This article presents an A-Z list of unusual psychiatric disorders that may present in primary care from Paris syndrome to Trichotillomania. This is part three of a three-part article.
31. Munchausen’s syndrome by proxy
Originally described by Dr Roy Meadow in 1977,1 Munchausen’s syndrome by proxy is a severe form of factitious illness, wherein the patient creates illness in another individual, usually a dependent, for no extrinsic gain.2 Because the patient reports symptoms within another person, Munchausen’s by proxy is invariably linked to abuse, and medical professionals are inevitably involved throughout, often as active, but unwitting, participants.3 The abuse usually takes a physical or emotional form, with neglect being more accurately described by the term Diogenes syndrome by proxy.4
A textbook case of Munchausen syndrome by proxy was reported in 2000, and involved a mother inducing hypoglycaemic episodes in her child through covert insulin administration.5 It is important to note that while this is a classic presentation, the perpetrators are not necessarily female, and the victims not necessarily children. Cases having been documented with male perpetrators and elderly victims respectively.5
- Meadow R. Munchausen syndrome by proxy, the hinterland of child abuse. The lancet 1977;310(8033):343.
- Semple D, Smyth R. Child abuse 1: general issues, Box 16.3 Munchausen's syndrome by proxy: factitious or induced illness syndrome (FIIS). Oxford Handbook of Psychiatry; 2012. p. 662.
- Cordess C. Munchausen syndrome by proxy abuse: a practical approach. Br J Psychiatry 2001;178(5):481
- O'Mahony D, Evans J. Diogenes syndrome by proxy. Brit J Psych 1994;164(5):705.
- Zylstra R, Miller K, Stephens W. Munchausen syndrome by proxy: a clinical vignette. Prim Care Companion J Clin Psychiatry 2000;2(2):42
32. Neuroleptic malignant syndrome
Neuroleptic malignant syndrome (NMS) is a life-threatening complication of antipsychotic medications.1 The pathophysiology of NMS is not well established, but it is suspected that the dopamine-blocking effects of antipsychotic medications leads to a state of hypodopaminergia.2,3,4 Diagnostically, patients may present with an altered mental state e.g. confusion, delirium, stupor and also have muscle rigidity, autonomic dysfunction and hyperthermia.5
Neuroleptic malignant syndrome typically occurs within about two weeks of starting an antipsychotic or increasing its dose. It is characterised by:
- Raised temperature
- Muscle rigidity, which can be severe and interfere with speaking, eating and swallowing
- Altered mental status; mental status can fluctuate through the day, varying from confusion to coma
- Autonomic instability; irregular pulse rate, blood pressure fluctuation, excessive sweating, heart rhythm disturbances and urinary incontinence may be an early sign
- Raised creatine kinase; excessive skeletal muscle breakdown can cause myoglobinuria and acute renal failure. The creatine kinase level in neuroleptic malignant syndrome is typically very much higher than that associated with exertion and physical contact (especially during restraint)
Neuroleptic malignant syndrome should be differentiated from serotonin syndrome. Muscle rigidity, leucocytosis and raised creatine kinase may be absent in serotonin syndrome.
A high index of clinical suspicion should lead clinicians to terminate antipsychotic medications and provide supportive and corrective measures. These include the administration of fluids, correcting electrolyte disturbances and utilising cooling methods to correct hyperthermia.2,6 There is little evidence to suggest pharmacological treatment has a role in ameliorating symptoms or improving recovery.7 This medical emergency presents significant challenges on both diagnostic and therapeutic levels, with mortality rates standing at 10% per episode.8 Combinations of antipsychotics, or concomitant use of antipsychotics and lithium or antidepressants, may increase the risk of NMS. The onset of clozapine-induced NMS does not tend to follow the classic pattern, with a reduced likelihood of tremor and rigidity.
Rarely, NMS is linked with withdrawal or reduction in dose of dopamine agonists such as levodopa, amantadine or bromocriptine. Metoclopramide and domperidone have been reported to cause NMS in some patients.
