Parkinsonism in a patient with AIDS.

Since the description of the "shaking palsy" by James Parkinson in 1817, Parkinson's disease (PD) has been established as the most commonextrapyramidal syndromethat has becomebest understood with distinct correlations with the pathology, biochemistry, and therapy. The core syndromeconsists of resting tremor, rigidity, poverty and slowness of voluntary movement, stooped posture, and festination. The modern era of correlating of striatal dopamine deficiency with PD was disclosed by Hornykiewicz in 1960 (1), hence the high-dose levodopa therapy was introduced by Cotzias in 1967 with a great success (2). Since then, improvements in pharmacotherapy have been challenged with the use of decarboxylase inhibitors and dopamine receptor agonist. Efforts to uncover the etiology of PDhave been intensified in recent years with the discovery of a-synuclein gene (3) and parkin gene (4) in familial cases of PD, but so far the real etiology has not yet been clarified. During this historical course, various disorders which mimic the clinical symptoms of PDhave been reported and the term parkinsonism refers to the broad category of these pathophysiologic processes. There are many causes for parkinsonism such as postencephalitic, drug-or toxin-induced and other degenerative diseases, so called "parkinsonism-plus". Amongthose disorders, parkinsonism in association with CNSinfections is a postencephalitic parkinsonism after encephalitis lethargica (von Economo's disease), which has been well known throughout the world since 1915. But the disease essentially disappeared from the world in 1940 when the diagnosis of encephalitis lethargica was relaced by the more inclusive term, acute infectious encephalitis. Encephalitis lethargica is a somnolentophthalmoplegic encephalitis but the viral agent was never been discovered. But clinical and pathologic features were typical of viral encephalitis with CSF pleocytosis and elevation of protein. The unique symptomswere markedsomnolenceand ophthalmoplegia-oculogyric crisis. Postencephalitic parkinsonism of von Economo's type usually appears after the disease, months to years following the acute illness. The pathology in the acute phase was also typical of viral etiology, with cellular infiltration principally in the midbrain, subthalamus and hypothalamus. The autopsy findings of the chronic stage were depigmentation of the substantia nigra and locus ceruleus with nerve cell destruction and glial proliferation in the substantia nigra, oculomotor and adjacent nuclei (5). Parkinsonian syndrome maybe seen with a variety of encephalitides, such as western and eastern equine, Coxsackie, measles, chicken pox, Murray Valley and Japanese B encephalitis. In Japan, Japanese B encephalitis-related parkinsonism has been frequently described in detail with clinical signs and autopsy pathology. But these encephalitis-related parkinsonisms are a distinctly different entity from true postencephalitic parkinsonism due to von Economo's disease. The former syndrome is usually less severe, non-progressive, and is apparent at the time of acute phase without any latent period. Amongother infection-related parkinsonisms, neurosyphilis and AIDShave been reported in addition to postencephalitic parkinsonism and transient parkinsonism after acute viral encephalitides and Creutzfeldt-Jakob disease. In this issue of the journal, Murakami et al (6) reported, "Parkinsonian symptoms as an initial manifestation in a Japanese patient with AIDSand toxoplasma infection".