Anatomical Links between White Matter Hyperintensity and Medial Temporal Atrophy Reveal Impairment of Executive Functions.

Although several studies have demonstrated correlation between white matter hyperintensities (WMH) and impairment of executive functions, the underlying anatomical-functional relationships are not fully understood. The present study sought to investigate the correlations between the volume of WMH and medial temporal lobe atrophy (MTA) using quantitative magnetic resonance image (MRI) and a variety of executive function assessments. A total of 91 patients ranging in age from 58 to 90 years with mild cognitive impairment (MCI) due to Alzheimer's disease (AD) or early phase AD were recruited from the outpatient clinic at the Department of Neurology of Nagoya City University Hospital. We administered neuropsychological batteries evaluating verbal memory, orientation, spatial ability, sustained attention, and a variety of executive functions, including verbal fluency, flexibility, inhibition, and working memory. Quantitative MRI analyses were performed using Dr. View/Linux software and a voxel-based specific regional analysis system. Significant correlations were observed between WMH, as well as MTA, and some executive function scores. Regression analysis revealed that MTA was the strongest predictor of flexibility and verbal fluency. These findings provide new insight into the relationship between quantitative MRI analyses and various types of executive dysfunction in elderly people with MCI due to AD and/or early phase AD. When cognitive function is examined in elderly patients with MCI due to AD or early phase AD, it is important to consider the involvement of WMH and MTA, which is indicative of AD pathology in cognitive dysfunction, particularly executive function.

Temporary deterioration of executive function after subthalamic deep brain stimulation in Parkinson's disease.

OBJECTIVE: Selective impairment of executive function has been shown in Parkinson's Disease (PD) patients undergoing Deep Brain Stimulation (DBS) of the Subthalamic Nucleus (STN). However, some patients experience difficulties in daily life, such as dissension in interpersonal relationships or a loss of lifestyle balance, in the short term after surgery. Our hypothesis is that these difficulties might be related to executive dysfunction. To elucidate the involvement of executive dysfunction in these difficulties, we assessed motor and executive function in the short term and long term after surgery. METHODS: We examined motor function and executive function in 30 patients who underwent bilateral STN-DBS for medically refractory PD. Patients were evaluated for executive function 1 month before surgery, 1 month after surgery, and 12 months after surgery using the Trail Making Test (TMT), the Modified Stroop Color Word Interference Test (MST) and tests of Verbal Fluency (VF). RESULTS: TMT-B, TMT (B/A), MST-B, VF-phonemic and VF-semantic scores were significantly poorer 1 month after STN-DBS. TMT-B, TMT (B/A) and VF-phonemic recovered to preoperative levels by 12 months after surgery. A reduction in dopaminergic medication 1 month after surgery was significantly correlated with deterioration of TMT (B/A). CONCLUSION: Temporary deterioration of executive function may occur in the short term after STN-DBS, whereas motor function is usually improved. PD patients undergoing STN-DBS should be managed during this period to better predict temporary executive dysfunction. Excessive reduction of dopaminergic medication after surgery might, at least in part, result in this deterioration of executive function.

Impaired ability to shift weight onto the non-paretic leg in right-cortical brain-damaged patients.

BACKGROUND: : Stroke patients experience postural instability that can impede functional improvements in their gait. However, the precise functions of the dominant and non-dominant hemispheres in controlling static standing posture and weight-bearing remain unclear. OBJECTIVE: : To investigate differences in balancing ability between right-handed patients with right and left hemispheric lesions. METHODS: : Weight shifting was quantitatively evaluated to determine the ability of patients to control their balance in a static posture and during conscious weight shifting onto the paretic or non-paretic leg. Participants were enrolled from a consecutive series of stroke patients attending a rehabilitation program (n=49; 31 male, 18 female; mean age 69.3+/-9.4 years). Age-matched normal controls were recruited as volunteers (n=12; 4 male, 8 female; mean age 67.9+/-4.9 years). RESULTS: : Patients with cortical lesions in the right hemisphere were able to shift less weight onto the non-paretic leg than patients with cortical lesions in the left hemisphere (p<0.05). There were no correlations between the existence of unilateral spatial neglect and the percentage of weight shifted onto the non-paretic leg, static standing posture (r=0.27, p=0.40) or dynamic standing posture (r=-0.37, p=0.24). In contrast, there was a significant correlation between the percentage of weight consciously shifted onto the non-paretic leg and the existence of anosognosia (r=0.74, p=0.006), but not between static standing posture and anosognosia (r=-0.15, p=0.63). CONCLUSION: : Patients with right cortical hemispheric lesions were able to shift less body weight onto their non-paretic leg. These patients should be encouraged to practice shifting their weight towards their non-paretic leg to improve their balance.

Apraxia of eyelid opening after subthalamic deep brain stimulation may be caused by reduction of levodopa.

Apraxia of eyelid opening (ALO) is an infrequent side effect of deep brain stimulation (DBS) of the subthalamic nucleus (STN) for Parkinson's disease (PD). However, the pathogenesis of ALO after STN DBS is not well understood. We report on two patients who suffered from disabling ALO after bilateral STN DBS. Their ALO improved by resuming the levodopa medication that had been discontinued after the surgery. Although ALO after STN DBS is considered as an adverse effect of STN stimulation, postoperative modification of dopaminergic medication may be a cause of ALO after STN DBS.