“Lower-half parkinsonism,” as mentioned earlier, has been applied to a pattern of slowed, sometimes shuffling gait in the absence of any abnormalities of the upper extremities, but the cause is rarely idiopathic Parkinson disease. The term “marche à petits pas” is also used as a description for an advanced form of the frontal lobe gait disorder and has been particularly associated with vascular damage to the white matter.
In frontal lobe disorders of gait there is a need to seek support from a companion’s arm or nearby furniture. The initiation of walking becomes progressively more difficult; in advanced cases, the patient makes only feeble, abortive stepping movements in place, unable to move his feet and legs forward; eventually, the patient can make no stepping movements whatsoever, as though his feet were glued to the floor. These late phenomena have been referred to as “magnetic feet” and the difficulty initiating gait as “slipping clutch” syndrome (Denny-Brown) or “gait ignition failure” (Atchison et al). In some patients, difficulty in the initiation of gait may be an early and apparently isolated phenomenon but invariably, with the passage of time, the other features of the frontal lobe gait disorder become evident. Finally, the resemblance to NPH is notable and these patients become unable to stand or even to sit; without support, they fall helplessly backward or to one side.
Until the late stages of the process, these patients, while seated or supine are able to make complex movements with their legs, such as drawing imaginary figures or pedaling a bicycle and, quite remarkably, to simulate the motions of walking, all at a time when their gait is seriously impaired. Eventually, however, all movements of the legs become slow and awkward, and the limbs, when passively moved, offer variable counterresistance (paratonia or gegenhalten). As with Parkinson disease, difficulty in turning over in bed may eventually become impossible.
These advanced motor disabilities are usually associated with dementia, but the gait and mental disorders need not evolve in parallel. Thus, some patients with Alzheimer disease may show a serious degree of dementia for several years before a gait disorder becomes apparent; in other conditions, such as NPH and Binswanger disease, the opposite pertains. Or both the dementia and gait disorder may progress more or less together. Grasping, groping, hyperactive tendon reflexes, and Babinski signs may or may not be present. The end result in some cases is a “cerebral paraplegia in flexion” (Yakovlev’s term), in which the patient lies curled up in bed, immobile and mute, with the limbs fixed by contractures in an attitude of flexion.
On the basis of bilateral but isolated frontal lobe infarction in the territory of the anterior cerebral artery (medial frontal lobes), the existence of a “gait center” has been proposed as mentioned in the introduction (see Della Sala). In the most severe and localized instance of complete gait failure from a frontal lobe stroke we have observed, the lesion was situated in the left pericallosal, medial supplementary motor area. Benson and colleagues have reported in an analysis of MRIs from a selected group of stroke patients that periventricular frontal and occipitoparietal ischemic lesions in the deep white matter are associated with deterioration of gait. Isolated pontine ischemic changes were associated with gait disequilibrium in another study by Kwa and colleagues of the Amsterdam Vascular Medicine Group. The clinical validity of all of these observations in regard to localization is uncertain but generally converges on the notion that ischemic damage at any of the aforementioned sites in the white matter can alter walking.
In addition to NPH and Alzheimer disease, the causes of the frontal lobe gait disorder include large neoplasms (meningioma, infiltrating glioma—gliomatosis cerebri), subcortical arteriosclerotic encephalopathy (Binswanger disease; see Thompson and Marsden), frontotemporal lobar degeneration (formerly Pick disease), and frontal lobe damage from trauma, stroke, or the residual of a ruptured anterior communicating aneurysm.