The main, conscious geniculocalcarine pathway, is the long pathway from
the retina via the lateral geniculate nucleus (LGN) to the primary visual cortex
(=V1). The subcortical, tectal pathway transfers information to superior
colliculus (SC), many nuclei in the brain stem and via pulvinar (PU) to the visual
associative functions. From V1 visual information flows upwards as the dorsal
stream (DS) and toward the inferotemporal lobe as the ventral stream (VS).
Lesions at different locations cause different functional losses. The two
main types of nerve fibres in the optic nerve are the parvo- (P) and the
magnocellular (M) fibres.
This diagram is an extreme oversimplification to show how visual information
is transferred from primary visual cortex (=V1) to different higher visual centres,
V2, V3, V4 and V5 (or MT). Note that visual information transferred by the
tectal pathway (TP) (tectal pathway = superior colliculus and pulvinar) reaches only
some higher visual functions, not all of them.
When the lesion is in the optic nerve (ON), the change in visual function
occurs only in that eye.- When it is close to the chiasm (CH) in the optic tract
(OT), it causes loss of visual field on the opposite side. If both optic
tracts are damaged, the person has no visual perception but light related diurnal
rhythm is still possible, if visual information can get to the pineal body via the
small suprachiasmatic nucleus (supra=above, nucleus above the chiasm).
When the lesion is in the optic tracts close to the lateral geniculate nucleus, visual information can enter the tectal pathway and via it to cortical functions in the parietal lobe that are related to spatial awareness of the visual space and visuomotor functions. This information has not gone through form analysis in the primary visual cortex and in the ventral stream so recognition of forms is poor although detection of long lines (grating acuity at different contrast levels) may be good.
When the lesion is in the optic radiation (OR), total damage to the pathway
is rare. More often there are small lesions causing a Swiss cheese like loss of
fibers with corresponding patchy loss of visual field.
When the lesion is in the visual cortex, it results in loss of part or one
half of the contralateral visual field (visual half field on the opposite
side). Diffuse metabolic changes may cause loss of certain type of information
without permanent field defects.
When the changes are in the secondary or higher visual analysis, they lead
to losses of specific functions, not to visual field defects. Damage to
the temporal, or ventral, stream (VS) results in agnosias, losses of
different recognition functions, whereas loss of function in the parietal,
dorsal stream leads to changes in visuomotor and oculomotor functions, and
egocentric orientation. Visual apraxia is a rare clinical entity caused by
changes in this part of visual pathways.
The ventral stream functions are sometimes called "what" functions, and the
dorsal stream functions "where" functions. This is an oversimplification
because we need recognition of the environment to orient in it although during
the movement we do not analyse in detail the structure of the body part moving
or the environment. The two main types of vision combine their functions and
support them with information from visual memory.
In most cases of brain damage there are lesions in several parts of the visual patways and often also motor and auditory functions. Sometimes the lesion is confined to the posterior part of the optic radiation and to the ventral stream functions (for slide click here).
Visual pathway transfers different types of visual information from the retina
via different nerve fibers. Parvocellular (P) fibers transfer colour and high
contrast black&white detail information. Magnocellular fibers (M) transfer
motion information and low contrast black&white information. The dichotomy is
present already at the retinal level, where cone cell and rod cell based vision
affect each other.
The presence of parallel visual pathways and functions is typical to the visual
system. This feature makes it possible that some visual functions are lost or
altered by a lesion and at the same time other visual functions remain normal.
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