- Email: [email protected]
Pituitary apoplexy as a cause of internal carotid artery occlusion
480
Case Reports / Journal of Clinical Neuroscience 15 (2008) 480–483
thalami. Atrophy of the mamillary bodies and cerebellar vermis are also reported.1 DWI has been cited as a superior modality of MRI due to the shorter acquisition time.5 However, DWI preferentially demonstrates lesions in the thalami but not in the periaqueductal regions, which are highlighted on T2-weighted and FLAIR images.2 This is thought to be due to the difference in the degree of oedema.2 A neuropathological study of non-alcoholic WE has shown that neuronal change appears to predominate in the thalamic regions with relative preservation in the periventricular regions and mamillary bodies, which may account for this interesting radiological feature as observed in our patient.4 Thalamic involvement in WE correlates with the extent of disturbance in consciousness and may be indicative of a more severe disease.2 Our case highlights that while the clinical index of suspicion should be high in such patients, neuroimaging is a useful adjunctive diagnostic tool and employing several modalities of MRI better delineates the brain lesions seen in WE. The DWI highlighted the thalamic lesions, whereas the periaqueductal lesions were demonstrated on the FLAIR sequence using the more rapid echoplanar acquisition. The routine FLAIR sequence was not interpretable in our patient due to gross movement artifacts. Echoplanar-acquired FLAIR should be considered in pa-
tients who are unable to tolerate a prolonged period in the scanner. Parenteral high-dose thiamine can arrest disease progression and reverse the neurological deficits within hours, highlighting the need for early diagnosis.3 A carefully tailored MRI with the appropriate sequences can provide useful information that can be of particular importance in aiding in the diagnosis of atypical cases of WE. References 1. Zhong C, Jin L, Fei G. MR imaging of nonalcoholic Wernicke encephalopathy: A follow-up study. Am J Neuroradiol 2005;26: 2301–5. 2. White ML, Zhang Y, Andrew LG, et al. MR imaging with diffusionweighted imaging in acute and chronic Wernicke encephalopathy. AJNR Am J Neuroradiol 2005;26:2306–10. 3. Yamamoto T. Alcoholic and non-alcoholic Wernicke’s encephalopathy. Be alert to the preventable and treatable disease. Intern Med 1996;35:754–5. 4. Gui QP, Zhao WQ, Wang LN. Wernicke’s encephalopathy in nonalcoholic patients: clinical and pathologic features of three cases and literature reviewed. Neuropathology 2006;26:231–5. 5. Kashihara K, Irisawa M. Diffusion weighted magnetic resonance imaging in a case of acute Wernicke’s encephalopathy. J Neurol Neurosurg Psychiatry 2002;73:181.
doi:10.1016/j.jocn.2007.03.007
Pituitary apoplexy as a cause of internal carotid artery occlusion Seref Dogan *, Hasan Kocaeli, Faruk Abas, Ender Korfali Department of Neurosurgery, Uludag˘ University School of Medicine, Gorukle, 16059 Bursa, Turkey Received 6 July 2006; accepted 20 August 2006
Abstract Occlusion of intracranial arteries by pituitary apoplexy with resulting infarction is a rare occurrence. A 50-year-old man who presented with a history of sudden onset of frontal headache and visual impairment was admitted to another medical centre and MRI revealed a non-enhancing sellar lesion with suprasellar and infrasellar extension. Thereafter, the patient’s consciousness deteriorated progressively and he showed signs of herniation; he was then referred to our centre for further evaluation. CT scanning revealed infarction of the left internal carotid artery territory. Transcranial resection of the tumour followed by a large decompressive craniotomy restored the blood flow in the internal carotid artery. Histological examination revealed the tumour to be a pituitary adenoma that contained formed blood elements. The patient’s neurological status did not improve and he died on the ninth postoperative day despite vigorous treatment for controlling intracranial pressure. This case study documents a rare presentation of pituitary apoplexy that caused signs of raised intracranial pressure due to mechanical obstruction of an internal carotid artery with resulting infarction. Ó 2007 Elsevier Ltd. All rights reserved. Keywords: Cerebral infarction; Decompressive craniectomy; Pituitary apoplexy; Vascular occlusion
*
Corresponding author. Tel.: +90 224 4428081; fax: +90 224 4429263. E-mail addresses: [email protected] (S. Dogan).
