Article Type
Changed
Tue, 04/20/2021 - 10:11

 

Schizophrenia patients with parkinsonism show unique neurodevelopmental signatures on imaging that involve the sensorimotor system, according to MRI data from 73 adult schizophrenia patients.

Although sensorimotor abnormalities are common in patients with schizophrenia, the neurobiology of parkinsonism in particular is not well understood. Aberrant neurodevelopment is considered a potential mechanism of action for the emergence of such abnormalities, wrote Robert Christian Wolf, MD, of Heidelberg (Germany) University, and colleagues.

In a multimodal MRI study published in Schizophrenia Research, the investigators identified 38 adults with schizophrenia and parkinsonism (SZ-P), 35 schizophrenia patients without parkinsonism (SZ-nonP), and 20 healthy controls.

Parkinsonism was defined as scores of 4 or higher on the Simpson-Angus Scale, while non-Parkinsonism schizophrenia patients had scores of 1 or less.

The researchers examined cortical and subcortical gray-matter volume, as well as three cortical surface markers related to neurodevelopment: cortical thickness (CTh), complexity of cortical folding (CCF), and sulcus depth.

Overall, the SZ-P patients showed increased CCF in the left supplementary motor cortex (SMC) and decreased left postcentral sulcus depth, compared with SZ-nonP patients (P < .05). The left SMC also showed increased CCF, compared with healthy controls – but that difference was not significant.

Both SZ-P and SZ-nonP patients showed higher levels of activity in the left SMC, compared with controls, and activity was higher in SZ-nonP patients, compared with SZ-P patients. In addition, parkinsonism severity was negatively associated with left middle frontal CCF and left anterior cingulate cortex CTh, Dr. Wolf and colleagues reported.

“Overall, the data support the notion that cortical features of distinct neurodevelopmental origin, particularly cortical folding indices such as CCF and sulcus depth, contribute to the pathogenesis of parkinsonism in SZ,” the researchers said.

The study findings were limited by several factors, including the cross-sectional design, the challenges of using the potential restraint inherent in the Simpson-Angus Scale to diagnose parkinsonism, the inability to gauge the impact of lifetime exposure to antipsychotics, and the inability to identify changes in brain stem nuclei, the researchers noted. However, the results suggest the impact of cortical development on parkinsonism in schizophrenia,.

“Cortical surface changes in the sensorimotor system suggest abnormal neurodevelopmental processes that are associated with increased risk for intrinsic sensorimotor abnormalities in SZ and related psychotic disorders,” they concluded.

The study was supported by the German Research Foundation and the German Federal Ministry of Education and Research. The researchers disclosed no financial conflicts.

Publications
Topics
Sections

 

Schizophrenia patients with parkinsonism show unique neurodevelopmental signatures on imaging that involve the sensorimotor system, according to MRI data from 73 adult schizophrenia patients.

Although sensorimotor abnormalities are common in patients with schizophrenia, the neurobiology of parkinsonism in particular is not well understood. Aberrant neurodevelopment is considered a potential mechanism of action for the emergence of such abnormalities, wrote Robert Christian Wolf, MD, of Heidelberg (Germany) University, and colleagues.

In a multimodal MRI study published in Schizophrenia Research, the investigators identified 38 adults with schizophrenia and parkinsonism (SZ-P), 35 schizophrenia patients without parkinsonism (SZ-nonP), and 20 healthy controls.

Parkinsonism was defined as scores of 4 or higher on the Simpson-Angus Scale, while non-Parkinsonism schizophrenia patients had scores of 1 or less.

The researchers examined cortical and subcortical gray-matter volume, as well as three cortical surface markers related to neurodevelopment: cortical thickness (CTh), complexity of cortical folding (CCF), and sulcus depth.

Overall, the SZ-P patients showed increased CCF in the left supplementary motor cortex (SMC) and decreased left postcentral sulcus depth, compared with SZ-nonP patients (P < .05). The left SMC also showed increased CCF, compared with healthy controls – but that difference was not significant.

