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Correlation of transcranial color Doppler to n20 somatosensory evoked potential detects ischemic penumbra in subarachnoid hemorrhage.

Di Pasquale P, Zanatta P, Morghen I, Bosco E, Forini E - Open Neurol J (2011)

Bottom Line: Both ratios became <0.65 (p <0.01) when patients showed unilateral images of ischemic penumbra and returned >0.65 if penumbra disappeared.Variations of interhemispheric ratios of MCA resistance and cortical N20 amplitude correlate closely in SAH and allow identification of the reversible ischemic penumbra threshold, when both ratios become <0.65.The correlation is lost when structural damage develops.

View Article: PubMed Central - PubMed

Affiliation: Anaesthesia and Intensive Care Department, Rovigo Hospital, Viale 3 Martiri, 140, 45100 Rovigo, Italy.

ABSTRACT

Background: Normal subjects present interhemispheric symmetry of middle cerebral artery (MCA) mean flow velocity and N20 cortical somatosensory evoked potential (SSEP). Subarachnoid haemorrhage (SAH) can modify this pattern, since high regional brain vascular resistances increase blood flow velocity, and impaired regional brain perfusion reduces N20 amplitude. The aim of the study is to investigate the variability of MCA resistances and N20 amplitude between hemispheres in SAH.

Methods: Measurements of MCA blood flow velocity (vMCA) by transcranial color-Doppler and median nerve SSEP were bilaterally performed in sixteen patients. MCA vascular changes on the compromised hemisphere were calculated as a ratio of the reciprocal of mean flow velocity (1/vMCA) to contralateral value and correlated to the simultaneous variations of interhemispheric ratio of N20 amplitude, within each subject. Data were analysed with respect to neuroimaging of MCA supplied areas.

Results: Both interhemispheric ratios of 1/vMCA and N20 amplitude were detected >0.65 (p <0,01) in patients without neuroimages of injury. Both ratios became <0.65 (p <0.01) when patients showed unilateral images of ischemic penumbra and returned >0.65 if penumbra disappeared. The two ratios no longer correlated after structural lesion developed, as N20 detected in the damaged side remained pathological (ratio <0.65), whereas 1/vMCA reverted to symmetric interhemispheric state (ratio >0.65), suggesting a luxury perfusion.

Conclusion: Variations of interhemispheric ratios of MCA resistance and cortical N20 amplitude correlate closely in SAH and allow identification of the reversible ischemic penumbra threshold, when both ratios become <0.65. The correlation is lost when structural damage develops.

No MeSH data available.


Related in: MedlinePlus

Patient No. 2 showed parallel courses of very low N20 and 1/v MCA ratio (<0.65) detected in the first three examinations (a, points 1to 3), corresponding with CT image of hypodesity of the right capsula (b, point 2); in the subsequent examinations, the divergent courses of N20 (< 0.65) and 1/vMCA (>0.65) and non correlated ratios (p= 0.2 r = 0.46, C.I. for r : -0.28 to 0.86) corresponded with CT and MRI images of structural infarct in the same area (b, point 4 and 8). Right N20 amplitude was < 1.2µV at points 1to 3 and 6 to7 (see examinations 2,3,4,7,8 in Table 3) and =< 1.5 µV at points 4,5, 8and 9 (see examinations 5,6,9,10 in Table 3); right MCA vasospasm (BFV >120 <180 cm/sec) was detected at points 1to 6. Clinical hemiparesis was always evident. (N20 amplitude is expressed in µV and MCA blood flow velocity in cm/sec).
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Figure 10: Patient No. 2 showed parallel courses of very low N20 and 1/v MCA ratio (<0.65) detected in the first three examinations (a, points 1to 3), corresponding with CT image of hypodesity of the right capsula (b, point 2); in the subsequent examinations, the divergent courses of N20 (< 0.65) and 1/vMCA (>0.65) and non correlated ratios (p= 0.2 r = 0.46, C.I. for r : -0.28 to 0.86) corresponded with CT and MRI images of structural infarct in the same area (b, point 4 and 8). Right N20 amplitude was < 1.2µV at points 1to 3 and 6 to7 (see examinations 2,3,4,7,8 in Table 3) and =< 1.5 µV at points 4,5, 8and 9 (see examinations 5,6,9,10 in Table 3); right MCA vasospasm (BFV >120 <180 cm/sec) was detected at points 1to 6. Clinical hemiparesis was always evident. (N20 amplitude is expressed in µV and MCA blood flow velocity in cm/sec).

