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Cerebral venous angioma of the pons complicated by nonhemorrhagic infarction. Case report.

The authors emphasize an unusual complication of venous angiomas in the brain: venous infarction. The patient in this case is a 32-year-old man who presented with a clinical history of headache followed by a worsening of his neurological status. Neuroimaging studies demonstrated a brain infarct in the posterior fossa, which was related to thrombosis of the draining vein of a cerebral venous angioma. A conservative treatment approach without anticoagulation therapy was followed and the patient completely recovered. Nonhemorragic venous infarction caused by thrombosis of a venous angioma is exceptional and only nine previous cases have been reported in the literature.

Adult↗

Distribution and in situ proliferation patterns of intravenously injected immortalized human neural stem-like cells in rats with focal cerebral ischemia.

Neural stem cells are considered as a candidate for cell replacement therapy in various neurological diseases. To investigate whether human neural stem cells can migrate into the adult ischemic rat brain, we transplanted immortalized human neural 'tem-like' cells intravenously 24 h after focal cerebral ischemia. The intravenously injected human neural stem-like cells were found around the infarcted area, differentiated into neurons and astrocytes in the lesioned areas, and survive up to 56 days after transplantation. The number of the injected cells increased between 7 and 14 days after transplantation with incorporating BrdU. Our findings show that intravenously injected human neural stem-like cells may incorporate into the ischemic brain, and undergo proliferation responding to the endogenous mitotic signal during the acute period of focal ischemia.

Animals↗

Correlation of lymphocyte heat shock protein 70 levels with neurologic deficits in elderly patients with cerebral infarction.

PURPOSE: To assess the association between heat shock protein 70 (HSP70) levels and the severity of ischemic stroke in elderly patients. METHODS: We conducted a case-control study to investigate the changes in lymphocyte HSP70 levels by immunoblot in 65 elderly patients with mild (n = 22), intermediate (n = 21), or severe (n = 22) stroke, and in 34 healthy controls. We analyzed correlations between HSP70 levels and neurologic deficit scores on days 1, 15, and 30 after the onset of stroke. RESULTS: Mean (+/- SD) HSP70 levels were higher in all stroke patients compared with controls (mild stroke: 709 +/- 194 units; intermediate: 585 +/- 165 units; severe: 421 +/- 124 units; controls: 86 +/- 34 units on day 1). Patients with mild stroke had higher levels at day 1 and 15 than did patients with severe stroke. HSP70 levels decreased rapidly from days 1 to 30 in all patients, except in patients with severe stroke, in whom levels decreased slowly between days 15 and 30. There were significant negative correlations between HSP70 levels and neurologic deficit scores in patients on days 1 (r = -0.53, P < 0.001) and 15 (r = -0.54, P < 0.001), but a positive correlation on day 30 (r = 0.49, P < 0.001). CONCLUSION: These data suggest that HSP70 may be a marker for neuroprotection in the early stage of ischemic stroke and a marker for a crisis in the later stages of severe cerebral infarction. Further studies on the use of lymphocyte HSP70 levels in predicting clinical outcomes and underlying mechanisms in cerebral infarction are warranted.

Aged↗

Distinguishing silent lacunar infarction from enlarged Virchow-Robin spaces: a magnetic resonance imaging and pathological study.

We studied clinicopathological correlations between magnetic resonance imaging (MRI) appearances of postmortem brains and pathological findings in 12 patients to identify simple criteria with which to distinguish lacunar infarctions from enlarged Virchow-Robin spaces. In vivo MRI was also available for 6 of the 12 patients. We focused on small, silent, focal lesions including lacunar infarctions and enlarged Virchow-Robin spaces that were confirmed pathologically. From a total of 114 lesions, enlarged Virchow-Robin spaces were most often found in the basal ganglia and had a round or linear shape. Lacunar infarctions also were most frequent in the basal ganglia, but 47% of these were wedge-shaped. In the pathological studies, excluding lesions from the lower basal ganglia region, enlarged Virchow-Robin spaces were usually smaller than 2 x 1 mm. The shapes and sizes of the lesions determined by MRI (in vivo and postmortem) concurred with the pathological findings, except that on MRI the lesions appeared to be about 1 mm larger than found in the pathological study. When lesions from the lower basal ganglia and the brain stem regions are excluded, the sensitivity and specificity for discriminating enlarged Virchow-Robin spaces from lacunar infarctions are optimal when their size is 2 x 1 mm or less in the pathological study (79%/75%, respectively), 2 x 2 mm or less in both of the MRI studies: postmortem (81%/90%), and in vivo (86%/91%). In conclusion, we were able to differentiate most lacunar infarctions from enlarged Virchow-Robin spaces on MRI on the basis of their location, shape and size. We stress that size is the most important factor used to discriminate these lesions on MRI.

