Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 77-year-old man complained of headache, dizziness and tactile hallucination. Based on those clinical signs and the findings of computed tomography scanning and magnetic resonance imaging, he was diagnosed as having pituitary adenoma. Clinical signs and symptoms of Cushing's disease had not been apparent because of the occurrence of the disease at an old age. An increase in serum cortisol and adrenocorticotropic hormone indicated the presence of Cushing's disease. Physical findings obtained thereafter were also compatible with the disease. While the patient was being prepared for surgery, pituitary apoplexy and intraventricular hemorrhage occurred. Massive ascites appeared as a result of tuberculous peritonitis. In spite of treatment for these complications, his general condition progressively deteriorated and he died 39 days after the intraventricular hemorrhage. This case presents the difficulty in the treatment of masked Cushing's disease in the elderly population.
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PMID:Masked Cushing's disease in an aged man associated with intraventricular hemorrhage and tuberculous peritonitis. 192 Sep 64

The classical subclavian steal syndrome is a larcenous vertebrobasilar insufficiency, secondary to retrograde flow in the vertebral artery. The authors present their experience with an unusual variant of subclavian steal in which the ipsilateral vertebral artery was completely or partially occluded, or arose from the aortic arch. These patients had symptoms typical of vertebrobasilar insufficiency--dizziness or brain stem transient ischemic attacks--despite steal through relatively small cervical collaterals to the obstructed subclavian artery. Physical findings of diminished pulses and blood pressure in the involved upper extremity are similar to those in the common form of subclavian steal. The alternate collaterals found in these patients are documented by angiography and other potential collaterals are reviewed. All three symptomatic patients were treated successfully by carotid-subclavian bypass or anastomosis of the subclavian to the common carotid artery. They have remained asymptomatic for 1 1/2 to 3 years following operation. The potential for development of subclavian steal in the absence of a vertebral artery to provide collateral flow adds another reason for abandoning vertebral artery ligation as an alternative treatment for the subclavian steal syndrome.
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PMID:Subclavian steal with ipsilateral vertebral artery occlusive disease. 372 45

Computerized tomography (CT) and magnetic resonance imaging (MRI) allow accurate anatomical localization of large thromboembolic cerebellar infarcts in the territories of the cerebellar arteries and their branches. In addition, MRI and CT show very small cerebellar infarcts as discrete foci of signal change that are not easily localizable within well-defined arterial territories. They could be border zone infarcts. Their anatomy, mechanism and clinical features have not been studied. By reviewing our CT and MRI files over a 2-year period, we found 47 patients with very small cerebellar infarcts; 23 patients had angiography. Infarcts were cortical (32 patients), deep (10 patients) and both (five patients). Most lesions corresponded to border zone cerebellar infarcts. The mechanisms of infarction were (i) global hypoperfusion due to cardiac arrest (two patients); (ii) small or end (pial) artery disease due to intracranial atheroma or hypercoagulable states (nine patients); (iii) focal cerebellar hypoperfusion due to large artery (vertebral or basilar) occlusive disease (16 patients) or brain embolism (11 patients) resulting in infarcts in the watershed areas (27 patients total); (iv) unknown mechanism (nine patients, 19%). Large artery occlusive disease was more frequently observed in deep than in cortical infarcts (9 out of 15 versus 11 out of 37; P < 0.0001). The most frequent symptoms were dizziness, lightheadedness, unsteadiness with axial lateropulsion, dysarthria and limb clumsiness. These symptoms were either transient or recurrent, at times related to positional changes of the head or trunk. Position-related symptoms often persisted for weeks or months after the ischaemic event, and occurred mainly in patients with combined carotid and vertebrobasilar occlusive disease. Physical findings were either absent or included wide-based gait, lateropulsion, mild ipsilateral dysmetria, dysarthria or dysdiadochokinesia. We conclude that very small cerebellar infarcts are often found on CT and MRI. Their border zone distribution and frequent posturally related symptoms most often result from large or pial artery disease rather than from systemic hypotension.
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PMID:Very small (border zone) cerebellar infarcts. Distribution, causes, mechanisms and clinical features. 845 55