CO2-related vasoconstriction superimposed on ischemic medullary brain autonomic nuclei may contribute to sudden death.

INTRODUCTION: In 2015, a multinational randomized controlled phase IV clinical trial of adaptive servoventilation for the management of heart failure with central sleep apnea was halted in progress because more patients in the study group were dying than in the control group. One year later, another large clinical trial reported results on the effectiveness of continuous positive airway pressure (CPAP) in preventing sudden death and other cardiovascular events such as heart attack and stroke in patients with preexisting vascular disease as well as obstructive sleep apnea. BACKGROUND: Sudden unexpected death has been associated with many types of small and nonmalignant medullary brain lesions, like demyelination plaques - largely asymptomatic until they caused sudden death. Many such medullary lesions, typically without hemorrhage or mass effect, have in themselves been previously considered relatively harmless - in cases where they have been known to be present. DISCUSSION: Why did not the improved pulmonary ventilation and subsequently improved gas exchange provided during the CPAP and servoventilation clinical trials help to resolve any ischemic lesions that may have been present both in the heart and in the medulla, thereby tending to normalize interactions between the vagal neural structures and the heart? CO2 is a potent dilator of brain vasculature, thereby increasing blood flow to the brain. When ventilation is increased, even if only to improve it back toward normal from a depressed steady-state level, the alveolar partial pressure of carbon dioxide is decreased, likely resulting in a converse relative vasoconstriction in the brain, thereby reducing blood flow in the brain, especially in watershed areas like the solitary tract nucleus. In normal physiology, this is demonstrated impressively by the ability of hyperventilation to induce loss of consciousness. CONCLUSIONS: The findings of several clinical trials recently reported, taken together with neuropathology case studies reported elsewhere, suggest that additional research is warranted in regard to the mechanisms by which focal medullary autonomic brain ischemia may be related to sudden death in general medical illnesses - and how it may additionally be influenced by changes in arterial CO2 levels.

Infarto isquémico mesencefálico: síndrome de Weber / Ischemic mesencephalic infarction: Weber's syndrome

La enfermedad cerebrovascular constituye la tercera causa de muerte en la población adulta, la primera causa de discapacidad a escala mundial y la segunda causa de demencia, problema de salud actual relacionado con otras enfermedades crónicas no transmisibles. Se presenta un caso de un infarto isquémico mesencefálico aterotrombótico en una anciana de 77 años con la expresión clínica de un síndrome de Weber. El síndrome de Weber es uno de los síndromes cruzados o alternos de la clínica y la neurología por lesión peduncular. Es poco frecuente y a la vez, el más frecuente de los alternos de tronco encefálico(AU)

Cerebrovascular disease is the third leading cause of death in the adult population, the leading cause of disability worldwide and the second cause of dementia. It is a current health problem related to other chronic noncommunicable diseases. We present a case of atherothrombotic mesencephalic ischemic infarction in a 77-year-old woman with the clinical expression of Weber syndrome, which is a crossed or alternating clinical syndrome and neurology by pedicle injury. It is rare and, at the same time, the most frequent alternating brainstem(AU)

Bilateral medial medullary infarction: a systematic review.

Bilateral infarction of the medial medulla (MMI) is rare. Limited information is available on clinical characteristics, etiology, and prognosis. High-resolution neuroimaging has a major role in elucidating the underlying stroke mechanism. The aim of this systematic review was to analyze the clinical presentations, stroke mechanisms, and outcomes in patients with bilateral MMI. We performed a systematic review of the literature from 1992-2011 that reported on clinical presentations, stroke mechanism, and/or outcomes in patients with magnetic resonance imaging-proven bilateral MMI. Medline, EMBASE, and Web of Science Scholars Portal were searched without language restriction. Two reviewers independently assessed identified studies to determine eligibility, validity, and quality. The primary outcome was inpatient mortality; a secondary outcome was case fatality at 12 months. We identified 138 articles from Medline, EMBASE, and Scholars Portal including the MeSH terms "brainstem infarction," "medulla," and "bilateral." Twenty-nine articles met our inclusion criteria, including a total of 38 cases with bilateral MMI, and included in our study. These 38 patients had a mean age of 62.2 years and were predominately male (74.2%). The most common clinical presentations were motor weakness in 78.4%, dysarthria in 48.6%, and hypoglossal palsy in 40.5%. The most common vascular pathology was vertebral artery atherosclerosis, in 38.5%. The clinical outcome was poor (mortality, 23.8%; dependency, 61.9%). Bilateral medial medullary infarction is a rare stroke syndrome. Clinical presentations were mostly rostral medullary lesions. Large-artery atherosclerosis and branch disease were the most common stroke mechanisms. The clinical outcome was usually poor.

