Symptoms of the occipital lobe

Destruction of the projection area of the analyzer (cuneus gyrus lingualis and deep sections of sulcus calcarinus) entails the appearance of the homonymous hemianopsia. Lighter degrees of damage cause not a complete hemianopsia. Hemiopic disorders can be partial. Thus, in the defeat of cuneus, only the lower quadrants in the fields of vision fall out, and the foci in the gyrus lingualis give the upper square hemianopsia.

In cortical (occipital) lesions, the central fields of vision are usually retained, which distinguishes them from visual pathway lesions (tr. Opticus). Lesions of the outer surfaces of the occipital lobes lead not to blindness, but to visual agnosia-the recognition of objects by their visual images. Foci on the border of the occipital lobe with parietal causes alexia (lack of understanding of written speech) and acalculia (break accounts).

Contralateral ataxia (disruption of the function of the occipital-bridge-cerebellar path) can occur, disrupt the combined movement of the eyes, change the width of the pupils and the accommodation disorder.

The irritation of the inner surface of the occipital lobe results in the appearance of simple visual sensations (photomata) - flashes of light, lightning, colored sparks, etc. More complex visual sensations (such as cinematographic pictures) appear when the outer surfaces of the occipital lobes are irritated.

Another disorder occurs when the occipital lobes are affected - metamorphosis (distorted perception of the shape of visible objects - their contours seem broken, curved, they appear too small - a microscope - or, on the contrary, too large - a macropsy). Most likely, the appearance of such distorted perceptions depends on the violation of the joint work of the visual and statokineesthetic analyzers.

Syndromes of local injuries of the occipital lobes

I. Medial departments

1. Defects of the field of view
2. Visible agnosia
3. Visual hallucinations
4. Alexia without agraphy
5. Anton (Anton) syndrome (negation of blindness)

II. Lateral (convectional) departments

1. Alexia with agraea
2. Violation of optokinetic nystagmus
3. Ipsilateral deterioration of follow-up movements of the eyeball.

III. Epileptic phenomena, characteristic for the occipital localization of epileptic foci

I. Medial departments.

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

The extensive lesion of the inner (medial) surface of the occipital lobe in the fissurae calcarinae region leads in typical cases to the fallout of the opposite fields of vision of both eyes, that is, to the development of the full hemianopsia of the same name. Local defeat over fissurae calcarinae, that is, in the cuneus region, leads to a quadrant hemianopsia of the opposite lower quadrants; with local lesions below this furrow (gyrus lingualis), the fields of the opposite upper quadrants fall out. Fires of even smaller size lead to the appearance of cattle in opposite fields of vision (in both fields of vision and in the quadrants of the same name). Color sensations in opposite fields of vision drop out earlier, therefore research of fields of sight not only on white, but also on blue and red colors at early stages of some diseases gets the important value.

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

Spotting agnosia in its expanded form is less common and more typical for bilateral involvement of the occipital lobe. In this case, the patient is not blind in the literal sense of the word; he sees all the objects, but loses the ability to recognize them. The nature of visual disorders in such cases is very variable. A bilateral homonymous hemianopsia is possible. Pupils, their reflex reactions and the fundus are normal.

The patient ceases to recognize and written, that is, develops alexia (partial or complete inability to read). Alexia is found in two main forms: "pure alexia" (or alexia without agraphy) and alexia with agraea. "Pure alexia" develops when the medial surface of the occipital lobe is damaged, which interrupts the connections of the visual cortex to the left (dominant) temporal-parietal region. These are usually lesions located behind and below the posterior horn of the lateral ventricle. With "pure alexia", visual acuity in most patients is normal, although a quadrant hemianopia or complete hemianopsia can occur. Non-verbal stimuli (any other objects and faces) can be recognized normally. Alexia with agrarians is typical for damage to the convexital surface of the occipital lobe, closer to the temporal lobe, and is manifested not only by a violation of reading, but also by defects in the letter, which is most often found in patients with various forms of aphasia.

