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At least 19 recordsLinked to original sources
PubMed1997

[Fatal brain stem infarction due to rupture of a brain abscess: a case report].

We report a case of a brain abscess which initially presented with subcortical hematoma and ultimately resulted in fatal brain stem infarction due to its rupture into the subarachnoid space. A 50-year-old male was admitted to a nearby hospital with complaints of headache, fever, and sensory aphasia. He had ventricular septal defect found 15 years previously, sinusitis, and liver cirrhosis. Computerized tomographic (CT) scan revealed a left temporal subcortical hematoma. Gadolinium-DTPA enhanced magnetic resonance imaging (MRI) showed faint ring-like enhancement at the margin of the lesion. The left internal carotid angiogram demonstrated the vascular blush and early venous filling of the vein of Labbé. Administration of antibiotics and predonine resulted in resolution of fever within five days. MRI obtained 17 days after the onset showed typical ring-like enhancement. The mass was just adjacent to the lateral ventricle. The patient was transferred to our hospital for further examination and treatment 21 days after the onset. Fever had recurred 2 days before admission to our hospital. One day after admission, the patient began to vomit. About 15 hours following this symptom, he suddenly became comatose and tetraplegic. CT scan demonstrated a rupture of the abscess. Emergent drainage from the lateral ventricle and the abscess cavity was undertaken. Follow-up CT scan revealed multiple infarctions involving the upper brain stem and the bilateral thalamus. He died on the 29th day after the onset. The mechanisms of hemorrhage with a brain abscess and cerebral infarction after rupture of brain abscess are discussed. Hemorrhage with brain abscess is extremely rare. However, brain abscess should be considered as a possible etiology of an atypical hematoma. To avoid fatal rupture of the brain abscess, immediate treatment is essential. Once the rupture of the brain abscess occurs, its contents might cause vasospasm severe enough to cause cerebral infarction.

Brain Abscess↗
PubMed1993

Ipsilateral hypohidrosis in brain stem infarction.

BACKGROUND AND PURPOSE: The brain stem is the most important autonomic processing center, but very little attention has been given to clinical manifestations of autonomic failure in brain stem stroke. Our purpose was to evaluate the prevalence, characteristics, and prognostic significance of sweating dysfunction in brain stem infarctions. METHODS: We carried out a prospective study using quantitative evaporimetry to investigate spontaneous and heat-stimulated sweating in 18 healthy control subjects and 18 patients with ischemic brain stem stroke in the acute phase and at 1 and 6 months after infarction. RESULTS: The sweating response induced by a heating stimulus was significantly lower on the ipsilateral side to the infarction than on the contralateral side. Constant ipsilateral hypohidrosis was established in 83% of the patients in the acute phase, in 100% at 1 month, and in 76% at 6 months after infarction. No differences of sweating response were found between medullary and pontine infarcts. CONCLUSIONS: Hypohidrosis throughout the whole ipsilateral side of the body, a long-lasting phenomenon that has not previously been described, is an essential feature of autonomic failure in brain stem infarction.

Adult↗
PubMed1997

[Clinical and image diagnostics of brain stem infarction].

Clinical features and image diagnostic characteristics of brain stem infarction were studied in 28 patients to facilitate early diagnosis. Crossed hemiparesis was found in all the patients with medulla oblongata and midbrain infarction. Pontine infarction had a variety of clinical syndromes as follows: (1) crossed-hemiparesis in 8 cases (44.4%) and ipsilateral hemiataxia in one case. (2) tetraplegia in 3 cases (16.7%). (3) pure hemiparesthesia in 4 cases. (4) hemiparesis and hemiparesthesia without cranial nerve palsy in 3 cases (16.7%). MRI was found to be a very useful diagnostic measure for brain stem infarction with a positive rate of 82.6%. However, brain stem infarction was sometimes not revealed by MRI. Brain stem infarction could not be diagnosed by CT, but brainstem hemorrhage might be excluded by CT.

Adult↗
PubMed1989

Transcranial Doppler in acute brain stem infarction.

Two patients with acute brain stem infarctions were examined angiographically and with the transcranial Doppler. One patient had a patent basilar artery but worsened clinically. The second patient had a thrombosis of the left vertebral artery which was dislodged with the angiographic catheter. Thrombolytic therapy was initiated. Serial transcranial Doppler examinations showed persistent patency of the vertebrobasilar system although the patient failed to improve. The usefulness of the transcranial Doppler in the management of acute stroke is discussed in the context of these patients.

