[MRI in patients with cerebral infarct and chronic cerebral circulation insufficiency].
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The importance of MRI (magnetic resonance imaging) for the diagnosis of brainstem infarction.
As experience with it accumulates, high resolution MRI seems more capable of representing morphological alterations of the central nervous system than cranial computer tomography (CCT). The question thus arises whether the detection of brainstem infarctions with MRI might not be easier than with CCT and how the topography of brainstem lesions demonstrated with MRI correlate with clinical symptoms and signs. 16 patients with definite clinical symptoms of brainstem infarction were examined by MRI. The examination took place between the 10th and 14th day after the occurrence of the infarction. Using MRI, we found pathological results in only 8 of these cases. In only 5 of these cases a clear relationship between the neurological picture and the topography of the lesion could be shown. These findings demonstrate that despite the high quality of the MRI images, the clinical examination for symptoms and signs is more important than imaging in the brainstem infarction.
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A case of cerebellar infarction occurred with the 8th cranial nerve symptoms.
A rare case, 32-year-old man, of cerebellar infarction with the occurrence of the 8th cranial nerve symptoms was reported. On the neuro-otological examination, hearing test and caloric test showed a severe hearing loss and no response on the right side, respectively, and the spontaneous horizontal nystagmus fixed to the left direction was observed. Magnetic resonance (MR) imaging showed the infarctions in the areas of anterior inferior cerebellar artery (AICA) and posterior inferior cerebellar artery (PICA) on the right side. On the 14th illness day, the 8th cranial nerve symptoms disappeared, and on the 12th illness day, right hearing level and caloric response were significantly improved. We suggested that such an early recovery of the subjective symptoms and neuro-otological findings may be attributable to the recanalized circulation disturbance or the development of collateral circulation.
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Infarction of superior cerebellar artery presenting as cerebellar symptoms.
BACKGROUND: MRI of the brain has facilitated the diagnosis of cerebellar infarction in the territory of the superior cerebellar artery (SCA). We analyzed the data on patients with SCA infarction who presented with only cerebellar symptoms in an attempt to define its underlying pathophysiology. SUMMARY OF REPORT: Ten patients with SCA infarction who presented with cerebellar symptoms were studied by brain MRI, angiography, and underlying pathology. Brain MRI demonstrated an infarct in the SCA territory in the anterior rostral cerebellum of all patients. None had abnormalities in the brain stem. In four patients, a hemorrhagic infarct was present in the same region. Cerebral angiography revealed no obvious SCA occlusion or atherosclerotic vascular disease in any patient. Eight of the 10 patients had heart disease, such as atrial fibrillation or old myocardial infarction. The presumed diagnosis was occlusion of the SCA in its periphery due to cardiogenic embolism. CONCLUSIONS: When a patient presents with only cerebellar symptoms and has cerebellar infarction demonstrated by brain MRI, the SCA branch is probably occluded by cardiogenic embolism.
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Neurophysiologic syndromes in stroke as predictors of outcome.
Outcomes in self-care following rehabilitation in 226 patients were correlated with 11 stroke syndromes, reflecting several pathophysiologic disturbances subsequent to either infarction or hemorrhage in cerebral or vertebro-basilar vessels. Self-care was scored on a 20-point scale for bed movements, transfers, feeding, dressing, personal hygiene, and bathing. Interjudge error among therapists did not exceed 2.5%. Mean score in left cerebral infarction without aphasia was used as a referent value. Scores in left cerebral infarction with aphasia and right parietal lobe syndrome with and without spatial agnosia were similar to the referent. Brain stem dysfunction with spasticity and right cerebral infarction with paresis and spatial agnosia fell below the referent value (Pless than 0.05). Higher levels were achieved in the syndromes of left and right anterior cerebral artery territories, brain stem dysfunction with ataxia, and left parietal lobe syndrome with comprehension aphasia, although t-values were not significant. Length of stay among the 11 groups was fairly uniform except for the group with brain stem dysfunction with spasticity and the group with left hemiplegia with spatial agnosia. These groups indicated rather severe disabilities. Aside from neurologic dysfunction the range of scores was influenced by associated cardiopulmonary involvement.
