spreading depression. One discrepancy is that the symptoms of migraine normally do not spread as far as the cortical spreadingwave, suggesting that the strength of the wave falls below anactivation threshold in the unaffected region (Dahlem & Had-jikhani, 2009). Since the first neural effect of cortical spreading depression is thought to be transient excitation, it is interesting that a variety ofevidence suggests that the brains of migraineurs with aura arechronically hyperexcitable between attacks (Aurora & Wilkinson,2007). For example, thresholds for phosphene generation by TMSare reduced in subjects who experience migraine aura (Aurora,Ahmad, Welch, Bhardhwaj, & Ramadan, 1998; Fierro et al., 2003;Mulleners, Chronicle, Palmer, Koehler, & Vredeveld, 2001; Mul-leners, Chronicle, Vredeveld, & Koehler, 2002). Psychophysicalevidence consistent with hyperexcitability or hypo-inhibition hasbeen adduced by Chadaide et al., 2007; Chronicle, Wilkins, and Coleston (1995); Mulleners, Aurora, et al. (2001); Palmer, Chron-icle, Rolan, and Mulleners (2000); and Wilkinson, Karanovic, and Wilson (2008). Epilepsy In epilepsy, like migraine, many unusual events are possible, depending on the cortical locus of the seizure. Compared to mi-graine, epileptic hallucinations are brief, with typical durations ofseveral seconds rather than many minutes (a strong diagnosticdiscriminator between migraine aura and petit mal occipital epi-lepsy; Panayiotopoulos, 1999). This is consistent with electrophys-iological findings that epileptiform activity is orders of magnitudefaster than the 3 mm/min cortical spread of migraine (Chervin,Pierce, & Connors, 1988; Penfield & Rasmussen, 1950). Thepercentage of epilepsy cases with visual symptoms (about 11% in Penfield & Kristiansen, 1951) seems surprisingly small (given theshare of cortex involved in some ways with vision); symptomsrange from simple phosphenes to the complicated scenic halluci-nations of temporal lobe epilepsy (Fried, Spenser, & Spenser,1995; Penfield & Kristiansen, 1951; Wilkinson, 2004; Williamson, Thadani, Darcey, Spenser, & Mattson, 1992). Phosphenes have avariety of simple shapes (stars, streaks, spots, annuli, wedges, andoccasionally a zigzag like a piece of a fortification illusion) andmay be strongly colored. In occipital epilepsy, circular phosphenesand annular forms (e. g., doughnut phosphenes) seem particularlyprevalent (Panayiotopoulos, 1999). Single-wedge and double-wedge (butterfly or bow-tie) phosphenes are also seen. Wilkin-son's (2004) review found that “components may be stationary andlong-lasting, but more commonly flicker, pulsate, twinkle or move. Several patterns of motion (translational, rotary, expansion, con-traction and random) have been described” (p. 311). If a subjecthas a characteristic epileptic aura, it can often be triggered by focalelectrical stimulation during neurosurgery (Penfield & Rasmussen,1950). Occipital epilepsy and its associated hallucinations can becontrolled by medicines that dampen neuronal excitability (e. g.,carbamazepine; Panayiotopoulos, 1999). Ocular-Pressure-Induced Forms It has been known since antiquity that illusory images are induced by applying pressure to the eyeballs; a light spot (phos-phene) appears opposite the point of pressure (if localized) and canbe seen in the dark. Some believed that ocular pressure createdinternal light, but Descartes and Newton correctly anticipated thatpressure mechanically stimulates the retina (Gru ¨sser & Hagner, 1990; Wade & Brozek, 2001). Phosphenes can sometimes be seenduring eye movements and accommodation in the dark, or whenocular pressure is abruptly raised (e. g., sometimes by coughing;Gru¨sser & Landis, 1991). The immediate retinal effect of ocular pressure is to activate retinal on-center ganglion cells (after a delayof 0. 2 s) and inhibit off-center ganglion cells, resulting in percep-tion of a light increment (Gru ¨sser, Gru ¨sser-Cornhels, Kusel, & Przybyzewski, 1989; Gru ¨sser, Hagner, & Przybyswewski, 1989). Gru¨sser and colleagues (Gru ¨sser, Gru ¨sser-Cornhels, et al., 1989; Gru¨sser, Hagner, & Przybyswewski, 1989) theorized that defor-Table 1 Conditions That Trigger Hallucinations and the Nature of the Resulting Hallucinations Condition Geometric pattern Fortification Phosphene Complex Drugs O, C, D Sa S O,C,D Photopic O, C, D Va S, C Vb Ocular pressure O, C, D OMigraine S, C O, C, D S, C SEpilepsy S, C S a S, C, D S Hypoglycemia S Sa Transcranial magnetic stimulationc O, C, D O Electrical (cortex)d S, P O, D Se Electrical (retina)f CO Charles Bonnet syndrome O O O, CSensory deprivation O O S Note. O/H11005often; S /H11005sometimes; V /H11005very seldom; C /H11005colored; D /H11005dynamic; P /H11005pinwheel (usually small and rotating). a Sometimes a serrated form resembling a fortification illusion occurs but is usually stationary and usually does not flash. b If only one eye is stimulated by flicker while the other eye is kept dark, binocular rivalry between the eyes leads to switching between the geometric hallucinations and dark-phase hallucinations, which are swirling amorphous structures (Smythies, 1959a). c Noninvasive focal electrical stimulation of neural tissue, by induction, using a temporally alternating, spatially focused magnetic field. d Usually done with implanted electrodes as part of visual prosthesis studies, or during surgery. e Depends on which cortical area is stimulated. f Usually done with current applied to entire orb. 747 HALLUCINATIONS AND CORTICAL PATTERN FORMATION