Aged↗

Neurologic, audiologic, and electrophysiologic sequelae of bilateral temporal lobe lesions.

A 67-year-old woman with demonstrated intact peripheral and brain-stem auditory pathways presented with sudden deafness secondary to sequential bilateral temporal lobe infarcts. Initial examination revealed no behavioral response to sounds and a mild Wernicke's aphasia. Hearing gradually returned but auditory agnosia persists. Changes seen on the computed tomographic scan and the middle latency auditory evoked response over a seven-month period were analyzed and suggest that the peak component of the middle latency response arises from Heschl's gyrus.

Aged↗

Cardiac arrhythmias in acute stroke.

Cardiac arrhythmias were more frequent (p less than 0.001) in 312 stroke patients admitted to an intensive care stroke unit, than in 92 patients admitted to the unit and subsequently found not to have strokes. This significant difference remained when a stroke subgroup and the non-stroke group were matched for age, sex and duration of stay in the unit (P less than 0.005). Hypertension and hypertensive cardiac disease were more common in the stroke than in the non-stroke patients (P less than 0.001). Ectopic beats and atrial fibrillation, as well as other arrhythmias, were most frequent in patients with cerebral hemisphere infarction, and patients with hemispheric lesions had significantly more arrhythmias than those with brain stem lesions (P less than 0.05). The arrhythmias were rarely (2%) responsible for hemodynamic ischemic cerebrovascular lesions, but may have been associated with cerebral embolism in up to 17% of cases. The cardiac arrhythmias appeared to have little influence on the course of the subsequent recovery from stroke. Although these arrhythmias frequently reflect the high incidence of cardiac disease in stroke patients, in some cases they are secondary to the acute cerebrovascular lesion itself.

Acute Disease↗

Diagnosis of retrocochlear and central vestibular disease by magnetic resonance imaging.

Magnetic resonance imaging has become the study of choice for the diagnosis of retrocochlear and central vestibular disease. Three groups of lesions, each characterized by a specific site of origin, have been recognized: 1) petrous apex lesions such as congenital cholesteatomas and cholesterol granulomas involving the eighth cranial nerve within the internal auditory canal; 2) cerebellopontine angle tumors, mainly acoustic neuromas and meningiomas; and 3) CNS disease involving the brain stem and the central auditory and vestibular pathways such as tumors, multiple sclerosis, infarcts, and hemorrhage.

Auditory Diseases, Central↗

Cerebral and retinal vascular complications of inflammatory bowel disease.

Recurrent retinal branch artery occlusions, carotid thromboembolism, cerebral venous thrombosis, transient brainstem ischemia, and massive brainstem and cerebral infarction complicated the course of inflammatory bowel disease in 5 patients. Three patients had ulcerative colitis and 2 had regional enteritis. The usual risk factors for stroke were absent. Neuropathological examination in 1 patient showed in situ thrombosis of small cerebral and brainstem arteries and veins. Coagulation studies showed thrombocytosis, short partial thromboplastin times, and elevation of fibrinogen and Factor VIII levels. Platelet counts and coagulation factors returned toward normal after control of intestinal inflammation in each of the 4 surviving patients. Inflammatory bowel disease can be accompanied by a hypercoagulable state that predisposes to stroke.

Adult↗

Early proliferative changes in astrocytes in postischemic noninfarcted rat brain.

