Hostname: page-component-cd9895bd7-gvvz8 Total loading time: 0 Render date: 2024-12-28T02:01:04.410Z Has data issue: false hasContentIssue false

TCD Diastolic Velocity Decay and Pulsatility Index Increment in PVS Cases

Published online by Cambridge University Press:  23 September 2016

Jesús Perez-Nellar
Affiliation:
Hermanos Ameijeiras Hospital, Service of Neurology
Calixto Machado*
Affiliation:
Institute of Neurology and Neurosurgery, Department of Clinical Neurophysiology, Havana, Cuba
Claudio E. Scherle
Affiliation:
Hermanos Ameijeiras Hospital, Service of Neurology
Mauricio Chinchilla
Affiliation:
Hermanos Ameijeiras Hospital, Service of Neurology
*
Institute of Neurology and Neurosurgery, Apartado Postal 4268, Ciudad de La Habana, 10400, Cuba
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

Functional neuroimaging has provided new insights for assessing cerebral function in persistent vegetative state patients (PVS). Compared to controls, positron emission tomography and single photon emission tomography have shown a substantial reduction of global brain cerebral glucose metabolism and perfusion in PVS. Doppler ultrasonography (TCD) assesses local blood flow velocity and direction in the proximal portions of large intracranial arteries; it is a noninvasive technique, and it can be carried out at the bedside. To date, few studies have applied TCD to study PVS.

Methods:

We assessed intracranial circulation by TCD in five PVS patients. The cause of brain insult was hypoxic encephalopathy in four cases, and the other suffered an embolic cerebral infarct causing a top of the basilar artery syndrome. The sample volume was set at 12 mm; power output and gain settings were maximized as needed. The temporal bone acoustic window was not suitable for intracranial vessel insonation in all patients. As an alternative, the internal carotid artery siphon was assessed by orbital insonation between 55-70 mm.

Results:

Systolic velocity was within a normal range, between 44 and 62 cm/second in all cases. However, the diastolic amplitude was reduced, as well as the end diastolic velocity, and the pulsatility index was increased in all patients.

Conclusions:

We conclude that TCD diastolic velocity decrement and PI augmentation in our cases might be related to uncoupling of cerebral blood flow and cerebral metabolic rate, arising from reduced cerebral glucose consumption and oxygen uptake, after extensive brain injury.

Résumé

RésuméContexte:

La neuroimagerie fonctionnelle a fourni de nouvelles avenues pour l'évaluation de la fonction cérébrale chez les patients en état végétatif persistant (EVP). La tomographie par émission de positons et la tomographie par émission d'un seul photon ont démontré une diminution substantielle du métabolisme et de la perfusion cérébrale du glucose dans tout le cerveau chez les patients en EVP par rapport aux sujets témoins. L'échographie Doppler (ED) évalue la vélocité du flux sanguin local et sa direction dans les portions proximales des grosses artères intracrâniennes. C'est une technique non effractive et elle peut être effectuée au chevet du patient. Cependant peu d'études ont utilisé l'ED pour étudier l'EVP.

Méthodologie:

Nous avons évalué la circulation intracrânienne par ED chez 5 patients en EVP. Une encéphalopathie hypoxique était la cause du dommage cérébral chez 4 patients et l'autre avait subi un infarctus cérébral par embolie à la bifurcation du tronc cérébral (top of the basilar artery syndrome). Le volume de l'échantillon était fixé à 12 mm et le réglage de la puissance de sortie et du gain étaient maximisés au besoin. La fenêtre acoustique de l'os temporal n'était pas propice à l'échographie des vaisseaux intracrâniens chez tous nos patients. Le siphon de la carotide interne a été évalué par échographie orbitaire entre 55-70 mm chez ces patients.

Résultats:

La vélocité systolique était dans l'écart normal, entre 44 et 62 cm par seconde, chez tous les patients. Cependant, l'amplitude diastolique était réduite de même que la vélocité en fin de diastole et l'indice de pulsatilité (IP) était diminué chez tous les patients.

Conclusions:

Nous concluons que la diminution de la vélocité diastolique à l'ED et l'augmentation de l'IP chez nos patients pourraient être reliées à un découplage du flux sanguin cérébral et du taux de métabolisme cérébral suite à une consommation réduite de glucose et d'oxygène au niveau du cerveau après un dommage cérébral important.