Case Reports / Journal of Clinical Neuroscience 15 (2008) 480–483
1. Introduction Various definitions have been proposed for pituitary apoplexy. Although patients with pituitary tumours may have silent haemorrhages, the term pituitary apoplexy should be reserved for the clinical syndrome of an apoplectic event characterized by the sudden onset of headache associated with neurological or endocrinological abnormalities attributed to a massive haemorrhage or infarction in a pituitary tumour. The syndrome often occurs in patients with no antecedent history suggestive of a pituitary tumour, and it may be the first definite indication that a pituitary tumour is present.1,2 Up to 25% of pituitary tumour haemorrhages are not associated with a clinical apoplectic event. Approximately 17% of all pituitary tumours removed surgically reveal histological evidence of infarction, and 7% of all patients with pituitary adenomas develop pituitary apoplexy.3 We report a case of pituitary apoplexy, in which the patient developed massive cerebral infarction due to direct compression of the internal carotid artery (ICA). We also review reported cases in the literature and discuss treatment options.
481
a pituitary adenoma that contained formed blood elements (Fig. 3). Postoperatively, the patient’s neurological status did not improve and he developed diabetes insipidus. As all of the patient’s preoperative pituitary hormone levels were very low, desmopressin and glucocorticoid treatment was initiated and the patient’s fluid balance was strictly controlled. Despite decompression and control of intracranial pressure (ICP) with monitoring and ventricular drainage, the patient died on the ninth postoperative day. 3. Discussion Pituitary apoplexy is associated with acute enlargement of a pituitary adenoma produced by infarction and/or
2. Case report A 50-year-old man presented at another hospital with a history of sudden onset of frontal headache and visual impairment MRI revealed a heterogeneous nonenhancing 5 3 cm sellar mass that was isointense and slightly hyperintense relative to the brain parenchyma on T1-weighted and T2-weighted images, respectively. The mass also extended into the sphenoid sinus as well as the suprasellar recess, displacing the optic nerves superiorly (Fig. 1a). The MRI findings were consistent with haemorrhagic macroadenoma of the pituitary compressing the right optic nerve and chiasm and occluding the supraclinoid portion of the ICA (Fig. 1b). On the day of admission, the patient’s consciousness deteriorated progressively and he showed signs of herniation; he was then referred to our centre for further evaluation. On admission, the patient was in a coma, requiring ventilatory support. Neurological examination revealed left-sided pupillary dilation, no light reflex in the left pupil, extensor motor response on the left, and no response in the right extremities. CT was performed to assess the patient’s rapidly deteriorating neurological status, and revealed a nonenhancing heterogeneous sellar mass and massive infarction in the left ICA territory (Fig. 2). The patient underwent a large left frontotemporoparietal craniotomy, which revealed a brain edema and compression and elevation of the ICA by an encapsulated sellar mass. The capsule was punctured and a haemorrhagic tumour was completely removed. After removal of the tumour, the left ICA began to pulsate. The patient’s bone flap was not replaced, rather it was stored in a deep-freezer. Microscopic examination revealed the tumour to be
Fig. 1. (a) Sagittal T1-weighted MRI with contrast showing an unenhancing sellar mass with suprasellar and sphenoidal sinus extension. (b) Axial T1-weighted image without contrast showing an isointense sellar mass lesion that has occluded the left internal carotid artery (arrow).
482
Case Reports / Journal of Clinical Neuroscience 15 (2008) 480–483
Fig. 2. Preoperative axial unenhanced CT scan showing a hyperdense haemorrhagic sellar lesion with infarction of the left frontotemporal region.
