Frontal Lobe Symptoms Research Articles

Clinical and tomographic findings in vascular dementia.

Vascular dementia (VD) may arise as a sequel to any form of cerebrovascular disease. Since only some patients with cerebrovascular disease will eventually develop dementia, we studied the morphological and clinical findings associated with dementia in cerebrovascular patients. The relationship between these factors and the dementia syndrome was evaluated in 25 patients with VD, and 68 non demented subjects with a history of cerebral ischemic attacks. We found that VD was significantly associated with white matter lesions and atrophy on CT-scan, and a high prevalence of frontal lobe symptoms and signs.

Progressive frontal dysfunction.

A number of causes of progressive mental impairment show a preponderance of frontal lobe symptoms. It is proposed that these disorders can be subdivided into primary and secondary frontal dementias, based on the symptomatology and the site of major pathological disruption. An anatomical explanation, based on variations in cortical and subcortical influences, aids in understanding the clinical differences.

Why do frontal lobe symptoms predominate in vascular dementia with lacunes?

We studied 30 necropsy cases of vascular dementia with a lacunar state. Manifestations included dementia, lack of volition, emotional lability, small-stepped gait, dysarthria, urinary incontinence, grasp reflex, pyramidal signs, paraplegia in flexion, and akinetic mutism. Pathologically, there was diffuse incomplete softening of white matter in all cases. Both lacunes and diffuse softening were found predominantly in the frontal lobes. The prominent clinical features were therefore frontal lobe symptoms, with good correlation between the symptoms and the distribution of pathologic lesions.

Why do frontal lobe symptoms predominate in vascular dementia with lacunes?

We studied 30 necropsy cases of vascular dementia with a lacunar state. Manifestations included dementia, lack of volition, emotional lability, small-stepped gait, dysarthria, urinary incontinence, grasp reflex, pyramidal signs, paraplegia in flexion, and akinetic mutism. Pathologically, there was diffuse incomplete softening of white matter in all cases. Both lacunes and diffuse softening were found predominantly in the frontal lobes. The prominent clinical features were therefore frontal lobe symptoms, with good correlation between the symptoms and the distribution of pathologic lesions.

Amnesic Syndrome: A Lesion-Specific Disorder?

This paper reviews various lines of evidence which suggest that organic amnesia stemming from lesions of the temporal lobe region produce an amnesia that is qualitatively different from that produced by diencephalic lesions. Differences between these two classes of amnesia were found within five dimensions of performance; (a) insight, concern and confabulation, (b) retrograde amnesia, (c) forgetting rate, (d) frontal lobe symptoms, (e) sensitivity to interference in short term memory. The range of differences found suggest that temporal lobe and diencephalic amnesics should not be considered as suffering from the same type of “amnesic syndrome”. It is proposed that future experimental work on amnesia should take full account of neuropathological differences between amnesic patients.