Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-five cases of berry aneurysm on the supraclinoid portion of internal carotid artery were reviewed on the viewpoint of oculomotor palsy. 27 of 65 patients (42%) showed oculomotor palsy. Most cases of complete oculomotor paralysis developed immediately after having subarachnoid hemorrhage, whereas the case of gradually developing oculomotor palsy tended to manifest diplopia first, and followed with blephaloptosis. The recovery rate from oculomotor palsy seemed to be correlated with the duration from the onset of symptom to surgery. The recovery from the complete oculomotor paralysis lasting for a long time seemed to be unsatisfactory unless the surgical direct procedure to the aneurysm was successful in early stage.
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PMID:[Oculomotor palsy due to aneurysm of internal carotid artery (author's transl)]. 49 66

The management of pituitary apoplexy with reference to both diagnosis and operative sequelae remains a major challenge. Acute onset of retro-orbital headache in association with visual loss and ophthalmoplegia are the cardinal symptoms; however, obtundation and signs of subarachnoid hemorrhage also may be present. Good quality plain skull radiographs and complete angiography prove sufficient for preoperative radiographic studies. Preoperative endocrine preparation focuses on supplemental glucocorticoids since these patients must be presumed deficient in cortisol reserve. Residual visual deficit appears to be more a function of the extent of damage at the time of ictus rather than rapidity of decompression. Our experience indicates that transsphenoidal decompression in appropriate cases offers an ideal opportunity to minimize mortality and morbidity. The acute onset of severe retro-orbital headache in association with stupor and ocular palsies would alert most physicians to the potential diagnosis of spontaneous subarachnoid hemorrhage. The association of complex ophthalmoplegias and visual defects in this constellation of symptoms should, in addition, alert one to the possibility of an acute intrasellar or parassellar expansile process. During the past two years, we have had the opportunity to care for 8 such patients with confirmed diagnoses of acute hemorrhagic infarction of the pituitary enabling us to formulate diagnostic and therapeutic schemata with reference to management of this problem.
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PMID:Pituitary apoplexy, therapeutic assessment. 103 16

A syndrome of combined right lateral gaze palsy and right internuclear ophthalmoplegia, followed by a left exotropia in a case of subarachnoid hemorrhage is presented. At necropsy a single small pontine end-zone infarction was found, involving the medial part of the right paramedian pontine reticular formation, the tectospinal tract and the ventral part of the right medial longitudinal fasciculus. The fila radicularia of the right abducens nerve passed through the necrotic area. The mechanism of these characteristic ocular motor disturbances in relation to the post mortem findings and the topopathogenesis of the pontine infarction are discussed.
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PMID:Paralytic pontine exotropia in subarachnoid hemorrhage. A clinicopathological correlation. 123 38

The authors present an extremely rare case of aspergillosis of the central nervous system (CNS) causing subarachnoid hemorrhage (SAH). A 78-year-old female developed facial pain, progressive deterioration in left visual acuity, and left total ophthalmoplegia. Computed tomography demonstrated a heterogeneously enhanced mass extending from the sphenoid sinus to the left cavernous sinus and left orbit, and angiography showed luminal narrowing and irregularity of the left internal carotid artery at its siphon. Biopsy of the left orbital and sphenoid sinus mass resulted in the diagnosis of Aspergillus granuloma. Despite combined administration of amphotericin-B and 5-FC, she became comatose from brainstem infarction and finally, suddenly died. Postmortem examination revealed massive SAH due to a ruptured mycotic aneurysm of the basilar artery. Aspergillosis of the CNS is a growing problem with the wider use of immunosuppressants and antibiotics. To the authors' knowledge, however, only 13 cases of CNS aspergillosis causing SAH have been reported. The prognosis is absolutely bad, with all patients dying from rupture of major intracranial arteries such as the internal carotid artery and basilar artery. Early diagnosis and vigorous chemotherapy are important.
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PMID:Aspergillosis of the central nervous system causing subarachnoid hemorrhage from mycotic aneurysm of the basilar artery--case report. 170 41

