ABSTRACT
Acute mountain sickness is an illness caused by climbing to a high altitude without prior acclimatization. Neurological consequences, like parkinsonism following acute mountain sickness without lesion of brain MRI have been reported rarely. A healthy 56-year-old man presented with dysarthria and gait disturbance. Neurological examination revealed tremor of hands, limb rigidity, and bradykinesia. The symptoms developed approximately 30 days following a 3,500 m climb of the Annapurna in the Himalayas. Brain MRI did not reveal any abnormalities including globus pallidus. The parkinsonism symptoms persisted for about 3 months before a complete recovered was made. We suggest that parkinsonism can develop after climbing to a high altitude but that the symptoms can be transient if a brain MRI detects no abnormalities.
ABSTRACT
Isolated pulsatile tinnitus is a rare condition in patients with neurological disorders but can be the only clue to a potentially life-threatening disease such as intracranial vascular malformation. We report a patient with pulsatile tinnitus caused by an arteriovenous fistula of the external carotid artery, which was successfully treated with coil embolization.
Subject(s)
Humans , Angiography , Arteriovenous Fistula , Carotid Artery, External , Nervous System Diseases , Tinnitus , Vascular MalformationsABSTRACT
BACKGROUND: The purpose of this study is to identify the differences of risk factors and stroke mechanism between early and late recurrence in patients with long-term antiplatelet therapy for stroke prevention. METHODS: We enrolled 114 consecutive patients with recurrent infarction who had been taking antiplatelet agents regularly since previous noncardioembolic cerebral infarction. Total 81 patients (49 men and 32 women) were met to the inclusion criteria through standardized evaluation. Subjects were classified into two groups depending on the time-to-recurrence after antiplatelet therapy: early antiplatelet failure (within 2 years, n=41, hereafter as "EAF") and later antiplatelet failure (after 2 years, n=40, hereafter as "LAF"). We investigated the differences of clinical factors between two groups using univariate and multivariate analysis. RESULTS: Family history of stroke (29.3% in EAF vs. 10% in LAF, p=0.029) was more frequent in EAF group. Low HDL-cholesterol and High total cholesterol/HDL-cholesterol ratio were associated with the LAF group (p=0.042, 0.005 respectively). Multivariate analysis showed that family history of stroke (OR=5.283, 95%CI 1.178-23.699, p=0.030) and previous infarction classified as large artery atherosclerosis (OR=8.497, 95%CI 1.444-50.015, p=0.018) were significant predictors for EAF whereas total cholesterol/HDL-cholesterol ratio (OR=2.002, 95%CI 1.183-3.389, p=0.010) was for LAF. CONCLUSIONS: This study suggests that family history of stroke and cerebral infarction due to large artery atherosclerosis are more responsible for the early recurrence while dyslipidemic condition is more related to the late recurrence during long-term antiplatelet therapy in patients with previous cerebral infarction.
Subject(s)
Humans , Male , Arteries , Atherosclerosis , Cerebral Infarction , Infarction , Multivariate Analysis , Platelet Aggregation Inhibitors , Recurrence , Risk Factors , Stroke , Treatment FailureABSTRACT
No abstract available.
Subject(s)
Autoantibodies , Brain Diseases , Hashimoto Disease , Status EpilepticusABSTRACT
A 70-year-old man presented with acute dysarthria and dizziness. He denied any history of trauma or cervical manipulations within several weeks before symptom onset. We could make a presumptive diagnosis of left Wallenberg syndrome through the results of neurologic examination, which include left limb ataxia, alternating hyp(o)esthesia, spontaneous nystagmus to right side, and left side Honer's syndrome. Initial diffusion weighted imaging performed at admission showed small and discrete high signal lesions in left lateral medulla, left cerebellar hemisphere, and bilateral occipital areas. Contrast enhanced MRA demonstrated a filling defect in long segment of distal left vertebral artery. On 4th days after symptom onset, the patient developed a severe form of ipsilateral hemiparesis. Follow-up brain MRI showed a downward extension of the initial ischemic lesion in upper medulla to upper cervical region. This case suggests that a severe form of ipsilateral hemiparesis may be complicated in the clinical setting of acute lateral medullary infarction with vertebral artery occlusion.