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)

In a group of 281 cases of subarachnoid haemorrhages including 105 cases of intracranial aneurysms confirmed on autopsy or by angiography the authors analyse the symptoms preceding subarachnoid haemorrhage and suggesting presence of aneurysm. The most frequent symptom suggesting presence of intracranial aneurysm were headaches, especially associated with other symptoms such as dizziness, nausea, paraesthesiae of extremities, visual disturbances. A careful analysis of these symptoms and early radiological examination may help in establishing the diagnosis of aneurysm before its rupture.
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PMID:[Symptoms preceding rupture of subarachnoid aneurysms: an analysis]. 68 25

Temporal bone changes are described in a 57-year-old man who had sudden onset of dizziness and unilateral deafness two months before death. The patient suffered from hypertension, and congestive and renal failure. At autopsy, subarachnoid hemorrhage with punctate cortical hemorrhages and arteriolar thickening involved the right superior cerebellar hemisphere. The pathological changes involved primarily the right cochlea, saccule and posterior ampulla, and were consistent with vascular embarrassment of the temporal bone of two months duration. The cochlea demonstrated total loss of the organ of Corti and severe degenerative changes of the stria vascularis, spiral ligament, outer sulcus cells and distal cochlear nerve fibers. The saccule demonstrated loss of its macula and nerve fibers. The posterior ampulla showed evidence of previous rupture of its membranous wall with fibrosis and beginning bone formation. Fresh hemorrhage, present in some areas of both temporal bones, was related to the patient's terminal subarachnoid hemorrhage.
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PMID:Sudden deafnfess of vascular origin: a human temporal bone study. 125 20

In the Danish Aneurysm Study 1076 patients (pts.) were admitted with an aneurysmal subarachnoid hemorrhage in the 5-year period 1978-83. A warning leak (WL), defined as a sudden episode of headache, vomiting, nuchal pain, dizziness or drowsiness, was identified in 166 pts. (15.4%). In 99 of these the episode was evaluated by a physician but misdiagnosed. A 2-year follow-up examination of the 99 pts. showed that 30 pts. had a normal mental outcome and 43 pts. were dead. If these patients were correctly diagnosed after the WL, when they were in Hunt grade 1-2, the outcome-figures would probably have been significantly better. A theoretical transfer of the outcome-probabilities for pts. in Hunt grade 1-2 to the above mentioned 99 pts. would result in 66 pts. with a normal mental outcome and 25 dead pts. This shows the importance of recognition of a WL episode.
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PMID:Importance of the recognition of a warning leak as a sign of a ruptured intracranial aneurysm. 201 46

Increasing recognition of the importance of calcium in the pathogenesis of cardiovascular disease has stimulated research into the use of calcium channel blocking agents for treatment of a variety of cardiovascular diseases. The favorable efficacy and tolerability profiles of these agents make them attractive therapeutic modalities. Clinical applications of calcium channel blockers parallel their tissue selectivity. In contrast to verapamil and diltiazem, which are roughly equipotent in their actions on the heart and vascular smooth muscle, the dihydropyridine calcium channel blockers are a group of potent peripheral vasodilator agents that exert minimal electrophysiologic effects on cardiac nodal or conduction tissue. As the first dihydropyridine available for use in the United States, nifedipine controls angina and hypertension with minimal depression of cardiac function. Additional members of this group of calcium channel blockers have been studied for a variety of indications for which they may offer advantages over current therapy. Once or twice daily dosage possible with nitrendipine and nisoldipine offers a convenient administration schedule, which encourages patient compliance in long-term therapy of hypertension. The coronary vasodilating properties of nisoldipine have led to the investigation of this agent for use in angina. Selectivity for the cerebrovascular bed makes nimodipine potentially useful in the treatment of subarachnoid hemorrhage, migraine headache, dementia, and stroke. In general, the dihydropyridine calcium channel blockers are usually well tolerated, with headache, facial flushing, palpitations, edema, nausea, anorexia, and dizziness being the more common adverse effects.
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PMID:Differential effects of 1,4-dihydropyridine calcium channel blockers: therapeutic implications. 332 59