- Strawn JR, Keck PE Jr, Caroff SN. Neuroleptic Malignant Syndrome. AM J Psychiatry. 2007; 164:870-876
- Buckley P, Adityanjee M, Sajatovic M. Neuroleptic malignant syndrome. In: Katirji B, Kaminski HJ, Preston DC, et al, eds. Neuromuscular disorders in clinical practice. Boston, MA: Butterworth-Heinemann; 2002:1264-1275
- Caroff SN, Mann SC. Neuroleptic malignant syndrome. Med Clin North Am. 1993;77:185-202
- Lazarus A, Mann SC, Caroff SN. The neuroleptic malignant syndrome and related conditions. Washington, DC: American Psychiatric Press; 1989
- Velamoor VR, Norman RM, Caroff SN, et al. Progression of symptoms in neuroleptic malignant syndrome. J Nerv Ment Dis. 1994;182:168-173
- Heiman-Patterson TD. Neuroleptic malignant syndrome and malignant hyperthermia: important issues for the medical consultant. Med Clin North Am. 1993;77:477-492
- Hasan S, Buckley P. Novel antipsychotics and the neuroleptic malignant syndrome: a review and critique. Am J Psychiatry. 1998;155:1113-1116
Nymphomania is a term which refers specifically to women, who have an uncontrollable, excessive or insatiable drive to engage in coitus. There is no medical or scientific definition for a female described as a nymphomaniac, and there is a considerable debate about whether it can even be termed a disease or clinical condition.1 The concept of nymphomania dates back to the Victorian era when it was described as ‘female pathology of over-stimulated genitals’. Some of the behaviours that led to this classification include women removing their clothes in public, grabbing at the first man they see, bearing children out of wedlock or getting caught engaging in masturbation.2
In psychiatry today it is uncertain where the line is drawn between personal preferences and habits and an illness that truly affects the well-being of an individual.3 This has led to the implementation of hypersexuality disorders into the ICD and DSM classification of disease, in an attempt to distinguish between true hyper-sexuality pathologies and out-dated terms such as nymphomania.
- Goldberg, A. Sex, Religion, and the Making of Modern Madness. New York: Oxford University Press, 1999
- Grant JE, Potenza MN. The Oxford Handbook of Impulse Control Disorders. Oxford University Press; 2011
- Kingston, D., & Firestone, P. (2008). Problematic Hypersexuality: A Review of Conceptualization and Diagnosis Sexual Addiction & Compulsivity, 15 (4), 284-310
Onychophagia, in lay terms is known as chronic nail biting. It is a common behaviour with prevalence estimated between 20-50%.1 It peaks in childhood/adolescence.2 It is partly impulsive and partly compulsive.1 Onychophagia’s aetiology is unknown but there are genetic and environmental contributions and associations with some psychiatric disorders such as anxiety and obsessive compulsive disorder (OCD).2 Onychophagia can vary in its level of severity, although there is not a clear categorisation of severity.3 Generally it is split into mild and severe:
- Mild: nail biting is used to self-groom and control nail length
- Severe: nails are bitten below the soft tissue border.3
Behaviour modification methods can be used to prevent or stop Onychophagia such as habit reversal or aversion techniques.1 Relaxation training may also be useful in the management of onychophagia.3
- Koritzky G, Yechiam E. On the value of nonremovable reminders for behavior modification: An application to nail-biting (Onychophagia). Behavior Modification 2011;35(6):511-30
- Halteh P, Scher RK, Lipner SR. Onychophagia: A nail-biting conundrum for physicians. Journal of Dermatological Treatment 2016:1-7
- Wells JH, Haines J, Williams CL, Brain KL. The self-mutilative nature of severe onychophagia: A comparison with self-cutting. The Canadian Journal of Psychiatry / La Revue canadienne de psychiatrie 1999;44(1):40-7
35. Orthorexia nervosa
Orthorexia nervosa is defined as malnutrition resulting from extreme diets which are intended for health reasons,1 ritualised eating patterns and avoidance of foods believed to be unhealthy.2 It most commonly occurs in adolescence.3 It was first defined in 1997 by Steven Bratman.4 The two main diagnostic criteria for orthorexia nervosa are:
- an obsessive focus on dietary practices believed to promote optimum health
- consequent impairment to health.4
Image disturbance and body weight concerns are not required for diagnosis.4
There is a diagnostic overlap between orthorexia nervosa and other psychiatric conditions such as anorexia nervosa and obsessive compulsive disorder (OCD).2 Current management guidance suggests cognitive-behavioural therapy and psychoeducation in addition to medical management, including selective serotonin reuptake inhibitors.2
- Dunn TM, Bratman S. On orthorexia nervosa: A review of the literature and proposed diagnostic criteria. Eating Behaviors 2016;21:11-7
- Koven NS, Abry AW. The clinical basis of orthorexia nervosa: Emerging perspectives. Neuropsychiatric Disease and Treatment 2015;11
- Hyrnik J, Janas-Kozik M, Stochel M, Jelonek I, Siwiec A, Rybakowski JK. The assessment of orthorexia nervosa among 1899 Polish adolescents using the ORTO-15 questionnaire. International Journal of Psychiatry in Clinical Practice 2016;20(3):199-203
- Cuzzolaro M, Donini LM. Orthorexia nervosa by proxy? Eating and Weight Disorders 2016;21(4):549-51
36. Paris syndrome
Paris syndrome is a transient psychological disorder precipitated by the shock that Paris does not live up to the romanticised city that is portrayed. It usually occurs in Japanese tourists and is characterised by delusions, hallucinations, feelings of persecution, derealisation and depersonalisation.1 2 In severe cases, psychosomatic symptoms such as tachycardia, excessive perspiration and vomiting may be seen.3
It was first recognized in 1986 by Professor Hiroaki Ota; and since then an average of 12 victims per year have been identified and repatriated.3-4 Subsequently, the Japanese embassy in Paris has established a 24-hour hotline for people suffering from the syndrome.4
Two subsets of the syndrome have been identified:
- Type 1 (Classic) describes an individual with a psychiatric background whose basis for visiting Paris revolves around delusional motives. The onset of symptoms occurs soon after arrival to Paris, and may even be triggered by stepping into Charles de Gaulle Airport.