Fig. 3. Photomicrograph of a tumour specimen obtained during surgery showing formed blood elements and round tumour cells with hyperchromatic nuclei (haematoxylin-eosin stain, 200).
haemorrhage. Haemorrhage may also occur in the absence of clinical features or with a subacute course, but the term apoplexy is properly reserved for those cases with an abrupt onset of typical symptoms and signs, that is, sudden headache, usually accompanied by nausea and vomiting.2,4 The headaches may be caused by pressure on the diaphragma sellae or irritation of the basal meninges.2,5 Suprasellar tumour expansion leads to compression of the visual apparatus, which may produce precipitous deterioration in visual acuity, reduction in visual fields or blindness.2,4 Less commonly, the optic tract can be compressed in a prefixed chiasm, resulting in a homonymous hemianopsia. Conversely, compression of the optic nerve in a postfixed chiasm can produce central scotoma, impaired
monocular visual acuity, and pain on eye movement. Hypothalamic involvement may also produce hypotension, disturbances of temperature regulation, cardiac and respiratory dysrhythmias, and diabetes insipidus. Less extensive haemorrhages might not lead to apoplexy, but might produce only a sudden drop in hormone levels.2 Various factors have been proposed as the precipitating events leading to pituitary apoplexy, including sudden trauma,6 use of bromocriptine,2 irradiation,2,6 hypertension,4 aspirin therapy,4 surgical procedures,7 neuroendocrinological manipulation,8 pregnancy,9 general anaesthesia10 and lumbar puncture.11 It has been suggested that the tendency to develop pituitary apoplexy may depend on the histological type of the adenoma. Apoplexy is thought to be more frequently associated with eosinophilic adenomas.12 The majority of adenomas undergoing apoplexy have been described as nonfunctional.1,4,13 Decreased visual acuity or visual field defects are the hallmarks of pituitary apoplexy.4 Also, upward enlargement of the adenoma can be extensive enough to compress the middle and anterior cerebral arteries, leading to focal ischaemic deficits.14,15 Lateral enlargement of the tumour into the cavernous sinuses may lead to extraocular ophthalmoplegia and ICA compression. Compression of the ICA, either in the cavernous sinus or in the supraclinoid portion, can cause hemispheric ischaemic deficits and altered consciousness.8,14–19 While signs of focal cerebral hemispheric dysfunction are uncommon in pituitary apoplexy, hemiplegia as the presenting sign is extremely unusual.8,14–20 The mechanism has been postulated to be cerebral ischaemia resulting either from mechanical obstruction of an intracranial artery by the enlarging mass, or mostly secondary to haemorrhage or spasm. Vasospasm could result from extravasation of blood from the pituitary tumour into the subarachnoid space and/or the interaction of a vasoactive agent released from the pituitary tumour into the hypothalamohypophyseal area.20,21 Mechanical obstruction of large cerebral arteries by pituitary expansion, with consequent hemiplegia and altered consciousness, has been previously described in only six cases.8,14–19 With an alert patient presenting with ophthalmoplegia in the absence of visual field deficit or impaired acuity, the surgical role is less clearly defined and many advocate conservative management.22 In patients who are stable or improving without diminished consciousness or signs of chiasmal or optic nerve compression, conservative management has also been suggested.8 Patients with severe visual or mental impairment or those with progressive deterioration and focal ischaemic deficit require urgent surgical decompression.2 Emergency transsphenoidal16,17 and transcranial decompression14,18 reportedly reverse visual compromise and restore ICA blood flow with varying clinical outcomes. Two of the six patients mentioned above were managed nonoperatively: one died15 and the other improved.8 Clark et al.8 suggested conservative treatment in patients with established infarcts at the time of presentation because of the risk of haemorrhagic transformation following decom-
Case Reports / Journal of Clinical Neuroscience 15 (2008) 483–486
pression, but they did not address how to manage raised ICP. We undertook a more radical decompressive approach for reduction of raised ICP, as early decompressive craniectomy has been reported to be associated with better outcomes in patients with cerebral artery infarction.23 4. Conclusion In patients with pituitary apoplexy who present with signs of raised ICP, a CT scan may provide additional clues about evolving intracranial pathologies and guide the choice of surgical approach. In cases with established cerebral infarcts, a transcranial approach not only provides decompression of the visual apparatus and ICA flow but also permits decompressive craniotomy for reducing elevated ICP. The present case demonstrates that pituitary apoplexy is a neurosurgical emergency that requires surgical intervention at the time of diagnosis. References 1. Bills DC, Meyer FB, Laws Jr ER, et al. A retrospective analysis of pituitary apoplexy. Neurosurgery 1993;33:602–69. 2. Cardoso ER, Peterson EW. Pituitary apoplexy: A Review. Neurosurgery 1984;14:363–73. 3. Wakai S, Fukushima T, Teramoto A, et al. Pituitary apoplexy: Its incidence and clinical significance. J Neurosurg 1981;55:187–93. 4. Randeva HS, Schoebel J, Byrne J, et al. Classical pituitary apoplexy: clinical features, management and outcome. Clin Endocrinol 1999;51:181–8. 5. David NJ, Gargano FP, Glaser JS. Pituitary apoplexy in clinical perspective. In: Glaser JS, Smith JL, editors. Neuro-ophthalmology VIII. St. Louis: Mosby; 1975. p. 140–65. 6. Ebersold MJ, Laws Jr ER, Scheithauer BW, et al. Pituitary apoplexy treated by transsphenoidal surgery. A clinicopathological and immunocytochemical study. J Neurosurg 1983;58:315–20. 7. Wiesmann M, Gliemroth J, Kehler U, et al. Pituitary apoplexy after cardiac surgery presenting as deep coma with dilated pupils. Acta Anaesthesiol Scand 1999;43:236–8.
