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Indice/Contents Nº 4

 

ACUTE BRAINSTEM INFARCT: MULTIDISCIPLINARY MANAGEMENT

Dr. Francisco Mena G., Dr. Manuel Fruns Q., Dra. Andrea Contreras S., Dr. Francisco Soto S, Dr. Ismael Mena G.

Centro Cerebro-Vascular
Clínica Las Condes
Santiago, Chile.

Correspondence:

Author’s address:

fmena@cybercenter.cl

Cita/Reference:
Mena, F. et al. Acute Brainstem Infarct: Multidisciplinary Management. Alasbimn Journal2(5): October 1999. http://www.alasbimnjournal.cl/revistas/5/mena.htm

 

Vertebro-basilar thrombosis has a high mortality rate between 75% to 86% (1). The clinical diagnosis of these patients is sometimes difficult and their medical management is not well defined. Prospective, multicenter, controlled studies have demonstrated that intravenous thrombolysis as well as intra-arterial are valid and efficacious for the treatment of acute cerebral infarct (2-3). Neuro-endovascular therapy has acquired an increasingly more active role in the treatment of brain attack (4).

We present a clinical case of acute thromboembolic occlusion of the basilar artery secondary to a traumatic dissection of the vertebral artery, which had an unusually long presentation and difficult diagnosis. The patient received a multidisciplinary medical management, which required intra-arterial thrombolysis. We discuss the clinical presentation of vertebro-basilar isquemia, the technique of intra-arterial thrombolysis, and medical management of hemodynamic factors and also the utility of brain HMPAO SPECT study in the medical management of acute brain infarct.

 

CLINICAL CASE:

The patient is an 18 year old male, without past medical history, transferred to Clinica Las Condes (CLC) from a small city in southern Chile called Villarica, arriving in neurologic and respiratory compromise, on mechanical ventilation. 48 hours before he had fell while playing soccer without suffering loss of consciousness. That same night he began experiencing disarthria, headache, and transient hemiparesis. The following day he was hospitalized in a local hospital. An initial brain computed tomography (CT) scan was normal. To follow, he had a generalized seizure, and his neurological state worsened and was transferred to CLC. Upon arrival to the CLC hospital, the patient was on mechanical ventilation and had been in coma for about one hour. A new CT scan only showed a possible small area of hypodensity in the pons without hemorrhage. Retrospectively, it is possible to distinguish a "hyperdense basilar artery" (Figure 1a). Immediately we performed a cerebral angiogram since we had a clinical suspicion of a possible carotid or vertebral dissection considering the history of trauma. When we began the angiogram he had been about two hours in coma, had fixed and dilated pupils, and had extensor pronation in all four extremities upon painful stimuli. In addition, he had bilateral repetitive myoclonic discharges related to brainstem ischemia.

The initial cerebral angiogram demonstrated complete occlusion of the superior segment of the basilar artery. Also, the distal segment of the right vertebral artery showed a focal stenosis and irregularity of the vessel wall, which corresponded to a dissection. Intra-arterial thrombolysis was initiated advancing a microcatheter to the occlusion at the basilar artery. A total of 700,000 units of Urokinase (UK) were infused over 30 minutes, achieving complete recanalization of the basilar artery and its principal branches. Lastly, the right vertebral artery was therapeutically occluded with GDC coils at the C2 level, just proximal to the dissection (Figure 2). Immediately post-thrombolysis, the patient once again had symmetric and reactive pupils, and localized to painful stimuli with all four extremities. A control brain CT scan showed hyperdensity in the center and left side of the pons, corresponding to a small asymptomatic hemorrhage post-thrombolysis (Figure 1b). The patient was transferred to the ICU and began hemodilution, hypervolemic, and hypertensive therapy with mean arterial pressure (MAP) of 120mm of Mercury (Hg). He was not anticoagulated.


Figure 1
Figure 1 (click=zoom)
Figure 2
Figure 2 (click= zoom)

The HMPAO brain SPECT exam performed the following day demonstrated a region of hypoperfusion 2 and 4 standard deviations below the mean in the brainstem, more extensive than the area of hemorrhage and infarct in the pons and left cerebral peduncle (Figure 3a). This finding was interpreted as a region of ischemic penumbra, which was treated with hypervolemic and hypertensive therapy. A brain magnetic resonance scan showed an infarct in most of the pons, predominantly on the left side, with only the most lateral right side remaining normal (Figure 4). During the following days, the patient made a progressive recovery.
Figure 3
Figure 3 (click =zoom)
Figure 4
Figure 4 (click=zoom)
 

