- Email: [email protected]
Conflicting images
CASE REPORT
Case report
Conflicting images Miguel Viana Baptista, Philippe Maeder, Annelise Dewarrat, Julien Bogousslavsky A 76-year-old man with long-standing hypertension and no previous history of neurological disease was admitted to hospital in August, 1997, with sudden onset of unsteadiness of gait and clumsiness of his left hand. Neurological examination showed left facio-brachial hemiparesis with an extensor plantar response, and diminished light touch and pinprick sensation with the same distribution. Blood pressure was 140/60 mm Hg. Brain computed tomography (CT) scan showed a frontoparietal infarct. A 95% internal-carotid-artery stenosis on the right was detected by doppler ultrasonography and confirmed by angiography. 3 months later, he had recovered apart from increased tone and a distal 4+/5 paresis of his left arm. Carotid endarterectomy was done without complications. 36 h later, he had focal motor seizures with clonic movements of his left leg. Clonazepam 2 mg/day intravenously was started. Progressive neurological deterioration developed, with drowsiness, Cheyne-Stokes respiration, and worsening left hemiparesis with diminished response to painful stimuli. Brain CT scan showed diffuse white-matter oedema in the right hemisphere with mass effect and a small 2 cm haemorrhage (figure, A). T2-weighted (T2W) magnetic resonance imaging (MRI) confirmed these findings (figure, B), suggesting a cerebral infarction. Diffusion-weighted MRI showed no acute ischaemic lesion (figure, C) and perfusion-imaging MRI showed no alteration of the local cerebral blood volume in the right hemisphere (figure, D). Duplex scan confirmed patency of the right internal carotid artery. Transcranial doppler did not show significant differences in blood-flow velocities and pulsatility indexes when compared with preoperative results. He was treated with antiepileptics, diuretics, and antihypertensives. When last seen in November, 1997, his condition was the same as before the operation. Hyperperfusion syndrome is a complication of carotid endarterectomy.1,2 Typically, it occurs 5 to 8 days after surgery and includes headache, fits, focal neurological signs, intracerebral haemorrhage, and brain oedema.3 Although increased blood-flow velocities have been correlated with this syndrome, transcranial doppler was normal, questioning once more this technique’s predictive power in this situation.4 White-matter oedema in the hyperperfusion syndrome may be overlooked or misinterpreted as infarction on CT scans.3 Our case shows that T2W MRI may also be ambiguous. However,
A: Transverse CT Diffuse hypodensity in white matter of right hemisphere compatible with oedema and 2 cm hyperdensity corresponding to haemorrhage.
B: Fast spin echo T2 transverse MRI Diffuse hypersignal in white matter of right hemisphere with oedema.
C: Diffusion-weighted MRI There is no hypersignal suggestive of cytotoxic oedema.
D: Perfusion image (Integration of 40 single-shot echo-planar images acquired during a bolus of Gadolinium.) Density represents local relative values of cerebral blood volume. There is no asymmetry of perfusion from side to side.
diffusion-weighted MRI showed that the severe whitematter oedema, associated with focal neurological signs, did not correspond to evolving infarction. As in other reports,4,5 outcome was good. The absence of changes on diffusion-weighted MRI, which detects changes in the diffusion of water molecules associated with cytotoxic oedema, suggests that clinical deterioration, at a reversible stage of the hyperperfusion syndrome, is probably related to interstitial oedema. Therefore, separating cytotoxic and interstitial oedema may be feasible with this technique, as was recently reported in a patient with eclampsia.5 Perfusion MRI deserves further attention, as this technique suggested that the “hyperperfused” brain had a normal blood flow. We propose that the term “reperfusion syndrome” should be used instead of hyperperfusion syndrome. References 1
2
Lancet 1998; 351: 414
3
Departments of Neurology (M V Baptista MD, A Dewarrat MD, J Bogousslavsky MD) and Neuroradiology (P Maeder MD), Centre Hospitalier Universitaire Vaudois, CH-1011 Lausanne, Switzerland
4
Correspondence to: Dr Julien Bogousslavsky (e-mail: [email protected])
414
5
Regli L, Piepgrass D, Bogousslavsky J. Carotid endarterectomy. In: Ginsberg M, Bogousslavsky, eds. Cerebravascular disease, pathology, diagnosis and treatment. Boston: Blackwell Publ (in press). Sundt TM, Sharbrough FW, Piepgras DG, Kearns TP, Messick HJM, O’Fallan WM. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy. Mayo Clin Proc 1981; 56: 533–43. Breen JC, Caplan LR, DeWitt LD, et al. Brain edema after carotid surgery. Neurology 1996; 46: 175–81. Powers SD, Smith RR. Hyperperfusion syndrome after carotid endarterectomy: a transcranial doppler evaluation. Neurosurgery 1990; 26: 56–60. Schaefer PW, Buonanno FS, Gonzalez RG, Schwamm L. Diffusionweighted imaging descriminates between cytotoxis and vasogenic edema in eclampsia. Stroke 1997; 28: 1002–85.