Both SZ-P and SZ-nonP patients showed higher levels of activity in the left SMC, compared with controls, and activity was higher in SZ-nonP patients, compared with SZ-P patients. In addition, parkinsonism severity was negatively associated with left middle frontal CCF and left anterior cingulate cortex CTh, Dr. Wolf and colleagues reported.

“Overall, the data support the notion that cortical features of distinct neurodevelopmental origin, particularly cortical folding indices such as CCF and sulcus depth, contribute to the pathogenesis of parkinsonism in SZ,” the researchers said.

The study findings were limited by several factors, including the cross-sectional design, the challenges of using the potential restraint inherent in the Simpson-Angus Scale to diagnose parkinsonism, the inability to gauge the impact of lifetime exposure to antipsychotics, and the inability to identify changes in brain stem nuclei, the researchers noted. However, the results suggest the impact of cortical development on parkinsonism in schizophrenia,.

“Cortical surface changes in the sensorimotor system suggest abnormal neurodevelopmental processes that are associated with increased risk for intrinsic sensorimotor abnormalities in SZ and related psychotic disorders,” they concluded.

The study was supported by the German Research Foundation and the German Federal Ministry of Education and Research. The researchers disclosed no financial conflicts.

 

Schizophrenia patients with parkinsonism show unique neurodevelopmental signatures on imaging that involve the sensorimotor system, according to MRI data from 73 adult schizophrenia patients.

Although sensorimotor abnormalities are common in patients with schizophrenia, the neurobiology of parkinsonism in particular is not well understood. Aberrant neurodevelopment is considered a potential mechanism of action for the emergence of such abnormalities, wrote Robert Christian Wolf, MD, of Heidelberg (Germany) University, and colleagues.

In a multimodal MRI study published in Schizophrenia Research, the investigators identified 38 adults with schizophrenia and parkinsonism (SZ-P), 35 schizophrenia patients without parkinsonism (SZ-nonP), and 20 healthy controls.

Parkinsonism was defined as scores of 4 or higher on the Simpson-Angus Scale, while non-Parkinsonism schizophrenia patients had scores of 1 or less.

The researchers examined cortical and subcortical gray-matter volume, as well as three cortical surface markers related to neurodevelopment: cortical thickness (CTh), complexity of cortical folding (CCF), and sulcus depth.

Overall, the SZ-P patients showed increased CCF in the left supplementary motor cortex (SMC) and decreased left postcentral sulcus depth, compared with SZ-nonP patients (P < .05). The left SMC also showed increased CCF, compared with healthy controls – but that difference was not significant.

Both SZ-P and SZ-nonP patients showed higher levels of activity in the left SMC, compared with controls, and activity was higher in SZ-nonP patients, compared with SZ-P patients. In addition, parkinsonism severity was negatively associated with left middle frontal CCF and left anterior cingulate cortex CTh, Dr. Wolf and colleagues reported.

“Overall, the data support the notion that cortical features of distinct neurodevelopmental origin, particularly cortical folding indices such as CCF and sulcus depth, contribute to the pathogenesis of parkinsonism in SZ,” the researchers said.

The study findings were limited by several factors, including the cross-sectional design, the challenges of using the potential restraint inherent in the Simpson-Angus Scale to diagnose parkinsonism, the inability to gauge the impact of lifetime exposure to antipsychotics, and the inability to identify changes in brain stem nuclei, the researchers noted. However, the results suggest the impact of cortical development on parkinsonism in schizophrenia,.

“Cortical surface changes in the sensorimotor system suggest abnormal neurodevelopmental processes that are associated with increased risk for intrinsic sensorimotor abnormalities in SZ and related psychotic disorders,” they concluded.

The study was supported by the German Research Foundation and the German Federal Ministry of Education and Research. The researchers disclosed no financial conflicts.

Publications
Publications
Topics
Article Type
Sections
Article Source

FROM SCHIZOPHRENIA RESEARCH

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads