The impact of pre-ictal statin use on vasospasm and outcome in aneurysmal subarachnoid hemorrhage.

BACKGROUND: Pleiotropic effects of statins may be beneficial in alleviating cerebral vasospasm (VS) and improving outcome after aneurysmal subarachnoid hemorrhage (aSAH). Initiation of statin treatment at aSAH is not recommended; however, the effect of pre-ictal and continued statin use is not fully investigated. METHODS: Retrospective study comparing aSAH patients admitted in 2012 to 2021 with pre-ictal statin use versus those not using statins. Patient entry variables, radiological/sonological VS, symptomatic VS, and radiologically documented delayed cerebral ischemia (DCI) were registered. Outcome was scored in terms of mortality, modified Rankin score, Glasgow outcome score extended, and levels of fatigue. Patients were compared on group level and in a case-control design. RESULTS: We included 961 patients, with 204 (21.2%) statin users. Statin users were older and had more often hypertension. Severe radiological/sonological VS, symptomatic VS, and DCI were less frequent in statin users, and their length of stay was shorter. Mortality, functional outcome, and levels of fatigue were similar in both groups. When analyzing 89 pairs of statin users and non-statin users matched for age, aSAH severity, gender, and hypertension, we confirmed decreased radiological/sonological and symptomatic VS as well as shorter length of stay in statin users. They also had more often a favorable functional outcome and lower levels of fatigue. CONCLUSIONS: Patients with pre-ictal and continued use of statins have a reduced occurrence of radiological/sonological and symptomatic VS, shorter length of stay, and more often favorable functional outcome, whereas mortality is similar to non-statin users. Even though larger multicenter studies with common, strict protocols for prevention, diagnosis, and treatment of vasospasm are needed to finally establish the value of statins in aSAH, continuation of pre-ictal statin use seems worthwhile.

Case report: a troublesome ophthalmic artery aneurysm.

Objective and Importance When treating large unruptured ophthalmic artery (OA) aneurysms causing progressive blindness, surgical clipping is still the preferred method because aneurysm sac decompression may relieve optic nerve compression. However, endovascular treatment of OA aneurysms has made important progress with the introduction of stents. Although this development is welcomed, it also makes the choice of treatment strategy less straightforward than in the past, with the potential of missteps. Clinical Presentation A 56-year-old woman presented with a long history of progressive unilateral visual loss and magnetic resonance imaging showing a 20-mm left-sided OA aneurysm. Intervention Because of her long history of very poor visual acuity, we considered her left eye to be irredeemable and opted for endovascular therapy. The OA aneurysms was treated with stent and coils but continued to grow, threatening the contralateral eye. Because she failed internal carotid artery (ICA) balloon test occlusion, we performed a high-flow extracranial-intracranial bypass with proximal ICA occlusion in the neck. However, aneurysm growth continued due to persistent circulation through reversed blood flow in distal ICA down to the OA and the cavernous portion of the ICA. Due to progressive loss of her right eye vision, we surgically occluded the ICA proximal to the posterior communicating artery and excised the coiled, now giant, OA aneurysm. This improved her right eye vision, but her left eye was permanently blind. Conclusion This case report illustrates complications of the endovascular and surgical treatment of a large unruptured OA aneurysm.

Cranioplasty with autologous cryopreserved bone after decompressive craniectomy: complications and risk factors for developing surgical site infection.