- Type 2 (Delayed Expression) is usually observed in patients without a psychiatric history, whose intentions for visiting Paris were ‘normal’. Symptoms occur much later (three months or more) into their stay in Paris.1
Symptoms are provoked by certain cultural encounters such as confusion caused by language barriers, and feelings of ostracization due to contrasting manners and attitudes. These cumulative factors, combined with the anguish of combatting the mismatch between the fantasized Paris and its reality, lead to a rapid deterioration in mental state - that is Paris syndrome.3,4
It is said that there is only one cure: to leave Paris and never to return.5
- Viala A, Ota H, Vacheron MN, Martin P, Caroli F. Les Japonais en voyage pathologique à Paris: un modèle original de prise en charge transculturelle. Nervure. Jun 2004;5:31-4. (Translated to English).
- Katada T. Reflexions on a case of Paris syndrome. Journal of the Nissei Hospital. 1998;26(2):127-32
- Swallow D. Paris Syndrome: Shocking Reality. Cross- Cultural Differences, Culture Shock and Stuff, East Asia, Europe, General. July 2011. (Accessed Jan 2017.) Available at: http://www.deborahswallow.com/2011/07/11/paris-syndrome-shocking-reality/#more-2428
- Griffiths M. French connections: A beginner’s guide to Paris Syndrome. Nov 2013. (Accessed Feb 2017) Available at: https://drmarkgriffiths.wordpress.com/2013/11/13/french-connections-a-beginners-guide-to-paris-syndrome/
- Wyatt C. Paris syndrome Strikes Japanese. BBC news. Dec 2006. (Accessed Jan 2017.) Available at: http://news.bbc.co.uk/1/hi/6197921.stm
Pica is an eating disorder characterised by an intense urge to consume non-nutritional objects, or substances which are not culturally defined as food. The term ‘Pica’ is derived from the Latin for magpie; a bird that collects an assortment of non-food items.1 It was first reported by Hippocrates in 400 BC and has since been recorded world-wide.2
According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), for such behaviour to be considered Pica, non-food items must be eaten at least once a month at an age for which it is developmentally inappropriate, and these compulsions must be inconsistent with social or cultural norms.3 Three main subtypes of non-nutritional substances prevail in Pica:
- earth substances such as clay or dirt (geophagia)
- paper products including wallpaper or toilet paper (amylophagia
- or ice (pagophagia).
- Nevertheless, items consumed vary depending on what may be available, and chalk, soap, cloth, coal, hair and paint have also been reported.4,5
The prevalence of Pica is relatively unknown, although it is predominantly reported in people from humid countries. It is common amongst pregnant women, children, people with developmental disabilities, and may coexist with a primary eating disorder.3,6
Patients with Pica can present with a varied spectrum of clinical features, sometimes manifestations of lead poisoning, and deficiencies in iron and zinc.2 Thus, complications may be benign or life threatening, highlighting the importance of identifying the ingested items.
- Johnson BE. Pica. In: Clinical Methods: The History, Physical, and Laboratory Examinations, 3rd edition, Walker HK, Hall WD, Hurst JW. (Eds), Butterworths, Boston 1990
- Young SL. Pica in pregnancy: new ideas about an old condition. Annu Rev Nutr 2010; 30:403
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), American Psychiatric Association, Arlington, VA 2013
- Simpson E, Mull JD, Longley E, East J. Pica during pregnancy in low-income women born in Mexico. The Western journal of medicine. 2000 Jul 1;173(1):20
- Kettaneh A, Eclache V, Fain O, Sontag C, Uzan M, Carbillon L, Stirnemann J, Thomas M. Pica and food craving in patients with iron-deficiency anemia: a case-control study in France. The American journal of medicine. 2005 Feb 28;118(2):185-8
- Young SL, Sherman PW, Lucks JB, Pelto GH. Why on earth?: Evaluating hypotheses about the physiological functions of human geophagy. The Quarterly review of biology. 2011 Jun 1;86(2):97-120
Porphyria’s most famous patient is King George III, although more recent evaluation of evidence suggests that he was more likely to have suffered from manic-depressive psychosis rather than attacks of acute porphyria.1 The porphyrias are a group of rare haematological metabolic disorders which are due to reduced activity of any of the enzymes in the heme- biosynthetic pathway.
