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)

A 67-year-old woman experienced a severe headache and vomiting. A computed tomographic (CT) scan showed a mild subarachnoid hemorrhage. Cerebral angiography revealed a saccular aneurysm at the apex of the basilar artery. Several days later, she noticed mild hemiparesis of the left extremities. She underwent a clipping operation on the aneurysm by approaching from the right temporal love. Postoperatively, she developed diplopia and dilatation of the left pupil. Cerebral angiography revealed an occlusion of the left posterior cerebral artery. She was admitted to another hospital in order to continue rehabilitation. General physical examination was normal. Neurological examination revealed paralysis of the left medial and left inferior rectus muscles and palsy of the left inferior oblique muscle. The pupil of the left eye was dilated, measuring 5 mm in diameter, and it did not constrict to any stimuli. The left superior rectus and levator palpebrae superioris functioned normally. Visual acuity and visual fields were normal except for the influence of a senile cataract. She had a mild left hemiparesis, slight left ataxia and slurred speech. She had numbness of the left half of the body. A CT scan showed small low density areas in the right thalamus and left cerebellar hemisphere. Her ophthalmologic findings were compatible with the inferior branch palsy of the oculomotor nerve. The ophthalmoplegia of this case seems to be due to partial damage of the oculomotor nerve induced by ischemia of vascular supply. It is supposed to be caused by a vasospasm of the left posterior cerebral artery following a clipping operation of the basilar apex aneurysm.
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PMID:[Inferior branch palsy of the oculomotor nerve following clipping of basilar apex aneurysm]. 831 94

Cavernous sinus dural arteriovenous shunt (CdAVS) usually presents with exophthalmos, conjunctival chemosis, ophthalmoplegia, headache, bruit, or pulsatile tinnitus. Intracranial hemorrhage associated with CdAVS is rare. We describe a patient with CdAVS presenting with subarachnoid hemorrhage and acute subdural hematoma. A 65-year-old woman presented headache and temporary loss of consciousness and was transferred to our hospital. On admission, the patient was alert and complained of a left-sided temporal headache. There were no ocular symptoms. A CT scan revealed subarachnoid hemorrhage and left acute subdural hematoma. When we prepared for cerebral angiography, the patient presented loss of consciousness following sudden onset of severe headache. Urgent angiography revealed left CdAVS, which was fed by both the internal carotid artery and the external carotid artery and drained only into ipsilateral (left) vein of the sylvian fissure. Aneurysmal dilatation of the draining veins and leptomeningeal drainage were present. No cerebral aneurysms were detected. After the angiography, a CT scan showed enlarged subdural hematoma, so left fronto-temporo-parietal craniotomy was immediately performed. On opening the dura mater, arterial bleeding from Sylvian fissure appeared and was uncontrollable. Unfortunately, the patient died 3 days after the operation. We concluded that subarachnoid hemorrhage and subdural hematoma were due to the rupture of engorged cortical veins. Our case report suggests that CdAVS with angiographic findings such as aneurysmal dilatation of the draining veins and leptomeningeal drainage should be treated urgently because of the high risk of the life-threatening complications resulting from a surgically uncontrollable hemorrhage.
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PMID:[Cavernous sinus dural arteriovenous shunt presenting with subarachnoid hemorrhage and acute subdural hematoma: a case report]. 1144 19

Two patients with primary oculomotor nerve palsy due to direct mild head injury are reported. They presented with internal ophthalmoplegia, dilated nonreactive pupils, and very mild disturbance in consciousness. Except for the persistent oculomotor nerve palsy, both the patients recovered fully within one week. Neither demonstrated a history that was suggestive of a cause for their oculomotor nerve palsy. Initial CT scans demonstrated localized subarachnoid hemorrhage around the brain stem. One of the patients had sustained a fracture of the anterior clinoid process. As the underlying pathophysiologic mechanism underlying the oculomotor nerve palsy we suspected mild injury to the pupillomotor fibers at the anterior petroclinoidal ligament and that of the pupillary fibers at the posterior petroclinoidal ligament. We speculate that these perforating fibers at the anterior petroclinoidal liqament acted as a fulcrum due to downward displacement of the brainstem at the time of impact.
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PMID:[Primary oculomotor nerve palsy due to mild head injury--report of two cases]. 1823 37

