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PubMed1999

Vertebrobasilar artery territory infarction as an initial manifestation of systemic lupus erythematosus.

Cerebral infarction is a well-documented complication of systemic lupus erythematosus (SLE), that usually occurs several years after the diagnosis of SLE. To our knowledge, however, strokes associated with vertebrobasilar artery involvement were not reported to present as an initial manifestation of SLE. We report two patients, who presented with vertebrobasilar territory infarction as an initial manifestation of SLE. Patient 1 was a 16-year-old girl, who developed dysarthria and ataxia. MRI showed multiple infarcts in the pons, cerebellum and thalamus. Four-vessel cerebral angiography showed multifocal stenoses in the vertebral and basilar arteries with beaded appearance. Patient 2 was a 26-year-old woman, who developed headache associated with dysarthria, dizziness and ataxia. MRI showed multiple infarcts in the cerebellum, medulla, pons, midbrain and thalamus. Cerebral angiography revealed occlusion of both vertebral arteries at the first cervical vertebral level with non-visualization of the basilar artery. Both patients were diagnosed as having SLE supported by laboratory results. Although rare, posterior circulation stroke can present as an initial manifestation of SLE, which may be attributed to vasculitis or dissection in the vertebral/basilar artery.

Adolescent↗
PubMed1995

[Isolated angiitis of the central nervous system. Clinical and neuropathological study of 2 cases].

Isolated angiitis of the central nervous system (IAC) is an idiopatic, recurrent vasculitis confined to the CNS involving small blood vessels. We describe the clinical, angiographic, and neuropathological data in two patients with IAC and delineate the main clinical and neuropathological features in both cases as well as the importance of a complete autopsy for discovering subclinical vasculitic lesions outside the CNS. Patient 1 concerned a 40 year-old-man that evolved for the last three years, initially with focal seizures, headache, and neurological focal deficits, later on the left sided hemihyposthesia and preferentially left parieto-occipital dysfunctions. He presented an oligoclonal band in CSF with slight hyperproteinorraquia and 25 lymphocytes. A cerebral angiography was compatible with angiitis and a leptomeningeal/cerebral biopsy showed lymphocytic vasculitis in the leptomeningeal and intraparenchymatous cerebral small vessels. These results lead to start a treatment with Cyclophosphamide associated to high dose of steroids. The patient clearly improved and now is almost asymptomatic. Patient 2 concerned a 67 year-old-man that evolved for 4 years with encephalic ischemic lesions distributed and confined throughout the brain stem and cerebellum, temporary remissions occurred and the patient required high-dose steroids and Cyclophosphamide to improve. Conventional and MRI angiographies only suggested the diagnosis that was confirmed at autopsy. The patient died after a massive pulmonary thromboembolism and a complete necropsic study showed abundant lymphocytic infiltrates, without granulomatous lesions, in the intraparenchymatous and leptomeningeal cerebral small vessels specially at the brain stem and cerebellar level where many demyelinated greyish areas and few infarctions were to be seen. The inflammatory cells were, in both cases, predominantly CD4+ T lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1981

Central auditory battery testing in brain stem disease.

The CAT scan and the BERA have revolutionized the practice of otology. There is a tendency to accept a negative scan report as indicating a lack of pathology. The authors have found cases where central battery testing has indicated progressing brain stem disease in the presence of a normal CAT scan. In one case, the abnormal test preceded a hemiplegia by two weeks. This raises the possibility of delaying or aborting an infarct if the correct diagnosis is made early.

Audiometry↗
PubMed1975

The electrocardiogram in infratentorial infarcts.

Sixty-nine patients with infratentorial infarcts were studied with respect to associated electrocardiographic (ECG) abnormalities. ECG changes were encountered in about 70% of the patients, the most frequent abnormalities being arrhythmias, conduction disturbances and ST-T changes. No relationship was found between the localization of the brain-stem lesion and the accompanying ECG pattern. It is concluded that ischaemic lesions within the central nervous system do not per se affect the ECG and that associated ECG changes are merely coincidental, reflecting the same basic vascular disease.

Adult↗
PubMed1980

Vertebral-basilar distribution infarction following chiropractic cervical manipulation.