Transient cerebral ischemia in rats was produced by permanent occlusion of the vertebral arteries and 30-minute occlusion of the common carotid arteries. This model produces ischemic necrosis of neurons in the corpus striatum, cerebral cortex, and hippocampus; infarcts, with necrosis of neuropil, astrocytes, and blood vessels, are rare. Changes in striatal astrocytes at 40 minutes and 3 hours of reperfusion were evaluated by electron microscopy, and quantitative estimates of increases in cytoplasmic and mitochondrial area were performed. In areas of corpus striatum with moderate ischemic cell change, the percentage of astrocytic nuclei increased from 10.79% in controls to 17.76% at 40 minutes after ischemia (p less than 0.01) and 19.86% at 3 hours (p less than 0.01). Astrocytic cytoplasm was expanded and contained increased numbers of mitochondria, many of which were pleomorphic and had dilated intracristal spaces and condensed matrix. Rough endoplasmic reticulum was increased. Total mitochondrial area and number of mitochondrial profiles rose significantly in the astrocytic perikarya and foot processes at 3 hours postischemia. The greater number of astrocytes, the increases in mitochondria and rough endoplasmic reticulum and the configurational changes in the mitochondria suggest increased metabolic activity of astrocytes in postischemic, noninfarcted brain.

Animals↗

Survival after traumatic ponto-medullary tear.

Two children (aged 10 and 12 years) were admitted unconscious to the neurosurgical department after traffic accidents. Both developed a 6th nerve paralysis on the next day. One patient was able to communicate from the 2nd day and died on the 8th day in an anuric state without major neurological deficit. The second patient remained deeply comatose, tetraplegic, and required intermittent artificial respiration: She died of pneumonia on the 26th day. Neuropathological examination revealed a ponto-medullary rent in each case: additionally there was avulsion of small arteries over the pyramids, haemorrhage and small focal infarcts in the distribution of perforating arteries in the medulla and pons, and abundant retraction balls in longitudinal fibre tracts of the brain stem. The cases show for the first time that traumatic ponto-medullary tears are not always rapidly fatal, and demonstrate that primary focal brain stem trauma may occur in the absence of diffuse trauma of the white substance.

Cerebral Arteries↗

Isolated cranial nerve palsies due to brainstem lesions.

Isolated cranial nerve palsies are often attributed to lesions of the respective nerves along their extraaxial courses. There are a significant number of reports of individual patients with cranial nerve palsies, mostly of the 3rd and 6th nerves, as the sole manifestation of brainstem lesions proven by magnetic resonance imaging (MRI) or computer-assisted tomography (CT). An intraaxial basis may still be underestimated if based on MRI only, as electrophysiological abnormalities indicating brainstem lesions (masseter reflex, blink reflex, DC electrooculography) may be independent from MRI-documented morphological lesions. This article reviews the evidence that ischemic and demyelinating brainstem lesions are an important and underestimated cause of clinically isolated cranial nerve palsies. Especially in middle-aged and elderly people with 3rd and 6th nerve palsies, small pontine and mesencephalic infarctions seem to be more frequent than small-vessel ischemic infarctions of the extraaxial nerves.

Aged↗

A case of pontine lacunar infarction with ulcerative colitis.

We present the case of a young man who experienced a sudden onset of pure motor hemiplegia in association with ulcerative colitis. Based on a review of earlier reports, ulcerative colitis was suspected to be the background disease leading to cerebral infarction. A cerebral infarction of the lacunar type in the right ventromedial aspect of the upper pons was seen on magnetic resonance images. These images detected small lesions in the brain stem, and were used to follow-up their transitions.

Adolescent↗

A rapid, reliable, and valid method for measuring infarct and brain compartment volumes from computed tomographic scans.

