Visual agnosia

Introduction Brain damage can sometimes cause obvious and specific obstacles in behavior. One of the most rare cases is that you can't get to know everyday items. This kind of disorder is called visual agnosia. Agnosia refers to the inability to understand the clinical symptoms of the body parts and familiar objects through organs without sensory insufficiency, mental decline, unconsciousness, and inattention.

Cause

The occipital lobe is the visual cortical center, which is mainly related to visual acuity and visual memory. The lesions in the 18th and 19th districts cause visual agnosia. The main causes of aphasia are intracranial tumors, cerebrovascular diseases and craniocerebral trauma.

The primary sensory areas such as the visual, auditory, and somatosensory aspects of the brain in the sensory area receive different stimuli, and non-formed visual anomalies such as flashes of eyes, sparks, and discoloration may occur. The ears hear silk, shasha, rumble. "The abnormal sound, limb numbness, acupuncture, touch and other physical sensations are different. The destruction of the primary sensory area makes the incoming impulse unable to produce a feeling in the brain."

an examination

Including object agnosia, appearance agnosia, simultaneous agnosia, color agnosia, visual spatial agnosia and so on.

(1) Object agnosia: The patient cannot recognize the common items that are clearly seen, such as hats, gloves, pens, etc.

(2) Appearance agnosia: The patient does not know the appearance of familiar people (including the closest people such as wives and children).

(3) Simultaneous agnosia: also known as comprehensive agnosia. The patient can understand all parts of the matter, but cannot understand the whole picture of things. For example, if two people perform baseball practice on one painting, they can't identify the two people who vote for the ball.

(4) Color misrecognition: The name and difference of the color cannot be recognized.

(5) Visual space agnosia: The spatial position of the object and the spatial relationship between the objects cannot be recognized.

Differential diagnosis

Visual misrecognition needs to be identified as follows:

Perceptive visual agnosia: Perceptual visual agnosia refers to the fact that patients can avoid obstacles encountered while walking, but in many ways they are blind. Patients cannot name the object they are presented, they cannot be drawn, nor can they pick the same object from a series of object samples. The patient cannot indicate the item that the examiner has informed, but the patient's vision and vision are normal, and the patient can also distinguish small changes in the intensity and brightness of the light source. Their shortcomings are obstacles to visual pattern recognition. Some patients complain that they cannot see static objects. Once these objects start to move, the patient can recognize them from the background. Distal sulcus or occipital lesions (mostly ischemic lesions) often cause this loss of recognition, and appear in the recovery period of the cortex. Tissues other than the striate cortex visual pathway, such as the thalamic occipital, superior and parietal lobe, also play a role in cognitive light and motion.

Associative visual agnosis: Associative visual agnosis means that the patient cannot visually recognize the object, but can draw the object, and can also point out the object from a series of object samples, indicating that the patient's vision is normal. The recognition of pictures is more difficult than the identification of objects. During the recovery period, this type of loss of recognition will gradually decrease. Optical aphasia means that the patient cannot name the object that has been recognized, but the patient can correctly explain the use of the object.

The above two types of misidentification are accompanied by right-sided hemianopia, pure dyslexia and color naming defects. Mostly caused by lesions in the medial side of the left occipital lobe and the corpus callosum, the most common ischemic lesions. Visual misrepresentation also includes color misrecognition and face recognition.

Color agnosis: Patients with color blindness (achromatopsia) cannot recognize different colors. Acquired color blindness is the lesion of the lower part of the occipital lobe on both sides or dominant hemisphere involving the lingual and shuttle, but the distance cortex is spared. Color loss can occur when the lesion under the cortical surface affects 1/3 of the tongue and the lesion under the cortical surface affects the white matter behind and behind the lateral ventricle. The occipital branch of the posterior cerebral artery is blocked, but color blindness can occur when the distance branch supplying the original visual cortex is unobstructed. The structure of the brain that handles color perception is different from the structure of processing depth and spatial perception. Each side of the hemisphere visual combined with the lower cortex mediates color half-blind patients who represent the upper and lower 1/4 of the field of view. The color blunt is often blinded by the upper 1/4 quadrant because of the striated hypodermis and visual radiation involvement. Patients with unilateral occipital infarction may have lower color blindness and have upper 1/4 quadrant blindness.

