Brainstem hypoperfusion in severe symptomatic vasospasm following aneurysmal subarachnoid hemorrhage: role of basilar artery vasospasm.

BACKGROUND: The hemodynamic effects of vertebrobasilar vasospasm are ill defined. The purpose of this study was to determine the effects of basilar artery (BA) vasospasm on brainstem (BS) perfusion. METHODS: Forty-five patients with delayed ischemic neurological deficits (DIND) following aneurysmal subarachnoid hemorrhage (SAH) underwent cerebral angiography prior to decision-making concerning endovascular treatment. BA diameter was compared with baseline angiogram. Regional brainstem (BS) cerebral blood flow (CBF) was qualitatively estimated by (99m)Tc ethyl cysteinate dimer single photon emission computed tomography (ECD-SPECT). FINDINGS: Delayed BS hypoperfusion was found in 22 (48.9%) of 45 patients and BA narrowing of more than 20% was found in 23 (51.1%). Seventeen of 23 (73.9%) patients with BA narrowing of more than 20% experienced BS hypoperfusion compared to 6 of 22 (27.3%) patients with minimal or no narrowing (p = 0.0072). Patients with severe and moderate BS hypoperfusion had higher degree of BA narrowing compared to patients with normal BS perfusion and mild BS hypoperfusion (p < 0.001). The three-month outcome of patients n-22) with BS hypoperfusion was significantly worse compared to patients (n-23) with unimpaired (p = 0.0377, odd ratio for poor outcome 4, 1.15-13.9 95% confidence interval). INTERPRETATION: These findings suggest that the incidence of BA vasospasm in patients with severe symptomatic vasospasm is high and patients with significant BA vasospasm are at higher risk to experience BS ischemia. Further studies should be done to evaluate the effects of endovascular therapy on BS perfusion and the impact of BS ischemia on morbidity and mortality of patients with severe symptomatic vasospasm.

Assessment: transcranial Doppler ultrasonography: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.

OBJECTIVE: To review the use of transcranial Doppler ultrasonography (TCD) and transcranial color-coded sonography (TCCS) for diagnosis. METHODS: The authors searched the literature for evidence of 1) if TCD provides useful information in specific clinical settings; 2) if using this information improves clinical decision making, as reflected by improved patient outcomes; and 3) if TCD is preferable to other diagnostic tests in these clinical situations. RESULTS: TCD is of established value in the screening of children aged 2 to 16 years with sickle cell disease for stroke risk (Type A, Class I) and the detection and monitoring of angiographic vasospasm after spontaneous subarachnoid hemorrhage (Type A, Class I to II). TCD and TCCS provide important information and may have value for detection of intracranial steno-occlusive disease (Type B, Class II to III), vasomotor reactivity testing (Type B, Class II to III), detection of cerebral circulatory arrest/brain death (Type A, Class II), monitoring carotid endarterectomy (Type B, Class II to III), monitoring cerebral thrombolysis (Type B, Class II to III), and monitoring coronary artery bypass graft operations (Type B to C, Class II to III). Contrast-enhanced TCD/TCCS can also provide useful information in right-to-left cardiac/extracardiac shunts (Type A, Class II), intracranial occlusive disease (Type B, Class II to IV), and hemorrhagic cerebrovascular disease (Type B, Class II to IV), although other techniques may be preferable in these settings.

Withdrawal of support in intracerebral hemorrhage may lead to self-fulfilling prophecies.

BACKGROUND: Withdrawal of support in patients with severe brain injury invariably leads to death. Preconceived notions about futility of care in patients with intracerebral hemorrhage (ICH) may prompt withdrawal of support, and modeling outcome in patient populations in whom withdrawal of support occurs may lead to self-fulfilling prophecies. METHODS: Subjects included consecutive patients with supratentorial ICH. Radiographic characteristics of the hemorrhage, clinical variables, and neurologic outcome were assessed. Attitudes about futility of care were examined among members of the departments of neurology and neurologic surgery through a written survey and case presentations. RESULTS: There were 87 patients with supratentorial ICH; overall mortality was 34.5% (30/87). Mortality was 66.7% (18/27) in patients with Glasgow Coma Score < or = 8 and ICH volume > 60 cm(3). Medical support was withdrawn in 76.7% (23/30) of patients who died. Inclusion of a variable to account for the withdrawal of support in a model predicting outcome negated the predictive value of all other variables. Patients undergoing surgical decompression were unlikely to have support withdrawn, and surgery was less likely to be performed in older patients (p < 0.01) and patients with left hemispheric hemorrhage (p = 0.04). Survey results suggested that practitioners tend to be overly pessimistic in prognosticating outcome based upon data available at the time of presentation. CONCLUSIONS: The most important prognostic variable in determining outcome after ICH is the level of medical support provided. Withdrawal of support in patients felt likely to have a "poor outcome" biases predictive models and leads to self-fulfilling prophecies. Our data show that individual patients in traditionally "poor outcome" categories can have a reasonable neurologic outcome when treated aggressively.