BACKGROUND AND PURPOSE: Clinical stroke trials require objective and reproducible end point variables. Morphometry of cerebral structures, including infarct volume, provides numerical measures that represent the amount of tissue damaged and potentially salvaged by therapy. However, morphometry may be time-consuming and labor-intensive, and it requires standardization across multiple centers, which may be difficult to achieve in large multicenter trials. We developed a brain morphometry method that is unbiased, rapid, reliable, and based on well-accepted stereological techniques. We now extend this method to analysis of routine computed tomographic (CT) scans such as might be obtained during a clinical stroke trial. METHODS: We studied CT scans from 18 stroke patients and 14 asymptomatic control patients obtained over 5 years at the San Diego Veterans Administration Medical Center. Three observers independently measured the volume of the cranial vault, cerebrum, cortex, white matter, deep gray structures, ventricle, sulcal cerebrospinal fluid space, visible infarction, and cerebellum/brain stem. RESULTS: The two patient groups were well matched demographically. The intracranial volume of 1400 +/- 40 mL in control subjects was not different from the 1311 +/- 41 mL in patients. Cerebral volume was 1250 +/- 36 mL compared with 1070 +/- 36 mL (control subjects versus patients, P < .001), and infarction volume was 55 +/- 16 mL in patients. For all structures, intraclass correlation coefficients among the observers ranged from 0.87 to 0.03; the best agreement was found for lesion, ventricle, and intracranial volume. White matter and cortex volume predicted the National Institutes of Health Stroke Scale score but not the late outcome scores on the Barthel Index or Rankin Scale. Each scan required 70 to 90 minutes for analysis. CONCLUSIONS: We developed a stereological method for cerebral morphometry from CT scans that is reliable, rapid, and simple. The measurements are unbiased, can be made on slices of any known thickness, and are independent of machine variables. Our results are remarkably similar to values obtained with more labor-intensive methods. This method should be of use in large-scale, multicenter trials of stroke therapy.

Aged↗

[A case of symptomatic cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)].

We here report a 42-year-old woman diagnosed cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) by age, family history, neurological findings, and neuro imagings. Magnetic resonance imaging well demonstrated the multiple lesions in the cerebrum including the brain stem, which was characteristic findings in CADASIL.

Adult↗

Pure motor hemiparesis in a case of vertebrobasilar arterial ectasia.

A case of pure motor hemiparesis due to a pontine lacunar infarct is reported. Infarction was related to vertebrobasilar ectasia identified on CT, MRI and MR angiography. MR studies provide accurate information on anatomical location, residual lumen, partial thrombosis, mass effect on brain stem and CSF pathways and vascular complications.

Aged↗

Balloon-in-stent technique for the constructive endovascular treatment of "ultra-wide necked" circumferential aneurysms.

INTRODUCTION: Circumferential aneurysms, which incorporate >180 degrees of the circumference of the parent vessel, present a unique therapeutic challenge, particularly in circumstances in which a deconstructive treatment strategy is not feasible. We detail a novel technique for endovascular parent vessel reconstruction with aneurysm embolization. METHODS: We performed a retrospective review of the prospectively maintained databases of our two institutions to identify cases in which a balloon-in-stent technique had been used to treat circumferential aneurysms. During the first stage of this technique, a stent (Neuroform [Boston Scientific, Natick, MA], Multilink Vision [Guidant, Indianapolis, IN], or Bx Velocity [Cordis, New Brunswick, NJ]) is placed across the neck of the aneurysm to achieve parent vessel reconstruction. During the second stage, aneurysm coil embolization is performed with a compliant temporary occlusion balloon (Sentry [Boston Scientific, Natick, MA] or Hyperglide [Microtherapeutics, Irvine, CA]) placed within the stent to unambiguously demarcate and protect the parent vessel. In some cases, during the course of the embolization, coils project over and obscure the parent vessel in both working views. Before each coil detachment, the protection balloon is deflated under blank fluoroscopic roadmap visualization. The absence of shifting of any portion of the coil mass during balloon deflation indicates that the introduced coil is external to the stent-reconstructed parent vessel (i.e., within the aneurysm) and can be detached. This process is repeated until satisfactory aneurysm embolization is achieved. After embolization, the balloon catheter may be exchanged for a stent delivery system to facilitate the placement of a second stent. RESULTS: Seven patients underwent balloon-in-stent-assisted embolization over a 15-month period. Three were performed for internal carotid aneurysms, three for basilar trunk or basilar apex aneurysms, and one for a dissecting/fusiform V4 segment vertebral artery aneurysm. In three cases, the presence of the inflated balloon facilitated the manipulation of the image intensifier into a position which produced a "down-the-barrel" view of the parent vessel. In the four additional cases, for anatomic reasons, this view could not be achieved and coil mass projected over the reconstructed parent vessel in both views. Partial aneurysm occlusion (75-90%), was achieved in five cases, and near complete (>95%) occlusion was achieved in two cases. Complications included two significant retroperitoneal hematomas and two brainstem infarcts, both of which resulted in hemisensory symptoms. CONCLUSION: The balloon-in-stent technique provides a practical and safe treatment strategy for the management of circumferential aneurysms that are not amenable to deconstructive embolization.