Aneurysm of the vertebrobasilar system is not a rare lesion but constituting 5-10% of all intracranial aneurysms. Aneurysm at the peripheral part of the anterior inferior cerebellar artery (AICA), however, is rare and only 20 cases have been reported previously. In this report, two cases of aneurysm arising at the junction between the AICA and internal auditory artery and extending into the internal auditory meatus are reported. The first patient was a 51-year-old male who was admitted because of sudden onset of dizziness, rt. tinnitus and deafness. Left vertebral angiograms demonstrated an AVM in the rt. cerebellar hemisphere and two aneurysms on the feeding arteries, one on the superior cerebellar artery and the other on the meatal loop of the rt. AICA. Removal of the AVM and neck clipping of the aneurysms, which were found unruptured, were performed through the rt. suboccipital approach. The second patient was a 42-year-old female who was admitted because of sudden onset of severe headache and vomiting followed by rt. tinnitus, deafness and double vision. CT scan showed subarachnoid clot mainly located in the rt. cerebellopontine angle. Repeated vertebral angiograms revealed an aneurysm at the meatal loop of the rt. AICA. Complete neck clipping was carried out. The clinical features of the aneurysms of this location can be divided into three subgroups according to the characters of onset: sudden onset with subarachnoid hemorrhage, insidious onset of the VII th, VIII th, nerve palsies by the mass effect of the aneurysm, intermittent episodes of the VIII th nerve disfunction due to the insufficiency of the internal auditory artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Aneurysm of the anterior inferior cerebellar artery at the internal auditory meatus: report of two cases]. 378 69

This 74-year-old female suddenly complained of severe headache, nausea, vomiting and dizziness on June 19, 1981. She was brought to nearby hospital. During the following six days, the state of consciousness gradually worsened and left-sided hemiparesis and convulsion attack arose and she was admitted to our clinic on June 25, 1981. Cerebral angiograms revealed an aneurysm of the right middle cerebral artery. Diagnosis of subarachnoid hemorrhage due to the rupture of an aneurysm was tentatively made and conservative therapy was done. On the second hospital day, she had nasal bleeding and began to excrete tar-like stool. Laboratory examination revealed thrombocytopenia, increase of FDP and prolongation of prothrombin time. Her liver and renal functions gradually worsened after this episode. On the 13th hospital day, she expired. General autopsy showed wide spread adenocarcinoma with metastases to the lung, lymph nodes and bones. Examination of the head revealed an unruptured aneurysm and bilateral diffuse subdural clotted hemorrhage. The dura was tightly adherent to the skull and partially thickened. No abnormal findings were found in the brain. On microscopical examination of the dura, there were fresh hemorrhage and many of the innumerable dilated small vessels contained tumor in the inner dural layer. Even by extensive examination, the origin of the malignancy could not be identified. We concluded that the initial symptoms just like of subarachnoid hemorrhage were due to the dural metastasis and subdural hematoma. Sixteen cases of subdural hematoma secondary to metastatic neoplasm were reported previously. We made some discussion about the pathogenesis and symptomatology of this type of subdural hematoma.
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PMID:[Subdural hematoma due to metastatic dural carcinomatosis associated with DIC--a case report]. 662 89

The AA relate a case of a complex malformation of the AICA characterized by aneurysm of the internal auditory artery developed inside the internal acoustic channel associated with an angioma fed by the cerebellar branch of the same artery. During a long period with dizziness, tinnitus, headache in the occipital region, mild sensoneural retrocochlear hearing loss a subarachnoid hemorrhage occurred. The vascular malformations were visualized by a vertebral angiography and the axial projection resulted to be the most important clue. The AA report the case for its rarity and emphasize the vascular origin of certain unexplained kinds of vestibular syndromes in young patients.
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PMID:[Rare malformation of the anterior-inferior cerebellar artery. Cerebellar hemisphere angioma and aneurysm of the labyrinthine artery]. 718 95

