DOCSLIB.ORG

Tumors of the Pituitary Gland

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Tumors of the Pituitary Gland CHAPTER 31 Tumors of the Pituitary Gland John W. Gittinger, Jr. ANATOMY OF THE PITUITARY COMPLEX PITUITARY CARCINOMA PITUITARY ADENOMAS METASTASES TO THE SELLA TURCICA AND PITUITARY General Considerations GLAND Types of Pituitary Adenomas MIMICS OF PITUITARY ADENOMAS Ophthalmic Manifestations of Pituitary Tumors PITUITARY ABSCESS Treatment of Pituitary Adenomas Hypophysitis Visual Prognosis in Patients with Pituitary Adenomas Tumors of the pituitary gland are so important from a histopathologic features of pituitary tumors, the clinical pre- neuro-ophthalmologic standpoint that they are considered in sentations of patients with pituitary tumors, the various a separate chapter. In this chapter, we discuss the normal modes of treatment of pituitary tumors, and the prognosis anatomy of the pituitary endocrine unit, the endocrine and in patients with various types of pituitary tumors. ANATOMY OF THE PITUITARY COMPLEX The hypophysis cerebri or pituitary gland lies at the weighs about 0.6 g, and may double in size during pregnancy base of the brain below the third ventricle nestled in a (1). The larger anterior lobe or glandular portion is the ade- ‘‘Turkish saddle’’ (sella turcica) of bone that is part of nohypophysis; the posterior lobe or neural portion is the the body of the sphenoid. Lying above the pituitary is a neurohypophysis. The hormones of the neurohypophysis are sheet of dura, the diaphragma sellae, that connects the oxytocin and vasopressin. Those of the adenohypophysis are clinoid attachments of the tentorium cerebelli. This is discussed below. The adenohypophysis is derived from an perforated by a hole that allows the infundibular stem or evagination of stomodeal ectoderm called Rathke’s pouch, stalk of the neural portion of the gland to connect to the remnants of which are thought to give rise to craniopharyngi- hypothalamus (Fig. 31.1). omas. Adenohypophyseal cells give rise to pituitary adeno- .mm, mas and the much rarer pituitary carcinomas 6 ן 9 ן The gland itself normally measures 12 PITUITARY ADENOMAS GENERAL CONSIDERATIONS especially the chiasm, and the ocular motor cranial nerves The characteristic pituitary tumor is the adenoma. Uncom- in the cavernous sinus (Fig. 31.2 mon in children (2), its incidence increases with age and may TYPES OF PITUITARY ADENOMAS approach 30% in an older population (3). Pituitary adenomas constitute 6–12% of all symptomatic intracranial tumors Pituitary adenomas are arbitrarily grouped by size into (4,5). Most are sporadic, but pituitary adenomas are a com- microadenomas (less than 10 mm in greatest diameter) and ponent of multiple endocrine neoplasia type 1, a familial macroadenomas. They are also classified according to their endocrine cancer syndrome characterized by primary hyper- secretory function, although a single tumor may secrete more parathyroidism, endocrine enteropancreatic tumors, and ad- than one hormone. Many tumors that secrete hor- renocortical and thymic/bronchial neuroendocrine tumors mones—prolactin, growth hormone (somatotrophin), adre- (6). As a pituitary adenoma grows and extends beyond the nocorticotropic hormone (ACTH or corticotrophin), and thy- sella turcica, it may then impinge upon the visual pathways, roid-stimulating hormone (TSH)—present clinically as 1531 1532 CLINICAL NEURO-OPHTHALMOLOGY Figure 31.1. The location of the pituitary gland. A, Schematic drawing showing the relationship of the pituitary gland to the intracranial optic nerve (ON) and chiasm (C). The heavily stippled portion of the gland is the adenohypophysis; the lightly stippled portion is the neurohypophysis. The arrows point to the diaphragma sellae. B, A postmortem specimen cut midsagittally through the pituitary gland, showing its relationships. (From Renn WH, Rhoton AL Jr. Microsurgical anatomy of the sellar region. J Neurosurg 1975;43Ϻ288–298.) Figure 31.2. Coronal section through the pituitary gland, showing its relationship to the optic chiasm, internal carotid arteries, sphenoid sinus, and cavernous sinuses. The open white arrows on the right side of photograph indicate the boundaries of the cavernous sinus. The open white arrows on the left side of photograph outline the boundaries of cranial nerves. 