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Table of Contents    
LETTERS TO EDITOR
Year : 2018  |  Volume : 66  |  Issue : 3  |  Page : 868-871

Hypersexuality following anterior communicating artery aneurysm rupture


1 Department of Endocrinology, IGMC, Shimla, Himachal Pradesh, India
2 Department of Psychiatry, Maharishi Markendaeshwar University, Solan, Himachal Pradesh, India
3 Department of Neurosurgery, Post Graduate Institute Medical Education and Research, Chandigarh, India
4 Department of Endocrinology, Post Graduate Institute Medical Education and Research, Chandigarh, India

Date of Web Publication15-May-2018

Correspondence Address:
Dr. Anil Bhansali
Department of Endocrinology, Post Graduate Institute Medical Education and Research, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.232289

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How to cite this article:
Jarial KD, Purkayastha M, Dutta P, Mukherjee KK, Bhansali A. Hypersexuality following anterior communicating artery aneurysm rupture. Neurol India 2018;66:868-71

How to cite this URL:
Jarial KD, Purkayastha M, Dutta P, Mukherjee KK, Bhansali A. Hypersexuality following anterior communicating artery aneurysm rupture. Neurol India [serial online] 2018 [cited 2018 May 20];66:868-71. Available from: http://www.neurologyindia.com/text.asp?2018/66/3/868/232289




Sir,

Human sexuality encompasses biological, physical, cultural, and psychological dimensions of the personality and behavior, and brain injuries can lead to altered sexual behavior.[1] Hypoactive sexual desire disorder is a well-known comorbidity associated with brain injury, while hypersexuality with disinhibition has been recognized as a rare condition.[2] Sexual outcome might depend upon the volume and areas of brain involved, and it provides an opportunity to understand pathobiology of human sexual behavior.[2],[3] Sexual disorders after stroke are similar in type, frequency, and range to those seen following traumatic brain injuries.[4],[5] Hypersexual behavior is rare following stroke and is associated with damage to the specific areas of the brain such as lacunar infarcts affecting the thalamus, frontolimbic connections, subthalamic nuclei, frontal lobe involving the orbito-frontal circuit, and lesions of the temporal lobe.[3],[6],[7],[8] We report a case of hypersexuality without social disinhibition following anterior communicating artery aneurysmal rupture and subsequent bleed into the left frontal cerebral hemisphere.

A 40-year old male, right handed, smoker, and alcoholic for last 15 years and with no other comorbidities presented with acute-onset headache. Contrast-enhanced computed tomography (CT) scan and CT angiography of the brain showed subarachnoid hemorrhage due to anterior communicating artery aneurysm rupture [Figure 1]a and [Figure 1]b. Right pterional craniotomy and clipping of the anterior communicating artery aneurysm was performed and the patient was discharged from the hospital after 3 weeks in hemodynamically stable condition, without any sensory or motor deficit. Mental status examination at discharge showed significant cognitive impairment.
Figure 1: (a and b) CT angiography showing anterior communicating artery aneurysm

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At follow-up, he presented with abnormal behavior; the patient's wife complained that he was having increased sexual urge, restlessness, increased appetite, apathy along with social withdrawal, and he had started smoking excessively. Detailed interview with wife revealed he was requesting her repeatedly for sexual intercourse, multiple times a day; however, there was no violent behavior on refusal. He always insisted on performing the sexual act; however, he was socially aware of circumstances where not to insist for the sexual act. On repeated performance of the sexual act, ejaculation time had increased from 5 to 10 min to approximately one 1 hour, with less amount of ejaculate. There was also insistence to perform unnatural sex. His sexual activities were confined to his wife only; there was no exhibitionism or masturbation in an open place. He was having shy behavior in front of other female subjects and no other paraphilias were reported.

