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• W1985210008 abstract "To the Editor: Cerebrovascular disease in the older patient is usually attributed to atherosclerosis, especially when risk factors for atherosclerosis other than age, such as diabetes mellitus, hypertension, or smoking, are present.1 When stroke occurs in such a patient, a diagnosis of giant cell (temporal) arteritis (GCA) is frequently not entertained initially. The insidious course of GCA and failure to appreciate its role in the development of stroke may then have fatal consequences. An older patient with presumed vasculopathy, who developed multiple cerebral infarctions in the course of giant cell (temporal) arteritis, is described. A 69-year old woman with a 10-year history of uncomplicated non-insulin-dependent diabetes mellitus was admitted to our hospital after she was found unconscious in her nursing home. No information was available with regard to the circumstances that led to the collapse, but it was learned later that a prodromal phase had preceded the present event. During the previous 6 months, the patient had begun to complain of headache, malaise, jaw claudication, and pain in the shoulder girdle. She had been treated by her general practitioner with calciumcarbasalate and codeine, which had resulted in disappearance of headache. During the last 2 months, however, the patient had become progressively passive and her appetite had decreased, resulting in a weight loss of 12 kg. Her children had noted an amnestic disorder and a dejected mood. One week before admission, the patient had experienced a transient paresis of the right leg. On admission, she was an anemic patient with blood pressure 100/60 mm Hg, pulse rate 78 bpm, and temperature 37.2°C. Except for a systolic murmur at the lower left sternal border and diminished vibratory sense of both lower legs, no abnormalities were found on physical examination. Temporal artery pulses were palpable and non- tender. On neurological examination, consciousness was clear, but the patient was brady-phrenic and apathetic with repetitive yawning. Eye movements were saccadic, and the nasolabial fold was absent on the right side. Walking was difficult as a result of bradykinesia, gait apraxia, and paratonia. There was a generalized areflexia, indifferent plantar reflexes, a snout reflex, and bilateral palmomental reflexes. Laboratory results showed an elevated ESR (98 mm/hour), microcytic anemia (Hb 5.5 mmol/L, MCV 74 fL), slight thrombocytosis (358 × 10e9/L), hyperglycemia (14.5 mmol/L), with normal values for leukocytes, CPK, urea, creatinine, and protein. The ECG showed sinus rhythm with repolarization abnormalities in leads V2-V3. The chest radiograph was normal except for a slightly enlarged heart. On the basis of these data, no definite diagnosis could be established. The neurological signs and symptoms were attributed to a chronic organic brain syndrome, a lesion in the left-sided corticospinal tract, and polyneuropathy. A CT scan of the brain disclosed bilateral infarctions in the basal ganglia and a small infarction lateral of the sella media. Echocardiography was normal. MRI of the brain showed multiple focal lesions periventricularly and in the basal ganglia (Figure 1). These findings of symmetrically located infarctions were interpreted as an unspecified cerebral vasculitis. Although clinical examination of both temporal arteries was unremarkable, temporal artery biopsy was performed the next day. The findings at microscopical examination were typical of GCA, showing obliteration of the vessel lumen with granulomatous infiltration of lymphocytes, histiocytes and multinucleated giant cells, and a fragmented lamina elastica interna. Therefore, prednisone, 60 mg/day, was added to the calciumcarbasalate 1 week after admission. Although a slight clinical improvement was noted at first, the patient collapsed again 3 weeks after admission and died subsequently, attributable to an acute inferolateral myocardial infarction. Permission for autopsy was not obtained. . A transverse FLAIR T2-weighted image shows symmetrical areas of high attenuation (edema) in periventricular regions in both hemispheres representing infarctions. This case illustrates the difficulties and pitfalls in the approach to the older patient with stroke and presumed vascular disease. In our patient, GCA was diagnosed and proven with temporal artery biopsy. Treatment with corticosteroids and salicylates failed to induce clinical remission, and the patient died in the course of the disease. Both patient's and doctor's delay probably accounted for the dramatic results because, in retrospect, the patient had experienced premonitory signs and symptoms for several months. The vague signs and symptoms on admission were at first ascribed to ischemic cerebral infarctions as manifestations of atherosclerosis. However, clues from the patient's history, abnormal laboratory results including increased ESR and normocytic anemia, and the findings of CT and MRI prompted additional diagnostic steps leading to a diagnosis of biopsy proven giant cell (temporal) arteritis. Multiple bilateral infarctions were detected on MRI, most notably in both basal ganglia that are supplied by the lenticulo-striate arteries, which arise from the middle cerebral arteries. The temporal relationship between the strokes and symptoms of GCA suggested a causal relationship. The localization, extent, and symmetrical nature of the intracerebral lesions were considered atypical for atherosclerotic thromboembolism, and the lesions were interpreted as manifestations of intracerebral vasculitis. Similarly, the fatal myocardial infarction was thought to be the result of coronary arteritis. Unfortunately, definite proof for the presence of intracerebral and coronary arteritis could not be obtained. Giant cell arteritis is a panarteritis that affects large and medium-sized arteries of the aortic arch preferentially.2 Although cerebral infarction is known to complicate GCA, it rarely is the presenting symptom.3 In the latter case, differentiation from atherosclerotic disease may be difficult. The precise relationship between GCA and cerebral infarction is poorly understood. Intracerebral arteritis associated with GCA is considered rare because only vessels within 5 mm of the dura are affected.4 This is thought to be related to the fact that arteries penetrating into the cranium lose their lamina elastica interna, which is thought to be the target for the presumed autoimmune response underlying GCA. Nevertheless, cases of GCA with intracranial vasculitis have been documented, and our patient may represent a similar example.5 If not caused by intracerebral vasculitis, stroke due to GCA probably results from thromboembolism arising in upstream extracranial vessels. As an illustration, basilar artery thrombosis is a frequent cause of death in patients with GCA.6 With both atherosclerosis and GCA favoring thromboembolism, patients suffering from both conditions may be particularly prone to develop stroke. Pathological findings from various studies have indeed shown clinically relevant atherosclerosis and GCA to be present simultaneously, both in the same and in different cranial and systemic vessels.6–9 In addition, the inflammatory infiltrate in GCA produces potentially procoagulant cytokines such as TNF-alpha.10 Furthermore, it is conceivable that the infiltrate itself may lead to critical narrowing of the vessel lumen or disruption of atheromatous plaques. Collateral circulation may become insufficient under these circumstances in patients with atherosclerosis, thus predisposing for ischemic infarction. GCA is treated with corticosteroids. As a rule, prednisone 1 mg/kg body weight is given, which usually results in a dramatic clinical amelioration parallel to a decrease in ESR. Some authors advocate the concomitant use of salicylates or anticoagulants inasmuch as they observed an increase in the number of thromboembolic events after initiation of corticosteroid therapy.11,12 However, stroke occurring in a patient with GCA probably heralds a fatal disease course, as illustrated by the present case, despite treatment, and few reports exist of a beneficial effect in such cases.13,14 The present case report suggests that GCA may precipitate cerebrovascular accidents in older patients who are at high risk because of atherosclerosis. Recognition of premonitory signs and symptoms may lead to the correct diagnosis and subsequent prompt treatment before irreversible damage has been done." @default.
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• W1985210008 date "1998-06-01" @default.
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• W1985210008 title "STROKE: ATHEROSCLEROSLS OR ARTERITIS?" @default.
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• W1985210008 doi "https://doi.org/10.1111/j.1532-5415.1998.tb03828.x" @default.
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