3, oculomotor nerve; 4, trochlear nerve; VI, ophthalmic division of the trigeminal nerve; VII, maxillary division of the trigeminal nerve; 6, abducens nerve; V.N., vidian nerve. (Courtesy of Dr. William F. Hoyt.) TUMORS OF THE PITUITARY GLAND 1533 endocrinopathies. As a result, secreting tumors are often di- enous hypercortisolism, the differential of which remains a agnosed while still microadenomas. clinical challenge (16). Nonsecreting tumors are usually recognized when they Cushing’s disease, a disorder much more common in have grown large enough to produce visual symptoms or women than men, refers to excess secretion of ACTH by a headache, thus tending to present as macroadenomas. By the pituitary adenoma that results in secondary adrenal hyperpla- mid-1990s, these nonfunctional tumors represented about sia and hypercortisolism. The majority of persons not taking 10% of clinically diagnosed pituitary adenomas (7). The corticosteroids with Cushing’s syndrome have Cushing’s widespread use of imaging has led to the discovery of silent disease, but significant minorities have adrenocortical or microadenomas, termed ‘‘incidentalomas’’ (8), measuring other tumors, especially small cell carcinoma of the lung, as small as 2–3 mm and present in 10–20% of the general that secrete ACTH (17). population (9). The prevalence of microadenomas at autopsy When adenomas were difficult to detect prior to modern may be as high as 30%. The imaging procedure of choice neuroimaging, many patients underwent bilateral adrenalec- in the detection of parasellar tumors, including pituitary ade- tomies for their Cushing’s disease. Freed from the restraint nomas, is high-field magnetic resonance (MR) imaging per- of hypercortisolism on corticotropin secretion and tumor formed both with and without gadolinium (10). growth, such patients often develop progressive cutaneous melanosis (Nelson’s syndrome) (18). In about 30% of per- Prolactin-Secreting Adenomas sons with Nelson’s syndrome, a large aggressive pituitary tumor is eventually recognized (7). Galactorrhea is normal following pregnancy. When women who have not recently been pregnant develop galac- Somatotroph (Growth Hormone-Secreting) Adenomas torrhea, its is most often caused by a prolactin-secreting ade- noma. Such tumors account for about 40% of all pituitary Growth hormone-secreting tumors cause acromegaly and tumors (11). Galactorrhea, in this setting, is frequently asso- giantism. Most such tumors are pituitary adenomas, but ec- ciated with amenorrhea (Forbes-Albright syndrome). Be- topic acromegaly from growth hormone-secreting carcinoid cause the prolactinomas are usually small, there are no visual or pancreatic islet cell tumors also stimulates pituitary hyper- symptoms or signs. plasia that mimics an adenoma on imaging studies (19,20). Normal serum prolactin levels are below 25 ng/mL in The differential diagnosis is made even more difficult be- women and below 20 ng/mL in men. Levels increase 10- cause both neuroendocrine tumors and pituitary adenomas fold in pregnancy. Adenomas that do not secrete prolactin are features of multiple endocrine neoplasia type 1 (21). and other parasellar processes may compress the pituitary Because the characteristic coarsening of facial features stalk, decreasing the normal dopaminergic inhibition and and other bodily changes—enlargement of the hands and increasing prolactin secretion. In this instance, the serum feet (the literal meaning of ‘‘acromegaly’’), hirsutism, der- prolactin level is only moderately elevated. Other, nonneo- mopathy, and hypertrophic arthropathy—are gradual, they plastic causes of moderately elevated prolactin levels include may not be noticed until far advanced. Review of old photo- pregnancy, medications that affect dopamine metabolism graphs may reveal evolution of acromegaly over a decade (e.g., phenothiazines, metoclopramide, risperidone, vera- or more (Fig. 31.3). Proximal myopathy and carpal tunnel pamil), renal failure, and primary hypothyroidism (12). Pro- syndromes are sometimes the first clinical manifestations lactinomas are generally associated with prolactin levels (22), and headaches, not necessarily related to tumor growth, above 200 ng/mL and, in some cases, exceed 10,000 ng/mL. are common. Diabetes is observed in persons with acromeg- Pregnancy may result in enlargement of a prolactin-secret- aly because of growth hormone’s effects on insulin recep- ing adenoma, but the risk of visual loss during pregnancy tors, as are hypertension and premature vascular disease. from a microadenoma is low (13). In contrast to pregnant As