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Results for “Brain Stem Infarctions”

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At least 55 records · Page 3Linked to original sources
PubMed2003

Vertebrobasilar artery dissection presenting with simultaneous subarachnoid hemorrhage and brain stem infarction: case report.

BACKGROUND: Intracranial dissecting aneurysms have been associated with subarachnoid hemorrhage (SAH) or cerebral ischemia. We encountered a patient presenting with simultaneous subarachnoid hemorrhage and brainstem infarction caused by a dissecting aneurysm of the vertebrobasilar artery, which was diagnosed by magnetic resonance imaging (MRI) but did not show abnormal findings on cerebral angiography. CASE DESCRIPTION: A 55-year-old man had sudden onset of headache and left abducens palsy. Computed tomography revealed a subarachnoid hemorrhage localized in the left prepontine cistern and the left cerebellomedullary fissure. Cerebral angiography showed neither a saccular aneurysm nor fusiform dilatation causing the subarachnoid hemorrhage. MRI demonstrated a small infarction in the left dorsal pons, and an intramural hematoma of the left vertebral artery and lower basilar artery. CONCLUSION: This is a rare case of a vertebrobasilar dissecting aneurysm that simultaneously caused both SAH and brain stem infarction. MRI should be performed in the acute phase of SAH of unknown origin to determine the possible coexistence of a dissecting aneurysm, as occurred in this case.

Aortic Dissection↗
PubMed2003

[Vertebrobasilar artery dissection with subarachnoid hemorrhage after brain stem infarct showing an improvement on angiography: case report].

A 66-year-old male presented with dysarthria and right hemiparesis. Cerebral angiography at onset showed obliteration of the basilar artery and dilatation in the left vertebral artery. The patient's clinical symptoms were exaggerated and he was finally diagnosed to as suffering locked-in syndrome. Magnetic resonance imaging showed a brain stem infarction from the pons to the left middle cerebellar peduncle. We determined that the patient suffered dissection of the left vertebral artery at the basilar artery and treated, using the conservative therapy him of strict blood pressure control. A second angiography 13 days after onset showed recanalization of the basilar artery. At 29 days after onset, the patient fell into a coma with subarachnoid hemorrhage and acute hydrocephalus. Cerebral angiography revealed improvement in the irregularity and dilatation of the basilar artery, but the point of rupture could not be clearly identified. After performing proximal occlusion of the left vertebral artery by intravascular surgery, both right STA-SCA anastomosis and proximal occlusion of the right vertebral artery were carried out. Unfortunately, the patient died. Based on there data, it is appointed out that patients with a dissection of the vertebrobasilar artery must be followed up by serial angiography, and even if an angiographical improvement of the dissection is observed, the risk of subarachnoid hemorrhage still exists in patients suffering ischemic stroke.

Aged↗
PubMed1999

Transient mutism resolving into cerebellar speech after brain stem infarction following a traumatic injury of the vertebral artery in a child.

A 3.7-year-old girl presented with an anterior neck injury followed by progressive subcutaneous emphysema and loss of consciousness. After resuscitation, a laceration on the first tracheal cartilage was closed surgically. As she was extubated one week later, she was found to have right hemiplegia and muteness. MRI showed a T2-bright lesion on the tegmentum of the left midbrain down to the upper pons. Right vertebral angiography disclosed an intimal flap with stenosis at the C3 vertebral level presumably caused by a fracture of the right C3 transverse process later confirmed in a cervical 3D-CT scan. Her muteness lasted for 10 days, after which she began to utter some comprehensible words in a dysarthric fashion. Her neurological deficits showed improvement within 3 months of her admission. Transient mutism after brain stem infarction has not been reported previously. We discuss the anatomical bases for this unusual reversible disorder in the light of previous observations and conclude that bilateral damage to the dentatothalamocortical fibers at the decussation of the superior cerebellar peduncle may have been responsible for her transient mutism.

Brain Mapping↗
PubMed1994

Aberrant distribution of tyrosine hydroxylase and substance P in infants with brain-stem infarction.

The distribution of tyrosine hydroxylase (TH) and substance P (SP) was examined in the brain-stem of 4 infants with respiratory abnormalities associated with remote brain-stem or cerebellar infarction utilizing immunohistochemical methods. TH-immunoreactive cells and SP-immunoreactive fibers were found in and around the area of the infarction in the tegmentum, in amounts and sites different from that seen in controls. The aberrant localization of SP and TH may represent an altered repair process associated with resolution of the infarction and may be related to abnormal respiratory control or sudden death.

Brain Stem↗
PubMed1988

[Experimental study of brain stem infarction in dogs--effect on BAEP, SSEP, blink reflex and EEG of perforator occlusion].

Assessment of the lesion in the brain stem by evoked potentials has not been well established. We have already developed a model of brain stem ischemia by occluding the perforators of the posterior cerebral arteries of the dog. The ischemic lesions locates mainly in the ventral side of the midbrain. Using this model, we assessed brain stem function by brain stem auditory evoked potential (BAEP), surface- and depth-recorded (in medial lemniscus) short latency somatosensory evoked potential (SSEP), blink reflex (BR) and electroencephalography (EEG), and investigated the correlation between the electrophysiological abnormalities and the lesion in the brain stem. The studies were performed for 6 hours after perforator occlusion. Furthermore, depth-recorded SSEP and regional cerebral blood flow (rCBF) were measured under induced hypotension by withdrawal of arterial blood. BAEP did not change in 13 of 16 animals. Surface-recorded SSEP remained unchanged in all 6 animals. The results are probably due to the fact that the lesion does not involve the auditory and somatosensory pathways and the accompanying events such as edema does not affect the both pathways. Depth-recorded SSEP remained unchanged after occlusion and did not disappear even when rCBF fell below 10 ml/100 g/min. It may be suggested that the threshold for electrical failure in the brain stem is much lower than that in the cortex. In BR, R1 did not change but ipsilateral R2 became nearly invisible immediately after perforator occlusion in all animals. The fact that the ischemic lesion did not involve the pons and disturbed reticular formation in the midbrain may probably account for the remaining of R1 and the disappearance of ipsilateral R2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Buspirone treatment for apneustic breathing in brain stem infarct.

We report a case of brainstem infarction resulting in apneustic breathing, which was alleviated with buspirone. We discuss apneusis, review the literature, and speculate about the benefit of serotonin 1A receptor agonists in the treatment of apneusis and other respiratory disorders.

Apnea↗