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Pituitary adenoma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

Synonyms and keywords:: Pituitary macroadenoma; Pituitary microadenoma; Pituitary adenomas, Adenoma of the pituitary gland; Pituitary non-functioning adenoma; Gonadotropic adenoma; Thyrotropic adenoma; TSH-oma; Plurihormonal pituitary adenoma; Null cell adenomas

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

Overview

Pituitary adenomas are tumors that occur in the pituitary gland and account for about 10% of intracranial neoplasms. Pituitary adenomas are often remain undiagnosed. Small pituitary adenoms are found in 6 to 24 percent of adults at autopsy. Pituitary adenomas arise within the anterior lobe (adenohypophysis) of the gland. Pituitary adenomas may be classified according to the size of the adenoma and type of hormone secretion. Pituitary adenomas subtypes include corticotrophic, somatotrophic, thyrotrophic, gonadotrophic, and lactrotrophic adenomas. Adenomas less than 10mm are called microadenomas. There are no established causes for pituitary adenoma. Patients with pituitary adenoma may progress to develop lethargy, headache, nausea, and vomiting. Common complications of pituitary adenoma include bitemporal hemianopia, anosmia, acromegaly, gigantism, and Cushing’s syndrome. Prognosis is generally good, and approximately 18% of patients with macroadenoma require further treatment. Pharmacologic medical therapy is recommended among patients with prolactinoma, thyrotrophic, somatotrophic, and adrenocorticotropic adenomas. The transsphenoidal microsurgical approach is the mainstay of treatment for growth hormone-(GH) producing adenomas, adrenocorticotropic hormone-(ACTH) producing adenomas, and macroadenomas.

Historical Perspective

Pituitary adenoma was first described by Pierre Marie, a French neurologist in 1886.[1]

Classification

Congenital adrenal hyperplasia due to 21-hydroxylase deficiency may be classified into several subtypes based on severity, time of onset (mild, moderate, and severe), and the presence of virilization (stage I to stage V).

Pathophysiology

On gross pathology, a well circumscribed suprasellar mass is a characteristic finding of pituitary adenoma. On microscopic histopathological analysis, a monomorphic expansion of usually one cell type with lack of reticulin network among neoplastic cells is a characteristic finding of pituitary adenoma.

Causes

There are no established causes for pituitary adenoma.

Differential Diagnosis

Pituitary adenoma must be differentiated from other diseases such as craniopharyngioma, meningioma, arachnoid cyst, and pituitary carcinoma.

Epidemiology and Demographics

The prevalence of pituitary adenoma is approximately 100 per 100,000 individuals worldwide. In the USA, the incidence pituitary adenoma is approximately 3.12 per 100,000 individuals.

Risk Factors

The most potent risk factor in the development of pituitary adenoma is a positive family history of either pituitary tumor, multiple endocrine neoplasia type 1 (MEN1), or McCune-Albright syndrome.

Pituitary adenoma natural history, complications, and prognosis

Patients with pituitary adenoma may progress to develop lethargy, headache, nausea, and vomiting. Common complications of pituitary adenoma include bitemporal hemianopia , anosmia, acromegaly, gigantism, and Cushing’s syndrome. Prognosis is generally good, and approximately 18% of patients with macroadenoma require further treatment.

Diagnosis

Staging

According to the American Joint Committee on Cancer classification and staging system for pituitary tumors, there is no staging system available for pituitary adenoma.[2]

History and Symptoms

The hallmark of pituitary adenoma is increased intracranial pressure. A positive history of visual field defect, headache, and menstrual irregularities is suggestive of pituitary adenoma. The most common symptoms of pituitary adenoma include galactorrhea, oligomenorrhea , erectile dysfunction, and loss of libido.

Physical Examination

The presence of altered mental status, nausea, lethargy, and visual filed defect (bitemporal hemianopsia) on physical examination is suggestive of pituitary adenoma.

Laboratory Findings

Laboratory findings consistent with the diagnosis of pituitary adenoma include elevated serum prolactin level and elevated or decreased serum levels of other pituitary hormones.