We report a case of a 32-year-old man who presented with subarachnoid hemorrhage. As revealed by lumbar puncture, the cerebrospinal fluid had low glucose, high protein levels, and pleocytosis with 5% of eosinophils. Cultures were negative. Enzyme-linked immunosorbent assay and complement fixation reactions for cysticercosis in cerebrospinal fluid were positive. An angiogram revealed an aneurysm of the right anteroinferior cerebellar artery. At surgery, the aneurysm was found to be surrounded by thickened leptomeninges, which histologically presented dense inflammation and remains of Cysticercus. The aneurysm could not be clipped, and it was wrapped. Postoperatively, the patient had dizziness and right ear tinnitus. He received prednisone therapy on alternate days and subsequently received albendazole for subarachnoid cysticerci. At the 4-year follow-up, the patient was asymptomatic and had normal cerebrospinal fluid. Although we cannot rule out a congenital aneurysm, its location inside an area of severe arachnoiditis around a cysticercus suggests an inflammatory origin. This type of vascular lesion not reported before should be suspected in patients with chronic cysticercotic meningitis.
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PMID:Subarachnoid hemorrhage secondary to a ruptured inflammatory aneurysm: a possible manifestation of neurocysticercosis: case report. 874 71

Although there is general agreement that chronic ingestion of alcohol poses great risks for normal cardiovascular functions and peripheral-vascular homeostasis, a direct cause and effect between the real phenomena of alcohol-induced headache and risk of brain injury and stroke is not appreciated. "Binge drinking" of alcohol is associated with an ever-growing number of strokes and sudden death. It is becoming clear that alcohol ingestion can result in profoundly different actions on the cerebral circulation (e.g., vasodilation, vasoconstriction-spasm, vessel rupture), depending upon dose and physiologic state of host. Using rats, it has been demonstrated that acute, high doses of ethanol can result in stroke-like events concomitant with alterations in brain bioenergetics. We review recent in vivo findings obtained with 31P-NMR spectroscopy, optical reflectance spectroscopy, and direct in vivo microcirculatory studies on the intact brain. Alcohol-induced hemorrhagic stroke is preceded by a rapid fall in brain intracellular free magnesium ions ([Mg2+]i) followed by cerebrovasospasm and reductions in phosphocreatine (PCr)/ATP ratio, intracellular pH, and the cytosolic phosphorylation potential (CPP) with concomitant rises in deoxyhemoglobin (DH), mitochondrial reduced cytochrome oxidase aa3 (rCOaa3), blood volume, and intracellular inorganic phosphate (Pi). Using osmotic mini-pumps implanted in the third cerebral ventricle, containing 30% ethanol, it was found that brain [Mg2+]i is reduced 30% after 14 days; brain PCr fell 15%, whereas the CPP fell 40%. Such animals became susceptible to stroke from nonlethal doses of ethanol. Human subjects with mild head injury have been found to exhibit early deficits in serum ionized Mg (IMg2+); the greater the degree of early head injury (30 min-8 h), the greater and more profound the deficit in serum IMg2+ and the greater the ionized Ca (ICa2+) to IMg2+ ratio. Patients with histories of alcohol abuse or ingestion of alcohol prior to head injury exhibited greater deficits in IMg2+ (and higher ICa2+/IMg2+ ratios) and, unlike the subjects without alcohol, did not leave the hospital for at least several days. Women, for some unknown reason, exhibit a much higher incidence of morbidity and mortality from subarachnoid hemorrhage (SAH) than men. Data on 105 men and women with different types of stroke indicate that, on the average, a 20% deficit in serum IMg2+ is seen; total Mg (TMg) or blood pH is usually near normal. Women with SAH, however, exhibit much lower IMg2+ and higher ICa2+/IMg2+ ratios; the presence of ethanol in the blood is associated with even more depression in IMg2+ in SAH in women. It is possible that prior alcohol ingestion is, in large measure, responsible for a great deal of this unexplained higher incidence of SAH in women. It has recently been reported that the cyclical changes in estrogenic hormones appear to control the serum IMg2+ level in young women. A surge in estrogenic levels prior to SAH could thus precipitate, in part, the SAH. In other human studies, it has been shown that migraines and headache, dizziness, and hangover, which accompany ethanol ingestion, are associated with rapid deficits in serum IMg2+ but not in TMg. The former, and the alcohol-associated headache, can be ameliorated with IV administration of MgSO4. Premenstrual tension-headache (PTH) and its exacerbation by alcohol in women is also accompanied by deficits in IMg2+, and elevation in serum ICa2+/IMg2+; IV MgSO4 corrects the PTH and the serum deficit in IMg2+. Animal experiments show that IV Mg2+ can prevent alcohol-induced hemorrhagic stroke and the subsequent fall in brain [Mg2+]i, [PCr], pHi, and CPP. Other recent data indicate that alcohol-induced cellular loss of [Mg2+]i is associated with cellular Ca2+ overload and generation of oxygen-derived free radicals; chronic pretreatment with vitamin E prevents alcohol-induced vascular injury and pathology in the brain. (ABSTRACT TRUNCATED)
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PMID:Association of alcohol in brain injury, headaches, and stroke with brain-tissue and serum levels of ionized magnesium: a review of recent findings and mechanisms of action. 1054 55