Diagnosis is by investigation of stool or urine porphyrin levels in an attack and diagnosis may subsequently require offers of genetic family screening. Out of the various subtypes of porphyrias, four have neuropsychiatric manifestations: acute intermittent porphyria, plumboporphyria, hereditary coproporphyria and variegate porphyria.2 Many are autosomal dominant but with poor penetrance so may never be clinically significant for the patient.
The porphyrias have a varied clinical course, with episodic and bizarre features. Symptoms include abdominal pain, skin lesions including photosensitivity, peripheral neuropathy, muscle weakness, vomiting and constipation. Psychiatric symptoms described in porphyrias are anxiety, hysteria, restlessness, insomnia, depression and psychosis. Psychiatric symptoms can present in a range of ways, from aggression and impulsive behaviour, to social withdrawal and persecutory delusions.3 Electrolyte disorders may occur. The porphyrias are easy to misdiagnose or miss, due to the variety of symptoms and attacks range from very acute to patients with chronic deficits. Porphyrias also mimic other medical and psychiatric disorders.2 Described as the ‘little imitator’, compared with syphilis being the ‘big imitator’, these rare disorders should not be forgotten about.3
- Peters TJ, Beveridge A. The madness of King George III: a psychiatric re-assessment. Hist Psychiatry. 2010;21(81 Pt 1):20-37
- Gonzalez-Arriaza HL, Bostwick JM. Acute porphyrias: a case report and review. Am J Psychiatry. 2003;160(3):450-9
- Crimlisk HL. The little imitator--porphyria: a neuropsychiatric disorder. J Neurol Neurosurg Psychiatry. 1997;62(4):319-28
39. Q Fever
Coxiella burnetii, a gram-negative obligate intracellular bacterium, is the aetiological agent of human Q fever. Q fever can manifest as an acute or chronic illness. Acute disease is typically a self-limiting febrile illness during which pneumonia or hepatitis can occur.1 Chronic disease, although rare, is a severe illness that usually manifests as endocarditis and occasionally as vascular infection, osteomyelitis, or chronic hepatitis.2 Infections with this zoonotic pathogen occur worldwide. Q fever is considered an occupational hazard associated with domestic livestock operations.1
People can become infected by inhaling contaminated particles of air, or through contact with the milk, urine, faeces, vaginal mucus, or semen of infected animals. People who have frequent contact with livestock face a significantly higher risk of developing Q fever. This includes farmers, veterinarians, stablehands, meat packers, and slaughterhouse workers. Living near a farm or farming facility may increase the risk. The bacteria can also be airborne.3
A number of studies4 have shown symptoms of mood disorders, depression, anger, and other neurocognitive problems were evident is human sufferers of Q fever.
- Maurin, M., and D. Raoult.1999. Q fever. Clin. Microbiol. Rev. 12:518-553.
- Raoult, D., T. Marrie, and J. Mege. 2005. Natural history and pathophysiology of Q fever.Lancet Infect. Dis. 5:219-226
- Medical News Today: http://www.medicalnewstoday.com/articles/191799.php
- Fatigue following Acute Q-Fever: A Systematic Literature Review (Morroy et al, 2016) http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0155884
Satyriasis also known as hyper sexuality or nymphomania colloquially can be defined as “exhibiting unusual or excessive concern with indulgence in sexual activity”.1 ICD-10 classification includes “Excessive Sexual Drive” which is subdivided into satyriasis and nymphomania for males and females respectively.2 Hyper sexuality can be a primary condition itself or present as a symptom of an underlying disorder or disease. Causes of hyper sexuality are suggested to be due to hormonal imbalances or a defect in the limbic system.3 The frontal lobe, the area of the brain responsible for our personality and inhibition if damaged can also give rise to loss of inhibition, and sexually inappropriate behaviour thus neurodegenerative disorders such as patients with dementia can present with it.4 Side effects from cognitive enhancers used in the treatment of dementia and other medication such as dopamine agonists used in Parkinson’s disease have also been implicated in hyper sexuality in these groups of patients.5
Other disorders which may present with hyper sexuality as a symptom are bipolar disorder, schizophrenia and neurosis. Personality disorders may also give rise to symptoms. The aetiology needs to be considered as this will affect the treatment offered. If secondary to organic disease, good management of the underlying disease may improve symptoms whereas if due to a borderline personality disorder psychotherapy should be offered.3
- Hypersexual – Definition of hypersexual by Merriam-Webster.merriam-webster.com
- 2012 ICD-10 Diagnosis Code F52.7 : Excessive sexual drive.
