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Frontal lobe disorder, also frontal lobe syndrome, is an impairment of the frontal lobe of the brain due to disease or frontal lobe injury. [5] The frontal lobe plays a key role in executive functions such as motivation, planning, social behaviour, and speech production.
Following a frontal lobe injury, an individual's abilities to make good choices and recognize consequences are often impaired. Memory impairment is another common effect associated with frontal lobe injuries, but this effect is less documented and may or may not be the result of flawed testing. [ 3 ]
The purpose of this study was to scan the brains in three dimensions and to identify the extent of both cortical and subcortical lesions in more detail. The study also sought to locate the exact site of the lesion in the frontal lobe in relation to what is now called Broca's area with the extent of subcortical involvement. [7]
Research shows that the most common areas to have focal lesions in non-penetrating traumatic brain injury are the orbitofrontal cortex (the lower surface of the frontal lobes) and the anterior temporal lobes, areas that are involved in social behavior, emotion regulation, olfaction, and decision-making, hence the common social/emotional and ...
Right hemiparesis, or right-sided paralysis, may coincide with TMoA if the lesion in the anterior frontal lobe is large enough and extends into the posterior frontal lobe. [1] There are some other forms of aphasia that relate to TMoA. For instance, adynamic aphasia is a form of TMoA that is characterized by sparse speech.
Frontal lobe signs usually involve the motor system and may include many special types of deficit, depending on which part of the frontal lobe is affected: [citation needed] unsteady gait (unsteadiness in walking) muscular rigidity, resistance to passive movements of the limbs
Pontine lesions can typically be distinguished from supranuclear lesions in the frontal lobe based on clinical neurologic findings. Gaze palsies secondary to frontal lobe lesions can be temporarily relieved with rapid, passive horizontal head rotation, which also directly stimulates the sixth nerve nucleus through the vestibuloocular reflex ...
This was seen in patients with Moyamoya disease who had bilateral frontal lobe infarctions which resulted in UB. Upon treatment, the UB was resolved due to 60–70% shrinkage of the anterior lobe hypodensities. [5] Concerning general frontal lobe damage, rehabilitation is known to help a patient function with their disorder.