Adult↗

Nestin-expressing neural stem cells identified in the scar following myocardial infarction.

Nerve fiber innervation of the scar following myocardial damage may have occurred either via the growth of pre-existing fibers and/or the mobilization of neural stem cells. The present study examined whether neural stem cells were recruited to the infarct region of the rat heart following coronary artery ligation. The neural stem cell marker nestin was detected in the infarct region of 1-week post-myocardial infarct (MI) male rats and cultured scar-derived neural-like cells. By contrast, nestin staining was undetected in either scar myofibroblasts or cardiac myocytes residing in the non-infarcted left ventricle. Reactive astrocytes were isolated from the infarct region and characterized by the co-expression of nestin, glial fibrillary acidic protein, and vimentin. Specific staining of oligodendrocytes and neurons was also detected in the infarct region and cultured scar-derived neural-like cells. Furthermore, neurofilament-M positive fibers were identified in the scar and tyrosine hydroxylase immunoreactivity was observed in peripherin-positive neurons. Neurite formation was induced in PC12 cells treated with the conditioned-media of primary passage scar-derived cells, highlighting the synthesis and secretion of neurotrophic factors. Nerve growth factor (NGF) and brain-derived neurotrophic factor were detected in myofibroblasts and neural cells, and both cell types expressed the NGF receptors trkA and p75. These data highlight the novel observation that neural stem cells were recruited to the infarct region of the damaged rat heart and may contribute in part to nerve fiber growth and subsequent innervation of the scar.

Animals↗

[Asymptomatic multiple sclerosis - 3 cases (author's transl)].

Multiple Sclerosis (MS) cases found at autopsy in patients who had died from other diseases and in whom no sign or symptom could be related to MS are called "asymptomatic". Three cases are reported. The first patient was a 62 year old man who presented with a slowly progressive disturbance of gait, incontinence and deterioration of intellectual function. A falx meningioma was surgically removed. The patient died 3 years later with an acute respiratory illness. Examination of the brain disclosed evidence of the operation and numerous old plaques disseminated through the cerebral hemispheres (centrum semi-ovale, periventricular regions, internal thalamus and junction between cortex and white matter) and in the brain stem. The second case, a 77 year old woman with diabetes mellitus and hypertension, presented with cortical blindness and disturbances of memory of acute onset. She died one year later. Examination of the brain showed multiple infarcts involving the territories of both posterior cerebral arteries and the left middle cerebral artery. Numerous old plaques were seen in the periventricular regions, in the corpus callosum and in the left middle cerebellar peduncle. The third case, a 60 year old woman with mitral and aortic stenosis, presented with cortical deafness and transient right hemiparesis. She died 5 years later. Brain examination showed infarcts involving both middle cerebral artery territories. There was also many old plaques in the periventricular areas, thalamus, internal capsule, centrum semi-ovale, brain stem and right nucleus dentatus. In the 3 cases, the optic tracts were normal. The spinal cord, examined only in the first case, was also normal. The asymptomatic character of these MS cases can be explained first by the location of the plaques and the lack of spinal cord and optic tract involvement. It could also be due to the small size of the plaques and to axonal preservation. Such features are rare since our 3 observations have been selected from a pathological collection of 125 MS cases and 9,300 general neuropathological records. Six other cases have been previously reported by other authors.

Aged↗