1. Alcoholic hallucinosis

George Bramham

Alcoholic hallucinosis can occur in patients with chronic alcohol abuse; both during heavy alcohol consumption and on stopping alcohol suddenly. The ICD-10 classifies alcoholic hallucinosis as a psychotic disorder due to the use of alcohol1,2 of rapid onset intense hallucinations, predominantly auditory in nature, which cannot be solely explained by acute intoxication or by delirium tremens. Patients may hear voices or music. Delusion and mood change can occur, but this is not the prominent feature. Patients with alcoholic hallucinosis usually have insight into the condition and fluctuation in consciousness does not usually occur.3

It was first named in 1919 by the Swiss psychiatrist Eugen Bleuler,4 following descriptions of cases from as early as 1847, where a syndrome named ‘folie d’ivrogne’, meaning ‘drunken madness’, was noted by the French author C.N.S Marcel.5 Since the discovery, relatively little research has been conducted into alcoholic hallucinosis and the evidence base is recognised as poor.6, 7 This disorder occurs worldwide; with incidences of 0.4-12.36% in alcohol dependent patients, depending on the study quoted,8-10 although it is thought that true incidence is probably around 0.4%, due to issues with the design of the studies quoting higher values.7 The aetiology of alcoholic hallucinosis is unknown; evidence currently available has found no conclusive evidence of a genetic link to schizophrenia, and imaging studies have been unable to identify a cause for this disorder.7 One study discovered increased levels of the excitatory neurotransmitters glutamate and aspartate, and reduced levels of inhibitory GABA and glycine in these patients.11 Several studies have examined the efficacy of different antipsychotics in managing alcoholic hallucinosis, but conclusive results have yet to be drawn.

Currently, abstinence from alcohol and antipsychotic medication is the mainstay of treatment, but more extensive evidence needs to be carried out in this area.7 One Indian study quoted that in a study of 52 patients with alcoholic hallucinosis, 13.5% continued to hallucinate even though patients had remained abstinent, and 21% of patients did not have relapse, even though they continued to consume alcohol.3 This reinforces the view that further study of alcoholic hallucinosis is required to be able to understand and manage this disorder effectively.


1. Moore DP, Puri BK, Arnold A. Textbook of Clinical Neuropsychiatry and Behavioral Neuroscience. 2012;70(6):786-804.
2. International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10)-WHO Version 2016 at http://apps.who.int/classifications/icd10/browse/2016/en#/F10-F19 (accessed 14/01/2017).
3. Perme B, Vijaysagar KJ, Chandrasekharan R. Indian J. Psychiatry 2003;45(4):244-46.
4. Bleuler E. Textbook of psychiatry, 1916:341. (The individual mental diseases).
5. Glass IB. Br J Addict 1989;84(2):151-64.
6. Engelhard CP, Touquet G, Tansens A, De Fruyt J. Tijdschrift voor psychiatrie 2014;57(3):192-201.
7. Jordaan GP, Emsley R. Metab Brain Dis 2014;29(2):231-43.
8. Soyka M. Eur Arch Psychiatry Clin Neurosci 2008;258:317-18.
9. Perälä J, Kuoppasalmi K, Pirkola S, Härkänen T, Saarni S, Tuulio-Henriksson A. Br. J. Psychiatry 2010;197(3):200-6.
10. Sedain CP. J Nepal Health Res Counc 2013;11(23):66-9.
11. Aliyev ZN, Aliyev NA. Narcology (Russian) 2004;12:48-53.


2. Alice in Wonderland syndrome

Nasreen Desai

“I can’t explain myself sir, because I’m not myself you see1” - Lewis Carroll, Alice in Wonderland1

Alice in Wonderland syndrome describes a rare neurological disorder, first described in 1955 as a perceptual disorder characterised by distortions of visual perception (metamorphopsias), the body schema, and the experience of time.2 Dr John Todd, a British psychiatrist, gave the disorder its name, noting that the misperceptions resemble Lewis Carroll’s descriptions of what happened to Alice.3 The main symptom is of altered body image; there is a distortion in the sufferers’ perception of the size of various objects, much like Alice.2,4 During an episode, some objects appear to get smaller (micropsia), making the sufferer feel larger, while for others, objects get larger (macropsia) making the sufferer feel smaller.4 Objects can also get further away or get closer.

Occurring in children more than adults, symptoms usually occur at night. The hallmark feature of this syndrome is a migraine, which patients usually experience prior to the abnormal perceptions. Looking at the causes of Alice in Wonderland syndrome, there are several theories. It is thought to be caused by a change in the way the brain processes perceptions of the environment, other causes include temporal lobe epilepsy, psychoactive drugs, brain tumours and Epstein Barr virus encephalitis.2 Patients are referred for investigation (bloods, EEG, MRI brain), but a large number will have normal investigations.