Type
Original Articles
Copyright
Copyright © The Canadian Journal of Neurological 2010

References

1. Giacino, J, Whyte, J. The vegetative and minimally conscious states: current knowledge and remaining questions. J Head Trauma Rehabil. 2005; 20:3050.10.1097/00001199-200501000-0000515668569Google Scholar
2. Jennett, B, Plum, F. Persistent vegetative state after brain damage. A syndrome in search of a name. Lancet. 1972; 1:734–7.Google Scholar
3. Vanhaudenhuyse, A, Noirhomme, Q, Tshibanda, LJ, Bruno, MA, Boveroux, P, Schnakers, C, et al. Default network connectivity reflects the level of consciousness in non-communicative braindamaged patients. Brain. 2010; 133(Pt 1):161–71.10.1093/brain/awp31320034928Google Scholar
4. Giacino, JT, Malone, R. The vegetative and minimally conscious States. Handb Clin Neurol. 2008; 90:99111.18631819Google Scholar
5. Owen, AM, Coleman, MR. Detecting awareness in the vegetative state. Ann N Y Acad Sci. 2008; 1129:130–8.10.1196/annals.1417.01818591475Google Scholar
6. Tshibanda, L, Vanhaudenhuyse, A, Boly, M, Soddu, A, Bruno, MA, Moonen, G, et al. Neuroimaging after coma. Neuroradiology. 2010; 52(1):1524.10.1007/s00234-009-0614-819862509Google Scholar
7. Monti, MM, Coleman, MR, Owen, AM. Neuroimaging and the vegetative state resolving the behavioral assessment dilemma? Ann NY Acad Sci. 2009; 1157:81–9.10.1111/j.1749-6632.2008.04121.x19351358Google Scholar
8. Machado, C, Korein, J, Aubert, E, Bosch, J, Alvarez, MA, Rodríguez, R, et al. Recognizing a mother’s voice in the persistent vegetative state. Clin EEG Neurosci. 2007; 38(3):124–6..10.1177/15500594070380030617844939Google Scholar
9. Machado, C. Brain death. A reappraisal. New York: Springer; 2007: p. 1223.Google Scholar
10. Machado, C. Persistent vegetative and minimally conscious states. Rev Neurosci. 2009; 20(3–4):203–20.20157991Google Scholar
11. Laureys, S, Owen, AM, Schiff, ND. Brain function in coma, vegetative state, and related disorders. Lancet Neurol. 2004; 3:537–46.10.1016/S1474-4422(04)00852-X15324722Google Scholar
12. Boly, M, Faymonville, ME, Schnakers, C, Peigneux, P, Lambermont, B, Phillips, C, et al. Perception of pain in the minimally conscious state with PET activation: an observational study. Lancet Neurol. 2008; 7(11):1013–20.10.1016/S1474-4422(08)70219-918835749Google Scholar
13. Nakayama, N, Okumura, A, Shinoda, J, Nakashima, T, Iwama, T. Relationship between regional cerebral metabolism and consciousness disturbance in traumatic diffuse brain injury without large focal lesions: an FDG-PET study with statistical parametric mapping analysis. J Neurol Neurosurg Psychiatry. 2006; 77(7):856–62.10.1136/jnnp.2005.0805231654941510.1136/jnnp.2005.080523Google Scholar
14. Owen, AM, Coleman, MR, Menon, DK, Johnsrude, IS, Rodd, JM, Davis, MH, et al. Residual auditory function in persistent vegetative state: a combined PET and fMRI study. Neuropsychol Rehabil. 2005; 15:290306.10.1080/0960201044300057916350973Google Scholar
15. Beuthien-Baumann, B, Holthoff, VA, Rudolf, J. Functional imaging of vegetative state applying single photon emission tomography and positron emission tomography. Neuropsychol Rehabil. 2005; 15:276–82.10.1080/0960201044300029016350971Google Scholar
16. Friedlich, D, Agner, C, Boulos, AS, Mesfin, F, Feustel, P, Bernardini, GL, et al. Retrospective analysis of parenteral magnesium sulfate administration in decreased incidence of clinical and neuroradiological cerebral vasospasm: a single center experience. Neurol Res. 2009; 31(6):621–5.10.1179/174313209X3823219660191Google Scholar
17. White, H, Venkatesh, B. Applications of transcranial Doppler in the ICU: a review. Intensive Care Med. 2006; 32(7):981–94.10.1007/s00134-006-0173-y1679166110.1007/s00134-006-0173-yGoogle Scholar
