Preliminary diagnosis of Parkinson's disease by olfactory bulb pathology.
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Humans↗
Biomedical subjects
S E Daniel
Publications and source records attributed to S E Daniel.
Alpha-tocopherol levels in brain are not altered in Parkinson's disease.
alpha-Tocopherol (vitamin E) levels in normal brain were lower in the cerebellum than in the cerebral cortex or basal ganglia. There was no difference in alpha-tocopherol levels in the cerebellum, basal ganglia, or cerebral cortex between control subjects and patients with Parkinson's disease.
Aged↗
Diffuse Lewy body disease presenting with supranuclear gaze palsy, parkinsonism, and dementia: a case report.
A 67-year-old man with a family history of parkinsonism had visual complaints due to difficulty in convergence, which was followed 2 years later by development of bradykinesia and rigidity. The diagnosis of Steele-Richardson-Olszewski syndrome was made on the basis of a supranuclear gaze palsy, bradykinesia, rigidity, and poor response to levodopa. However, subsequent neuropathological examination revealed diffuse Lewy body disease with no evidence of neurofibrillary tangles involving either subcortical or brain stem structures.
Aged↗
Brain, skeletal muscle and platelet homogenate mitochondrial function in Parkinson's disease.
The recent discovery of mitochondrial complex I deficiency in the substantia nigra of patients with idiopathic Parkinson's disease has provided new understanding into the possible mechanisms that may underlie this neurodegenerative disorder. The biochemical defect is identical to that induced in humans, primates and mice exposed to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. We have studied mitochondrial respiratory chain function in various brain regions, in skeletal muscle and in blood platelets from patients with idiopathic Parkinson's disease and from matched controls. We provide evidence suggesting that the complex I deficiency in Parkinson's disease is limited to the brain and that this defect is specific for the substantia nigra. The tissue specificity of the complex I deficiency in Parkinson's disease and its localization to the substantia nigra support the proposition that complex I deficiency may be directly involved in the cause of dopaminergic cell death in Parkinson's disease. An understanding of the molecular basis of this biochemical defect will provide valuable insight into the cause of Parkinson's disease. Our findings of normal mitochondrial function in platelet homogenates suggests that this tissue cannot be used to develop a 'diagnostic test' for Parkinson's disease.
Aged↗
The dopaminergic response in multiple system atrophy.
Fifteen of 23 pathologically confirmed cases of multiple system atrophy (MSA) showed some initial response to levodopa and eight of these remained at least partially responsive at the time of death. Eleven developed motor oscillations, and drug-induced dyskinesias, often involving the face and jaw, were also seen in 11 cases. Acute levodopa and apomorphine challenges were administered to 11 patients with clinical MSA who were considered levodopa responsive. A short duration relatively small amplitude response with associated dyskinesias occurred in six and a further three developed dyskinesias without any motor response. Following levodopa withdrawal, a delayed deterioration occurred after three to six days in six patients, five of whom had shown no short duration motor response to the acute challenges. The occurrence of levodopa-induced dyskinesias without a concomitant motor response and delayed deterioration several days after levodopa withdrawal may be more typical of patients with MSA than Parkinson's disease.
Adult↗
Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases.
Few detailed clinico-pathological correlations of Parkinson's disease have been published. The pathological findings in 100 patients diagnosed prospectively by a group of consultant neurologists as having idiopathic Parkinson's disease are reported. Seventy six had nigral Lewy bodies, and in all of these Lewy bodies were also found in the cerebral cortex. In 24 cases without Lewy bodies, diagnoses included progressive supranuclear palsy, multiple system atrophy, Alzheimer's disease, Alzheimer-type pathology, and basal ganglia vascular disease. The retrospective application of recommended diagnostic criteria improved the diagnostic accuracy to 82%. These observations call into question current concepts of Parkinson's disease as a single distinct morbid entity.
Adult↗
What features improve the accuracy of clinical diagnosis in Parkinson's disease: a clinicopathologic study.