Activities of Daily Living↗
The vascular territories in the cerebellum and brainstem: CT and MR study.
More than 100 CT and 15 MR studies of infarcts in the cerebellum and brainstem were reviewed to define the most typical distribution of infarcts in the different vascular territories. Posterior inferior cerebellar artery and anterior inferior cerebellar artery territories are variable in size and are in a sort of equilibrium with each other. The posterior inferior cerebellar artery territory in transverse sections reveals a characteristic posterior crescent caused by its cranial posterior extension. The anterior inferior cerebellar artery territory may be limited to the lateral inferior pontine and floccular regions but usually extends over the whole petrosal surface of the cerebellum up to the lateral angle. Superior cerebellar artery territory is the most extensive territory and includes the largest part of the deep white matter. Infarcts in a single-branch distribution, vermian or hemispheric, have a characteristic sagittal or oblique orientation. Watershed cerebellar infarcts can also be recognized. In the brainstem, paramedian, lateral, and dorsal penetrating arteries have characteristic distributions at the medullary, pontine, and mesencephalic levels. With MR, lateral medullary infarcts can be demonstrated. Paramedian penetrating arteries are paired, and symmetric and small infarcts at medullary and pontine levels are sharply delimited on the midline. At the mesencephalic level, infarcts in this distribution usually involve all the arteries originating from the tip of the basilar artery and from the precommunicating segment of the posterior cerebral arteries, resulting in a central mesencephalic infarct with bilateral upward extension in the thalami. The different vascular territories in the cerebellum and in the brainstem are illustrated in schematic drawings in transverse, coronal, and sagittal planes. Knowledge of the vascular territories gained by the multiplanar capabilities of MR, and knowledge of the CT patterns of enhancement and evolution, will improve recognition and definition of infarcts.
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Magnetic resonance imaging in ischaemic accidents of the brain stem.
Seven cases of ischaemic accident affecting the brain stem are reported. There were two lacunar infarctions and five infarctions due to occlusion of major arteries (two lateral medullary infarctions, one pontine infarction and two thalamo-mesencephalic infarctions). In every case the abnormalities detected at MRI were concordant with the clinical findings. The authors underline the value of MRI in establishing clinico-topographic correlations in vivo and in differentiating lacunar infarctions from infarctions due to stenosis of major arteries in the vertebro-basilar system.
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[Results of treatment of cerebellar infarctions].
PURPOSE: The aim of this study is to assess the treatment results in patients with cerebellar infarctions and attempt to determine the features influencing the results. MATERIAL AND METHODS: We have analysed 12 patients with cerebellar infarctions treated from 1987 to 1996. The patients were admitted to hospital in the period between 24 hours and 37 days after onset. The level of consciousness on admission was assessed according to the Glasgow Coma Scale and results of treatment were assessed according to the Glasgow Outcome Scale at the time of discharge. The CT, MR, angio-MR, cerebral arteriography, USG-Doppler and ECHO were the main diagnostic methods. All patients were treated medically; temporary external ventricular drainage or ventriculoperitoneal shunt were used when hydrocephalus had been found. The influence of the level of consciousness, stroke localisation and presence of hydrocephalus on the results of treatment were analysed. RESULTS: 2 patients were in coma on admission, 3 patients scored 13-14 points in GCS and 7 patients did not demonstrate any consciousness disturbances. On neurological examination patients showed cerebellar signs in 9 cases, hemiparesis in 4 cases, lower cranial nerve dysfunction in 3 cases, eyeball movement disorders, compulsory gaze deviation, hemihypoaesthesia, trigeminal nerve dysfunction, peripheral facial palsy in 2 cases each and deafness in 1 case. Infarctions were localised in the cerebellar hemisphere only in 7 cases, in the cerebellar hemisphere with vermian extension in 2 cases and in 3 cases in cerebellum with brain stem extension. Based on additional investigations atherosclerotic occlusion in 3 cases and embolism mechanism in 4 cases were found as causes of the stroke; in 5 cases the cause of stroke remained unknown. The hydrocephalus resulting from the obstruction of cerebrospinal flow pathways was found in 5 patients. 1 patient died, permanent neurological deficits (GOS: SD) were found in 2 patients, the treatment results were successful (GOS: MD + GR) in 9 patients. The infarctions with brain stem extension had the greatest influence on treatment results among all analysed features. The level of consciousness on admission and presence of hydrocephalus had less influence on treatment results. CONCLUSIONS: In all patients with consciousness disturbances the hydrocephalus was found. The stroke localisation had a great influence on treatment results: worst results were obtained in patients with infarcts extending onto the brain stem. The consciousness disturbances on admission and the presence of hydrocephalus had only a slight influence on the results of treatment.