Pituitary apoplexy describes the clinical syndrome characterised by headache, visual impairment and ophthalmoplegia caused by sudden enlargement of a pituitary adenoma. This is usually due to extensive tumour infarction or haemorrhage. Pituitary apoplexy is rare, mimics spontaneous intracranial bleeding, and thus may be easily mistaken for acute subarachnoid haemorrhage. Urgent surgical intervention and hormone replacement therapy are required.
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PMID:Bleeding intracranial aneurysm? Pituitary apoplexy! 179 4

A case of fungal aneurysm associated with presumed Tolosa-Hunt syndrome is reported. A 57-year-old man was admitted to our hospital with complaints of left blepharoptosis, headache and weight loss. Neurological examination revealed left ophthalmoplegia without facial hypesthesia. Visual acuity was normal. Laboratory studies showed raised ESR, 4+ glycosuria, and a blood sugar of 351mg/dl. Computerized tomography (CT) scan and left carotid angiography were considered normal. Left orbital venography showed no filling of the left cavernous sinus. Diabetic ophthalmoplegia was suspected by a neurologist. The patient was treated with insulin therapy, but visual acuity worsened, and hypesthesia was noted in the first and second divisions of the left trigeminal nerve. Subsequent CT scan demonstrated a high density lesion, which was homogeneously enhanced, in the left cavernous portion and the superior orbital fissure. The patient was presumed of Tolosa-Hunt syndrome, and prednine therapy (30mg/day) was started. On the second day after the administration of prednine, hypesthesia of the first and second division of the left trigeminal nerve improved. After 9 days of prednine therapy, the patient suddenly complained of severe headache, and lapsed into a coma. Massive hemorrhage with subarachnoid hemorrhage was recognized on the CT scan, with a marked midline shift to the right. The hematoma was immediately removed. A ruptured cerebral aneurysm was found at the bottom of the hematoma. The aneurysm was located in the distal portion of the left middle cerebral artery. Aneurysm clipping with external decompression and bilateral ventricular drainage was performed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A fungal aneurysm in a patient with presumed Tolosa-Hunt syndrome]. 185 58

Of 37 patients with 44 intracavernous carotid artery aneurysms (ICCAAns) diagnosed between 1976 and 1988, patients with 20 aneurysms were followed without treatment for 5 months to 13 years (median, 2.4 years). Ten of the 20 ICCAAns were asymptomatic at diagnosis, and 10 were symptomatic. Three of the asymptomatic ICCAAns were symptomatic at follow-up. One of these required clipping because of a progressing cavernous sinus syndrome; the other 2 were minimally symptomatic and have not required treatment. Of the 10 initially symptomatic ICCAAns, 2 had not changed, 4 became more symptomatic, and 4 had symptomatically improved by follow-up. One patient with an ICCAAn that had not changed clinically was lost to follow-up 6 months after diagnosis. Of the 4 ICCAAns that became more symptomatic, 2 continue to be monitored, and 2 required intervention: one with detachable balloon occlusion of the aneurysm with preservation of the internal carotid artery lumen, and the other with gradual cervical internal carotid artery occlusion. The clinical course of this selected group of patients with ICCAAns suggests that the natural history of ICCAAns can be quite variable. Although clinical progression does occur, symptomatic ICCAAns also can improve spontaneously. Therapeutic intervention for asymptomatic ICCAAns should be reserved for patients with aneurysms arising at the anterior genu of the carotid siphon and/or extending into the subarachnoid space, where subarachnoid hemorrhage is most likely. Intervention for symptomatic ICCAAns should be reserved for patients with subarachnoid hemorrhage, epistaxis, severe facial or orbital pain, evidence of radiographic enlargement, progressive ophthalmoplegia, or progressive visual loss.
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PMID:Aneurysms of the intracavernous carotid artery: natural history and indications for treatment. 236 71

