Stroke-induced aphasia refers to the inability to speak or unclear speech.
Based on anatomical knowledge of the brain, it is recognized that stroke-induced aphasia caused by cerebrovascular diseases is the result of damage to the cerebral cortex. Clinically, it can be divided into motor aphasia, sensory aphasia, naming aphasia, and semantic aphasia according to the damaged area of the cerebral cortex. If two or more types of aphasia occur simultaneously, it is called mixed aphasia.
What is motor aphasia?
Motor aphasia occurs when the fronto-inferior region of the cerebral cortex, also known as the motor speech center, is stimulated or damaged by either cerebral hemorrhage or thrombosis. Patients with motor aphasia can understand what others are saying, but cannot speak for themselves.
What is semantic aphasia?
Semantic aphasia occurs when the junction of the three lobes of the cerebral cortex (temporal, parietal, and occipital) is stimulated pathologically. This part of the cerebral cortex is responsible for integrating visual, auditory, and linguistic information to generate semantics, as well as speech symbols and syntactic codes that can express these semantics. The characteristic of semantic aphasia is the inability to understand complex grammatical structures. For example, patients cannot distinguish the meanings of “brother’s father” and “father’s brother.” They cannot comprehend passive voice sentences like “The apple was eaten by the child,” resulting in confusion about who ate whom.
What is sensory aphasia?
Sensory aphasia occurs when the posterior part of the temporal lobe, which is the sensory language center, is stimulated by the lesion in stroke patients. That is, patients can speak autonomously, but they are unclear about the meaning of their own words, and they cannot understand what others are saying. Therefore, they often give answers that are not relevant to the question, and their language has no logicality and even babbles. In this situation, relatives and others should show sympathy and understanding towards the patient, realizing that this is a pathological condition. Only through active treatment can sensory aphasia gradually recover.
What is nominal aphasia?
Nominal aphasia occurs when the posterior part of the temporal lobe and the inferior part of the parietal lobe are damaged. Patients lose the ability to name objects and can only describe their purposes instead of their names. For example, when showing a pencil, the patient can only say it is a “writing tool” but cannot call it a “pencil.”
One study on stroke-induced aphasia in Europe
One study on stroke-induced aphasia in Europe is the research conducted by the Department of Neurology at the University Hospital Frankfurt, Goethe University Frankfurt, in Germany. This study focused on the neuroanatomical correlates of aphasia following stroke, particularly investigating the relationship between the location and extent of brain damage and the severity and type of aphasia experienced by patients.
- The study aimed to elucidate the neural substrates of aphasia by examining patients who had suffered from ischemic strokes affecting language-related areas of the brain. The researchers used advanced neuroimaging techniques, such as diffusion tensor imaging (DTI) and functional MRI (fMRI), to map the damage and its impact on language functions. They also assessed the patients’ language abilities using standardized aphasia tests to categorize the type and severity of their aphasia.
- The study revealed specific patterns of brain damage associated with different types of aphasia. For instance, damage to the left frontal and temporal lobes often resulted in expressive aphasia, while damage to the left parietal lobe was linked to receptive aphasia. The extent of damage, as measured by DTI, was found to correlate with the severity of aphasia symptoms. Furthermore, the study suggested that certain neural networks, particularly those involving the left hemisphere and possibly cross-hemispheric connections, play crucial roles in language processing and recovery.
This research not only contributes to the understanding of the neurobiology of aphasia but also has implications for clinical practice, potentially guiding therapeutic interventions tailored to the specific neural deficits of individual patients.
