The visual pathway and its disorders

Visual pathway

Visual disorders in humans can occur as a result of damage to the following anatomical structures:

• retina
• optic nerve
• optic chiasm
• optic tract
• lateral geniculate body
• geniculate-occipital tract
• the visual center of the occipital cortex of the cerebral hemispheres

Affected areas	Visual field defects	Schematic representation
1. Unilateral lesion of the optic nerve	Blindness of the affected eye
2. The lesion is in the optic chiasm (chiasma)	Bitemporal hemianopsia ("blinders")
3. Unilateral lesion of the visual tract	Contralateral homonymous hemianopsia
4. Unilateral lesion of visual radiance in the Meyer loop (anterior part of the temporal lobe)	Contralateral upper quadrant anopsia ("pie in the sky")
5. Unilateral lesion of visual radiance, medial part	Contralateral lower quadrant anopsia
6. Lesion of the occipital lobe	Homonymous hemianopsia
7. Lesion of the occipital pole (cortical zones)	Homonymous hemianopic central scotoma

Retinal lesions cause the appearance of arcuate scots (focal loss of the visual field), defined as islands of loss of the visual field, which are directed towards the blind spot or originate from it. Arcuate defects (damage to the bundle of nerve fibers) have a distinct border along the horizontal midline, and with its extensive size, they lead to the loss of half of the field of vision. Damage papillomacular beam, providing a Central fixation, leads to a Central (defeat the point of gaze fixation) or centrically (defeat the point of gaze fixation and the blind spot) scotoma. In the case of macular lesions, a small central scotoma often leads to impaired vision, visual perception, characterized by distortion of the shape and size of visible objects, especially straight lines (metamorphopsy), which distinguishes macular lesions from damage to the optic nerve.

A centrocecal scotoma is a frequent specific sign of optic nerve damage, the causes of which can be both internal (demyelinating, infiltrating, degenerative processes) and external compression (aneurysms, tumor) factors. Toxic effects (methyl alcohol, quinine, some phenothiazine-type tranquilizers)and eating disorders (tobacco and alcohol blindness) lead to the formation of relatively symmetrical bilateral central or centrocecal cattle. Progressive generalized narrowing of the peripheral isopters with relative preservation of the central vision may be a consequence of the annular compression of the tumor, as, for example, in meningioma of the optic nerve sheath. Spiral constriction or tube vision of inorganic origin (in hysteria, simulation) persists when examining vision from any distance. In the case of organic lesions, the outer diameter of the visual field defect will increase with the distance between the eye and the object under study.

A visual field defect that is localized in one half of the visual field of each eye is called hemianopsia. At the same time, there is a clear border along the vertical line.

Bitemporal hemianopsia indicates a lesion of the intersecting fibers of the nasal part of the retina in the area of the visual cross, usually due to compression of the chiasm (with a pituitary tumor, craniopharyngioma, meningioma of the Turkish saddle diaphragm, suprasellar aneurysm of the arteries of the Willis circle).

Homonymous hemianopsia (loss of the left or right halves of the visual fields) occurs when the visual pathway is affected above the intersection and in the case of complete hemianopsia, it does not allow to determine the exact localization. Incomplete homonymous hemianopsia more specifically indicates the possible site of the lesion:

• if the visual field defects are identical on both sides, it is most likely that the lesion is localized in the cortex of the groove
• if there is a mismatch of defects (asymmetry), then most likely the fibers of the optic tract, the lateral geniculate body, or the visual radiance of the parietal or temporal lobe have been damaged

Lesions of the visual tract are characterized by the development of asymmetric homonymous hemianopsia. Chronic damage to the tract is accompanied by an impaired afferent reaction of the pupil to light and transverse atrophy of the optic nerve on the opposite side.

In the case of lesions of the visual pathway above the lateral geniculate body, pupillary reflexes are preserved.

Nerve fibers from the lower quadrants of the retina project into the temporal lobe, so damage to this lobe can cause homonymous upper quadrant hemianopsia. Lesions of the parietal lobes affect the lower quadrants more than the upper quadrants; this can also lead to the occurrence of hemianopsia due to inattention.

Complete homonymous hemianopsia with the destruction of the fibers coming from the macula develops if the cortical parts of the large hemispheres are damaged in the area of the spur furrow on one side. The preservation of the macula is often due to imperfect fixation.

Bilateral homonymous hemianopsia occurs as a result of bilateral lesions of the visual cortex, usually of an ischemic nature, in the areas of blood supply to the posterior cerebral arteries. Persistent cortical blindness may develop. In such patients, Anton's syndrome is observed: bilateral blindness, denial of vision loss, normal pupillary reflexes, and bilateral infarcts in the occipital-parietal regions.

Other disorders of central vision include various types of image distortion, in which objects appear either too small (micropsia), or excessively large (macropsia), or curved. With bilateral symptoms, the temporal lobes are most likely to be affected; in this case, visual disorders occur at the time of epilepsy attacks and may be accompanied by complex visual hallucinations or other manifestations of temporal epilepsy.