Lateral bulbar infarction due to intracranial dissection and subarachnoid haemorrhage

INTRODUCTION: Intracranial vertebral artery dissecting aneurysms are a recognized cause of subarachnoid hemorrhage and the hemorrhagic recurrence risk after a first rupture of the dissecting aneurysm is high and of poor prognosis. However, when the dissection is discovered in a patient with vertebrobasilar territory ischemia, little is known about the risk of hemorrhagic rupture risk and there is no consensus on management. OBSERVATION: We report the case of a 49-year-old man who developed subarachnoid hemorrhage 48 hours after the occurrence of a latero-bulbar syndrome caused by a spontaneous dissection with occlusion of the right vertebral artery. The subsequent angiography showed a V4 dissecting aneurysm of the right vertebral artery which was treated by stenting and coiling without any complications. CONCLUSION: This case underlines the hemorrhagic risk of an intradural vertebral artery dissection and its possible progression to aneurysm. Subsequent angiographic imaging must be carefully examined to search for aneurysms which may require early specific treatment because of the high risk of recurrent bleeding.     

Two cases with unilateral lateral medullary infarction associated with central respiratory failure

We reported two patients with unilateral lateral medullary infarction involving severe, long-term respiratory failure. The first patient is an 86-year-old man presenting with gait disturbance, hoarseness and dysphagia. A right lateral medullary infarction was revealed by brain MRI. On the fifth hospitalized day, acute respiratory failure occurred. His condition failed to recover, and he was still attached to a ventilator 10 months after the onset. The second patient is an 83-year-old woman mainly presenting with dysphagia. A tiny infarction in the right lateral medulla was revealed by brain MRI. On the third day after the onset, acute respiratory failure occurred, which was not changed even at 8 months later. Although the symptoms and the lesion in the medulla were quite different between two patients, dysphagia and respiratory failure occurred in both patients. Therefore, it is postulated that the lesion that causes dyspnea may be approximate to the lesion that causes dysphagia. Many previously reported cases presenting respiratory failure seemed to suffer swallowing difficulty as well. We conclude that elderly patients suffering from unilateral lateral medullary infarction with dysphagia can present respiratory failure a few days after the onset, demonstrating the need to observe them under intensive attention.     

Transient upbeat nystagmus due to unilateral focal pontine infarction

Upbeat nystagmus is known to be caused by an imbalance of the vertical vestibulo-ocular reflex (VOR), favoring downward VOR activity, due to bilateral lesions of the medulla, ventral tegmentum, anterior cerebellar vermis, adjacent brachium conjunctivum and the midbrain. We report on two patients who had transient upbeat nystagmus due to unilateral pontine infarction that may have disrupted bilateral upward VOR pathways running in the ventral tegmental tracts.     

急性脑梗塞与单侧多汗症

出汗异常是自主神经功能障碍中最常见的症状之一。本文报道５例脑梗塞伴对侧躯体出汗异常患者。３例为大脑中动脉区梗塞、２例为脑岛皮层区梗塞。出汗部位以额和前臂明显，持续１～４天，未发现其它自主神经功能障碍。本文就５例患者并结合有关文献对其预防、临床特征、发病机理及临床意义作一讨论。     

Primary position upbeat nystagmus due to unilateral medial medullary infarction

We report on a patient who developed primary position upbeat nystagmus (ppUBN) due to a unilateral medial medullary infarction. On oculography, the slow phases of the nystagmus sometimes had an exponentially decreasing velocity waveform, indicating that the nystagmus was due to impairment of the vertical position-to-velocity neural integrator. On magnetic resonance imaging, the lesion was caudal to the vestibular nuclei and to the most rostral of the perihypoglossal nuclei, the nucleus intercalatus, a structure that was also involved in a previously reported case of ppUBN due to a unilateral medullary lesion. On the basis of these imaging and oculographic observations, we propose that a unilateral lesion of the nucleus intercalatus is sufficient to cause ppUBN and that the nucleus intercalatus is a part of the vertical position-to-velocity neural integrator in the human ocular–motor system.     

Acute mania due to a right hemisphere infarction

A 67-year-old woman who developed acute secondary mania immediately after a mixed (perforating and cortical) embolic brain infarction in the territory of the right middle cerebral artery is described. According to neuroradiological findings ischemic lesions involving the basal and medial areas of the temporal lobe and the head of the caudate as well as the putamen were evident. In the pathogenesis of secondary mania due to cerebrovascular disease, the pattern of involved structures is unique and underlines the significance of lesion location after damage of the minor hemisphere.     

Respiratory failure and unilateral caudal brainstem infarction

We report clinicotopographic correlations in 2 patients with central hypoventilation and unilateral infarct in the caudal brainstem. One patient had nearly complete loss of ventilation involving both automatic and voluntary components. He showed no ventilator response during a CO2 retention test (PaCO2 62 mm Hg, PaO2 82 mm Hg), while consciousness was preserved until death. The infarct involved the reticular formation, nucleus tractus solitarius, nucleus ambiguus, and nucleus retroambiguus on the right but spared the dorsal motor nucleus of the tenth cranial nerve, and sensory and corticospinal tracts. The second patient showed hypoventilation more selectively involving automatic responses (Ondine's curse). The infarct involved the medullary reticular formation and nucleus ambiguus but spared the nucleus tractus solitarius. We suggest that unilateral involvement of pontomedullary reticular formation and nucleus ambiguus is sufficient for generating loss of automatic respiration, while associated lesion of the nucleus tractus solitarius may lead to more severe respiratory failure involving both automatic and voluntary responses.     

Memory impairment due to a small unilateral infarction of the fornix

A 52-year-old man suffered sudden anterograde and retrograde amnesia without any focal neurological deficit. Assessment using Wechsler Memory Scale-Revised test revealed significant memory impairment with a marked decline of delayed recall and preserved attention and concentration. Wechsler Adult Intelligent Scale-Third Edition indicated poor intelligent quotients. MRI revealed a small infarction at the anterior column of the left fornix. His memory loss persisted for more than 3 months with only slight improvement. This rare case indicates that isolated damage to the anterior column of the unilateral fornix is sufficient to cause significant memory disturbance, and that cerebral infarction should be considered in the differential diagnosis of a patient presenting with amnesia as the only symptom.     

Acute hemichorea due to infarction in the corona radiata

Summary A 66-year-old hypertensive man presented with acute hemichorea. Magnetic resonance imaging disclosed an infarct, confined to the contralateral corona radiata, that interrupted excitatory corticostriate fibres. The movement disorder may have been caused by subcortical lesion without direct involvement of the basal ganglia.     

Acute failure of automatic respirations secondary to a unilateral brainstem infarct

A case of failure of automatic respiration with sleep apnea is described in a patient with a unilateral lateral medullary tegmental lesion. This case is the first known with autopsy confirmation in which a unilateral lesion has caused this syndrome.     

Bilateral wallerian degeneration of the middle cerebellar peduncles due to unilateral pontine infarction

We report the case of a patient with bilateral and symmetrical T2 hyperintensities of the middle cerebellar peduncles. She had a history of left pontine infarction 8 months before. This was attributed to bilateral Wallerian degeneration. MR Spectroscopy showed decreased N-acetyl aspartate/Creatine (NAA/Cr) ratio in the cerebellar peduncles as well as in the whole cerebellum. We hypothesize that this could reflect neuronal degeneration following a stroke.