PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Brain Stem Infarctions”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources

[Trigeminotrophic ulceration of the ala nasi in Wallenberg syndrome].

A patient developed a trophic ulceration of the nose after an acute bulbar ischemia with infarction of the right trigeminal nuclei. Neurologic examination showed symptoms of a Wallenberg syndrome including ipsilateral hyp- and paresthesia of the second trigeminal branch and disturbed sensibility and temperature sense on the contralateral half of the body. The right ala nasi showed the characteristic sickle-shaped defect (ulcération en arc). The differential diagnosis and therapeutic approaches are discussed.

Aged↗

Claude's syndrome in association with posterior cerebral artery stenosis.

BACKGROUND: We report a case of a 61 year old man with midbrain infarction causing Claude's syndrome attributable to stenosis of the posterior cerebral artery. CASE DESCRIPTION: The patient presented with a pupil-sparing left third nerve palsy and contralateral ataxia. A background history of treated hypertension and cigarette smoking was obtained. Magnetic resonance imaging revealed an area of infarction involving the left medial midbrain. Magnetic resonance angiography revealed significant stenosis of the left posterior cerebral artery. Antiplatelet therapy was instituted and the patient made a satisfactory recovery. CONCLUSIONS: This is the first reported case of Claude's syndrome arising in association with stenosis of the posterior cerebral artery. Intracranial large vessel disease should be considered as a potential aetiologic factor in patients with similar midbrain ischaemia.

Ataxia↗

[A case of intracranial dural arteriovenous fistula presenting with brainstem infarction].

A 68-year-old female presented with the disturbance of brainstem function. Brain T2 weighted and FLAIR (fluid-attenuated inversion recovery) magnetic resonance imaging revealed the hyperintensity signal of the medulla oblongata, which led to diagnosis of brainstem infarction. Diagnostic cerebral angiography showed the dural arteriovenous fistula (DAVF) developed on the left transverse sinus (TS). Venous drainage route was consisted of retrograde leptomeningieal venous reflux of the cerebrum and spinal perimedullary vein via superior petrosal sinus. Venous hypertension of the brainstem was relieved by transvenous platinum coil selective embolization of superior petrosal sinus. The correct analysis of venous drainage pattern is essential for the curative endovascular surgery.

Aged↗

Brainstem stroke following uncomplicated cervical epidural steroid injection.

BACKGROUND: Cervical epidural steroid injection treatment of radicular pain has become a common procedure. OBJECTIVES: To describe the clinical, radiologic, and autopsy findings of a 41-year-old patient treated with methylprednisolone acetate cervical epidural steroid injection, who developed a fatal hemorrhagic brainstem infarction and to discuss the possible mechanisms involved. DESIGN: Case report. SETTING: Pain management center and tertiary care hospital. RESULTS: Immediately following a seemingly uncomplicated epidural steroid injection at C5-6, the patient developed progressive symptoms of extensive brainstem and thalamic infarction (documented by magnetic resonance imaging and autopsy) with hemorrhagic conversion and hydrocephalus. Hemorrhage within the adventitia of the left vertebral artery, but no dissection, was found at the C5 vertebral level at necropsy. CONCLUSIONS: This case report shows the possibility of serious intracranial pathology resulting from cervical epidural steroid injection despite use of fluoroscopic guidance. Vascular spasm distant to the site of injection is a possible mechanism.

Adult↗

Bilateral Wallerian degeneration of the medial cerebellar peduncles after ponto-mesencephalic infarction.

Three patients with acute large paramedian ponto-mesencephalic infarctions developed a bilateral retrograde degeneration of the medial cerebellar peduncles within 4 months after the insult. In an initial magnetic resonance imaging (MRI) within the first 2 weeks, the medial cerebellar peduncles showed normal intensities, but a control MRI after 4 months showed bright hyperintensities in the T2-TSE weighted images, and moderately increased signal intensities in echo planar imaging-diffusion weighted imaging were seen, possibly representing bilateral Wallerian degeneration of the cerebellar-pontine fibers.

Aged↗

Modelling oculomotor data with decision tree induction.

