Working Memory Deficits After Lesions Involving the Supplementary Motor Area.
Ikusi/ Ireki
Data
2018Egilea
Cañas, Alba
Juncadella, Montserrat
Lau, Ruth
Gabarrós, Andreu
Hernández, Mireia
Cañas A, Juncadella M, Lau R, Gabarrós A and Hernández M (2018) Working Memory Deficits After Lesions Involving the Supplementary Motor Area. Front. Psychol. 9:765. doi: 10.3389/fpsyg.2018.00765
Laburpena
The Supplementary Motor Area (SMA)—located in the superior and medial aspects of
the superior frontal gyrus—is a preferential site of certain brain tumors and arteriovenous
malformations, which often provoke the so-called SMA syndrome. The bulk of the
literature studying this syndrome has focused on two of its most apparent symptoms:
contralateral motor and speech deficits. Surprisingly, little attention has been given to
working memory (WM) even though neuroimaging studies have implicated the SMA in
this cognitive process. Given its relevance for higher-order functions, our main goal was
to examine whether WM is compromised in SMA lesions. We also asked whether WM
deficits might be reducible to processing speed (PS) difficulties. Given the connectivity
of the SMA with prefrontal regions related to executive control (EC), as a secondary
goal we examined whether SMA lesions also hampered EC. To this end, we tested
12 patients with lesions involving the left (i.e., the dominant) SMA. We also tested 12
healthy controls matched with patients for socio-demographic variables. To ensure that
the results of this study can be easily transferred and implemented in clinical practice,
we used widely-known clinical neuropsychological tests: WM and PS were measured
with their respective Wechsler Adult Intelligence Scale indexes, and EC was tested
with phonemic and semantic verbal fluency tasks. Non-parametric statistical methods
revealed that patients showed deficits in the executive component of WM: they were
able to sustain information temporarily but not to mentally manipulate this information.
Such WM deficits were not subject to patients’ marginal PS impairment. Patients also
showed reduced phonemic fluency, which disappeared after controlling for the influence
of WM. This observation suggests that SMA damage does not seem to affect cognitive
processes engaged by verbal fluency other than WM. In conclusion, WM impairment
needs to be considered as part of the SMA syndrome. These findings represent the
first evidence about the cognitive consequences (other than language) of damage to the
SMA. Further research is needed to establish a more specific profile of WM impairment
in SMA patients and determine the consequences of SMA damage for other cognitive
functions.