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Objective:To describe the relation between gaze and posture/gait control in Parkinson disease (PD) and to determine the role of the mesencephalic locomotor region (MLR) and cortex-MLR connection in saccadic behavior because this structure is a major area involved in both gait/postural control and gaze control networks.Methods:We recruited 30 patients with PD with or without altered postural control and 25 age-matched healthy controls (HCs). We assessed gait, balance, and neuropsychological status and separately recorded gait initiation and eye movements (visually guided saccades and volitional antisaccades). We identified correlations between the clinical and physiologic parameters that best characterized patients with postural instability. We measured resting-state functional connectivity in 2 pathways involving the frontal oculomotor cortices and the MLR and sought correlations with saccadic behavior.Results:Patients with PD with postural instability showed altered antisaccade latencies that correlated with the stand-walk-sit time (r = 0.78, p < 0.001) and the duration of anticipatory postural adjustments before gait initiation (r = 0.61, p = 0.001). Functional connectivity between the pedunculopontine nucleus (PPN) and the frontal eye field correlated with antisaccade latency in the HCs (r = −0.54, p = 0.02) but not in patients with PD.Conclusions:In PD, impairment of antisaccade latencies, a simple and robust parameter, may be an indirect marker correlated with impaired release of anticipatory postural program. PPN alterations may account for both antisaccade and postural impairments.

To investigate the potential causes of excessive daytime sleepiness in patients with PD-poor sleep quality, abnormal sleep-wakefulness control, and treatment with dopaminergic agents.The authors performed night-time polysomnography and daytime multiple sleep latency tests in 54 consecutive levodopa-treated patients with PD referred for sleepiness, 27 of whom were also receiving dopaminergic agonists.Sleep latency was 6.3 +/- 0.6 minutes (normal8 minutes), and the Epworth Sleepiness score was 14.3 +/- 4.1 (normal10). A narcolepsy-like phenotype (or = 2 sleep-onset REM periods) was found in 39% of the patients, who were sleepier (4.6 +/- 0.9 minutes) than the other 61% of patients (7.4 +/- 0.7 minutes). Periodic leg movement syndromes were rare (15%, range 16 to 43/h), but obstructive sleep apnea-hypopnea syndromes were frequent (20% of patients had an apnea-hypopnea index15/h; range 15.1 to 50.0). Severity of sleepiness was weakly correlated with Epworth Sleepiness score (r = -0.34) and daily dose of levodopa (r = 0.30) but not with dopamine-agonist treatment, age, disease duration, parkinsonian motor disability, total sleep time, periodic leg movement, apnea-hypopnea, or arousal indices.In patients with PD preselected for sleepiness, severity of sleepiness was not dependent on nocturnal sleep abnormalities, motor and cognitive impairment, or antiparkinsonian treatment. The results suggest that sleepiness-sudden onset of sleep-does not result from pharmacotherapy but is related to the pathology of PD.

To prospectively evaluate the impact of subthalamic nucleus (STN) stimulation on social adjustment in patients with Parkinson disease (PD).Before and 18 to 24 months after bilateral STN stimulation, the authors assessed 29 patients with PD for motor disability, cognition (Mattis dementia rating scale, frontal score), psychiatric morbidity (Mini-5.0.0, MADRS, BAS), quality of life (PDQ-39), social adjustment (Social Adjustment Scale), and psychological status using unstructured in-depth interviews.Despite marked improvement in parkinsonian motor disability, the absence of significant changes in cognitive status, and improvement of activities of daily living and quality of life by the end of the study, social adjustment did not improve. Several kinds of problems with social adjustment were observed, affecting the patients' perception of themselves and their body, marital situation, and professional life. Marital conflicts occurred in 17/24 couples. Only 9 out of 16 patients who had a professional activity before the operation went back to work after surgery.After STN stimulation, patients experienced difficulties in their relations with themselves, their spouses, their families, and their socio-professional environment. The authors suggest a multidisciplinary psychosocial preparation and follow-up to help patients and their entourage cope with the sudden changes in their existence following successful neurosurgery.