We studied relationships between oculomotor test results and the site of lesion in the data set containing patient cases with operated cerebello-pontine angle tumour, operated hemangioblastoma, infarction of cerebello-brainstem or Meniere's disease and control subjects. Several classification models were generated by decision tree induction to find parameter combinations which are efficient in classification. The studied data were characterised by missing values and scarcity of example cases. This study suggested that decision tree induction can be a useful method even in problematic real world classification tasks. Models generated by decision tree induction and evaluated by an expert physician may give information that is beneficial for research.

Brain Stem Infarctions↗

Virtual arterial endoscopy as a diagnostic aid in a patient with basilar artery fenestration and thromboembolic pontine infarct.

Focal signal intensity loss of the basilar artery on MR angiograms obtained in a 69-year-old man was considered to be caused by an embolus, and thrombolytic therapy was initiated. On the follow-up MR angiograms, the same oval signal intensity loss of the basilar artery was observed. On the basis of a virtual endoscopic look into the basilar artery, the diagnosis of a rare vascular anomaly--a fenestration of the basilar artery--was confirmed and the presence of a thrombus at the site of the signal intensity loss was excluded.

Aged↗

[Unilateral sudden deafness as a primary symptom of brainstem and cerebellar infarction].

We report a case with a unilateral sudden sensorineural hearing loss caused by an infarction of brainstem and cerebellum. The patient was a 74-year-old male presented with a sudden onset of hearing loss and tinnitus in the right ear and dizziness. Steroid was administered on suspicion of idiopathic sudden deafness. However, the initial symptoms were deteriorated approximately 2 weeks later. He newly complained of the numbness of the right face and double vision, and he was transferred to our hospital for further evaluation. Neurological examination demonstrated horizontal nystagmus, diminution in the right facial sensation, right peripheral facial palsy, right hearing loss and cerebellar ataxia. Urgent MRI disclosed fresh infarctions of the right middle cerebellar peduncle and cerebellum localized in the territory of anterior inferior cerebellar artery. In general, idiopathic sudden deafness and Meniere's disease are frequent diagnosis in cases of sudden hearing loss with vertigo, but these symptoms may rarely be caused by cerebrovascular disorder. In patients with risk factors for arteriosclerosis, cerebrovascular disorder should be taken into consideration even if idiopathic sudden deafness may be suspected clinically. We emphasize the diagnostic importance of careful observation on neurological findings and early detection of radiological abnormalities on MRI.

Aged↗

Watershed infarcts in the fetal and neonatal brainstem. An aetiology of central hypoventilation, dysphagia, Möibius syndrome and micrognathia.

Watershed zone infarcts of the human cerebral cortex at the overlapping junctions of the anterior and middle cerebral arterial territories are well known. Another watershed zone exists in the brainstem tegmentum, between the terminal perfusion zones of the paramedian penetrating and long circumferential arteries, which are paired segmental vessels arising from the basilar artery. The vertebrobasilar circulation achieves its mature configuration and caudorostral flow by 9 weeks gestation. Systemic hypotension and other conditions of reduced basilar perfusion in the fetus, either early or late in gestation, may result in symmetrical longitudinal columns of infarction in the midbrain and tegmentum of the pons and medulla oblongata and laminar necrosis of the midbrain tectum. Within this zone are cranial nerve nuclei III-XII, the nucleus and tractus solitarius or central pneumotaxic center, as well as the nucleus ambiguus and other somatic motor nuclei that subserve muscles of swallowing, mastication and tongue movement. Watershed infarcts in the human fetal and neonatal brainstem are clinically expressed as multiple cranial neuropathies, failure of central respiratory drive and apnea, dysphagia and aspiration, Möbius syndrome and Pierre Robin sequence. MRI is sometimes helpful, but most of the involved neuroanatomical structures are beneath the resolution of present imaging techniques, and the diagnosis during life depends upon clinical neurological examination of the neonate, sometimes supported by evoked potential studies. Postmortem examination confirms the diagnosis and dates the lesions, but also contributes to better understand transient or persistent vascular insufficiencies in the fetal and neonatal brainstem.

Brain Stem Infarctions↗

Brainstem infarction after delayed thrombosis of a stented vertebral artery fusiform aneurysm: case report.

