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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pituitary adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion. Pituitary adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications, hypertension, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86

A 66-year-old man suddenly developed bilateral ptosis after awaking from a nap. He did not experience nausea, vomiting or headache. In the emergency room, high blood pressure was noted. On examination, his consciousness was clear. Ptosis was present bilaterally and worse on the right side. The pupils promptly constricted to light. He could fully adduct his eyes during conjugate gaze movements, but convergence was impaired in the right eye. There was no diplopia or nystagmus. The assessment of the motor and sensory systems revealed no significant findings. Computed tomographic scanning and magnetic resonance imaging of the brain showed a small hematoma in the midbrain. Six months later, ptosis improved; however, the convergence deficit remained.
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PMID:Midbrain hemorrhage presenting as bilateral ptosis without hemiplegia: a case report. 775 61

A 62-year-old man with a history of diabetes mellitus, hypertension and liver damage has sudden diplopia on Nov. 4, 1992. Ocular movements of this right eye were normal, but his left eyelid was completely ptotic, and left pupil was dilated and nonreactive to light. In primary position, his left eye deviated outward, and could not move to any direction. He was diagnosed as having total oculomotor nerve palsy of the left side without any other neurological signs or symptoms; his consciousness level was alert and mental state was normal. The present case showed normal facial sensation, no facial palsy and no tongue deviation. Deep tendon reflexes were hypoactive bilaterally. Pyramidal tract sign, cerebellar sign, and gait disturbance were not observed. Superficial sensation of the extremity was normal. Brain CT scan revealed a small mesencephalic hemorrhage extending to the tegmentusm ventral to the cerebral aqueduct of the left side. Brain magnetic resonance imaging demonstrated a high-intensity area in the left oculomotor nucleus and its fascicles in the midbrain on T1- and T2-weighted image. The oculomotor nerve palsy of the left eye gradually improved, but mydriasis, adduction impairment and downward gaze palsy continued, and oculomotor nerve palsy of the left eye was compatible with so-called inferior branch palsy of the oculomotor nerve. Moreover, contralateral eye movements were normal except for mild upward gaze palsy. Oculomotor nerve palsy of this type was consistent with the syndrome of oculomotor nucleus described by Pierrot-Deseillingny in 1981. It was presumed that the superior rectus muscle is innervated by the contralateral oculomotor nerve nucleus in man as well as in animals.
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PMID:[Isolated oculomotor nerve palsy caused by mesencephalic hemorrhage]. 783 46

Seventy-two patients (69 women and 3 men) with benign intracranial hypertension were examined. Besides general clinical signs, such as headache in 71, giddiness in 29, vomiting in 19, poor health in general in 18, painful movements of the eyeballs in 11, unsteady walking in 10, ringing in the ears in 9, noise in the head in 3, all the patients developed changes in the organ of vision. Congestive optic disks were detected in all the cases. Obnubilations were detected in 34 (47.2%) patients, diplopia in 5 (6.9%). Vision acuity was reduced in 33 (45.8%) patients, visual field was limited in 23 (31.9%). Forty-three patients completely recovered, negligible residual symptoms of benign intracranial hypertension persisted in 16, and all symptoms of the condition were virtually unchanged in 13 patients. Vision acuity remained reduced in 10 (13.9%) patients, and one female patient developed amaurosis of both eyes.
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PMID:[Visual functional disorders in benign intracranial hypertension]. 807 84

A 74-year-old woman, with hypertension and dilated cardiomyopathy, presented with sudden onset of diplopia without vertigo and other neurological symptom. Examination revealed left inferior rectus muscle paresis. Other neurological findings were normal. She had no cerebellar ataxia and sensori-motor dysfunction. Magnetic resonance imaging showed increased signal intensity on T2-weighted and proton density-weighted images in the right ventral midbrain, compatible with infarction involving the fascicular oculomotor fibers. Complete resolution of the diplopia and normal ocular motility were noted 3 months after the onset of the diplopia. Focal ischemic midbrain lesions should be considered in cases of isolated partial oculomotor nerve paresis.
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PMID:[Isolated inferior rectus muscle paresis from midbrain infarction]. 837 Feb 6

