Common clinical symptoms and signs of damage in cerebral cortical lesions
Cerebral cortex is the last receiving station involved along a line of stations that receive information from eyes, ears and other organs responsible for general sensations. Lesions of the cerebral cortex are due to tumours, vascular accidents (Stroke) and trauma. However, cerebral cortex has the remarkable ability to reorganize itself, once part of it, is damaged.
Lesions in the Cerebral cortex
Cortical damage in motor areas results in the paralysis of contralateral side of the cerebral cortex. Damage to the secondary motor area causes difficulty in performing skilled tasks. Jacksonian march is due to an irritative lesion of the primary motor area.
Discrete lesions in primary motor cortex results in little change in the muscle tone. However larger lesions involving both primary and secondary motor cotices result in muscle spasm. Secondary motor areas transmit inhibitory impulses to the extrapyramidal system that tend to lower the muscle tone. But primary motor cortex seems to increase the muscle tone.
Frontal eye field
Destruction to the frontal eye field causes deviation to the side of the lesion with inability to turn the eyes to the opposite side. Involuntary tracking movements are not involved. Irritable lesion in frontal eye field cause the two eyes to move to the opposite side.
Lesions in Brocas speech area
This lesion causes loss of ability to produce speech. However they can think the words they wish and can write them. They can understand the spoken words also.
Lesions in Wernicke’s area
This lesion causes loss of ability to understand spoken or written language. However speech is unaffected. But patient is unaware of the meaning, may use nonexistent words, incorrect words and he/she is also unaware of any mistakes.
Lesions in both areas (Brocas and Wernicke’s) cause global aphasia. Lesions involving insula of the cortex can have difficulty in producing phonemes in their proper order.
Lesion in dominant angular gyrus in the posterior parietal lobe result in inability to read and write, due to the division of the connection between visual association area and the anterior part of the Wernicke’s area.
Lesion in prefrontal cortex can result in losing initiative and judgment. In addition it can cause euphoria. Patient usually does not conform to the acceptable social behavior and becomes careless of dress and appearance.
Lesions in Sensory cortex
Sensory cortex is necessary for the appreciation of spatial recognition, recognition of relative intensity, and recognition of similarity and difference.
Lesions of the primary somesthetic area of the cortex result in contralateral sensory disturbances, which is most severe in distal limbs. Other crude stimuli are recognized at the thalamic level. However the patient is unable to judge weights of the objects. Loss of muscle tone may also occur with sensory cortex damage. Lesions of secondary somesthetic area do not cause recognizable sensory defects.
Lesion in Somesthetic association area of the superior parietal lobule may result in inability to combine touch, pressure, and proprioceptive impulses. This is called astereognosis. E.g. a patient may unable to identify a key placed in his hand when the eyes are closed.
The Primary visual area
Lesions involving posterior part of the calcarine sulcus, results in loss of sight in the opposite visual field. But central visual field is spared and it is called macular sparing. It is may be due to the fact that patient shifting his/her eyes very slightly. So other non-affected macular area is used to assess the affected visual field. Lesions in upper half can cause inferior quandrantic hemianopia. Lesions in below the calcrine sulcus may result in superior quandrantic hemianopia. Lesions in occipital pole causes central scotomas. Lesions in secondary visual area results in loss of ability to recognize objects in opposite visual field.
Lesions in Unilateral Primary Auditory area can cause bilateral loss of hearing, but loss is greater in the opposite ear. But the main defect would be to identify the location of sound. Bilateral lesions cause complete deafness.
Lesions in secondary auditory area (lesion in cortex posterior to the primary auditory area) in the lateral sulcus could cause pure word deafness.
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