BACKGROUND: Renewed interest has developed in decompressive craniectomy, and improved survival is shown when this treatment is used after malignant middle cerebral artery infarction. The aim of this study was to investigate the frequency and possible risk factors for developing surgical site infection (SSI) after delayed cranioplasty using autologous, cryopreserved bone. METHODS: This retrospective study included 74 consecutive patients treated with decompressive craniectomy during the time period May 1998 to October 2010 for various non-traumatic conditions causing increased intracranial pressure due to brain swelling. Complications were registered and patient data was analyzed in a search for predictive factors. RESULTS: Fifty out of the 74 patients (67.6 %) survived and underwent delayed cranioplasty. Of these, 47 were eligible for analysis. Six patients (12.8 %) developed SSI following the replacement of autologous cryopreserved bone, whereas bone resorption occurred in two patients (4.3 %). No factors predicted a statistically significant rate of SSI, however, prolonged procedural time and cardiovascular comorbidity tended to increase the risk of SSI. CONCLUSIONS: SSI and bone flap resorption are the most frequent complications associated with the reimplantation of autologous cryopreserved bone after decompressive craniectomy. Prolonged procedural time and cardiovascular comorbidity tend to increase the risk of SSI.

Aspects of intracerebral hematomas--an update.

BACKGROUND: In Norway, there are approximately 16000 strokes each year and 15% of these are caused by intracerebral hematomas. Intracerebral hemorrhage (ICH) results from the rupture of blood vessels within the brain parenchyma. ICH occurs as a complication of several diseases, the most prevalent of which is chronic hypertension. When hemorrhage develops in the absence of a pre-existing vascular malformation or brain parenchymal lesion, it is denoted primary ICH. Secondary ICH refers to hemorrhage complicating a pre-existing lesion. Primary ICH is the most common type of hemorrhagic stroke, accounting for approximately 10% of all strokes. Despite aggressive management strategies, the 30-day mortality remains high, at almost 50%, with the majority of deaths occurring within the first 2 days. At 6 months, only 20-30% achieve independent status. MATERIAL AND METHODS: This article is based on clinical experience, modern therapeutic guidelines for the treatment of intracerebral hematomas and up-to-date medical literature found in Medline. The article discusses the pathophysiology, clinical aspects, treatment, and the prognosis of intracerebral hematomas. RESULTS AND DISCUSSION: Advances in diagnosis, prognosis, pathophysiology, and treatment over the past few decades have significantly advanced our knowledge of ICH; however, much work still needs to be carried out. Future genetic and epidemiologic studies will help identify at-risk populations and hopefully allow for primary prevention. Randomized controlled studies focusing on novel therapeutics should help to minimize secondary injury and hopefully improve morbidity and mortality.

Surgical treatment of aneurysmal subarachnoid haemorrhage in the presence of 24-h endovascular availability: management and results.

Endovascular treatment of ruptured intracranial aneurysms increasingly supersedes surgical repair. This study focuses on the management and results in 109 individuals treated surgically when both treatment modalities were available. The management principles were immediate identification of the origin of haemorrhage, early aneurysm repair, minimal brain retraction during surgery and rigorous prevention of secondary brain damage. Predominantly, aneurysms located on the middle cerebral artery and those of the posterior communicating artery were allocated to surgery. Despite of ultra-swift care, aneurysm rebleeds remained a challenge. Although one-third of the patients presented in a poor clinical grade, outcome was good with 87 (80%) of the individuals being independent, 16 (15%) being dependent and six patients (6%) dying. Results of surgical aneurysm repair are good presupposed the untiring ongoing efforts of an inter-disciplinary team of dedicated physicians and nurses.

Association among intracranial compliance, intracranial pulse pressure amplitude and intracranial pressure in patients with intracranial bleeds.

