U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Impotence

MedGen UID:
1720680
Concept ID:
CN208474
Finding
Synonyms: Difficulty getting a full erection; Difficulty getting an erection
 
HPO: HP:0000802

Definition

Inability to develop or maintain an erection of the penis. [from HPO]

Term Hierarchy

Conditions with this feature

Sandhoff disease
MedGen UID:
11313
Concept ID:
C0036161
Disease or Syndrome
Sandhoff disease comprises a phenotypic continuum encompassing acute infantile, subacute juvenile, and late-onset disease. Although classification into these phenotypes is somewhat arbitrary, it is helpful in understanding the variation observed in the timing of disease onset, presenting manifestations, rate of progression, and life span. Acute infantile Sandhoff disease (onset age <6 months). Infants are generally normal at birth followed by progressive weakness and slowing of developmental progress, then developmental regression and severe neurologic impairment. Seizures are common. Death usually occurs between ages two and three years. Subacute juvenile Sandhoff disease (onset age 2-5 years). After attaining normal developmental milestones, developmental progress slows, followed by developmental regression and neurologic impairment (abnormal gait, dysarthria, and cognitive decline). Death (usually from aspiration) typically occurs in the early to late teens. Late-onset Sandhoff disease (onset older teen years or young adulthood). Nearly normal psychomotor development is followed by a range of neurologic findings (e.g., weakness, spasticity, dysarthria, and deficits in cerebellar function) and psychiatric findings (e.g., deficits in executive function and memory). Life expectancy is not necessarily decreased.
Adrenoleukodystrophy
MedGen UID:
57667
Concept ID:
C0162309
Disease or Syndrome
X-linked adrenoleukodystrophy (X-ALD) affects the nervous system white matter and the adrenal cortex. Three main phenotypes are seen in affected males: The childhood cerebral form manifests most commonly between ages four and eight years. It initially resembles attention-deficit disorder or hyperactivity; progressive impairment of cognition, behavior, vision, hearing, and motor function follow the initial symptoms and often lead to total disability within six months to two years. Most individuals have impaired adrenocortical function at the time that neurologic disturbances are first noted. Adrenomyeloneuropathy (AMN) manifests most commonly in an individual in his twenties or middle age as progressive stiffness and weakness of the legs, sphincter disturbances, sexual dysfunction, and often, impaired adrenocortical function; all symptoms are progressive over decades. "Addison disease only" presents with primary adrenocortical insufficiency between age two years and adulthood and most commonly by age 7.5 years, without evidence of neurologic abnormality; however, some degree of neurologic disability (most commonly AMN) usually develops by middle age. More than 20% of female carriers develop mild-to-moderate spastic paraparesis in middle age or later. Adrenal function is usually normal.
Fragile X-associated tremor/ataxia syndrome
MedGen UID:
333403
Concept ID:
C1839780
Disease or Syndrome
FMR1 disorders include fragile X syndrome (FXS), fragile X-associated tremor/ataxia syndrome (FXTAS), and fragile X-associated primary ovarian insufficiency (FXPOI). Fragile X syndrome occurs in individuals with an FMR1 full mutation or other loss-of-function variant and is nearly always characterized in affected males by developmental delay and intellectual disability along with a variety of behavioral issues. Autism spectrum disorder is present in 50%-70% of individuals with FXS. Affected males may have characteristic craniofacial features (which become more obvious with age) and medical problems including hypotonia, gastroesophageal reflux, strabismus, seizures, sleep disorders, joint laxity, pes planus, scoliosis, and recurrent otitis media. Adults may have mitral valve prolapse or aortic root dilatation. The physical and behavioral features seen in males with FXS have been reported in females heterozygous for the FMR1 full mutation, but with lower frequency and milder involvement. FXTAS occurs in individuals who have an FMR1 premutation and is characterized by late-onset, progressive cerebellar ataxia and intention tremor followed by cognitive impairment. Psychiatric disorders are common. Age of onset is typically between 60 and 65 years and is more common among males who are hemizygous for the premutation (40%) than among females who are heterozygous for the premutation (16%-20%). FXPOI, defined as hypergonadotropic hypogonadism before age 40 years, has been observed in 20% of women who carry a premutation allele compared to 1% in the general population.