A week later, when the patient was placed in the erect position for the first time during his rehabilitation session, he had an acute neurologic decline with increased hemiparesis and transient bilateral myoclonic discharges related to the hemodynamic effect of orthostatic hypotension. A brain CT did not demonstrate any significant change in the size of the brainstem infarct (Figure 1c). This event was interpreted as hemodynamic in origin, secondary to hypoperfusion in a zone of ischemic penumbra in the pons, which was immediately and energetically controlled with hypervolemic therapy. The patient completely recovered of these symptoms in a few days. At day 18, he began oral intake, and had partially recovered movements of his vocal cords. Controls with brain HMPAO SPECT scan showed cerebellar diasquesis with hypoperfusion of the inferior right cerebellar hemisphere. There was also increased uptake in the pons, which was interpreted as secondary to breakdown of the blood brain barrier (Figure 3b). The rest of the study was normal. After two months of inpatient rehabilitation, the patient made almost a complete recovery and was discharged.

DISCUSSION

The clinical presentation of basilar artery thrombosis is variable, but its evolution is commonly bad. Out patient had an atypical prolonged presentation of approximately 48 hours, with symptoms of transient and recurrent vertebro-basilar ischemia, including disarthria, hemiplagia, headache and vertigo and finally loss of consciousness. He arrived in a state of coma of about 1-2 hours in duration prior to the procedure.

The medical management of the patient upon arrival to our institution included stabilizing his cardiorespiratory function. The etiology of the clinical presentation of our patient was immediately evident. In fact, the clinical presentation of vertebro-basilar isquemia can be sometimes nonspecific. In this patient, the initial symptoms were not specific, and considering that the patient had 48 hours of symptomatology, it was possible to consider other etiologies in addition to isquemia, including an inflammatory process. Nevertheless, we opted to investigate the most urgently treatable etiology first, like a cerebro-vascular occlusion, possibly related to an arterial dissection considering the history of trauma. The cerebral angiogram showed a basilar occlusion embolic in origin, related to a traumatic vertebral dissection at the skull base level. Considering the poor prognosis of this lesion and also that the patient had been in coma for only 1-2 hours with no or minimal brain CT changes, we elected to perform intra-arterial thrombolysis. In the posterior circulation, there does not exist a limit as to the amount of time elapse from the beginning of the symptoms to perform thrombolysis, like exists in the anterior circulation of 3-6 hours. This is because thrombosis of the basilar artery has extremely high mortality and therefore thrombolysis is the only viable therapeutic alternative. Also, as an anecdotal observation, it may be that neuronal tissue in the pons, which is predominantly axonal, may be less vulnerable to isquemia. It is therefore, the clinical presentation and not the time elapse that directs the therapeutic conduct. If the patient is still not in coma, or if in coma, only for a short duration, the patient is a candidate for thrombolysis. We decided to perform thrombolysis intra-arterially and not intravenously, since the intra-arterial route of administration is associated with a higher recanalization rate (60-90% intra-arterial versus 30-50% intravenous) (12-13).

After having achieved an excellent result of recanalization, we decided to occlude the right vertebral artery proximal to the region of the dissection, in order to eliminate the possibility of another thrombus dislodging from the dissection site and the antegrade flow causing another thromboembolic occlusion of the basilar artery. It was possible to occlude the right vertebral artery since the right posterior inferior cerebellar artery (PICA) filled from retrograde flow from the left vertebral artery (Figure 2). A case report similar to ours was recently published which instead of occluding the damaged vessel with the dissection, it was possible to stabilize the segment with the dissection with angioplasty and stenting (7).

The first clinical series of intra-arterial thrombolysis for acute vertebro-basilar isquemia was published by Zeumer et al in 1983 (11). The results of clinical series of intra-arterial thrombolysis in the posterior circulation show a mortality of approximately of 25-50% (1,6). Patients that present in coma, like our case, have a higher mortality (1,6). In the series of Bercker et al. (6) there was a 100% mortality (3/3) for patients who presented in coma, even when a successful recanalization was obtained with intra-arterial thrombolysis. Other factors which are associated to a higher mortality rate include inability to obtain recanalization with thrombolysis, rethrombosis and hemorrhage post thrombolysis. The incidence of hemorrhage post vertebro-basilar thrombolysis is 0 - 15% (1,5). In the series of Bercke (6) 8 of 9 patients with imaging signs of infarct before thrombolysis did not have a hemorrhagic event post-thrombolysis. Our patient developed a small hemorrhage in the region of the infarct in the pons, without clinical manifestations.

