Stuttering pituitary apoplexy resembling meningitis.
Stuttering pituitary apoplexy resembling meningitis.
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口吃垂体中风类似于脑膜炎。
DOI：
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发表时间：
1990
影响因子：
11
通讯作者：
G. Plant
中科院分区：
文献类型：
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作者：
J. Winer;G. Plant
Brougham等人在第一次明确描述垂体卒中时提出，该综合征应考虑为突然出现头痛、弱视、复视、嗜睡、意识不清或昏迷。这些临床特征现已得到充分证实然而，Brougham等人提到了一例脑垂体肿瘤出血，导致颅内动脉瘤破裂，眼麻痹延迟了几天我们已经看到两个病例延误诊断发生由于亚急性发作的症状。高细胞性脑脊液（CSF）的发现进一步混淆了临床表现。第一个病例是一名50岁的仓库服务员，他有5天的全身性头痛和呕吐史，2天复视。亲戚们注意到他的右眼皮断断续续地下垂。他以前健康状况良好，除了在童年早期的“冷脓肿”引流。他每周喝大约20品脱啤酒。检查显示轻度发热（37.5 '），颈部屈曲受限，但无颈部僵硬。他有部分左第三神经麻痹，左侧瞳孔扩张但反应性强，左侧部分上睑下垂。视野无缺损，眼外运动完整。四肢的力量和音调正常。强化可引起肱二头肌反射，但肌腱反射均不存在。足底屈肌反应正常，感觉测试正常。进行非增强CT扫描以排除脓肿。腰椎穿刺显示脑脊液在19 cms压力下呈乳白色，含有77 mg%的蛋白，52个白细胞（5%多形细胞，910%淋巴细胞，4%巨噬细胞）。没有看到微生物，糖的浓度也很正常。脑电图显示主要向后分布的过量慢波。初步临床诊断为亚急性脑膜脑炎，并开始静脉注射阿昔洛韦和硫胺素治疗。在接下来的三天里，他的临床状况恶化，体温上升到39度。他出现双侧上睑下垂，双眼内收和上仰受损。右眼视力下降到一米以内数不清手指，右眼纵向视野缺损，延伸至水平子午线以下。眼眶高分辨率增强CT扫描显示垂体腺瘤伴鞍上延伸。立即开始强的松龙治疗，视力迅速改善至6/7.5。内分泌检查显示泌乳素正常（< 65单位），但TSH （0.2 uU/L）和游离T4 （5.5 pm/L）较低。随后他进行了平稳的经蝶窦垂体切除术，病理检查结果与垂体腺瘤梗死的最终诊断一致。第二个病例是一名45岁的打印机助理，双侧出现腕管综合征症状。一年后，人们注意到他的手很大，而且有肢端肥大症的其他特征。CT扫描证实垂体腺瘤。在等待经蝶窦垂体切除术时，他突然出现额部头痛并呕吐。第二天，他稍微好了一点，但三天后，他开始感到困惑，并抱怨视力受损。他被送往当地一家医院，在那里他被发现颈部僵硬，体温高达40度。腰椎穿刺显示脑脊液黄色，压力升高，蛋白浓度升高，混合性多细胞增多。第二天，他出现眼眶周围和结膜下水肿和双侧第六神经麻痹。他的深腱反射消失，意识水平开始下降。他被转移到一个专科病房，在那里他被发现迷失了时间和地点，并且发烧。眼眶周围水肿，左眼周围瘀伤，颈部明显僵硬。他的右视敏度是3/60，左视敏度是6/18他无法识别石原的任何一块测试板。左眼见颞部偏盲，颜色偏浅，右眼见密集的中央暗斑。轻度椎间盘肿胀，无静脉搏动。侧直肌完全无力，右眼双侧和向上运动受限。唯一的其他异常发现是完全反射。全血细胞计数正常，尿素正常，但血清钠低至126毫米/升。脑脊液中含有1-2 G/L的蛋白，压力为30 cm脑脊液，白细胞计数为900 (106/L)，其中7900为多态性，其余为淋巴细胞。红细胞20个（106/L），脑脊液葡萄糖正常。尿液和血清渗透压提示ADH分泌异常。颅骨平片显示垂体窝肿大，蝶窦混浊。CT扫描显示鞍上肿块呈外侧延伸。血清皮质醇低（60 mu/L），总甲状腺素、TSH、催乳素、FSH和LH水平也低，证实了全垂体功能低下。随机估计生长激素略高（16.6 mu/L）。鉴于症状和细胞脑脊液的逐渐演变，转诊医院临时诊断为脑膜炎。停用抗生素并静脉注射类固醇和甲状腺素治疗后，脑脊液无菌，野区缺损和脑神经征象消失。在一些脑垂体中风的病例中，脑脊液中存在炎症改变，这在文献中有很好的记载。Bjerre和Lindholm最近强调“无菌性脑膜炎”的发生是垂体中风的一个重要特征，并报告了6例脑脊液检查显示白细胞和/或多态性计数升高的病例。文献中还引用了另外四个案例。在典型急性发作的患者中，脑脊液多细胞症的存在通常很少引起诊断关注，而诊断是通过紧急CT扫描确认的。在我们的病例中，亚急性或口吃的发作使诊断变得困难，并促使本报告。在第一种情况下，没有现场缺陷的表现加剧了诊断的困难。在第二个病例中，尽管先前诊断为垂体瘤，但由于缺乏对垂体卒中的这种表现模式的认识，延迟了准确诊断的建立。
In the first clear description of pituitary apoplexy Brougham et al' suggested that the syndrome should be considered as the abrupt development of headache, amblyopia, diplopia, drowsiness, confusion or coma. These clinical features have now become well established.23 However, Brougham et al mention one case of haemorrhage into a pituitary tumour simulating rupture of an intracranial aneurysm where ophthalmoplegia was delayed several days.4 We have seen two cases where delay in diagnosis occurred as a result of the subacute onset of symptoms. The clinical picture was further confused by the finding of a highly cellular cerebrospinal fluid (CSF). The first case was a 50 year old warehouse attendant who had a five day history of generalised headache and vomiting with two days of double vision. His relatives had noticed an intermittent droop of the right eyelid. He had previously been in good health apart from the drainage ofa "cold abscess" in early childhood. He drank about 20 pints of beer each week. Examination revealed a slight pyrexia (37 5') with limitation of neck flexion but no neck stiffness. He had a partial left third nerve palsy with a dilated but reactive left pupil and a partial left ptosis. There was no field defect and extra-ocular movements appeared full. Power and tone was normal in the limbs. The biceps reflexes could be elicited on reinforcement but otherwise tendon reflexes were all absent. Plantar responses were flexor and sensory testing was normal. An unenhanced CT scan was performed to exclude an abscess. Lumbar puncture revealed opalescent CSF under 19 cms pressure which contained a concentration of 77 mg% of protein with 52 white cells (5% polymorphs, 910% lymphocytes, 4% macrophages). No organisms were seen and the concentration ofsugar was normal. An EEG showed an excess of mainly posteriorly distribute slow waves. A provisional clinical diagnosis of a subacute meningoencephalitis was made and treatment was started with intravenous Acyclovir and thiamine. Over the next three days there was a deterioration in his clinical state with a rising pyrexia to 39'C. He developed bilateral ptosis with impaired adduction and