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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a 24 year old man with a 22 year history of attacks of migraine without aura and attacks of ophthalmoplegic migraine. A persistent right 3rd nerve palsy appeared after the 17th attack. Although its existence has been debated, ophthalmoplegic migraine is recognized as such in the International Headache Society (IHS) classification. A review of published cases satisfying the IHS diagnostic criteria for ophthalmoplegic migraine is presented.
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PMID:[Opthalomoplegic migraine]. 207 17

A patient with a history of facial myokymia presented with apoplectic headache and a 3rd nerve palsy. Initial CT, lumbar puncture, and cerebral angiogram were unremarkable, but subsequent CSF examination revealed oligoclonal bands. MRI displayed over 30 white matter lesions. This case demonstrates that multiple sclerosis may present with severe headache and a 3rd nerve palsy, simulating the clinical picture of a posterior communicating artery aneurysm.
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PMID:Apoplectic headache and oculomotor nerve palsy: an unusual presentation of multiple sclerosis. 199 90

10 cases are presented in which a posterior cerebral artery (PCA) deficit developed suddenly in dramatic fashion with headache, visual symptoms, sensory and motor deficits, and signs of 3rd nerve involvement. There were 9 females and 1 male, ranging in age from 18-51 years with 7 cases under age 35. In 9 of the 10 patients, headache was prominent at the onset; 6 patients reported being dramatically stricken with a severe, sharp localized pain in the forehead or occiput. Visual symptoms were prominent at the onset in 7 patients -- 4 patients experiencing blindness and 3 patients a hemianoptic deficit. Hemisensory symptoms or deficit occurred in 6 instances, a hemiparesis in 3, combined weakness and sensory deficit in 1. Evidence of a 3rd nerve palsy was found in 3 cases. A persisting neurologic deficit occurred in 10 cases -- visual field defect, 6 cases; hemiplegia, 1; slight weakness, 1; and a sensory deficit, 2. A movement disorder developed on the involved side in 7 cases. Evidence of infarction in 1 or both occipital lobes was obtained in 6 patients. 1 patient did not have impaired visual fields, and the other 3 were examined before the days of nuclear medicine and CT scanning. Conventional angiography was performed in 8 patients with the following results: retrothalamic occlusion of 1 PCA (1 patient); distal occlusion of 1 PCA (1 patient); retrothalamic narrowing of 1 PCA (1 patient); irregularity of the wall of the upper basilar artery and both PCAs (1 patient); and in 4 angiography was normal. A digital subtraction angiogram in 1 patient was normal; 1 patient did not have an arteriogram. A history of accompanied migraine was obtained in 3 patients. 1 patient was pregnant; 1 patient was 3 months postpartum. 1 patient was taking oral contraceptives; 1 patient had taken 1 contraceptive pill, and 1 patient was receiving injections of estrogen. These cases represent involvement of the territory of the PCA. They share the same features in varied combinations. The onset or evolution is dramatic, distinctive, or alarming. The cases do not fall easily into any commonly recognized category of cerebrovascular disturbances. The process that most likely applies to this group of cases is migraine. If that is so, the term "catastropic migraine" or "cataclysmic migraine" may have some currency. If it is assumed that the process is ischemic and since vascular obstruction was found in 2 cases, the possibility of using heparin therapy might be considered. In most of the present cases, steroid therapy was used to control brain swelling. If the pathologic process is temporary vasospasm, the use of hemodilution or hyperbaric oxygen could be an option.
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PMID:Unusual vascular events in the territory of the posterior cerebral artery. 395 50

The patient was a 48-year-old housewife, who had a sudden onset of severe headache followed by loss of consciousness for a few hours on the day of admission. Initially she showed slight restlessness due to headache, neck stiffness and subhyaloid hemorrhage. Four-vessel study revealed a basilar aneurysm on right retrograde brachial angiography and anterior communicating aneurysm on left carotid angiography. Two weeks after the onset, when she had no neurological deficit except for intermittent appearance of disorientation, both aneurysms were successfully clipped through right pterional approach of Yasargil. The subarachnoid hemorrhage was apparently due to basilar bifurcation aneurysm. Postoperatively, she showed right hemiparesis including her face, aniscocoria (left, 4 mm, oval: right, 1.5 mm, round) and conjugate deviation toward the left. The disturbance of conjugate eye movement and the hemiparesis completely disappeared in 2 and 7 days respectively. The patient was discharged 4 weeks postoperatively with mild left 3rd nerve palsy. At present, one year postoperatively, she is fully engaged in her housewife life without any neurological deficits. A case of superior Foville syndrome combined with Weber syndrome after clipping of basilar bifurcation aneurysm was reported and its anatomicoclinical mechanism was reviewed. The pathogenesis was supposed to be left midbrain ischemic lesion due to circulatory disturbance of P-1 perforators (P-1: proximal posterior cerebral artery); e.g., occlusion on clipping of vasospasm. This P-1 perforator syndrome after aneurysmal clipping has been reported only little. The importance of preservation of these perforators with careful dissection and manipulation under microscopy was emphasized.
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PMID:[Superior Foville syndrome after clipping of basilar bifurcation aneurysm--case report (author's transl)]. 724 18

A patient with a history of migraine without aura developed a complete left III nerve palsy a day after the onset of bilateral throbbing headache associated with vegetative symptoms. Magnetic resonance imaging showed a hemorrhagic pituitary adenoma as the probable cause of the symptoms, presumably by a compressive mechanism. This case suggests a further possible cause of ophthalmoplegia associated with migraine and confirms the clinical utility of magnetic resonance imaging in the differential diagnosis of ophthalmoplegic migraine and other conditions in which the symptomatology is secondary to intracranial lesions.
Headache 1994 Sep
PMID:Ophthalmoplegic migraine-like syndrome due to pituitary apoplexy. 796 Jul 35

