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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the incidence of neurosyphilis has declined dramatically after the World War II because of the development of antibiotics, it is recently increasing a little bit. There has been few reports on the neuroimaging of general paresis. We studied a fresh case of general paresis by X-ray CT (XCT), MRI and PET scans, and report the changes of neuroimages before and after the therapy. A 38-year-old man was admitted with disorientation, thought disorder and personality change. He also had insomnia and megalomania. There were neither obvious neurological signs nor particular changes of the XCT scan abnormalities on admission. His clinical symptoms were gradually worsened within three months, when the XCT and MRI scans showed moderate brain atrophy especially in the frontal and temporal lobes with mild dilatation of the lateral ventricles. In the PET study, the cerebral blood flow was decreased in the entire brain, especially in the frontal lobes, although the thalamus and the basal ganglia had normal levels. By immunological procedures and the cerebrospinal fluid (CSF) studies, the diagnosis of general paresis was made. He was treated with penicillin G and other antibiotics. In one year after his first therapy, many symptoms vanished. Although the cerebral atrophy was a little advanced, the cerebral blood flow was dramatically increased. As far as we know, this is the first PET study of general paresis before and after penicillin treatments.
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PMID:[A case of general paresis with marked improvement of cerebral blood flow after antiluetic therapy--case report]. 141 41

A 38-year-old man presented with personality change, postural tremor of the right arm and leg, and right hemidysesthesia. MR imaging (MRI) revealed left hemisphere dominant brain atrophy and leuko-araiosis in the deep white matter. Serological test of serum and cerebrospinal fluid demonstrated high titers of antibodies to Treponema pallidum. He was diagnosed as Lissauer's general paresis based on the clinical symptoms and signs, and MRI findings. This disorder is characterized by focal cerebral atrophy, corresponding to focal neurologic signs. Neuropathological features in Lissauer's general paresis are spongiform atrophy of the cerebral cortex and demyelination of the white matter. Leuko-araiosis on MRI in our case may represent demyelination of the white matter. Although MRI findings in general paresis are usually nonspecific, this is, as far as we know the first case report of general paresis with MRI showing focal cerebral atrophy and leuko-araiosis.
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PMID:[A case of Lissauer's general paresis with left hemisphere dominant brain atrophy and leuko-araiosis in the deep white matter on MRI]. 866 36

MRI was performed in 7 patients with general paresis before or at a very early stage of treatment. A large dose of antibiotics, mainly penicillin, was given to all patients, and the effects of treatment, the patients' outcome, and MRI findings were investigated. Three of the 7 patients had MRI findings of atrophy of the medial temporal lobe including the hippocampus. In the medial temporal lobe atrophy group, a personality change or general dementia remained even after the treatment was completed, and outcome in social functioning was poor. Medial temporal lobe atrophy may be a poor prognostic sign in general paresis.
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PMID:Relationship between MRI findings and prognosis for patients with general paresis. 1100 4

We here report an autopsy case of meningovascular neurosyphilis associated with Fischer's plaques, a demyelinating lesion which is typical of the late stage general paresis. A Japanese male who was 59 years old at the time of death, developed personality change and dementia. He was clinically diagnosed as having neurosyphilis by serological tests of the blood and the cerebrospinal fluid. Despite the administration of Penicillin, psychiatric symptoms were unchanged and the patient died of aspiration pneumonia after the clinical course of 18 month. The weight of brain was 1485 g. Postmortem pathological examination of the brain revealed extensive leukocyte infiltration into the meninges, in particular, around the meningeal vessels. Perivascular leukocyte infiltration, though less severe, was also noted in the brain parenchyma in the temporal and frontal cortices. Brain atrophy and neuronal cell loss were absent. The primary pathology of this case was, thus, considered to be meningeal and vascular inflammation consistent with the stage III meningovascular neurosyphilis. However, we also found in the frontal and parietal cortices a few small demyelinating lesions, which were referred to as Fischer's plaques. Fischer's plaque is a hallmark of advanced stage of general paresis where the principal lesion exists in the brain parenchyma. We speculate that, in patients with chronic progressive neurosyphilis, meningovascular and parenchymal lesions coexist during the transitional stage. Attention has to be paid for the occurrence of atypical neurosyphilis in association with increased immuologically compromised hosts and frequent usage of antibiotics.
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PMID:[Autopsy case of meningovascular neurosyphilis associated with Fischer's plaques]. 1766 52