Previous case reports of vertebral-basilar system infarction following chiropractic cervical manipulation have emphasized the role of predisposing factors such as cervical spondylosis, atherosclerosis, and congenital asymmetry of the posterior circulation. Ten patients without prior neurologic symptoms had vertebral-basilar system infarction promptly after chiropractic maneuvers. One patient, who was free of clinical and radiographic evidence of predisposing factors, subsequently died. Autopsy studies revealed massive nonhemorrhagic brainstem infarction due to bilateral vertebral artery thrombosis. Nine patients survived with residual neurologic deficits due to lesions in various locations of the posterior circulation. No patient received anticoagulants. Previous case reports are summarized and the kinetic anatomy of the vertebral arteries is reviewed to clarify the potential mechanisms involved in the pathogenesis of this entity. Although a causal relationship may be difficult to establish in individual cases, cervical manipulation seems to be the major identifiable factor in the pathogenesis of stroke in some patients.

Adolescent↗
PubMed1980

Parkinsonism in patients with cerebral infarcts.

From 220 necropsies of patients with cerebral infarcts, 5 were selected, in which the clinical history revealed typical parkinsonian symptoms with a progressive course of the extrapyramidal disorder. No correlation could be found between the location and the size of the infarcts on the one hand and the signs of parkinsonism on the other hand. In the 5 cases presented, the substantia nigra showed patchy areas of neuronal degeneration without any Lewy bodies nor neurofibrillary changes, around a pronounced status cribrosus in areas irrigated by paramedian branches of the mesencephalic arteries. Similar neuropathologic findings were present, but to a minor degree, in 2 of 5 cases of pseudo-bulbar palsy. Some extrapyramidal features were also present. It is proposed that is some rare instances, status cribrosus may be responsible for nigral degeneration and for the occurrence of parkinsonism.

Aged↗
PubMed1988

Leukoencephalopathy in elderly depressed patients referred for ECT.

Using brain magnetic resonance imaging (MRI) and high-resolution computed tomography (CT), we identified changes in the subcortical white matter in 44 of 67 elderly depressed inpatients (66%) referred for electroconvulsive therapy (ECT). This "leukoencephalopathy" was frequently associated with other structural brain changes, including cortical atrophy, lateral ventricular enlargement, and lacunar infarctions of the basal ganglia and thalamus. Many (58%) of the patients had developed late-onset depressive disorders, and the majority (86%) had been refractory to and/or intolerant of antidepressant drug therapy. Nevertheless, all but 1 of the 44 patients subsequently responded to a course of ECT, which in general was well tolerated. Although the precise etiology of the leukoencephalopathy remains unclear, clinical data suggest that it may result from arteriosclerotic disease of the medullary arteries that supply the subcortical brain regions. Several lines of evidence suggest that leukoencephalopathy may have implications for the pathophysiology of depressive illness, at least in some elderly patients.

Aged↗
PubMed1992

[MR study of the brain stem in elderly subjects].

Findings in patients in whom brain stem lesions were suspected were studied by a high-field-strength (1.5 T) MR imager. MR scans were obtained in 97 patients over a 10-month period. The mean age was 71 years (range, 39-94 years). A high incidence of infarction and lesions showing a high signal on T2-weighted image, but an almost normal signal on the T1-weighted image were observed at the pons in elderly cases. Furthermore, cases in which these two findings were observed, had a high incidence of lesion at other regions than pons. Cases with a past history of hypertension had higher incidence of lesions at the pons than normotensive patients (alpha less than 0.01). These findings suggest that MRI examination in the elderly could detect a high incidence abnormal lesions at the brain stem as well as in basal ganglia.

Aged↗
PubMed1995

Neurosurgical management of cerebellar haematoma and infarct.

The clinical features, treatment, and outcome were reviewed for 48 patients with a haematoma and 71 patients with an infarct in the posterior fossa in order to develop a rational plan of management. Clinical features alone were insufficient to make a diagnosis in about half of the series. Patients with a haematoma were referred more quickly to the neurosurgical unit, were more often in coma, and more often had CT evidence of brain stem compression and acute hydrocephalus. Ultimately, 75% of the patients with a haematoma required an operation. By contrast, most patients with an infarct were managed successfully conservatively. Early surgical management in both cerebellar haemorrhage and infarct (either external ventricular drainage or evacuation of the lesion), associated with early presentation and CT signs of brain stem compression and acute hydrocephalus, led to a good outcome in most patients. Of the patients with cerebellar haematoma initially treated by external drainage, over half subsequently required craniectomy and evacuation of the lesion; but, in some cases, this failed to reverse the deterioration. In patients with a cerebellar infarct, external drainage was more often successful. The guidelines, findings, and recommendations for future management of patients with posterior fossa stroke are discussed.

Adult↗
PubMed1989

[Blunt injury of the vertebral artery: report of three cases].