We present a case with bilateral internal carotid artery hypoplasia and multiple posterior circulation aneurysms who was diagnosed following a subarachnoid hemorrhage. The patient was admitted to our clinic with a history of sudden and severe headache with short-term loss of consciousness and being unable to open the right eyelid five days ago. Nuchal rigidity and right partial ophthalmoplegia were found during the examination. Computed tomography revealed a subarachnoid hemorrhage. Digital subtraction angiography showed bilateral internal carotid artery hypoplasia while three-dimensional computed tomographic angiography showed bilateral internal carotid artery hypoplasia and multiple posterior circulation aneurysms. The aneurysms arising from the right posterior cerebral artery (P1 segment) and left superior cerebellar artery region were clipped using the right modified pterional approach. Asymptomatic unilateral or bilateral internal carotid artery hypoplasia may not be an important problem. However, other concurrent anomalies may be potentially life-threatening. These aneurysms must be treated due to the marked hemodynamic stress even if they have not ruptured and are asymptomatic. It may not be possible to see the aneurysm with digital subtraction angiography in these cases due to superimposition. Three-dimensional computed tomographic angiography provides more detailed diagnostic information.
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PMID:Bilateral internal carotid artery hypoplasia and multiple posterior circulation aneurysms. Importance of 3DCTA for the diagnosis. 1943 Nov 29

Several anatomical studies indicate that the intracranial pachimeninges consist of two dural layers joined together, which divide while bordering the venous sinuses, therefore located in an interdural space. We present here an uncommon case of haematoma due to rupture of an infraclinoidal internal carotid artery aneurysm. The dome of the aneurysm leaned against the posterior wall of the cavernous sinus and, following laceration, pierced the inner dural layer and caused its detachment from the periosteal layer, thus determining a truly interdural haematoma which progressively involved the whole posterior fossa. A 42-year-old female was admitted to our institution with a recent history of thunderclap headache and right ophthalmoparesis. Two cerebral computerised scan tomographies performed elsewhere tested negative for subarachnoid haemorrhage. A cerebral magnetic resonance imaging (MRI) showed a thin collection of blood adjacent to the clivus and all along the wall of the posterior fossa and foramen magnum. A right infraclinoid internal carotid artery aneurysm was also diagnosed, subsequently better highlighted on angiography. The patient underwent surgery with aneurysm clipping. Post-operative course was uneventful, and control angiography showed complete exclusion of the aneurysm from blood circulation. The patient was discharged 5 days later. At 3 months follow-up ophthalmoplegia had disappeared, and the patient had fully recovered. The possibility of a truly interdural location, particularly in cases of non-traumatic parasellar or clival haematomas, must be included in the differential diagnosis of posterior fossa extra-axial haemorrhages. MRI is the test of choice for diagnostic purposes.
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PMID:Interdural haemorrhage of the posterior fossa due to infraclinoidal carotid artery aneurysm rupture. 2147

Aneurysms of the A1 segment of the anterior cerebral artery are rare and represent less than 1% of intracranial aneurysms. There are few reports available in the literature describing the role of endovascular management of these rare aneurysms. In the present series we describe five patients with A1 aneurysms presenting at our institution with various clinical presentations, treated successfully by endovascular method with a good clinical outcome. From January 2008 to July 2011, five patients (two males and three females) with A1 aneurysms were treated by endovascular means. Four of the patients presented with subarachnoid hemorrhage due to rupture of the A1 aneurysm and one patient presented with symptoms of mass effect in the form of headache and ophthalmoplegia. The age group ranges from eight to 52 years with a mean age of 34.2 years. Four of the patients were treated by coiling without any assisted technique whereas one patient who had a dissecting fusiform aneurysm was treated with stent-assisted coiling. Technical success was achieved in all the patients.We did not encounter any procedure-related complications in any of our cases. All the patients had an uneventful course with good clinical outcome. Angiographic follow-up was available in four patients (80%). Endovascular treatment of this rare group of aneurysms is an effective and safe treatment modality, however large series are required to support our findings.
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PMID:Endovascular treatment of A1 aneurysms. A series of five cases with a brief literature review. 2402 88