Hereditary sensory and autonomic neuropathy type 1B
MedGen UID:
330880
Concept ID:
C1842586
Disease or Syndrome
The hereditary sensory and autonomic neuropathies (HSAN), which are also referred to as hereditary sensory neuropathies (HSN) in the absence of significant autonomic features, are a genetically and clinically heterogeneous group of disorders associated with sensory dysfunction. For a discussion of genetic heterogeneity of HSAN, see HSAN1A (162400).
Hemochromatosis type 4
MedGen UID:
340044
Concept ID:
C1853733
Disease or Syndrome
Hemochromatosis type 4 (HFE4) is a dominantly inherited iron overload disorder with heterogeneous phenotypic manifestations that can be classified into 2 groups. One group is characterized by an early rise in ferritin (see 134790) levels with low to normal transferrin (190000) saturation and iron accumulation predominantly in macrophages. The other group is similar to classical hemochromatosis, with high transferrin saturation and prominent parenchymal iron loading (summary by De Domenico et al., 2005). For general background information and a discussion of genetic heterogeneity of hereditary hemochromatosis, see 235200.
Hemochromatosis type 3
MedGen UID:
388114
Concept ID:
C1858664
Disease or Syndrome
TFR2-related hereditary hemochromatosis (TFR2-HHC) is characterized by increased intestinal iron absorption resulting in iron accumulation in the liver, heart, pancreas, and endocrine organs. Age of onset is earlier than in HFE-HHC. The majority of individuals present with signs and symptoms of iron overload in the third decade (e.g., weakness, fatigue, abdominal pain, hepatomegaly, arthritis, arthralgia, progressive increase in skin pigmentation). Others present as young adults with nonspecific symptoms and abnormal serum iron studies or as adults with abnormal serum iron studies and signs of organ involvement including cirrhosis, diabetes mellitus, and arthropathy.
Adult-onset autosomal dominant demyelinating leukodystrophy
MedGen UID:
356995
Concept ID:
C1868512
Disease or Syndrome
LMNB1-related autosomal dominant leukodystrophy (ADLD) is a slowly progressive disorder of central nervous system white matter characterized by onset of autonomic dysfunction in the fourth to fifth decade, followed by pyramidal and cerebellar abnormalities resulting in spasticity, ataxia, and tremor. Autonomic dysfunction can include bladder dysfunction, constipation, postural hypotension, erectile dysfunction, and (less often) impaired sweating. Pyramidal signs are often more prominent in the lower extremities (e.g., spastic weakness, hypertonia, clonus, brisk deep tendon reflexes, and bilateral Babinski signs). Cerebellar signs typically appear at the same time as the pyramidal signs and include gait ataxia, dysdiadochokinesia, intention tremor, dysmetria, and nystagmus. Many individuals have sensory deficits starting in the lower limbs. Pseudobulbar palsy with dysarthria, dysphagia, and forced crying and laughing may appear in the seventh or eighth decade. Although cognitive function is usually preserved or only mildly impaired early in the disease course, dementia and psychiatric manifestations can occur as late manifestations. Affected individuals may survive for decades after onset.
Amyloidogenic transthyretin amyloidosis
MedGen UID:
414031
Concept ID:
C2751492
Disease or Syndrome
