Mycoplasma pneumoniae infection may cause striatal lesions leading to acute neurologic dysfunction

Reversible parkinsonism and dystonia following probable mycoplasma pneumoniae infection

“…Movement disorders associated with MP infection have been described in two previous reports (12,16). AlMateen et al (12) described a 9-year-old girl with encephalitis lethargica-like symptoms.…”

“…Although diagnosis of MP infection requires fourfold rising of the serologic titer (17), temporal relationship of MP antibody titer with clinical and radiological changes suggests that the patient's neurologic symptoms are related to MP infection. All other investigations were nonrevealing, and the clinical course of this patient excluded the possibility of mitochondria1 cytopathy or other progressive metabolic disorders.In the literature, neurologic manifestations associated with MP infection include meningitis (2), meningoencephalitis (2,3,7,9,10,14), encephalomyelitis ( 1 3 , psychosis (l), seizures (3,12,14,16), polyradiculitis (2,3,13), acute cerebellar ataxia (3, brain stem dysfunction (4), and myelitis (6,ll). Considering the clinical course, imaging studies, and negative culture studies, the neurologic manifestations of at least some of these patients were believed to be immune or toxin mediated (7,11,14,17) rather than due to direct invasion of the organism.…”

Mycoplasma pneumoniae as an Under- Recognized Agent of Vasculitic Disorders

“…It has been reported in association with M. pneumoniae infection [Sakoulas, 2001;Saitoh et al, 1993;van Buiren & Uhl, 2003;Zambrino et al, 2000]. Chorea or choreiform movements may be a neurological consequence of striatal damage [Al-Mateen et al, 1988;Decaux et al, 1980;Zambrino et al, 2000].…”

“…It can reasonably be postulated that the pathomechanism underlying striatal necrosis must be local vasculitis induced by M. pneumoniae through the operation of cytokines and chemokines and leading eventually to vascular occlusion. In fact, cerebrospinal fluid from a patient with this disease was found to contain the genome of M. pneumoniae [Saitoh et al, 1993], which suggested a direct mechanism. Moreover, two reported cases of the involuntary movement disorder Tourette syndrome have been accompanied by the detectable presence of the M. pneumoniae genome in cerebrospinal fluid [Müller et al, 2000].…”

“…Firstly, M. pneumoniae is not always present at the site of vascular damage, except in conditions associated with direct vascular occlusion such as striatal necrosis and stroke, where a tiny amount of M. pneumoniae may be detected in cerebrospinal fluid by culture [Sočan et al, 2001] or by polymerase chain reaction [Padovan et al, 2001;Saitoh et al, 1993]. Secondly, respiratory samples such as oropharyngeal swabs, which are routinely utilized for molecular detection of infectious organisms, are not always adequate for the diagnosis of extrapulmonary manifestations with very little or no respiratory symptoms such as cough and sputa.…”