483
8. Clark JD, Freer CE, Wheatley T. Pituitary apoplexy: an unusual cause of stroke. Clin Radiol 1987;38:75–7. 9. Onesti ST, Wisniewski T, Post KT. Clinical versus subclinical pituitary apoplexy: presentation, surgical mamagement, and outcome in 21 patients. Neurosurgery 1990;26:980–6. 10. Barber SG. Hypopituitarism and artificial ventilation. Acta Endocrinol 1979;90:211–6. 11. Symon L, Mohandy S. Hemorrhage in pituitary tumors. Acta Neurochir 1982;65:41–9. 12. Werner PL, Shah JH, Kukreja SC, et al. Recurrence of acromegaly after pituitary apoplexy. JAMA 1982;247:2816–8. 13. Semple PL, Webb MK, de Villiers JC, et al. Pituitary apoplexy Neurosurgery 2005;56:65–72. 14. Majchrzak H, Wencel T, Dragan T, et al. Acute hemorrhage into pituitary adenoma with subarachnoid hemorrhage and anterior cerebral artery occlusion. J Neurosurg 1983;58:771–3. 15. Schnitker KT, Lehnert HB. Apoplexy in a pituitary chromophobe adenoma producing the syndrome of middle cerebral artery thrombosis. J Neurosurg 1952;9:201–13. 16. Bernstein M, Hegele RA, Gentili F, et al. Pituitary apoplexy associated with a triple bolus test. J Neurosurg 1984;61:586–90. 17. Lath R, Rajshekhar V. Massive cerebral infarction as a feature of pituitary apoplexy. Neurol India 2001;49:191–3. 18. Rosenbaum TJ, Houser OW, Laws ER. Pituitary apoplexy producing internal carotid artery occlusion. Case report. J Neurosurg 1977;47:599–604. 19. Rodier G, Meotien Y, Battaglia F, et al. Bilateral stroke secondary to pitıitary apoplexy. J Neurol 2003;250:491–5. 20. Pozzati E, Frank G, Nasi MT, et al. Pituitary apoplexy, bilateral carotid vasospasm, and cerebral infarction in a 15-year-old boy. Neurosurgery 1987;20:56–9. 21. Cardoso ER, Peterson EW. Pituitary apoplexy and vasospasm. Surg Neurol 1983;20:391–5. 22. Thompson D, Powell M, Foster O. Atypical presentation of vascular events in pituitary tumors: ‘‘non-apoplectic” pituitary apoplexy. J Neurol Neurosurg Psychiatry 1994;57:1441–2. 23. Cho D-Y, Chen T-C, Lee H-C. Ultra-early decompressive craniectomy for malignant middle cerebral artery infarction. Surg Neurol 2003;60:227–33.
doi:10.1016/j.jocn.2006.08.020
Evacuation of a 14-vertebral-level cervico-thoracic epidural abscess and review of surgical options for extensive spinal epidural abscesses M. Payer a,*, H. Walser b a
Spine and Pain Clinic Zu¨rich, Witellikerstrasse 40, 8008, Zu¨rich, Switzerland b Neurology Center Hirslanden, Zu¨rich, Switzerland Received 17 November 2006; accepted 17 December 2006
*
Corresponding author. Tel.: +044 387 37 41; fax: +044 387 37 45. E-mail addresses: [email protected] (M. Payer).
