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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various combinations of hypertension, convulsion, severe headache, and cerebral haemorrhage appeared in eight thalassaemic patients after they had received 3--7 units of blood in preparation for splenectomy. Intracranial haemorrhage definitely developed in four patients, three of whom died. At necropsy the brains showed changes similar to those of hypertensive cerebral haemorrhage and hypertensive encephalopathy. It is believed that hypertension initiates this syndrome. Since the episodes often occurred days, as long as 15 days, after the last unit of blood was transfused, hypertension did not seem to result from volume overload, but probably from vasopressive substances provided by or occurring in association with multiple blood-transfusions. Host factors may also contribute.
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PMID:A syndrome of hypertension, convulsion, and cerebral haemorrhage in thalassaemic patients after multiple blood-transfusions. 8 May 27

Benign intracranial hypertension, an unusual case of headaches, was associated with pregnancy in a gravid female with the chief complaint of headache. Symptoms resolved after three days of prednisone therapy. In benign intracranial hypertension, the possibilities of intracranial mass lesions, intracranial infection, obstruction of the cerebral ventricles, and hypertensive encephalopathy are excluded by evaluation with skull films, computerized axial tomography, electroencephalography and lumbar puncture. The only symptom may be headache and the only physical sign, papilledema. Therefore, neurological examination must include visualization of the fundi.
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PMID:Benign intracranial hypertension in pregnancy. 45 93

A 49-year-old female with a 30-year history of untreated essential hypertension was noted to have a blood pressure of 290/175 mmHg during evaluation for elective gynecological surgery. At the time of hospitalization she complained chiefly of chronic frontal headaches. Physical examination revealed grade two hypertensive retinopathy, and laboratory studies showed left ventricular hypertrophy. Over the next 12 days the patient's blood pressure was successfully lowered to 178/106 mmHg. During revision of her therapy her mean blood pressure rose to 244/144 mm Hg (88% of the admission level) over 36 hours and she developed hypertensive encephalopathy with papilledema, headaches and projectile vomiting. Concomitant resolution of neurological symptoms and control of blood pressure occurred over the next nine days. The course of this patient suggests that autoregulation of cerebral blood flow may be acutely reversed and that the occurrence of hypertensive encephalopathy depends not only on the magnitude and duration of the blood pressure elevation but, more important, on the rate at which that blood pressure is attained.
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PMID:Iatrogenically induced hypertensive encephalopathy. 45 3

The clinical and pathologic findings in 20 patients with hypertensive encephalopathy were reviewed. The dominant central nervous system (CNS) symptoms were altered state of consciousness and severe headache. Nausea, vomiting, and visual disturbances were less common. Seizures and focal signs were infrequent. The changes seen were invariably accompanied both by the characteristic ophthalmoscopic alterations of malignant hypertension and by uremia. The neuropathologic changes consisted of severe vascular alterations (fibrinoid necrosis of arterioles, thrombosis of arterioles and capillaries), and of parenchymal lesions (microinfarcts, petechial hemorrhages) secondary to the vascular lesions. The vascular changes were not confined to the brain but were diffuse, affecting the eyes, kidneys, and other organs. In the CNS the brainstem was most severely affected. Cerebral edema was not observed, even in those patients who had increased cerebrospinal fluid pressure and papilledema.
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PMID:Hypertensive encephalopathy: a clinicopathologic study of 20 cases. 56 64

Hypertensive encephalopathy is a dramatic syndrome characterized by severe elevation of blood pressure, headache, visual disturbances, altered mental status, and convulsions. Although the syndrome is uncommon, to recognize and treat it promptly is important or the condition may prove to be fatal. Hypertensive encephalopathy should be distinguished from other cerebral complications of severe hypertension by obtaining careful history and performing thorough physical examination. The only definitive criterion for the diagnosis of this syndrome is its prompt response to therapy. If the patient's condition does not improve with hypotensive therapy, the physician should immediately search for alternate diagnoses. Potent drugs are available for prompt reduction of blood pressure. There are few medical emergencies in which the objective response to therapy is so strikingly apparent as in hypertensive encephalopathy.
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PMID:Hypertensive encephalopathy: recognition and management. 71 53