Angiografic factors which are associated with a better outcome are the localization of the occlusion in the basilar in its distal segment, and the presence of bilateral posterior communicating arteries since from these can arise small perforating vessels that also supply the territory of thalamoperforators, in addition to the both posterior cerebral arteries. Also important is the location and severity of the brainstem infarct. Our patient had an excellent recovery even in the presence of a large pontine infarct.

The medical management of our patient after the thrombolysis included hypervolemic and hypertensive therapy. This type of treatment was maintained for about a week, keeping MAP between 100-120mm/Hg. Even several weeks after the pontine infarct event, the patient remained dependent on normal arterial pressures and was sensitive to any orthostatic hypotension event. After an abrupt neurological decline in relation to a hemodynamic event during a rehabilitation session, the patient responded rapidly to hypervolemic therapy.

The aggressive hemodynamic management was essential in order to better provide blood flow to the zone of isquemic penumbra around the infarct region in the pons. The zone of isquemic penumbra was first seen on the initial brain HMPAO SPECT study, and later controlled with other follow-up exams. The brain SPECT technology is able to identify a zone of hypoperfusion in the cerebral hemispheres (8-10). This case demonstrated that NeuroSPECT is also able to evaluate the perfusion of the brainstem.

CONCLUSION

Vertebro-basilar thrombosis has a very high mortality rate. Our patient, who presented in coma secondary to a thromboembolic occlusion of the basilar artery 48 hours in evolution, had a successful recovery after an aggressive multidisciplinary management, which included endovascular recanalization of the occlusion with intra-arterial thrombolysis. This clinical recovery was possible even in the presence of an established pontine infarct. The brain HMPAO SPECT studies were an important aid in estimating the zone of isquemic penumbra and thus helps direct the hemodynamic factors of the medical management.

 

REFERENCES

1. Hacke W, Zeumer H, Ferbert A, Bruckmann H, del Zoppo GJ. Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar disease. Stroke 1988; 19:1216-1222.

2. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;333:1581-1587.

3. Furlan AJ, Higashida RT, Wechsler L, Schulz, PROACT II Inverstigators. PROACT II: recombinant Prov-U- Sep (r-ProUK) in acute cerebral thromboembolism. Initial trial results. Stroke 1999;30:234. Abstract.

4. Mena F, Viñuela F. Terapia endovascular del ataque cerebral. Rev Médica Clínica Las Condes 1998;9(2):49-53.

5. Zeumer H, Freitag HJ, Zanella F, Thie A, Arning C. Local intra-arterial fibrinolytic therapy in patients with stroke: urokinase versus recombinant tissue plasminogen activator (r-TPA). Neuroradiology 1993;35:159-162.

6. Becker KJ, Monsein LH, Ulatowske J, Mirski M, Williams M, Hanley DF. Intraarterial Trombolysis in Vertebrobasilar Occlusion. AJNR 1996;17:255-262.

7. Price RF, Sellar R, Leung C, O´Sullivan MJ. Traumatic vertebral arterial dissection and vertebrobasilar arterial thrombosis successfully treated with endovascular trombolysis and stenting. AJNR 1998;19:1677-1680.

8. Mena F, Mena I, Soto F, Ducci H, Contreras A, Fruns M. Neuro-SPECT evaluation of carotid stenosis before and after angioplasty and stenting. Alasbimn Journal 1999,1(4). http://www.alasbimnjournal.cl/revistas/4/mena.htm

9. Ueda T, Hatakeyama T, Kumon Y, Sakaki S, Uraoka T. Evaluation of risk of hemorrhagic transformation in local intra-arterial trombolysis in acute ischemic stroke by initial SPECT. Stroke 1994;25(2):298-303.

10. Alexandrov AV, Masdeu JC, Devous MD, Black SE, Grotta JC. Brain Single-Photon Emission CT with HMPAO and safety of trombolytic therapy in acute ischemic stroke. Stroke 1997;28(9):1830-1834.

11. Zeumer H, Hacke W, Ringelstein EB: Local intraarterial thrombolysis in vertebrobasilar thromboembolic disease. AJNR 1983;4:401-404.

12. Boysen G, Overgaard K: Thrombolysis in ischaemic stroke—how far from a clinical breakthrough? J Intern Med 1995;237:95-103.

13. Brott T, Kothari R, Broderick J. Thrombolytic therapy for cerebral infarction, in Cerebrovascular disease, HH Batjer, Editor. 1997, Lippincott-Raven: Philadelphia p535-546. 

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