18. Rasulo, EA, De Peri, E, Lavinio, A. Transcranial Doppler ultrasonography in intensive care. Eur J Anaesthesiol Suppl. 2008; 42:167–73.18289437Google Scholar
19. Conti, A, Iacopino, DG, Spada, A, Cardali, SM, Giusa, M, La Torre, D, et al. Transcranial Doppler ultrasonography in the assessment of cerebral circulation arrest: improving sensitivity by transcervical and transorbital carotid insonation and serial examinations. Neurocrit Care. 2009; 10:326–35.10.1007/s12028-009-9199-719238589Google Scholar
20. Shan, G, Yining, H, Xia, H, Yicheng, Z, Bo, W, Shunwei, L. Transcranial Doppler characteristics in persistent vegetative status, locked-in syndrome and brain death. Chin Med Sci J. 1999; 14:211–14.12894893Google Scholar
21. Shiogai, T, Koshimura, M, Uebo, C, Makino, M, Mizuno, T, Nakajima, K. Acetazolamide vasoreactivity in persistent vegetative state and vascular dementia evaluated by transcranial harmonic perfusion imaging and Doppler sonography. Acta Neurochir Suppl. 2003; 87:63–9.14518526Google Scholar
22. Giacino, JT, Kalmar, K, Whyte, J. The JFK Coma Recovery Scale-Revised: measurement characteristics and diagnostic utility. Arch Phys Med Rehabil. 2004; 85:2020–9.10.1016/j.apmr.2004.02.03315605342Google Scholar
23. Aggarwal, S, Brooks, DM, Kang, Y, Linden, PK, Patzer, JF 2nd. Noninvasive monitoring of cerebral perfusion pressure in patients with acute liver failure using transcranial doppler ultrasonography. Liver Transpl. 2008; 14:1048–57.10.1002/lt.2149918581484Google Scholar
24. Perez-Nellar, J, Scherle, C, Machado, C. TCD systolic spikes in a malignant MCA infarct. Neurocrit Care. 2009; 11:94–6.10.1007/s12028-009-9216-x19381882Google Scholar
25. Miao, J, Benkeser, PJ, Nichols, FT. A computer-based statistical pattern recognition for Doppler spectral waveforms of intracranial blood flow. Comput Biol Med. 1996; 26:5363.10.1016/0010-4825(95)00029-18654053Google Scholar
26. Jorgensen, LG. Transcranial Doppler ultrasound for cerebral perfusion. Acta Physiol Scand Suppl. 1995; 625:144.Google Scholar
27. Brinck, HP, Gran, L, Larsen, JL. [Delay of retinal fluorescence as a death criterion]. Can Anaesth Soc J. 1979; 26:309–12.10.1007/BF03006292509347Google Scholar
28. Larsen, FS, Pott, F, Hansen, BA, Ejlersen, E, Knudsen, GM, Clemmesen, JD, et al. Transcranial Doppler sonography may predict brain death in patients with fulminant hepatic failure. Transplant Proc. 1995; 27:3510–11.8540074Google Scholar
29. Larsen, FS, Strauss, G, Knudsen, GM, Herzog, TM, Hansen, BA, Secher, NH. Cerebral perfusion, cardiac output, and arterial pressure in patients with fulminant hepatic failure. Crit Care Med. 2000; 28:9961000.10.1097/00003246-200004000-0001410809272Google Scholar
30. Strauss, GI, Høgh, P, Møller, K, Knudsen, GM, Hansen, BA, Larsen, FS. Regional cerebral blood flow autoregulation in patients with fulminant hepatic failure. Liver Transpl. 2000; 6:795800.10.1053/jlts.2000.1870511084071Google Scholar
31. Hassler, W, Steinmetz, H, Pirschel, J. Transcranial Doppler study of intracranial circulatory arrest. J Neurosurg. 1989; 71:195201.10.3171/jns.1989.71.2.0195266409Google Scholar
32. Martinelli, O, Benedetti-Valentini, F. Trancranial Doppler: value in clinical practice. Int Angiol. 2009; 28(4):249–53.19648867Google Scholar
33. Gur, AY, Kesler, A, Shopin, L, Bornstein, NM. Transcranial Doppler for evaluation of idiopathic intracranial hypertension. Acta Neurol Scand. 2007; 116:239–42.10.1111/j.1600-0404.2007.00861.x17824902Google Scholar
34. Calleja, S, Tembl, JI, Segura, T; Sociedad Española de Neurosonología. [Recommendations of the use of transcranial Doppler to determine the existence of cerebral circulatory arrest as diagnostic support of brain death]. Neurologia. 2007; 22(7):441–7.17853962Google Scholar