OBJECTIVE AND IMPORTANCE: Recent technological advances have provided clinicians with stents that can be navigated throughout the tortuous proximal vessels of the posterior intracranial circulation. There have been few reports of fusiform and wide-necked aneurysms treated with stents. Of the known risks involved in stent placement in the intracranial circulation, delayed stent thrombosis has not been well described. CLINICAL PRESENTATION: A 34-year-old man who experienced the sudden onset of a severe headache with increasing lethargy was found on computed tomographic imaging to have a subarachnoid hemorrhage. Angiography revealed a left vertebral artery fusiform aneurysm that incorporated the posteroinferior cerebellar artery origin. INTERVENTION: A low-porosity Magic Wallstent (Boston Scientific, Natick, MA) was placed in the left vertebral artery across the aneurysm and the origin of the posteroinferior cerebellar artery. Angiography performed 9 days later revealed significant reduction in filling of the aneurysm. The patient returned 3 months after stent placement with severe neurological deterioration from a brainstem infarction caused by complete thrombotic occlusion of the left vertebral artery at the stented segment of the vessel. CONCLUSION: Stenting of fusiform aneurysms has provided an alternative to surgical clipping or parent vessel reconstruction. With the increasing frequency of intracranial stent placement for various cerebrovascular disease entities, we must become aware of potential complications associated with these procedures. Such awareness may influence decision-making processes regarding treatment and follow-up care.

Adult↗

Medial medullary infarction: abnormal ocular motor findings.

In 20 consecutive patients with isolated medial medullary infarction, abnormal ocular motor findings included nystagmus (n = 8), ocular contrapulsion (n = 5), and contralesional ocular tilt reaction (n = 2). The nystagmus was ipsilesional (n = 4), gaze-evoked (n = 5), upbeating (n = 4), and hemiseesaw (n = 1). The ocular motor abnormalities may be explained by involvements of the nucleus prepositus hypoglossi, medial longitudinal fasciculus or efferent fibers from the vestibular nuclei, climbing fibers, and cells of the paramedian tracts.

Adult↗

Author's experience of lateral medullary infarction--thermal perception and muscle allodynia.

The patient, the author (S.K.), is a 67-year-old male. He has the typical dissociated pain, altered temperature sensation and ataxia often encountered by patients with lateral medullary infarction. This started at the time of his admission to hospital. Several weeks after discharge, he experienced the withdrawal reaction to high temperature, first mentioned by Rousseaux (Stroke 30 (1999) 2223), and movement allodynia as described by Bowsher (J Neurol Neurosurg Psychiatry 61 (1996) 62). The article describes his personal experience of the symptoms of central post-stroke pain and allodynia. A difference between muscle allodynia and conventional allodynia caused by dermal stimulation is proposed. Follow-up evaluation of sensory symptoms that appear several weeks after discharge is essential to ensure measures to alleviate them are provided.

Aged↗

Improved early stroke detection: wavelet-based perception enhancement of computerized tomography exams.

Nonenhanced computerized tomography (CT) exams were used to detect acute stroke by notification of hypodense area. Infarction perception improvement by data denoising and local contrast enhancement in multi-scale domain was proposed. The wavelet-based image processing method enhanced the subtlest signs of hypodensity, which were often invisible in standard CT scan review. Thus improved detection efficiency of perceptual ischemic changes was investigated. Data processing became more effective by initial segmentation of brain tissue and extraction of regions susceptible to tissue density changes. The new method was experimentally verified. Sensitivity of stroke diagnosis increased to 56.3% in comparison to 12.5% of standard CT scan preview.

Acute Disease↗

Dissecting aneurysm of the vertebral artery causing subarachnoid hemorrhage after non-hemorrhagic infarction--case report.

A 45-year-old male presented with lateral medullary infarction. Cerebral angiography showed dissecting aneurysm as pearl and string sign in the right vertebral artery (VA). Conservative treatment was administered with antiplatelet agent. However, subarachnoid hemorrhage occurred 2 days after admission, inducing coma. Intraaneurysmal embolization and proximal occlusion of the right VA by intravascular surgery resulted in only mild neurological deficits. Conservative treatment including strict control of blood pressure is the first choice of treatment. Antiplatelet therapy and anticoagulant therapy should not be administered. Patients must be followed up by serial angiography and surgery considered if signs of aneurysmal progression are seen.

