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Results for “Brain Stem Infarctions”

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PubMed2000

Diaschisis and acetazolamide reactivity in brainstem infarction.

Regional cerebral blood flows (rCBF) were studied in 6 patients with lateral medullary infarction and 4 patients with pontine infarction, using stable xenon computed tomography method. In lateral medullary infarction, the rCBF and acetazolamide reactivity were decreased in the ipsilateral cerebellum and the rCBF was decreased with normal acetazolamide reactivity in the contralateral frontal lobe in one patient accompanying ipsilateral cerebellar infarction. rCBF was decreased with normal acetazolamide reactivity in the cerebellum in 3 patients, and both rCBF and acetazolamide reactivity were decreased in the whole brain in 2 patients. In pontine infarction, rCBF was decreased in ipsilateral frontal lobe and contralateral cerebellum in one patient, rCBF was decreased in the cerebellum with normal acetazolamide reactivity in the other patients. The hypoperfusion with normal acetazolamide reactivity was considered to be due to diaschisis. The rCBF decrease in the remote areas in patients with brainstem infarction was considered to be due to diaschisis or underlying arteriosclerosis.

Acetazolamide↗
PubMed2000

Aspiration subsequent to a pure medullary infarction: lesion sites, clinical variables, and outcome.

BACKGROUND: Aspiration as a symptom of dysphagia and its apparent sequela, aspiration pneumonia, are common consequences of a stroke in the medulla. Previous reports that focused on dysphagia due to a medullary lesion were studies of single cases or a relatively small number of patients with multiple lesion loci. Moreover, the interval between the onset of stroke and the evaluation time of swallowing was not controlled and varied largely among patients. Thus, prediction of the swallowing status of patients with a medullary lesion has not been tenable. OBJECTIVES: To investigate the relation between the loci of pure medullary lesions and aspiration, to examine swallowing function over time, and to explore clinical variables that can predict aspiration. METHODS: We investigated 23 patients with pure medullary infarctions using the videofluoroscopic swallowing study and compared the airway status findings with the lesion location as determined with magnetic resonance imaging. The patients were classified by 6 medullary lesion-level categories (lower, lower-middle, middle, lower-middle-upper, middle-upper, and upper) and by 5 intralevel lesion loci (inferior-dorsal, large inferior-dorsolateral, para-median, midlateral, and dorsolateral). From the results of the videofluoroscopic swallowing studies, 2 patient groups were formed: one with aspiration and the other without aspiration. The clinical variables related to aspiration and outcome measures were also explored. RESULTS: Ten (44%) of the 23 patients manifested aspiration on swallowing: 9 (69%) of 13 with only middle-level lesions or lesions in multilevels, including the middle level; 1 (33%) of 3 with only upper-level lesions; and 0 (0%) of 7 with only lower-level medullary lesions. A lesion running the length of the middle and the lower medullary levels always resulted in aspiration. When an upper-level lesion was additionally involved, the incidence of aspiration depended on the horizontal extension of the lesion. We were able to discriminate the 2 patient groups with 95.7% accuracy using such variables as dysphonia, soft palate dysfunction, and facial hypesthesia. Most of the patients with aspiration symptoms due to a pure medullary infarction recovered rather quickly. CONCLUSIONS: Medullary infarctions often cause aspiration, but the occurrence may depend on the levels along the neuraxis and intralevel lesion loci. When different lesion levels and loci and their related clinical findings are considered as possible variables, aspiration becomes predictable. The outcome data prove that systematic control of evaluation time of swallowing was critical as we engaged in this study, since many aspirators with pure medullary infarctions resolve their swallowing difficulties rather quickly.

Adult↗
PubMed2001

Localization of clinical syndromes using DWI: two examples of the "capsular" warning syndrome.

The capsular warning syndrome (CWS) is a subtype of transient ischemic attack characterized by its recurrent nature, absence of cortical signs, and high probability of early capsular stroke. Currently, standard imaging techniques have identified only internal capsule lesions in this entity. The authors present 2 cases with an otherwise typical CWS in whom a brainstem stroke was detected by diffusion-weighted imaging (DWI). DWI's ability to differentiate between acute and chronic infarcts may assist in more accurate localization of clinical syndromes.

Aged↗
PubMed1991

Surgical treatment of space-occupying cerebellar infarctions--4 1/2 years post-operative follow-up.

Case reports of three patients with cerebellar infarction causing brain stem dysfunction and obstructive hydrocephalus as seen in computed tomography are presented. Surgical treatment, either ventricular puncture with drainage or suboccipital craniectomy and resection of the necrotic cerebellar tissue, was carried out. Indications for surgical treatment of space-occupying cerebellar infarction and post-operative follow-up of 4 1/2 years are discussed.

Adult↗
PubMed2002

Brainstem infarctions with normal MRI.