OBJECTIVE: To investigate the association among intracranial compliance (ICC), intracranial pulse pressure amplitude and intracranial pressure (ICP) in patients with intracranial bleeds. METHODS: Five patients with intracranial bleeds had their ICC and ICP monitored during days 1-8 after ictus. The recordings were stored as raw data files and analysed retrospectively. The parameters mean ICC, mean ICP wave amplitude and mean ICP were determined and average values were calculated in 1 hour time periods. RESULTS: A total of 262 1 hour recordings were analysed. There was a significant correlation between mean ICC and mean ICP wave amplitude and between mean ICC and mean ICP. The mean ICP wave amplitude was significantly higher during the 1 hour periods with mean ICC<0.5 ml/mmHg and significantly lower during 1 hour periods with mean ICC 1.5-3.0 ml/mmHg. Correspondingly, in the 159 1 hour recordings with mean ICP wave amplitude> or =5.0 mmHg, mean ICC was significantly lower than in the 103 recordings with mean ICP wave amplitude<5.0 mmHg. Mean ICP was normal (i.e. <20 mmHg) in 260 of 262 (99.2%) of the 1 hour recordings; in the 49 1 hour recordings with mean ICP>15 mmHg, mean ICC was significantly lower than in the 213 recordings with mean ICP<15.0 mmHg. CONCLUSION: In this cohort of pressure recordings, there was a strong association between ICC and intracranial pulse pressure amplitude. There also was a strong association between ICC and mean ICP, but mean ICP was normal in 260 of 262 1 hour recordings (99.2%).

Association between intracranial, arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients.

OBJECTIVE: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation. METHODS: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1-14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording. RESULTS: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p

BNCT for recurrent intracranial meningeal tumours - case reports.

OBJECTIVES: The investigation was designed to explore the efficacy of boron neutron capture therapy (BNCT) as treatment for recurrent intracranial meningeal tumours. MATERIALS AND METHODS: Three patients with meningeal tumours, recurring after initial surgery, radiation therapy and several reoperations, were evaluated for treatment with BNCT by determination of the accumulation of boronophenylalanine fructose (BPA-F) in tumour and in surrounding tissue. Two of these patients were subsequently treated by BNCT. RESULTS: The present results indicate that BNCT could be effective in prolonging time to recurrence, and thus in extending survival time, for patients with recurrent intracranial meningeal tumours. CONCLUSIONS: BNCT is potentially an effective radiation treatment modality for malignant intracranial meningeal tumours, which could increase progression-free survival, thus reducing the need for additional surgical interventions. Indications for BNCT would be even larger if recurrent grade II meningiomas could be treated, as indicated by the results of the boron uptake study.

From intracranial pressure to intracranial pressure wave-guided intensive care management of a patient with an aneurysmal subarachnoid haemorrhage.

We report on a 65-year-old female with an aneurysmal subarachnoid hemorrhage (SAH) that was followed clinically, radiologically and electrophysiologically before and after converting from intracranial pressure (ICP)-guided to ICP wave-guided intensive care management. Intracranial pressure-guided management is aimed at keeping mean ICP < 15-20 mmHg, while ICP wave-guided management is aimed at keeping mean ICP wave amplitude < 5 mmHg. The aims of management were obtained by adjusting cerebrospinal fluid (CSF) draining volume from her external ventricular drain. No improvement was seen clinically or in cerebral magnetic resonance imaging (MRI) scans during the ICP-guided management. Clinical, MRI and neurophysiologic (electroencephalography and auditory evoked responses) improvements were obvious within 2 days after converting from ICP- to ICP wave-guided management. This case report describes how we used various ICP parameters to guide intensive care management of an aneurysmal SAH patient.

Intracranial pressure levels and single wave amplitudes, Glasgow Coma Score and Glasgow Outcome Score after subarachnoid haemorrhage.