The authors reported three cases, whose vertebral arteries had been injured by blunt trauma to the neck which was followed by cerebello-brainstem infarctions. Case 1: a 32-year-old man, who developed severe vertigo and nausea 7 days after a traffic accident. He showed neck pain and horizontal nystagmus on admission. Three days later, he became drowsy. CT scan of the head demonstrated right-side cerebellar infarction, and the angiography revealed an occlusion of the right vertebral artery at C4-5 level. After the removal of the right cerebellar hemisphere, he recovered neurologically and was discharged from the hospital, able to walk. Case 2: a 47-year-old man, who suddenly became comatose 6 hours after an accident. Plain CT demonstrated a highly dense basilar artery. Angiography revealed the occlusion of the left vertebral artery, and severe stenosis of the right vertebral artery. The basilar artery was not visualized. Anticoagulant therapy was started immediately. He survived, but he developed locked-in syndrome. Case 3: a 53-year-old man, who developed transient apnea after an injury. On admission, neurological examination showed horizontal nystagmus, weakness of his right upper limb, and sensory disturbance in the left side of the body. Neck traction was done for spinal C1 and C2 fractures. Twenty-one hours after the injury, he became comatose suddenly. The four-vessels angiography revealed the occlusion of both vertebral arteries. The basilar artery was visualized through the posterior communicating arteries. He died on the 6th day after the trauma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Acute space-occupying processes in the posterior cranial fossa. Clinical aspects and computerized tomographic findings].

Ascending transtentorial herniation and compression of the brain stem are very severe sequelae of acute space-occupying lesions of the posterior fossa such as hematoma, infarction and tumours. The symptoms, course and outcome of these acute space - occupying lesions are discussed on the basis of 50 patients. For correct diagnosis of transtentorial herniation, CT studies are essential. The signs can be divided into early and alarming, and the time course into a biphasic and foudroyant form. Early detection of transtentorial herniation or impending incarceration is of crucial importance for successful therapy.

Acute Disease↗
PubMed1995

HMPAO single-photon emission computed tomography in posterior circulation infarcts.

The sensitivity of single-photon emission computed tomography (SPECT) in evaluating posterior circulation infarcts compared with that of computed tomography (CT) or magnetic resonance imaging (MRI) remains unknown. In a hospital-based population, the authors studied SPECT, CT, and MRI in 35 consecutive patients presenting with acute infarction clinically localized in the thalamus (7), posterior cerebral artery (PCA) territory (15), brainstem (19), and cerebellum (3). Multiple infarcts were noted in 8 patients. Overall, the SPECT sensitivity was lower than that of MRI (21% vs 93%, p = 0.004) and CT (42% vs 65%, p = 0.046). The SPECT and CT sensitivities were not significantly different (67% vs 73%) for PCA infarcts. Performed within 24 hours, SPECT showed a relevant hypoperfusion in all PCA infarcts. For brainstem infarcts, CT (33%, p = 0.074) and MRI (91%, p = 0.004) were more sensitive than SPECT, which showed no hemispheric hypoperfusion. The sensitivity of the three imaging techniques was 100% for large cerebellar infarcts. For the small group of thalamic infarcts, the SPECT, CT, and MRI sensitivities were 14, 71, and 100%, respectively. Thus, SPECT compared to CT and MRI is not helpful in the subacute phase to localize PCA and cerebellar infarcts and is of limited value for thalamic infarcts. In the first hours, the absence of cerebral hypoperfusion in brainstem infarcts may help to differentiate them from hemispheric infarcts usually associated with profound hypoperfusion.

Aged↗
PubMed2002

The injured brain interacts reciprocally with neural stem cells supported by scaffolds to reconstitute lost tissue.

Hypoxic-ischemic injury is a prototype for insults characterized by extensive tissue loss. Seeding neural stem cells (NSCs) onto a polymer scaffold that was subsequently implanted into the infarction cavities of mouse brains injured by hypoxia-ischemia allowed us to observe the multiple reciprocal interactions that spontaneously ensue between NSCs and the extensively damaged brain: parenchymal loss was dramatically reduced, an intricate meshwork of many highly arborized neurites of both host- and donor-derived neurons emerged, and some anatomical connections appeared to be reconstituted. The NSC-scaffold complex altered the trajectory and complexity of host cortical neurites. Reciprocally, donor-derived neurons were seemingly capable of directed, target-appropriate neurite outgrowth (extending axons to the opposite hemisphere) without specific external instruction, induction, or genetic manipulation of host brain or donor cells. These "biobridges" appeared to unveil or augment a constitutive reparative response by facilitating a series of reciprocal interactions between NSC and host, including promoting neuronal differentiation, enhancing the elaboration of neural processes, fostering the re-formation of cortical tissue, and promoting connectivity. Inflammation and scarring were also reduced, facilitating reconstitution.

