OBJECTIVE: To compare the pattern of cortical excitability between early onset major depression (MD) and vascular depression (VD). BACKGROUND: Changes in Transcranial Magnetic Stimulation-related parameters of cortical excitability have been associated with MD. Conversely, although the clinical and neuroradiological profile of VD has been well depicted, neurophysiological studies providing direction of causation between the white matter lesions and the late onset depression are scarce. DESIGN/METHODS: Patients with recurrent MD (n=11), VD (n=11) and healthy controls (n=11) underwent a bilateral study of resting motor threshold (rMT), cortical silent period, intracortical inhibition and facilitation (ICF) at interstimulus intervals (ISI) of 1, 3, 5, 7, 10 and 15 ms. All the MD patients were receiving antidepressant medication at the time of the study. RESULTS: The Wilcoxon test used for the comparison between left and right hemisphere of patients and controls showed a statistically significant increase of rMT in the left hemisphere compared to the right in MD patients. An enhancement of ICF at ISI of 15 ms was observed in the right hemisphere of VD patients. No other differences among the groups and between the two hemispheres were found. CONCLUSIONS: Our study provides a neurophysiological explanation for the different neurobiological and neurochemical processes underlying VD and MD. The enhanced ICF observed in VD patients might be probably related to a glutamate-dependent compensatory plasticity in response to vascular damage of the frontal cortical–subcortical loops implicated in mood regulation and cognition. The asymmetry in cortical excitability, as indexed by the rMT, in MD patients is consistent with a global imbalance of both excitatory and inhibitory circuits.On the contrary, neither significant intercortical asymmetry nor involvement of the inhibitory GABAergic intracortical circuits were found in VD patients. Taken together, these findings support the “vascular depression hypothesis” as a different syndrome with respect to MD.

Distinctive pattern of cortical excitability in vascular depression and major depression

Valentina Puglisi;Carmen Concerto
Secondo
;
Luisa Vinciguerra;Giuseppe Lanza;Manuela Pennisi;Riccardo Ricceri;Bella R;Eugenio Aguglia
Penultimo
;
Giovanni Pennisi
Ultimo
2013

Abstract

OBJECTIVE: To compare the pattern of cortical excitability between early onset major depression (MD) and vascular depression (VD). BACKGROUND: Changes in Transcranial Magnetic Stimulation-related parameters of cortical excitability have been associated with MD. Conversely, although the clinical and neuroradiological profile of VD has been well depicted, neurophysiological studies providing direction of causation between the white matter lesions and the late onset depression are scarce. DESIGN/METHODS: Patients with recurrent MD (n=11), VD (n=11) and healthy controls (n=11) underwent a bilateral study of resting motor threshold (rMT), cortical silent period, intracortical inhibition and facilitation (ICF) at interstimulus intervals (ISI) of 1, 3, 5, 7, 10 and 15 ms. All the MD patients were receiving antidepressant medication at the time of the study. RESULTS: The Wilcoxon test used for the comparison between left and right hemisphere of patients and controls showed a statistically significant increase of rMT in the left hemisphere compared to the right in MD patients. An enhancement of ICF at ISI of 15 ms was observed in the right hemisphere of VD patients. No other differences among the groups and between the two hemispheres were found. CONCLUSIONS: Our study provides a neurophysiological explanation for the different neurobiological and neurochemical processes underlying VD and MD. The enhanced ICF observed in VD patients might be probably related to a glutamate-dependent compensatory plasticity in response to vascular damage of the frontal cortical–subcortical loops implicated in mood regulation and cognition. The asymmetry in cortical excitability, as indexed by the rMT, in MD patients is consistent with a global imbalance of both excitatory and inhibitory circuits.On the contrary, neither significant intercortical asymmetry nor involvement of the inhibitory GABAergic intracortical circuits were found in VD patients. Taken together, these findings support the “vascular depression hypothesis” as a different syndrome with respect to MD.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/100273
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