Aortic Dissection↗

Episodic pain syndrome restricted cheiro-oral region associated with pontine lesion.

Other than from the thalamus and sensory cortex, episodic pain is an extremely rare neurological manifestation in the central compartment. This study reports a middle-aged man who experienced an acute onset of episodic oscillatory burning pain restricted to the cheiro-oral region, who was found to have a singular infarct at the left tegmental pons. A close relationship between his pain attack and an elevation of arterial blood pressure was clearly observed. Blood adenohypophyseal hormones and electroencephalogram did not reveal an abnormality in the ictus. Neuroimaging and clinical studies did not support involvement of the thalamus, periaqueductal gray matter, hypothalamus or regional structure. Therefore, episodic pain may be an isolated manifestation with a pontine lesion. A relapsing expansion of focal cerebral oedema with fluid retention may have corresponded to the oscillation of his sensory deficit. This accumulating, devastating calamity by a repetitive and paroxysmal offense after a blood-brain barrier breakdown should be cautiously reviewed.

Acute Disease↗

[Anti-GD1b IgG antibody-related Guillain-Barré syndrome initially mimicking brainstem infarction].

We described a 58-year-old woman with Guillain-Barré syndrome, who initially showed rapid progression of brainstem infarction-like signs. She developed superficial sensory disturbance on the left side, dysarthria, and left-predominant limb weakness within a few hours. She showed bilateral extensor plantar responses and head CT scan detected no abnormality. It was difficult to be distinguished from brainstem infarction until symmetrical limb weakness and generalized areflexia appeared. Serum anti-GD1b IgG antibody with cross-reactivity with GM1b was detected. Cerebrospinal fluid examination revealed albuminocytologic dissociation on day 5. After 5 sessions of immunoadsorption therapy, her symptoms gradually lessened. Anti-GD1b antibody has been detected in patients with sensory ataxic neuropathy. Our patient, however, was characterized with early involvement of brainstem with ataxia of cerebellar type. Our case suggests that anti-GD1b antibody-associated neuropathy has a broad spectrum of clinical features, which are related to cross-reactivity of this antibody.

Brain Stem Infarctions↗

Benign segmental myoclonus: electrophysiological evidence of transient dysfunction in the brainstem.

We present a 66-year-old patient with segmental myoclonus evoked by a brainstem infarction. The myoclonus appeared soon after a cerebrovascular accident and it was evident in the soft palate, jaw, neck, shoulders and upper limbs. Brain MRI showed infarction in the left pons and left cerebellum. Small amounts of orally administered clonazepam were remarkably effective. Electroencephalogram (EEG) and auditory brainstem response (ABR) were normal. Somatosensory evoked potential (SSEP) revealed delays in P 14 and N19 recorded at C3 by right median nerve stimulation. These findings were normalized in 4 days. Seg-mental myoclonus is thought to be evoked by olivary hypertrophy following cerebrovascular accident in the brainstem and is said to be resistant to medication. The limited involvement of the brainstem in our patient may account for the transient segmental myoclonus. The prognosis for this type of segmental myoclonus is excellent.

Aged↗

Etiology and long-term prognosis of unilateral paramedian pontine infarction with progressive symptoms.

Progressive pure motor hemiparesis is a common feature in paramedian pontine infarction. To assess the etiology, clinical course and long-term prognosis of this stroke subtype, we identified 26 patients with progressive symptoms in a retrospective study, treated in our hospital between 1993 and 1998. All patients had more than one stroke risk factor, and in 20, basilar branch disease, an atherosclerotic occlusion of basilar perforating arteries, was causative. Most patients developed severe hemiparesis after a mean time of 3 days, nearly 50% showed deterioration in connection with a fall in systolic blood pressure. The patients were followed up for 4-9 years: 4 patients had further strokes, 5 died, and 17 patients were independent, which may be interpreted as a good long-term prognosis.

Aged↗