Alice in Wonderland syndrome is a distortion of perception4 not an optical problem, a hallucination nor a physiological change to the body’s systems. The diagnosis can be presumed if all other causes of neurological disease have been ruled out and there is an association between symptoms and the onset of migraines.4

There is no known treatment of this condition, with patient reassurance being key. It is important to emphasise that these perceptions are not harmful and do not require treatment; the perceptions usually disappear with time.2,5 Abnormal perceptions can recur several times a day, and may only become less frequent as a child increases in age, and can be frightening and alarming for patients to experience.5

1. http://www.goodreads.com/quotes/333914-i-m-afraid-i-can-t-explain-myselfsir-because-i-am
2. https://well.blogs.nytimes.com
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4909520/
4. https://en.wikipedia.org/wiki/Alice_in_Wonderland_syndrome
5. http://www.neurologytimes.com/headache-and-migraine/alice-wonderland-syndrome


3. Anti-NMDA receptor encephalitis

George Bramham

Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis consists of acute psychiatric symptoms including hallucinations, delusions, agitation and aggression or catatonia. There may also be speech dysfunction, seizures, memory deficits, dyskinesias, autonomic instability, central hypoventilation, and reduced levels of consciousness. 1,2 These receptors are ion channels found in the nervous system and involve the chemicals glycine and glutamate. They have been implicated in many neurological diseases, but in anti-NMDA receptor encephalitis there is an autoimmune reaction resulting in severe encephalitis with mental deterioration of the patient. The first description was in 2005 in four women with ovarian teratomas and was originally named ‘teratoma-associated encephalitis’.3 The antibodies against the NMDAR, which are responsible for the condition, were isolated in 2007 following more reported cases and the syndrome was named by Josep Dalmau and colleagues 4.

One large study identified it as responsible for 4% of confirmed cases of encephalitis in the UK,5 and another showing that in 1% of all ITU admissions with encephalitis, NMDAR antibodies were discovered. Almost all of these patients present with psychiatric symptoms within the first month.2 A multi-institutional cohort study6 revealed that anti-NMDAR encephalitis is more common in women (81%) and is prevalent across all age groups, but predominantly in patients under age 45 (95%) with a median age of 21 years. Tumours were identified in 38% of the patients and 94% of these tumours were ovarian teratomas, with the majority occurring between the ages of 12-45. As expected, there is a female increased incidence of 4:1 females to males. The remaining tumours identified included lung, breast, testicular, ovarian carcinoma, thymic carcinoma, and pancreatic cancer with no more than two cases of either. This study and others7 identified that although there is an association between tumour presence and the syndrome, in the majority a tumour is not identified and no cause is found for the presence of antibodies against the NMDAR.

Definitive diagnosis is by detection of NMDAR antibodies, which should be present in cerebrospinal fluid.9 If present, these antibodies are very specific for anti-NMDAR encephalitis.10, 11 The characteristic course of the illness12 emphasises the rapid mental deterioration and complications.

Treatment involves immunotherapy first-line and removal of any tumours present, with second-line immunotherapy if there is a poor response. With regards to prognosis within 24 months: the mortality rate is 6%, the probability of making a good recovery is 81% and the relapse rate is approximately 12%. Like any encephalitis, some patients are left with intellectual or other mental long-term sequelae.


1. Dalmau J, Gleichman AJ, Hughes EG, Rossi JE, Peng X, Lai M, et al. Lancet Neurol 2008;7(12):1091-8.
2. Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R. Lancet Neurol 2011;10(1):63-74.
3. Vitaliani R, Mason W, Ances B, Zwerdling T, Jiang Z, Dalmau J. Ann Neurol. 2005;58(4):594-604.
4. Dalmau J, Tüzün E, Wu HY, Masjuan J, Rossi JE, Voloschin A, et al. Ann Neurol 2007;1(61).
5. Granerod J, Ambrose HE, Davies NW, Clewley JP, Walsh AL, Morgan D, et al. Lancet Infec Dis 2010;10(12):835-44.
6. Titulaer MJ, McCracken L, Gabilondo I, Armangué T, Glaser C, Iizuka T, et al. Lancet Neurol 2013;12(2):157-65.
7. Irani SR, Bera K, Waters P, Zuliani L, Maxwell S, Zandi MS. Brain 2010;133(6):1655-67.
8. Graus F, Titulaer MJ, Balu R, Benseler S, Bien CG, Cellucci T. Lancet Neurol 2016;15(4):391-404.
9. Gresa-Arribas N, Titulaer MJ, Torrents A, Aguilar E, McCracken L, Leypoldt F. Lancet Neurol 2014;13(2):167-77.
10. Planagumà J, Leypoldt F, Mannara F, Gutiérrez-Cuesta J, Martín-García E, Aguilar E. Brain 2014;138(1):94-109.
11. Moscato EH, Peng X, Jain A, Parsons TD, Dalmau J, Balice-Gordon RJ. Ann Neurol 2014;76(1):108-19.
12. S Kayser M, Dalmau J. Curr Psychiatry Rev 2011;7(3):189-93.