Brain SPECT used to evaluate vasospasm after subarachnoid hemorrhage: correlation with angiography and transcranial Doppler.

PURPOSE: The primary objective of this study was to correlate Tc-99m HMPAO and ethyl cysteine dimer perfusion brain SPECT imaging with angiography and transcranial Doppler (TCD) to identify vasospasm after subarachnoid hemorrhage. METHODS: A retrospective analysis of consecutive patients who had cerebral blood flow SPECT imaging for subarachnoid hemorrhage and aneurysm clipping was made. Flow velocity measurements were correlated using TCD and cerebrovascular angiography. RESULTS: Of the 129 patients were included in this study, 84 were female and 45 were male, with a mean age of 51.9 years and a median age of 51 years (range, 9 to 84 years). Eighty-nine patients had brain SPECT evidence of hypoperfusion. Concordance was found between SPECT and TCD with vasospasm in 57 of 89 (64%) patients and nonconcordance was evident in 32 patients (36%). Eleven patients who had concordance between SPECT and TCD had nonconcordant results of angiography for vasospasm. CONCLUSIONS: These findings suggest that all three methods are complementary to each other in the evaluation of patients with vasospasm after subarachnoid hemorrhage. Concordance of 64% between SPECT and TCD is acceptable and explicable by the differences in technique and measurement of cerebral blood flow compared with vascular narrowing, respectively.

Use of structural allografts in spinal osteomyelitis: a review of 47 cases.

OBJECT: The use of structural allografts in spinal osteomyelitis remains controversial because of the perceived risk of persistent infection related to a devitalized graft and spinal hardware. The authors have identified 47 patients over the last 3.5 years who underwent a surgical decompression and stabilization procedure in which fresh-frozen allografts were used after aggressive removal of infected and devitalized tissue. The patients subsequently underwent 6 weeks of postoperative antibiotic therapy (12 months for those with tuberculosis [TB]). METHODS: Follow-up data included results of serial clinical examinations, radiography, laboratory analysis (erythrocyte sedimentation rate and white blood cell count), and clinical outcome questionnaires. Of the original 47 patients (14 women and 33 men, aged 14-83 years), 39 were available for follow up. The average follow-up period at the time this article was submitted was 17 +/- 9 months (median 14 months, range 6-45 months). In the majority of cases (57%), a Staphylococcus species was the infectious organism. Predisposing risk factors included intravenous drug abuse (IVDA), previous surgery, diabetes, TB, and concurrent infections. During the follow-up period only two patients suffered recurrent infection at a contiguous level; both had a history of IVDA and one also had a chronic excoriating skin condition. No other recurrent infections have been identified, and no patient has required reoperation for persistent infection or allograft/hardware failure. CONCLUSIONS: It is the authors' opinion that the use of structural allografts in combination with aggressive tissue debridement and adjuvant antibiotic therapy provide a safe and effective therapy in cases of spinal osteomyelitis requiring surgery.

Neurotoxicity in organotypic hippocampal slices mediated by adenosine analogues and nitric oxide.