elevation of both eyes. Visual acuity in the right eye was reduced to counting fingers at one metre and a right altitudinal field defect developed which extended below the horizontal meridian. A high resolution enhanced CT scan of the orbits revealed a pituitary adenoma with some suprasellar extension. Treatment with Prednisolone was started immediately with rapid improvement ofvisual acuity to 6/7.5 in the effected eye. Endocrine studies revealed a normal prolactin (< 65 units) but low TSH (0 2 uU/L) and free T4 (5 5 pm/L). He subsequently had an uneventful transphenoidal hypophysectomy and pathological examination of the specimen was consistent with the eventual diagnosis of infarction in a pituitary adenoma. The second case was a 45 year old printer's assistant who presented with symptoms ofthe carpal tunnel syndrome bilaterally. It was noted, a year later, that he had large hands and other features of acromegaly. A pituitary adenoma was confirmed on CT scan. Whilst awaiting a transphenoidal hypophysectomy he awoke with sudden onset frontal headache and vomited. The following day he was a little better but three days later he became confused and complained of visual impairment. He was admitted to a local hospital where he was found to have neck stiffness and a temperature of40'C. A lumbar puncture revealed CSF which was xanthochromic and under increased pressure with raised protein concentration and a mixed pleocytosis. The following day he developed peri-orbital and subconjunctival oedema and bilateral sixth nerve palsies. His deep tenden reflexes were absent and his conscious level began to deteriorate. He was transferred to a specialist unit where he was found to be disoriented in time and place and pyrexial. Periorbital oedema, bruising around the left eye and marked neck stiffness were noted. Visual acuity was 3/60 on the right and 6/18 on the left and he was unable to identify any of the Ishihara test plates. There was a temporal hemianopia to colour in the left eye and a dense central scotoma on the right on confrontation. There was mild disc swelling with absent venous pulsation. Lateral rectus weakness was complete and bilateral and upward movement of the right eye was limited. The only other abnormal finding was total areflexia. The full blood count was normal as was the urea although the serum sodium was low at 126 mm/L. The CSF contained 1-2 G/L of protein with a pressure of 30 cms ofCSF and a white cell count of 900 (106/L) of which 7900 were polymorphs and the rest lymphocytes. There were 20 (106/L) red cells and a normal CSF glucose. Urine and serum osmolarities suggested inappropriate secretion of ADH. A plain skull radiograph showed an enlarged pituitary fossa and opacification of the sphenoid sinus. CT scan revealed a suprasellar mass with lateral extension. Serum cortisol was low (60 mu/L) as were levels of total thyroxine, TSH, prolactin, FSH and LH confirming panhypopituitarism. A random estimation of growth hormone was slightly elevated (16 6 mu/L). In view ofthe gradual evolution of symptoms and the cellular CSF a provisional diagnosis of meningitis was made by the referring hospital. The CSF proved to be sterile and field defects and cranial nerve signs resolved when antibiotics were withdrawn and he was treated with intravenous steroids and thyroxine. The presence of inflammatory changes in the CSF in some cases ofpituitary apoplexy is well documented in the literature. Bjerre and Lindholm' have recently emphasised the occurrence of "sterile meningitis" as an important feature of pituitary apoplexy and report six cases where CSF examination revealed an elevated leucocyte and or polymorph count. Four further cases in the literature are cited. The presence of CSF pleocytosis usually presents little diagnostic concern in patients with a typical acute onset where the diagnosis is confirmed by urgent CT scanning. The subacute or stuttering onset in our cases made diagnosis difficult and prompted this report. In the first case the absence of a field defect on presentation compounded the difficulty in diagnosis. In the second case the lack of awareness of this mode of presentation of pituitary apoplexy delayed establishing an accurate diagnosis despite the previous diagnosis of a pituitary tumour.