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The clinical and pathological features of 28 fatal cases of acute uncomplicated massive cerebellar infarction are reviewed. Although infarcts may involve any portion of the cerebellum, they predominantly involve the posteroinferior half of one cerebellar hemisphere. The frequency of acute uncomplicated fatal cerebellar infarction is much greater than previously appreciated, approximating that of acute fatal cerebellar hemorrhage. All patients were past middle age. Atherosclerosis and acute vertebral artery occlusion were the most common etiological factors. The onset was sudden in most cases, with vomiting, dizziness, vertigo, and cerebellar dysfunction. All patients died with progressive brain stem dysfunction and medullary respiratory failure secondary to compression by a swollen cerebellum. Death usually occurred between the third and sixth days following the onset of symptoms, but only six to 30 hours after the onset of obtundation; therefore, decompressive therapy must be instituted promptly.
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PMID:Cerebellar infarction. A clinicopathological study. 113 Oct 69

Computerized tomography of the head was done in 5021 patients aged 21 to 81 years from various neurological, neurosurgical and neurotraumatological indications. Brain atrophy as an only finding (primary) was noted in 11.5%- and in 5.4% of cases it was associated with other changes. The neurological-radiological correlations were established in 200 cases of primary strophy. History data included: headaches in 54.5%, dizziness in 15.0%, epilepsy in 24.5%. Objective examination showed: slight hemiparesis in 37.5%, spastic-atactic gait disturbances in 31.5%, isolated damage to the corticospinal tracts with signs limited to one side of the body was more frequent in cortical atrophy, and these signs associated with ataxia were more frequent in subcortional atrophy. The authors explain this as a loss of cortical cells or damage to the paraventricularly coursing nerve fibres. A probable aetiology of "primary" atrophy was established in 405% of cases (hypertension, atherosclerosis, minor craniocerebral trauma). No signs or neurological syndromes were observed which could be regarded as more or less characteristic of brain atrophy.
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PMID:[Brain atrophy: radiological-neurological correlations]. 213 53

A 34 year old female had a history of dizziness and presyncope. She had many risk factors for atherosclerosis including smoking 30 packs of cigarettes/year, using oral contraceptives (OCs) for almost 10 years, somewhat elevated blood sugars, strong family history of heart disease and diabetes, and hypertension. During an examination in 1983, she had an elevated blood pressure in the right arm but a reading could not be found in the left arm. The physician heard a grade III rough, blowing systolic bruit over the right subclavian artery moving into the right carotid artery. Pulses of both carotid arteries were normal. Heart sounds were normal. While the right brachial and radial pulses were fine, there were none on the left side. Laboratory tests showed a serum cholesterol of 258 mg/dl, a fasting blood sugar of 92 mg/dl, a white blood cell count of 8400, and a normal differential count. The arch aortogram showed a 50-60% stenosis beginning at the innominate artery and a completely occluded left subclavian artery at its origin. Physicians performed an aortoinnominate bypass operation using a Dacron prosthetic graft. This operation alleviated the symptoms, but 2 years later she had bilateral dysesthesias in her upper arms and vertigo returned. Her right arm became more and more limp while her left arm did so mildly. The aortoinnominate graft and the left subclavian artery were occluded. Physicians did coronary angioplasty using the right transfemoral route and corrected both lesions in her brachiocephalic system. they used a technique which eased safe crossing of the occluded subclavian segment (covering the catheter tip with a J curve guidewire). Following the operation, the patient had superb brachial and radial pulses in both arms. Physicians advised her to discontinue using OCs and tobacco products. At months 1 and 5, the symptoms were gone and vital signs were fine.
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PMID:Percutaneous transluminal angioplasty for innominate artery stenosis and total occlusion of subclavian artery in Takayasu's-type arteritis. 256 38

