Chronic arterial hypertension as unique symptom of brainstem astrocytoma

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The ACTOBAT group also raised concerns about the potential duration of the suppression of the pituitary-thyroid axis after TRH. However, this abnormality is probably transient and does not result in sustained alterations of thyroxine in the newborn infant.5 Several controlled trials of antenatal TRH and glucocorticoids including surfactant therapy as part of the study design are in progress or planned, and these will providea final answer on the issue of antenatal TRH for prevention of neonatal respiratory disease. *Fernando R Moya, Andres Maturana *Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA; and Universidad de Chile, Santiago, Chile 1

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Schellenberg JC, Liggins GC, Manzai M, Kitterman JA, Lee H. Synergistic hormonal effects on lung maturation in fetal sheep. J Appl Physiol 1988; 65: 94-100. Moya F, Mena P, Foradori A, Becerra M, Inzunza A, Germain A. Effect of maternal administration of thyrotropin-releasing hormone on the preterm fetal pituitary-thyroid axis. J Pediatr 1991; 119: 966-71. Roti E, Gardini E, Minelli R, Bianconi L, Alboni A, Braverman LE. Thyrotropin-releasing hormone does not stipulate prolactin release in the preterm human fetus. Acta Endocrinol 1990; 122: 462-66. Torres J, Foradori A, Salinas R, et al. Dose-related response of the fetal pituitary-thyroid axis to maternal administration of thyrotropinreleasing hormone (TRH). Pediatr Res 1995; 37: 241A. Torres BA, Stromquist CI, Moya FR, DeClue T. Prenatal administration of thyrotropin-releasing hormone and postnatal thyroxine values. Lancet 1994; 343: 730.

Chronic arterial hypertension as unique symptom of brainstem astrocytoma SiR-Although the association between lesions of the posterior cranial fossa and arterial hypertension is well known, we report a case of particular interest because of arterial hypertension that remained the only symptom of a low-grade astrocytoma of the brainstem for 16 years. At 20 years of age, our patient presented with arterial hypertension (160-180/100-120 mm Hg) unresponsive to medical treatment. Physical examination and pertinent laboratory investigations, including urinary excretion of 4hydroxy-3-methoxymandelic acid and renal angiography, were normal. At age 36, he developed acute respiratory failure that required emergency orotracheal intubation. On admission, the patient was alert and breathed freely through the orotracheal tube. Blood pressure was 170/110 mm Hg and heart rate 115/min. Neurological examination showed left cerebellar syndrome and palsy of cranial nerves IX, X, and XII on the left side. There were no ocular signs of intracranial hypertension. Magnetic resonance imaging (MRI) revealed a mass in the medulla oblongata (figure A). The tumour was partly resected with a suboccipital craniotomy. Histology showed a grade II astrocytoma. Postoperatively, the patient developed severe arterial hypotension that required dopamine infusion. 2 weeks later, the blood pressure was normal (140-150/70-80 mm Hg) and dopamine was discontinued. He was unable to maintain his airway so tracheostomy and gastrostomy were done. Postoperative MRI showed residual tumour in the upper medulla (figure B). 1 month after surgery, the patient started rehabilitation. 10 months later, he is alive and his blood pressure remains stable without medication. Only one similar case has been reported. Evans et al’ described a 10-year-old boy with a 1-year history of arterial hypertension and palsy of left cranial nerves V, VII, IX, XI, and XII, who harboured an unresectable astrocytoma of the medulla. Mechanisms responsible for arterial hypertension in posterior cranial fossa lesions include raised intracranial pressure,2 increased catecholamine production,’ and direct

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Figure: Preoperative (A) T1-weighted sequence

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postoperative (B) MRls in sagittal

A=non-enhancing hypointense lesion of medulla oblongata that bulges dorsally in lower half of IV ventricle (arrow); B shows extent of surgical resection.

stimulation of the cardiovascular centred In the case reported by Evans et al’ and in our patient, the cranial nerves were affected only on the left side. This finding supports the hypothesis that compression/distortion of the left side of the medulla may cause arterial hypertension.’,’ *R Pallini, L Lauretti, E Fernandez Institute of

Neurosurgery, Catholic University School

of Medicine, 00168 Rome,

Italy 1 2

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Evans CH, Westfall V, Atuk NO. Astrocytoma mimicking the features of pheochromocytoma Med Intell 1972; 26: 1397-99. Cushing H. Some experimental and clinical observations concerning states of increased intracranial tension. Am J Med Sci 1902; 124: 375-400. Dickinson CJ. Neurogenic hypertension. Oxford: Blackwell Scientific, 1965. Jannetta PJ, Segal R, Wolfson SK. Neurogenic hypertension: etiology and surgical treatment, II: observations in an experimental nonhuman primate model. Ann Surg 1985; 202: 253-61. Naraghi R, Gaab MR, Walter GF, et al. Arterial hypertension and neurovascular compression at the ventrolateral medulla: a comparative microanatomical and pathological study J Neurosurg 1992; 77: 103-12.

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