OBJECT: To relate intracranial pressure (ICP) levels and single ICP wave amplitudes to the acute clinical state (Glasgow Coma Score, GCS) and final clinical outcome (Glasgow Outcome Score, GOS) in patients with subarachnoid haemorrhage (SAH). METHODS: Twenty-seven consecutive patients with severe SAH had their ICP and arterial blood pressure (ABP) continuously monitored during days 1-6 after SAH. The acute clinical state could be assessed in 11 non-sedated cases using the Glasgow Coma Scale, while outcome was assessed in all cases after 6 months using the Glasgow Outcome Scale. The ICP/ABP recordings were stored as raw data files and analyzed retrospectively. For every consecutive 6 seconds time window, mean ICP, mean cerebral perfusion pressure (CPP) and the mean ICP wave amplitude were computed. RESULTS: The GCS during days 1-6 after SAH was significantly related to the mean ICP wave amplitude, but not to the mean ICP or mean CPP. There was also a strong relationship between the mean ICP wave amplitude and GOS 6 months after SAH, with mean ICP wave amplitudes being significantly lower in those with moderate disability/good recovery, as compared with those with severe disability and death. Mean ICP was significantly higher in those who died than in the group with moderate disability/good recovery whereas mean CPP was not different between outcome groups. CONCLUSIONS: In this small patient group the mean ICP wave amplitude during days 1-6 after SAH was related to the acute clinical state (GCS) as well as to the clinical outcome (GOS) 6 months after SAH. Similar relationships were not found for mean ICP or the mean CPP, except for a higher mean ICP in those who died than in those with moderate disability/good recovery.

Preoperative spinal hydrodynamics versus clinical change 1 year after shunt treatment in idiopathic normal pressure hydrocephalus patients.

Nineteen consecutive cases treated for idiopathic normal pressure hydrocephalus (iNPH) with ventriculo-peritoneal shunts were clinically followed prospectively. Change in clinical state one year after shunt surgery was assessed as change on a 15-3 score NPH Grade Scale. Preoperative spinal hydrodynamics were assessed using a constant-rate lumbar infusion test. The pressure recordings were stored as raw data files and analysed retrospectively with regard to the mean cerebrospinal fluid pressure (CSFP), as well as mean CSFP wave amplitudes. Changes in NPH score 1 year after shunt surgery correlated significantly with the levels of single CSFP wave amplitudes, but not with the lumbar resistance to CSF outflow (R(out)). Mean CSFP wave amplitude was thus, in this cohort, a better predictor of clinical change one year after shunt treatment than R(out).

The ELANA technique: constructing a high flow bypass using a non-occlusive anastomosis on the ICA and a conventional anastomosis on the SCA in the treatment of a fusiform giant basilar trunk aneurysm.

A patient with a partially thrombosed fusiform giant basilar trunk aneurysm presented with devastating headache and symptoms of progressive brain stem compression. Having an aneurysm inaccessible for endovascular treatment, and after failing a vertebral artery balloon occlusion test, he was offered bypass surgery in order to exclude the aneurysm from the cerebral circulation and relieve his symptoms. A connection between the intracranial internal carotid artery and the superior cerebellar artery was created whereupon the basilar artery was ligated just distally to the aneurysm. The proximal anastomosis on the internal carotid artery was made using the excimer laser-assisted non-occlusive anastomosis (ELANA) technique, while a conventional end-to-side anastomosis was used for the distal anastomosis on the superior cerebellar artery. Intra-operative flowmetry showed a flow through the bypass of 40 ml/min after ligation of the basilar artery. An angiogram 24 hours later showed normal filling of the bypass and the vessels supplied by it, but also disclosed a subtotal occlusion of the proximal ipsilateral middle cerebral artery with delayed filling distally. The patient, who had a known thrombogenic coagulopathy, died the following day. Autopsy showed no signs of ischemia in the territories supplied by the bypass, but a thrombus in the proximal middle cerebral artery and massive acute hemorrhagic infarction with swelling in its territory and uncal herniation. Multiple fresh thrombi were found in the lungs. The ELANA anastomosis showed re-endothelialisation without thrombus formation on the inside.

Effect of Guglielmi detachable coil placement on intraaneurysmal pressure: experimental study in canines.