Antihypertensive Agents↗
Bilateral cerebellar ataxia as the sole manifestation of a unilateral rostral pontine tegmental infarct.
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Brain Stem↗
Cerebrovascular reactivity before and after carotid endarterectomy.
BACKGROUND: The hemodynamic relevance of internal carotid artery (ICA) stenosis often does not correlate with anatomic features, as angiographically defined. The cerebrovascular reactivity (CVR) has been advocated as a means of defining the cerebral hemodynamic impairment. METHODS: We assessed the results of pre- and postoperative CVR evaluation, using the CO2 transcranial doppler method, in 25 patients with high-grade ICA stenosis. The patients with history of stroke, evidence of cerebral CT infarction or symptoms from the contralateral circulation or the brain stem were excluded to avoid the effects of cerebral infarction on the hemodynamic studies. Statistical analysis was used to evaluate the CVR changes after carotid endarterectomy. RESULTS: Preoperative evaluation showed that CVR was generally well correlated with the degree of ICA stenosis and concomitant contralateral carotid steno-occlusion. Before endarterectomy the mean CVR value was 66.5% (moderately reduced). After surgery the overall mean value of CVR was 84.1% (normal), with a statistically significant improvement. CONCLUSION: The results of this study suggest that the CVR evaluation allows one to obtain hemodynamic information of clinical interest in the patients with ICA stenosis and that carotid endarterectomy is effective to restore the CVR in patients with cerebral hemodynamic impairment.
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[Cerebellar infarctions and their mechanisms].
Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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[Clinical analysis of diffuse axonal injury].
Sixty cases of diffuse axonal injury were analysed in this paper. All cases were caused by traffic accident; the mortality was 53.12%. Clinical manifestations were post-traumatic immediate and continuous coma with severe dysfunction of brain stem. MRI is helpful for clinical diagnosis. Pathological findings include the diffuse axonal injury of cortical while matter, corpus callosum, brain stem, and focal hemorrhage and infarction. The early use of hyperbaric oxygen combined with neuro-growth factor as an effective therapy is recommended.
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A prospective analysis of risk factors for white matter disease in the brain stem: the Cardiovascular Health Study.
BACKGROUND AND PURPOSE: White matter disease (WMD) in the brain stem may be a predictor of poor clinical outcome, independent of WMD in the periventricular and subcortical areas of the brain. Many cardiovascular risk factors such as older age, hypertension, and smoking have been suggested as risk factors for WMD in the periventricular and subcortical areas of the brain. However, no epidemiologic study has examined the associations between cardiovascular risk factors and WMD in the brain stem. METHODS: A total of 789 participants, aged 65 years or older, from the Cardiovascular Health Study constituted the present study population. WMD, defined as hyperintensive lesions on magnetic resonance imaging (MRI), in the brain stem was measured in 1992/1993 and 1997/1998. RESULTS: Of the 789 participants, 212 (26.9%) had WMD in the brain stem in 1997/1998. In multivariate logistic regression analysis, the presence of WMD in the brain stem in 1997/1998 was significantly associated with several variables measured in 1992/1993: an increase by 5 years of age (OR = 1.51, 95% CI: 1.25-1.83), a 10-pack-years increase in smoking (OR = 1.12, 95% CI: 1.04-1.21), a 0.1-liter increase in first-second forced expiratory volume (OR = 0.95, 95% CI: 0.92-0.99), a 1 micromol/l increase in fibrinogen level (OR = 1.13, 95% CI: 1.03-1.23), and MRI infarction (OR = 2.58, 95% CI: 1.78-3.74). Excluding those (n = 167) with WMD in the brain stem in 1992/1993, the pattern remained. Hypertension was not associated with WMD in the brain stem. CONCLUSIONS: Increased age, smoking, lower forced expiratory volume, increased fibrinogen level, and MRI infarction, but not hypertension, may be independent risk factors for WMD in the brain stem in older adults.