Mentions: During the survey all 16 patients were eligible. A total of 66 bilateral SSEP and TCCD were performed with the criteria of simultaneousness. Values of the 1/v MCA and N20 amplitude recorded on the compromised hemisphere of each patient, expressed as ratios of their respective contralaterals and compared to CT/MRI scan images of the corresponding MCA supplied area, N20 amplitude absolute value, presence/absence of vasospasm and lateralizing symptoms are shown in Tab.3. The 1/vMCA and N20 interhemispheric ratio of 40 examinations were analyzed in respect of 40 images of CT/MRI scan performed on the same day as the TCCD and SSEP. Sixteen examinations in eleven patients (group 1: patients No. 1,3,5,6,9,10,12,13,14,15,16) matched CT/MRI image of no brain damage in the area supplied by the MCA: all subjects showed a high level of symmetry between interhemispheric values of 1/vMCA and N20 amplitude (Fig. 1); both interside ratios were always >0,65 and showed correlation (p< 0,01, r = 078, 95% CI = 0,46 to 0,92). In this group, MCA unilateral vasospasm (mean flow velocity > 120 < 150 cm /sec, L.I.>3) or almost symmetric bilateral vasospasm (< 180 cm/sec, L.I.>3) was detected in 18,7% of examinations; N20 amplitudes were still bilaterally normal (>1,2 μV) and symmetric. Patients did not show lateralizing neurological defects or consciousness alteration at clinical evaluation (Table 4). Fourteen examinations in seven patients (group 2: patients No. 2,3,5,7,12,15,16) matched CT/MRI images of tissue alterations in unilateral MCA area (shift, oedema, tissue hypodensity, cloth) or hydrocephalus. Both values of 1/vMCA and N20 amplitude on the compromised side were lower than contralateral and both interhemi-spheric ratios were always <0,65 in all these patients (p <0,01 r = 0,67, 95% CI = 0,23 to 0,88) (Fig. 2). Unilateral MCA vasospasm (mean flow velocity > 120 < 180 cm/sec and L.I. >3) was detected in 57% of overall examinations. N20 amplitudes on the compromised hemisphere were much lower than those on the contralateral in all patients, but still > 1,2 μV, except in patient No.2, who reached pathological amplitude (<1,2 μV) in several examinations. Corresponding lateralizing neurological defect of muscular strength or conciousness alteration was detected at clinical examination in all these patients (Table 5). Ten examinations in four patients (group 3: patients No.2,4,8,11) matched unilateral CT/MRI brain structural ischemic or hemorrhagic damage evidence; in all of them, resistance (1/vMCA) on the compromised side reverted to a high ratio to the contralateral (>0,65) and no longer correlated to the persistent interhemispheric asymmetry of N20 amplitude (ratio < 0,65) (Fig. 3); in this group correlation between the interhemispheric ratios of 1/MCA and N20 was lost (p=0.88, r = -0.05, 95% CI = -0.66 to 0.59). MCA vasospasm (mean flow velocity > 120< 165 cm /sec) was detected in 33,3% of examinations. The N20 value on the compromised hemispheres was pathologic (<1,2 μV) or absent in 9 examinations and all patients had stable hemiparesis or hemiplegia (Table 6). Patients No. 2, 3,5,12,15 belong to more than one group at different times, as a consequence of modification of their brain CT/MRI images during the survey; patient No.2 shifted from group 2 to 3; patients No. 3 and No.5 shifted from group 2 to 1; patients No.12 and No.15 shifted from group 1 to 2 and back to 1 again. In addition, we examined the course and correlation between the two interhemispheric ratios in those patients, seven in all, who were submitted to more than three examinations on different days. Statistic correlation (p<0.01) emerged in patient No. 9 (Fig. 4), who had no CT modifications and in those who showed transient unilateral alterations on CT/MRI in MCA supplied brain area and resumed a normal picture (patients No. 3, 5,12,15; Figs. 5-8). Interhemispheric modifications of 1/vMCA and N20 amplitude did not correlate in patients who had morphological brain damage on CT scan immediately after SAH (patient No.11, p = 0.89) (Fig. 9) or who subsequently developed brain injury (patient No.2, p = 0.2) (Fig. 10a,b).