Many authorities have drawn attention to the difficulties in clinically distinguishing Parkinson's disease (PD) from other parkinsonian syndromes. We assessed the clinical features of 100 patients diagnosed prospectively by a group of consultant neurologists as having idiopathic PD according to their pathologic findings. Seventy-six percent of these cases were confirmed to have PD. By using selected criteria (asymmetrical onset, no atypical features, and no possible etiology for another parkinsonian syndrome) the proportion of true PD cases identified was increased to 93%, but 32% of pathologically confirmed cases were rejected on this basis. These observations suggest that studies based on consultant diagnosis of PD, using standard diagnostic criteria, will include cases other than PD, thus distorting results from clinical trials and epidemiologic studies. The strict use of additional criteria can reduce misdiagnosis but at the cost of excluding genuine PD cases.
Adult↗
Idiopathic Parkinson's disease combined with multiple system atrophy. A clinicopathological report.
The clinical and postmortem findings of a patient with Lewy body pathology combined with multiple-system atrophy are described. When alive the patient was diagnosed as having Parkinson's disease. Pathological examination found evidence of striatonigral and olivopontocerebellar degeneration, together with Lewy bodies at a number of sites characteristic for idiopathic Parkinson's disease. Taken together, the clinical history and histological findings support the coexistence of two disease processes.
Astrocytes↗
Alterations in the levels of iron, ferritin and other trace metals in Parkinson's disease and other neurodegenerative diseases affecting the basal ganglia.
Levels of iron, copper, zinc and manganese were measured by inductively coupled plasma spectroscopy in frozen postmortem brain tissue from patients with Parkinson's disease (PD), progressive supranuclear palsy (PSP), multiple system atrophy with strionigral degeneration (MSA), and Huntington's disease (HD) compared with control subjects. Total iron levels were found to be elevated in the areas of basal ganglia showing pathological change in these disorders. In particular, total iron content was increased in substantia nigra in PD, PSP and MSA, but not in HD. Total iron levels in the striatum (putamen and/or caudate nucleus) were increased in PSP, MSA and HD but not in PD. Total iron levels were decreased in the globus pallidus in PD. There were no consistent alterations of manganese levels in basal ganglia structures in any of the diseases studied. Copper levels were decreased in the substantia nigra in PD, and in the cerebellum in PSP, and were elevated in the putamen and possibly substantia nigra in HD. Zinc levels were only increased in PD, in substantia nigra and in caudate nucleus and lateral putamen. Levels of the iron binding protein ferritin were measured in the same patient groups using a radio-immunoassay technique. Increased iron levels in basal ganglia were generally associated with normal or elevated levels of ferritin immunoreactivity, for example, the substantia nigra in PSP and possibly MSA, and in putamen in MSA. The exception was PD where there was a generalized reduction in brain ferritin immunoreactivity, even in the substantia nigra. An increase in total iron content appears to be a response to neurodegeneration in affected basal ganglia regions in a number of movement disorders. However, only in PD was there an increased total iron level, decreased ferritin content, decreased copper content, and an increased zinc concentration in substantia nigra. These findings suggest an alteration of iron handling in the substantia nigra in PD. Depending on the form in which the excess iron load exists in nigra in PD, it may contribute to the neurodegenerative process.
Aging↗
Granular cell tumours of the orbit.
Granular cell tumours are uncommon benign tumours, occurring in various sites in the body, and very rarely in the orbit or ocular adnexa. Four cases of orbital granular cell tumour are described, with detailed light and electron microscopic description of one tumour arising in the orbital apex of a child. The histogenesis of granular cell tumour is uncertain, with many authors proposing an origin from Schwann cells. In central nervous system granular cell tumours, an astrocytic cell origin has been proposed. Evidence is presented for an origin from astrocytes in a child whose tumour arose in or adjacent to the optic nerve.
Adult↗
Neuropathological features of Alzheimer's disease in non-demented parkinsonian patients.
Two patients with levodopa-responsive Parkinson's syndrome had numerous cortical and striatal senile plaques and some neurofibrillary tangles at necropsy. In addition neurons in the pars compacta of the substantia nigra were severely depleted but there were no Lewy bodies or other neuropathological changes to account for parkinsonism. Neither patient was demented. These pathological findings have not previously been described as a cause of Parkinson's syndrome without associated dementia of Alzheimer's disease type.