A series of 12 patients with cerebellar infarcts diagnosed by computerized tomography are reviewed. The clinical features of cerebellar infarctions cover a wide spectrum, mimicking symptoms and signs from an acute labyrinthitis to a rapidly expanding posterior fossa mass lesion with brain stem and cerebral dysfunction. Two patients were asymptomatic and three showed signs of cerebellar dysfunction only. Three patients had evidence of brain stem dysfunction with cranial nerve palsies accompanying the cerebellar deficit. Two presented a pseudovestibular form with sudden onset of nausea, vomiting, rotary dizziness and ataxia. A pseudotumoral form with intracranial hypertension was found in two cases, in which softening tissue acts as a rapidly expanding posterior foss mass lesion. It is difficult to identify the exact artery involved in a cerebellar infarct because of the collateral circulation and connections between the three major arteries. Atherosclerosis and general decrease in blood flow can be regarded as the most likely factors precipitating focal cerebellar infarction. Surveillance is necessary during the first days with anti-edematous therapy. Rapid deterioration of consciousness should be considered a sign of increasing intracranial pressure progressing with the development of hydrocephalus. If necessary, surgical decompression by external drainage or by direct access to the posterior fossa can be carried out.
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PMID:[Cerebellar infarct. Clinical presentation and x-ray computed tomography of the brain]. 394 88

Sulocton effect was evaluated in 33 patients with symptoms of brain ischaemia during atherosclerosis. Thirty patients received the drug orally for 2 months in doses of 100 mg thrice daily. Three patients discontinued the treatment earlier (two of them discontinued it because of side effects). After two months of treatment a significant improvement was observed in such disturbances important for wellbeing and social contacts as: anxiety and fear, mood depression, disequilibrium of emotion, motivation and initiative. In many patients headaches, dizziness and gait disturbances disappeared or diminished. Sulocton was useful in the treatment of patients with cerebral atherosclerosis.
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PMID:[Evaluation of sulocton action in patients with atherosclerotic brain ischemia]. 629 59

In a 55-year-old man, attacks of spontaneous angina were associated with dizziness and syncope. Holter ECG monitoring disclosed evidence of sinus node dysfunction. Dizziness and syncope were corrected by a permanent ventricular demand pacemaker. Coronary cineangiography showed spontaneous, severe, diffuse spasm in a dominant left coronary artery and localized spasm in a nondominant right coronary artery. The patient died of pump failure shortly after cardiac catheterization. An autopsy disclosed only minimal coronary atherosclerosis. This patient's condition shows that (1) coronary spasm may cause sinus node dysfunction, dizziness, and syncope, (2) severe spasm that involves all the coronary artery branches may be fatal, and (3) severe spasm occur in minimally diseased coronary arteries confirmed by pathologic examination.
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PMID:Coronary artery spasm with sinus node dysfunction and syncope. 711 92

ON the basis of analyzing the clinical picture of the disease in 280 patients suffering from atherosclerosis with transitory disturbances of the circulation in the vertebrobasilar system the author comes to a conclusion that in patients with truncal strokes the clinical picture usually includes symptoms of preceding transitory ischemic episodes. In patients with an ischemic lesion in the basin of the posterior cerebral arteries, the lesion localization and the preceding transitory cerebral circulation disturbances are usually not in agreement: the episodes are characterized by a considerable polymorphism and not infrequently point to a circulatory insufficiency in the arteries of the truncal or the carotid systems. the character, frequency, duration, and number of episodes are of no decisive diagnostic importance as regards the possibility of an ischemic stroke development. One can only speak of a more favourable course of the disease in patients with attacks of systemic dizziness, and of a less favourable course in patients with attacks of unconsciousness and transitory global amnesia.
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PMID:[Prognostic value of different clinical symptoms in transient circulatory disorders in the vertebro-basilar system]. 732 78

This study included 125 cases of cerebellar infarction followed during an average period of 4.3 years. The diagnosis was made by CT or MRI. Infarctions localized to the territory of the superior cerebellar artery (SCA) and the territory of the posterior inferior cerebellar artery (PICA) occurred with the same frequency. Transient ischemic attacks preceded infarction in 26% of cases. Symptoms and signs were usual with sudden association of headache, dizziness, unsteadiness and vomiting. Vestibular signs were more important in infarctions of the PICA territory; cerebellar signs and dysarthria were more frequent in infarction of the SCA territory. A decreased level of consciousness developed in only 21% of cases. Surgical operation was required in 9 cases. Investigations have showed the large responsibility of cardiac embolisms and atherosclerosis. Short term outcome was more often favourable: 116 patients were alive at the end of the first month; 80% of survivors were independent one year later. At 5 years, 73% of patients were alive. After the acute period, mortality was mainly due to cerebro-vascular and cardiac events.
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PMID:[Clinical and evolutive aspects of cerebellar infarction]. 786 66

