Cases reported "Brain Stem Infarctions"

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1/42. Ipsilateral facial weakness in upper medullary infarction-supranuclear or infranuclear origin?

    We describe two patients with upper medullary infarctions showing ipsilateral facial weakness and relative sparing of the upper facial muscles. Electrophysiological follow-up using transcranial magnetic stimulation of the motor cortex in combination with stimulation of the peripheral facial nerve disclosed a supranuclear (corticofacial) tract lesion in one patient and a partial nuclear/infranuclear intra-axial facial nerve lesion in another.
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2/42. Concomitant post-traumatic craniocervical junction epidural hematoma and pontomedullary junction infarction: clinical, neurophysiologic, and neuroradiologic features.

    STUDY DESIGN: A case report. OBJECTIVES: To report and discuss a case of post-traumatic epidural hematoma of the craniocervical junction with concomitant brain stem infarction. SUMMARY OF BACKGROUND DATA: Post-traumatic epidural hematoma of the cervical spine and brain stem post-traumatic infarction are very rare disorders. Post-traumatic epidural hematoma is usually located dorsally in the epidural space. methods: The clinical, neuroradiologic, and neurophysiologic findings in one patient with post-traumatic epidural hematoma located ventrally at the cervicomedullary junction and associated with medial infarction at the pontomedullary junction are reported. RESULTS: The main clinical finding in this patient was bilateral corticospinal and corticobulbar tract involvement. A magnetic resonance image showed displacement and flattening of the medulla oblongata and of the most cranial portion of cervical cord, which were caused by the epidural hematoma associated with an ischemic lesion of the pontomedullary junction. Results of central motor conduction studies indicated that the abnormality of the central motor pathways was localized at brain stem level, and that there was normal conduction from the cervicomedullary junction to spinal cord. CONCLUSION: This is the first reported case of spinal epidural hematoma located ventrally in the cervical spine at the cervicomedullary junction level and concomitant infarction at the pontomedullary junction resulting from whiplash injury.
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3/42. Abnormal vergence with upper brainstem infarcts: pseudoabducens palsy.

    BACKGROUND: Infarcts of the rostral brainstem often cause vertical gaze palsies but may also produce inappropriate convergence that manifests as pseudoabducens palsy and convergence-retraction nystagmus (CRN). Although the substrate for vergence has been defined in the monkey as lying dorsal and lateral to the oculomotor nucleus, the human homologue is unknown.Method:- The authors reviewed the clinical features, ocular findings, and CT or MR lesions in seven patients with pseudoabducens palsy and "top-of-the-basilar" infarction. They reviewed the literature for infarcts causing pseudoabducens palsy or CRN with precise autopsy localization. The authors then mapped the location of the infarcts on anatomic templates. RESULTS: The smallest MR infarct produced an ipsilateral pseudoabducens palsy and CRN, and was located just rostral to the oculomotor nucleus, near the midbrain-diencephalic junction. Two patients with only contralateral pseudoabducens palsy had both subthalamic and thalamic infarction. Four patients with bilateral pseudoabducens palsy had larger infarcts involving the midbrain. All patients with pseudoabducens palsy had upgaze palsy. Two patients with CRN from the literature had small infarcts near the midbrain-diencephalic junction at autopsy. CONCLUSIONS: Lesions near the midbrain-diencephalic junction are important for the development of pseudoabducens palsy. Pseudoabducens palsy and CRN are probably both manifestations of abnormal vergence activity. Inhibitory descending pathways for convergence may pass through the thalamus and decussate in the subthalamic region.
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4/42. Bilateral medial medullary infarction.

    We present a case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging (MRI) and review 12 previously reported cases. We classify these 13 cases (including the present case) into two groups according to the extent of the ischemic region: type 1, the ischemic lesion developed from the medullary pyramid to the medial longitudinal fasciculus; type 2, the lesion was confined to the medullary pyramid.A 71 year old man presented with slight disturbance of consciousness, dysarthria, disturbance of leftward gaze, no gag reflex and tetraparesis. He developed nearly complete horizontal ophthalmoplegia. MRI revealed upper medial medullary infarction bilaterally that extended to the pontomedullary junction. We propose that the prognosis of type 2 bilateral medial medullary infarction is better than that of type 1. Furthermore, the prognosis of bilateral medial medullary infarction itself may be better than previously indicated.
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5/42. 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.
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6/42. 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.
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7/42. Massive pontine hemorrhagic infarction associated with embolic basilar artery occlusion.

    We report here an autopsy case of massive pontine hemorrhagic infarction secondary to embolic basilar artery occlusion. A large embolus appeared to have traversed the vertebral artery into the basilar artery as a result of basilarization of the vertebral artery due to severe stenosis of the contralateral vertebral artery. Extensive ischemia due to embolic occlusion of the entire length of the basilar artery, and migration of the embolus are assumed to have resulted in a massive pontine hemorrhagic infarction.
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8/42. Venous infarction of brainstem and cerebellum.

    The authors describe 2 cases of posterior fosa venous infarction. A 56-year-old woman with essential thrombocytemia presented with fluctuating complaints of headache, nausea, vomiting, left-sided numbness-weakness, and dizziness and became progressively stuporous. Cranial magnetic resonance imaging (MRI) showed bilateral parasagittal fronto-parietal and left cerebellar contrast-enhancing hemorrhagic lesions. On magnetic resonance venography, the left transverse and sigmoid sinuses were occluded. The second patient, a 39-year-old woman, presented with acute onset of diplopia, numbness of the tongue, vertigo, and right-sided weakness following a gestational age stillbirth. MRI revealed lesions in the right half of midbrain and pons and in the superior part of the right cerebellar hemisphere. Digital subtraction angiography showed right transverse and sigmoid sinus occlusion. The authors suggest that one should investigate the possibility of venous infarction in the presence of posterior fossa lesions that are often hemorrhagic and are not within any arterial territory distribution but respect a known venous drainage pattern. Recognition of the observed clinical and neuroimaging features can lead to earlier diagnosis and, potentially, more effective management.
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9/42. Medial medullary infarction: a role of diffusion-weighted magnetic resonance imaging for stroke rehabilitation.

    We report a patient with medial medullary infarction who could be diagnosed in an early stage, and we discuss the role of diffusion-weighted magnetic resonance imaging (MRI) for stroke rehabilitation. In the case of our patient, the infarction was difficult to diagnose because the patient had atypical features and a past history of head injury. Nonetheless, we could diagnose the medial medullary infarction easily using diffusion MRI within several hours of onset. Then, a rehabilitation program was started the day after onset. We believe that diffusion MRI can be used as a useful method for very early stage diagnosis and to execute rehabilitation for early stroke patients.
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10/42. 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.
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