[Treatment and prognosis of brainstem infarction].
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Brain Stem↗
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The electroencephalogram in brain stem vascular disease; some observations relating electroencephalographic findings to various combinations of infarction and vascular insufficiency.
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Brain Diseases↗
[Basilar artery rostral occlusion syndrome. Clinico-radiological assessment of 56 patients].
We studied 56 patients, 30 women and 26 men ranging from 30 to 79 years of age (average age 64.5 +/- 10.4), who were admitted to our hospital between 1982 and August 1995 with clinical features compatible with occlusion at the level of the bifurcation of the basilar artery. The patients were selected following clinical and neuro-radiological criteria. All patients included in the study had two or more recent infarcts in the vertebro-basilar territory, related to involvement of the rostral region of the basilar artery. The diagnosis was confirmed by CT or MR scanning. The infarcts were in the thalamus, brain-stem, cerebellum and parieto-occipital lobe. A thalamic infarct associated with an infarct in another region was the most frequent lesion. The CT-MR findings in the 56 cases were: 29 patients presented with a unilateral thalamic infarct associated with another infarct (23 occipital, 8 parietal, 6 brain-stem and 2 cerebellum). There were eight patients with bilateral thalamic infarcts and seven with bilateral occipital infarcts. In six patients the occipital infarct was associated with another infarct at a different level (parietal or cerebellar) and six patients had cerebellar infarcts together with an infarct of the mid-brain. In 22 of the patients, lesions were found in three or more areas. The commonest clinical findings were: Motor deficit (69.6%), abnormal eye movements (44.5%), cerebellar dysfunction (42.8%), altered level of consciousness (32.1%), visual field defects (28.5%), pupil anomalies (19.6%). The most frequently associated risk factors were: Arterial hypertension (58.9%), a history of ACV (32.1%) and atrial fibrillation (21.4%). Mortality was 5.7%. In contrast to the classical descriptions, motor defecit was the commonest symptom in our series.
Adult↗
Diffuse leptomeningeal gliomatosis associated with multifocal CNS infarcts.
BACKGROUND: Widespread dissemination of astrocytoma throughout the cerebrospinal fluid is unusual, especially as the initial presentation in a patient, and association with cerebral infarcts is rare. CASE DESCRIPTION A 47-year-old man subacutely developed progressive headache and backache, vomiting, altered consciousness, and numbness in both arms. Brain computerized axial tomography showed calcification in the fourth ventricle and magnetic resonance imaging demonstrated diffuse meningeal enhancement, a lesion in the canal of Magendie, and T2-weighted hyperintense lesions in several locations. Angiography showed vasospasm/vasculopathy involving multiple cerebral vessels. Biopsy of the fourth ventricular mass revealed a subependymoma with an overlying leptomeningeal anaplastic astrocytoma with numerous Rosenthal fibers. The patient was treated with three doses of intrathecal methotrexate via lumbar puncture but suddenly became unresponsive and died 6 days later, 8 weeks after initial symptoms. Autopsy demonstrated the subependymoma and a widespread leptomeningeal anaplastic astrocytoma, which showed no clear-cut origin from the subependymoma, but microscopically infiltrated the left medial temporal lobe. Multiple subacute and acute infarcts of the brain, brain stem, and upper spinal cord were seen only in areas with leptomeningeal tumor. CONCLUSION Glioma cells surrounding and focally permeating central nervous system vessels without lumenal occlusion can lead to vasospasm and widespread infarcts.
Arachnoid↗
Cerebellar infarction resulting from traumatic occlusion of a vertebral artery. Case report.
A case is reported of a patient who suffered a gunshot wound of the neck which resulted in occlusion of a vertebral artery. Within a few hours he deteriorated neurologically to a comatose state with a gaze paresis and a facial paresis ipsilateral to the occluded vertebral artery. The diagnosis of cerebellar infarction with brain-stem compression was made clinically, and a posterior fossa decompression was carried out promptly. The patient has made an excellent recovery. Cerebellar infarction, like cerebellar hemorrhage, may act as a posterior fossa mass requiring neurosurgical decompression. This report emphasizes that such a pathological process may occur after certain injuries that are likely to result in occlusion of a vertebral artery.