Visual hallucinations can be of the nature of simple photos or more complex visual images (the latter more often with the stimulation of the lateral sections of the cortex of the occipital lobe) and can be observed in isolation or in the form of an aura of epileptic seizure. Ignoring or denying (anosognosia) of blindness in some patients with visual agnosia (cortical blindness) is called Anton syndrome (Anton). Patients with the syndrome of Anton confabulate their visual environment and refuse to recognize their visual defect. Anton's syndrome is more common in cortical blindness of vascular genesis.

In general, the causes of cortical blindness are diverse; it is described in vascular (stroke, complication of angiography), infectious (meningitis, encephalitis), degenerative (MELAS syndrome, Lee's disease, adrenoleukodystrophy, metochromatic leukodystrophy, Creutzfeldt-Jacob disease), immune (multiple sclerosis, subacute sclerosing panencephalitis), metabolic (hypoglycemia , poisoning with carbon monoxide, uremia, hemodialysis), toxic (mercury, lead, ethanol), iatrogenic (vincristine) and other pathological conditions (transitory ictal or postictal phenomenon, eclampsia, hydrocephalus I, a brain tumor, a traumatic brain injury, electric injury, porphyria, brain edema).

II. Lateral sections.

The defeat of the lateral (convectional) parts of the occipital lobe may also be accompanied by a change in the optokinetic nystagmus and a deterioration in the tracking movements of the eyes, which is revealed in special instrumental studies. Extensive damage to the occipital cortex with partial involvement of the parietal lobe can lead to special forms of metamorphosis, including palinopsy (perseveration of the visual image), alle- sia (false orientation of the object in space), monocular diplopia or triplopia, and even polyopia (one object is perceived as two or more). In these cases, such phenomena as memory impairment for visual stimuli, worsening of topographic memory, problems in visually spatial orientation are also possible.

Prosopagnosia (impaired recognition of the face) can be caused by bilateral occipital-parietal lesions. One-sided optical ataxia on the side opposite to parieto-occipital damage can be observed in isolation without other components of the Balint syndrome.

Color achromatopsia is manifested by a violation of the recognition of color shades (posterior damages of the right hemisphere).

The list of the main neurological syndromes in the defeat of the occipital lobe looks as follows.

Any (right or left) occipital lobe.

1. Contralateral homonymous defect of the visual field: scotoma, hemianopsia, quadrant hemianopsia.
2. One-sided optical ataxia

Non-dominant (right) occipital lobe.

1. Color agnosia
2. Spectacular oculomotor disorders (violations of follow-up movements of the eyes)
3. Deterioration of the visual orientation
4. Decay of topographic memory

Dominant (left) occipital lobe.

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

Both occipital lobes

1. Bilateral scotoma
2. Cortical blindness
3. Syndrome of Anton.
4. The Balint syndrome
5. Various variants of visual agnosia (objects, persons, color).

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

Nuchal attacks are accompanied by elementary visual images (photomata), as well as negative phenomena (scotoma, hemianopsia, amavroz). More complex hallucinations are associated with the spread of epileptic discharge to the parietal or temporal region. Rapid forced blinking at the beginning of a seizure may be a sign of the occipital epileptic focus. Sometimes after visual hallucinations, the turn of the head and eyes develops in the opposite direction (involvement of the contralateral parietal-occipital region). The spread of convulsive discharges to the temporal region can lead to complex partial seizures, and the "leakage" of them into the parietal lobe may cause various somatosensory phenomena. Sometimes convulsive discharges from the occipital lobe extend to the anterior central gyrus or additional motor area with a corresponding clinical picture, which makes it difficult to correctly locate the epileptic focus.

Epileptic paroxysmal oblique deviation of the eyes (epileptic skew deviation) with nystagmus is described with lesion of the left occipital lobe.

Thus, the following nuchal epileptic phenomena occur:

1. Elementary visual seizures (the most frequent variant) with photomata or negative visual phenomena.
2. Perceptual illusions (polyopsy, metamorphosis).
3. Autoscopy.
4. Vertical movements of the head and eyes.
5. Fast forced blinking.
6. Evolution of simple partial seizures to more complex ones (with involvement of somatosensory, primary motor or additional motor cortex); secondary generalization.
7. Epileptic oblique deviation of the eyes and epileptic nystagmus.

[1], [2], [3]