A 68-year-old man with disturbed consciousness had repeatedly developed light-headedness and dizziness since the summer of 1996 and was admitted to a hospital for detailed examinations on October 8, 1996. On admission, he weighed 49 kg and showed subclinical hypothyroidism with low T3 syndrome. The adrenal function and serum electrolytes were normal. Since the stool samples were positive for occult blood, gastroscopy was performed. Examination of the biopsy specimens demonstrated gastric cancer. On October 21, blood examination showed hyponatremia (127 mEq/l). On October 22, marked disturbance of consciousness developed. On October 24, the serum Na level further decreased to 116 mEq/l. On November 8, he was referred to our hospital. On admission, his skin and tongue showed marked dehydration, and severe disturbance of consciousness and neck stiffness were observed. The central venous pressure was 4 cmH2O. In the cerebrospinal fluid, atypical cells were observed, and a diagnosis of meningeal carcinomatosis was made. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was excluded because of marked dehydration, a normal blood ADH level, and because plasma osmotic pressure was greater than urinary osmotic pressure. Considering the possibility of cerebral salt wasting syndrome (CSWS) or hypoadrenocorticism, Na supplementation and drip infusion of prednisolone (20 mg/day) were performed. The serum Na has normalized (140.1 mEq/l), and his consciousness improved. He died of aggravation of the general condition on December 16. Pathological examination demonstrated a small metastatic lesion in the infundibular part of the pituitary gland and a small metastatic lesion in the parenchyma of the bilateral adrenal glands. However, since neither hypotension nor hypoglycemia was observed before treatment, and the blood cortisol level and the serum K level were normal, hypoadrenocorticism was excluded. Hypoaldosteronism was also excluded because of a normal serum K level. CSWS has been reported to be caused by head trauma, subarachnoid hemorrhage, or trans-sphenoidal pituitary operation. This patient is a rare case of CSWS developed in the presence of meningeal carcinomatosis accompanied by a small pituitary metastatic lesion from gastric cancer. The aged with decreased ability to retain water and sodium in the body are more susceptible to CSWS than the young. In the aged with central hyponatremia, the possibility of CSWS should be considered, and early diagnosis and treatment are necessary.
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PMID:[A patient with meningeal carcinomatosis accompanied by a small pituitary metastatic lesion from gastric cancer who developed cerebral salt wasting syndrome]. 1057 52


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