Medial medullary infarction: clinical, imaging, and outcome study in 86 consecutive patients.

BACKGROUND AND PURPOSE: Clinical-imaging correlation and long-term clinical outcomes remain to be investigated in medial medullary infarction (MMI). METHODS: We studied clinical, MRI, and angiographic data of 86 consecutive MMI patients. The lesions were correlated with clinical findings, and long-term outcomes, divided into mild and severe (modified Rankin scale >3), were assessed by telephone interview. Central poststroke pain (CPSP) was defined as persistent pain with visual numeric scale > or = 4. RESULTS: The lesions were located mostly in the rostral medulla (rostral 76%, rostral+middle 16%), while ventro-dorsal lesion patterns include ventral (V, 20%), ventral+middle (VM, 33%), and ventral+middle+dorsal (VMD, 41%). Clinical manifestations included motor dysfunction in 78 patients (91%), sensory dysfunction in 59 (73%), and vertigo/dizziness in 51 (59%), each closely related to involvement of ventral, middle, and dorsal portions, respectively (P<0.001, each). Vertebral artery (VA) atherosclerotic disease relevant to the infarction occurred in 53 (62%) patients, mostly producing atheromatous branch occlusion (ABO). Small vessel disease (SVD) occurred in 24 (28%) patients. ABO was more closely related to VMD (versus V+VM) than was SVD (P=0.035). During follow-up (mean 71 months), 11 patients died, and recurrent strokes occurred in 11. Old age (P=0.001) and severe motor dysfunction at admission (P=0.001) were factors predicting poor prognosis. CPSP, occurring in 21 patients, was closely (P=0.013) related to poor clinical outcome. CONCLUSION: MMI usually presents with a rostral medullary lesion, with a good clinical ventro-dorsal imaging correlation, caused most frequently by ABO followed by SVD. A significant proportion of patients remain dependent or have CPSP.

Long-term outcome after suboccipital decompressive craniectomy for malignant cerebellar infarction.

BACKGROUND AND PURPOSE: Suboccipital decompressive craniectomy (SDC) is a life-saving intervention for patients with malignant cerebellar infarction. However, long-term outcome has not been systematically analyzed. METHODS: In this monocentric retrospective study we analyzed mortality, long-term functional outcome, and quality of life of all consecutive patients that were treated by SDC for malignant cerebellar infarction in our institution between 1995 and 2006. RESULTS: A total of 57 patients were identified. All of them were treated by bilateral SDC. An external ventricular drainage was inserted in 82%, necrotic tissue was evacuated in 56% of patients. There were no fatal procedural complications. Five patients were lost for follow-up. In the remaining 52 patients, the mean follow-up interval was 4.7 years (1 to 11 years). Within the first 6 months after surgery 16 of 57 patients (28%) had died. At follow-up, 21 of 52 patients (40%) had died and 4 patients (8%) lived with major disability (mRS 4 or 5). Twenty-one patients (40%) lived functionally independent (mRS 0 to 2). The presence of additional brain stem infarction was associated with poor outcome (mRS > or =4; hazard ratio: 9.1; P=0.001). Quality of life in survivors was moderately lower than in healthy controls. CONCLUSIONS: SDC is a safe procedure in patients with malignant cerebellar infarction. Infarct- but not procedure-related early mortality is substantial. Long-term outcome in survivors is acceptable, particularly in the absence of brain stem infarction.

Surgical and endovascular management of symptomatic posterior circulation fusiform aneurysms.