He was evaluated by a psychiatrist for hypersexuality and psychological tests were performed. Postgraguate Institute (PGI) battery of brain dysfunction was done (PGI memory scale, Bender Visuomotor Gestalt test, Alexander Pass, Koh's Block test), which showed mild executive dysfunction. He was taking multiple drugs such as haloperidol, risperidone, and fluoxetine without any improvement for almost 1 year. The patient was referred to endocrinology services for evaluation of hypersexuality. On examination, the testicular volume was 20 ml each, with normal pubic and axillary hair. Investigations revealed a normal hemogram, as well as renal and liver function tests. Hormonal workup showed thyroxine (T)3 1.73 ng/ml (normal: 0.8–2.0), T4 9.66 μg/dl (normal: 4.8–12.7), thyroid stimulating hormone 2.10 μIU/ml (normal: 0.27–4.2), luteinizing hormone 4.57 mIU/ml (normal: 2.4–12.6), follicle stimulating hormone 5.11 mIU/ml (normal: 1.5–12.4), testosterone 18.73 nmol/l (normal: 0.9–27), estradiol 61.9 pg/ml (normal: 7.6–42.6), prolactin 9.36 (normal: 4.0–15.2) ng/ml, and 08:00 h cortisol 491.1 nmol/l (normal: 171–536). The patient was started on medroxyprogesterone depot 150 mg intramuscularly every month. After 3 months of therapy, the patient had improvement in hypersexual behavior to near normal. Noncontrast CT on a follow-up visit showed gliotic changes in bilateral frontal lobes, left more than the right, with prominent ventricles [Figure 2].
Figure 2: Noncontrast CT head shows gliotic changes in left frontal lobe

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The neurological basis of human sexual response and its regulation are poorly understood. Most of the information on human sexual response comes from the studies in patients with traumatic brain injuries or neurological disorders such as Parkinson's disease, multiple sclerosis, Huntington's disease, and focal epilepsy. Hypersexuality has been rarely described following stroke, and is usually caused by thalamic or subthalamic infarcts and injuries to the frontal lobe or temporal lobe, usually associated with disinhibition and other cognitive dysfunctions.

Structural damage to different areas of the brain caused by stroke or brain injuries causes different types of hypersexual behavior [Table 1]. Hypersexuality and hemiballism occur as a result of subthalamic infarcts,[9] and disinhibition and hypersexuality occur with prefrontal and basal medial frontal lesions.[2],[7] Klüver–Bucy syndrome occurs as a result of temporal infarcts, and hypersexuality and hemiparesis result from basal ganglia (lentiform nuclei and head of caudate nucleus) infarct due to middle cerebral artery occlusion or due to hemorrhage.[10] Excessive masturbation and third nerve palsy have been described in bilateral thalamic infarct. Alien hand sign leading to excessive masturbation occurs due to lesions of the corpus callosum and frontal lobe due to anterior cerebral artery infarct.[11],[12]
Table 1: Cases of hypersexuality associated with brain lesions

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In vascular neurocognitive disorder, there is evidence of cerebrovascular disease from history, physical examination, and neuroimaging. This account for the onset of neurocognitive deficits, which are temporally related. The cognitive deficits can be attributed to disruption of cortical–subcortical circuits, and complex attention, particularly the speed of information processing and frontal executive functions, are likely to be affected.[13],[14],[15],[16],[17],[18],[19]

Frontotemporal neurocognitive disorder has an insidious onset and gradual progression with behavioral symptoms, including disinhibition, apathy, loss of empathy, perseverative, stereotyped or compulsive/ritualistic behavior, hyperorality, and decline in social cognition or executive abilities, or decline in language ability, in speech, word finding, object naming, grammar, or word comprehension. There is relative sparing of learning, memory, and perceptual-motor function. There may be neuroimaging evidence or of genetic mutation from either family history or genetic testing.[19]

Emotional lability has a number of organic causes including cerebrovascular accidents, head injury, epilepsy, Parkinson's disorder and other dementias, brain tumors, and multiple sclerosis. It is a common feature of frontal lobe syndrome, where it occurs with other signs of disinhibition (bad language, sexually inappropriate behavior, rage episodes), severe personality change (at the very least, loss of social graces and consideration for others), loss of initiative and ambition, and reduction in motor activity.[20]

