Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

A patient with a large, right-sided basilar artery aneurysm was evaluated. Major symptoms included progressive hearing loss, facial numbness, occipital headaches, dizziness, and diplopia of less than a year's duration. Audiologic results indicated a low-frequency sensorineural hearing loss with marked discrepancies between ascending and descending pure-tone thresholds for the ear ipsilateral to the lesion. Auditory brain-stem response demonstrated bilateral abnormalities, but the early waves were normal. Contralateral acoustic reflexes were absent on the right and elevated on the left. Electronystagmography results showed bilaterally absent caloric responses as well as gaze nystagmus and abnormal pursuit movements. Additional audiologic results as well as radiologic and medical findings are also presented.
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PMID:Audiologic and other clinical findings in a case of basilar artery aneurysm. 358 Jan 63

The patient was a 52-year-old woman who was initially admitted to our hospital with a recent history of diplopia, ptosis and visual impairment on the right, adding to 6 years history of the right orbital pain and temporal headache. She had gradually developed pain and fatigue of the right knee since childhood and had been suffered from multiple subcutaneous tumor in the both hands and the right foot from youth onward. On neurological examination, she has had right exphthalmos and 3rd and 6th cranial nerve palsies on the right. Skull X-ray and CT scan showed parasellar calcified mass on the right. In chromosome examination, the inversion of the No. 1 chromosome was disclosed by the Q- and C-band dyeing of her leucocytes and skin culture. Cavernous hemangioma of her skin lesion and enchondroma of the skeletal lesion were diagnosed by X-ray examination and histological specimen, indicating so-called Maffucci's syndrome. One year and a half later, she was readmitted to our institution, because of progressive visual loss on the right and left hemiparesis. Malignant change of the parasellar lesion was suspected by the clinical course and neuroradiological findings and was confirmed histologically by the second peration. During postoperative course, intratumoral hemorrhage had occurred twice and the patient died, and postmortem examination confirmed her clinical affair. This is the case which was clarified malignant transformation of enchondroma in the parasellar region, and is the first case verified the chromosome abnormalities in Maffucci's syndrome.
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PMID:[Maffucci's syndrome with intracranial manifestation and chromosome abnormalities--a case report]. 370 42

Twenty-three children (16 girls, 7 boys, aged 6-17 years) who presented with the specific complaint of blurred vision were diagnosed as having functional visual loss. Symptoms were intermittent in seven children. Associated signs and symptoms were common and included headaches, visual field loss, diplopia, micropsia, voluntary nystagmus, and spasm of the near reflex. Our treatment consisted of reassurance and follow-up. Resolution of symptoms occurred within 24 hours in one third and within two months in three-quarters of our patients. Parental support and encouragement were associated with more rapid resolution. Recurrence of symptoms and late onset of somatic complaints were rare. Conflicts related to family or school environment were common. Four children had been sexually or physically abused. Our experience suggests that, regardless of the duration or severity of symptoms, functional visual loss in children can usually be treated with reassurance. We believe that psychiatric referral is not necessary for most patients. Sexual or physical abuse should be considered as a possible predisposing factor.
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PMID:Functional visual loss in children. 370 8

A review of 78 cases of surgically managed pituitary adenomas revealed that haemorrhage had occurred in 13. Frank haemorrhage or haemorrhagic infarction caused increasing headache, drowsiness, diplopia and visual failure. The correct diagnosis was suggested by skull X-rays and contrast studies leading to prompt surgical decompression.
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PMID:Pituitary apoplexy and haemorrhage into adenomas. 374 28

In 12 patients with minimal oculomotor nerve deficits due to unruptured intracranial aneurysm, the nerve-related findings were incomplete and at least one element (ptosis, mydriasis, or extraocular muscle weakness) was spared in every patient. Although symptomatic, the affected cranial nerve III functions were only partially lost. Six patients had ptosis and mydriasis, three had ptosis and diplopia, two had mydriasis and diplopia, and one had mydriasis alone. Eleven patients had accompanying headaches that were remarkably variable and difficult to categorize. Cerebral angiography showed the aneurysms, but computed tomography missed one third of them. The symptomatic aneurysm arose from the internal carotid artery in six patients, and from the distal basilar artery in six. Fragments of a cranial nerve III palsy associated with recent onset and ipsilateral headache suggest an enlarging internal carotid or distal basilar artery aneurysm.
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PMID:Minimal oculomotor nerve paresis secondary to unruptured intracranial aneurysm. 375 62

A case of solitary neurinoma of oculomotor nerve is reported. A 40-year-old female had a sudden headache with nausea and vomiting in January, 1978. She complained of diplopia and right ptosis two months later and visited a neurosurgical clinic, but radiological examination was told to be normal. Headache and right ptosis diminished, but diplopia continued. She was admitted to our clinic on Aug. 30, 1984, complaining of diplopia and right ptosis which were noticed only when she was tired. On admission, she had no neurological deficits except for right oculomotor nerve palsy. There was no cutaneous manifestation of von Recklinghausen's disease. Plain skull radiogram and angiogram showed normal study. CT scan showed a solitaly enhancing mass in the right prepontine region. On Sept. 22, 1984, a right frontotemporal craniotomy was performed, and the tumor was totally removed by pterional approach. The tumor was located beside the right internal carotid artery and the oculomotor nerve was incorporated in the tumor. The histological diagnosis was Antoni B type neurinoma. The clinical features of fourteen reported cases of neurinoma of the oculomotor nerve in the literature were reviewed.
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PMID:[Neurinoma of the oculomotor nerve: case report]. 378 66

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

Chronic intracranial hypertension in the presence of hydrocephalus and/or arachnoiditis is a rare presentation of neurobrucellosis. The present case is exceptional because neither hydrocephalus nor arachnoiditis were present. Brucellosis was diagnosed by serological tests. The patient developed asthenia, anorexia, weight loss, violent headaches, explosive vomiting, bilateral papilloedema, diplopia with paralysis of the abducens nerves, left supranuclear facial paralysis and left hemiparesis. A skull radiograph showed destruction of the sella turcica. Rapid recovery was attained with the use of antibiotics. The pathogenesis of this intracranial hypertension syndrome with destruction of sella turcica is discussed.
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PMID:Chronic intracranial hypertension secondary to neurobrucellosis. 381 88

Lumbar puncture has been in widespread clinical use for nearly a century. It is used in emergency medicine primarily as a tool for the diagnosis of meningoencephalitis and subarachnoid hemorrhage. The development of computed tomography has changed the position that lumbar puncture has held in the diagnostic sequence of a number of clinical entities. The procedure is contraindicated if there is soft-tissue infection adjacent to the puncture site and if there are findings of increased intracranial pressure due to a mass lesion. Performance in the setting of a coagulopathy may also be hazardous. The most serious potential complication is cerebral herniation. The commonest complication is postlumbar puncture headache, which is due to CSF hypotension resulting from persistent spinal fluid leakage through the meningeal puncture site. Spinal hematoma, diplopia, and intraspinal dermoid tumor formation are less common complications. Meningitis has been found to follow lumbar puncture in children with bacteremia. The lumbar puncture is a useful test for providing information regarding the cellular, chemical, and microbiologic composition of the CSF. Fluid obtained should be evaluated for cell count, Gram's stain, bacterial culture, glucose and protein levels, and other tests as clinically indicated.
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PMID:Lumbar puncture. 383 22


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