BACKGROUND AND PURPOSE: Treatment of ruptured aneurysms with Guglielmi detachable coils (GDCs) has been shown to prevent repeat bleeding. To assess whether GDC coiling alters aneurysmal pressure, we measured intraaneurysmal pressure in two canine types of carotid artery aneurysms before and after GDC placement. METHODS: A 0.014-inch guidewire with a pressure transducer was inserted into parent arteries and domes of surgically created aneurysms. Intravascular static pressures were recorded before and during saline power injections (10, 20, and 30 mL over 1 and 2 s), before and after GDC placement. Common femoral arterial pressure was monitored. RESULTS: Saline power injections reproducibly and abruptly increased pressure in parent arteries and aneurysms. Mean intraaneurysmal pressure varied (18 +/- 4 [10 mL] to 75 +/- 15 mm Hg [30 mL]), independent of injection duration. Intraaneurysmal baseline pressures were higher after GDC placement (111 +/- 10 versus 93 +/- 15 mm Hg; P =.05). Aneurysmal pressure increases with saline injections were slightly higher after GDC placement, which dampened intraaneurysmal pressure amplitude at baseline (26.5 +/- 5.6 versus 19.6 +/- 7.4 mm Hg; P =.003) and during hypertension (25.3 +/- 5.4 versus 19.8 +/- 7.5 mm Hg, P =.002). The pressure increase slope with saline injection was delayed with GDC placement (0.24 +/- 0.1 versus 0.38 +/- 0.19 s; P <.001). CONCLUSION: Graded saline power injections into parent arteries can rapidly increase intraaneurysmal pressure. GDC treatment did not attenuate mean intraaneurysmal pressures, but both dampened the pressure amplitude and delayed pressure increases during locally induced hypertension.

[Resection of malignant tumors involving the anterior cranial fossa]. / Reseksjon av maligne svulster med relasjon til fremre skallgrop.

BACKGROUND: The craniofacial approach has greatly facilitated resections of tumours involving the base of the anterior cranial fossa when compared to either the transcranial or transfacial approach alone. MATERIAL AND METHODS: This approach was used in 11 patients with malignant tumours localized to the ethmoid sinus, orbit and bone or soft tissue of the base of the anterior part of the skull. By combining a low frontal or frontolateral craniotomy with resection of the facial skull, en bloc resections were accomplished. A frontogaleal periostal flap or a muscle flap from the temporal muscle was used to replace resected bone and to seal the skull base. RESULTS: There were no peri- or postoperative deaths. One patient died due to local recurrence, one patient is alive with residual tumour six years after surgery, and one is reoperated due to local recurrence. In addition one patient developed recurrence of a previously treated tumour of the maxillary sinus. Two patients developed meningitis and one pneumocephalus postoperatively. One patient has partial loss of vision and two patients underwent dacryocystorhinostomy due to epiphora. INTERPRETATION: The planning and execution of this type of surgery requires close interaction in an interdisciplinary team, in particular between neurosurgeon and head and neck surgeon.

Transcranial Doppler ultrasonography-guided management of internal carotid artery closure.

OBJECTIVE: To emphasize the integrated use of transcranial Doppler ultrasonography (TCD) in the management of internal carotid artery (ICA) closure. METHODS: Thirty-three patients being considered for ICA closure underwent TCD assessment, vasomotor reserve testing/estimation, and carotid artery test occlusion with concomitant middle cerebral artery (MCA) blood velocity (V(MCA)) monitoring, including calculation of the MCA pulsatility index. Twelve of these patients proceeded to undergo ICA sacrifice. Sequential TCD sonograms guided their postoperative treatment. RESULTS: ICA aneurysms and neck neoplasms affected the TCD results and vasomotor reserve insignificantly, whereas carotid-cavernous fistulae induced characteristic circulatory alterations. The 10 subjects who tolerated ICA sacrifice hemodynamically all showed an initial decrease in the ipsilateral V(MCA) to > or =60% of the preocclusion value and a progressively decreasing MCA pulsatility index during carotid artery test occlusion. The two patients who developed hemodynamic cerebral infarctions exhibited a decrease in V(MCA) to <60% and a MCA pulsatility index that remained stable after a vast initial reduction. Postoperative hypervolemic and hypertensive support was safely titrated in all patients who received postoperative TCD surveillance, providing an ipsilateral V(MCA) of > or =80% of the preocclusion value. ICA closure permanently altered the cerebral circulatory pattern. CONCLUSION: The hemodynamic outcome of ICA sacrifice can be correctly predicted by using the TCD occlusion test. TCD provides the means to titrate the extent of postoperative hypervolemic/hypertensive support.

