Ralf W. Baumgartner

Clinical and radiological predictors of recanalisation and outcome of 40 patients with acute basilar artery occlusion treated with intra-arterial thrombolysis

Objective: To define predictors of recanalisation and clinical outcome of patients with acute basilar artery occlusions treated with local intra-arterial thrombolysis (IAT). Methods: Vascular risk factors, severity of the neurological deficit graded by the National Institutes of Health stroke scale (NIHSS), and radiological findings were recorded at presentation. Outcome was measured using the modified Rankin scale (mRS) three months later and categorised as favourable (mRS 0–2), poor (mRS 3–5), or death (mRS 6). Results: 40 patients were studied. Median NIHSS on admission was 18. Mean time from symptom onset to treatment was 5.5 hours (range 2.3 to 11). Outcome was favourable in 14 patients (35%) and poor in nine (23%); 17 (42%) died. There were two symptomatic cerebral haemorrhages (5%). Recanalisation of the basilar artery was achieved in 32 patients (80%); it was complete (TIMI grade 3) in 20% and partial (TIMI grade 2) in 60%. In multivariate logistic regression analysis, low NIHSS score on admission (pu200a=u200a0.002) and vessel recanalisation (pu200a=u200a0.005) were independent predictors of favourable outcome. Recanalisation occurred more often with treatment within six hours of symptom onset (pu200a=u200a0.003) and when admission computed tomography showed a hyperdense basilar artery sign (pu200a=u200a0.007). In a univariate model, quadriplegia (pu200a=u200a0.002) and coma (pu200a=u200a0.004) were associated with a poor outcome or death. Conclusions: Low baseline NIHSS on admission and recanalisation of basilar artery occlusions predict a favourable outcome after intra-arterial thrombolysis. Early initiation of IAT and the presence of a hyperdense basilar artery sign on CT were associated with a higher likelihood of recanalisation.

Carotid dissection with and without ischemic events Local symptoms and cerebral artery findings

Objective: To study whether spontaneous dissections of the cervical internal carotid artery dissection (ICAD) with and without ischemia of the brain or retina differ in the prevalence of vascular risk factors, local neurologic signs and symptoms, and stenoses and occlusions of the cerebral arteries. Methods: The authors prospectively studied 181 consecutive patients with 200 ICAD. Diagnosis was based on ultrasonography and MRI or catheter angiography. Vascular risk factors, presenting local (headache, neck pain, Horner syndrome, pulsatile tinnitus, cranial nerve palsy on the side of the ICAD) and ischemic signs and symptoms, and ultrasonographic findings in the carotid and basal cerebral arteries were evaluated. Results: ICAD with ischemic events (n = 145) had a higher prevalence of hypercholesterolemia (p < 0.05), >80% stenoses and occlusions of the ICA (p < 0.0001), and intracranial obstructions (p < 0.001). ICAD without ischemic events (n = 55) had a higher prevalence of Horner syndrome (p < 0.001), cranial nerve palsy (p < 0.01), and normal ICA findings (p < 0.0001). Conclusions: These data suggest that ICAD causing high-grade stenosis and occlusion are more likely to lead to intracranial obstructions and cerebral or retinal ischemic events. Conversely, ICAD without luminal narrowing cause more local signs and symptoms.

Acute Mountain Sickness: Controversies and Advances

This review discusses the impact of recent publications on pathophysiologic concepts and on practical aspects of acute mountain sickness (AMS). Magnetic resonance imaging studies do not provide evidence of total brain volume increase nor edema within the first 6 to 10 h of exposure to hypoxia despite symptoms of AMS. After 16 to 32 h at about 4500 m, brain volume increases by 0.8% to 2.7%, but morphological changes do not clearly correlate with symptoms of AMS, and lumbar cerebrospinal fluid pressure was unchanged from normoxic values in individuals with AMS. These data do not support the prevailing hypothesis that AMS is caused by cerebral edema and increased intracranial pressure. Direct measurement of increased oxygen radicals in hypoxia and a first study reducing AMS when lowering oxygen radicals by antioxidants suggest that oxidative stress is involved in the pathophysiology of AMS. Placebo-controlled trials demonstrate that theophylline significantly attenuates periodic breathing without improving arterial oxygen saturation during sleep. Its effects on AMS are marginal and clearly inferior to acetazolamide. A most recent large trial with Ginkgo biloba clearly showed that this drug does not prevent AMS in a low-risk setting in which acetazolamide in a low dose of 2 x 125 mg was effective. Therefore, acetazolamide remains the drug of choice for prevention and the recommended dose remains 2 x 250 mg daily until a lower dose has been tested in a high-risk setting and larger clinical trials with antioxidants have been performed.