Case Reports / Journal of Clinical Neuroscience 15 (2008) 480–483
thalami. Atrophy of the mamillary bodies and cerebellar vermis are also reported.1 DWI has been cited as a superior modality of MRI due to the shorter acquisition time.5 However, DWI preferentially demonstrates lesions in the thalami but not in the periaqueductal regions, which are highlighted on T2-weighted and FLAIR images.2 This is thought to be due to the difference in the degree of oedema.2 A neuropathological study of non-alcoholic WE has shown that neuronal change appears to predominate in the thalamic regions with relative preservation in the periventricular regions and mamillary bodies, which may account for this interesting radiological feature as observed in our patient.4 Thalamic involvement in WE correlates with the extent of disturbance in consciousness and may be indicative of a more severe disease.2 Our case highlights that while the clinical index of suspicion should be high in such patients, neuroimaging is a useful adjunctive diagnostic tool and employing several modalities of MRI better delineates the brain lesions seen in WE. The DWI highlighted the thalamic lesions, whereas the periaqueductal lesions were demonstrated on the FLAIR sequence using the more rapid echoplanar acquisition. The routine FLAIR sequence was not interpretable in our patient due to gross movement artifacts. Echoplanar-acquired FLAIR should be considered in pa-
tients who are unable to tolerate a prolonged period in the scanner. Parenteral high-dose thiamine can arrest disease progression and reverse the neurological deficits within hours, highlighting the need for early diagnosis.3 A carefully tailored MRI with the appropriate sequences can provide useful information that can be of particular importance in aiding in the diagnosis of atypical cases of WE. References 1. Zhong C, Jin L, Fei G. MR imaging of nonalcoholic Wernicke encephalopathy: A follow-up study. Am J Neuroradiol 2005;26: 2301–5. 2. White ML, Zhang Y, Andrew LG, et al. MR imaging with diffusionweighted imaging in acute and chronic Wernicke encephalopathy. AJNR Am J Neuroradiol 2005;26:2306–10. 3. Yamamoto T. Alcoholic and non-alcoholic Wernicke’s encephalopathy. Be alert to the preventable and treatable disease. Intern Med 1996;35:754–5. 4. Gui QP, Zhao WQ, Wang LN. Wernicke’s encephalopathy in nonalcoholic patients: clinical and pathologic features of three cases and literature reviewed. Neuropathology 2006;26:231–5. 5. Kashihara K, Irisawa M. Diffusion weighted magnetic resonance imaging in a case of acute Wernicke’s encephalopathy. J Neurol Neurosurg Psychiatry 2002;73:181.
doi:10.1016/j.jocn.2007.03.007
Pituitary apoplexy as a cause of internal carotid artery occlusion Seref Dogan *, Hasan Kocaeli, Faruk Abas, Ender Korfali Department of Neurosurgery, Uludag˘ University School of Medicine, Gorukle, 16059 Bursa, Turkey Received 6 July 2006; accepted 20 August 2006
Abstract Occlusion of intracranial arteries by pituitary apoplexy with resulting infarction is a rare occurrence. A 50-year-old man who presented with a history of sudden onset of frontal headache and visual impairment was admitted to another medical centre and MRI revealed a non-enhancing sellar lesion with suprasellar and infrasellar extension. Thereafter, the patient’s consciousness deteriorated progressively and he showed signs of herniation; he was then referred to our centre for further evaluation. CT scanning revealed infarction of the left internal carotid artery territory. Transcranial resection of the tumour followed by a large decompressive craniotomy restored the blood flow in the internal carotid artery. Histological examination revealed the tumour to be a pituitary adenoma that contained formed blood elements. The patient’s neurological status did not improve and he died on the ninth postoperative day despite vigorous treatment for controlling intracranial pressure. This case study documents a rare presentation of pituitary apoplexy that caused signs of raised intracranial pressure due to mechanical obstruction of an internal carotid artery with resulting infarction. Ó 2007 Elsevier Ltd. All rights reserved. Keywords: Cerebral infarction; Decompressive craniectomy; Pituitary apoplexy; Vascular occlusion
*
Corresponding author. Tel.: +90 224 4428081; fax: +90 224 4429263. E-mail addresses: [email protected] (S. Dogan).