- Satyriasis from a contemporary perspective: A review of male hypersexuality. Moore, Stan L.; May, Michael Hillside Journal of Clinical Psychiatry, Vol 4(1), 1982, 83-93
- Robinson, Karen M. DNS, RN, CS, FAAN (January 2003). "Understanding Hypersexuality: A Behavioral Disorder of Dementia".Home Healthcare Nurse: the Journal for the Home Care and Hospice Professional.
- Uitti, R. J., Tanner, C. M., & Rajput, A. H. (1989). Hypersexuality with antiparkinsonian therapy.Clinical Neuropharmacology, 12, 375-383
41. Sleeping Beauty Syndrome
This uncommon sleeping disorder is also known as Kleine-Levin syndrome and can affect both males and females, but more commonly boys (4:1) and onset is usually in the teenage years.1 It has an unknown cause, with possible onset due to an infection or neurological event. Due to its periodic nature of presentation, prevalence of the disorder is unknown.2 It is a little known disease and so diagnosis is often delayed after ruling out other possibly disorders. Kleine-Levin syndrome can cause periodic behavioural and cognitive changes including hypersomnia, hyperphagia and hyper sexuality. Associated with the disorder and in some cases there can be irritability, confusion and a feeling of unrealness for surroundings. Episodes can last between 2 to 270 days but most commonly 10 days.3
Patients can recover spontaneously, rapidly and be lucid for several months, which is typical of Klein-Levin syndrome. Diagnosis is mainly clinical as MRI and CT imaging is usually normal. However functional imaging during an episode can show reduced perfusion of the thalamic region and hypothalamus. An EEG will often be abnormal showing a slow wave delta or theta or slowdown of in basic alpha rhythm. Unfortunately there has been evidence of one medication in the treatment of Klein-Levin syndrome. Stimulants such as modafinil have been shown to help, as well as other antipsychotics such as risperidone and benzodiazepines to help with anxiety.1
- Miglis MG, Guilleminault C. Kleine-Levin syndrome: a review. Nature and Science of Sleep. 2014;6:19-26
- Mudgal S, Jiloha RC, Kandpal M, Das A. Sleeping beauty: kleine-levin syndrome. Indian Journal Of Psychiatry. 2014;56(3):298-300
- Assi B, Yapo-Ehounoud C, Baby MBA, Aka-Diarra E, Amon-Tanoh M, Tanoh C. The Kleine-Levin Syndrome: A Rare Disease with Often Delay
42 Stendhal Syndrome
Stendhal syndrome is also known as Florence Syndrome and describes the phenomenon of being psychologically overwhelmed with the artistic greatness of Florence, Italy. First described by Stendhal in the early 19th Century, an Italian psychiatrist coined the title ‘Stendhal Syndrome’ in 1992, after writing a report of over 100 patients who experienced acute transient psychiatric symptoms after being exposed to some of the artwork Florence has to offer.1
This psychosomatic disorder causes rapid heartbeat, fainting, confusion and hallucinations in people who have viewed astonishing artwork.2 The condition is not limited to the cultural offerings of Florence so other places of artistic beauty are likely to cause such symptoms. There is dispute amongst psychiatrists whether this is an actual psychiatric condition, but whether or not it is included in official diagnostic criteria, staff in Florence hospitals have become familiar with dealing with distressed and confused tourists who have revered the artwork of their city.1,2
- Nicholson TR, Pariante C, McLoughlin D. Stendhal syndrome: a case of cultural overload. BMJ Case Rep. 2009;2009
- Squires N. Scientists investigate Stendhal Syndrome–fainting caused by great art. Daily Telegraph. 2010
43. Stockholm Syndrome
Psychological explanation for the development of a bond created between the captor and the hostage. It is thought to be a form of adaptation, which provides hope for the victim.1 This conscious coping strategy has been seen many times and described as “an intense bond with the captor.” First named in 1973, as “Capture bonding”, after four hostages were taken during a bank robbery. The victims defended the captors and refused to testify. The strong emotions that develop are usually amongst the abuse and beating experienced by the victim.2
The bond is thought to be created by the extreme fear which develops into love and attachment to cope in the hostage situation. The hostage may often feel sympathy for the captors’ cause and begin to believe what they say. This strategy helps to aid survival, and commonly these feelings continue after being released from the hostage situation.3
- Celia Jameson (2010) The “Short Step” from Love to Hypnosis: A Reconsideration of the Stockholm Syndrome, Journal for Cultural Research, 14:4, 337-355
- Mackenzie, Ian K. "The Stockholm Syndrome Revisited: Hostages, Relationships, Prediction, Control, and Psychological Science". Journal For Police Crisis Negotiations. 4: 5–21
- Sundaram, Chandar S. (2013). "Stockholm Syndrome". Salem Press Encyclopedia– via Research Starters
Synaesthesia is a neuropsychological phenomenon in which sensory perceptions become mixed up, such as words being visualised as colour internally. This can be commonly manifested by the conversion of learned semantic memory into a sensory stimulus1 so certain words (e.g. Wednesday) can be visualised as a colour (e.g. dark red with a scaly blue tinge on the outside). The synaesthetic perceptions are always internalised; synaesthetes understand that they are not hallucinating but instead perceiving stimulus in a multimodal manner.