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Vascular pseudoparkinsonism.
Vascular pseudoparkinsonism may be confused with idiopathic Parkinson's disease. Patients may be unnecessarily treated with anti-parkinsonian drugs while their underlying vascular disease is ignored. We investigated 250 parkinsonian patients seen in our Movement Disorders Clinic for a possible vascular etiology. After excluding those with a known secondary cause such as drug-induced parkinsonism, progressive supranuclear palsy, multiple system atrophy and hyperparathyroidism, brain computed tomography and/or magnetic resonance imaging were performed on those who showed poor or no response to levodopa. In those with an ischemic lesion demonstrated on neuroimaging, anti-parkinsonian drugs were stopped and the patients were reassessed. Eleven patients (4.4%) had ischemic brain lesions accounting for their parkinsonism. All were initially diagnosed as Parkinson's disease because of the prominence of bradykinesia and rigidity. Gait disturbance was also common, but resting tremor was distinctly absent. Three anatomical patterns with different prognosis were identified. Three patients with basal ganglia lacunar infarct recovered spontaneously, three with frontal lobe infarcts remained static and five with periventricular and deep subcortical white matter lesions had progressive deterioration. Autopsy in one patient confirmed bilateral frontal lobe watershed infarcts and the absence of brain stem Lewy bodies. Parkinsonian patients with poor or no response to levodopa therapy should be investigated for a vascular etiology.
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Palatal myoclonus and denervation supersensitivity in the central nervous system.
We postulate that palatal myoclonus after infarction of the brainstem or cerebellum, or both, is the manifestation of denervation supersensitivity secondary to lesions involving the dentatorubroolivary system. Two cases of our own and 31 from the English and French literature were analyzed in order to determine the delay between the occurrence of presumed anatomical lesions and the recognition of palatal myoclonus. The intervals varied from 2 to 49 months with the median between 10 and 11 months. The natural history of palatal myoclonus following brainstem infarction seemed consistent with the hypothesis.
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[Cerebellar infarct: clinical picture, diagnosis and treatment].
Cerebellar infarctions are a relatively rare disorder, the diagnosis of which even based on clinical, angiographical and ventriculographic studies is rather difficult. Of big service in such conditions are computer tomographies. In extensive isolated cerebellar infarctions with signs of developing occlusional hydrocephaly with brain stem compressions, there may be indications to surgical operations. The paper contains the literary review, where problems of diagnosis and treatment of cerebellar infarctions are considered. The paper also contains a description of one case where a surgical operation was performed with a good outcome.
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[Evoked potentials in diagnosis of ischemic brain stem lesions].
We present an overview on the impact of evoked potentials in diagnosis of ischemic brainstem lesions. Brainstem auditory evoked potentials and somatosensory evoked potentials depict abnormalities, whereas visual evoked potentials are normal in most cases. In patients with basilar artery thrombosis and primary pontine hemorrhage these evoked potentials are mostly abnormal and can indicate the location of the lesion. Furthermore, they are of prognostic value. Whether evoked potentials are abnormal in strokes with branch occlusion of the basilar artery, depends on the location of the infarction. In infarctions of the basis pontis BAEP and SEP may be normal. Hemiparesis in brainstem strokes are associated with abnormalities in transcranial magnetic stimulation. However, no further evaluation of the level of the pyramidal tract lesion is possible by this method. During fibrinolytic therapy of basilar artery thrombosis a continuous monitoring is possible by means of BAEP. Thus, information can be obtained that is not available from neurological examination of the patient under sedative drugs.
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Computerized tomography in infarctions of the vertebral-basilar system.
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