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This year, the field of neuroscience celebrates the 50th anniversary of Mountcastle's discovery of the cortical column. In this review, we summarize half a century of research and come to the disappointing realization that the column may have no function. Originally, it was described as a discrete structure, spanning the layers of the somatosensory cortex, which contains cells responsive to only a single modality, such as deep joint receptors or cutaneous receptors. Subsequently, examples of columns have been uncovered in numerous cortical areas, expanding the original concept to embrace a variety of different structures and principles. A "column" now refers to cells in any vertical cluster that share the same tuning for any given receptive field attribute. In striate cortex, for example, cells with the same eye preference are grouped into ocular dominance columns. Unaccountably, ocular dominance columns are present in some species, but not others. In principle, it should be possible to determine their function by searching for species differences in visual performance that correlate with their presence or absence. Unfortunately, this approach has been to no avail; no visual faculty has emerged that appears to require ocular dominance columns. Moreover, recent evidence has shown that the expression of ocular dominance columns can be highly variable among members of the same species, or even in different portions of the visual cortex in the same individual. These observations deal a fatal blow to the idea that ocular dominance columns serve a purpose. More broadly, the term "column" also denotes the periodic termination of anatomical projections within or between cortical areas. In many instances, periodic projections have a consistent relationship with some architectural feature, such as the cytochrome oxidase patches in V1 or the stripes in V2. These tissue compartments appear to divide cells with different receptive field properties into distinct processing streams. However, it is unclear what advantage, if any, is conveyed by this form of columnar segregation. Although the column is an attractive concept, it has failed as a unifying principle for understanding cortical function. Unravelling the organization of the cerebral cortex will require a painstaking description of the circuits, projections and response properties peculiar to cells in each of its various areas.

Thalamic nuclei are thought to funnel sensory information to the brain's primary cortical areas, which in turn transmit signals afresh to higher cortical areas. Here we describe a direct projection in the macaque monkey from the lateral geniculate nucleus (LGN) to the motion-selective middle temporal area (MTor V5), a cortical area not previously considered 'primary'. The constituent neurons are mostly koniocellular, send virtually no collateral axons to primary visual cortex (V1) and equal about 10% of the V1 population innervating MT. This pathway could explain the persistence of motion sensitivity in subjects following injury to V1, suggesting more generally that residual perception after damage in a primary area may arise from sparse thalamic input to 'secondary' cortical areas.

Primary and secondary visual cortex (V1 and V2) form the foundation of the cortical visual system. V1 transforms information received from the lateral geniculate nucleus (LGN) and distributes it to separate domains in V2 for transmission to higher visual areas. During the past 20 years, schemes for the functional organization of V1 and V2 have been based on a tripartite framework developed by Livingstone & Hubel (1988) . Since then, new anatomical data have accumulated concerning V1's input, its internal circuitry, and its output to V2. These new data, along with physiological and imaging studies, now make it likely that the visual attributes of color, form, and motion are not neatly segregated by V1 into different stripe compartments in V2. Instead, there are just two main streams, originating from cytochrome oxidase patches and interpatches, that project to V2. Each stream is composed of a mixture of magno, parvo, and konio geniculate signals. Further studies are required to elucidate how the patches and interpatches differ in the output they convey to extrastriate cortex.