Studies from Cambridge, England found a 6:1 ratio of females to males, a prevalence of 1 in 2000, and a familial link.2
Historically, synaesthetes that were open about their experiences were shunned and given a diagnosis of a mental health disorder (some demographic and socio-cultural aspects of synaesthesia).
Neurological imaging has been done to see whether there is a biological basis for this unusual sensory information mix up. Studies by Paulesu et al3 and Gray et al4 found that when subjects with synaesthesia were given an auditory stimulus, imaging showed activation of the visual cortex. This supports the theory that there are abnormal connections in the brain between cortical regions.
The impact of this experience is entirely individual – for most people the association with words and colours can provide a different way of working memory and be used in a positive, if not pleasant style. However, there are examples of synaesthetes who not only visualise sounds but can interpret visual stimulus audibly, and find it distressing to be in a ‘loud’ colour environment.
- Hochel M, Milan EG. Synaesthesia: the existing state of affairs. Cogn Neuropsychol. 2008;25(1):93-117
- Baron-Cohen S, Burt L, Smith-Laittan F, Harrison J, Bolton P. Synaesthesia: prevalence and familiality. Perception. 1996;25(9):1073-9.
- Paulesu E, Harrison J, Baron-Cohen S, Watson JD, Goldstein L, Heather J, et al. The physiology of coloured hearing. A PET activation study of colour-word synaesthesia. Brain. 1995;118 ( Pt 3):661-76
- Gray J, Nunn J, Williams S, Baron-Cohen S. "Synaesthesia", in Synaesthesia: Classic and Contemporary Readings Eds S Baron-Cohen, J Harrison. (Oxford: Basil Blackwell). 1997
This chronic hair pulling condition is illustrated by repeated pulling of hair from one’s body, either with hands or tweezers, leading to substantial hair loss. This condition is more prevalent in women than men, and studies suggest that 0.6-3.6% of adults are affected by it.1
Trichotillomania is described as an impulse control disorder and studies have investigated links between this condition and anxiety and obsessive-compulsive disorders.2
It is included in DSM-5 under Obsessive-Compulsive and Related Disorders, where five criteria are required:
- the person purposefully removes hair from any region of the body
- the person has tried to decrease or stop the pulling
- The person suffers distress and impairment in functioning
- the hair pulling cannot be accredited to another medical condition e.g. skin disorders
- the hair pulling cannot be better explained by the symptoms of a different mental disorder (for example, in body dysmorphic disorder).3
Shame and low self-esteem are commonly suffered by those with trichotillomania. Medical professionals tend to have insufficient knowledge on this condition, leading to poor care and confusion over treatment.1
- Woods DW, Houghton DC. Diagnosis, evaluation, and management of trichotillomania. Psychiatr Clin North Am. 2014;37(3):301-17
- Grzesiak M, Reich A, Szepietowski JC, Hadrys T, Pacan P. Trichotillomania Among Young Adults: Prevalence and Comorbidity. Acta dermato-venereologica. 2016
- Association AP. Diagnostic and statistical manual of mental disorders: DSM-5. 5th ed. Washington DC
46. Wendigo Syndrome
Wendigo Syndrome, or Wendigo Psychosis, is the culture-bound psychotic syndrome of having an intense hunger for human flesh, despite other food being available and is commonly associated with cannibalism.
The term ‘Wendigo’ comes from a North American (Algonquian) folk tale about an evil spirit which possessed people and caused them to become cannibals. The spirit was believed to possess an individual if they became too greedy or selfish and forced them to become ‘wild’ and ’savage’ and eventually attack their family and loved ones. This tale was thought to promote a behaviour of selflessness amongst their people but was often taken very literally as well.1
Despite this being only a folk tale, the north American indians were also the first to report a true psychological phenomenon where members of their tribes would suddenly become violent and aggressive, threatening others and claiming they craved human flesh. The similarity to their tale of the Wendigo led to sufferers being executed if their native healers could not cure the illness, believing the cause to be an evil spirit.2
The first written descriptions of this phenomenon appeared during the colonisation of North America in the 17th and 18th Century. French travellers would often describe, in detail, accounts of men becoming ‘rabid’ and attacking their loved ones with the aim to consume their flesh. The most well-known case, ‘Swift Runner’ in 1878 describes a man who murdered and consumed his wife and five children during an intense storm, despite an emergency food supply only being a few miles away. This was the first written account to specifically describe the cause being ‘Wendigo Psychosis’.3
Wendigo Psychosis has only ever been reported in North America, leading it to be known as a ‘culture-bound’ syndrome. This also led to it’s actual existence being called into question and heavily disputed in the 1960’s after reports of this syndrome became incredibly infrequent. However, due to the number of cases and eye-witness accounts, some form of psychotic origin to these reports cannot be ignored.