Adult↗
Neuroradiologic findings in polyarteritis nodosa.
PURPOSE: To demonstrate the neuroradiologic findings in patients with polyarteritis nodosa. METHODS: A review of hospital records for a 10-year period revealed 50 patients with a discharge diagnosis of polyarteritis nodosa. Thirteen patients had undergone neuroimaging, and abnormal findings were found in 5 cases; these were the subjects of this study. RESULTS: All 5 patients had abnormal findings on CT scans, 3 had abnormal findings on MR images, and 1 had an abnormal finding on a cerebral angiogram. All patients had cerebral cortical or subcortical infarctions, and 1 also had small infarctions within the brain stem and cerebellum. One patient had cerebral angiographic findings of arteritis. The diagnosis of arteritis was considered probable or possible in 3 other patients. Three patients had echocardiographic evidence of concentric hypertrophy and a hypocontractile left ventricle resulting from polyarteritis nodosa-related hypertension. Cardiogenic embolism was considered the likely cause in 1 patient. CONCLUSION: Small peripheral cerebral infarctions, consistent with an arteritis involving medium-sized and small arteries, were the most common finding. However, cardiogenic embolism should also be considered as a possible cause of cerebral infarction in patients with polyarteritis nodosa who have left ventricular dysfunction.
Adult↗
Brain stem stroke causing baroreflex failure and paroxysmal hypertension.
BACKGROUND: Paroxysmal neurogenic hypertension has been associated with a variety of diseases affecting the brain stem but has only rarely been reported after brain stem stroke. The mechanism is thought to involve increased sympathetic activity and baroreflex dysfunction. We undertook microneurographic recordings of muscle sympathetic nerve activity (MNSA) during beat-to-beat blood pressure (BP) monitoring to investigate this hypothesis. CASE DESCRIPTION: We investigated a 75-year-old woman who developed paroxysmal hypertension (BP 220/110 mm Hg) after a large left-sided medullary infarct. The paroxysms were triggered by changes in posture and were accompanied by tachycardia, diaphoresis, and headache. Serum catecholamines were substantially increased (norepinephrine level, 23.9 nmol/L 9 days after stroke; normal level, <3.8 nmol/L), and heart rate variability, measured by spectral analysis, was decreased in both low- and high-frequency domains (0.04 and 0.06 ms(2), respectively; normal level, 0.14+/-0.02 ms(2)). MNSA was increased in frequency (61 bursts per minute; normal level, 34+/-18 bursts per minute), and the burst amplitude was not inversely related to diastolic BP. BP and MNSA responses to cold pressor and isometric handgrip stimuli were intact. CONCLUSIONS: Extensive unilateral infarction of the brain stem in the region of the nucleus tractus solitarius may result in partial baroreflex dysfunction, increased sympathetic activity, and neurogenic paroxysmal hypertension.
Aged↗
[A 71-year-old man with Cushing reflex].
BACKGROUND: The Cushing reflex in comatose intensive care patients usually indicates that intracranial perfusion is about to be abolished. MATERIAL AND METHODS: A 71-year-old man suffered an attack during which he became comatose. After 14 hours he developed polyuria, dilated fixed pupils and Cushing reflex. The cause was believed to be a global anoxic brain oedema. Coma, apnoea and absent brain stem reflexes suggested brain death. RESULTS: Angiography with contrast injected into the aortic arch showed preserved circulation in both internal carotid, middle and anterior cerebral arteries, but absence of basilar artery circulation. A cerebral CT scan was initially normal, but 14 hours later a new scan demonstrated infarction of the brain stem, cerebellum and occipital lobes. The Norwegian criteria for organ donation were not fulfilled as these require stop of all intracranial circulation. The respirator was disconnected and the patient died. INTERPRETATION: The Cushing reflex can be seen after profound ischaemia in the posterior cerebral circulation with preserved circulation to the forebrain. Ischaemia of the brain stem alone may be sufficient to elicit the Cushing reflex.
Aged↗
Fatal ethibloc embolization of vertebrobasilar system following percutaneous injection into aneurysmal bone cyst of the second cervical vertebra.