Correlation of transcranial color Doppler to n20 somatosensory evoked potential detects ischemic penumbra in subarachnoid hemorrhage.

Di Pasquale P, Zanatta P, Morghen I, Bosco E, Forini E - Open Neurol J (2011)

Patient No. 2 showed parallel courses of very low N20 and 1/v MCA ratio (<0.65) detected in the first three examinations (a, points 1to 3), corresponding with CT image of hypodesity of the right capsula (b, point 2); in the subsequent examinations, the divergent courses of N20 (< 0.65) and 1/vMCA (>0.65) and non correlated ratios (p= 0.2 r = 0.46, C.I. for r : -0.28 to 0.86) corresponded with CT and MRI images of structural infarct in the same area (b, point 4 and 8). Right N20 amplitude was < 1.2µV at points 1to 3 and 6 to7 (see examinations 2,3,4,7,8 in Table 3) and =< 1.5 µV at points 4,5, 8and 9 (see examinations 5,6,9,10 in Table 3); right MCA vasospasm (BFV >120 <180 cm/sec) was detected at points 1to 6. Clinical hemiparesis was always evident. (N20 amplitude is expressed in µV and MCA blood flow velocity in cm/sec).
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Figure 10: Patient No. 2 showed parallel courses of very low N20 and 1/v MCA ratio (<0.65) detected in the first three examinations (a, points 1to 3), corresponding with CT image of hypodesity of the right capsula (b, point 2); in the subsequent examinations, the divergent courses of N20 (< 0.65) and 1/vMCA (>0.65) and non correlated ratios (p= 0.2 r = 0.46, C.I. for r : -0.28 to 0.86) corresponded with CT and MRI images of structural infarct in the same area (b, point 4 and 8). Right N20 amplitude was < 1.2µV at points 1to 3 and 6 to7 (see examinations 2,3,4,7,8 in Table 3) and =< 1.5 µV at points 4,5, 8and 9 (see examinations 5,6,9,10 in Table 3); right MCA vasospasm (BFV >120 <180 cm/sec) was detected at points 1to 6. Clinical hemiparesis was always evident. (N20 amplitude is expressed in µV and MCA blood flow velocity in cm/sec).
Mentions: During the survey all 16 patients were eligible. A total of 66 bilateral SSEP and TCCD were performed with the criteria of simultaneousness. Values of the 1/v MCA and N20 amplitude recorded on the compromised hemisphere of each patient, expressed as ratios of their respective contralaterals and compared to CT/MRI scan images of the corresponding MCA supplied area, N20 amplitude absolute value, presence/absence of vasospasm and lateralizing symptoms are shown in Tab.3. The 1/vMCA and N20 interhemispheric ratio of 40 examinations were analyzed in respect of 40 images of CT/MRI scan performed on the same day as the TCCD and SSEP. Sixteen examinations in eleven patients (group 1: patients No. 1,3,5,6,9,10,12,13,14,15,16) matched CT/MRI image of no brain damage in the area supplied by the MCA: all subjects showed a high level of symmetry between interhemispheric values of 1/vMCA and N20 amplitude (Fig. 1); both interside ratios were always >0,65 and showed correlation (p< 0,01, r = 078, 95% CI = 0,46 to 0,92). In this group, MCA unilateral vasospasm (mean flow velocity > 120 < 150 cm /sec, L.I.>3) or almost symmetric bilateral vasospasm (< 180 cm/sec, L.I.>3) was detected in 18,7% of examinations; N20 amplitudes were still bilaterally normal (>1,2 μV) and symmetric. Patients did not show lateralizing neurological defects or consciousness alteration at clinical evaluation (Table 4). Fourteen examinations in seven patients (group 2: patients No. 2,3,5,7,12,15,16) matched CT/MRI images of tissue alterations in unilateral MCA area (shift, oedema, tissue hypodensity, cloth) or hydrocephalus. Both values of 1/vMCA and N20 amplitude on the compromised side were lower than contralateral and both interhemi-spheric ratios were always <0,65 in all these patients (p <0,01 r = 0,67, 95% CI = 0,23 to 0,88) (Fig. 2). Unilateral MCA vasospasm (mean flow velocity > 120 < 180 cm/sec and L.I. >3) was detected in 57% of overall examinations. N20 amplitudes on the compromised hemisphere were much lower than those on the contralateral in all patients, but still > 1,2 μV, except in patient No.2, who reached pathological amplitude (<1,2 μV) in several examinations. Corresponding lateralizing neurological defect of muscular strength or conciousness alteration was detected at clinical examination in all these patients (Table 5). Ten examinations in four patients (group 3: patients No.2,4,8,11) matched unilateral CT/MRI brain structural ischemic or hemorrhagic damage evidence; in all of them, resistance (1/vMCA) on the compromised side reverted to a high ratio to the contralateral (>0,65) and no longer correlated to the persistent interhemispheric asymmetry of N20 amplitude (ratio < 0,65) (Fig. 3); in this group correlation between the interhemispheric ratios of 1/MCA and N20 was lost (p=0.88, r = -0.05, 95% CI = -0.66 to 0.59). MCA vasospasm (mean flow velocity > 120< 165 cm /sec) was detected in 33,3% of examinations. The N20 value on the compromised hemispheres was pathologic (<1,2 μV) or absent in 9 examinations and all patients had stable hemiparesis or hemiplegia (Table 6). Patients No. 2, 3,5,12,15 belong to more than one group at different times, as a consequence of modification of their brain CT/MRI images during the survey; patient No.2 shifted from group 2 to 3; patients No. 3 and No.5 shifted from group 2 to 1; patients No.12 and No.15 shifted from group 1 to 2 and back to 1 again. In addition, we examined the course and correlation between the two interhemispheric ratios in those patients, seven in all, who were submitted to more than three examinations on different days. Statistic correlation (p<0.01) emerged in patient No. 9 (Fig. 4), who had no CT modifications and in those who showed transient unilateral alterations on CT/MRI in MCA supplied brain area and resumed a normal picture (patients No. 3, 5,12,15; Figs. 5-8). Interhemispheric modifications of 1/vMCA and N20 amplitude did not correlate in patients who had morphological brain damage on CT scan immediately after SAH (patient No.11, p = 0.89) (Fig. 9) or who subsequently developed brain injury (patient No.2, p = 0.2) (Fig. 10a,b).

