Symptoms of occipital lobe lesions

Destruction of the analyzer projection zone (cuneus gyrus lingualis and deep sections of sulcus calcarinus) entails the appearance of the eponymous hemianopsia. Milder degrees of damage cause incomplete hemianopsia. Hemiopic disorders can be partial. Thus, with damage to the cuneus, only the lower quadrants in the visual fields fall out, and foci in the gyrus lingualis cause upper quadrant hemianopsia.

In cortical (occipital) lesions, the central visual fields are usually preserved, which distinguishes them from lesions of the visual pathways (tr. opticus). Lesions of the outer surfaces of the occipital lobes do not lead to blindness, but to visual agnosia - failure to recognize objects by their visual images. Lesions on the border of the occipital lobe with the parietal cause alexia (failure to understand written language) and acalculia (impaired counting).

Contralateral ataxia (disruption of the occipito-ponto-cerebellar tract), disturbance of combined eye movements, changes in pupillary width, and accommodation disorders may occur.

Stimulation of the inner surface of the occipital lobe results in the emergence of simple visual sensations (photomes) - flashes of light, lightning, colored sparks, etc. More complex visual sensations (like cinematic pictures) appear when the outer surfaces of the occipital lobes are stimulated.

Another disorder occurs when the occipital lobes are damaged - metamorphopsia (distorted perception of the shape of visible objects - their contours seem broken, curved, they seem too small - micropsia - or, conversely, too large - macropsia). Most likely, the occurrence of such distorted perceptions depends on the disruption of the joint work of the visual and statokinesthetic analyzers.

Syndromes of local damage of the occipital lobes

I. Medial sections

1. Visual field defects
2. Visual agnosia
3. Visual hallucinations
4. Alexia without agraphia
5. Anton's syndrome (denial of blindness)

II. Lateral (convexital) sections

1. Alexia with agraphia
2. Violation of optokinetic nystagmus
3. Ipsilateral impairment of pursuit eye movements.

III. Epileptic phenomena characteristic of occipital localization of epileptic foci

I. Medial sections.

Lesions of the occipital lobes usually result in a variety of visual disturbances in the form of visual field defects, including hemianopsia, visual agnosia ("cortical blindness"), and visual hallucinations.

An extensive lesion of the inner (medial) surface of the occipital lobe in the fissurae calcarinae region typically results in loss of the opposite fields of vision of both eyes, i.e., in the development of complete homonymous hemianopsia. A local lesion above the fissurae calcarinae, i.e., in the cuneus region, results in quadrant hemianopsia of the opposite lower quadrants; with a local lesion below this groove (gyrus lingualis), the fields of the opposite upper quadrants are lost. Even smaller lesions result in the appearance of scotomas in the opposite fields of vision (in both fields of vision and in the homonymous quadrants). Color sensations in the opposite fields of vision are lost earlier, so the study of the fields of vision not only for white, but also for blue and red colors is of great importance in the early stages of some diseases.

Bilateral lesions of the medial surfaces of the occipital lobe rarely lead to complete blindness: usually the so-called central or macular vision is preserved.

Visual agnosia in its expanded form is less common and is more typical for bilateral occipital lobe lesions. In this case, the patient is not literally blind; he sees all objects, but loses the ability to recognize them. The nature of visual impairment in such cases is quite variable. Bilateral homonymous hemianopsia is possible. The pupils, their reflex reactions, and the fundus remain normal.

The patient stops recognizing what is written, i.e. alexia (partial or complete inability to read) develops. Alexia occurs in two main forms: "pure alexia" (or alexia without agraphia) and alexia with agraphia. "Pure alexia" develops with damage to the medial surface of the occipital lobe, which interrupts the connections of the visual cortex with the left (dominant) temporoparietal region. Usually these are lesions located behind and below the posterior horn of the lateral ventricle. With "pure alexia", visual acuity is normal in most patients, although quadrant hemianopsia or complete hemianopsia may occur. Non-verbal stimuli (any other objects and faces) can be recognized normally. Alexia with agraphia is typical for damage to the convexital surface of the occipital lobe, closer to the temporal lobe, and is manifested not only by reading impairment, but also by writing defects, which is most often found in patients with various forms of aphasia.

