Patients with advanced Parkinson's disease with and without freezing of gait: a comparative analysis of vascular lesions using brain MRI.

INTRODUCTION: Freezing of gait (FOG) is one of the most disabling and enigmatic symptoms in Parkinson's disease. Vascular lesions, observed in magnetic resonance imaging (MRI) scans, may produce or exacerbate this symptom. PATIENTS AND METHODS: The study includes 22 patients with Parkinson's disease subjects, 12 with freezing of gait and 10 without. All patients underwent an MRI scan and any vascular lesions were analysed using the modified Fazekas scale. RESULTS: Patients with FOG scored higher on the modified Fazekas scale than the rest of the group. Although the two groups contained the same percentage of patients with vascular lesions (50% in both groups), lesion load was higher in the group of patients with FOG. Vascular lesions in the periventricular area and deep white matter seem to be the most involved in the development of FOG. DISCUSSION: Vascular lesions may contribute to the onset or worsening of FOG in patients with PD. This study suggests that cerebral vascular disease should be considered in patients with FOG.

[Freezing of gait unresponsive to dopaminergic stimulation in patients with severe Parkinsonism]. / Bloqueos de la marcha sin respuesta al estímulo dopaminérgico con apomorfina en pacientes parkinsonianos graves.

INTRODUCTION: Freezing of gait unresponsive to dopaminergic stimulation in patients with severe Parkinsonism. The freezing of gait episodes (FOG) normally appear during the off period and generally improve with dopaminergic stimulus, at the same time as improving other Parkinsonian symptoms. PATIENTS AND METHODS: We report a group of 10 patients with severe Parkinson's disease. All patients suffered motor fluctuations, dyskinesias and episodes of FOG during the on and off state. The patients received a subcutaneous apomorphine bolus, without other dopaminergic medication; an effective dose of apomorphine was considered as one that induced a reduction of at least a 60% in the UPDRS motor scale. RESULTS: The baseline motor UPDRS was 61.3 +/- 4.7, which dropped to 21 +/- 4.3 after the apomorphine injection. The mean dose of apomorphine was 5.5 mg (3-7 mg). The bolus of apomorphine improved the parameters of the gait related to bradykinesia and the tapping tests of the limbs, but the episodes of FOG did not vary significantly between the off and on state. CONCLUSIONS: We present a group of 10 patients with freezing of gait episodes that did not improve with treatment and persisted during the on period induced by dopaminergic stimulus with apomorphine.