it is harder to recognize the dysmorphic changes asso- women with known macroadenomas, where formal visual ciated with excessive growth hormone than galactorrhea or fields should probably be obtained at least once a trimester, the stigmata of Cushing’s syndrome, somatotroph adenomas women with microadenomas do not require routine field test- are less often detected as microadenomas. The frequency of ing during pregnancy (14). suprasellar extension and visual field defects in somatotroph Men with prolactinomas become impotent and infertile. adenomas is therefore intermediate between prolactin- and They may be obese with gynecomastia but do not usually corticotropin-secreting tumors and nonsecreting adenomas have galactorrhea. Because the
Load more

Recommended publications
  • An Unusual Presentation of Subfrontal Meningioma: a Case Report and Literature Review for Foster Kennedy Syndrome
    Intern Emerg Med (2011) 6:267–269 DOI 10.1007/s11739-010-0437-y CE - MEDICAL ILLUSTRATION An unusual presentation of subfrontal meningioma: a case report and literature review for Foster Kennedy syndrome Shahram Lotfipour • Kris Chiles • J. Akiva Kahn • Tareg Bey • Scott Rudkin Received: 17 December 2009 / Accepted: 13 July 2010 / Published online: 26 August 2010 Ó SIMI 2010 Introduction head trauma. She admitted to abusing crack cocaine for 13 years with her last use 4 months ago. She denied any Foster Kennedy syndrome, named after neurologist Robert trouble with ambulation, dizziness, and changes in hearing or Foster Kennedy (1884–1952), describes unilateral ipsilat- other alterations in sensation. She denied any suicidal or eral optic atrophy and contralateral papilledema from an homicidal ideation. The patient denied any auditory halluci- intracranial mass. This syndrome is unreliably associated nations, but did report that she had been experiencing with anosmia and ipsilateral proptosis [1]. It originates visual hallucinations and visual disturbances for at least from variety of intracranial pathologies, but most often a 6–8 months. She reported complete blindness in the left eye, subfrontal mass. We present a case of Foster Kennedy and shadow perception in her right for an unknown length of syndrome and review its etiology, pathology and incidence time. Her past medical history was notable for major in intracranial tumors. depression. The patient did not have a previous history of hallucinations or psychosis, and had never been hospitalized for psychiatric reasons. The patient was not on any medica- Case report tions, and was allergic to penicillin and codeine.
    [Show full text]
  • HYPOPITUITARISM YOUR QUESTIONS ANSWERED Contents
    PATIENT INFORMATION HYPOPITUITARISM YOUR QUESTIONS ANSWERED Contents What is hypopituitarism? What is hypopituitarism? 1 What causes hypopituitarism? 2 The pituitary gland is a small gland attached to the base of the brain. Hypopituitarism refers to loss of pituitary gland hormone production. The What are the symptoms and signs of hypopituitarism? 4 pituitary gland produces a variety of different hormones: 1. Adrenocorticotropic hormone (ACTH): controls production of How is hypopituitarism diagnosed? 6 the adrenal gland hormones cortisol and dehydroepiandrosterone (DHEA). What tests are necessary? 8 2. Thyroid-stimulating hormone (TSH): controls thyroid hormone production from the thyroid gland. How is hypopituitarism treated? 9 3. Luteinizing hormone (LH) and follicle-stimulating hormone (FSH): LH and FSH together control fertility in both sexes and What are the benefits of hormone treatment(s)? 12 the secretion of sex hormones (estrogen and progesterone from the ovaries in women and testosterone from the testes in men). What are the risks of hormone treatment(s)? 13 4. Growth hormone (GH): required for growth in childhood and has effects on the entire body throughout life. Is life-long treatment necessary and what precautions are necessary? 13 5. Prolactin (PRL): required for breast feeding. How is treatment followed? 14 6. Oxytocin: required during labor and delivery and for lactation and breast feeding. Is fertility possible if I have hypopituitarism? 15 7. Antidiuretic hormone (also known as vasopressin): helps maintain normal water Summary 15 balance. What do I need to do if I have a pituitary hormone deficiency? 16 Glossary inside back cover “Hypo” is Greek for “below normal” or “deficient” Hypopituitarism may involve the loss of one, several or all of the pituitary hormones.