We describe the clinical course of two cases of envenoming by the many-banded krait (Bungarus multicinctus). A man developed generalized paralysis and respiratory failure with transient hypertension. Nerve conduction studies revealed normal motor and sensory conduction velocities with reduced motor unit action potential amplitudes consistent with neuromuscular blockade. He showed a slight transient response to the banded krait (B. fasciatus) antivenom but required ventilatory support for 8 days. After the fourth day, there was some response to treatment with anticholinesterase. Another man developed diplopia, dysphagia and leg weakness but recovered spontaneously after 48 hours.
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PMID:Evenoming by Bungarus multicinctus (many-banded krait) in Hong Kong. 854 31

In a patient who developed clinical signs of intracranial hypertension, bilateral papilledema and diplopia, in association with mild hypotension, hyponatremia and hyperkalemia, the hypothesis of Addison's disease was raised and confirmed. Substitutional therapy led to complete recovery. The present paper represents the first report of pseudotumor cerebri as the only clinical sign of an Addisonian crisis.
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PMID:Pseudotumor cerebri as presenting syndrome of Addisonian crisis. 862 16

We describe a 13-year-old girl who presented with an acute febrile disease accompanied by headache, dizziness, nausea, decreased visual acuity, and diplopia. Examination showed papilledema, enlarged blind spots, and visual field defects with an otherwise normal neurological examination. The diagnosis of idiopathic intracranial hypertension was confirmed by increased intracranial pressure (cerebrospinal pressure > 200 mm water) in the absence of any abnormal radiological findings of the brain. Initially, only positive serology tests showing elevated titers of anti-DNA antibodies and positive tests for anti-Sm and anti-RNP antibodies were found; however, 6 mo later clinical and laboratory findings were compatible with systemic lupus erythematosus (SLE). Our patient illustrates that the possibility of SLE needs to be considered in the differential diagnosis of idiopathic intracranial hypertension.
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PMID:Systemic lupus erythematosus presenting as idiopathic intracranial hypertension. 882 3

A girl with HIV infection acquired at birth by blood transfusion, was admitted at the age of 10 years for diplopia, vomiting, headache and papilledema. CT scan was negative. A lumbar puncture revealed clear CSF, protein 0.40 g/l, glucose 2 mmol/l, 5 mononuclear cells/mm3. The Indian ink preparation and the latex agglutination antigen test were positive for Cryptococcus n. Treatment with amphotericin B and flucytosine was started. After 10 days, since the in vitro susceptibility testing of the isolates showed resistence to both drugs, fluconazolo (400 mg/day) was started. Acetazolamide, furosemide and spironolactone were then added to the antifungal therapy for the persistence of severe intracranial hypertension. Diuretics were maintained for 10 weeks. The patient returned to school two and half months after the admission to the hospital. After 19 months, she is doing well and she is on maintenance of fluconazole (200 mg/day). We hypothesized that the increased intracranial pressure would be due to an impaired CSF reabsorption probably as a consequence of a direct cryptococcal infiltration of the villi.
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PMID:Intracranial hypertension and cryptococcal meningitis in a girl with AIDS. 887 56

A 7-year-old boy presented with a 4-week history of daily headache. His parents reported that he was unable to attend school the week prior to presentation. Intermittent nausea without vomiting was reported, but no blurred vision, photophobia, or diplopia were described. There was no history of trauma or recent systemic illness. The physical examination showed mild neck discomfort, no papilledema, and normal cranial nerve, motor and sensory functioning. Both a CT scan of the sinuses and an MRI of the brain were normal. Although the opening pressure was elevated, the cerebrospinal fluid was also normal. In previous accounts of idiopathic intracranial hypertension in children, concomitant papilledema, visual symptoms and/or palsy of the sixth cranial nerve are described. This case demonstrates that idiopathic intracranial hypertension in a young child can present as a daily headache without any visual symptoms or signs.
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PMID:Idiopathic intracranial hypertension in a young child without visual symptoms or signs. 891 68


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