11/22. Oligoclonal banding in the cerebrospinal fluid of patients with postencephalitic Parkinsonism. Two recent sporadic cases of progressive Parkinsonism after encephalitis are described. Both patients had two oligoclonal protein bands in their CSF. These bands were not present in patients with idiopathic Parkinson's disease and might, therefore, be useful for diagnostic purposes, particularly when the history of encephalitis is uncertain. ( info) |
12/22. Oculogyric crises and parkinsonism. A case of recent onset. Oculogyric crisis in association with postencephalitic parkinsonism has been reported only following encephalitis lethargica (Economo's disease). Generally, it has been assumed that this phenomenon would fade away with the demise of these postencephalitic patients. Therefore, we report a case of recent onset of persistent oculogyric crisis with parkinsonism in a 35-year-old man following an apparent attack of encephalitis in 1972. ( info) |
13/22. Parkinson's disease of post-encephalitic type following general paresis--an autopsied case. A clinico-pathological report is given of a case of Parkinson's disease following a general paresis. A 66-year-old male, with no previous history of febrile disease or viral encephalitides, developed a dementing illness. The general paresis was diagnosed from serological studies at the age of 45. He underwent a series of penicillin plus fever therapies as treatment for neurosyphilis. He also developed generalized rigidity and slow mobility 12 years after the diagnosis of general paresis. An anti-Parkinson drug was given. Finally he fell in a state of muteness and became bedridden. He had been hospitalized for 21 years and died from bronchopneumonia. The pathological findings were strikingly similar to post-encephalitic parkinsonism in addition to a healed state of general paresis. They consisted of a widespread nerve cells loss, gliosis and the presence of Alzheimer's neurofibrillary tangles in the substantia nigra. In the cerebral cortex, a diffuse loss of nerve cells and the presence of a weak positive iron reaction were observed. The coexistence of general paresis and post-encephalitic parkinsonism is unusual and the authors discussed the etiological relationship between the two different conditions. ( info) |
14/22. Early onset of the "on-off" phenomenon in children with symptomatic Parkinsonism. Many patients with idiopathic Parkinson's disease treated with levodopa for more than five years develop fluctuations in their clinical response to this drug. Such fluctuations may be unpredictable, but more commonly occur in a regular pattern related to the size and timing of the levodopa dosage. Theories as to their cause have emphasised both the progression of the underlying Parkinson's disease and the possibility of a late side-effect of levodopa. We report two children with Parkinsonism, one after recurrent obstructive hydrocephalus and the other following an encephalitic illness. Both patients had striking improvement with levodopa, but developed predictable and unpredictable dramatic response fluctuations within weeks of starting levodopa therapy. This suggests that neither the pathology of idiopathic Parkinson's disease, nor the long-term use of levodopa are essential for the development of predictable or unpredictable fluctuations in response to levodopa therapy. ( info) |
15/22. Frequency of Alzheimer's neurofibrillary tangle in the brains of progressive supranuclear palsy, postencephalitic parkinsonism, Alzheimer's disease, senile dementia and non-demented elderly person. The frequency and the distribution of Alzheimer's neurofibrillary tangles were examined in those cases of progressive supranuclear palsy (one case), postencephalitic parkinsonism (one case), Alzheimer's disease (two cases), senile dementia (two cases) and non-demented elderly person (three cases). The light microscopic pattern of Alzheimer's neurofibrillary tangles seen in progressive supranuclear palsy was similar to those in postencephalitic parkinsonism, Alzheimer's disease, senile dementia and non-demented elderly person. Some differences in the frequency and the distribution of Alzheimer's neurofibrillary tangles were demonstrated. ( info) |