Cerebral artery blood velocity in normal subjects during acute decreases in barometric pressure.

To investigate the effect of acute changes in barometric pressure on regional cerebral perfusion we studied the middle cerebral artery (MCA) blood velocity in five healthy male volunteers by means of a low-pressure chamber. The MCA blood velocity, arterial blood and respiratory gases were measured at the barometric pressures of 1, 0.8, 0.65, and 0.5 atmospheres. The observed blood velocity (Vo) showed no systematic changes. Decreases in barometric pressure induced hypoxia and hypocapnia. When normalizing the MCA blood velocity (Vn) to a standard P(CO2) (5.3 kPa), thereby correcting for the hypoxic induced hypocapnia, we obtained an inverse relationship between cerebral artery blood velocity and arterial blood oxygen content (CaO2). The oxygen supply to the brain, estimated as the product of Vo and CaO2, decreased with lowering of the barometric pressure. However, the product of Vn and CaO2 remained constant. This suggests the existence of a regulatory mechanism attempting to maintain a constant oxygen supply to the brain during acute changes in CaO2, if the hyperventilation induced decrease in PCO2 can be omitted. In the artificial situation of a low pressure chamber, our findings are quite similar to those obtained at sea level. This indicates that the underlying mechanisms of control of cerebral blood flow do not change during acute exposure to altitude.

Varying impact of common carotid artery digital compression and internal carotid artery balloon test occlusion on cerebral hemodynamics.

BACKGROUND: The purpose of this study was to compare the cerebral hemodynamic changes brought about by common carotid artery (CCA) digital compression and angiographic internal carotid artery (ICA) balloon occlusion. METHODS: Bilateral transcranial Doppler ultrasonographic monitoring of the middle cerebral artery blood velocity (VMCA) was performed in 12 subjects with neck neoplasms or traumatic carotid-cavernous fistulas. The MCA pulsatility index (PIMCA) and hemodynamic tension (Uhem MCA) were calculated. RESULTS: Common carotid artery compression provoked the largest drop in ipsilateral VMCA, PIMCA, and Uhem MCA. Common carotid artery compression caused a steal of blood from the intra- to the extracranial circulation, with the discrepancy in hemodynamic findings between CCA and ICA test occlusions being dependent on the quantity of reversed ipsilateral ICA blood flow. CONCLUSION: If the carotid artery is to be sacrificed, permanent ICA closure is the procedure of choice with respect to the occurrence of cerebral ischemic lesions in patients with neck neoplasms and ICA flow reversal during CCA compression.

Cerebral haemodynamics in internal carotid artery trial occlusion.