Aged↗
Anatomic and disease specificity of NADH CoQ1 reductase (complex I) deficiency in Parkinson's disease.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is thought to produce parkinsonism in humans and other primates through its inhibition of complex I. The recent discovery of mitochondrial complex I deficiency in the substantia nigra of patients with Parkinson's disease has provided a remarkable link between the idiopathic disease and the action of the neurotoxin MPTP. This article shows that complex I deficiency in Parkinson's disease is anatomically specific for the substantia nigra, and is not present in another neurodegenerative disorder involving the substantia nigra. Evidence is also provided to show that there is no correlation between L-3,4-dihydroxyphenylalanine therapy and complex I deficiency. These results suggest that complex I deficiency may be the underlying cause of dopaminergic cell death in Parkinson's disease.
Citrate (si)-Synthase↗
Degeneration and regeneration in the superior cervical sympathetic ganglion after Latrodectus venom.
The effects of the venom of the spider Latrodectus mactans hasselti on the superior cervical ganglion were studied in the guinea pig. Under anaesthesia the ganglion was bathed in venom solution for 15 min. Shortly afterwards animals salivated profusely and later developed unilateral ptosis and enophthalmos. Postoperative survival times ranged from 15 min to 10 weeks. Electron microscopy showed acute swelling of preganglionic cholinergic nerve terminals, followed by degeneration with separation of synapses. Other ganglionic elements appeared to be undamaged, although after detachment of synapses the dendritic postsynaptic specializations were reduced in number. Recovery was very rapid; axon growth cones were identifiable at 18 h and synapse reformation was well established by 2 weeks. With longer survival times there was progressive restoration of normal morphology such that by 8 weeks regeneration appeared complete. These experiments indicate that the preganglionic cholinergic nerve terminals are selectively affected by Latrodectus venom and have a considerable capacity for appropriate regeneration.
Animals↗
Chronic basal meningitis and vasculitis in acquired immunodeficiency syndrome. A possible role for human immunodeficiency virus.
We describe the clinical and postmortem findings in a 57-year-old man with human immunodeficiency virus who presented with neurologic symptoms attributed to stroke. In addition to multiple foci of ischemic necrosis, pathologic examination of the brain showed chronic basal meningitis and vasculitis. No microorganisms were found. The association of meningitis and vasculitis in patients with acquired immunodeficiency syndrome is unusual and the possibility that these conditions may be due to primary human immunodeficiency virus infection is raised.
Acquired Immunodeficiency Syndrome↗
Malignant angioendotheliosis involving the nervous system: support for a lymphoid origin of the neoplastic cells.
The clinical and post mortem findings of a case of malignant angioendotheliosis are described. The patient presented with neurological signs attributable to repeated episodes of cerebral and spinal cord infarction. Histological examination showed multifocal intravascular proliferation of mononuclear cells. Immunocytochemical characterisation of these neoplastic cells supports the recent suggestion that this disease represents an unusual form of intravascular lymphoma, which appears to show a predilection for blood vessels of the nervous system.
Antigens, Neoplasm↗
Primary intracranial histiocytic lymphoma with Langerhans' granules. A light microscopic and ultrastructural study.
An intracranial tumor classified as a histiocytic lymphoma was studied with light and electron microscopic examination and immunocytochemical methods. The characteristics of the malignant mononuclear phagocyte cells are described. The presence of some cells containing Langerhans' granules suggests differentiation towards a specialized cell of the mononuclear phagocyte system: the Langerhans' cell.
Adult↗
Encephalomyeloneuropathy in the absence of a detectable neoplasm. Clinical and postmortem findings in three cases.
The clinical and postmortem findings in three cases of encephalomyeloneuropathy are reported. Two patients presented with subacute sensory neuropathy and one with amnesia and confusion. In none of these cases was a tumour detected clinically or at autopsy. Neuropathological examination showed inflammatory lesions in the brain, spinal cord and posterior root ganglia indistinguishable from encephalomyeloneuropathy occurring as a remote effect of carcinoma.
Aged↗
Rhino-orbital zygomycosis.
A 63-year-old diabetic man presented with sinusitis with orbital and intracranial signs progressing over one week, due to zygomycosis. Despite control of the diabetes, surgical excision of infected tissue and antifungal therapy he died in the fifth week of illness. Pathological study showed extensive fungal infiltration of periorbital structures and mycotic thrombosis of many blood vessels with associated necrosis and infarction of fat and extraocular muscles.
Diabetes Mellitus, Type 2↗