    [Show full text]
  • A Radiologic Score to Distinguish Autoimmune Hypophysitis from Nonsecreting Pituitary ORIGINAL RESEARCH Adenoma Preoperatively
    A Radiologic Score to Distinguish Autoimmune Hypophysitis from Nonsecreting Pituitary ORIGINAL RESEARCH Adenoma Preoperatively A. Gutenberg BACKGROUND AND PURPOSE: Autoimmune hypophysitis (AH) mimics the more common nonsecret- J. Larsen ing pituitary adenomas and can be diagnosed with certainty only histologically. Approximately 40% of patients with AH are still misdiagnosed as having pituitary macroadenoma and undergo unnecessary I. Lupi surgery. MR imaging is currently the best noninvasive diagnostic tool to differentiate AH from V. Rohde nonsecreting adenomas, though no single radiologic sign is diagnostically accurate. The purpose of this P. Caturegli study was to develop a scoring system that summarizes numerous MR imaging signs to increase the probability of diagnosing AH before surgery. MATERIALS AND METHODS: This was a case-control study of 402 patients, which compared the presurgical pituitary MR imaging features of patients with nonsecreting pituitary adenoma and controls with AH. MR images were compared on the basis of 16 morphologic features besides sex, age, and relation to pregnancy. RESULTS: Only 2 of the 19 proposed features tested lacked prognostic value. When the other 17 predictors were analyzed jointly in a multiple logistic regression model, 8 (relation to pregnancy, pituitary mass volume and symmetry, signal intensity and signal intensity homogeneity after gadolin- ium administration, posterior pituitary bright spot presence, stalk size, and mucosal swelling) remained significant predictors of a correct classification. The diagnostic score had a global performance of 0.9917 and correctly classified 97% of the patients, with a sensitivity of 92%, a specificity of 99%, a positive predictive value of 97%, and a negative predictive value of 97% for the diagnosis of AH.
    [Show full text]
  • Synchronous Morphologically Distinct Craniopharyngioma and Pituitary
    orders & is T D h e n r Bhatoe et al., Brain Disord Ther 2016, 5:1 i a a p r y B Brain Disorders & Therapy DOI: 10.4172/2168-975X.1000207 ISSN: 2168-975X Case Report Open Access Synchronous Morphologically Distinct Craniopharyngioma and Pituitary Adenoma: A Rare Collision Entity Harjinder S Bhatoe*, Prabal Deb and Sudip Kumar Sengupta Institute of Neuroscience, Max Super Speciality Hospital, New Delhi, India Abstract While pituitary tumors and craniopharyngiomas share a common lineage, their simultaneous occurrence is distinctly rare. We present one such patient, an adult male with two distinct tumors, that were excised by two different approaches. Relevant literature is briefly reviewed. Keywords: Brain tumor; Collision tumor; Craniopharyngioma; Pituitary tumor Introduction Simultaneous occurrence of morphological distinct, discreet intracranial tumors sharing the same cell lineage is a rarity. Pituitary tumors and craniopharyngiomas share a common lineage. Simultaneous occurrence of these two tumors in the same patient is rare and has been reported only nine times so far (Table 1). While pituitary tumours are centred in the sella, craniopharyngiomas may occur anywhere from the pituitary gland to the third ventricle. Association of intra-third ventricular craniopharyngioma and growth hormone- Figure 1: Contrast MRI (T1-weighted sagittal) showing intra-third-ventricular secreting pituitary macroadenoma as two distinct, unconnected tumors craniopharyngioma and pituitary adenoma. occurring synchronously has not been reported so far. Case Report A 35-year-old male was admitted with six-month-history of generalized headache, gradual loss of vision and intermittent generalized tonic clonic seizures. Clinically, he had acromegaly and optic atrophy with no perception of light.
