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» Home » CAD » Neurology » Demyelinating Disease » Frontal lobe syndrome
Background
Frontal lobe syndrome is a clinical condition caused by prefrontal cortex damage and decreased function, a significant association region of the frontal lobe essential for brain functioning functions such as planning, motivation, social conduct, and language or speech production. The lateral prefrontal cortex, orbitofrontal cortex, frontal poles, and anterior cingulate may all be implicated.
Lesions in the orbitofrontal regions, which are often recognized to cause frontal lobe personality, induce drastic behavioral changes, leading to impulsivity and a lack of judgment. Brodmann’s Area lesions are related to a lack of inhibition, emotional lability, and an inability to perform correctly in social relationships.
Epidemiology
The underlying etiology determines the prevalence of frontal lobe syndrome. Recent research suggests that degenerative causes of frontal lobe dysfunction may be under-reported.
Previous research in Japan discovered about 12,000 frontal lobe syndrome cases, indicating that the condition is not as uncommon as previously assumed.
Anatomy
Pathophysiology
According to human and animal research with frontal lobe lesions, the ventromedial orbitofrontal cortex and dorsolateral convexity have received particular attention. Both lesions, however, have differing effects on behavior. As previously noted, dorsolateral lesions can result in abulic and apathetic states.
On the other hand, ventromedial orbitofrontal lesions produce impulsive unconstrained behavior and potentially harmful judgments. Bilateral lesions typically result in more severe impairments. A difference has also been noted between right and left frontal lesions.
Lesions on the left are linked to depression-like symptoms, whereas right-side lesions are linked to mania. However, this syndrome encompasses many activities that do not adhere to rigid guidelines.
Etiology
Frontal lobe abnormalities are caused by a variety of diseases, including severe head trauma, which can induce orbitofrontal cortex injury, cerebrovascular disease, tumors capsulizing the frontal lobe, and neurodegenerative disease. Other reasons include frontal lobe epilepsy, multiple sclerosis, HIV, and early-onset dementia.
Genetics
Prognostic Factors
The prognosis is better for reversible and curable causes like brain infections and resectable tumors than for progressive neurodegenerative conditions such as frontotemporal dementia.
In the later instances, treatment centers on symptom management, and eventually, patients die due to complications.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK532981/
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» Home » CAD » Neurology » Demyelinating Disease » Frontal lobe syndrome
Frontal lobe syndrome is a clinical condition caused by prefrontal cortex damage and decreased function, a significant association region of the frontal lobe essential for brain functioning functions such as planning, motivation, social conduct, and language or speech production. The lateral prefrontal cortex, orbitofrontal cortex, frontal poles, and anterior cingulate may all be implicated.
Lesions in the orbitofrontal regions, which are often recognized to cause frontal lobe personality, induce drastic behavioral changes, leading to impulsivity and a lack of judgment. Brodmann’s Area lesions are related to a lack of inhibition, emotional lability, and an inability to perform correctly in social relationships.
The underlying etiology determines the prevalence of frontal lobe syndrome. Recent research suggests that degenerative causes of frontal lobe dysfunction may be under-reported.
Previous research in Japan discovered about 12,000 frontal lobe syndrome cases, indicating that the condition is not as uncommon as previously assumed.
According to human and animal research with frontal lobe lesions, the ventromedial orbitofrontal cortex and dorsolateral convexity have received particular attention. Both lesions, however, have differing effects on behavior. As previously noted, dorsolateral lesions can result in abulic and apathetic states.
On the other hand, ventromedial orbitofrontal lesions produce impulsive unconstrained behavior and potentially harmful judgments. Bilateral lesions typically result in more severe impairments. A difference has also been noted between right and left frontal lesions.
Lesions on the left are linked to depression-like symptoms, whereas right-side lesions are linked to mania. However, this syndrome encompasses many activities that do not adhere to rigid guidelines.
Frontal lobe abnormalities are caused by a variety of diseases, including severe head trauma, which can induce orbitofrontal cortex injury, cerebrovascular disease, tumors capsulizing the frontal lobe, and neurodegenerative disease. Other reasons include frontal lobe epilepsy, multiple sclerosis, HIV, and early-onset dementia.
The prognosis is better for reversible and curable causes like brain infections and resectable tumors than for progressive neurodegenerative conditions such as frontotemporal dementia.
In the later instances, treatment centers on symptom management, and eventually, patients die due to complications.
https://www.ncbi.nlm.nih.gov/books/NBK532981/
Frontal lobe syndrome is a clinical condition caused by prefrontal cortex damage and decreased function, a significant association region of the frontal lobe essential for brain functioning functions such as planning, motivation, social conduct, and language or speech production. The lateral prefrontal cortex, orbitofrontal cortex, frontal poles, and anterior cingulate may all be implicated.
Lesions in the orbitofrontal regions, which are often recognized to cause frontal lobe personality, induce drastic behavioral changes, leading to impulsivity and a lack of judgment. Brodmann’s Area lesions are related to a lack of inhibition, emotional lability, and an inability to perform correctly in social relationships.
The underlying etiology determines the prevalence of frontal lobe syndrome. Recent research suggests that degenerative causes of frontal lobe dysfunction may be under-reported.
Previous research in Japan discovered about 12,000 frontal lobe syndrome cases, indicating that the condition is not as uncommon as previously assumed.
According to human and animal research with frontal lobe lesions, the ventromedial orbitofrontal cortex and dorsolateral convexity have received particular attention. Both lesions, however, have differing effects on behavior. As previously noted, dorsolateral lesions can result in abulic and apathetic states.
On the other hand, ventromedial orbitofrontal lesions produce impulsive unconstrained behavior and potentially harmful judgments. Bilateral lesions typically result in more severe impairments. A difference has also been noted between right and left frontal lesions.
Lesions on the left are linked to depression-like symptoms, whereas right-side lesions are linked to mania. However, this syndrome encompasses many activities that do not adhere to rigid guidelines.
Frontal lobe abnormalities are caused by a variety of diseases, including severe head trauma, which can induce orbitofrontal cortex injury, cerebrovascular disease, tumors capsulizing the frontal lobe, and neurodegenerative disease. Other reasons include frontal lobe epilepsy, multiple sclerosis, HIV, and early-onset dementia.
The prognosis is better for reversible and curable causes like brain infections and resectable tumors than for progressive neurodegenerative conditions such as frontotemporal dementia.
In the later instances, treatment centers on symptom management, and eventually, patients die due to complications.
https://www.ncbi.nlm.nih.gov/books/NBK532981/
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