A 69-year-old, right-handed, Japanese male patient presented with pure agraphia with topographical disorientation after hemorrhage in the right parietal lobe. Upon developing cerebral hemorrhage, he was referred to our hospital for close examination of agraphia. There was no paresis or clumsiness in his extremities. His speech was fluent and well-articulated. Neither aphasia nor reading impairments was found, although there was a clear writing impairment with effort and hesitation. His writing of both kanji and kana letters contained additional, absent or deformed strokes or parts. No hemianopia, prosopagnosia, constructional disturbances and dressing apraxia were found. He could recognize familiar buildings or landscapes, but often lost his way around well-known areas. MR images revealed subcortical lesions of precuneus, superior and inferior parietal lobules in the right hemisphere, around the posterior horn of the lateral ventricle. He revealed pure agraphia and topographical disorientation after the right brain haemorrhage, without dementia or personality change. These findings indicate that the right parietal lobe participates in the kinesthetic movements of writing. Some authers have been documented cases of aphasic agraphia or alexia with agraphia caused by right hemisphere damage in dextrals, but pure agraphia caused by the lesion in the right hemisphere is very rare.
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PMID:[Pure agraphia with topographical disorientation caused by right hemisphere lesion]. 1871 86

A 48-years-old man presented with slowly progressive bradykinesia, personality change and rapidly progressive left hemiparesis. On admission, he presented dementia, poor judgment, left hemiparesis. MRI revealed a widespread high intensity area in right hemisphere and MRA was almost normal. Serological tests of serum and CSF demonstrated high titers of antibodies to Treponema pallidum. He was treated for syphilis with daily penicillin injections without improvement. He died of sepsis eight months after admission. At autopsy, the brain weighed 1,100 g and the right cerebral hemisphere was atrophic, especially in frontal base, temporal, parietal, angular, and posterior regions covered by thickened, fibrotic leptomeninges. Microscopically, chronic meningoencephalitis was observed. Severe neuronal loss with gliosis was seen in the right cerebral cortices. Scattered rod-shaped microglia and inflammatory cell infiltration were visible in the cerebral parenchyma. The dorsal column of the spinal cord was not involved and meningovascular syphilis was unclear. The distribution of the encephalitic lesions was well correlated with the clinical and neuroradiological findings. This was a rare autopsy case presenting Lissauer's general paresis, clinically manifesting as rapidly progressive stroke-like episode.
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PMID:[Autopsy case of Lissauer's general paresis with rapidly progressive left hemiparesis]. 1961 44

Familial idiopathic basal ganglia calcification (Fahr`s disease) is a rare neurodegenerative disorder characterized by symmetrical and bilateral calcification of the basal ganglia. Calcifications may also occur in other brain regions such as dentate nucleus, thalamus, and cerebral cortex. Both familial and non-familial cases of Fahr`s disease have been reported, predominantly with autosomal-dominant fashion. The disease has a wide range of clinical presentations, predominantly with neuropsychiatric features and movement disorders. Psychiatric features reported in the literature include: cognitive impairment, depression, hallucinations, delusions, manic symptoms, anxiety, schizophrenia-like psychosis, and personality change. Other clinical features include: Parkinsonism, ataxia, headache, seizures, vertigo, stroke-like events, orthostatic hypotension, tremor, dysarthria, and paresis. Fahr`s disease should be considered in the differential diagnosis of psychiatric symptoms, particularly when associated with movement disorder. The disease should be differentiated from other conditions that can cause intracranial calcification. No specific treatment is currently available. Further research is needed to bridge the gap existing in our current knowledge of the prevalence, etiology, symptoms, and treatment of Fahr`s disease.
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PMID:Familial idiopathic basal ganglia calcification (Fahr`s disease). 2498 77