    [Show full text]
  • From Isolated GH Deficiency to Multiple Pituitary Hormone
    European Journal of Endocrinology (2009) 161 S75–S83 ISSN 0804-4643 From isolated GH deficiency to multiple pituitary hormone deficiency: an evolving continuum – a KIMS analysis M Klose, B Jonsson1, R Abs2, V Popovic3, M Koltowska-Ha¨ggstro¨m4, B Saller5, U Feldt-Rasmussen and I Kourides6 Department of Medical Endocrinology, Copenhagen University Hospital, PE2131, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark, 1Department of Women’s and Children’s Health, Uppsala University, SE-75185 Uppsala, Sweden, 2Department of Endocrinology, University of Antwerp, Antwerp, Belgium, 3Neuroendocrine Unit, Institute of Endocrinology, University Clinical Center Belgrade, Belgrade, Serbia, 4KIMS Medical Outcomes, Pfizer Endocrine Care, Sollentuna, Sweden, 5Pfizer Endocrine Care Europe, Tadworth, UK and 6Global Endocrine Care, Pfizer Inc., New York, New York 10017, USA (Correspondence should be addressed to M Klose; Email: [email protected]) Abstract Objective: To describe baseline clinical presentation, treatment effects and evolution of isolated GH deficiency (IGHD) to multiple pituitary hormone deficiency (MPHD) in adult-onset (AO) GHD. Design: Observational prospective study. Methods: Baseline characteristics were recorded in 4110 patients with organic AO-GHD, who were GH naı¨ve prior to entry into the Pfizer International Metabolic Database (KIMS; 283 (7%) IGHD, 3827 MPHD). The effect of GH replacement after 2 years was assessed in those with available follow-up data (133 IGHD, 2207 MPHD), and development of new deficiencies in those with available data on concomitant medication (165 IGHD, 3006 MPHD). Results: IGHD and MPHD patients had similar baseline clinical presentation, and both groups responded similarly to 2 years of GH therapy, with favourable changes in lipid profile and improved quality of life.
    [Show full text]
  • Pituitary Adenomas and Ophthalmology
    1 Pituitary Adenomas and Ophthalmology Santiago Ortiz-Perez and Bernardo Sanchez-Dalmau Hospital Clinic, University of de Barcelona, Ophthalmology department Spain 1. Introduction Pituitary gland, also called hypophysis, is a neuroendocrine organ placed in the “sella turcica” in the skull base. This gland consists of 2 main areas, the anterior and medial part constitute the adenohypophysis, the posterior part is called neurohypophysis. Pituitary gland is in charge of the internal constancy, homeostasis and reproductive function; this is why pituitary abnormalities cause a wide spectrum of signs and symptoms. Pituitary adenomas are a common pathology; they represent about 10% of all intracranial tumours and between 50-80% of pituitary tumours. Necropsy and imaging studies estimate an incident of 20-25% of pituitary adenomas in general population; however, only about 1/3 of them are clinically evident (Asa & Ezzat, 2009). The majority of these tumours have monoclonal origin (mutation of a single gonadotropic cell), but there are still some discrepancies about the pathogenesis of these neoplasms. The most common mutations seem in other human neoplasms are not frequent in pituitary adenomas, and only a minimum proportion of them are associated to other genetic disorders, such as MEN1 syndrome (multiple endocrine neoplasms type 1) or the Carney complex, due to mutations of the genes MEN1 and PRKAR1A (protein kinase A regulatory subunit 1A) respectively (Beckers & Daly, 2007). Hormones and growth factors involve in normal pituitary function can be also related to the growth of these tumours, although evident connection with the pathogenesis has not been demonstrated. Symptoms related to pituitary tumours are secondary to several factors.
    [Show full text]
  • Annual Report Research Activity 2019
    Annual Report Research Activity 2019 Division of Clinical Neuroscience University of Oslo and Oslo University Hospital 0 Contents Oslo University Hospital and the University of Oslo .................................................................................... 4 From Division Director Eva Bjørstad ........................................................................................................... 4 Division of Clinical Neuroscience (NVR) Organizational Chart ..................................................................... 5 Department of Physical Medicine and Rehabilitation Rehabilitation after trauma....................................................................................................................... 6 Group Leader: Nada Andelic Painful musculoskeletal disorders .............................................................................................................. 9 Group Leader: Cecilie Røe Department of Refractory Epilepsy - National Centre for Epilepsy Complex epilepsy .................................................................................................................................... 11 Group Leader: Morten Lossius Department of Neurosurgery Neurovascular-Hydrocephalus Research Group ..................................................................................... 16 Group Leader: Per Kristian Eide Oslo Neurosurgical Outcome Study Group (ONOSG) ................................................................................. 19 Group Leaders: Eirik Helseth and Torstein
    [Show full text]
  • Clinical Characteristics of Pain in Patients with Pituitary Adenomas
