Freezing of gait (FOG) is a frequent, disabling symptom of Parkinson's disease (PD). FOG usually lasts a few seconds. It refers to brief paroxysmal events during which a subject is unable to start or continue locomotion. Despite its frequency, FOG pathophysiology is unclear. Because a frontal lobe dysfunction or a disconnection between the frontal lobe and basal ganglia has been implicated in FOG, we explored frontal functions in PD patients using neuropsychological tests. Thirteen early-stage PD patients [Hoehn & Yahr score (H&Y) < or = 2.5] with freezing during "on " state (FOG+), and 15 age-, H&Y score-, and disease-duration-matched PD patients without freezing (FOG-) were investigated. No patient was demented or depressed. Assessment included the Unified Parkinson's Disease Rating Scale (UPDRS), FOG questionnaire, Mini Mental State Examination (MMSE), frontal assessment battery (FAB), phonemic verbal fluency, Stroop test (parts II and III), and ten-point clock test (TPCT). UPDRS and MMSE scores did not differ between the two groups. FAB, verbal fluency, and TPCT scores were significantly lower in FOG+ patients than in FOG- patients (FAB: P = 0.008; phonemic verbal fluency: P = 0.011; TPCT: P = 0.024). FOG correlated with lower scores at frontal tests in patients with early-stage PD.

Lateral trunk flexion is a very common clinical observation in patients affected by Parkinson's disease. Postural control is known to depend on vestibular, visual, and somatosensory information. The aim of this study was to investigate whether impairment of vestibular function can account for the postural alterations observed in parkinsonian patients with lateral trunk flexion. We evaluated vestibular function in 11 parkinsonian patients with lateral trunk flexion and in 11 age-, sex-, and disease duration-matched patients without lateral trunk flexion. The following vestibular tests were performed: infrared videonystagmography including fast and slow ocular movements, spontaneous-positional and evoked nystagmus search with and without visual fixation, fast positioning maneuvers, the bithermal caloric test, and the vibration test. A peripheral, unilateral vestibular hypofunction was identified in all patients with lateral trunk flexion. The vestibular hypofunction was ipsilateral to the leaning side and contralateral to the most affected parkinsonian side in all patients. In the control group, 7 subjects had no vestibular signs; 4 subjects had unilateral vestibular hypofunction without clinically evident lateral trunk flexion. Two of the latter patients subsequently developed lateral trunk flexion ipsilateral to the vestibular deficit and contralateral to the side most affected by Parkinson's disease. The processing of vestibular information was impaired in parkinsonian patients affected by lateral trunk flexion. The impairment was at least in part responsible for the patients' postural abnormality. We propose that the acronym PISA (Postural Imbalance Syndrome with vestibular Alterations) be used to describe the specific postural change observed in parkinsonian patients affected by a vestibular defect and lateral trunk flexion.

Clinical features and evoked potentials are useful predictors of long-term recovery of responsiveness in patients with prolonged postanoxic VS.

We reported for the first time a 2-year prospective study on non-motor symptoms before and after starting therapy in newly diagnosed PD patients. Even if non-motor symptoms are very frequent in early stage, they tend to remain stable during the early phase of disease, being only few non-motor symptoms affected from dopaminergic therapy and, specifically, by the use of dopamine agonists.