CT

On head CT scan may be helpful in the diagnosis of pituitary adenoma. Findings on CT scan suggestive of pituitary adenoma include a large suprasellar mass that invades surrounding structures, calcification, and rarely hemorrhage.

MRI

On brain MRI, pituitary adenoma is characterized by a large mass with heterogeneous signal. Other findings may include remodeling of the floor of the sella and deviation of the pituitary infundibulum to the opposite side.

Other Imaging Studies

Historically, before the advent of MRI, lateral skull x-rays were performed to look for remodelling of the pituitary fossa.[3]

Other Diagnostic Studies

Inferior petrosal sinus sampling may be performed to detect hormonally active pituitary microadenoma.

Treatment

Medical Therapy

Pharmacologic medical therapy is recommended among patients with prolactinoma, thyrotrophic, somatotrophic, and adrenocorticotropic adenomas.

Surgery

The transsphenoidal microsurgical approach is the mainstay of treatment for growth hormone-(GH) producing adenomas, adrenocorticotropic hormone-(ACTH) producing adenomas, and macroadenomas.

Primary Prevention

There are no primary preventive measures available for pituitary adenoma.

Secondary Prevention

Secondary prevention strategies following pituitary adenoma include a regular check up of pituitary hormones serum levels and regular neuro-ophthalmic examination.

References

  1. ↑ Marie P. Hyertrophie singuliere non congenital des extremites superieures, inferieures et cephalique. Rev Medicine. 1886;6:297–333.
  2. ↑ Pituitary adenoma (2015). http://www.cancer.gov/types/pituitary/hp/pituitary-treatment-pdq#section/_96. Accessed on 9/28/2015. Invalid parameter “cancer” in <ref> tag. The supported parameters are: dir, follow, group, name.
  3. ↑ Pituitary Microadenoma. Dr Amir Rezaee and Dr Frank Gaillard. Radiopaedia.org 2015. http://radiopaedia.org/articles/pituitary-microadenoma

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

Overview

Pituitary adenoma was first described by Pierre Marie, a French neurologist in 1886.[1]

Historical Perspective

Pituitary adenoma was first described by Pierre Marie, a French neurologist in 1886.[1]

References

  1. ↑ 1.0 1.1 Marie P. Hyertrophie singuliere non congenital des extremites superieures, inferieures et cephalique. Rev Medicine. 1886;6:297–333.

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

Overview

Pituitary adenoma may be classified according to the size of the adenoma and type of hormone secretion, subtypes include corticotrophic, somatotrophic, thyrotrophic, gonadotrophic, and lactrotrophic adenomas.

Classification

  • Historically, pituitary tumors were classified as basophilic, acidophilic, or chromophobic based on the positivity of hematoxylin and eosin stain.
  • Newer classification is based on either the size or the functional status of the adenoma (secretory vs. non-secretory).

Classification based on hormone secretion and immunohistochemical staining

Type of adenoma Secretion Staining Pathology
Corticotrophic adenomas Adrenocorticotropic hormone (ACTH) and pro-opiomelanocortin (POMC) Basophilic Cushing’s disease
Somatotrophic adenomas Growth hormone (GH) Acidophilic Acromegaly (gigantism)
Thyrotrophic adenomas (rare) Thyroid-stimulating hormone (TSH) Basophilic Occasionally hyperthyroidism/Asymptomatic
Gonadotrophic adenomas Luteinizing hormone (LH), follicle-stimulating hormone (FSH) and their subunits Basophilic Asymptomatic
Lactrotrophic adenomas or prolactinomas (most common) Prolactin Acidophilic Galactorrhea, hypogonadism, amenorrhea, infertility, and impotence
Null cell adenomas Do not secrete hormones May stain positive for synaptophysin

Classification based on the size of the adenoma

Pituitary adenoma may be classified into 4 grades based on radioanatomical:[1]

