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10: Over-reliance on negative test results using none toattach none with web,windows application Visual Studio Development Tools and Languages Figure 10.4 Ocul none none ar motility testing in a 52-year-old homemaker with a painful third nerve palsy. There is marked left upper lid ptosis and minimal movement of the left eye except for abduction.

Notice also anisocoria, left pupil larger than right.. Headache and third nerve palsy Case: A 52-year- none for none old homemaker experienced sudden onset of a left-sided headache that increased in severity over two days. On the second day she noticed oblique diplopia followed by progressive drooping of her left upper lid. She had been previously healthy and speci cally had no history of diabetes, hypertension or hypercholesterolemia.

Examination showed a nearly complete left third nerve palsy with pupil involvement (Figure 10.4)..

Table 10.4 Causes of acute isolated and painful third nerve palsy Compressive lesi none for none on aneurysm tumor pituitary apoplexy Ischemic microvascular disease vasculitis carotid dissection brainstem stroke In ammatory sarcoidosis, tuberculosis, systemic lupus idiopathic Meningeal disease infectious neoplastic Trauma. Which diagnostic possibilities should be addressed rst The list of poss none none ible causes of an isolated acute third nerve palsy is lengthy (Table 10.4), but in this patient, some etiologies are more likely than others. The very acute onset speaks against a skull base tumor or in ltrative process such as nasopharyngeal carcinoma or chronic meningitis.

An ischemic brainstem stroke can cause a third. nerve palsy, but most cases are not accompanied by pain. The etiologies that should be addressed most urgently in this case are a posterior communicating artery aneurysm, pituitary apoplexy and. 10: Over-reliance on negative test results Figure 10.5 Neur o-imaging of the above patient. (A) Axial non-contrast T1-weighted MRI and (B) MRA maximum intensity projection reconstruction of the circle of Willis showed no cause for this patient s acute third nerve palsy.

. carotid dissecti none for none on, because in these conditions the outcome is most strongly in uenced by the timeliness of treatment. An MRI and MRA of the head were obtained and both were reportedly normal (Figure 10.5).

Based on her negative neuro-imaging, vasculopathic and in ammatory etiologies were considered. Serologic tests for systemic in ammatory diseases were all normal and the patient was treated with 60 mg per day of oral prednisone for a presumptive diagnosis of idiopathic in ammatory disease (see 6, Painful ophthalmoplegia). Her pain resolved in a few days but her extraocular muscle palsy and ptosis persisted.

Eight weeks later, her examination was essentially unchanged and at that time she was referred for neuro-ophthalmic consultation.. What additional test should be obtained Although her pai none none n improved with steroids, suggesting the possibility of Tolosa Hunt syndrome,. her motility did not show the expected recovery, effectively eliminating this diagnosis. Is her clinical course at this point consistent with a vasculopathic third nerve palsy Failure to show some degree of recovery eight weeks after onset speaks strongly against an ischemic cranial nerve palsy (see 11, Acute isolated sixth nerve palsy). At this point no cause for this patient s third nerve palsy has been found, despite a variety of ancillary tests, and we must therefore reconsider the diagnoses that have previously been excluded.

Of these possibilities, the most threatening is a cerebral aneurysm and it is important to ask if this diagnosis has been fully excluded. The essence of this case is whether a negative MRA truly rules out an aneurysm. An acute, painful, pupil-involving third nerve palsy in a young or middle-aged adult with no vascular risk factors is so strongly suggestive of a posterior communicating artery aneurysm that we must go the extra mile to exclude it.

This patient therefore had a conventional carotid arteriogram that did reveal an aneurysm at the junction of the. 10: Over-reliance on negative test results Figure 10.6 Left internal carotid arteriogram (catheter study) of the same patient. A bilobed saccular aneurysm projects inferiorly from the posterior communicating artery (arrow).

In retrospect, the more proximal lobe of the aneurysm is in fact present on the MRA reconstruction (Figure 10.5)..

left internal ca none none rotid and posterior communicating arteries (Figure 10.6). The source lms from the original MRA were subsequently reviewed by the neuroradiologist who had performed the catheter angiogram and the aneurysm was identi able.

The patient underwent clipping of her aneurysm and her third nerve palsy showed partial resolution over the next six months. Discussion: As the sensitivity of non-invasive imaging improves, the need for conventional arteriography decreases. At this point, magnetic resonance angiography (MRA) and computed tomography angiography (CTA) are extremely sensitive for the detection of cerebral aneurysms, but have not yet achieved 100% accuracy.

A recent study comparing MRA techniques to catheter angiography in patients with third nerve palsy due to an unruptured posterior communicating artery aneurysm found a sensitivity of 92% using reformatted images and 98% using source image. analysis. Studie s using CTA have reported a similarly high sensitivity for the detection of symptomatic aneurysms. The sensitivity of these techniques depends in part on the size of the aneurysm.

The ability of MRA or CTA to detect an aneurysm approaches 100% for aneurysms larger then 5 mm; however, the risk of aneurysmal rupture for aneurysms smaller than 5 mm can approach 10%. In addition, and perhaps more importantly, clinicians must be cautious in applying data from published series to their own practice. The level of non-invasive technology available at a particular community hospital may not be equivalent to that of a tertiary care center.

This disparity is due to several factors, including differences in magnet strength and other aspects of instrumentation, imaging acquisition and processing, and the expertise of the person who interprets the images. Although MRA and CTA are not quite as sensitive as catheter angiography, not all negative studies should be followed by an angiogram. As in all such medical decisions, the risks of each study must be weighed against its bene ts.

In patients with a low likelihood of harboring an aneurysm, and particularly in those who also have a relatively high risk for complications from an arteriogram, an MRA or CTA is the more appropriate study. Patients who would be considered to have a relatively low risk of aneurysm would include those who are being screened for an aneurysm because of polycystic kidney disease or because of a family member with an aneurysm. Those who have a similarly low risk of aneurysm and, additionally, a high risk of complications from invasive angiography, are older patients with vascular risk factors who develop an acute pupil-sparing but partial third nerve palsy or a complete palsy with slight pupil involvement.

In such cases, a negative MRA or CTA is usually suf cient, with the caveat that the patient be monitored for possible development of pupillary involvement over the next 7 to 10 days. In patients with an otherwise complete but pupil-sparing, isolated third nerve palsy with vascular risk factors, no imaging is needed. These patients can be followed expectantly,.

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