Human Immunodeficiency Virus
The association of human immunodeficiency virus (HIV) infection and movement disorders has been recognized since the first descriptions of neurological complications of HlV-associated AIDS
(58). Secondary parkinsonism has been reported by various authors as case reports, but Mattos et al.
(59) have reported movement disorders in 28 HIV patients of whom 14 patients had parkinsonism. The mean age at onset of parkinsonism was 37.2 yr (range 25-63). They report mean Hoehn and Yahr scale of 2.5 (range of 1-5). The clinical features included tremor, and rapid progression of parkinsonian symptoms with time of onset to death being five mo in eight patients. Five patients were levodopa responsive. Imaging study with CT scans showed hydrocephalus ex-vacuo, and one patient had toxo-plasmosis involving the basal ganglia. One patient with T1 enhancement on the MRI of the brain had ipsilateral ophthalmoplegia and contralateral parkinsonism. Only two of the patients with parkinsonism had other parkinsonian risk factors such as metaclopramide exposure and neurotoxoplasmosis (59). Maggi et al. (60) described parkinsonism in a patient with AIDS and toxoplasmosis with abulia, VII cranial nerve impairment, hypomimia, speech impairment, difficulty arising from a chair, stooped posture, short stepped gait and freezing of gait, cogwheel rigidity, and bradykinesia in association with toxoplasma lesion in the bilateral lenticular nucleii and the right frontobasal region (60). Presence of parkinsonism and tremor has been reported by other authors, and the management involves treatment of opportunistic infections, symptomatic treatment of parkinsonism, and antiretroviral therapy (61). Bradykinesia, postural instability, gait disorder, and hypomimia are common features of HIV-related parkinsonism with dementia. Parkinsonian features have been reported in association with dopamine receptor antagonists, opportunistic infections such as toxoplasmosis, or HIV itself. Some patients with HIV have clinical features identical to idiopathic PD (62). Dopaminergic medication has been thought to accelerate the course of HIV viral infection as shown in the study of levodopa and selegiline in the SIV-infected (Simian immunodeficiency virus) macaque model (63).
Subacute sclerosing panencephalitis (SSPE), a slow viral disease caused by measles virus with a mutated M-protein, has been long recognized to cause parkinsonism, myoclonus, dystonia, chorea, athetosis, stereotypies, and a variety of other movement disorders. Sawaishi et al. (64) reported a case of SSPE with documented lesions in the substantia nigra as well as the putamen, globus pallidus, and caudate nuclei, seen on the MRI scans of the brain. Parkinsonian symptoms described in SSPE include bradykinesia and rigidity. Previous descriptions of MRI findings include lesions in the putamen and caudate, but sparing the globus pallidus and thalamus (64). Treatment with levodopa and amantadine has been reported to provide some symptomatic relief (65).
Mycoplasma pneumoniae has been reported to cause parkinsonism in a young boy with flulike symptoms, followed by parkinsonism with bradykinesia, hypomimia, hypophonia, and dystonia with MRI findings of increased signal (T1 or T2) in the basal ganglia (66). The patient had elevated mycoplasma antibody levels and his symptoms and MRI abnormalities spontaneously resolved. Postencephalitic encephalitis has been associated with parkinsonism since the epidemic in early 1900s. Although the incidence of postencephalitic parkinsonism has markedly decreased, well-documented cases have been reported recently, including those caused by the West Nile virus (67,68).
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