  • Stage I involves microadenomas (<1 cm) without sella expansion
  • Stage II involves macroadenomas (≥1 cm) and may extend above the sella
  • Stage III involves macroadenomas with enlargement and invasion of the floor or suprasellar extension
  • Stage IV involves macroadenomas that cause destruction of the sella

References

  1. ↑ Pituitary adenoma (2015). http://www.cancer.gov/types/pituitary/hp/pituitary-treatment-pdq#section/_96. Accessed on 9/28/2015. Invalid parameter “cancer” in <ref> tag. The supported parameters are: dir, follow, group, name.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

Overview

On gross pathology, a well circumscribed suprasellar mass is a characteristic finding of pituitary adenoma. On microscopic histopathological analysis, a monomorphic expansion of usually one cell type with lack of reticulin network among neoplastic cells is a characteristic finding of pituitary adenoma.

Pathology

Pathological feature

Pituitary adenoma may be classified into 4 grades based on radioanatomical findings:[1]

  • Stage I involves microadenomas (<1 cm) without sella expansion
  • Stage II involves macroadenomas (≥1 cm) and may extend above the sella
  • Stage III involves macroadenomas with enlargement and invasion of the floor or suprasellar extension
  • Stage IV involves macroadenomas that cause destruction of the sella

Microadenoma

  • Pituitary microadenomas are defined as adenomas less than 10 mm in size.[2]
  • Most frequently diagnosed as a result of investigating hormonal imbalance.
  • They are confined to the sella and have no scope to produce mass effect related symptoms.

Microscopic Pathology

  • Histopathological image of pituitary adenoma with GH production. Acidophilic cell type. Hematoxylin & esoin stain.[3]
    Histopathological image of pituitary adenoma with GH production. Acidophilic cell type. Hematoxylin & esoin stain.[3]
  • Histopathological image of pituitary adenoma with GH production. Acidophilic cell type. Hematoxylin & esoin stain.[3]
    Histopathological image of pituitary adenoma with GH production. Acidophilic cell type. Hematoxylin & esoin stain.[3]

Macroadenoma

  • Pituitary macroadenomas are the most common suprasellar mass in adults.[4]
  • They are defined as adenomas greater than 10 mm in size and are most frequently diagnosed due to compression of the surrounding structures, such as the optic chiasm.
  • Larger adenomas can lead to hormonal imbalance due to mass effect rather than secretion.
  • Hypopituitarism or moderately elevated prolactin are both seen, the latter due to stalk effect. Prolactin release (unlike other pituitary hormones) is tonically inhibited by prolactin inhibitory hormone (dopamine) and as such compression of the pituitary infundibulum can result in elevation of systemic prolactin levels due to interruption of normal inhibition.
  • Macroadenomas are approximately twice as common as micoadenoma.

Microscopic Pathology

  • Histopathological image of nonfunctioning pituitary adenoma. Hematoxylin & eosin stain.[5]
    Histopathological image of nonfunctioning pituitary adenoma. Hematoxylin & eosin stain.[5]

References

  1. ↑ Pituitary adenoma (2015). http://www.cancer.gov/types/pituitary/hp/pituitary-treatment-pdq#section/_96. Accessed on 9/28/2015. Invalid parameter “cancer” in <ref> tag. The supported parameters are: dir, follow, group, name.
  2. ↑ pituitary micro adenoma Dr Amir Rezaee and Dr Frank Gaillard. 2015 http://radiopaedia.org/articles/pituitary-microadenoma
  3. ↑ 3.0 3.1 https://en.wikipedia.org/wiki/Pituitary_adenoma#/media/File:Pituitary_adenoma_%281%29_GH_production.jpg
  4. ↑ Pituitary adenoma. Dr Amir Rezaee and Dr Yuranga Weerakkody. Radiopaedia.org 2015.http://radiopaedia.org/articles/pituitary-adenoma
  5. ↑ https://en.wikipedia.org/wiki/Pituitary_adenoma#/media/File:Nonfunctioning_pituitary_adenoma_%281%29.jpg

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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

Overview

There are no established causes for pituitary adenoma.

Causes

There are no established causes for pituitary adenoma.