Case Reports / Journal of Clinical Neuroscience 15 (2008) 480–483
1. Introduction Various definitions have been proposed for pituitary apoplexy. Although patients with pituitary tumours may have silent haemorrhages, the term pituitary apoplexy should be reserved for the clinical syndrome of an apoplectic event characterized by the sudden onset of headache associated with neurological or endocrinological abnormalities attributed to a massive haemorrhage or infarction in a pituitary tumour. The syndrome often occurs in patients with no antecedent history suggestive of a pituitary tumour, and it may be the first definite indication that a pituitary tumour is present.1,2 Up to 25% of pituitary tumour haemorrhages are not associated with a clinical apoplectic event. Approximately 17% of all pituitary tumours removed surgically reveal histological evidence of infarction, and 7% of all patients with pituitary adenomas develop pituitary apoplexy.3 We report a case of pituitary apoplexy, in which the patient developed massive cerebral infarction due to direct compression of the internal carotid artery (ICA). We also review reported cases in the literature and discuss treatment options.
481
a pituitary adenoma that contained formed blood elements (Fig. 3). Postoperatively, the patient’s neurological status did not improve and he developed diabetes insipidus. As all of the patient’s preoperative pituitary hormone levels were very low, desmopressin and glucocorticoid treatment was initiated and the patient’s fluid balance was strictly controlled. Despite decompression and control of intracranial pressure (ICP) with monitoring and ventricular drainage, the patient died on the ninth postoperative day. 3. Discussion Pituitary apoplexy is associated with acute enlargement of a pituitary adenoma produced by infarction and/or
2. Case report A 50-year-old man presented at another hospital with a history of sudden onset of frontal headache and visual impairment MRI revealed a heterogeneous nonenhancing 5 3 cm sellar mass that was isointense and slightly hyperintense relative to the brain parenchyma on T1-weighted and T2-weighted images, respectively. The mass also extended into the sphenoid sinus as well as the suprasellar recess, displacing the optic nerves superiorly (Fig. 1a). The MRI findings were consistent with haemorrhagic macroadenoma of the pituitary compressing the right optic nerve and chiasm and occluding the supraclinoid portion of the ICA (Fig. 1b). On the day of admission, the patient’s consciousness deteriorated progressively and he showed signs of herniation; he was then referred to our centre for further evaluation. On admission, the patient was in a coma, requiring ventilatory support. Neurological examination revealed left-sided pupillary dilation, no light reflex in the left pupil, extensor motor response on the left, and no response in the right extremities. CT was performed to assess the patient’s rapidly deteriorating neurological status, and revealed a nonenhancing heterogeneous sellar mass and massive infarction in the left ICA territory (Fig. 2). The patient underwent a large left frontotemporoparietal craniotomy, which revealed a brain edema and compression and elevation of the ICA by an encapsulated sellar mass. The capsule was punctured and a haemorrhagic tumour was completely removed. After removal of the tumour, the left ICA began to pulsate. The patient’s bone flap was not replaced, rather it was stored in a deep-freezer. Microscopic examination revealed the tumour to be
Fig. 1. (a) Sagittal T1-weighted MRI with contrast showing an unenhancing sellar mass with suprasellar and sphenoidal sinus extension. (b) Axial T1-weighted image without contrast showing an isointense sellar mass lesion that has occluded the left internal carotid artery (arrow).
482
Case Reports / Journal of Clinical Neuroscience 15 (2008) 480–483
Fig. 2. Preoperative axial unenhanced CT scan showing a hyperdense haemorrhagic sellar lesion with infarction of the left frontotemporal region.
Fig. 3. Photomicrograph of a tumour specimen obtained during surgery showing formed blood elements and round tumour cells with hyperchromatic nuclei (haematoxylin-eosin stain, 200).