Color-deficient patients can see maps of different colors, but can't name colors, nor can they pick out the color of the inspector's instructions. However, the question about the color of the spoken language is correct, and if you can correctly answer "What color is the sky"? The inner surface of the superior hemisphere occipital lobe is most likely to be color-deficient, so patients with color misidentification often have right-sided hemianopia and pure dyslexia. The dyslexia is due to the involvement of the left occipital lobe transition. The inside of the compartment; hemianopia is due to involvement of the left geniculate body, visual radiation or the cortical cortex.

Prosopagnosia: Lesions in the lower part of the occipital lobe can also cause difficulty in visually discerning faces, while discerning visually similar objects, such as specific vehicles in parking lots. The patient loses the ability to select a particular individual from a general object. Patients with face disrespect can't even visually identify their relatives, only the relatives' voices identify them. But patients can still recognize faces and distinguish between different faces. Patients with face disrespect are also having difficulty recognizing photos of well-known people, and they cannot even identify themselves in the face of their own photos. In severe cases, the patient sat in front of the mirror to see that he could not recognize himself. Most autopsy patients found that the face was identified as a bilateral fusiform lesion or a disconnection. The fusiform gyrus can be considered as a visual joint zone for recognizing a face, and its defect may be a partial visual memory deficit.

Some face-deficient patients have better ability to recognize objects than faces, and some patients have the opposite. In addition, the unilateral right occipital temporal lobe lesions may also have facial dissonance, which may be due to the identification of the main body of the left occipital cortex, while the right main face is identified.

Patients with face disapproval also have misidentification of the non-classical shape of the object. If the folded glasses are not recognized, they can be confirmed when they are opened. Sometimes it is a strange "paradonical knowledge" that occurs when a patient sees a celebrity photo or a portrait. When he sees a Guanyin portrait, he says, "This may not be Guanyin."

Patients with central blindness may develop Charcot-Wilbrant syndrome with visual memory impairment, the patient cannot recall the color of the object, or cannot remember the shape of the familiar object.

Visual simultanagnosia: Visual image combination misrecognition means that the patient cannot recognize and understand the meaning of the entire visual image, but there is no obstacle to the understanding and understanding of the various components of the image. The patient can correctly understand and understand the various subunits of a complex portrait, but the meaning of the whole portrait cannot be understood. If the patient can't calculate the total value of the coins scattered on the table, but can tell the representative value of each coin.

A visually imaged combination of unidentified patients may also have a visual field defect (single or bilateral lower 1/4 quadrant). The visual image combination misidentification may be an obstacle to the eye movement required for the integration of spatial objects, or it may be an obstacle to the spatial and temporal interaction of the whole process of visual impulse conduction, so that there may be a lack of continuous visual space attention, or it may be related to structural composition. The visual object encodes an obstacle to the positioning process.

A visually imaged combination of unidentified patients may appear to be "turning a blind eye" and static objects disappear when viewed directly. This phenomenon is caused by the occipital lobe on both sides as a result of combined cortical lesions. Visual images combined with unidentified patients are often accompanied by other symptoms of Balint syndrome.

Visual image combination unidentified patients may be the first or prominent clinical manifestations of Alzheimer's disease. These patients are referred to as the visual variant of Alzheimer's disaese, whose cortical atrophy is heavier in the hemisphere. This type of patient is often seen in the ophthalmology department. The patient has normal vision, no color misrecognition, good insight, and a sense of humor. He also has language barriers, can't read, and has visual obstacles. Imaging showed bilateral cortical atrophy, with the parietal lobe as a prominent.

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