References

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Differentiating Pituitary adenoma from other Diseases

Differentiating Pituitary adenoma from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Overview

On the basis of seizure, visual disturbance, and constitutional symptoms, pituitary adenoma must be differentiated from oligodendroglioma, meningioma, hemangioblastoma, astrocytoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

Differentiating pituitary adenoma from other Diseases

Differentiating pituitary adenoma from other diseases on the basis of seizure, visual disturbance, and constitutional symptoms

On the basis of seizure, visual disturbance, and constitutional symptoms, pituitary adenoma must be differentiated from oligodendroglioma, meningioma, hemangioblastoma, astrocytoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

Diseases Clinical manifestations Para-clinical findings Gold
standard 		Additional findings
Symptoms Physical examination
Lab Findings MRI Immunohistopathology
Head-
ache 		Seizure Visual disturbance Constitutional Focal neurological deficit
Adult primary brain tumors
Pituitary adenoma
[1][2][3] 		− − + Bitemporal hemianopia − −
  • It is associated with MEN1 disease.
      Glioblastoma multiforme
      [4][5][3]       		+ +/− +/− − + −
      • Pseudopalisading appearance
      Oligodendroglioma
      [6][7][8]       		+ + +/− − + −
      • Chicken wire capillary pattern
      • Fried egg cell appearance
      Meningioma
      [9][10][11]       		+ +/− +/− − + −
      • Well circumscribed
      • Extra-axial mass
      • Whorled spindle cell pattern
      • May be associated with NF-2
      Hemangioblastoma
      [12][13][14][15]       		+ +/− +/− − + −
      Schwannoma
      [16][17][18][19]       		− − − − + −
      • Split-fat sign
      • Fascicular sign
      • Often have areas of hemosiderin
      • S100+
      Primary CNS lymphoma
      [20][21]       		+ +/− +/− − + −
      • Single mass with ring enhancement
        Childhood primary brain tumors
        Pilocytic astrocytoma
        [22][23][24]         		+ +/− +/− − + −
        Medulloblastoma
        [25][26][27]         		+ +/− +/− − + −
        • Homer wright rosettes
        Ependymoma
        [28][3]         		+ +/− +/− − + −
        • Hydrocephalus
        • Causes an unusually persistent, continuous headache in children.
        Craniopharyngioma
        [29][30][31][3]         		+ +/− + Bitemporal hemianopia − +
        Pinealoma
        [32][33][34]         		+ +/− +/− − + vertical gaze palsy
        • May cause prinaud syndrome (vertical gaze palsy, pupillary light-near dissociation, lid retraction and convergence-retraction nystagmus
        Vascular
        AV malformation
        [35][36][3]         		+ + +/− − +/− −
        Brain aneurysm
        [37][38][39][40][41]         		+ +/− +/− − +/− −
        • MRA and CTA
        Infectious
        Bacterial brain abscess
        [42][43]         		+ +/− +/− + +
        • Central hypodense signal and surrounding ring-enhancement in T1
        • Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding edema in T2
        • History/ imaging
        Tuberculosis
        [44][3][45]         		+ +/− +/− + +
        • Lab data/ Imaging
        Toxoplasmosis
        [46][47]         		+ +/− +/− − +
        • History/ imaging
        Hydatid cyst
        [48][3]         		+ +/− +/− +/− +
        • Imaging
        CNS cryptococcosis
        [49]         		+ +/− +/− + +
        • We may see numerous acutely branching septate hyphae
        • Lab data/ Imaging
        CNS aspergillosis
        [50]         		+ +/− +/− + +
        • Multiple abscesses
        • Ring enhancement
        • Peripheral low signal intensity on T2
        • We may see numerous acutely branching septate hyphae
        • Lab data/ Imaging
        Other
        Brain metastasis
        [51][3]         		+ +/− +/− + + −
        • Based on the primary cancer type we may have different immunohistopathology findings.
        • History/ imaging