haemorrhage. Haemorrhage may also occur in the absence of clinical features or with a subacute course, but the term apoplexy is properly reserved for those cases with an abrupt onset of typical symptoms and signs, that is, sudden headache, usually accompanied by nausea and vomiting.2,4 The headaches may be caused by pressure on the diaphragma sellae or irritation of the basal meninges.2,5 Suprasellar tumour expansion leads to compression of the visual apparatus, which may produce precipitous deterioration in visual acuity, reduction in visual fields or blindness.2,4 Less commonly, the optic tract can be compressed in a prefixed chiasm, resulting in a homonymous hemianopsia. Conversely, compression of the optic nerve in a postfixed chiasm can produce central scotoma, impaired
monocular visual acuity, and pain on eye movement. Hypothalamic involvement may also produce hypotension, disturbances of temperature regulation, cardiac and respiratory dysrhythmias, and diabetes insipidus. Less extensive haemorrhages might not lead to apoplexy, but might produce only a sudden drop in hormone levels.2 Various factors have been proposed as the precipitating events leading to pituitary apoplexy, including sudden trauma,6 use of bromocriptine,2 irradiation,2,6 hypertension,4 aspirin therapy,4 surgical procedures,7 neuroendocrinological manipulation,8 pregnancy,9 general anaesthesia10 and lumbar puncture.11 It has been suggested that the tendency to develop pituitary apoplexy may depend on the histological type of the adenoma. Apoplexy is thought to be more frequently associated with eosinophilic adenomas.12 The majority of adenomas undergoing apoplexy have been described as nonfunctional.1,4,13 Decreased visual acuity or visual field defects are the hallmarks of pituitary apoplexy.4 Also, upward enlargement of the adenoma can be extensive enough to compress the middle and anterior cerebral arteries, leading to focal ischaemic deficits.14,15 Lateral enlargement of the tumour into the cavernous sinuses may lead to extraocular ophthalmoplegia and ICA compression. Compression of the ICA, either in the cavernous sinus or in the supraclinoid portion, can cause hemispheric ischaemic deficits and altered consciousness.8,14–19 While signs of focal cerebral hemispheric dysfunction are uncommon in pituitary apoplexy, hemiplegia as the presenting sign is extremely unusual.8,14–20 The mechanism has been postulated to be cerebral ischaemia resulting either from mechanical obstruction of an intracranial artery by the enlarging mass, or mostly secondary to haemorrhage or spasm. Vasospasm could result from extravasation of blood from the pituitary tumour into the subarachnoid space and/or the interaction of a vasoactive agent released from the pituitary tumour into the hypothalamohypophyseal area.20,21 Mechanical obstruction of large cerebral arteries by pituitary expansion, with consequent hemiplegia and altered consciousness, has been previously described in only six cases.8,14–19 With an alert patient presenting with ophthalmoplegia in the absence of visual field deficit or impaired acuity, the surgical role is less clearly defined and many advocate conservative management.22 In patients who are stable or improving without diminished consciousness or signs of chiasmal or optic nerve compression, conservative management has also been suggested.8 Patients with severe visual or mental impairment or those with progressive deterioration and focal ischaemic deficit require urgent surgical decompression.2 Emergency transsphenoidal16,17 and transcranial decompression14,18 reportedly reverse visual compromise and restore ICA blood flow with varying clinical outcomes. Two of the six patients mentioned above were managed nonoperatively: one died15 and the other improved.8 Clark et al.8 suggested conservative treatment in patients with established infarcts at the time of presentation because of the risk of haemorrhagic transformation following decom-
Case Reports / Journal of Clinical Neuroscience 15 (2008) 483–486
pression, but they did not address how to manage raised ICP. We undertook a more radical decompressive approach for reduction of raised ICP, as early decompressive craniectomy has been reported to be associated with better outcomes in patients with cerebral artery infarction.23 4. Conclusion In patients with pituitary apoplexy who present with signs of raised ICP, a CT scan may provide additional clues about evolving intracranial pathologies and guide the choice of surgical approach. In cases with established cerebral infarcts, a transcranial approach not only provides decompression of the visual apparatus and ICA flow but also permits decompressive craniotomy for reducing elevated ICP. The present case demonstrates that pituitary apoplexy is a neurosurgical emergency that requires surgical intervention at the time of diagnosis. References 1. Bills DC, Meyer FB, Laws Jr ER, et al. A retrospective analysis of pituitary apoplexy. Neurosurgery 1993;33:602–69. 2. Cardoso ER, Peterson EW. Pituitary apoplexy: A Review. Neurosurgery 1984;14:363–73. 3. Wakai S, Fukushima T, Teramoto A, et al. Pituitary apoplexy: Its incidence and clinical significance. J Neurosurg 1981;55:187–93. 4. Randeva HS, Schoebel J, Byrne J, et al. Classical pituitary apoplexy: clinical features, management and outcome. Clin Endocrinol 1999;51:181–8. 5. David NJ, Gargano FP, Glaser JS. Pituitary apoplexy in clinical perspective. In: Glaser JS, Smith JL, editors. Neuro-ophthalmology VIII. St. Louis: Mosby; 1975. p. 140–65. 6. Ebersold MJ, Laws Jr ER, Scheithauer BW, et al. Pituitary apoplexy treated by transsphenoidal surgery. A clinicopathological and immunocytochemical study. J Neurosurg 1983;58:315–20. 7. Wiesmann M, Gliemroth J, Kehler U, et al. Pituitary apoplexy after cardiac surgery presenting as deep coma with dilated pupils. Acta Anaesthesiol Scand 1999;43:236–8.