A 4-year-old boy developed progressive neck pain and an expansile osteogenic lesion of C2; the diagnosis was an aneurysmal bone cyst. An image-guided biopsy with 3D CT planning was performed followed by Ethibloc injection into the aneurysmal bone cyst. Subsequent CT and MR images demonstrated embolization material in the vertebrobasilar system, and the patient died of brain stem and cerebellar infarction 23 hours after the intervention. The course of events and technical considerations are discussed.
Basilar Artery↗
MR contrast enhancement in brainstem and deep cerebral infarction.
MR imaging with IV administration of gadopentetate dimeglumine was performed in 89 patients with 100 clinically and radiologically documented brainstem or deep cerebral (basal ganglia/internal capsule) infarctions to determine the patterns and time course of contrast enhancement. By location, there were 61 deep cerebral, eight midbrain, 23 pontine, and eight medullary infarctions. The age of the infarctions ranged from 1 day to 3 1/2 years, with 22% of the patients scanned within 4 days and 43% scanned within 2 weeks of clinical ictus. Abnormalities on T2-weighted images were encountered in every case. Mass effect was seen in 10 infarctions, most commonly noted between days 2 and 6, but persisting to day 20 in a single case. Parenchymal contrast enhancement was seen in 43 cases, occurring predominately between days 2 and 80. By postinfarction day 3 only half the strokes enhanced, although all did after day 6. Intravascular enhancement within the vertebral or basilar arteries was noted in five cases; all were brainstem infarctions imaged during the first week following ictus. Meningeal enhancement adjacent to the infarction was not seen in any case. Our results indicate that MR contrast enhancement of brainstem and deep cerebral infarctions typically occurs over a period from about 3 days to 3 months following ictus. Lack of both parenchymal and intravascular enhancement is thus to be expected for several days after a brainstem or deep cerebral infarction.
Adult↗
Spontaneous vertebral artery dissection initially mimicking myocardial infarction.
BACKGROUND AND PURPOSE: Vertebral and carotid artery dissections may present with very different signs and symptoms, making early recognition difficult. However, diagnosis should be established as soon as possible to prevent unnecessary diagnostic investigations and to institute adequate treatment. CASE DESCRIPTION: A 46-year-old man presented with severe intermittent pain of his left upper arm and general discomfort. During extensive cardiological evaluation for suspected myocardial infarction, a severe brain stem syndrome occurred. Ultrasound Doppler studies detected vertebral artery dissection, which was confirmed by angiography. CONCLUSIONS: The unusual initial presentation of vertebral artery dissection delayed an early diagnosis and adequate treatment. Because noninvasive methods are available today, their applications are recommended in similarly uncharacteristic circumstances.
Aortic Dissection↗
Bilateral latero-pontine infarction: a rare syndrome, an unusual imaging.
The authors present one case of bilateral infarction of the brain stem, in the territory of the antero-inferior cerebellar artery. Besides the fact that such bilateral ischaemic lesions are rare, the initial clinical presentation mimicking a vestibular neuronitis indicates that this latero-pontine syndrome may appear as a peripheral disorder. It also reminds clinicians that careful and repeated examinations should always be performed in all patients suffering from vertigo. An unusual iconography is also presented.
Cerebral Infarction↗
[Cerebellar infarction, clinical presentation, diagnosis and treatment].
Cerebellar infarction is relatively infrequent and accounts for about 2% of all strokes. Its clinical presentation and course are variable. It may resemble vestibulitis in mild cases, but the presentation may be more dramatic in other cases. Cerebellar infarction may cause life-threatening complications such as acute hydrocephalus or brain stem compression, resulting from their mass effect in the posterior fossa or extension of the infarct to the brain stem. Clinical features alone are insufficient for the diagnosis and for follow-up of patients with cerebellar infarction. However the advent of CT and MRI and their availability enable early diagnosis of cerebellar infarction, and early recognition of the development of acute hydrocephalus or brain stem compression which require surgical decompression. The prognosis of most cases is good when treatment is appropriate.
Aged↗
Electroencephalography in lacunar infarction.