        ABBREVIATIONS

        CNS=Central nervous system, AV=Arteriovenous, CSF=Cerebrospinal fluid, NF-2=Neurofibromatosis type 2, MEN-1=Multiple endocrine neoplasia, GFAP=Glial fibrillary acidic protein, HIV=Human immunodeficiency virus, BhCG=Human chorionic gonadotropin, ESR=Erythrocyte sedimentation rate, AFB=Acid fast bacilli, MRA=Magnetic resonance angiography, CTA=CT angiography

        References

        1. ↑ Kucharczyk W, Davis DO, Kelly WM, Sze G, Norman D, Newton TH (December 1986). “Pituitary adenomas: high-resolution MR imaging at 1.5 T”. Radiology. 161 (3): 761–5. doi:10.1148/radiology.161.3.3786729. PMID 3786729.
        2. ↑ Syro LV, Scheithauer BW, Kovacs K, Toledo RA, Londoño FJ, Ortiz LD, Rotondo F, Horvath E, Uribe H (2012). “Pituitary tumors in patients with MEN1 syndrome”. Clinics (Sao Paulo). 67 Suppl 1: 43–8. PMC 3328811. PMID 22584705.
        3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
        4. ↑ Sathornsumetee S, Rich JN, Reardon DA (November 2007). “Diagnosis and treatment of high-grade astrocytoma”. Neurol Clin. 25 (4): 1111–39, x. doi:10.1016/j.ncl.2007.07.004. PMID 17964028.
        5. ↑ Pedersen CL, Romner B (January 2013). “Current treatment of low grade astrocytoma: a review”. Clin Neurol Neurosurg. 115 (1): 1–8. doi:10.1016/j.clineuro.2012.07.002. PMID 22819718.
        6. ↑ Smits M (2016). “Imaging of oligodendroglioma”. Br J Radiol. 89 (1060): 20150857. doi:10.1259/bjr.20150857. PMC 4846213. PMID 26849038.
        7. ↑ Wesseling P, van den Bent M, Perry A (June 2015). “Oligodendroglioma: pathology, molecular mechanisms and markers”. Acta Neuropathol. 129 (6): 809–27. doi:10.1007/s00401-015-1424-1. PMC 4436696. PMID 25943885.
        8. ↑ Kerkhof M, Benit C, Duran-Pena A, Vecht CJ (2015). “Seizures in oligodendroglial tumors”. CNS Oncol. 4 (5): 347–56. doi:10.2217/cns.15.29. PMC 6082346. PMID 26478444.
        9. ↑ Zee CS, Chin T, Segall HD, Destian S, Ahmadi J (June 1992). “Magnetic resonance imaging of meningiomas”. Semin. Ultrasound CT MR. 13 (3): 154–69. PMID 1642904.
        10. ↑ Shibuya M (2015). “Pathology and molecular genetics of meningioma: recent advances”. Neurol. Med. Chir. (Tokyo). 55 (1): 14–27. doi:10.2176/nmc.ra.2014-0233. PMID 25744347.
        11. ↑ Begnami MD, Palau M, Rushing EJ, Santi M, Quezado M (September 2007). “Evaluation of NF2 gene deletion in sporadic schwannomas, meningiomas, and ependymomas by chromogenic in situ hybridization”. Hum. Pathol. 38 (9): 1345–50. doi:10.1016/j.humpath.2007.01.027. PMC 2094208. PMID 17509660.
        12. ↑ Lonser RR, Butman JA, Huntoon K, Asthagiri AR, Wu T, Bakhtian KD, Chew EY, Zhuang Z, Linehan WM, Oldfield EH (May 2014). “Prospective natural history study of central nervous system hemangioblastomas in von Hippel-Lindau disease”. J. Neurosurg. 120 (5): 1055–62. doi:10.3171/2014.1.JNS131431. PMC 4762041. PMID 24579662.
        13. ↑ Hussein MR (October 2007). “Central nervous system capillary haemangioblastoma: the pathologist’s viewpoint”. Int J Exp Pathol. 88 (5): 311–24. doi:10.1111/j.1365-2613.2007.00535.x. PMC 2517334. PMID 17877533.
        14. ↑ Lee SR, Sanches J, Mark AS, Dillon WP, Norman D, Newton TH (May 1989). “Posterior fossa hemangioblastomas: MR imaging”. Radiology. 171 (2): 463–8. doi:10.1148/radiology.171.2.2704812. PMID 2704812.