Visual hallucinations may be simple photomes or more complex visual images (the latter more often with stimulation of the lateral parts of the occipital lobe cortex) and may be observed in isolation or as an aura of an epileptic seizure. Ignorance or denial (anosognosia) of blindness in some patients with visual agnosia (cortical blindness) is called Anton's syndrome. Patients with Anton's syndrome confabulate their visual environment and refuse to acknowledge their visual defect. Anton's syndrome is more common in cortical blindness of vascular genesis.

In general, the causes of cortical blindness are varied; it has been described in vascular (stroke, angiography complication), infectious (meningitis, encephalitis), degenerative (MELAS syndrome, Leigh disease, adrenoleukodystrophy, metachromatic leukodystrophy, Creutzfeldt-Jakob disease), immune (multiple sclerosis, subacute sclerosing panencephalitis), metabolic (hypoglycemia, carbon monoxide poisoning, uremia, hemodialysis), toxic (mercury, lead, ethanol), iatrogenic (vincristine) and other pathological conditions (transient ictal or postictal phenomenon, eclampsia, hydrocephalus, brain tumor, traumatic brain injury, electrical injury, porphyria, cerebral edema).

II. Lateral sections.

Damage to the lateral (convexital) sections of the occipital lobe may also be accompanied by changes in optokinetic nystagmus and deterioration of tracking eye movements, which is revealed by special instrumental studies. Extensive damage to the occipital cortex with partial involvement of the parietal lobe may lead to special forms of metamorphosis, including palinopsia (perseveration of a visual image), allesthesia (false orientation of an object in space), monocular diplopia or triplopia, and even polyopia (one object is perceived as two or more). In these cases, such phenomena as deterioration of memory for visual stimuli, deterioration of topographic memory, and problems in visual spatial orientation are also possible.

Prosopagnosia (facial recognition impairment) may be caused by bilateral occipito-parietal lesions. Unilateral optic ataxia on the side opposite the parieto-occipital lesion may occur in isolation without other components of Balint's syndrome.

Color achromatopsia is characterized by impaired recognition of color shades (posterior damage to the right hemisphere).

The list of the main neurological syndromes associated with damage to the occipital lobe is as follows.

Any (right or left) occipital lobe.

1. Contralateral homonymous visual field defect: scotoma, hemianopsia, quadrant hemianopsia.
2. Unilateral optic ataxia

Non-dominant (right) occipital lobe.

1. Color agnosia
2. Gaze oculomotor disorders (impaired pursuit eye movements)
3. Deterioration of visual orientation
4. Impairment of topographic memory

Dominant (left) occipital lobe.

1. Color anomie (inability to correctly name a color)
2. Alexia without agraphia (with damage to the posterior parts of the corpus callosum)

Both occipital lobes

1. Bilateral scotomas
2. Cortical blindness
3. Anton's syndrome.
4. Balint's syndrome
5. Various types of visual agnosia (objects, faces, colors).

III. Epileptic phenomena characteristic of occipital localization of epileptic foci.

Occipital seizures are accompanied by elementary visual images (photomas) and negative phenomena (scotoma, hemianopsia, amaurosis). More complex hallucinations are associated with the spread of epileptic discharge to the parietal or temporal region. Rapid forced blinking at the onset of a seizure may be a sign of an occipital epileptic focus. Sometimes, visual hallucinations are followed by a turn of the head and eyes to the opposite side (involvement of the contralateral parieto-occipital region). The spread of convulsive discharges to the temporal region may lead to complex partial seizures, and their "flow" into the parietal lobe may cause various somatosensory phenomena. Sometimes convulsive discharges from the occipital lobe spread to the anterior central gyrus or additional motor region with a corresponding clinical picture, which complicates the correct localization of the epileptic focus.

An epileptic paroxysmal skew deviation with nystagmus is described in the case of damage to the left occipital lobe.

Thus, the following occipital epileptic phenomena occur:

1. Elementary visual seizures (the most common variant) with photomas or negative visual phenomena.
2. Perceptual illusions (polyopsia, metamorphopsia).
3. Autoscopy.
4. Versive movements of the head and eyes.
5. Rapid forced blinking.
6. Evolution of simple partial seizures to more complex ones (involving the somatosensory, primary motor or supplementary motor cortex); secondary generalization.
7. Epileptic oblique deviation of the eyes and epileptic nystagmus.

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