Is the Concept of Frontal–Subcortical Dementia Relevant to Schizophrenia?

1992 ◽  
Vol 160 (4) ◽  
pp. 442-460 ◽  
Author(s):  
Christos Pantelis ◽  
Thomas R. E. Barnes ◽  
Hazel E. Nelson

A syndrome of subcortical dementia has been described in conditions predominantly affecting the basal ganglia or thalamus, structures that have also been implicated in the pathogenesis of schizophrenia. There are similarities between subcortical dementia and the type II syndrome of schizophrenia, in terms of clinical features, pattern of neuropsychological deficits, pathology, biochemistry and data from brain-imaging studies. These similarities raise the possibility that certain schizophrenic symptoms, particularly negative symptoms and disturbance of movement, may reflect subcortical pathology. Neuropsychological deficits of presumed frontal lobe origin have been reported in some schizophrenic subjects. The occurrence of such deficits in a condition in which frontal lobe pathology has not been clearly demonstrated may be explicable in terms of a subcortical deafferentation of the pre-frontal cortex.

2011 ◽  
Vol 26 (S2) ◽  
pp. 2154-2154
Author(s):  
J.-L. Martinot ◽  
E. Artiges ◽  
C. Leroy ◽  
M.-L. Paillère Martinot ◽  
S. Mana ◽  
...  

1/In juvenile patients, a cross-sectional ALE meta-analysis of both brain structure and function regional deviations in 270 articles allowed to cluster the diagnosed disorders into three sets with respectively marked affective, cognitive, and psychomotor phenomenology. The group with affective phenomenology was characterized by abnormalities of the frontal-limbic regions; the group with “cognition deficits” (incl. schizophrenia) mainly related to cortex abnormalities; and the psychomotor condition was associated with abnormalities in the basal ganglia. Therefore, early regional brain abnormalities might interact with the analysis of subsequent treatments effects in MR studies of brain structure and function of chronic mental disorders. 2/In chronic patients, brain imaging studies of antipsychotic drugs using dopamine receptor radioligands &PET scanner have consistently demonstrated the prevalence of their dose-dependent action in basal ganglia. This information has led to theoretical windows for optimal drug dosage. Recent measures of the dopamine transporter in chronic antipsychotic treatment, or in chronic use of drugs of addiction (e.g. tobacco, cannabis) suggest opposite changes of the adioligand uptake in both conditions. Therefore, control for the associated confounding addictions is required for in vivo analysis of antipsychotic action on the dopamine regulation in cortex and subcortical regions. 3/In treatment-resistant patients, MR & PET imaging studies have detected deviations of both brain structure and function, therefore suggesting biomarker of treatment response. 4/Conclusion: stage of illness, addictions, multimodal imaging, should be considered as covariates for brain imaging determinations of treatment effects in patients with chronic mental disorders.


1989 ◽  
Vol 154 (5) ◽  
pp. 596-614 ◽  
Author(s):  
W. R. G. Gibb

Recent research into the dementia of Parkinson's disease has exposed a complex area in which it has not always been possible to match clinical and pathological observations. Certain neuropsychological deficits result from a disruption of basal ganglia and frontal lobe interactions. These are unrelated to a global dementia, the prevalence of which exceeds twice that in the normal population. The associated pathological lesions comprise cortical pathology, either Alzheimer's disease or Lewy bodies, in combination with moderate degeneration of the subcortical, cholinergic, basal nucleus of Meynert.


2021 ◽  
Vol 11 (3) ◽  
pp. 299
Author(s):  
Yeong Jin Kim ◽  
Tae-Young Jung ◽  
In-Young Kim ◽  
Shin Jung ◽  
Kyung-Sub Moon

Postoperative complications after brain tumor surgery occur occasionally and it is important for clinicians to know how to properly manage each complication. Here, we described a rare case of late-onset, subdural fluid collection localized at the resection cavity that caused motor weakness after convexity meningioma resection, requiring differentiation from an abscess, to help clinicians determine treatment strategies. A 58-year-old right-handed female was admitted to the hospital with a headache and posterior neck pain. Brain computed tomography (CT) scans and magnetic resonance (MR) images showed a homogeneously enhanced, calcified, and multi-lobulated mass adjacent to the right motor strip without perilesional edema. The patient underwent surgery without incident or residual deficit and was discharged from the hospital in good condition. Six weeks after surgery, the patient complained of left arm monoparesis without infection-related symptoms. Brain imaging studies showed a localized fluid collection in the resection cavity with an enhanced margin and perilesional edema. Diffusion restriction was not detected. After three months of conservative treatment without surgery or antibiotics, she recovered from the neurologic deficits, and brain imaging studies showed the spontaneous regression of the fluid collection and perilesional edema. Late-onset, localized fluid collection at the resection cavity, which is similar to an abscess, could occur three to eight weeks after meningioma resection. When there are predisposing factors, including blood components and hemostatic materials in the surgical cavity, it is important for clinicians to understand this type of complication and choose conservative management as a feasible strategy.


1989 ◽  
Vol 155 (S7) ◽  
pp. 93-98 ◽  
Author(s):  
Nancy C. Andreasen

When Kraepelin originally defined and described dementia praecox, he assumed that it was due to some type of neural mechanism. He hypothesised that abnormalities could occur in a variety of brain regions, including the prefrontal, auditory, and language regions of the cortex. Many members of his department, including Alzheimer and Nissl, were actively involved in the search for the neuropathological lesions that would characterise schizophrenia. Although Kraepelin did not use the term ‘negative symptoms', he describes them comprehensively and states explicitly that he believes the symptoms of schizophrenia can be explained in terms of brain dysfunction:“If it should be confirmed that the disease attacks by preference the frontal areas of the brain, the central convolutions and central lobes, this distribution would in a certain measure agree with our present views about the site of the psychic mechanisms which are principally injured by the disease. On various grounds, it is easy to believe that the frontal cortex, which is specially well developed in man, stands in closer relation to his higher intellectual abilities, and these are the faculties which in our patients invariably suffer profound loss in contrast to memory and acquired ability.” Kraepelin (1919, p. 219)


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