    C Dimopoulou and others Pain in patients with 171:5 581–591 Clinical Study pituitary adenomas Clinical characteristics of pain in patients with pituitary adenomas C Dimopoulou1, A P Athanasoulia1,3, E Hanisch1, S Held1, T Sprenger2,4,5, T R Toelle2, J Roemmler-Zehrer3, J Schopohl3, G K Stalla1 and C Sievers1 1Department of Endocrinology, Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany, Correspondence 2Department of Neurology, Technische Universita¨ tMu¨ nchen, Munich, Germany, 3Medizinische Klinik und Poliklinik should be addressed IV, Ludwig-Maximilians-University, Munich, Germany, 4Department of Neurology, University Hospital Basel, Basel, to C Sievers Switzerland and 5Division of Neuroradiology, Department of Radiology, University Hospital Basel, Basel, Email Switzerland [email protected] Abstract Objective: Clinical presentation of pituitary adenomas frequently involves pain, particularly headache, due to structural and functional properties of the tumour. Our aim was to investigate the clinical characteristics of pain in a large cohort of patients with pituitary disease. Design: In a cross-sectional study, we assessed 278 patients with pituitary disease (nZ81 acromegaly; nZ45 Cushing’s disease; nZ92 prolactinoma; nZ60 non-functioning pituitary adenoma). Methods: Pain was studied using validated questionnaires to screen for nociceptive vs neuropathic pain components (painDETECT), determine pain severity, quality, duration and location (German pain questionnaire) and to assess the impact of pain on disability (migraine disability assessment, MIDAS) and quality of life (QoL). Results: We recorded a high prevalence of bodily pain (nZ180, 65%) and headache (nZ178, 64%); adrenocorticotropic adenomas were most frequently associated with pain (nZ34, 76%). Headache was equally frequent in patients with macro- and microadenomas (68 vs 60%; PZ0.266).
    [Show full text]
  • Incidental Pituitary Adenomas
    Neurosurg Focus 31 (6):E18, 2011 Incidental pituitary adenomas WALAVAN SIVAKUMAR, M.D.,1 ROUKOZ CHAMOUN, M.D.,1 VINH NGUYEN, M.D.,2 AND WILLIAM T. COULdwELL, M.D., PH.D.1 Departments of 1Neurosurgery and 2Radiology, University of Utah, Salt Lake City, Utah Object. Pituitary incidentalomas are a common finding with a poorly understood natural history. Over the last few decades, numerous studies have sought to decipher the optimal evaluation and treatment of these lesions. This paper aims to elucidate the current evidence regarding their prevalence, natural history, evaluation, and management. Methods. A search of articles on PubMed (National Library of Medicine) and reference lists of all relevant ar- ticles was conducted to identify all studies pertaining to the incidence, natural history, workup, treatment, and follow- up of incidental pituitary and sellar lesions, nonfunctioning pituitary adenomas, and incidentalomas. Results. The reported prevalence of pituitary incidentalomas has increased significantly in recent years. A com- plete history, physical, and endocrinological workup with formal visual field testing in the event of optic apparatus involvement constitutes the basics of the initial evaluation. Although data regarding the natural history of pituitary incidentalomas remain sparse, they seem to suggest that progression to pituitary apoplexy (0.6/100 patient-years), visual field deficits (0.6/100 patient-years), and endocrine dysfunction (0.8/100 patient-years) remains low. In larger lesions, apoplexy risk may be higher. Conclusions. While the majority of pituitary incidentalomas can be managed conservatively, involvement of the optic apparatus, endocrine dysfunction, ophthalmological symptoms, and progressive increase in size represent the main indications for surgery.
    [Show full text]
  • References Briskly Compared with the Fellow Eye
    LETTERS TO THE JOURNAL 367 frontal tumour. The optic atrophy is commonly felt to Sir, result from optic nerve compression and the contralateral Apraclonidine in the Management of Glaucomatocy­ 1.2 papilloedema from increased intracranial pressure. clitic crisis Another mechanism suggests that Foster Kennedy syn­ Glaucomatocyclitic cnSlS (Posner-Schlossman syn­ drome is due to bilateral direct optic nerve compression by drome) is a unilateral inflammation of the uveal tract in a midline basal mass or less commonly by long-standing which signs of an acute increase in intraocular pressure increased intracranial pressure without direct com­ predominate. As the aetiology is doubtful, numerous treat­ pression of either nerve.3 ments have been suggested, the main aim being to reduce Since the early cases of Foster Kennedy syndrome, the exceptionally high intraocular pressure which, left many cases have been reported in the literature caused by untreated, will cause permanent optic nerve damage. other tumours, especially meningiomas such as olfactory Apraclonidine hydrochloride I %, a clonidine deriva­ groove and sphenoid ridge meningiomas, with gliomas tive and a peripheral alpha-adrenergic agonist. was devel­ occasionally reported.�-7 To our knowledge, nasopharyn­ oped to lower intraocular pressure while minimising geal carcinoma is rarely reported in the literature as a systemic side effects. It has specificrecept or-binding and cause of Foster Kennedy syndrome. physico chemical properties that limit its access to the cen­ Other terms have been used in the literature to describe tral nervous system. In normal human volunteers it pro­ atypical cases of Foster Kennedy syndrome. 'Pseudo Fos­ duces a significant fall in intraocular pressure.