THE LANCET • Vol 351 • February 7, 1998
Case report
Conflicting images Miguel Viana Baptista, Philippe Maeder, Annelise Dewarrat, Julien Bogousslavsky A 76-year-old man with long-standing hypertension and no previous history of neurological disease was admitted to hospital in August, 1997, with sudden onset of unsteadiness of gait and clumsiness of his left hand. Neurological examination showed left facio-brachial hemiparesis with an extensor plantar response, and diminished light touch and pinprick sensation with the same distribution. Blood pressure was 140/60 mm Hg. Brain computed tomography (CT) scan showed a frontoparietal infarct. A 95% internal-carotid-artery stenosis on the right was detected by doppler ultrasonography and confirmed by angiography. 3 months later, he had recovered apart from increased tone and a distal 4+/5 paresis of his left arm. Carotid endarterectomy was done without complications. 36 h later, he had focal motor seizures with clonic movements of his left leg. Clonazepam 2 mg/day intravenously was started. Progressive neurological deterioration developed, with drowsiness, Cheyne-Stokes respiration, and worsening left hemiparesis with diminished response to painful stimuli. Brain CT scan showed diffuse white-matter oedema in the right hemisphere with mass effect and a small 2 cm haemorrhage (figure, A). T2-weighted (T2W) magnetic resonance imaging (MRI) confirmed these findings (figure, B), suggesting a cerebral infarction. Diffusion-weighted MRI showed no acute ischaemic lesion (figure, C) and perfusion-imaging MRI showed no alteration of the local cerebral blood volume in the right hemisphere (figure, D). Duplex scan confirmed patency of the right internal carotid artery. Transcranial doppler did not show significant differences in blood-flow velocities and pulsatility indexes when compared with preoperative results. He was treated with antiepileptics, diuretics, and antihypertensives. When last seen in November, 1997, his condition was the same as before the operation. Hyperperfusion syndrome is a complication of carotid endarterectomy.1,2 Typically, it occurs 5 to 8 days after surgery and includes headache, fits, focal neurological signs, intracerebral haemorrhage, and brain oedema.3 Although increased blood-flow velocities have been correlated with this syndrome, transcranial doppler was normal, questioning once more this technique’s predictive power in this situation.4 White-matter oedema in the hyperperfusion syndrome may be overlooked or misinterpreted as infarction on CT scans.3 Our case shows that T2W MRI may also be ambiguous. However,
A: Transverse CT Diffuse hypodensity in white matter of right hemisphere compatible with oedema and 2 cm hyperdensity corresponding to haemorrhage.
B: Fast spin echo T2 transverse MRI Diffuse hypersignal in white matter of right hemisphere with oedema.
C: Diffusion-weighted MRI There is no hypersignal suggestive of cytotoxic oedema.
D: Perfusion image (Integration of 40 single-shot echo-planar images acquired during a bolus of Gadolinium.) Density represents local relative values of cerebral blood volume. There is no asymmetry of perfusion from side to side.
diffusion-weighted MRI showed that the severe whitematter oedema, associated with focal neurological signs, did not correspond to evolving infarction. As in other reports,4,5 outcome was good. The absence of changes on diffusion-weighted MRI, which detects changes in the diffusion of water molecules associated with cytotoxic oedema, suggests that clinical deterioration, at a reversible stage of the hyperperfusion syndrome, is probably related to interstitial oedema. Therefore, separating cytotoxic and interstitial oedema may be feasible with this technique, as was recently reported in a patient with eclampsia.5 Perfusion MRI deserves further attention, as this technique suggested that the “hyperperfused” brain had a normal blood flow. We propose that the term “reperfusion syndrome” should be used instead of hyperperfusion syndrome. References 1
2
Lancet 1998; 351: 414
3
Departments of Neurology (M V Baptista MD, A Dewarrat MD, J Bogousslavsky MD) and Neuroradiology (P Maeder MD), Centre Hospitalier Universitaire Vaudois, CH-1011 Lausanne, Switzerland
4
Correspondence to: Dr Julien Bogousslavsky (e-mail: [email protected])
414
5
Regli L, Piepgrass D, Bogousslavsky J. Carotid endarterectomy. In: Ginsberg M, Bogousslavsky, eds. Cerebravascular disease, pathology, diagnosis and treatment. Boston: Blackwell Publ (in press). Sundt TM, Sharbrough FW, Piepgras DG, Kearns TP, Messick HJM, O’Fallan WM. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy. Mayo Clin Proc 1981; 56: 533–43. Breen JC, Caplan LR, DeWitt LD, et al. Brain edema after carotid surgery. Neurology 1996; 46: 175–81. Powers SD, Smith RR. Hyperperfusion syndrome after carotid endarterectomy: a transcranial doppler evaluation. Neurosurgery 1990; 26: 56–60. Schaefer PW, Buonanno FS, Gonzalez RG, Schwamm L. Diffusionweighted imaging descriminates between cytotoxis and vasogenic edema in eclampsia. Stroke 1997; 28: 1002–85.
THE LANCET • Vol 351 • February 7, 1998