Most studies on brainstem infarctions included only patients with lesions documented by CT or MRI. The aim of this study was to analyse the clinical symptomatology in patients with the classical signs of brainstem infarcts and normal MRI results. Frequencies of MR-positive and negative infarctions should be analysed according to their location. In a series of 30 consecutive patients with acute clinical symptoms of ischemic brainstem lesions and persistence of the symptomatology for more than 10 days, 8 patients had normal MRI. In these patients the location of the lesion was established by clinical and electrophysiological criteria. The lesions in the 8 patients with normal MRI were situated in medulla oblongata (n=3), in pons (n = 2), and in midbrain (n = 3). In each of these patients the clinical symptoms corresponded to one of the classical alternating syndromes, which are pathognomic for brainstem infarctions (1 Wallenberg, 1 Avellis, 1 Jackson, 2 Millard-Gubler, and 3 Weber). The clinical course of the infarctions with normal MRI was favourable, the symptoms disappeared within few weeks. Our study proved that the clinical diagnosis of brainstem infarction, particularly in lesions of midbrain and caudal tegmentum pontis, can not be excluded by normal MRI.

Aged↗
PubMed2006

Peri-infarct reorganization of motor function in patients with pontine infarct.

OBJECTIVES: Combined functional MRI (fMRI) and diffusion tensor tractography (DTT) imaging provides a powerful vehicle for the investigation of motor recovery mechanisms. Using this combined method, we investigated the motor recovery mechanism in patients with pontine infarct. DESIGN: We evaluated six healthy control subjects and two patients with pontine infarct at 6 months from onset. fMRI was performed at 1.5 T with timed hand grasp-release movements. For DTT, we used each of the 32 noncollinear diffusion-sensitizing gradients. Three-dimensional reconstructions of the fiber tracts were obtained with FA <0.3, angle >45 degrees as termination criteria. RESULTS: fMRI data revealed activation only in the contralateral primary sensorimotor cortex during movement of either hand. DTI findings from controls and the unaffected hemisphere of the patients showed that the corticospinal tract descended through the known corticospinal tract pathway. However, the tracts of the affected hemisphere in the patients were observed to pass along peri-infarct areas (patient 1: lateral, patient 2: posterior) in the pons. CONCLUSIONS: It seems that the peri-infarct areas compensate for corticospinal tract damage at the pons; this may be one mechanism of motor recovery for patients with pontine infarct.

Adult↗
PubMedDate not supplied

[Traumatic heart rupture or infarct?].

A 70-year-old motorist driving on the wrong side of the road caused a car-to-car head-on collision and died some minutes later. The autopsy revealed a lethal rupture of the right heart ventricle. The insurance company argued that driving on the wrong side was an act of gross negligence so that the damage was not covered by the full comprehensive insurance. Surprisingly, the microscopic examination of the myocardium performed by a clinical pathologist brought to light a severe myofibrillar degeneration (MFD) which was interpreted as diagnostic of acute myocardial infarction. It was supposed that this could have caused an incapacity of the driver to control his car, which in turn would commit the insurance to payment. A critical re-evaluation of the heart tissue material, however, revealed the pattern of trauma-induced hypercontraction banding of the myocardium along the cleft edges but no findings suggestive of myocardial infarction. Thus, the accident was not the result of a cardiac attack. But there was a severe preexisting pathology including cardiac hypertrophy, scarring of the myocardium, siderophages of the lungs, and an infarction of the pons, so that a cerebral dysfunction was the most plausible explanation for the accident. Thus, gross negligence had to be denied, and the insurance company was obliged to pay. This observation points to the existence of two different variants of MFD: Clinical pathologists are familiar with "tyical" MFD occurring in reperfusion after ischemia, in catecholamine toxicity, and around infarct necroses. But hypercontraction banding, regularly found along penetrating heart lesions and well known to forensic pathologists, is uncommon in clinical pathology.

Accidents, Traffic↗
PubMed2003

Cognitive functioning in patients with a small infarct in the brainstem.

Earlier findings in patients with a small supratentorial white matter infarct demonstrated subtle impairments of cognition. This is in line with reported difficulties in regaining premorbid level of functioning in daily life activities, even though any physical neurological deficits are no longer present. Either a "bystander effect" of adjoining gray matter or a long distance effect through hypometabolism or other neurochemical changes might underlie these impairments. To find the best explanation, a group of 17 patients with a lacunar infarct in the brainstem was neuropsychologically evaluated and compared with a closely matched control group. The patients demonstrated significantly impaired task performance on a constellation of neuropsychological tasks that was very similar to the findings previously found in patients with a supratentorial lacunar infarct (Boston Naming Test, TEA visual elevator, category fluency, Trailmaking Test). We conclude that a small white-matter infarct may affect cognitive functioning in a nonspecific way independently of its location.

Adult↗
PubMed1993

[Cerebellar hemorrhage and cerebellar infarct: retrospective study of 125 cases].

In a retrospective study of 125 patients, symptoms, diagnosis, and clinical course of 64 cases of cerebellar infarction and 61 cerebellar hemorrhage were studied retrospectively. Neurologically, cerebellar signs were present in 50% of hemorrhages and 7%, of infarctions, while 50% of patients with cerebellar hemorrhage and 37% of patients with cerebellar infarction showed brain stem symptoms or cranial nerve deficits; at least slight disturbance of consciousness was present in all patients. The state of consciousness, as estimated by the Innsbruck Coma Scale, together with diagnostic imaging (CT and/or MRT) allowed precise indication for surgical intervention. Over-all lethality was 11% for cerebellar infarction, and 31%, for cerebellar hemorrhage. Comparison of clinical outcome and state of consciousness at time of surgery suggests, that decompressive craniotomy should be performed even in deeply comatose patients with signs of decerebration.

Adolescent↗