Hereditary transthyretin (ATTR) amyloidosis is characterized by a slowly progressive peripheral sensorimotor and/or autonomic neuropathy as well as non-neuropathic changes of cardiomyopathy, nephropathy, vitreous opacities, and CNS amyloidosis. The disease usually begins in the third to fifth decade in persons from endemic foci in Portugal and Japan; onset is later in persons from other areas. Typically, sensory neuropathy starts in the lower extremities with paresthesias and hypesthesias of the feet, followed within a few years by motor neuropathy. In some persons, particularly those with early-onset disease, autonomic neuropathy is the first manifestation of the condition; findings can include: orthostatic hypotension, constipation alternating with diarrhea, attacks of nausea and vomiting, delayed gastric emptying, sexual impotence, anhidrosis, and urinary retention or incontinence. Cardiac amyloidosis is mainly characterized by progressive cardiomyopathy. Individuals with leptomeningeal amyloidosis may have the following CNS findings: dementia, psychosis, visual impairment, headache, seizures, motor paresis, ataxia, myelopathy, hydrocephalus, or intracranial hemorrhage.
Hemochromatosis type 1
MedGen UID:
854011
Concept ID:
C3469186
Disease or Syndrome
HFE hemochromatosis is characterized by inappropriately high absorption of iron by the small intestinal mucosa. The phenotypic spectrum of HFE hemochromatosis includes: Persons with clinical HFE hemochromatosis, in whom manifestations of end-organ damage secondary to iron overload are present; Individuals with biochemical HFE hemochromatosis, in whom transferrin-iron saturation is increased and the only evidence of iron overload is increased serum ferritin concentration; and Non-expressing p.Cys282Tyr homozygotes, in whom neither clinical manifestations of HFE hemochromatosis nor iron overload are present. Clinical HFE hemochromatosis is characterized by excessive storage of iron in the liver, skin, pancreas, heart, joints, and anterior pituitary gland. In untreated individuals, early symptoms include: abdominal pain, weakness, lethargy, weight loss, arthralgias, diabetes mellitus; and increased risk of cirrhosis when the serum ferritin is higher than 1,000 ng/mL. Other findings may include progressive increase in skin pigmentation, congestive heart failure, and/or arrhythmias, arthritis, and hypogonadism. Clinical HFE hemochromatosis is more common in men than women.
Multiple system atrophy 1, susceptibility to
MedGen UID:
811503
Concept ID:
C3714927
Finding
Multiple system atrophy (MSA) is a distinct clinicopathologic entity that manifests as a progressive adult-onset neurodegenerative disorder causing parkinsonism, cerebellar ataxia, and autonomic, urogenital, and pyramidal dysfunction in various combinations. Two main subtypes are recognized: 'subtype C,' characterized predominantly by cerebellar ataxia, and 'subtype P,' characterized predominantly by parkinsonism. MSA is characterized pathologically by the degeneration of striatonigral and olivopontocerebellar structures and glial cytoplasmic inclusions (GCIs) that consist of abnormally phosphorylated alpha-synuclein (SNCA; 163890) or tau (MAPT; 157140) (Gilman et al., 1998; Gilman et al., 2008; Scholz et al., 2009). 'Subtype C' of MSA has been reported to be more prevalent than 'subtype P' in the Japanese population (65-67% vs 33-35%), whereas 'subtype P' has been reported to be more prevalent than 'subtype C' in Europe (63% vs 34%) and North America (60% vs 13%, with 27% of cases unclassified) (summary by The Multiple-System Atrophy Research Collaboration, 2013). MSA is similar clinically and pathologically to Parkinson disease (PD; 168600) and Lewy body dementia (127750). See also PARK1 (168601), which is specifically caused by mutation in the SNCA gene. Pure autonomic failure manifests as orthostatic hypotension and other autonomic abnormalities without other neurologic involvement. Although there is some phenotypic overlap, the relationship of pure autonomic failure to MSA is unclear (Vanderhaeghen et al., 1970; Schatz, 1996).
Moyamoya disease with early-onset achalasia
MedGen UID:
816733
Concept ID:
C3810403
Disease or Syndrome
Moyamoya disease-6 is a progressive vasculopathy characterized by occlusion of the terminal portion of the internal carotid arteries and its branches, and the formation of compensatory neovascularization and the moyamoya, or 'puff of smoke,' appearance of these vessels on angiogram. Affected individuals may present with ischemic strokes, intracerebral hemorrhage, or transient ischemic attacks. Patients with MYMY6 usually present early in life with achalasia. Hypertension and Raynaud phenomenon may be associated features (summary by Wallace et al., 2016; Herve et al., 2014). For a general phenotypic description and a discussion of genetic heterogeneity of moyamoya disease, see MYMY1 (252350).