16/22. Distribution and ultrastructure of Alzheimer's neurofibrillary tangles in postencephalitic Parkinsonism of Economo type. The distribution and ultrastructure of Alzheimer's neurofibrillary tangles (ANT) in the brain stem, hypothalamus, and Ammon's horn were studied in four patients with postencephalitic parkinsonism of Economo type (PEPE). The distribution of ANT was as previously reported; the pattern of distribution resembled to that of amine-containing nerve cells. Ultrastructurally, ANT revealed twisted tubules (TT), but straight tubules (ST) of 150 A width were also found in the locus ceruleus of three cases; sometimes, TT and ST were mixed in a single neuron. Whether the coexistence of TT and ST in the locus ceruleus is a characteristic ultrastructural feature of ANT in PEPE or a regional peculiarity could not be determined. Ultrastructurally, ANT in PEPE were identical to those found in the brains of patients with Alzheimer's disease or senile dementia. ( info) |
17/22. Juvenile parkinsonism caused by chronic meningoencephalitis: a clinicopathological study. After a six-year history of poor concentration, intellectual and growth retardation, and a one-year history of absences, an 11-year-old girl developed parkinsonism and thereafter had a progressive, predominantly extrapyramidal disorder for the next nine years, until her death at age 20. Other clinical features included pyramidal signs, peripheral neuropathy and sideroblastic anemia. Despite a clinical course suggestive of a degenerative condition, the principal findings on examination of the brain were chronic meningitis, brainstem encephalitis and mild diffuse cerebral gliosis. Extensive investigations failed to demonstrate an infective agent, either in life or by post mortem examination. ( info) |
18/22. Pathological overlap in cases of parkinsonism associated with neurofibrillary tangles. A study of recent cases of postencephalitic parkinsonism and comparison with progressive supranuclear palsy and Guamanian parkinsonism-dementia complex. In recent years a number of patients suffering from long-standing postencephalitic parkinsonism have donated their brains to the United Kingdom Parkinson's disease Society Brain Bank, in london. In view of the paucity of detailed neuropathological reports of the disease since the 1940s, we have carried out a clinicopathological study of eight recent cases. A spectrum of pathological change was seen, with highly variable involvement of cortical, subcortical and brainstem structures. There was no correlation between severity of disease and severity of pathology. The anatomical distribution of lesions was compared with that seen in progressive supranuclear palsy and Guamanian Parkinson-dementia complex. No definite histological features were identified that could distinguish any of the three disease entities. While the pathogenesis of postencephalitic parkinsonism, progressive supranuclear palsy and Guamanian Parkinson-dementia complex remains unknown, the presence of similar pathologies in these conditions suggests a common disease mechanism, despite the distinctive clinical features. ( info) |
19/22. Tic douloureux, Parkinson's disease and the herpes connection. Several cases encountered in psychiatric practice are described in which herpetic involvement of the trigeminal nerve appeared to be crucial to the pathophysiology of the patient's illness. A brief history of herpes is discussed in terms of the anatomy and physiology of the trigeminal nerve. Particular attention is given to the effects of intraneuronal herpes on gasserian ganglion and spinal nuclei discharge thresholds, as well as viral pathways directly impacting the substantia nigra. Evidence characterizing Parkinson's disease as one of several important manifestations of CNS herpes is covered. ( info) |
20/22. Primary sensory symptoms in parkinsonism. Forty-three of 101 outpatients with parkinsonism reported that they regularly experienced primary sensory symptoms, i.e., spontaneous abnormal sensations not caused by somatic disease. This is in contrast to similar symptoms reported by only 8 percent of a control population. The most striking and severe symptom was burning of the trunk and proximal extremities, occurring in 11 patients. Twenty-nine patients reported spontaneous pain; a variety of other paresthesialike sensations, e.g., tingling, numbness, and formication, occurred in 32 patients. These subjective sensory phenomena were not associated with sensory loss or autonomic or motor signs. In 20 percent of affected individuals (9 percent of the total), sensory symptoms preceded the onset of the movement disorder, causing difficulty in diagnosis. It is concluded that at least some sensory symptoms originate within the nervous system as a manifestation of the disease process and are not secondary effects of the motor disorder. ( info) |