483
8. Clark JD, Freer CE, Wheatley T. Pituitary apoplexy: an unusual cause of stroke. Clin Radiol 1987;38:75–7. 9. Onesti ST, Wisniewski T, Post KT. Clinical versus subclinical pituitary apoplexy: presentation, surgical mamagement, and outcome in 21 patients. Neurosurgery 1990;26:980–6. 10. Barber SG. Hypopituitarism and artificial ventilation. Acta Endocrinol 1979;90:211–6. 11. Symon L, Mohandy S. Hemorrhage in pituitary tumors. Acta Neurochir 1982;65:41–9. 12. Werner PL, Shah JH, Kukreja SC, et al. Recurrence of acromegaly after pituitary apoplexy. JAMA 1982;247:2816–8. 13. Semple PL, Webb MK, de Villiers JC, et al. Pituitary apoplexy Neurosurgery 2005;56:65–72. 14. Majchrzak H, Wencel T, Dragan T, et al. Acute hemorrhage into pituitary adenoma with subarachnoid hemorrhage and anterior cerebral artery occlusion. J Neurosurg 1983;58:771–3. 15. Schnitker KT, Lehnert HB. Apoplexy in a pituitary chromophobe adenoma producing the syndrome of middle cerebral artery thrombosis. J Neurosurg 1952;9:201–13. 16. Bernstein M, Hegele RA, Gentili F, et al. Pituitary apoplexy associated with a triple bolus test. J Neurosurg 1984;61:586–90. 17. Lath R, Rajshekhar V. Massive cerebral infarction as a feature of pituitary apoplexy. Neurol India 2001;49:191–3. 18. Rosenbaum TJ, Houser OW, Laws ER. Pituitary apoplexy producing internal carotid artery occlusion. Case report. J Neurosurg 1977;47:599–604. 19. Rodier G, Meotien Y, Battaglia F, et al. Bilateral stroke secondary to pitıitary apoplexy. J Neurol 2003;250:491–5. 20. Pozzati E, Frank G, Nasi MT, et al. Pituitary apoplexy, bilateral carotid vasospasm, and cerebral infarction in a 15-year-old boy. Neurosurgery 1987;20:56–9. 21. Cardoso ER, Peterson EW. Pituitary apoplexy and vasospasm. Surg Neurol 1983;20:391–5. 22. Thompson D, Powell M, Foster O. Atypical presentation of vascular events in pituitary tumors: ‘‘non-apoplectic” pituitary apoplexy. J Neurol Neurosurg Psychiatry 1994;57:1441–2. 23. Cho D-Y, Chen T-C, Lee H-C. Ultra-early decompressive craniectomy for malignant middle cerebral artery infarction. Surg Neurol 2003;60:227–33.
doi:10.1016/j.jocn.2006.08.020
Evacuation of a 14-vertebral-level cervico-thoracic epidural abscess and review of surgical options for extensive spinal epidural abscesses M. Payer a,*, H. Walser b a
Spine and Pain Clinic Zu¨rich, Witellikerstrasse 40, 8008, Zu¨rich, Switzerland b Neurology Center Hirslanden, Zu¨rich, Switzerland Received 17 November 2006; accepted 17 December 2006
*
Corresponding author. Tel.: +044 387 37 41; fax: +044 387 37 45. E-mail addresses: [email protected] (M. Payer).