Animals↗
PubMed1991

[Pathological and etiological studies on cerebral infarction in the vertebrobasilar arterial system].

25 cases of cerebral infarcts in vertebrobasilar arterial system are reported. Those were divided into 4 groups: 1. Embolism (10), the causes were NBTE, pulmonary infarct, rheumatic or congenital heart disease, coronary artery disease, respectively, and 2 unknown. 2. Thrombosis (5), the causes were arteriosclerosis, vascular malformations in the basal part of cerebrum. 3. Inflammatory infarcts (3), those were verified from tuberculosis, syphilis and aspergillosis respectively. 4. Lacunar infarcts (7), the causes were considered from hypertension. Pathologically, it was noticed that the location of embolism often situated at the terminal of basilar artery, and that if the embolism was completely obliterated, often a hemorrhagic infarction would follow. But the thrombosis in basilar artery, even the lumen was completely obliterated, any infarct would not follow, if the related collateral circulation was satisfactory. Clinically, the embolism in basilar artery often showed sudden onset, and that the symptoms of brain stem would aggravate quickly, but the thrombosis in basilar artery, if the collateral circulation was satisfactory, and symptom of brain stem might not follow.

Adult↗
PubMed1982

Temporal profile of neuronal damage in a model of transient forebrain ischemia.

This study examined the temporal profile of ischemic neuronal damage following transient bilateral forebrain ischemia in the rat model of four-vessel occlusion. Wistar rats were subjected to transient but severe forebrain ischemia by permanently occluding the vertebral arteries and 24 hours later temporarily occluding the common carotid arteries for 10, 20, or 30 minutes. Carotid artery blood flow was restored and the rats were killed by perfusion-fixation after 3, 6, 24, and 72 hours. Rats with postischemic convulsions were discarded. Ischemic neuronal damage was graded in accordance with conventional neuropathological criteria. Ten minutes of four-vessel occlusion produced scattered ischemic cell change in the cerebral hemispheres of most rats. The time to onset of visible neuronal damage varied among brain regions and in some regions progressively worsened with time. After 30 minutes of ischemia, small to medium-sized striatal neurons were damaged early while the initiation of visible damage to hippocampal neurons in the h1 zone was delayed for 3 to 6 hours. The number of damaged neurons in neocortex (layer 3, layers 5 and 6, or both) and hippocampus (h1, h3-5, paramedian zone) increased significantly (p less than 0.01) between 24 and 72 hours. The unique delay in onset of ischemic cell change and the protracted increase in its incidence between 24 and 72 hours could reflect either delayed appearance of ischemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.

Animals↗
PubMed1982

Regional cerebral blood flow and glucose metabolism following transient forebrain ischemia.

Progressive brain damage after transient cerebral ischemia may be related to changes in postischemic cerebral blood flow and metabolism. Regional cerebral blood flow (rCBF) and cerebral glucose utilization (rCGU) were measured in adult rats prior to, during (only rCBF), and serially after transient forebrain ischemia. Animals were subjected to 30 minutes of forebrain ischemia by occluding both common carotid arteries 24 hours after cauterizing the vertebral arteries. Regional CBF was measured by the indicator-fractionation technique using 4-iodo-[14C]-antipyrine. Regional CGU was measured by the 2-[14C]deoxyglucose method. The results were correlated with the distribution and progression of ischemic neuronal damage in animals subjected to an identical ischemic insult. Cerebral blood flow to forebrain after 30 minutes of moderate to severe ischemia (less than 10% control CBF) was characterized by 5 to 15 minutes of hyperemia; rCBF then fell below normal and remained low for as long as 24 hours. Post-ischemic glucose utilization in the forebrain, except in the hippocampus, was depressed below control values at 1 hour and either remained low (neocortex, striatum) or gradually rose to normal (white matter) by 48 hours. In the hippocampus, glucose utilization equaled the control value at 1 hour and fell below control between 24 and 48 hours. The appearance of moderate to severe morphological damage in striatum and hippocampus coincided with a late rise of rCBF above normal and with a fall of rCGU; the late depression of rCGU was usually preceded by a period during which metabolism was increased relative to adjacent tissue. Further refinement of these studies may help identify salvageable brain after ischemia and define ways to manipulate CBF and metabolism in the treatment of stroke.

Animals↗