Bottom Line: Both ratios became <0.65 (p <0.01) when patients showed unilateral images of ischemic penumbra and returned >0.65 if penumbra disappeared.Variations of interhemispheric ratios of MCA resistance and cortical N20 amplitude correlate closely in SAH and allow identification of the reversible ischemic penumbra threshold, when both ratios become <0.65.The correlation is lost when structural damage develops.

View Article: PubMed Central - PubMed

Affiliation: Anaesthesia and Intensive Care Department, Rovigo Hospital, Viale 3 Martiri, 140, 45100 Rovigo, Italy.

ABSTRACT

Background: Normal subjects present interhemispheric symmetry of middle cerebral artery (MCA) mean flow velocity and N20 cortical somatosensory evoked potential (SSEP). Subarachnoid haemorrhage (SAH) can modify this pattern, since high regional brain vascular resistances increase blood flow velocity, and impaired regional brain perfusion reduces N20 amplitude. The aim of the study is to investigate the variability of MCA resistances and N20 amplitude between hemispheres in SAH.

Methods: Measurements of MCA blood flow velocity (vMCA) by transcranial color-Doppler and median nerve SSEP were bilaterally performed in sixteen patients. MCA vascular changes on the compromised hemisphere were calculated as a ratio of the reciprocal of mean flow velocity (1/vMCA) to contralateral value and correlated to the simultaneous variations of interhemispheric ratio of N20 amplitude, within each subject. Data were analysed with respect to neuroimaging of MCA supplied areas.

Results: Both interhemispheric ratios of 1/vMCA and N20 amplitude were detected >0.65 (p <0,01) in patients without neuroimages of injury. Both ratios became <0.65 (p <0.01) when patients showed unilateral images of ischemic penumbra and returned >0.65 if penumbra disappeared. The two ratios no longer correlated after structural lesion developed, as N20 detected in the damaged side remained pathological (ratio <0.65), whereas 1/vMCA reverted to symmetric interhemispheric state (ratio >0.65), suggesting a luxury perfusion.

Conclusion: Variations of interhemispheric ratios of MCA resistance and cortical N20 amplitude correlate closely in SAH and allow identification of the reversible ischemic penumbra threshold, when both ratios become <0.65. The correlation is lost when structural damage develops.

No MeSH data available.


Related in: MedlinePlus