    [Show full text]
  • Pituitary Disease Handbook for Patients Disclaimer This Is General Information Developed by the Ottawa Hospital
    The Ottawa Hospital Divisions of Endocrinology and Metabolism and Neurosurgery Pituitary Disease Handbook for Patients Disclaimer This is general information developed by The Ottawa Hospital. It is not intended to replace the advice of a qualified health-care provider. Please consult your health-care provider who will be able to determine the appropriateness of the information for your specific situation. Prepared by Monika Pantalone, NP Advanced Practice Nurse for Neurosurgery With guidance from Dr. Charles Agbi, Dr. Erin Keely, Dr. Janine Malcolm and The Ottawa Hospital pituitary patient advisors P1166 (10/2014) Printed at The Ottawa Hospital Outline This handbook is designed to help people who have pituitary tumours better understand their disease. It contains information to help people with pituitary tumours discuss their care with health care providers. This booklet provides: 1) An overview of what pituitary tumours are and how they are grouped 2) An explanation of how pituitary tumours are investigated 3) A description of available treatments for pituitary tumours What is the Pituitary Gland? The pituitary gland is a pea size organ located just behind the bridge of the nose at the base of the brain, in a bony pouch called the “sella turcica.” It sits just below the nerves to the eyes (the optic chiasm). The pituitary gland is divided into two main portions: the larger anterior pituitary (at the front) and the smaller posterior pituitary (at the back). Each of these portions has different functions, producing different types of hormones. Optic Pituitary Hypothalamus tumor chiasm Pituitary stalk Anterior Sphenoid pituitary gland sinus Posterior pituitary gland Sella Picture provided by turcica pituitary.ucla.edu 1 The pituitary gland is known as the “master gland” because it helps to control the secretion of various hormones from a number of other glands including the thyroid gland, adrenal glands, testes and ovaries.
    [Show full text]
  • Multiple Endocrine Neoplasia Type 1 (MEN1)
    Lab Management Guidelines v2.0.2019 Multiple Endocrine Neoplasia Type 1 (MEN1) MOL.TS.285.A v2.0.2019 Introduction Multiple Endocrine Neoplasia Type 1 (MEN1) is addressed by this guideline. Procedures addressed The inclusion of any procedure code in this table does not imply that the code is under management or requires prior authorization. Refer to the specific Health Plan's procedure code list for management requirements. Procedures addressed by this Procedure codes guideline MEN1 Known Familial Mutation Analysis 81403 MEN1 Deletion/Duplication Analysis 81404 MEN1 Full Gene Sequencing 81405 What is Multiple Endocrine Neoplasia Type 1 Definition Multiple Endocrine Neoplasia Type 1 (MEN1) is an inherited form of tumor predisposition characterized by multiple tumors of the endocrine system. Incidence or Prevalence MEN1 has a prevalence of 1/10,000 to 1/100,000 individuals.1 Symptoms The presenting symptom in 90% of individuals with MEN1 is primary hyperparathyroidism (PHPT). Parathyroid tumors cause overproduction of parathyroid hormone which leads to hypercalcemia. The average age of onset is 20-25 years. Parathyroid carcinomas are rare in individuals with MEN1.2,3,4 Pituitary tumors are seen in 30-40% of individuals and are the first clinical manifestation in 10% of familial cases and 25% of simplex cases. Tumors are typically solitary and there is no increased prevalence of pituitary carcinoma in individuals with MEN1.2,5 © eviCore healthcare. All Rights Reserved. 1 of 9 400 Buckwalter Place Boulevard, Bluffton, SC 29910 (800) 918-8924 www.eviCore.com Lab Management Guidelines v2.0.2019 Prolactinomas are the most commonly seen pituitary subtype and account for 60% of pituitary adenomas.
    [Show full text]