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We report a case of ruptured internal carotid artery aneurysm with contralateral oculomotor nerve paresis. A 69-year-old female experienced a sudden onset of severe headache. Left-sided mydriasis, absence of light reflex, disability of left ocular movement and ptosis were identified. Computed tomography scan revealed massive subarachnoid hemorrhage. Cerebral angiography showed a right internal carotid artery aneurysm. No abnormal finding was observed in the left internal carotid artery or basilar artery. Magnetic resonance imaging did not show thrombosed aneurysm. The oculomotor nerve paresis lasted for ten days. Ruptured right internal carotid artery aneurysm was surgically confirmed and repaired. We speculated that the contralateral oculomotor nerve paresis was the consequence of bloody jet flow from the ruptured aneurysm.
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PMID:[A case report of ruptured internal carotid artery aneurysm with contralateral oculomotor nerve paresis]. 1583 May 43

Two patients are described, the first with a giant aneurysm of the left carotid bifurcation previously treated by endovascular technique, the second with a bilateral intracavernous aneurysm: both were submitted to high-flow by-pass operation. The first patient was a 40 year-old woman who had presented subarachnoid hemorrhage 6 months before operation. She had been treated by means of a high-flow by-pass between the external carotid artery and the middle cerebral artery. Control angiograms performed 12 hours later showed a stenosis above the suture between the external carotid artery and the venous graft. Angioplasty was performed by endovascular route: new angiograms showed occlusion of the graft while dopplersonography demonstrated the presence of flow within the graft. Angiograms performed 1 week later showed marked vasospasm of the venous graft, of the internal carotid artery, the anterior cerebral artery and the middle cerebral artery. The evolution of spasm of the graft and of the intracranial arterial flow was monitored by dopplersonography and MR-angiography: the latter was performed 20 days after the last angiography and confirmed patency of the graft, while dopplersonography showed resolution of vasospasm. Finally, the aneurysm was embolized. The second patient was a 49 year-old woman with mild left palpebral ptosis and retro-orbital pain. She had already been submitted to high-flow by-pass operation 7 months earlier to treat a right intracavernous aneurysm; the left by-pass was necessary because the intracavernous aneurysm had become symptomatic. One week after surgery, spasm of the venous graft was documented by MR-angiography. In both cases, treatment consisted of calcium antagonists as well as hypertensive and hypervolemic medication, which was successful in treating vasospasm of the venous graft and its symptoms. Spasm of the venous graft, a well-known occurrence in cardiac revascularization, can also be observed in cerebral revascularization.
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PMID:Vasospasm of venous grafts in extra-intracranial by-pass. Report of two cases. 1628 93

Pituitary carcinomas are very rare tumors, nearly always presenting as widely invasive masses, although the hallmark of these lesions is the finding of distant metastases. One third of reported cases are prolactin (PRL)-secreting tumors. We report the case of a fatal pituitary carcinoma evolving within 4 years from a PRL-secreting microadenoma. A 22-year-old woman presented because of galactorrhea. Evaluation of the patient disclosed slight hyperprolactinemia and magnetic resonance imaging (MRI) showed a 7-mm intrapituitary lesion, which responded to treatment with cabergoline. About 4 years after the first evaluation she developed sudden headache, ptosis, and diplopia in the right eye. MRI disclosed the growth of a large pituitary mass, invading the right cavernous sinus. Despite two trans-sphenoidal surgical procedures followed by gamma-knife radiosurgery, the patient showed rapid local progression of the tumor and the occurrence of new lung lesions, probably of metastatic nature. The patient died 7 months after the development of her first neurological symptoms because of tumor apoplexy and subsequent subarachnoid hemorrhage. This case represents the first documented rapid evolution from a microprolactinoma initially responding to dopamine agonists to a fatal pituitary carcinoma.
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PMID:Evolution of a prolactin-secreting pituitary microadenoma into a fatal carcinoma: a case report. 1791 59

Valid parameters do not exist to predict oculomotor nerve palsy (ONP, ptosis and/or diplopia) intraoperatively. In 49 operations involving 46 patients with posterior communicating artery aneurysms, the oculomotor nerves were stimulated after the aneurysms were clipped. A quantitative analysis of evoked compound muscle action potential (CMAP) parameters (stimulus threshold, amplitude and latency) from the levator palpebrae superioris (LPS) muscle was performed. Absolute values of CMAP amplitude statistically correlated with initial and long-term oculomotor nerve function (ONF) after surgery (p<0.05). In addition, subarachnoid hemorrhage (SAH) significantly influenced the CMAP threshold (p<0.05). Monitoring of LPS muscle activity is valuable in the assessment of ONF, and the CMAP amplitude of LPS may be a reliable predictor of ONF. Moreover, SAH has an impact on the parameters of the LPS CMAP.
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PMID:Intraoperative oculomotor nerve monitoring predicts outcome following clipping of posterior communicating artery aneurysms. 2245 80

A 61-year-old male presented to the emergency department (ED) with painless diplopia, left-ptosis, and left downward gaze, 3 days after sustaining a fall from standing height with subsequent lumbar and head trauma. Prior to the ED consult, his only symptom was persistent generalized high intensity headache. On physical examination, no other neurological deficit was found. Computed tomography (CT) scan showed Fisher 4 subarachnoid hemorrhage (SAH). Cerebral angiogram and brain magnetic resonance imaging (MRI) were negative. Screening for possible secondary causes of isolated third-nerve palsy (TNP) were all negative. To our knowledge, this is the first report of a traumatic SAH with delayed onset of an isolated complete TNP as its manifestation.
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PMID:True- true- unrelated? A delayed onset, complete third-nerve palsy after traumatic subarachnoid hemorrhage. 2382 39