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In normal macaque monkeys a histochemical stain for cytochrome oxidase activity revealed a striking pattern of regularly spaced patches in primary visual (striate, area 17, V1) cortex. The patches were most obvious in layers II and III, but also in layers I, IV b, V and VI; only in layers IV c and IV a were they absent. The patches were oval shaped, about 250 by 150 pm and aligned into rows spaced about 350 pm apart. Along each row a patch was located about every 550 pm; often patches in neighbouring rows were aligned, creating a square array. T heir density was about one patch per 0.2 mm 2 (550 by 350 pm) in opercular cortex. The patches were also labelled preferentially by stains for lactate dehydrogenase, succinate dehydrogenase, acetylcholinesterase (AChE), and myelin. In V2, a coarser pattern of broad parallel stripes labelled by cytochrome oxidase, lactate dehydrogenase, and AChE was present. The cytochrome oxidase patches were absent in non-prim ate species like the cat, mink, tree shrew, mouse, rat, rabbit, and ground squirrel. However, they were present in all prim ate species examined, including the rhesus, cynomolgus, owl, and squirrel monkey, baboon, bushbaby, and hum an. While more species should be tested, it appears that the patches are a cytoarchitectonic feature unique to prim ate visual cortex. In the owl monkey patches of anterogradely transported horseradish peroxidase (HRP) were found in layers IV c a , III, and II after injection of the tracer into the lateral geniculate nucleus (l.g.n.). They coincided exactly with the position of patches in adjacent sections processed for cytochrome oxidase. A similar result was obtained in the macaque, except that patches were not present in layer IV c a . These experiments established that the cytochrome oxidase patches receive a direct, patchy projection from the lateral geniculate body. However, retrogradely filled layer VI cells in the owl monkey bore no regular relation to the patches. In the macaque, the ‘honeycomb’ of geniculate terminals in layer IV a matched a similar honeycomb pattern of cytochrome oxidase staining. In the Nissl stain three sublayers in layer IV a were identified: the honeycomb was located in layer IV a p . In V2, in the owl monkey the parallel stripes of enhanced cytochrome oxidase activity received a direct projection from l.g.n. or pulvinar. In the macaque, after intraocular injection of [ 3 H]proline, the rows of patches in layers II and III lay in register with ocular dominance columns seen by transneuronal radioautography in layer IV c. In another macaque, one eye was removed and the cortex stained for cytochrome oxidase, AChE and Nissl substance after six months survival. In layer IV c light and dark bands corresponding to the ocular dominance columns were visible; surprisingly the dark cytochrome oxidase bands matched the light AChE and Nissl bands. The set of bands belonging to the missing eye was determined by examining cytochrome oxidase staining and proline radioautographs in another macaque that sustained severe eye injury by [ 3 H]proline injection. In striate cortex, bands of radioactive label from the injured eye matched ocular dominance columns appearing more lightly stained by cytochrome oxidase. In the macaque tested six months after enucleation, in every other row the cytochrome oxidase patches appeared pale and shrunken. These lighter rows fit into precise register with the lighter ocular dominance columns in layer IV c, confirming the correspondence between rows of patches and ocular dominance columns demonstrated by proline injection. AChE staining of patches was similarly affected by eye removal. The effect of visual deprivation upon cytochrome oxidase staining was tested in two monocularly sutured macaques. In the l.g.n. no effect was detected. In visual cortex wide light columns alternating with thin dark columns were observed in layer IV. In one m acaque the ocular dominance columns were labelled independently by H R P injection into a deprived l.g.n. lamina. The H R P labelled ocular dominance columns fit within the pale cytochrome oxidase columns; this establishes that monocular deprivation causes a relatively greater loss of enzyme activity in ocular dom inance columns belonging to the closed eye. However, there was also loss of cytochrome oxidase staining along the borders of the normal eye dominance columns, indicating that ocular dominance columns in layer IV are subdivided into core zones flanked by border strips that are susceptible to loss of cytochrome oxidase activity with suture of either eye. The core zones are the same width as the rows of cytochrome oxidase patches and correspond to the dark bands seen in Liesegang stains of normal macaque striate cortex. In two adult cats the effect of monocular lid suture at 28 d old was assessed: no effect upon cytochrome oxidase staining in l.g.n. or cortex was observed. The optic disc representation in visual cortex was studied by 2-deoxyglucose radioautography and cytochrome oxidase staining after eye removal or lid suture in m acaque monkeys. It appeared as a pale oval, 1.65 times longer than the optic disc, a distortion probably required to m aintain overall isotrophy in magnification factor. Patches were present in the disc representation although ocular dominance columns are absent: they appeared rounder and more widely separated. In the temporal cresent patches were also present. They were larger, rounder, and less densely spaced than patches in binocular cortex. Deoxyglucose mapping in a macaque monkey monocularly stimulated with a display of parallel black and white stripes of irregular width and spacing rotated through all orientations has resulted in patches in the upper layers over ocular dominance columns corresponding to the open eye. These patches match cytochrome oxidase patches situated in every other row, thus suggesting that cells located in cytochrome oxidase patches respond to all orientations of stimulus. Macaques binocularly stimulated with vertical or horizontal stripes show a complicated pattern of deoxyglucose uptake, overlapping extensively with the pattern of cytochrome oxidase patches. In one monkey the right eye was removed and 18 d later the animal was stimulated with vertical stripes. Deoxyglucose radioautography and cytochrome oxidase staining combined in single tissue sections each revealed a matching pattern of ocular dominance columns in layer IV. In the upper layers, dots of radioautographic label were present, matching cytochrome oxidase patches in alternate rows. In foetal monkeys at E142-144 the laminar pattern of cytochrome oxidase staining in visual cortex was remarkable for a prominent wide band of intense activity in layer IV b and upper IV c a , absent in mature macaques. In tangential section, patches were visible in layers II, III and in layer IV b -IV c a , which indicates that patches form in monkey visual cortex before birth. The functional significance of the patches remains uncertain. It has been suggested that the visual field is analysed in visual cortex by small modules containing several hypercolumns of each stimulus variable. The cytochrome oxidase patches may constitute the anatomical correlate of these proposed modules.

The occipital lobes were obtained after death from six adult subjects with monocular visual loss. Flat-mounts were processed for cytochrome oxidase (CO) to reveal metabolic activity in the primary (V1) and secondary (V2) visual cortices. Mean V1 surface area was 2643 mm 2 (range, 1986 -3477 mm 2 ). Ocular dominance columns were present in all cases, having a mean width of 863 m. There were 78 -126 column pairs along the V1 perimeter. Human column patterns were highly variable, but in at least one person they resembled a scaled-up version of macaque columns. CO patches in the upper layers were centered on ocular dominance columns in layer 4C, with one exception. In this individual, the columns in a local area resembled those present in the squirrel monkey, and no evidence was found for column/patch alignment. In every subject, the blind spot of the contralateral eye was conspicuous as an oval region without ocular dominance columns. It provided a precise landmark for delineating the central 15°of the visual field. A mean of 53.1% of striate cortex was devoted to the representation of the central 15°. This fraction was less than the proportion of striate cortex allocated to the representation of the central 15°in the macaque. Within the central 15°, each eye occupied an equal territory. Beyond this eccentricity, the contralateral eye predominated, occupying 63% of the cortex. In one subject, monocular visual loss began at age 4 months, causing shrinkage of ocular dominance columns. In V2, which had a larger surface area than V1, CO stripes were present but could not be classified as thick or thin.

Idiopathic intracranial hypertension is the term to be adopted instead of pseudotumor cerebri. IIH remains an enigmatic diagnosis of exclusion. However, prompt diagnosis and thorough evaluation and treatment are crucial for preventing visual loss and improving associated symptoms.