Objective: To understand why some PD patients developed a cognitive decline in the year following STN-HFS. Background STN-HFS is efficient in alleviating parkinsonian motor signs. However, some patients developed a decline in cognitive function after surgery. Design/Methods: Between 02/1996 and 07/2009, 309 PD patients were operated for STN-HFS in the GHPS. Patients were evaluated before and one year after surgery with: 1) neuropsychological and 2) psychiatric tests, 3) parkinsonian disability scales (UPDRS parts I to VI). Precise location of stimulating contacts was obtained using an adjustable three-dimensional atlas of the basal ganglia. The stimulation parameters and levodopa equivalent dosage were reported. A voxel-based-morphometry was also performed on the pre-operative MRI of the patients. Postoperative cognitive decline was defined as a decrease more than 1 SD in the MDRS one year after surgery and/or MDRS Results: Two-hundred fifty-four patients were included in the final statistical analysis. Forty-five (21,5%) presented a decrease in the MDRS score more than 6 points (n=31) and/or a MDRS score under 130 (n=14). No statistical difference in the preoperative clinical characteristics was found between PD patients with vs without postoperative cognitive decline. Patients with postoperative cognitive decline presented a higher rate of postoperative confusion and/or psychiatric troubles. They showed a lower improvement in parkinsonian motor disability and activities of daily living with STN-HFS. The decrease in antiparkinsonian treatment and levodopa-induced complications was not different between the two patients groups. In patients with cognitive decline, the stimulating contacts were located more posteriorly and ventrally, and the frequency of stimulation was lower. Conclusions: STN-HFS may be deleterious for cognitive function, in particular when located in the more ventral part of the STN, thought to process cognitive and emotional information. Disclosure: Dr. Welter has nothing to disclose. Dr. Czernecki has nothing to disclose. Dr. Schupbach has received personal compensation for activities with Medtronic, Inc. and Lundbeck. Dr. Fernandez-Vidal has nothing to disclose. Dr. Karachi has nothing to disclose. Dr. Navarro has nothing to disclose. Dr. Cornu has nothing to disclose. Dr. Pidoux has nothing to disclose. Dr. Mallet has nothing to disclose. Dr. Dormont has nothing to disclose. Dr. Vidailhet has nothing to disclose. Dr. Grabli has nothing to disclose. Dr. Bonnet has nothing to disclose. Dr. Belaid has nothing to disclose. Dr. Houeto has nothing to disclose. Dr. Bardinet has nothing to disclose. Dr. Yelnik has nothing to disclose. Dr. Agid has nothing to disclose.

Objective: In this study, we aimed to understand the physiopathology of these higher level gait disorders. Background The gait and balance disorders with falls are a major public health problem in the elderly population. In 10-20% of elderly people, these disorders are of unknown cause, and the term Higher Level Gait Disorders (HLGD) has been proposed. Design/Methods: Precise clinical evaluation, gait initiation analysis and brain imaging was performed in 20 patients with HLGD (mean age : 77 ± 6,8 years, mean disease duration : 3,9 ± 2,9 years), in comparison to 20 age-matched controls (mean age :77,3 ± 6,4 years). Results: HLGD patients showed parkinsonian symptoms with in particular an axial involvement (rigidity, freezing of gait and falls), without dementia or dysautonomia or supranuclear palsy. In HLGD patients compared to controls, step length, velocity and braking capacity (balance control) during the first step were reduced (-25%, -55% and -45%, respectively). A positive correlation was found between parenchymal volumes and step length and velocity, and the midbrain surface and the braking index. Compared to controls, patients with HLGD had a midbrain and primary motor cortex atrophy. Conclusions: In patients with so-called HLGD, imaging data are in favor of a degeneration of the structures classically described as affected in progressive supranuclear palsy (PSP). These data suggest that HLGD may in fact represent a very slow progressive form of this disease which has been recently described. Disclosure: Dr. Welter has nothing to disclose. Dr. Demain has nothing to disclose. Dr. Westby has nothing to disclose. Dr. Bonneville has nothing to disclose. Dr. Do has nothing to disclose. Dr. Tezenas Du Montcel has nothing to disclose. Dr. Dormont has nothing to disclose. Dr. Agid has nothing to disclose. Dr. Fernandez-Vidal has nothing to disclose. Dr. Chastan has nothing to disclose.