To determine the occurrence and clinical implications of electroencephalographic (EEG) abnormalities in patients with acute lacunar infarction, we conducted a single-blinded EEG study in 55 patients. Twenty-nine (53%) had mild EEG abnormalities, which were focal and ipsilateral to the side of infarction in 7 patients (13%). Abnormalities were more common in patients with evidence of a prior stroke (10 of 12 patients, 83%). However, 43% (16 of 37 patients) of those without historical or radiologic evidence of a prior stroke also had mild EEG abnormalities. This represents a higher incidence of routine EEG abnormalities in lacunar infarction than is generally assumed. Indeed, these findings are more consistent with recent quantitative EEG studies that consistently have shown high rates of abnormalities in lacunar infarction. We did not find major EEG abnormalities, such as continuous or nearly continuous focal delta activity, in any patient with first lacunar infarction. We conclude that within the first 48 h after a first ischemic infarction, when computed tomography often fails to show abnormalities, an EEG that shows lateralized major abnormalities is useful in excluding the diagnosis of either lacunar infarction or infarction limited to the brain stem. Mild abnormalities occur more often than previously thought in lacunar infarction and do not exclude this diagnosis.
Aged↗
Vertebrobasilar insufficiency. Part 1: Microsurgical treatment of extracranial vertebrobasilar disease.
Extracranial vertebrobasilar artery thrombo-occlusive disease may cause repetitive transient ischemic episodes and, less frequently, brain-stem or cerebellar infarction. This report describes 40 patients who experienced repetitive vertebrobasilar ischemic symptoms despite maximal medical therapy. The natural history, pathogenesis, and treatment options for each causative lesion are reviewed. The operative approaches to symptomatic disease of the proximal vertebral arteries, arterial compression by cervical osteophytes, traumatic lesions of the vertebral arteries, and thrombo-occlusive pathology of the distal extracranial vertebral arteries are outlined. Specific anesthetic and surgical techniques that have proved successful while achieving zero operative mortality and low perioperative morbidity rates are reported.
Adolescent↗
Traumatic basilar artery occlusion caused by a fracture of the clivus--case report.
A 56-year-old man presented with a rare traumatic basilar artery occlusion caused by a fracture of the clivus. He fell from the height of 2 meters and immediately fell into a coma. Head computed tomography (CT) revealed an open depressed fracture, an acute epidural hematoma 1 cm thick in the left middle frontal fossa, and a longitudinal fracture of the clivus. Emergency removal of the hematoma was performed with cranioplasty. Head CT 8 hours 50 minutes after injury showed infarctions in the brain stem, cerebellum, and occipital lobes. Cerebral angiography revealed occlusion of the basilar artery in the middle part of the clivus. The patient died after 3 days. Autopsy revealed that the basilar artery was trapped in the clivus fracture site. Vertebrobasilar artery occlusion due to trapping in a clivus fracture has a very poor prognosis. Diagnosis is difficult and generally only confirmed at autopsy. Cerebral angiography is recommended in a patient in a deep coma without massive brain contusion at the early stage of head injury to identify the possibility of vertebrobasilar artery occlusion in a clivus fracture.
Accidental Falls↗
MR imaging of posterior fossa infarctions: vascular territories and clinical correlates.
Ischemic infarctions in certain vascular territories of the cerebellum and brain stem can produce some characteristic radiologic and clinical patterns. The cerebellum serves as a coordination center for the maintenance of equilibrium and muscle tone and refines the movements of the somatic muscles. The anatomy of the brain stem is extremely complex, and small infarcts can potentially be disastrous. MR imaging depicts the anatomy of the posterior fossa and infarcts in this region with greater accuracy than was previously possible. Familiarity with the vascular territories and patterns of infarction of the posterior fossa depicted with MR imaging and familiarity with the associated clinical symptoms of stroke in this region can help the radiologist recognize these infarcts and correlate clinical and radiologic findings. When patients are referred for MR imaging of the brain because of clinical findings suggestive of infarction, it may be useful to obtain coronal or sagittal views in addition to axial images to better depict the vascular distribution of a suspected ischemic lesion.
Brain Stem↗