The purpose of this study was to analyse the cerebral haemodynamic changes brought about by trial occlusion of the internal carotid artery (ICA). Sixteen patients with surgically inaccessible cerebral aneurysms, carotid cavernous fistulas or neck neoplasms were monitored with transcranial Doppler ultrasonography (TCD) during 90-120 s angiographic ICA balloon occlusion or ICA closure with a Selverstone clamp. The blood velocity (V) was registered continuously in both middle cerebral arteries (MCA) while the pulsatility index (PIMCA) and haemodynamic tension (Uhem MCA) were calculated. ICA closure led to an instantaneous drop in the ipsilateral VMCA, PIMCA and Uhem MCA. The VMCA thereafter increased gradually until reaching a stable level. The subjects were grouped into those with initial drops in VMCA to > or = 60% of pre-occlusion value (group 1) and those that fell to < 60% (group 2), respectively. In group 1 autoregulatory mechanisms made the PIMCA decline further, while the Uhem MCA remained unaltered during ICA closure. In group 2, however, the PIMCA did not change further, while the Uhem MCA increased slightly. The cerebral haemodynamic features during ICA test occlusion were thus essentially different in the two groups. On re-opening the ICA, there was an overshoot in VMCA and Uhem MCA. Contralaterally, the VMCA was increased during ICA occlusion. Seven of the patients later had their ICA closed permanently. While none of five group 1 patients developed haemodynamic complications, two group 2 individuals experienced haemodynamic stroke. Assuming ICA sacrifice is feasible when test occlusion results in an ipsilateral initial reduction in VMCA to > or = 60% of pre-occlusion value, the corresponding limit for the Uhem MCA is > or = 40%. In the pre-operative evaluation of the haemodynamic risk related to ICA loss, TCD emerges as a reliable method. It also seems to allow for the reduction of test occlusion time to 90-120 s.

Cerebral haemodynamic considerations in obstructive carotid artery disease.

46 subjects with obstructive carotid artery disease were investigated with transcranial Doppler ultrasonography. Their baseline blood velocities (V) in the middle, anterior and posterior cerebral artery (MCA, ACA and PCA) and in the extracranial internal carotid artery (ICA) were measured and the pulsatility index (PI) calculated for each vessel. Thereafter the vasomotor reserve in both MCAs was tested. Typical patterns of V, PI and vasomotor reactivity are presented. Arterial collaterals were recognized by their relatively increased velocities. We demonstrated a close association of the baseline variables V and PI and the total vasomotor reactivity (hypocapnic plus no, hypercapnic response) by calculating an index of Uhem related to the cerebrovascular tone. The Uhem index is expressed by: Uhem index = VMCA.PIMCA/VPCA.PIPCA The relationship between Uhem index and the total vasomotor reactivity seemed to correspond to a hyperbolic curve. The hyperbolic tangent of Uhem index and total vasomotor reactivity correlated highly significantly, r = 0.8203, p < 0.0001, n = 49, the best fit for the regression line was Y = -0.005 + Uhem index 51.3. On the 99% significance level an Uhem index > or = 0.94 indicated normal total cerebral vasomotor reactivity in contrast to an impaired reactivity when < or = 0.81. Findings in 20 patients investigated post hoc supported the validity of our concept.

Haemodynamic classification of symptomatic obstructive carotid artery disease.

63 subjects with symptomatic obstructive carotid artery disease were investigated with transcranial Doppler ultrasonography. Their blood velocities at rest (V) in the middle and posterior cerebral artery (MCA and PCA) and in the extracranial internal carotid artery were measured and the pulsatility index (PI) and Uhem index (VMCA.PIMCA/VPCA.PIPCA) calculated. The vasomotor responses in both MCAs were also tested. The subjects were divided into groups based on the findings on physical examination and cerebral computed tomography. In the patient group with lacunar/territorial infarction we found in the stroke hemisphere: VMCA > VPCA, PIMCA = PIPCA and normal values for the Uhem index and total vasomotor reactivity. In the patient group with watershed infarction this hemisphere was characterized by: VMCA < VPCA, PIMCA < PIPCA and subnormal scores for the Uhem index and total vasomotor reactivity. Displaying features from both stroke groups, we obtained in the hemisphere of interest in patients with transient ischaemic attacks: VMCA = VPCA, PIMCA < PIPCA and normal values for the Uhem index and total vasomotor reactivity. Five patients with clinical evidence of stroke but with negative cerebral computed tomography findings had scores similar to those of the watershed group of patients. For the stroke patients, individual measurements of V, PI and total vasomotor reactivity failed to clearly identify to which stroke group a subject might belong. However, such an identification was achieved in all subjects when using the Uhem index. The Uhem index data in patients with transient ischaemic attacks suggest two subgroups with different pathogenesis underlying, the ischaemic events.