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

Oppenheimer and Fischberg's vasoconstriction-hypothesis on the pathogenesis of hypertensive encephalopathy was subsequently supported by animal experiments. Later on the role of decompensation of the autoregulatory mechanism of the cerebral blood flow was revealed. The transient symptomatology comprises headache, seizures, focal cerebral symptoms (hemiplegia etc.), visual disturbances, mental disorders, papiledema etc. The age-dependency of the influence of edema is probably expressed by the predominance of seizures in childhood and the long duration of the symptoms in our third and fourth patient. The differentiation between hypertensive encephalopathy and a local complication of hypertension (hemorrhage) can be difficult, not at least because the first disturbance may be followed by the second (patient 3). Hypertension is not always present as initial symptom (patient 1 and 2). Hence a series of blood pressure readings is required in acute cerebral incidents in childhood. Steroid-treatment may lead, especially in patients suffering from a hypocomplementemic form of membranoproliferative glomerulonephritis, to a sudden rise of the blood pressure and subsequently to hypertensive encephalopathy (patients 2 and 3). Hypertensive encephalopathy is a neuropediatric emergency. The urgent treatment with dioxaside, fursemide and sodium nitroprusside is shortly reviewed.
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PMID:Hypertensive encephalopathy in childhood. Diagnostic problems. 98 19

A case is presented of neurilemmoma of the left oculomotor nerve occurring in a 64-year-old hypertensive woman. The incipient tumour produced ptosis, limited inwards rotation of the eyeball, and persistent pupillary dilatation on the left side. The mechanism of this process is discussed, having regard to the interruption of the fibres innervating these structures by the tumour, and considering the mode of occurrence of the ocular and pupillary impairments. The patient also had generalized athero-sclerosis and fusiform aneurysm of the terminal part of the left internal carotid artery. The symptoms of headache, seizure, coma, and temporary right hemiparesis were considered as manifestations of hypertensive encephalopathy unrelated to the tumour.
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PMID:Neurilemmoma of the oculomotor nerve. 112 61

Clinical and neuroimaging studies were made in twenty-one patients during the attack of eclampsia. Most frequent neurological signs and symptoms were the impairment of consciousness, headache, seizure and visual disturbance. Mean arterial blood pressure increased by 46 mmHg (n = 21) during the attacks. Eight of 9 patients studied by CT and/or MRI showed transient abnormalities on brain images during the attack in the occipital cortex, basal ganglia, and internal and external capsule. The findings were compatible with brain edema and were seen mainly in the white matter. Cerebral blood flow measured by SPECT method in one patient during an attack with visual disturbance showed increased blood flow in the occipital cortex. Acute increase in blood pressure, cerebral hyperperfusion and edema, similar to the pathophysiology of hypertensive encephalopathy, were considered to play an important role in the pathogenesis of eclampsia.
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PMID:[Neurological and neuroimaging studies of eclampsia]. 129 Nov 59

38 cases of Takayasu's arteritis were reported. The mean age of onset was 23.3 years with a female: male ratio of 1:1.7. The median delay between first symptom and time of diagnosis was 12.2 years. Headache was the most common symptom of neurologic manifestations (55%). Major neurologic events occurred in 52.7% patients in this group, including TIA, cerebral infarction, hypertensive encephalopathy, lacunar infarct, seizure, paraplegia, watershed infarct, cerebral hemorrhage, Moyamoya phenomenon, and confusion in the order of frequency. A variety of mechanisms that must be taken into account in explaining this neurologic events were proposed. The secondary hypertension and cardiac complications play an important role in causing neurologic symptoms. The formation of anastomotic networks has "Jekyll and Hyde" effect on brain both in preventing or limiting the ischemic injury and in producing some special symptoms and signs, that further widen the clinical spectrum of brain involvement.
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PMID:[Neurological manifestation of Takayasu's arteritis]. 136 36


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