Abstract
The sympathetic nervous system participates in the modulation of cerebrovascular autoregulation. The most important source of sympathetic innervation of the cerebral arteries is the superior cervical ganglion. The aim of this study was to investigate signs of the neurodegenerative alteration in the sympathetic ganglia including the evaluation of apoptosis of neuronal and satellite cells in the human superior cervical ganglion after ischemic stroke, because so far alterations in human sympathetic ganglia related to the injury to peripheral tissue have not been enough analyzed. We investigated human superior cervical ganglia from eight patients who died of ischemic stroke and from seven control subjects. Neurohistological examination of sympathetic ganglia was performed on 5 microm paraffin sections stained with cresyl violet. TUNEL method was applied to assess apoptotic cells of sympathetic ganglia. The present investigation showed that: (1) signs of neurodegenerative alteration (darkly stained and deformed neurons with vacuoles, lymphocytic infiltrates, gliocyte proliferation) were markedly expressed in the ganglia of stroke patients; (2) apoptotic neuronal and glial cell death was observed in the human superior cervical ganglia of the control and stroke groups; (3) heterogenic distribution of apoptotic neurons and glial cells as well as individual variations in both groups were identified; (4) higher apoptotic index of sympathetic neurons (89%) in the stroke group than in the control group was found. We associated these findings with retrograde reaction of the neuronal cell body to axonal damage, which occurs in the ischemic focus of blood vessels innervated by superior cervical ganglion.
Highlights
The sympathetic nervous system, the predominant innervation to the cerebral arteries, participates in the modulation of cerebrovascular autoregulation by controlling the intracranial pressure, blood volume, and cerebrospinal fluid production and protects cerebral blood flow and blood-brain barrier integrity by limiting cerebrovascular dilation during severe arterial hypertension, arterial hypoxia, and hypercapnia [1]
The present investigation showed that: [1] signs of neurodegenerative alteration were markedly expressed in the ganglia of stroke patients; [2] apoptotic neuronal and glial cell death was observed in the human superior cervical ganglia of the control and stroke groups; [3] heterogenic distribution of apoptotic neurons and glial cells as well as individual variations in both groups were identified; [4] higher apoptotic index of sympathetic neurons (89%) in the stroke group than in the control group was found
We associated these findings with retrograde reaction of the neuronal cell body to axonal damage, which occurs in the ischemic focus of blood vessels innervated by superior cervical ganglion
Summary
The sympathetic nervous system, the predominant innervation to the cerebral arteries, participates in the modulation of cerebrovascular autoregulation by controlling the intracranial pressure, blood volume, and cerebrospinal fluid production and protects cerebral blood flow and blood-brain barrier integrity by limiting cerebrovascular dilation during severe arterial hypertension, arterial hypoxia, and hypercapnia [1]. The most important source of sympathetic innervation of the cerebral arteries is the superior cervical ganglion (SCG). The pathway from SCG to all basal cerebral arteries lies along the internal carotid and vertebral arteries [4]. Acute cerebral ischemia and traumatic brain injury cause perivascular nerve fiber damage and contributes to vascular abnormalities in cerebral circulation [5, 6]. The studies on experimental animals revealed that the cerebral arterial occlusion by extraluminal electrocoagulation induced a marked decrease in the perivascular innervation including the catecholaminecontaining nerve fibers of the occluded middle cerebral artery [6]. The cellular response to axonal injury begins as Structural changes of the human superior cervical ganglion following ischemic stroke 391 central chromatolysis and might evolve as apoptotic cell death along a synchronous time course [8]
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