Contrast-induced encephalopathy (CIE) is an acute and reversible neurological disturbance associated with the intra-arterial administration of iodinated contrast medium during cardiac catheterisation. It may manifest with encephalopathy, motor and sensory disturbances; vision disturbances, including cortical blindness, ophthalmoplegia, aphasia; and seizures. Disruption of the blood-brain barrier and direct neuronal toxicity are believed to be implicated in the pathophysiology of the syndrome. Symptoms appear soon after contrast administration and resolve completely within 24-48 h. Risk factors may include hypertension, diabetes mellitus, renal impairment, the administration of large volumes of iodinated contrast, percutaneous coronary intervention or selective angiography of internal mammary grafts and previous adverse reaction to iodinated contrast. On cerebral imaging, CIE may mimic subarachnoid haemorrhage or cerebral ischaemia, but imaging may be normal. Prognosis is excellent with supportive management alone. CIE may recur, but re-challenge with iodinated contrast without adverse effects has been documented. CIE is a diagnosis of exclusion and is an important clinical entity to consider in the differential diagnosis of stroke following cardiac catheterisation. Physicians should be aware of it and consider it prior to initiating thrombolysis.
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PMID:Recurrent contrast-induced encephalopathy following coronary angiography. 2972 92

The classical term "pituitary apoplexy" (PA) describes a clinical syndrome usually characterized by abrupt onset of headache accompanied by neurologic and/or endocrinologic deterioration due to sudden expansion of a mass within the sella turcica as a result of hemorrhage or infarction within a pituitary tumor and adjacent pituitary gland. PA is a medical emergency and a difficult diagnosis to establish. Thus this article reviews the presenting symptoms of PA patients to help clinicians recognize or at least suspect this critical condition early on. PA commonly occurs in the setting of a preexisting adenoma, and several patients are unaware of its existence prior to the onset of apoplexy symptoms, which are mainly of a neurologic, ophthalmologic, and endocrinologic nature. Neurologic symptoms include sudden-onset severe headache and other symptoms of subarachnoid hemorrhage, symptoms from compression of the cavernous sinus contents, nausea/vomiting, impaired consciousness, and symptoms of meningeal irritation. Ophthalmologic symptoms include visual field defects, visual loss, diplopia, and ophthalmoplegia. Endocrinologic disturbances include pituitary adenoma symptoms, cortisol deficiency, panhypopituitarism, diabetes insipidus, and syndrome of inappropriate secretion of antidiuretic hormone. Magnetic resonance imaging is the imaging method of choice to aid the PA diagnosis. Its differential diagnoses include cerebrovascular accidents, infectious diseases, and other causes of endocrinologic imbalance. Transsphenoidal surgery is the treatment of choice, especially if there are associated visual abnormalities and ophthalmoplegia. Clinicians should be aware of the presenting symptoms because early diagnosis may reduce the morbidity and mortality of this neurosurgical emergency.
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PMID:Presenting Symptoms of Pituitary Apoplexy. 2843 13

Oculomotor nerve palsy (ONP) is an important and common clinical diagnosis. Its main features are diplopia and ptosis. Its aetiologies are various and complex. A number of different conditions have been reported to cause ONP, such as diabetes mellitus, aneurysm, tumours, painful ophthalmoplegia, pituitary lesions, cavernous sinus lesions, central nervous system infections, and subarachnoid haemorrhage. A patients needs to undergo several tests in order to establish the correct underlying pathology. In this review, we have summarized the aetiologies of the unilateral ONP, and discussed their relative clinical features, pathogenesis, diagnostic criteria, treatment options, and prognosis. We searched PubMed for papers related to ONP and its aetiologies, and selected the publications, which seemed appropriate.
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PMID:The aetiologies of the unilateral oculomotor nerve palsy: a review of the literature. 3059 40


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