Carotid dissection with permanent and transient occlusion or severe stenosis Long-term outcome

Objective: To compare the rate of ischemic events and intracranial hemorrhage in the long-term follow-up of patients with persistent and transient severe stenosis or occlusion of the internal carotid artery (ICA) due to spontaneous dissection (ICAD). Methods: One hundred and sixty-one consecutive patients with unilateral ICAD causing severe stenosis or occlusion were examined clinically and by ultrasound 1 year after symptom onset. Forty-six cases with persistent and 46 age- and latency-matched cases with transient (recanalization complete or less than 50% stenosis) severe stenosis or occlusion of the ICA were enrolled. Nine patients with surgical, endovascular, or fibrinolytic therapy for ICAD or associated stroke were excluded. Antithrombotic therapy was given at the discretion of the treating physician. Clinical follow-ups were done annually. Results: Antithrombotic therapy and follow-up were similar in patients with permanent (6.2 ± 3.4 years) and transient (7.2 ± 4.3 years) severe stenosis or occlusion of the ICA. Cases with permanent carotid stenosis or occlusion showed annual rates of 0.7% for ipsilateral carotid territory stroke and of 1.4% for any stroke. Cases with transient carotid stenosis or occlusion showed annual rates of 0.3% for ipsilateral carotid territory stroke and of 0.6% for any stroke. Conclusions: This study suggests that ICAD has a benign long-term prognosis with low rates of ipsilateral carotid territory and any stroke and that the stroke rate in ICAD is not related to the persistence of severe carotid stenosis or occlusion. These results question the rationale of surgical or catheter-based revascularization in patients with ICAD.

Emerging concepts in acute mountain sickness and high-altitude cerebral edema: from the molecular to the morphological.

Acute mountain sickness (AMS) is a neurological disorder that typically affects mountaineers who ascend to high altitude. The symptoms have traditionally been ascribed to intracranial hypertension caused by extracellular vasogenic edematous brain swelling subsequent to mechanical disruption of the blood–brain barrier in hypoxia. However, recent diffusion-weighted magnetic resonance imaging studies have identified mild astrocytic swelling caused by a net redistribution of fluid from the “hypoxia-primed” extracellular space to the intracellular space without any evidence for further barrier disruption or additional increment in brain edema, swelling or pressure. These findings and the observation of minor vasogenic edema present in individuals with and without AMS suggest that the symptoms are not explained by cerebral edema. This has led to a re-evaluation of the relevant pathogenic events with a specific focus on free radicals and their interaction with the trigeminovascular system. (Part of a multi-author review.)

Seizure Outcome after Resection of Supratentorial Cavernous Malformations: A Study of 168 Patients

Summary:u2002 Purpose: The optimal management of cerebral cavernous malformations (CCMs) with epileptic seizures is still a matter of debate. The aim of our study was to examine seizure outcome in the largest published series of surgically treated patients with epilepsy due to a supratentorial CCM, and to define predictors for good surgical outcome.

Middle cerebral artery occlusion and ocular fat embolism after autologous fat injection in the face

a nursing home where she now lives with severe dementia and myoclonus. The patient’s history reported by the family was normal except for minor sleep disturbances, which had occurred about 1 month before the onset of focal neurological symptoms. Thus, the onset of the first non-specific symptoms can be considered to be 7 weeks and the onset of the first neurological symptoms to be 3 weeks before admission to our hospital. The first measurement of NSE in the CSF (commercial kit Hoffmann LaRoche, Basle, Switzerland; normal value: 12.5 ng/ml) was done at admission and showed a level of 66.8 ng/ml. In a second measurement 15 days later, the NSE level was 97.2 ng/ml and a third measurement another day later showed a level of 100.0 ng/ml. The diagnosis of CJD was also supported by the detection of the 14-3-3 brain protein in the second CSF sample (Department of Neurology, University of Göttingen, Germany). 14-3-3 has also been reported to be a specific marker for CJD, although false-positive results may occur in some cases [1]. Our observation shows that NSE and the 14-3-3 brain protein can be elevated even a few weeks after onset of neurological symptoms of CJD. We conclude that in cases of possible or probable CJD it is useful to measure NSE and 14-3-3 in the CSF even in the early stages of the disease. Furthermore, this case supports the hypothesis that damage of brain cells leading to NSE elevation possibly starts before the onset of neurological symptoms or is extremely marked in the very early stage of the disease. References