A 66-year-old male was brought to our hospital following a car accident. He had subarachnoid hemorrhage, multiple rib fractures, and left hemopneumothorax. He was referred to the Cardiology Department for elevated troponin levels (42 ng/ml, reference 0-1 ng/ml). The electrocardiogram was free of ischemia, whereas the transthoracic echocardiography revealed dilated right heart chambers, enlarged tricuspid annulus and coaptation failure of the tricuspid valvular leaflets. There was rupture on the subvalvular apparatus of the anterior leaflet of the tricuspid valve with accompanying prolapse, causing severe tricuspid valvular regurgitation. The patient did not present right ventricular failure signs and symptoms; he was referred to surgery after the resolution of associated thoracic and cranial injuries.
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PMID:Posttraumatic tricuspid valve injury and severe tricuspid valve regurgitation. 2421 91

We describe isolated cranial nerve-III palsy as a rare clinical finding in a patient with perimesencephalic subarachnoid hemorrhage. In this unusual case, the patient presented with complete cranial nerve-III palsy including ptosis and pupillary involvement. Initial studies revealed subarachnoid hemorrhage in the perimesencephalic, prepontine, and interpeduncular cisterns. Angiographic studies were negative for an intracranial aneurysm. The patient's neurological deficits improved with no residual deficits on follow-up several months after initial presentation. Our case report supports the notion that patients with perimesencephalic subarachnoid hemorrhage have an excellent prognosis. Our report further adds a case of isolated cranial nerve-III palsy as a rare initial presentation of this type of bleeding, adding to the limited body of the literature.
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PMID:Isolated Cranial Nerve-III Palsy Secondary to Perimesencephalic Subarachnoid Hemorrhage. 2694 57

A 53-year-old woman experienced a right retrobulbar pain followed by ipsilateral extraocular palsies in all directions without dilated pupils or ptosis. Because a plain head computed tomography (CT) scan obtained on her initial visit showed no abnormal findings, such as subarachnoid hemorrhage or a giant cavernous aneurysm, her condition was provisionally diagnosed as Tolosa-Hunt syndrome and elective magnetic resonance (MR) imaging was scheduled. The day after her initial visit, however, she suddenly developed complete ptosis and a dilated pupil on the right side. Emergency MR imaging and angiography revealed a clover leaf-shaped aneurysm projecting to the cavernous sinus at the junction of the internal carotid artery and the posterior communicating artery. Her condition was diagnosed as impending rupture of the aneurysm, and she underwent emergency open surgery. Her symptoms completely resolved within the following 2 weeks. Our case demonstrated that a medium-sized internal carotid artery-posterior communicating artery aneurysm can cause simultaneous oculomotor and abducens nerve palsies with retrobulbar pain if the shape of the aneurysm is complicated. Although these symptoms are very similar to those of Tolosa-Hunt syndrome, we believe that prompt radiological examinations such as MR or 3D CT angiography should be performed to prevent subsequent rupture of the aneurysm.
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PMID:A Case of the Internal Carotid Artery-Posterior Communicating Artery Aneurysm Mimicking Tolosa-Hunt Syndrome. 2866 52

Acute non-traumatic headaches with neurological deficits alarm emergency department (ED) physicians. Typically, a sudden headache with oculomotor nerve palsy involving a pupil indicates the possibility of a subarachnoid hemorrhage (SAH) due to an aneurysm originating from the posterior communicating artery. For the ED physician, thinking beyond the possibility of an SAH can be crucial. Here, we report on a 59-year-old woman who presented to the ED with an intractable headache and right ptosis. She had previously received nicorandil for paroxysmal atrial fibrillation in the cardiology clinic. Her vital signs were stable upon ED arrival. Neurological examination revealed a mild anisocoria with a sluggish response to light stimuli in the right eye. Adduction, supraduction, and infraduction were also limited in the right eye. Nuchal rigidity was not apparent. An urgent brain magnetic resonance image (MRI) with angiography was requested to assess for possible SAH, but revealed no aneurysm. Cerebrospinal fluid analysis was also unremarkable. The patient's headache and oculomotor nerve palsy improved completely after discontinuation of nicorandil for 3 days. To the best of our knowledge, this is the first case report on side effects of nicorandil presenting as a severe headache with reversible oculomotor nerve palsy involving a pupil, symptoms which mimicked a possible SAH due to aneurysm.
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PMID:Acute intractable headache and oculomotor nerve palsy associated with nicorandil: A case report. 2928 97

The abrupt onset of acute, high-intensity headache, unlike any experienced before, can be an urgent medical condition, which requires attention. A 32-year-old female patient developed thunderclap headache attacks had applied with increasing intensity and frequency since 1 week. She had visited the emergency department several times, and cranial computed tomography findings were normal. On the last presentation, neurological examination showed complete oculomotor nerve palsy on the left. Brain magnetic resonance imaging together with intracranial brain angiography revealed left posterior communicating aneurysm compressing the ipsilateral oculomotor nerve, with no evidence of subarachnoid hemorrhage. The patient was treated with endovascular balloon-assisted coil embolization of the aneurysm under digital subtraction angiography. As a result, the headache resolved soon after the intervention. Furthermore, complete ptosis recovered by the third month. Although thunderclap headache has rarely been attributed to an enlarging unruptured cerebral aneurysm, early recognition and treatment are rather important as it may indicate a high risk of rupture.
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PMID:Unruptured aneurysm producing thunderclap headache treated with endovascular coil embolization. 3002 82


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