        15. ↑ Perks WH, Cross JN, Sivapragasam S, Johnson P (March 1976). “Supratentorial haemangioblastoma with polycythaemia”. J. Neurol. Neurosurg. Psychiatry. 39 (3): 218–20. PMID 945331.
        16. ↑ Donnelly, Martin J.; Daly, Carmel A.; Briggs, Robert J. S. (2007). “MR imaging features of an intracochlear acoustic schwannoma”. The Journal of Laryngology & Otology. 108 (12). doi:10.1017/S0022215100129056. ISSN 0022-2151.
        17. ↑ Feany MB, Anthony DC, Fletcher CD (May 1998). “Nerve sheath tumours with hybrid features of neurofibroma and schwannoma: a conceptual challenge”. Histopathology. 32 (5): 405–10. PMID 9639114.
        18. ↑ Chen H, Xue L, Wang H, Wang Z, Wu H (July 2017). “Differential NF2 Gene Status in Sporadic Vestibular Schwannomas and its Prognostic Impact on Tumour Growth Patterns”. Sci Rep. 7 (1): 5470. doi:10.1038/s41598-017-05769-0. PMID 28710469.
        19. ↑ Hardell, Lennart; Hansson Mild, Kjell; Sandström, Monica; Carlberg, Michael; Hallquist, Arne; Påhlson, Anneli (2003). “Vestibular Schwannoma, Tinnitus and Cellular Telephones”. Neuroepidemiology. 22 (2): 124–129. doi:10.1159/000068745. ISSN 0251-5350.
        20. ↑ Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ (December 1995). “Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy”. Radiology. 197 (3): 649–54. doi:10.1148/radiology.197.3.7480733. PMID 7480733.
        21. ↑ Paulus, Werner (1999). “Classification, Pathogenesis and Molecular Pathology of Primary CNS Lymphomas”. Journal of Neuro-Oncology. 43 (3): 203–208. doi:10.1023/A:1006242116122. ISSN 0167-594X.
        22. ↑ Sathornsumetee S, Rich JN, Reardon DA (November 2007). “Diagnosis and treatment of high-grade astrocytoma”. Neurol Clin. 25 (4): 1111–39, x. doi:10.1016/j.ncl.2007.07.004. PMID 17964028.
        23. ↑ Pedersen CL, Romner B (January 2013). “Current treatment of low grade astrocytoma: a review”. Clin Neurol Neurosurg. 115 (1): 1–8. doi:10.1016/j.clineuro.2012.07.002. PMID 22819718.
        24. ↑ Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
        25. ↑ Dorwart, R H; Wara, W M; Norman, D; Levin, V A (1981). “Complete myelographic evaluation of spinal metastases from medulloblastoma”. Radiology. 139 (2): 403–408. doi:10.1148/radiology.139.2.7220886. ISSN 0033-8419.
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        33. ↑ Sano, Keiji (1976). “Pinealoma in Children”. Pediatric Neurosurgery. 2 (1): 67–72. doi:10.1159/000119602. ISSN 1016-2291.
        34. ↑ Baggenstoss, Archie H. (1939). “PINEALOMAS”. Archives of Neurology And Psychiatry. 41 (6): 1187. doi:10.1001/archneurpsyc.1939.02270180115011. ISSN 0096-6754.
        35. ↑ Kucharczyk, W; Lemme-Pleghos, L; Uske, A; Brant-Zawadzki, M; Dooms, G; Norman, D (1985). “Intracranial vascular malformations: MR and CT imaging”. Radiology. 156 (2): 383–389. doi:10.1148/radiology.156.2.4011900. ISSN 0033-8419.
        36. ↑ Fleetwood, Ian G; Steinberg, Gary K (2002). “Arteriovenous malformations”. The Lancet. 359 (9309): 863–873. doi:10.1016/S0140-6736(02)07946-1. ISSN 0140-6736.