Professional guidelines

PubMed

Srivastava V, Mathur D, Rout S, Mishra BK, Pannu V, Anand A
Curr Alzheimer Res 2022;19(8):568-584. doi: 10.2174/1567205019666220805100008. PMID: 35929620
Podolej GS, Babcock C
Emerg Med Pract 2017 Jan;19(1):1-16. Epub 2017 Jan 1 PMID: 28027457
Bodner DR
Prim Care 1985 Dec;12(4):719-33. PMID: 3909176

Recent clinical studies

Etiology

Orimoloye OA, Feldman DI, Blaha MJ
Trends Cardiovasc Med 2019 Nov;29(8):458-465. Epub 2019 Jan 11 doi: 10.1016/j.tcm.2019.01.002. PMID: 30665816
Miner M, Kim ED
Asian J Androl 2015 Jan-Feb;17(1):3-4. doi: 10.4103/1008-682x.143753. PMID: 25532581Free PMC Article
Vlachopoulos C, Jackson G, Stefanadis C, Montorsi P
Eur Heart J 2013 Jul;34(27):2034-46. Epub 2013 Apr 24 doi: 10.1093/eurheartj/eht112. PMID: 23616415
Montorsi F, Adaikan G, Becher E, Giuliano F, Khoury S, Lue TF, Sharlip I, Althof SE, Andersson KE, Brock G, Broderick G, Burnett A, Buvat J, Dean J, Donatucci C, Eardley I, Fugl-Meyer KS, Goldstein I, Hackett G, Hatzichristou D, Hellstrom W, Incrocci L, Jackson G, Kadioglu A, Levine L, Lewis RW, Maggi M, McCabe M, McMahon CG, Montague D, Montorsi P, Mulhall J, Pfaus J, Porst H, Ralph D, Rosen R, Rowland D, Sadeghi-Nejad H, Shabsigh R, Stief C, Vardi Y, Wallen K, Wasserman M
J Sex Med 2010 Nov;7(11):3572-88. doi: 10.1111/j.1743-6109.2010.02062.x. PMID: 21040491
Ware JC
Clin Geriatr Med 1989 May;5(2):301-14. PMID: 2665913

Diagnosis

Papagiannopoulos D, Khare N, Nehra A
Asian J Androl 2015 Jan-Feb;17(1):11-6. doi: 10.4103/1008-682X.139253. PMID: 25370205Free PMC Article
Tapscott AH, Hakim LS
Urol Clin North Am 2013 Nov;40(4):521-43. Epub 2013 Sep 3 doi: 10.1016/j.ucl.2013.07.003. PMID: 24182973
Morgentaler A
Lancet 1999 Nov 13;354(9191):1713-8. doi: 10.1016/S0140-6736(99)06586-1. PMID: 10568586
Carlin BW
Metabolism 1988 Feb;37(2 Suppl 1):19-21. doi: 10.1016/0026-0495(88)90182-5. PMID: 3340009
Bodner DR
Prim Care 1985 Dec;12(4):719-33. PMID: 3909176

Therapy

Kathrins M
Fertil Steril 2020 Jan;113(1):95-96. doi: 10.1016/j.fertnstert.2019.10.020. PMID: 32033739
Shamloul R, Ghanem H
Lancet 2013 Jan 12;381(9861):153-65. Epub 2012 Oct 5 doi: 10.1016/S0140-6736(12)60520-0. PMID: 23040455
Williams SK, Melman A
Maturitas 2012 Jan;71(1):20-7. Epub 2011 Dec 7 doi: 10.1016/j.maturitas.2011.11.004. PMID: 22154078
Evans HC, Goa KL
Drugs Aging 2003;20(12):905-16; discussion 917-8. doi: 10.2165/00002512-200320120-00005. PMID: 14565784
Kursh ED, Bodner DR, Resnick MI, Althof SE, Turner L, Risen C, Levine SB
Urol Clin North Am 1988 Nov;15(4):625-9. PMID: 3055615

