Secondary degeneration of the mesencephalic substantia nigra after cerebral infarction
is widely known to occur in animal experiments, but has yet to be sufficiently investigated
in human cerebral infarction. This study investigated the background and features
of patients exhibiting secondary degeneration of the mesencephalic substantia nigra.
The subjects comprised 43 patients admitted to our hospital for cerebral infarction
between April 2007 and October 2010 showing secondary degeneration of the mesencephalic
substantia nigra on cranial magnetic resonance imaging (MRI). We investigated clinical
disease type, location of vascular occlusion, lesion site, and time from onset of
symptoms to lesion identification by MRI. The clinical disease type was cardiogenic
embolism in 29 patients (67%), atheromatous embolism (artery to artery) in 8 patients
(19%), embolism (origin unknown) in 2 patients (5%), infarction after coil embolization
for internal carotid aneurysm in 1 patient (2%), arterial dissection in 2 patients
(5%), and vasculitis due to Takayasu disease in 1 patient (2%). Magnetic resonance
angiography (MRA) identified the occluded vessel as the internal carotid artery in
19 patients (44%), the middle cerebral artery (M1) in 20 patients (47%), and the middle
cerebral artery (M2) in 3 patients (7%); MRA was not performed in 1 patient (2%).
The cerebral infarctions were striatal in 7 patients (16%) and striatal and cortical
in 36 patients (84%). Hyperintense regions in the mesencephalic substantia nigra were
observed in all patients after 7-28 days (mean, 13.3 days) on diffusion-weighted imaging
or fluid-attenuated inversion recovery and T2-weighted MRI. Most patients with secondary
degeneration of the substantia nigra demonstrated clinical disease comprising vascular
occlusion of the internal carotid artery or the neighborhood of the middle cerebral
artery, which was envisaged to cause a sudden drop in brain circulation across a wide
area. Striatal infarctions were observed in all patients. Secondary degeneration of
the substantia nigra appeared at 1-4 weeks after onset and disappeared after several
months.
Key Words
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References
- Wallerian degeneration after cerebral infarction: Evaluation with sequential MR imaging.Radiology. 1989; 172: 179-182
- MR imaging of Wallerian degeneration in the human brain stem after ictus.Neuroradiology. 1990; 32: 191-195
- Brainstem and cerebellar changes after cerebrovascular accidents: Magnetic resonance imaging.Eur Radiol. 2006; 16: 592-597
- MR appearance of hypertrophic olivary degeneration after contralateral cerebellar hemorrhage.AJNR Am J Neuroradiol. 1991; 12: 71-72
- Olivary degeneration after cerebellar or brain stem hemorrhage: MRI.Neuroradiology. 1993; 35: 335-338
- Hypertrophic olivary degeneration: MR imaging and pathologic findings.Radiology. 1994; 192: 539-543
- Secondary thalamic degeneration after cerebral infarction in the middle cerebral artery distribution: Evaluation with MR imaging.Radiology. 1997; 204: 255-262
- Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.Stroke. 1991; 22: 615-618
- Ipsilateral mamillary body atrophy after infarction of the posterior cerebral artery territory: MR imaging.Eur Radiol. 2005; 15: 2312-2315
- Cytoarchitecture of the substantia nigra in the rat.Am J Anat. 1970; 129: 417-438
- Decrease of glutamate decarboxylase (GAD) immunoreactive nerve terminals in the substantia nigra after kainic acid lesion of the striatum.J Histochem Cytochem. 1981; 29: 977-980
- Origin and distribution of glutamate decarboxylase in substantia nigra of the cat.Brain Res. 1974; 71: 77-92
- Delayed transneuronal death of substantia nigra neurons prevented by γ-aminobutyric acid agonist.Science. 1987; 235: 66-69
- Atrophy of the ipsilateral substantia nigra following middle cerebral artery occlusion in rats.Brain Res. 1990; 510: 154-157
- Astrocytic swelling in the ipsilateral substantia nigra after occlusion of the middle cerebral artery in rats.AJNR Am J Neuroradiol. 2001; 22: 660-663
- MR Detection of secondary changes remote from ischemia: Preliminary observations after occlusion of the middle cerebral artery in rats.AJNR Am J Neuroradiol. 1997; 18: 945-950
- Signal change of the substantia nigra on diffusion-weighted imaging following striatal infarction.Intern Med. 2010; 49: 65-68
- Degeneration of the ipsilateral substantia nigra after striatal infarction: Evaluation with MR imaging.Radiology. 1997; 204: 847-851
- Secondary degeneration of the substantia nigra and corticospinal tract after hemorragic middle cerebral artery infarction: Diffusion-weighted MR finding.Magn Reson Med Sci. 2002; 1: 175-178
- Diffusion abnormality of deep gray matter in external capsular hemorrhage.AJNR Am J Neuroradiol. 2005; 26: 229-235
- Degeneration of ipsilateral substantia nigra following cerebral infarction in the striatum.Stroke. 1992; 23: 328-332
- Secondary degeneration of substantia nigra following massive basal ganglia infarction.Clin Neurol. 1989; 29: 1352-1356
- Diffusion-weighted imaging of acute excitotoxic brain injury.AJNR Am J Neuroradiol. 2005; 26: 216-228
- Reaction of the substantia nigra to massive basal ganglia infarction.Acta Neuropathol. 1983; 62: 96-102
- Alteration of the free fatty acids in the thalamus following middle cerebral artery occlusion in the rat.Teikyo Med J. 2005; 28: 241-254
- FK506 protects against various immune responses and secondary degeneration following cerebral ischemia.Anat Record. 2009; 292: 1993-2001
Article info
Publication history
Published online: July 25, 2011
Accepted:
June 11,
2011
Received in revised form:
June 7,
2011
Received:
April 26,
2011
Identification
DOI: https://doi.org/10.1016/j.jstrokecerebrovasdis.2011.06.006
Copyright
© 2013 National Stroke Association. Published by Elsevier Inc. All rights reserved.