Patients with right frontal lobe hemispheric injury are less inhibited and aware of inappropriate social behavior. Patients with injuries involving these anatomical regions have reduced insight.[13] Frontal right or left hemispheric lesions usually present with hyposexual desire; however, some studies show more decline of sexual function in the left hemispheric stroke,[14],[15] while some studies show a greater decline in sexual function involving the right hemisphere stroke. However, higher sexual arousal and increased sexual activity following the right hemispheric lesions have been described in some cases.[16],[17]

Literature on brain imaging during sexual functioning is lacking. Diffusion tensor imaging (DTI), a magnetic resonance imaging technique, has been used to quantify white matter organization and integrity. DTI has been used in patients with kleptomania [18] and in compulsive sexual behavior, when high superior mean diffusivity on DTI is seen.[10]

The aim of management of inappropriate hypersexual behavior is to reduce the risk to other people in the society and risk of injuries to the patient.[11],[12],[13],[14],[15],[16],[17],[18] Antipsychotic drugs, antiandrogen medications, gonadotropin-releasing hormone-agonists, and estrogens have been used with variable results. Medroxyprogesterone acetate (MPA) has also been used to treat hypersexual behavior; it reduces the sexual drive by inhibiting gonadotropes and directly acts on testes, thus lowering testosterone levels. MPA is safe and efficacious and has been used in habitual sexual offenders and pedophiles.

The index case presented with hypersexuality with an intact insight and evidence of lesions in the left frontal hemisphere, which is contrary to the findings in the available literature.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Ponsford J. Sexual changes associated with traumatic brain injury, Neuropsychol Rehabil 2003;13:275-89.  Back to cited text no. 1
    
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Mutarelli EG, Omur MPA, Adoni T. Hypersexuality following bilateral thalamic infarction. Arq Neuropsiquiatr 2006;64:146-8.  Back to cited text no. 3
    
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Kaplan SM, Richard BK. Diagnosis, assessment, and treatment of hypersexuality. J Sex Res 2010;47;181-98.  Back to cited text no. 8
    
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Absher JR, Vogt BA, Clark DG, Flowers DL, Gorman DG, Keyes JW, et al. Hypersexuality and hemiballism due to subthalamic infarction. Neuropsychiatry Neuropsychol Behav Neurol 2000;13:220-9.  Back to cited text no. 9
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Libman RB, Wirkowski EJ. Hypersexuality and stroke: A role for the basal ganglia? Cerebrovasc Dis 1996;6:111-3.  Back to cited text no. 10
    
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Mondon K, Bonnaud I, Debiais S, Brunault P, Saudeau D, de Toffol B, et al. Abrupt onset of disturbed vigilance, bilateral third nerve palsy and masturbating behaviour: A rare presentation of stroke. Emerg Med J 2007;24:600-1.  Back to cited text no. 11
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Goddess E, Wagner N, Silverman, D. Post stroke sexual activity of CVA patients. Med Aspects Human Sex 1979;13:6-30.  Back to cited text no. 14
    
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Monga TN, Monga M, Raina MS. Hypersexuality in stroke. Arch Phys Med Rehabil 1986;67:415-7.  Back to cited text no. 16
    
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Coslett H, Heilman K. Male sexual function: Impairment after right hemisphere stroke. Arch Neurol 1986;43:1036-9.  Back to cited text no. 17
    
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Grant JE, Correaia S, Brennan-Krohn, T. White matter integrity in kleptomania: A pilot study. Psychiatry Res Neuroimaging 2006;147:233-7.  Back to cited text no. 18
    
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DSM-5. Diagnostic and statistical manual of mental disorders. APA. American Psychiatric Association. Arlington, VA; 2013. pp 614-22.  Back to cited text no. 19
    
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Byrne P, Byrne N. Psychiatry, Clinical cases uncovered. Wiley Blackwell; 2008. pp 106.  Back to cited text no. 20
    


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