. Hallucinations may be formed (eg, real objects such as animals, flowers, cars, or people) or unformed (eg, light, spots, dots, or geometric patterns).

Ocular Origin

Unlike illusions, hallucinations have no optical causes. Vitreous detachment with persistent vitreoretinal adhesions may produce colored shapes or vertical white flashes (so-called lightning streaks of Moore). Such hallucinations are often most apparent in a dark environment. Retinal detachment may produce persistent flashes and floaters with or without loss of vision.

Outer retinal diseases may result in photopsias (flashing lights) that tend to be continuous and persistent. Such flashes may be simple white lights, but often they form geometric webs that may take on colors, including silver and gold. Photopsia often heralds the onset of autoimmune retinopathy including cancer-associated retinopathy, a paraneoplastic process. Similarly, photopsia may accompany a variety of retinal, retinal pigment epithelium, and choroidal abnormalities (eg, multiple evanescent white dot syndrome, acute zonal occult outer retinopathy, or birdshot chorioretinopathy). For a complete description of these conditions, see BCSC Section 12, Retina and Vitreous.

Retinal vasospasm may produce loss of vision or unformed monocular images—colors, lines, or phosphenes (fleeting, bright flashes of light)—that last up to 45 minutes and may be followed by a headache. Sequelae are unusual, although a permanent scotoma may develop.

Alabduljalil T, Behbehani R. Paraneoplastic syndromes in ophthalmology. Curr Opin Ophthalmol. 2007;18(6):463–469.

Gass JD, Agarwal A, Scott IU. Acute zonal occult outer retinopathy: a long-term follow-up study. Am J Ophthalmol. 2002;134(3):329–339.

Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders. 2nd ed. Cephalalgia. 2004;24(Suppl 1):9–160.

Zaret BS. Lightning streaks of Moore: a cause of recurrent stereotypic visual disturbance. Neurology. 1985;35(7):1078–1081.

Optic Nerve Origin

Optic neuritis often produces phosphenes induced by eye movement or a dark setting. Patients with subacute or long-standing optic neuropathy may experience sound-induced photisms (sensations of color or light induced by stimulus to another sense). Such phenomena tend to be unformed and are triggered by various sounds heard in the ipsilateral ear. Sound-induced photisms are attributed to discharges from the lateral geniculate nucleus, which is also responsive to sound and is adjacent to the medial geniculate nucleus of the auditory system.

Cortical Origin

It is often taught that lesions affecting the anterior optic radiations (ie, the temporal lobe) cause formed hallucinations and that more posterior lesions (ie, in the parietal and occipital lobes) produce unformed hallucinations. However, this general pattern has many exceptions. In rare cases, lesions involving the mesencephalon may cause hallucinations (peduncular hallucinosis) that are formed and can be constant. These hallucinations are usually associated with an inverted sleep-wake cycle. Associated symptoms may occur if adjacent structures are affected (eg, oculomotor nerve fascicles, corticospinal tracts).

Palinopsia

Interesting cortical phenomena may occur with disorders of the nondominant parieto-occipital area. Palinopsia is visual perseveration after the removal of the original stimulus (multiple afterimages). The afterimages may be associated with a homonymous hemianopia in which the palinoptic images appear in the blind hemifield. Visual hallucinations may also be present. Migraine, hallucinogenic drugs such as lysergic acid diethylamide (LSD), and medications (eg, clomiphene, trazodone, nefazodone, topiramate) can produce similar symptoms.

Temporal, parietal, and occipital lobe lesions

Temporal lobe lesions most often produce olfactory and gustatory hallucinations. Visual phenomena from this area are usually complex, formed hallucinations in either the ipsilateral or the contralateral visual field. Epilepsy is the most common cause of hallucinations traced to this region. A visual aura implies that the seizure began focally.

In the parietal lobe, hallucinations may be either formed or unformed, whereas occipital lobe disorders commonly cause unformed hallucinations. Patients with occipital lobe lesions may describe white or colored flashes of light, kaleidoscopic colors, moving discs, flickering, or a hexagonal array (eg, chicken-wire or honeycomb pattern). A complete whiteout of vision suggests bilateral occipital lobe ischemia.

Patients sometimes describe hallucinations within a homonymous hemianopia or quadrantanopia. These images are generally complex and may be static or move throughout the visual field.

Celesia GG. Positive spontaneous visual phenomena. In: Celesia GG, ed. Handbook of Clinical Neurophysiology. Vol 5. Edinburgh: Elsevier; 2005:353–370.

Migraine

The visual phenomena of migraine are thought to be caused by abnormal excitatory activity in the cerebral cortex followed by a wave of depressed neuronal function (spreading depression of Leão).