        37. ↑ Chapman, Arlene B.; Rubinstein, David; Hughes, Richard; Stears, John C.; Earnest, Michael P.; Johnson, Ann M.; Gabow, Patricia A.; Kaehny, William D. (1992). “Intracranial Aneurysms in Autosomal Dominant Polycystic Kidney Disease”. New England Journal of Medicine. 327 (13): 916–920. doi:10.1056/NEJM199209243271303. ISSN 0028-4793.
        38. ↑ Castori M, Voermans NC (October 2014). “Neurological manifestations of Ehlers-Danlos syndrome(s): A review”. Iran J Neurol. 13 (4): 190–208. PMC 4300794. PMID 25632331.
        39. ↑ Schievink, W. I.; Raissi, S. S.; Maya, M. M.; Velebir, A. (2010). “Screening for intracranial aneurysms in patients with bicuspid aortic valve”. Neurology. 74 (18): 1430–1433. doi:10.1212/WNL.0b013e3181dc1acf. ISSN 0028-3878.
        40. ↑ Germain DP (May 2017). “Pseudoxanthoma elasticum”. Orphanet J Rare Dis. 12 (1): 85. doi:10.1186/s13023-017-0639-8. PMC 5424392. PMID 28486967.
        41. ↑ Farahmand M, Farahangiz S, Yadollahi M (October 2013). “Diagnostic Accuracy of Magnetic Resonance Angiography for Detection of Intracranial Aneurysms in Patients with Acute Subarachnoid Hemorrhage; A Comparison to Digital Subtraction Angiography”. Bull Emerg Trauma. 1 (4): 147–51. PMC 4789449. PMID 27162847.
        42. ↑ Haimes, AB; Zimmerman, RD; Morgello, S; Weingarten, K; Becker, RD; Jennis, R; Deck, MD (1989). “MR imaging of brain abscesses”. American Journal of Roentgenology. 152 (5): 1073–1085. doi:10.2214/ajr.152.5.1073. ISSN 0361-803X.
        43. ↑ Brouwer, Matthijs C.; Tunkel, Allan R.; McKhann, Guy M.; van de Beek, Diederik (2014). “Brain Abscess”. New England Journal of Medicine. 371 (5): 447–456. doi:10.1056/NEJMra1301635. ISSN 0028-4793.
        44. ↑ Morgado, Carlos; Ruivo, Nuno (2005). “Imaging meningo-encephalic tuberculosis”. European Journal of Radiology. 55 (2): 188–192. doi:10.1016/j.ejrad.2005.04.017. ISSN 0720-048X.
        45. ↑ Be NA, Kim KS, Bishai WR, Jain SK (March 2009). “Pathogenesis of central nervous system tuberculosis”. Curr. Mol. Med. 9 (2): 94–9. PMC 4486069. PMID 19275620.
        46. ↑ Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ (December 1995). “Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy”. Radiology. 197 (3): 649–54. doi:10.1148/radiology.197.3.7480733. PMID 7480733.
        47. ↑ Helton KJ, Maron G, Mamcarz E, Leventaki V, Patay Z, Sadighi Z (November 2016). “Unusual magnetic resonance imaging presentation of post-BMT cerebral toxoplasmosis masquerading as meningoencephalitis and ventriculitis”. Bone Marrow Transplant. 51 (11): 1533–1536. doi:10.1038/bmt.2016.168. PMID 27348541.
        48. ↑ Taslakian B, Darwish H (September 2016). “Intracranial hydatid cyst: imaging findings of a rare disease”. BMJ Case Rep. 2016. doi:10.1136/bcr-2016-216570. PMC 5030532. PMID 27620198.
        49. ↑ McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ (July 2014). “Mold infections of the central nervous system”. N. Engl. J. Med. 371 (2): 150–60. doi:10.1056/NEJMra1216008. PMC 4840461. PMID 25006721.
        50. ↑ McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ (July 2014). “Mold infections of the central nervous system”. N. Engl. J. Med. 371 (2): 150–60. doi:10.1056/NEJMra1216008. PMC 4840461. PMID 25006721.
        51. ↑ Pope WB (2018). “Brain metastases: neuroimaging”. Handb Clin Neurol. 149: 89–112. doi:10.1016/B978-0-12-811161-1.00007-4. PMC 6118134. PMID 29307364.