35. Smith, EE, Vijayappa, M, Lima, F, Delgado, P, Wendell, L, Rosand, J, et al. Impaired visual evoked flow velocity response in cerebral amyloid angiopathy. Neurology. 2008; 71:1424–30.10.1212/01.wnl.0000327887.64299.a418955685Google Scholar
36. Vokatch, N, Grótzsch, H, Mermillod, B, Burkhard, PR, Sztajzel, R. Is cerebral autoregulation impaired in Parkinson’s disease? A transcranial Doppler study. J Neurol Sci. 2007; 254:4953.Google Scholar
37. Weber, BB, Kerr, ME, Wechsler, LR, Marion, DW. Absence of a diastolic velocity notch does not indicate hyperemia in traumatic brain injured patients without elevated cerebral blood flow velocity. J Neurosurg Anesthesiol. 2002; 14:279–86.10.1097/00008506-200210000-0000212357084Google Scholar
38. Ingvar, DH, Lassen, NA. Cerebral function, metabolism and blood flow. News and trends from the VIIIth international CBF symposium in Copenhagen, June 1977. Acta Neurol Scand. 1978; 57:262–9.10.1111/j.1600-0404.1978.tb05874.x665148Google Scholar
39. Lassen, NA, Ingvar, DH. Brain regions involved in voluntary movements as revealed by radioisotopic mapping of CBF or CMR-glucose changes. Rev Neurol (Paris). 1990; 146:620–5.Google Scholar
40. Mintun, MA, Lundstrom, BN, Snyder, AZ, Vlassenko, AG, Shulman, GL, Raichle, ME. Blood flow and oxygen delivery to human brain during functional activity: theoretical modeling and experimental data. Proc Natl Acad Sci U S A. 2001; 98:6859–64.10.1073/pnas.11116439811381119Google Scholar
41. Paulson, OB, Hasselbalch, SG, Rostrup, E, Knudsen, GM, Pelligrino, D. Cerebral blood flow response to functional activation. J Cereb Blood Flow Metab. 2010; 30(1):214.10.1038/jcbfm.2009.18819738630Google Scholar
42. Owen, AM, Coleman, MR. Using neuroimaging to detect awareness in disorders of consciousness. Funct Neurol. 2008; 23:189–94.19331781Google Scholar
43. Owen, AM, Coleman, MR. Functional neuroimaging of the vegetative state. Nat Rev Neurosci. 2008; 9:235–43.10.1038/nrn233018285801Google Scholar
44. Coleman, MR, Davis, MH, Rodd, JM, Robson, T, Ali, A, Owen, AM, et al. Towards the routine use of brain imaging to aid the clinical diagnosis of disorders of consciousness. Brain. 2009; 132:2541–52.10.1093/brain/awp18319710182Google Scholar
45. Kassubek, J, Juengling, FD, Els, T, Spreer, J, Herpers, M, Krause, T, et al. Activation of a residual cortical network during painful stimulation in long-term postanoxic vegetative state: a 15O-H2O PET study. J Neurol Sci. 2003; 212:8591.10.1016/S0022-510X(03)00106-012810004Google Scholar
46. Conti, A, Iacopino, DG, Spada, A, Cardali, SM, Giusa, M, La Torre, D, et al. Transcranial Doppler ultrasonography in the assessment of cerebral circulation arrest: improving sensitivity by trancervical and transorbital carotid insonation and serial examinations. Neurocrit Care. 2009; 10:326–35.10.1007/s12028-009-9199-719238589Google Scholar
47. Kwon, JH, Kim, JS, Kang, DW, Bae, KS, Kwon, SU. The thickness and texture of temporal bone in brain CT predict acoustic window failure of transcranial Doppler. J Neuroimaging. 2006; 16:347–52.10.1111/j.1552-6569.2006.00064.x17032385Google Scholar
48. Kinney, HC, Samuels, MA. Neuropathology of the persistent vegetative state. A review. J Neuropathol Exp Neurol. 1994; 53:548–58.10.1097/00005072-199411000-000027964896Google Scholar
49. Adams, JH, Graham, DI, Jennett, B. The neuropathology of the vegetative state after an acute brain insult. Brain. 2000; 123(Pt 7):1327–38.10.1093/brain/123.7.132710869046Google Scholar
50. Graham, DI, Maxwell, WL, Adams, JH, Jennett, B. Novel aspects of the neuropathology of the vegetative state after blunt head injury. Prog Brain Res. 200 Google Scholar