As part of the Atherosclerosis Risk in Communities (ARIC) Study assessment of the etiology and sequelae of atherosclerosis, a standardized questionnaire on transient ischemic attack (TIA) and nonfatal stroke and a computerized diagnostic algorithm simulating clinical reasoning were developed and tested at the four ARIC field centers: Forsyth County, North Carolina; Minneapolis, Minnesota; Jackson, Mississippi; and Washington County, Maryland. The diagnostic algorithm used participant responses to a series of questions about six neurologic trigger symptoms to identify symptoms of TIA or stroke and their vascular distribution. Among 12,205 ARIO participants reporting their lifetime occurrence of one or more symptoms probably due to cerebrovascular causes, nearly half (47%) reported the sudden onset of at least one symptom sometime prior to their ARIC examination. Of those with at least one symptom, only 12.9% were classified by the computer algorithm as having symptoms of TIA or stroke. Dizziness/loss of balance was the most frequently reported symptom (36%); 1.2% of these persons were classified by the algorithm as having a TIA/stroke event. Positive symptoms of speech dysfunction were classified most often (77.%) as being symptoms of TIA or stroke. Symptoms suggesting TIA were reported more frequently than symptoms suggesting stroke by both sexes. TIA or stroke-like phenomena were more frequent (p < 0.001) in females (7%) than in males (5%) and increased with age in both sexes (p = 0.13 for females; p = 0.02 for males). In Forsyth County, TIA and stroke symptoms were greater in African Americans than in Caucasians (p = 0.05, controlling for sex). The association of algorithmically defined symptoms of TIA or stroke with traditional cerebrovascular risk factors is the subject of a companion paper.
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PMID:Self-reported transient ischemic attack and stroke symptoms: methods and baseline prevalence. The ARIC Study, 1987-1989. 889 Jun 63

Losartan potassium is the first of a new class of orally active antihypertensive drugs which antagonise the action of angiotensin (AT) II at the AT1 receptor subtype. Losartan potassium is converted by the liver to the active metabolite E-3174, which is a more potent antagonist at the AT1 receptor. E-3174 is responsible for most of the pharmacological effects of losartan potassium, and its long half-life contributes to the extended duration of action of the drug. Losartan potassium is effective as a once-daily antihypertensive agent. In mild to moderate hypertension, losartan potassium has similar efficacy to enalapril, atenolol and felodipine extended release. When losartan potassium is combined with hydrochlorothiazide there is a further reduction in blood pressure. Losartan potassium is well tolerated in mild, moderate and severe essential hypertension, with dizziness being reported as the only drug-related adverse effect. The overall rate of patient withdrawal from therapy due to adverse experiences with losartan potassium is lower (2.3%) than that of placebo (3.7%). First-dose hypotension is uncommon, perhaps due to the slower onset of action of the drug, and cough does not appear to be a significant problem. A number of areas concerning the safety and efficacy of losartan potassium remain to be clarified. In particular, long term tolerability studies are needed; cough only became apparent as an adverse effect of ACE inhibitors after 3 to 4 years of use. Postmarketing surveillance has shown that angioedema, a rare but life-threatening adverse effect of ACE inhibitors, also occurs with losartan potassium. Further data are needed on the use of losartan potassium in patients with renal impairment before accepting the recommendation that dosage adjustment is not necessary. The pharmacokinetics and pharmacodynamics of losartan potassium in patients with hepatic disease also require further investigation. Losartan potassium increases uric acid secretion and lowers plasma uric acid levels, which may be of benefit when losartan potassium is combined with a thiazide diuretic, but which may otherwise lead to uric acid stone formation and possibly to nephropathy. Simple control of blood pressure is no longer an adequate goal in the management of hypertension. Any new antihypertensive agent should also reduce cardiovascular events, prevent or cause regression of end-organ damage such as left ventricular hypertrophy, atherosclerosis and renal failure, and should not impair quality of life. Such data on losartan potassium are not currently available. Losartan potassium is likely to be used in patients who are intolerant of ACE inhibitors, but its future in the management of hypertension will depend on long term tolerability studies and data on its effects beyond simple blood pressure control.
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PMID:A risk-benefit assessment of losartan potassium in the treatment of hypertension. 901 Jun 43


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