Having delusions of craving human flesh and dreaming of cannibalism is frequently reported across the world as a symptom in cases of paranoid schizophrenia and psychotic depression. As Wendigo Syndrome is, by definition, only the ‘intense hunger’ for human flesh and not the cannibalistic act itself, these cases could therefore be described as Wendigo Syndrome.4
However, due to the dispute and lack of knowledge surrounding the syndrome, these delusions are only seen as a symptom of the psychotic illness and not described or reported as ‘Wendigo Syndrome’ itself.
In conclusion, Wendigo Syndrome, the delusion of craving human flesh, is most likely a true symptom still seen today. However, due to lack of knowledge, it is not described as the syndrome itself and only as a symptom of the overlying psychotic disorder.
- Jabbar, F., Kelly, B., & Casey, P. (2008). Mental disorders in specific cultures. Irish Medical Times, 42(43), 40
- Marano, L et al. (1982). Wendigo psychosis: The anatomy of an emic-etic confusion. Current Anthropology, vol. 23, no. 4
- Hay, T. (1971). Wendigo Psychosis: Psychodynamic, Cultural, and Social Factors in Abberant Behaviour. American Anthropologist, vol. 73, no.1.
- Ahenakew, C. (2011). The birth of the ‘Wendigo’: The construction of Aboriginal health in biomedical and traditional Indigenous models of medicine. Critical Literacy: Theories and Practices 5:1
47. Wilson’s Disease
Wilson’s disease is a rare inherited disorder of copper metabolism, first described by British neurologist Samuel Alexander Kinnier Wilson in 1912.1> Also known as hepatolenticular degeneration, Wilson’s causes hepatic copper accumulation and subsequent deposition in tissues and organs throughout the body; most notably the brain and liver. Inherited as an autosomal recessive trait, Wilson’s disease is caused by mutations in the ATP7B gene of chromosome 13 - a gene that would usually code for the binding of copper to caeruloplasmin and its excretion into bile.2,3 The typical onset is during the second or third decade of life, typically presenting as liver disease in children and adolescents, and as neuropsychiatric illness in young adults.4
The psychiatric features are present in approximately one-third of people with the disease, and can be the main presenting complaint involving abrupt behavioural changes, such as aggression, depression with suicidal ideation or psychosis.5 Neurological features involve tremor, ataxia or altered gait, dysphagia, dysarthria, dystonias and dykinesias. Hepatic features of the disease vary in severity from raised serum aminotransferases or hepatomegaly, to acute liver failure or even chronic hepatitis and cirrhosis. Other signs include Kayser-Fleischer rings (present in 95% of those with symptomatic disease), sunflower cataracts, haemolysis, blue lunulae (lunulae are the white part of the nail bed) and early-onset arthritis.6 Wilson’s disease should be considered as a differential diagnosis in any patient with unusual liver or neurological abnormalities. Diagnosis can be established via liver biopsy, or less invasively via clinical signs along with low serum caeruloplasmin or elevated 24-hour urinary copper excretion.7
Conservative management involves a copper-restricted diet. Lifelong oral chelating agents are the treatment for Wilson’s, penicillamine requires careful monitoring due to side effects (rash, nausea, fever pancytopenia) which are deemed intolerable for about one third of patients. Such patients commence zinc acetate or trientine therapy instead. Complications include liver failure; an indication for liver transplantation. Genetic screening in siblings is advisable as asymptomatic homozygotes also need treating.
Prognosis is dependent on the progression and manifestation of the disease and the timeliness of diagnosis as it is fatal if left untreated. Therefore prognosis can vary but many people go on to live a relatively normal life.
- WILSON, S. (1912). Progressive Lenticular Degeneration: A Familial Nervous Disease Associated With Cirrhosis Of The Liver. Brain, 34(4), pp.295-507
- Patient.info. (2017). Wilson's Disease; hepatolenticular degeneration. [online] Available at: https://patient.info/doctor/wilsons-disease-pro [Accessed 8 Jun. 2017]
- abtestsonline.org.uk. (2017). Wilson's Disease. [online] Available at: http://labtestsonline.org.uk/understanding/conditions/wilsons-diseases/ [Accessed 9 Jun. 2017]
- European Association for the Study of the Liver. (2012). Management of Wilson’s disease; https://www.easl.eu/medias/cpg/Wilsons-Disease/English-report.pdf [Accessed 8 Jun. 2017]
-  Rarediseases.info.nih.gov. (2017). Wilson disease | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program. [online] Available at: https://rarediseases.info.nih.gov/diseases/7893/wilson-disease [Accessed 10 Jun. 2017].
