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Ultrastructure and biochemistry of sympathetic ganglia in idiopathic orthostatic hypotension
Author(s) -
Petito Carol K.,
Black Ira B.
Publication year - 1978
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410040103
Subject(s) - postsynaptic potential , gliosis , spinal cord , endocrinology , medicine , pathology , chemistry , neuroscience , biology , receptor
The role of transsynaptic dysfunction in the pathogenesis of idiopathic orthostatic hypotension (IOH, or idiopathic autonomic insufficiency) was examined microsocopically and biochemically in autopsy specimens. Light microscopy of the sympathetic ganglia showed abnormalities in all 4 IOH patients, including focal phagocytosis of neurons, increased numbers of satellite cells, and perivascular lymphocytic infiltrates. Electron microscopy revealed proliferation and hypertrophy of satellite cells and abnormalities in the unmyelinated axons. In constrast, the spinal cord intermediolateral columns, containing the presynaptic neurons, were unremarkable in 1 patient, exhibited only mild gliosis in another, and showed neuron loss and fibrillary gliosis in 2 patients. Postsynaptic dopamine‐β‐hydroxylase (DBH) activity was decreased at least fourfold ( p < 0.02) in sympathetic ganglia of patients with IOH, while tyrosine hydroxylase (T‐OH) was normal. Ganglion choline acetyltransferase (ChAc) activity, an index of presynaptic function and integrity, was normal in the IOH group. A number of our observations suggest that presynaptic disease is not an absolute requirement for adrenergic abnormalities in IOH. The intermediolateral columns of the spinal cord were histologically normal in 2 of the patients with IOH, and ultrastructural abnormalities in sympathetic ganglia were consistent with primary adrenergic degeneration. In addition, presynaptic ChAc activity was normal in IOH ganglia, whereas postynaptic DBH activity was depressed. Finally, postsynaptic T‐OH activity, which is regulated by transsynaptic mechanisms, was normal in IOH ganglia.