title: [Vascular or "lower body Parkinsonism": rise and fall of a diagnosis].
abstract: The "arteriosclerotic parkinsonism", which is called vascular parkinsonism (VP), was first described by Critchley'. The broad based slow gait, reduced stride lenght, start hesitation, freezing and paratonia was mentioned as "lower body parkinsonism" (LBP) which can be associated by slow speech, dysexecutive syndrome, and hand tremor of predominantly postural character. In VP the DAT-scan proved normal dopamine content of the striatum in contrast with Parkinson's disease (PD). Additionally, Lewy bodies of brainstem type were not found in VR Probability of VP increases if central type pathologic gait is prominent; the hands are slightly involved, the MRI indicates transparent periventricular white substance and/or brain atrophy. In some cases differentiation of gait apraxia and parkinsonism could be challenging. There is no rigor of the lower limbs at rest in neither of them, the disturbance of movement is evoked by the gait itself. Three subtypes of "gait ignition failure" has been recently described: (1) ignition apraxia, (2) equilibrium apraxia and (3) mixed gait apraxia. The primary progressive freesing gait was considered as a Parkinson-plus syndrome. Freesing occurs more frequently in diseases with pakinsonism than in PD. The grade of ventricle dilatation and the frontal leukoaraiosis was similar in LBP and gait apraxia. In cases of normal pressure hydrocephalus the impaired gait may mimic PD. Pathologic gait in VP can be explained by the lesions of the senso-motor association pathways in dorsal paramedian white substance within the vulnerable borderzone region. These may be colocalized with the representation of the lower extremities in the posterior third of the supplementer motor area. Rektor2 proposed to change the name of LBP to "cerebrovascular gait disorder". Notwithstandig central type gait disorder develops also in many degenerative diseases other than cerebro-vascular origin. The neuronal net controling the regulation of movement is widespread, therefore several cortical and subcortical lesions could elicit large variations of pathologic gait, ie.: ataxia, apraxia, ignition failure, akinesis etc.
  
  
  CONCLUSIONS
  most of the central gait disorders regarding the pathology and their appearance can not be called "parkinsonism"; these are much closer related to the localization of lesions rather than to the diagnostic categories.
authors.affiliation: Semmelweis Egyetem, Neurológiai Klinika, Budapest. szirmaiimre@gmail.com
authors.forename: Imre
authors.initials: I
authors.lastname: Szirmai
mesh_terms: D001921:Brain / Q000503:physiopathology*; D003704:Dementia / Q000150:complications / Q000503:physiopathology; D003937:Diagnosis, Differential; D004298:Dopamine / Q000172:deficiency; D005684:Gait; D020235:Gait Apraxia / Q000209:etiology / Q000503:physiopathology; D020234:Gait Ataxia / Q000209:etiology / Q000503:physiopathology; D020233:Gait Disorders, Neurologic / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D035002:Lower Extremity / Q000503:physiopathology; D010300:Parkinson Disease / Q000175:diagnosis / Q000503:physiopathology; D010302:Parkinson Disease, Secondary / Q000097:blood / Q000150:complications* / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology
chemical_list: D004298:Dopamine