Hypoxia-Induced Acute Mountain Sickness is Associated with Intracellular Cerebral Edema: A 3 T Magnetic Resonance Imaging Study

Acute mountain sickness is common among not acclimatized persons ascending to high altitude; the underlying mechanism is unknown, but may be related to cerebral edema. Nine healthy male students were studied before and after 6-h exposure to isobaric hypoxia. Subjects inhaled room air enriched with N2 to obtain arterial O2 saturation values of 75 to 80%. Acute mountain sickness was assessed with the environmental symptom questionnaire, and cerebral edema with 3 T magnetic resonance imaging in 18 regions of interest in the cerebral white matter. The main outcome measures were development of intra- and extracellular cerebral white matter edema assessed by visual inspection and quantitative analysis of apparent diffusion coefficients derived from diffusion-weighted imaging, and B0 signal intensities derived from T2-weighted imaging. Seven of nine subjects developed acute mountain sickness. Mean apparent diffusion coefficient increased 2.12% (baseline, 0.80±0.09; 6 h hypoxia, 0.81 ± 0.09; P = 0.034), and mean B0 signal intensity increased 4.56% (baseline, 432.1 ±98.2; 6 h hypoxia, 450.7 ± 102.5; P < 0.001). Visual inspection of magnetic resonance images failed to reveal cerebral edema. Cerebral acute mountain sickness scores showed a negative correlation with relative changes of apparent diffusion coefficients (r = 0.83, P = 0.006); there was no correlation with relative changes of B0 signal intensities. In conclusion, isobaric hypoxia is associated with mild extracellular (vasogenic) cerebral edema irrespective of the presence of acute mountain sickness in most subjects, and severe acute mountain sickness with additional mild intracellular (cytotoxic) cerebral edema.

Good Outcomes in Ischemic Stroke Patients Treated With Intravenous Thrombolysis Despite Regressing Neurological Symptoms

Background and Purpose— We evaluated the clinical course of 19 acute stroke patients with rapid early improvement of neurological deficit within the 3-hour window, treated with intravenous thrombolytics. Results— No patient demonstrated a neurological deterioration during hospitalization. National Institutes of Health Stroke Scale (NIHSS) scores at therapy decision and discharge were 5 (4 to 6) and 0.5 (0 to 1.5), respectively. At 3-month follow-up, 1 patient had died; in remaining patients, NIHSS was 0 (0 to 1) and modified Rankin Scale 0.5 (0 to 1; ≤1 in 15 patients). Conclusions— Withholding of intravenous thrombolysis because of spontaneous early regression of neurological symptoms may not be justified.

A validation study on the intraobserver reproducibility of transcranial color-coded duplex sonography velocity measurements

Transcranial color-coded duplex sonography (TCCD) is a new method for the measurement of angle-corrected intracranial blood velocities. The insonation angle represents the most important technical variable affecting Doppler velocimetry. The present study was designed to evaluate the intraobserver reproducibility of TCCD for repeated examinations of blood velocity in the anterior, middle and posterior cerebral, basilar and vertebral arteries. Three examinations were performed by the same examiner in each of 20 healthy volunteers within 10 days, with a minimal interval of 2 days between two subsequent examinations. The observer was blinded to previous results. The reproducibility was evaluated by calculating the correlation coefficient (r) and the coefficient of variance (CV) of the difference between the values obtained from the second and the third examination vs. the first examination. The results showed good reproducibility of TCCD velocity measurements in all examined arteries: for maximal systolic velocity r was 0.80-0.94 (p < 0.001), and CV was 5.5-9.4%; for maximal end-diastolic velocities r was 0.89-0.94 (p < 0.001), and CV was 6.6-12.2%.