(Stroke. 1999;30:1974-1981.)
© 1999 American Heart Association, Inc.
Letters to the Editor |
Secondary Change in the Substantia Nigra Induced by Incomplete Infarct and Minor Hemorrhage in the Basal Ganglia Due to Traumatic Middle Cerebral Arterial Dissection
Department of Neurosurgery, Nara Prefectural Emergency Center
Department of Radiology, Nara Prefectural Nara Hospital, Nara, Japan
Key Words: dissection • magnetic resonance imaging • middle
cerebral artery
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Introduction |
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To the Editor:
Cerebral infarction caused by middle cerebral artery (MCA) occlusion (MCAO) can lead to secondary neuronal damage in discrete-remote brain areas, including the ipsilateral thalamus and substantia nigra.1 2 3 4 These neuronal changes have been considered to develop due to either anterograde or retrograde degeneration or transsynaptic injury after the initial ischemia.1 2 3 4 An early study of MRI showed that the lesion in the substantia nigra persisted for at least several months after the stroke.4 Transient changes in the substantia nigra on MRI have never been reported in patients after basal ganglionic ischemia.
We have investigated basal ganglia injuries after various types of transient brain energy failures in humans and rats using repeated MRI.5 6 7 8 Recently, we showed that a specific change in the caudate putamen of humans and rats on serial MRI represented an incomplete ischemic injury of selective neuronal death and gliosis associated with biochemical changes which affect the magnetic field.7 8 We present the first MRI study of the temporary change in the ipsilateral substantia nigra in a patient with minor hemorrhage and incomplete infarct in the basal ganglia after traumatic MCA dissection (MCAD).
An 18-year-old man received a head injury in a motorcycle accident on
May 29, 1997 (day 0). His neurological state was normal on his
admission to a local hospital. CT scans revealed no findings at that
time. However, left hemiparesis and dysarthria developed in the patient
on day 3. CT scans on day 3 demonstrated a low-density area in the
right putamen. He was referred to our hospital for further examination
on day 4. On admission, he was conscious and alert but suffered from
left hemiparesis and dysarthria. CT scans on day 4 showed low-density
lesions in the right putamen and cerebral cortex of the right frontal
lobe. Cerebral angiography revealed stenotic change of the
right MCA horizontal portion. The initial MRI on day 5 revealed
ischemic changes of hyperintensity/hyperintensity on
T1-weighted/T2-weighted (T1W/T2W) images, respectively, in the lateral
portion of the right putamen (we tentatively designated this area as
P1), hypointensity/hyperintensity in another portion of the right
putamen (P2), and linear ischemic change of
hypointensity/hyperintensity in the right cerebral cortex. The second
MRI on day 26 demonstrated lesions of hypointensity/hyperintensity on
T1-/T2-WI in the P1, hyperintensity/hyperintensity in the P2, and
hyperintensity/hyperintensity in the right cerebral cortex
(Figure
). Furthermore, the MRI on day 26
revealed delayed ischemic change of hyperintensity on T1W and
relative hypointensity on T2W images in the right globus pallidus
(Figure). Additionally, in the right substantia nigra, the MRI on day
26 revealed a late-onset change of isointensity/hyperintensity on
T1W/T2W images that the first MRI did not reveal (Figure). The third
MRI on day 39 showed hypointensity/hyperintensity in the P1,
hyperintensity/hyperintensity in the P2, hyperintensity/relative
hypointensity in the right globus pallidus, and linear change of
hyperintensity/hyperintensity in the right cerebral cortex. In the
right substantia nigra, the delayed change on MRI disappeared on day
39. The patient's neurological state improved gradually during
hospitalization. The patient could walk without any assistance,
although he had a slight left hemiparesis. He could communicate with
other persons without any speech disturbance. He left the
hospital on day 48 and was admitted to a rehabilitation center for
further neurological recovery. He resumed his university studies at the
beginning of October 1997.
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The neuroradiological data in our patient can be interpreted as follows. First, cerebral angiography demonstrated right MCA stenosis, which led to delayed neurological deficits after a mild head injury, suggesting traumatic dissection of the MCA. Second, repeated MRI revealed hemorrhagic infarction with subsequent cavitation in the right putamen P1. Third, MRI also showed evidence of a minor hemorrhage that was not evident on CT scans in the right putamen P2.5 Fourth, MRI depicted a delayed lesion of persistent hyperintensity/relative hypointensity on T1W/T2W images, respectively, in the right globus pallidus, suggestive of the presence of the incomplete ischemic injury, which had been reported previously in our clinical and experimental studies.7 8 Last, MRI exhibited a transient delayed change of isointensity on T1W and hyperintensity on T2W images in the right substantia nigra.