OBJECT: Patients with fusiform aneurysms can present with subarachnoid hemorrhage (SAH), mass effect, ischemia, or unrelated symptoms. The absence of an aneurysm neck impedes the direct application of a clip and endovascular coil deployment. To evaluate the effects of their treatments, the authors retrospectively analyzed a consecutive series of patients with posterior circulation fusiform aneurysms treated at Stanford University Medical Center between 1991 and 2005. METHODS: Forty-nine patients (mean age 53 years, male/female ratio 1.2:1) treated at the authors' medical center form the basis of the analysis. Twenty-nine patients presented with an SAH. The patients presenting without SAH had cranial nerve dysfunction (five patients), symptoms of mass effect (eight patients), ischemia (six patients), or unrelated symptoms (one patient). The aneurysms were located on the vertebral artery (VA) or posterior inferior cerebellar artery (PICA) (21 patients); vertebrobasilar junction (VBJ) or basilar artery (BA) (18 patients); and posterior cerebral artery (PCA) (10 patients). Pretreatment clinical grades were determined using the Hunt and Hess scale; for patients with unruptured aneurysms (Hunt and Hess Grade 0) functional subgrades were added. Outcome was evaluated using the Glasgow Outcome Scale (GOS) score during a mean follow-up period of 33 months. Overall long-term outcome was good (GOS Score 4 or 5) in 59%, poor (GOS Score 2 or 3) in 16%, and fatal (GOS Score 1) in 24% of the patients. In a univariate analysis, poor outcome was predicted by age greater than 55 years, VBJ location, pretreatment Hunt and Hess grade in patients presenting with SAH, and incomplete aneurysm thrombosis after endovascular treatment. In a multivariate analysis, age greater than 55 years was the confounding factor predicting poor outcome. Stratification by aneurysm location removed the effect of age. Of 13 patients with residual aneurysm after treatment, five (38%) subsequently died of SAH (three patients) or progressive mass effect/brainstem ischemia (two patients). CONCLUSIONS: Certain posterior circulation aneurysm locations (PCA, VA-PICA, and BA-VBJ) represent separate disease entities affecting patients at different ages with distinct patterns of presentation, treatment options, and outcomes. Favorable overall long-term outcome can be achieved in 90% of patients with PCA aneurysms, in 60% of those with VA-PICA aneurysms, and in 39% of those with BA-VBJ aneurysms when using endovascular and surgical techniques. The natural history of the disease was poor in patients with incomplete aneurysm thrombosis after treatment.

Aetiopathogenesis and long-term outcome of isolated pontine infarcts.

BACKGROUND AND PURPOSE: Isolated pontine strokes cause characteristic neurological syndromes and have a good short-term prognosis. The aim of this study was to examine the long-term survival, cumulative recurrence rate and clinical handicap of patients with isolated pontine infarcts of different aetiology. METHODS: One hundred consecutive patients with an isolated pontine infarction were identified by imaging studies and evaluated prospectively. After extensive study, cases were classified according to the aetiopathogenetic mechanisms: stroke due to basilar artery branch disease (BABD), small-artery disease (SAD) and large-artery-occlusive disease (LAOD). During a mean follow-up period of 46 months, stroke presentation and initial course, early and long-term mortality, disability and recurrence were evaluated. RESULTS: BABD was the most frequent cause of isolated pontine ischaemia (43%), followed by SAD (34%) and LAOD (21%). Hypertension was the most prominent risk factor, especially among patients with SAD (94.1%). Neurological impairment on admission was more severe in the LAOD group, followed by BABD. After 1 month patients with LAOD had the highest cumulative mortality (14.3%, p = 0.026) and more severe disability (61.1%, p = 0.001). Five-year mortality rate was 20.6%, 14% and 23.8% in the SAD-, BABD- and in LAOD-group respectively (p = 0.776). Cumulative 5-year recurrence rate was 2.3 % for BABD, 14.3 % for LAOD, and 29.4 % for SAD (p = 0.011). CONCLUSIONS: Overall long-term survival of patients with isolated pontine infarcts is good. Initial differences regarding short-term outcome in infarctions of different aetiology resolve with time. Effective secondary prevention among SAD patients may limit stroke recurrence and positively influence long-term prognosis.

Giant vertebrobasilar aneurysms: endovascular treatment and long-term follow-up.