48. Yellow fever and psychiatric sequelae
Yellow fever is a tropical virus (flavavirus) spread by mosquitos (mainly the Aedes and Haemogogus species.) It occurs most in tropical and subtropical parts of South America, parts of the Caribbean, and Africa (most common)1 . Initial Symptoms are non-specific and so can be difficult to diagnose: fever, chills, loss of appetite, nausea, muscle pains particularly in the back, and headaches. This is until the disease progresses, when the features include : liver and kidney damage, jaundice and bleeding from orifices.2
Although little research has been done on yellow fever alone and psychiatric sequelae, there is strong evidence from those suffering other types of flavavirus infection, go on to suffer from mental health problems years later. Examples of this include Dengue fever (causing higher incidence of mania, anxiety and depression3,4 and Japanese Encephalitis (30-50% of people develop neurological or psychiatric sequelae)5.
It may be possible that yellow fever is linked with psychiatry in a similar way, but it is difficult to study these possible long-term links because the death rate from yellow fever has been estimated as over 50%6 and many people die within 10 days.
Interestingly, Dr. Benjamin Rush, one of three Physicians who stayed in Philadelphia during the yellow fever outbreak of 1793, named the ‘Father of American Psychiatry’ was the first to conclude that mental illness was a disease of the mind. Perhaps Dr. Rush had determined this from experience of treating the probable psychiatric aspects of yellow fever at the time?
- Nordqvist, C. Yellow fever: Symptoms, causes, and prevention. Medical news today. Updated May 2017. Webpage access: http://www.medicalnewstoday.com/articles/174372.php#post
- http://www.who.int/mediacentre/factsheets/fs100/en/ Updated May 2016 [Date accessed: 18/05/2017]
- Hashmi,MD. Zeeshan, B, Zaidan, I, et al. Anxiety and Depression Symptoms in Patients with Dengue Fever and Their Correlation with Symptom Severity. International Journal of Psychiatry in Medicine. 2012, Vol.44(3), pp.199-210.
- Jhanjee, A ; Bhatia, M.; Srivastava, S. Industrial Psychiatry. 2011, Vol.20(1). p.56
- http://www.who.int/mediacentre/factsheets/fs386/en/ . Updated December 2015 [Date accessed: 18/05/2017]
- Tomori O .Yellow fever: the recurring plague. Crit Rev Clin Lab Sci. 41 (4): 391–427. (2004).
Zoophilia is classed as an ‘other disorder of sexual preference’ by ICD-10,1 so technically doesn’t have a specific diagnostic classification code. It is classified as a disorder of sexual preference involving sexual activity with animals. Sexual Activity involving animals has existed since primitive times.2 There is some blurring between the terms ‘zoophilia’ and ‘bestiality’, with the clearest distinction being that Zoophilia is a sexual desire towards animals (which may involve lust/fantasies and masturbation) whereas bestiality is the physical act of engaging in sexual activity with an animal.
Bestiality remains a criminal offence under the 1956 Sexual Offences Act.3 Several studies4,5 have shown a correlation between forensic offences, psychiatric inpatients and zoophilia, but the exact prevalence amongst the general population is unknown. In some of the studies there doesn’t seem to be any association between zoophilia and animal cruelty and dissocial personality disorder, suggesting the motives behind the behaviour may be sexually driven, rather than cruelty or a desire to inflict pain.
- The ICD-10 Classification of Mental and Behavioural Disorders 6th edition (2000) World Health Organisation. Geneva p220
- Ranger, R., & Fedoroff, P. (2014)."Commentary: Zoophilia and the Law". Journal of the American Academy of Psychiatry and the Law Online. 42 (4): 421– PMID 25492067
- Duffield et al (2015) Zoophilia in Young Sexual Abusers https://www.researchgate.net/profile/Angela_Hassiotis/publication/32886352_Zoophilia_in_Young_Sexual_Abusers/links/556eba7308aeab777226ab42.pdf?origin=publication_list (Date accessed 05/06/2017)
- Wellings, K., Field, J., Johnson, A. M. and Wadsworth, J, (1994) Sexual Behaviours in Britain: The National Survey of Sexual Attitudes and Lifestyles. Harmondsworth, Mx: Penguin
- Miller, K. S. and Knutson, J. F. (1997) ‘Reports of Severe Physical Punishment and Exposure to Animal Cruelty by Inmates Convicted of Felonies and by University Students’. Child Abuse and Neglect 21(1): 59-82
Medical students from the universities of Liverpool and Lancaster, under the guidance of Dr Jane Wilcock and Mr Nick Mullin, provide an A-Z of unusual psychiatric conditions that GPs might encounter. Illustrations by Grace Mutton.