Focal brain ischemia produces a severe ischemic core with the surrounding area of milder ischemia and a nonischemic region.9 In this case, we believe that MCAD led to severe ischemia (hemorrhagic infarction followed by cavitation) in the P1, relatively moderate ischemia (minor hemorrhage that could not be detected on CT scans)5 in the P2, and mild ischemia producing "delayed ischemic hyperintensity on T1W MRI" (DIH)7 8 in the globus pallidus. We showed that this DIH corresponded to selective neuronal death and gliosis without infarct or hemorrhage.8
An interesting finding in our patient is the late-onset change of isointensity/hyperintensity on T1W/T2W MRI, respectively, in the ipsilateral substantia nigra after the primary ischemic lesion in the basal ganglia. The consciousness level of our patient remained clear throughout his hospital stay. The MRI change in the substantia nigra could be detected on T2W images obtained on day 26 but not on day 5. Therefore, this MRI abnormality of delayed onset in the substantia nigra seemed to result from a remote effect of the ischemic lesion in the basal ganglia (secondary change through the striatonigral and/or nigrostriatal pathways) but not a direct effect of the initial head trauma.
Interestingly, the T2 hyperintensity of the substantia nigra
observed at day 26 cleared by day 39. Although remote effects of
central nervous system injuries have been seen on various MRI
sequences,4 10 this is the first observation of a remote
effect leading to transient MRI change within the substantia nigra of
humans. This distant effect from the basal ganglia might cause the
edematous change on MRI in the substantia nigra. Based on an early
experimental study,3 Nakane et al4 suggested
that the remote neuronal degeneration in the ipsilateral substantia
nigra of their patients were caused by a transsynaptic,
neurotransmitter-mediated disinhibition due to the loss of striatal
neurons of the striatonigral pathway. The loss of an
inhibitory 
-aminobutyric acidergic output from
the striatum to substantia nigra is considered to result in excessive
excitation sufficient to cause the neuronal damage in the substantia
nigra.3
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References |
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TopIntroductionReferences |
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1. Kataoka K, Hayakawa T, Yamada K, Mushiroi T, Kuroda R, Mogami H. Neuronal network disturbance after focal ischemia in rats. Stroke.. 1989;20:1226–1235.
2.
Tamura A, Tahira Y, Nagashima H, Kirino T, Gotoh O,
Hojo S, Sano K. Thalamic atrophy following cerebral infarction in the
territory of the middle cerebral artery. Stroke.. 1991;22:615–618.
3. Tamura A, Kirino T, Sano K, Takagi K, Oka H. Atrophy of the ipsilateral substantia nigra following middle cerebral artery occlusion in the rat. Brain Res.. 1990;510:154–157.[Medline] [Order article via Infotrieve]
4.
Nakane M, Teraoka A, Asato R, Tamura A. Degeneration
of the ipsilateral substantia nigra following cerebral infarction in
the striatum. Stroke.. 1992;23:328–332.
5. Fujioka M, Okuchi K, Sakaki T, Hiramatsu K, Miyamoto S, Iwasaki S. Specific changes in human brain following reperfusion after cardiac arrest. Stroke.. 1994;25:2091–2095.[Abstract]
6.
Fujioka M, Okuchi K, Hiramatsu K, Sakaki T, Sakaguchi
S, Ishii Y. Specific changes in human brain after hypoglycemic injury.
Stroke.. 1997;28:584–587.
7.
Fujioka M, Taoka T, Hiramatsu K-I, Sakaguchi S, Sakaki
T. Delayed ischemic hyperintensity on T1-weighted MRI in the
caudoputamen and cerebral cortex of humans after
spectacular shrinking deficit. Stroke.. 1999;30:1038–1042.
8.
Fujioka M, Taoka T, Matsuo Y, Hiramatsu K-I, Sakaki T.
Novel brain ischemic change on MRI: delayed ischemic
hyperintensity on T1-weighted images and selective neuronal death in
the caudoputamen of rats after brief focal
ischemia. Stroke.. 1999;30:1043–1046.
9. Hossmann K-A. Viability thresholds and the penumbra of focal ischemia. Ann Neurol.. 1994;36:557–565.[Medline] [Order article via Infotrieve]
10.
Ogawa T, Yoshida Y, Okudera T, Noguchi K, Kado H,
Uemura K. Secondary thalamic degeneration after cerebral infarction in
the middle cerebral artery distribution: evaluation with MR imaging.
Radiology.. 1997;204:255–262.
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