Aged↗
PubMed1985

Megadolichobasilar anomaly associated with brain stem infarction: a case report.

A rare case of megadolichobasilar anomaly associated with localized brain stem infarction showing right hemiparesis and disturbance of consciousness is described. The etiologic mechanisms of brain stem infarction in this anomaly are discussed. The tortuosity and dilatation of the basilar artery were thought to play an important role in the pathogenesis of the brain stem infarction.

Aged↗
PubMedDate not supplied

Xenon contrast-enhanced CT imaging of supratentorial hypoperfusion in patients with brain stem infarction.

BACKGROUND AND PURPOSE: The characteristics of hypoperfusion in the supratentorial region of patients with brain stem infarction are unclear. We investigated the relationships between the presence of hypoperfusion and the location, number, and size of the infarcts with xenon contrast-enhanced CT. METHODS: One hundred five patients with brain stem infarction detected by MR imaging underwent xenon contrast-enhanced CT to measure the regional CBF (rCBF) in the frontal, temporal, parietal, and occipital regions and in the putamen and thalamus. A decrease of more than 10% from the mean rCBF value for normal individuals was considered to indicate hypoperfusion. RESULTS: Thirty-six patients had supratentorial hypoperfusion. The mean rCBF values (measured in mL/100 g/minute) were as follows: frontal region, 36.2 +/- 5.1 (-14.8%, n = 28); parietal region, 42.3 +/- 4.7 (-19.1%, n = 29); temporal region, 41.5 +/- 2.8 (-12.6%, n = 12); and thalamus, 50.1 +/- 3.2 (-19.6%, n = 7). Supratentorial hypoperfusion was associated with pontine infarction in 33 patients (upper pons in 15, middle pons in 18, and lower pons in seven), midbrain infarction in two, and medulla infarction in one. Twenty-three patients had infarcts that were larger than 5 mm, and 11 had infarcts that were 2 to 5 mm. Only two had infarcts that were smaller than 2 mm. Seven patients each had one infarct, 13 each had two, and 16 each had three. CONCLUSION: Supratentorial hypoperfusion was associated with larger infarcts, with more infarcts, and with pontine infarction.

Aged↗
PubMed2001

[Diffusion-weighted magnetic resonance imaging (MRI) in acute brain stem infarction].

Diffusion-weighted magnetic resonance imaging (DWI) provides one of the earliest demonstrations of ischemic lesions. However, some lesions may be missed in the acute stage due to technical limitation of DWI. We therefore conducted the study to clarify the sensitivity of DWI to acute brain stem infarctions. Twenty-eight patients with the final diagnosis of brain stem infarction(midbrain 2, pons 9, medulla oblongata 17) who had been examined by DWI within 24 hours of onset were retrospectively analyzed for how sensitively the initial DWI demonstrated the final ischemic lesion. Only obvious(distinguishable with DWI alone without referring clinical symptoms and other informations) hyperintensity on DWI was regarded to show an ischemic lesion. Sixteen(57.1%) out of 28 patients had brain stem infarctions demonstrated by initial DWI. In the remaining 12 cases, no obvious ischemic lesion was evident on initial DWI. Subsequent MRI studies obtained 127 hours, on average after the onset showed infarction in the medulla oblongata in 11 cases and in the pons in one case. Negative findings of DWI in the acute stage does not exclude possibility of the brain stem infarction, in particulary medulla oblongata infarction.

Adult↗
PubMedDate not supplied

Respiratory rate and pattern disturbances in acute brain stem infarction.

Respiratory rates and patterns were studied in 23 patients with acute brain stem infarction using impedance pneumography. Autopsy was obtained in six of eight fatal cases. Pontine lesions were present in all patients, with coexistent infarction of midbrain in four and of medulla in nine. Respiratory rate and pattern abnormalities observed included Cheyne-Stokes respiration, Cheynb-Stokes variant pattern and tachypnea. Abnormalities of respiratory rate and pattern of varying duration were observed at some time in all patients. All patients in whom prominent Cheyne-Stokes respiration or tachypnea were observed had extensive bilateral pontine lesions involving both basal and tegmental portions. However, not all patients with large pontine infarcts had Cheyne-Stokes respiration or tachypnea. Cheyne-Stokes respiration was prominent in four patients (two fatal, two nonfatal). Cheyne-Stokes variant pattern was present frequently in four patients (one fatal, three nonfatal). Sustained tachypnea developed in five patients, four of whom died. In ten patients (one fatal, nine nonfatal), normal respiratory rate and pattern predominated with only rare or occasional apperance of Cheyne-Stokes respiration or Cheyne-Stokes variant pattern, especially during sleep. The types of respiratory rate and pattern abnormalities in acute brain stem infarction were not specifically related to the level of lesions, but rather to the size and bilaterality of the lesions. Respiratory alkalosis was present in varying degrees in most patients with either tachypnea or prominent CSR.