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        Epidemiology and Demographics

        Epidemiology and Demographics

        Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

        Overview

        The prevalence of pituitary adenoma is approximately 100 per 100,000 individuals worldwide. In the USA, the incidence pituitary adenoma is approximately 3.12 per 100,000 individuals.

        Epidemiology and Demographics

        Prevalence

        • The prevalence of pituitary adenoma is approximately 100 per 100,000 individuals worldwide.[1]
        • Autopsy prevalence of pituitary adenoma is approximately 15,000 per 100,000 individuals worldwide.[1]

        Incidence

        • In the USA, the incidence of the pituitary adenoma is approximately 3.12 per 100,000 individuals.[2]
        • The actual incidence is much higher as most patients remain asymptomatic for long time.[2]

        References

        1. ↑ 1.0 1.1 Pituitary adenoma. Dr Amir Rezaee and Dr Yuranga Weerakkody. Radiopaedia.org 2015.http://radiopaedia.org/articles/pituitary-adenoma
        2. ↑ 2.0 2.1 http://www.cancer.org/cancer/pituitarytumors/detailedguide/pituitary-tumors-key-statistics

        Template:WikiDoc Sources

        Risk Factors

        Risk Factors

        Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

        Overview

        The most potent risk factor in the development of pituitary adenoma is a positive family history of either pituitary tumor, multiple endocrine neoplasia type 1 (MEN1), or McCune-Albright syndrome.

        Risk Factors

        The most potent risk factor in the development of pituitary adenoma is a positive family history of either pituitary tumor, multiple endocrine neoplasia type 1 (MEN1), or McCune-Albright syndrome.

        References

        Template:WikiDoc Sources

        Natural History, Complications and Prognosis

        Natural History, Complications and Prognosis

        Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]

        Overview

        Patients with pituitary adenoma may progress to develop lethargy, headache, nausea, and vomiting. Common complications of pituitary adenoma include bitemporal hemianopia , anosmia, acromegaly, gigantism and Cushing’s syndrome. Prognosis is generally good, and approximately 18% of patients with macroadenoma require further treatment.

        Natural history, complications, and prognosis

        Natural history

        • Pituitary adenomas are generally benign.
        • Patients with micoradenoma usually asymptomatic and diagnosed incidentally. At later stage they may show signs and symptoms of hormonal disturbances.
        • Patients with macroadenoma usually present with visual field deficits and hormonal disturbances. Macroadenoma grows slowly and invades surrounding structure such as optic chiasm and olfactory tract.
        • Females tend to develop symptoms at an earlier stage than males due to menstrual irregularities associated with the disease.

        Complications

        Prognosis

        • The prognosis of pituitary adenoma is generally good. However, recurrent symptoms require further intervention.
        • Approximately 18% of patients with macroadenoma require further treatment.[4]

        References

        1. ↑ Pituitary adenoma https://en.wikipedia.org/wiki/Pituitary_adenoma. 9 29 2015
        2. ↑ Gigantism http://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/acromegaly-and-gigantism
        3. ↑ http://www.niddk.nih.gov/health-information/health-topics/endocrine/cushings-syndrome/Pages/fact-sheet.aspx#1
        4. ↑ Dr Amir Rezaee and Dr Yuranga Weerakkody http://radiopaedia.org/articles/pituitary-adenoma 2015. URL accessed on 9 30 2015

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        Diagnosis

        Diagnosis

        History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

        Treatment

        Treatment

        Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

        Case Studies

        Case Studies

        Case #1

        Related Chapters
        External links

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