Adenosine (ADO) and nitric oxide (NO) have been implicated in a variety of neurophysiological actions, including induction of long-term potentiation, regulation of cerebral blood flow, and neurotoxicity/neuroprotection. ADO has been shown to promote NO release from astrocytes by a direct effect on A1 and A2 receptors, thus providing a link between actions of NO and adenosine in the brain. However, while adenosine acts as an endogenous neuroprotectant, NO is believed to be the effector of glutamate neurotoxicity. To resolve this apparent paradox, we have further investigated the effects of adenosine and NO on neuronal viability in cultured organotypic hippocampal slices exposed to sub-lethal (20') in vitro ischemia. Up to a concentration of 500 microM ADO did not cause toxicity while exposures to 100 microM of the stable ADO analogue chloroadenosine (CADO) caused widespread neuronal damage when paired to anoxia/hypoglycemia. CADO effects were significantly prevented by the ADO receptor antagonist theophylline and blockade of NO production by L-NA (100 microM). Moreover, CADO effects were mimicked by the NO donor SIN-1 (100 microM). Application of 100 microM ADO following blockade of adenosine deaminase (with 10 microM EHNA) replicated the effects of CADO. CADO, ADO + EHNA but not ADO alone caused a prolonged and sustained release of nitric oxide as measured by direct amperometric detection. We conclude that at high concentrations and/or following blockade of its enzymatic catabolism, ADO may cause neurotoxicity by triggering NO release from astrocytes. These results demonstrate for the first time that activation of pathways other than those involving neuronal glutamate receptors can trigger NO-mediated neuronal cell death in the hippocampus.

Predicting length of hospital stay and cost by aneurysm grade on admission.

To determine the relationship between clinical grade on admission and treatment cost after aneurysm rupture, the authors retrospectively examined the length of hospital stay (LOS) and total hospitalization costs (excluding professional fees) for 543 patients admitted for aneurysm surgery between 1983 and 1993. The overall median LOS was 18 days, with a range of 1 to 165 days. Increased median LOS correlated with Hunt and Hess Grades 0 to IV on admission (p < 0.001). Median LOS for Grade V patients was reduced, in part, because of early mortality. Increased treatment cost also correlated with worse admission clinical grade (p < 0.001). A significant proportion of total expenditures occurred early in the hospitalization for patients in all clinical grades. Identification of additional factors affecting the cost of aneurysm treatment is indicated to complement treatment outcome studies.

The incidence of surgical complications is similar in good and poor grade patients undergoing repair of ruptured anterior circulation aneurysms: a retrospective review of 355 patients.

To determine how clinical grade after subarachnoid hemorrhage impacts operative characteristics and the incidence of intra- and postoperative surgical complications, we retrospectively compared the surgical management of all good grade (n = 224) and poor grade (n = 131) patients who suffered ruptured anterior circulation aneurysms between 1983 and 1993. The majority of good grade (74.2%) and poor grade (89.8%) patients underwent surgery < 3 days after subarachnoid hemorrhage. The results in this series demonstrate that severe cerebral swelling, often secondary to intracerebral hemorrhage, was significantly more frequent in poor grade patients. The incidence of complications, such as failure to occlude the aneurysm, major vessel occlusion, intraoperative aneurysm rupture, or surgical contusion, however, was similar in poor grade and good grade patients. We conclude, therefore, that except for severe cerebral swelling associated with intracerebral hemorrhage, the risk of surgical complications is similar in good and poor grade patients undergoing surgical repair of ruptured anterior circulation aneurysms.

Posterior instrumentation of the unstable cervicothoracic spine.

Fractures, tumors, and other causes of instability at the cervicothoracic junction pose diagnostic and treatment challenges. The authors report on 23 patients with instability of the cervicothoracic region, which was treated with posterior plate fixation and fusion between the lower cervical and upper thoracic spine. During operation AO reconstruction plates with 8- or 12-mm hole spacing were affixed to the spine using screws in the cervical lateral masses and the thoracic pedicles. Postoperative immobilization consisted of the patient's wearing a simple external brace for 2 months. The following parameters were analyzed during the pre- and postoperative treatment period: neurological status, spine anatomy and reconstruction, and complications. Follow up consisted of clinical and radiographic examinations (mean duration of follow up, 15.4 months; range, 6-41 months). No neurovascular or pulmonary complications arose from surgery. All patients achieved a solid arthrodesis based on flexion-extension radiographs. There was no significant change in angulation during the postoperative period, but one patient had an increase in translation that was not clinically significant. There were no hardware complications that required reoperation. One patient requested hardware removal in hopes of reducing postoperative pain in the cervicothoracic region. One postoperative wound infection required debridement but not hardware removal. The authors conclude that posterior plate fixation is a satisfactory method of treatment of cervicothoracic instability.

Adenosinergic modulation of CA1 neuronal tolerance to glucose deprivation in organotypic hippocampal cultures.