Acute Disease↗
PubMedDate not supplied

Characteristics and survival of patients with brain stem infarction.

A retrospective study of 141 patients whith ischemic brain stem infarction admitted to the Department of Neurology, University of Helsinki, during 1966 to 1973 was performed. The patients were contacted by mail in January and February, 1974; in case of death, the death certificates were procured. The follow-up period was from 4 to 99 months (median 46.5 months), during which a total of 39 patients had died. A life table analysis gave a 50% probability of a seven-year survival after the stroke. Survival was similar for men and women, and age appeared to have little influence on the prognosis with only a slightly higher case fatality in old age. Soft palate paralysis, disturbed sensorium, need of special treatment measures (feeding by gastric tube intravenous infusions, etc.) during the acute phase, abnormalities in the ECG (T-wave negativity, S-T segment depression), fasting blood glucose 100 mg/100 ml or higher, and an abnormal eeg (slowing down of alpha rythm alone or in association with paroxysmal and/or focal disturbances) were all associated with high case fatality. Preceding TIAs, blood pressure level, serum cholesterol and triglyceride values, and aortic arch angiogram findings, on the other hand, had no effect upon the prognosis. The effects of body build on prognosis remained obscure.

Adult↗
PubMed1999

Natural course of combined limb and palatal tremor caused by cerebellar-brain stem infarction.

After infarction of the left superior cerebellar peduncle and dentate nucleus, a patient developed tremor of the left upper limb beginning on the twelfth day followed by palatal tremor appearing 10 months after infarction. Surface electromyogram revealed a difference in the frequency of the tremor in the upper limb and soft palate. When the palatal tremor appeared, brain magnetic resonance T2-weighted images revealed high signal intensity of the contralateral, right inferior olivary nucleus. Subsequently, when the amplitude of palatal tremor became less severe, the high olivary signal intensity subsided whereas the hypertrophy of the nucleus remained. This patient provides useful information on the pathogenesis of skeletal and palatal tremor with brain stem or cerebellar lesions based on the differences in the onset and frequency of tremors and morphologic changes in the inferior olive.

Arm↗
PubMed1993

Brain stem infarction and diaschisis. A SPECT cerebral perfusion study.

BACKGROUND AND PURPOSE: We studied six patients suffering from pure, unilateral brain stem infarction to explore the association of remote cerebral and cerebellar blood flow changes with damage at different sites of this region of the brain. METHODS: We used single-photon emission computed tomography and [123I]iodoamphetamine to measure regional differences in tracer uptake. Qualitative image analysis and calculated asymmetry indexes were correlated to the location of the infarcted area on magnetic resonance imaging and to the patients' clinical findings. RESULTS: Significant perfusion asymmetries were noted in the two patients with infarction in the upper pons but not in those with lesions below this level. They comprised a contralateral cerebellar and ipsilateral supratentorial hypoactivity that was most marked in the frontoparietal cortex. There was no clear relation between the patterns of cerebral or cerebellar tracer uptake and specific neurological findings. CONCLUSIONS: Remote perfusion changes after pure brain stem infarction may be seen both infratentorially and supratentorially and depend on the lesion site rather than on the neurological deficit. In this context, our study confirmed damage to the corticopontocerebellar pathways as the key event in the genesis of a crossed cerebellar diaschisis. The exact mechanisms causing ipsilateral cerebral hemispheric diaschisis await further clarification.

Aged↗
PubMed1986

Brain stem infarction as a complication of giant-cell arteritis.

Two cases of brain stem infarction as an early and fatal complication of giant-cell arteritis are reported. These complications occurred despite adequate treatment with corticosteroids. The findings at autopsy are compared with those of the literature. The possible pathogenetic mechanisms of vertebro basilar occlusion and the therapeutical implications are discussed.

Aged↗