OBJECTIVE: To report long-term imaging follow-up and clinical outcome of 13 patients with a giant vertebrobasilar aneurysm treated by parent artery occlusion (PAO). METHODS: From 1994 to 2000, 13 consecutive patients with a giant vertebrobasilar aneurysm were treated by PAO. Symptoms were related to mass effect in nine patients and to a subarachnoid hemorrhage in four. Endovascular treatment consisted of aneurysm trapping in nine patients and occlusion of one or both vertebral arteries in four. We assessed the clinical outcome and imaging findings in all patients during a 28-month period. RESULTS: Endovascular treatment resulted in clinical improvements in eight patients, worsening of symptoms in four, and death in one. One woman with a ruptured vertebral aneurysm died from a rebleeding after PAO without trapping. One man developed a brainstem infarction after lower basilar artery occlusion and incurred hemiparesis. In three patients, symptoms of mass effect increased after the procedure. Long-term follow-up revealed good or excellent clinical outcome in all patients and a sharp decrease in size of the thrombosed aneurysm in nine patients. One basilar aneurysm recanalized despite selective coiling and subsequent bilateral vertebral artery occlusion; one vertebral aneurysm and one basilar aneurysm did not decrease in size despite complete occlusion. CONCLUSION: Giant vertebrobasilar aneurysms are rare and challenging lesions for both neurosurgeons and neurointerventionalists. Their treatment by endovascular PAO remains safe and effective. Early clinical worsening may be observed, but long-term follow-up shows good or excellent results in most patients. This treatment can be carried out with minimal morbidity and mortality using clinical and angiographic monitoring.

Management of acute cerebellar infarction: one institution's experience.

OBJECTIVE: The management of cerebellar infarctions is controversial. The aim of this study was to determine which patients require surgical treatment and which surgical procedure should be performed when a patient with a cerebellar infarction exhibits progressive neurological deterioration. METHODS: A total of 44 patients (24 male and 20 female patients; average age, 56 yr) were treated at our institution for cerebellar infarctions in the past 8 years. Twenty-five patients received conservative treatment; two patients who were deeply comatose received no treatment. The remaining 17 patients underwent emergency surgery. Of those 17 patients, 8 underwent external ventricular drainage alone, 5 underwent external ventricular drainage as the first treatment plus secondary suboccipital craniectomy, and 4 underwent suboccipital craniectomy, with removal of necrotic tissue, as the first treatment. RESULTS: Of the 25 conservatively treated patients, 20 experienced good outcomes, 4 experienced moderate outcomes, and 1 died as a result of pulmonary embolism. Of the 17 surgically treated patients, 10 experienced good functional recoveries (7 treated with external ventricular drainage only and 3 treated with drainage followed by suboccipital craniectomy) and 3 survived with mild neurological deficits (one patient underwent ventriculostomy, one suboccipital craniectomy plus external ventricular drainage, and one suboccipital craniectomy only). The overall mortality rate was 13.6% (6 of 44 patients). CONCLUSION: For patients with worsening levels of consciousness and radiologically evident ventricular enlargement, we recommend external ventricular drainage. We reserve surgical resection of necrotic tissue for patients whose clinical status worsens despite ventriculostomy, those for whom worsening is accompanied by signs of brainstem compression, and those with tight posterior fossae.

[Clinical presentation and prognosis of brain stem infarcts. An evaluation of the Stroke Databank of the German Stroke Foundation]. / Klinische Präsentation und Prognose von Hirnstamminfarkten. Eine Auswertung der Schlaganfall-Datenbank der Stiftung Deutsche Schlaganfall-Hilfe.

Due to the great variety of clinical classification systems and syndromes, a representative overview of the etiology and prognosis of brain stem infarctions is missing. From the German Stroke Data Bank we therefore investigated 455 patients with visible brainstem infarction on cerebral imaging in comparison to patients with other infarct localizations. Follow-up after 3 and 12 months assessed functional outcome and recurrence of cerebral ischemia. Of 455 patients with acute brainstem infarction, 115 had additional infarctions in other vascular territories. In the remaining 340 patients with isolated brainstem infarction, the classification was: small vessel disease in 36.2%, macroangiopathy in 22.6%, and cardioembolism in 11.2%. After 3 months, 10% of the patients with isolated brainstem infarction had died and 55.6% were functionally independent. Mortality was 43.5% in patients with combined brainstem infarction. Our study highlights the frequency of small vessel disease as well as the relatively favorable prognosis in isolated brainstem infarction and preserved consciousness.