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most cases in our experience have been of the combined type, and patients of both types are prone to falling Most patients, while seated or supine, are able to make complex movements with their legs, such as drawing imaginary gures 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 resistance (paratonia, or gegenhalten) Dif culty in turning over in bed is characteristic, and this maneuver may eventually become impossible These advanced motor disabilities are usually associated with dementia, but the gait and mental disorders need not evolve in parallel, as emphasized below 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 re exes, and Babinski signs may or may not be present The end result in some cases is a cerebral paraplegia in exion (Yakovlev), in which the patient lies curled up in bed, immobile and mute, with the limbs xed by contractures in an attitude of exion In addition to NPH and Alzheimer disease, the causes of this complex frontal lobe gait disorder include widespread neoplasm (meningioma, in ltrating glioma gliomatosis cerebri), subcortical arteriosclerotic encephalopathy (Binswanger disease; see Thompson and Marsden), Pick disease, progressive supranuclear palsy, and frontal lobe damage from trauma, stroke, or a ruptured anterior communicating aneurysm On the basis of success in a small controlled trial conducted by Baezner and colleagues, amantadine 100 mg daily or twice daily may be tried for cases of vascular white matter degeneration with prominent gait dif culty Selegiline has also been suggested from anecdotal experience.

Manganese poisoning results from the chronic inhalation and ingestion of manganese particles and occurs in miners of manganese ore and in workers who separate manganese from other ore Several clinical syndromes have been observed The initial stages of intoxication may be marked by a prolonged confusional-hallucinatory state Later, the symptoms are predominantly extrapyramidal They are often described as parkinsonian in type, but in the patients seen by the authors, the resemblance was not close: an odd gait ( cock walk), dystonia and rigidity of the trunk, postural instability, and falling backward were features seen in two South American miners Others, however, have reported stiffness and awkwardness of the limbs, often with tremor of the hands, cogwheel phenomenon, gross rhythmic movements of the trunk and head, and retropulsive and propulsive gait Corticospinal and corticobulbar signs may be added Progressive weakness, fatigability, and sleepiness as well as psychiatric symptoms (manganese madness) are other clinical features Rarely, severe axial rigidity and dystonia, like those of Wilson disease, are said to have been the outstanding manifestations Neuronal loss and gliosis, affecting mainly the pallidum and striatum but also the frontoparietal and cerebellar cortex and hypothalamus, have been described, but the pathologic changes have not been carefully studied Treatment The neurologic abnormalities have not responded to treatment with chelating agents In the chronic dystonic form of manganese intoxication, dramatic and sustained improvement has been reported with the administration of L-dopa; patients with the more common parkinsonian type of manganese intoxication have shown only slight if any improvement with L-dopa

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Each internal and external component is connected to the system board The system board, also referred to as the main board, the motherboard, or the planar board, is made of fiberglass and is typically brown or green, with a meshwork of copper lines, as shown

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