Paresis of the oculomotor nerve associated with subarachnoid haemorrhage is considered a hallmark of aneurysms located at the junction of the internal carotid artery and posterior communicating artery. Third nerve palsy can also be caused by those aneurysms located in the intracavernous part of the internal carotid artery, basilar artery, posterior cerebral artery and superior cerebellar artery. However, oculomotor nerve paresis caused by an anterior communicating artery aneurysm is a very uncommon occurrence. We report a case of an elderly female with sudden severe headache who developed an acute third nerve paresis. Angiography revealed an anterior communicating artery aneurysm. Management and the pertinent literature are reviewed along with the mechanism of third nerve compression.
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PMID:Unusual neuro-ophthalmic presentation of anterior communicating artery aneurysm with third nerve paresis. 1533 48

Pseudotumor cerebri is a clinical syndrome characterized by raised intracranial pressure with normal ventricular size, anatomy and position. Headache, vomiting and diplopia are the most common symptoms. Signs include those of raised intracranial pressure including papilledema and absence of focal neurological signs. A secondary cause is identifiable in 50% of children; the most common predisposing conditions are otitis media, viral infection and medications. Management is mainly directed towards identifying and treating the cause and measures to reduce the raised intracranial pressure. Though it is mostly a self limited condition, optic atrophy and blindness can occur. Oculomotor nerve palsy is very rarely associated with pseudotumor cerebri. We report a unique case of pseudotumor cerebri who had left Oculomotor palsy with sparing of the pupillary fibres, which resolved following treatment with oral acetazolamide.
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PMID:Pseudotumor cerebri with transient oculomotor palsy. 1638 55

Primary CNS lymphoma (PCNSL), a rare form of non-Hodgkin lymphoma that is confined to the brain, is usually of B-cell origin. Primary leptomeningeal lymphoma, regardless of T or B-cell origin, is an unusual site of presentation. Out of 100 consecutive PCNSL patients that we have followed up in our center during the last 10 years, five had T-cell lymphoma (5%). All presented with leptomeningeal involvement as the sole manifestation and four of them presented with neuronal lymphomatosis. Presenting symptoms included signs of elevated intracranial pressure with 6th nerve palsy; headache and bilateral 3rd nerve palsy; mononeuritis multiplex and unilateral hearing loss; bilateral 7th nerve paralysis and bilateral uveitis. Because neither the CSF nor the MRI were indicative, meningeal or nerve biopsies were required for conclusive diagnosis. Four patients died 10-19 months from disease onset and one patient is alive 36 months following the diagnosis. We conclude that T-cell PCNSL can present as an isolated leptomeningeal involvement which may be associated with neurolymphomatosis affecting cranial and peripheral nerves. These manifestations mimic other neurological conditions such as pseudotumor cerebri or vasculitis. Diagnosis is difficult and, as a result, frequently delayed. This calls for early consideration of meningeal or nerve biopsy whenever CSF findings are inconclusive.
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PMID:Primary T-cell CNS lymphoma presenting with leptomeningeal spread and neurolymphomatosis. 1859 37

Oculomotor nerve palsy (ONP) with subarachnoid hemorrhage (SAH) occurs usually when oculomotor nerve is compressed by growing or budding of posterior communicating artery (PcoA) aneurysm. Midbrain injury, increased intracranial pressure (ICP), or uncal herniation may also cause it. We report herein a rare case of ONP associated with SAH which was caused by middle cerebral artery (MCA) bifurcation aneurysm rupture. A 58-year-old woman with clear consciousness suffered from headache and sudden onset of unilateral ONP. Computed tomography showed SAH caused by the rupture of MCA aneurysm. The unilateral ONP was not associated with midbrain injury, increased ICP, or uncal herniation. The patient was treated with coil embolization, and the signs of oculomotor nerve palsy completely resolved after a few days. We suggest that bloody jet flow from the rupture of distant aneurysm other than PcoA aneurysm may also be considered as a cause of sudden unilateral ONP in patients with SAH.
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PMID:Oculomotor nerve palsy associated with rupture of middle cerebral artery aneurysm. 1944 51

To present a unique case of the internal carotid artery-posterior communicating artery (ICA-PcomA) aneurysm penetrating the oculomotor nerve presenting a pure acute subdural hematoma (ASDH) without any oculomotor dysfunction. A 71-year-old woman presented with a sudden headache and drowsiness. She had no history of head trauma and did not manifest any neurological deficits including oculomotor nerve palsy. Computed tomography (CT) of her head revealed left ASDH. Subsequent CT angiography showed an aneurysm originating from the left ICA with an inferior projection having continuity with the hematoma. Intraoperative inspection revealed ASDH observed mainly in middle fossa and no subarachnoid hemorrhage, while the aneurysm was confirmed to split the oculomotor nerve and to be fixed with the middle fossa. The aneurysm was obliterated by direct clip application and the patient's postoperative course was uneventful. Oculomotor nerve palsy is an important warning sign of imminent rupture of ICA-PcomA aneurysm. However, we should consider that the ICA-PcomA aneurysm could rupture causing ASDH without any oculomotor nerve palsy, even though the aneurysm penetrated the oculomotor nerve.
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PMID:Asymptomatic Penetration of Oculomotor Nerve by Internal Carotid-Posterior Communicating Artery Aneurysm Presenting Pure Acute Subdural Hematoma: A Case Report. 2937 86


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