Prognosis

Tzolos E, Dweck MR
Arterioscler Thromb Vasc Biol 2020 Jul;40(7):1620-1626. Epub 2020 May 7 doi: 10.1161/ATVBAHA.120.313785. PMID: 32375543Free PMC Article
Orimoloye OA, Feldman DI, Blaha MJ
Trends Cardiovasc Med 2019 Nov;29(8):458-465. Epub 2019 Jan 11 doi: 10.1016/j.tcm.2019.01.002. PMID: 30665816
Papagiannopoulos D, Khare N, Nehra A
Asian J Androl 2015 Jan-Feb;17(1):11-6. doi: 10.4103/1008-682X.139253. PMID: 25370205Free PMC Article
Shamloul R, Ghanem H
Lancet 2013 Jan 12;381(9861):153-65. Epub 2012 Oct 5 doi: 10.1016/S0140-6736(12)60520-0. PMID: 23040455
Hakim LS, Goldstein I
Endocrinol Metab Clin North Am 1996 Jun;25(2):379-400. doi: 10.1016/s0889-8529(05)70329-7. PMID: 8799705

Clinical prediction guides

Tzolos E, Dweck MR
Arterioscler Thromb Vasc Biol 2020 Jul;40(7):1620-1626. Epub 2020 May 7 doi: 10.1161/ATVBAHA.120.313785. PMID: 32375543Free PMC Article
Orimoloye OA, Feldman DI, Blaha MJ
Trends Cardiovasc Med 2019 Nov;29(8):458-465. Epub 2019 Jan 11 doi: 10.1016/j.tcm.2019.01.002. PMID: 30665816
Papagiannopoulos D, Khare N, Nehra A
Asian J Androl 2015 Jan-Feb;17(1):11-6. doi: 10.4103/1008-682X.139253. PMID: 25370205Free PMC Article
Shamloul R, Ghanem H
Lancet 2013 Jan 12;381(9861):153-65. Epub 2012 Oct 5 doi: 10.1016/S0140-6736(12)60520-0. PMID: 23040455
Vlachopoulos C, Terentes-Printzios D, Stefanadis C
Curr Vasc Pharmacol 2012 Nov;10(6):728-30. doi: 10.2174/157016112803520846. PMID: 23259567

Recent systematic reviews

Farook F, Al Meshrafi A, Mohamed Nizam N, Al Shammari A
Am J Mens Health 2021 May-Jun;15(3):15579883211007277. doi: 10.1177/15579883211007277. PMID: 34013796Free PMC Article
Kellesarian SV, Malignaggi VR, Feng C, Javed F
Int J Impot Res 2018 Jun;30(3):129-140. Epub 2018 May 25 doi: 10.1038/s41443-018-0017-7. PMID: 29795528
Chen LW, Chen MY, Lian ZP, Lin HS, Chien CC, Yin HL, Chu YH, Chen KY
Am J Mens Health 2018 Mar;12(2):370-379. Epub 2017 Oct 11 doi: 10.1177/1557988317734519. PMID: 29019272Free PMC Article
Kellesarian SV, Kellesarian TV, Ros Malignaggi V, Al-Askar M, Ghanem A, Malmstrom H, Javed F
Am J Mens Health 2018 Mar;12(2):338-346. Epub 2016 Mar 29 doi: 10.1177/1557988316639050. PMID: 27030114Free PMC Article
Semet M, Paci M, Saïas-Magnan J, Metzler-Guillemain C, Boissier R, Lejeune H, Perrin J
Andrology 2017 Jul;5(4):640-663. Epub 2017 Jun 16 doi: 10.1111/andr.12366. PMID: 28622464

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...