An attempt at transfemoral transarterial balloon occlusion of a high-flow spontaneous carotid-cavernous fistula was unsuccessful because the carotid artery rent was too small for this approach. During a subsequent transvenous approach to the cavernous sinus through the jugular vein, the inferior petrosal sinus was perforated. A minor subarachnoid hemorrhage occurred before the tear could be sealed by the deposition of three Gianturco coils in the vein. The patient was taken to the operating room for emergency obliteration of the fistula and petrosal sinus in order to remove the risk of further hemorrhage. Under the guidance of intraoperative digital subtraction angiography, isobutyl-2-cyanoacrylate was injected directly into the surgically exposed cavernous sinus. Successful obliteration of the fistula was achieved with preservation of the carotid artery, and the angiography catheter was removed safely from the petrosal sinus. Although initially after surgery the patient had nearly complete ophthalmoplegia, at her 1-year follow-up examination she had normal ocular motility and visual acuity. The transvenous approach to the cavernous sinus and alternative methods of treatment of carotid-cavernous fistulas are discussed.
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PMID:Venous rupture during transvenous approach to a carotid-cavernous fistula. Case report. 266 39

Although loss of normal pituitary function may be silent and asymptomatic, sudden loss of gland function (pituitary apoplexy) typically results in characteristic presentations. Sheehan's syndrome is the development of hypopituitarism after postpartum hemorrhage or shock. Patients with Sheehan's syndrome may have typical or atypical presentations based on the extent of pituitary gland destruction. Patients with typical symptoms fail to lactate after giving birth; subsequently these patients also develop symptoms and signs of hypopituitarism. Measuring the serum prolactin level after giving thyrotropin-releasing hormone is a reasonable first step in the diagnosis of this condition in patients who fail to lactate after giving birth. The diagnosis of hypopituitarism is delayed for up to 7 years in patients with atypical symptoms. Acute symptomatic failure of the pituitary gland (pituitary apoplexy) commonly occurs in patients who have asymptomatic pituitary tumors. Many patients with pituitary tumors do not have signs of abnormal endocrine gland secretion and have a normal appearance. Most patients have the following signs or symptoms: headache; acute disturbances in visual acuity or visual fields; ophthalmoplegia, and changes in the level of consciousness. The syndrome of pituitary apoplexy usually evolves over hours to days. Subarachnoid hemorrhage and acute bacterial meningitis are the two most important mimics of pituitary apoplexy. Intravenous steroids and prompt neurosurgical consultation are mandatory in cases of pituitary apoplexy since both steroids and surgery can improve vision. Testings for acute or chronic hypopituitarism is challenging in the Emergency Department setting; however, carefully chosen tests will aid in the subsequent early correct diagnosis after initial Emergency Department management.
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PMID:Adrenal and pituitary emergencies. 268 Apr 71

A 52-year-old woman was admitted to our hospital presenting with subarachnoid hemorrhage, left ophthalmoplegia, and right hemiparesis. Previous symptoms and signs suggested the presence of panhypopituitarism. A giant intracranial aneurysm of the internal carotid artery, diagnosed by magnetic resonance imaging, showed the characteristic flow void phenomenon with black appearance. Analysis of endocrine function disclosed panhypopituitarism and hyperprolactinemia. After proximal balloon occlusion of the aneurysm, diabetes insipidus developed. Pituitary function reassessed 6 months after initial admission confirmed anterior and posterior hypopituitarism and hyperprolactinemia. Possible mechanisms are discussed. A review of the literature on pituitary dysfunction caused by carotid artery aneurysms discloses that the pituitary-gonadal axis is the most frequently involved (67.5% of cases), followed by the pituitary-adrenal axis (48.6%) and the pituitary-thyroid axis (40.5%). These frequencies are very similar to those described in other types of hypopituitarism.
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PMID:Giant intrasellar aneurysm presenting with panhypopituitarism and subarachnoid hemorrhage: case report and literature review. 804 78


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