Glucose deprivation produced neuronal degeneration of CA1 pyramidal neurons in hippocampal slice cultures. The effects of the adenosine agonist cyclohexyladenosine (CHA) and antagonist cyclopentylxanthine (CPX) on CA1 neuronal loss following hypoglycemia was examined using propidium iodide fluorescence as an indicator of cell death. The intensity of propidium iodide fluorescence in hippocampal area CA1 was quantified using Optimas image analysis software. Following 2 or 3 h of glucose deprivation, CPX significantly enhanced injury in the CA1 region while CHA provided significant protection. These results suggest that adenosine plays an important role in endogenous neuronal protection during hypoglycemic injury, and also supports a role for the use of adenosine agonists as neuroprotective agents.

Severe symptomatic vasospasm: the role of immediate postoperative angioplasty.

The clinical success of angioplasty for symptomatic vasospasm following subarachnoid hemorrhage (SAH) depends on early intervention and can best be achieved after the aneurysm is occluded. However, patients presenting with unsecured ruptured aneurysms and established clinical vasospasm offer a dilemma for the surgeon. The authors describe the cases of five such patients who underwent acute clipping of aneurysms followed by immediate postoperative angioplasty between 1988 and 1992. All were referred at least 5 days after SAH. Severe vasospasm compatible with the clinical presentation was confirmed by angiography. The patients met the department's criteria for angioplasty but, because of unclipped aneurysms, were first taken patients met the department's criteria for angioplasty but, because of unclipped aneurysms, were first taken to the operating room for a craniotomy and aneurysm obliteration. Angiography was repeated immediately after surgery. Arterial narrowing had progressed during surgery in two patients. In all patients, postoperative mechanical dilatation was achieved with the use of a silicone microballoon. Following angioplasty, transcranial Doppler ultrasound flow velocities and single-photon emission computerized tomography evaluation indicated improved cerebral perfusion compared to preoperative determinations. Four patients improved clinically and made a good recovery. In this subgroup of patients presenting with proven symptomatic vasospasm and an unclipped but ruptured aneurysm, urgent surgical obliteration of the aneurysm followed by immediate postoperative angioplasty may be a safe and reasonable means to improve outcome.

Emergent aneurysm clipping without angiography in the moribund patient with intracerebral hemorrhage: the use of infusion computed tomography scans.

The authors report their experience with 25 patients (mean age, 44.3 +/- 12.1 years) with an intracerebral hematoma (ICH) from a ruptured aneurysm who were emergently operated on without angiography. Instead, preoperative high-resolution infusion computed tomography (CT) scans were used to identify the aneurysm causing the hemorrhage. In all patients, the preoperative Glasgow Coma Scale score was < 5 and brain stem compression was evident. ICH was present in the frontal or temporal lobe and was often associated with intraventricular hemorrhage (n = 17) and significant (> 1 cm) midline shift (n = 18). Infusion CT scans correctly identified the aneurysm in all patients (middle cerebral artery, 18; posterior communicating artery, 2; carotid bifurcation, 3; anterior communicating artery, 2). Partial evacuation of the hematoma guided by infusion CT scan was usually required first to clip the aneurysm definitively using standard microvascular techniques. Intraoperative rupture occurred twice, and temporary clips were used on four occasions. Lobectomy (n = 8), decompressive craniotomy (n = 15), and ventriculostomy (n = 8) were required to control cerebral swelling. All patients underwent postoperative angiography to confirm aneurysm obliteration. Eleven unruptured aneurysms were subsequently identified. Nine had been predicted by infusion scan. Twelve patients survived, eight of whom were only moderately disabled and were independent at 6-months' follow-up. Of the 13 patients who died, all except one died within 4 days of admission. The authors conclude that although angiographic verification before aneurysm surgery is preferable, in the moribund patient with intracerebral hemorrhage, infusion CT scanning provides sufficient information concerning vascular anatomy to allow rational emergency craniotomy and aneurysm clipping.

CT infusion scanning for the detection of cerebral aneurysms.

Computerized tomography (CT) infusion scanning can confirm the presence or absence of an aneurysm as a cause of spontaneous intracerebral hemorrhage. Eight patients who presented with spontaneous hemorrhage were examined using this technique. In five patients the CT scan showed an aneurysm which was later confirmed by angiography or surgery; angiography confirmed the absence of an aneurysm in the remaining three patients. This method is an easy effective way to detect whether an aneurysm is the cause of spontaneous intracerebral hemorrhage.