4. Binswanger disease

Nasreen Desai

Described by Otto Binswanger in 1894, Binswanger disease (BD) is a type of dementia caused by widespread, microscopic areas of damage to the deep layers of white matter in the brain.1 The damage is caused by atherosclerosis, thromboembolism and other diseases that obstruct blood vessels that supply the deep structures of the brain,2 leading to disruption of the subneural cortical circuits controlling executive cognitive functioning.1 This results in symptoms of deterioration in memory, organisation, mood, attention, decision making and behaviour1. Binswanger Disease usually affects males and females equally and presents late in the fourth decade and severity increases with age.

The most characteristic feature of Binswanger disease is psychomotor slowness – an increase in the length of time it takes, for example, for the fingers to turn the thought of a letter into the shape of a letter on a piece of paper.1 Other symptoms include forgetfulness, speech changes, changes in
personality or mood (apathy, irritability, and depression), and urinary symptoms in the absence of urological disease.1 CT or MRI scan reveals Binswanger disease damaged brain tissue and is essential for a positive diagnosis.1

Risk factors for Binswanger’s disease include:3

  • Hypertension
  • Smoking
  • Hypercholesterolemia
  • Coronary artery disease
  • Diabetes mellitus

There is no known treatment for Binswanger disease, so the long-term outlook is poor. Due to the vascular aetiology, the symptoms and signs may suddenly worsen due to small strokes, stabilise, and then improve for a short time, but the overall condition continues to advance as the blood vessels become increasingly obstructed.1 The aim of treatment is to reduce the rate of progression of symptoms. This is done by control of diet and increasing exercise, using anti-hypertensives to control blood pressure, statins for atherosclerosis, anti-platelet agents to reduce the risk of thromboembolism and optimising diabetes control.2 Additional medications can be given to control individual symptoms such as depression.


1. NIH, Binswanger’s Disease Information Page https://www.ninds.nih.gov/disorders/all-disorders/binswangers-disease-information-page (accessed 05/02/2017).
2. NORD, Binswanger Disease, https://rarediseases.org/rare-diseases/binswanger-disease (accessed 05/02/2017).
3. NIH, Binswangers disease https://rarediseases.info.nih.gov/diseases/5925/binswangers-disease/cases/24966 (accessed 05/02/2017).


5. Bouffée délirante

Sharna Bennett

Bouffée délirante is a well-known diagnosis in French psychiatry, described in the 1880s by the French psychiatrist Valentin Magnan,1 although information on this condition outside of France is minimal. It literally translates as “delusional flush”.2 It is a cultural disorder, seen mainly in younger males in West Africa and Haiti. The condition is an acute remitting psychosis, described as sudden, short-lived outbursts of aggression and agitation3 with accompanying “clouding of consciousness” in connection with emotional instability. Delusions with ever-changing themes are usually present and hallucinations may be co-existent. An episode may be triggered by a period of stress, although this is not essential for diagnosis. Patients often do not have any previous psychiatric history. Bouffée délirante influenced the ICD-10 label of “acute and transient psychotic disorders”, which are acute-onset psychotic disorders which resolve in less than 3 months. This condition generally has a good prognosis, as after an episode the patient will quickly return to their pre-morbid state, although relapses can occur after symptom-free periods.1


1. Pillmann F, Haring A, Balzuweit S, Bloink R, Marneros A. Australian & New Zealand Journal of Psychiatry 2003:37(3):327-333.
2. Rich M, Sujeeve S. Australian & New Zealand Journal of Psychiatry 2012:46(5):482-483.
3. Singh A, Swann A. International Journal of Geriatric Psychiatry 2007:22(8):817-819.


Briquet’s syndrome

Sharna Bennett

Briquet’s syndrome, named after the 19th century physician, Pierre Briquet, is now more commonly known as somatisation disorder.1 In the ICD-10 diagnostic criteria, it is described as a fluctuating and chronic disorder with a long history, involving frequent contact with primary and secondary care. Patients have several physical symptoms, for at least two years, which are recurrent and often changing in nature and can be related to any part of the body. Somatisation disorder can have a severe impact on the patient’s social functioning.2 Symptoms are widespread and pain may be felt in any area, but common locations are the chest, abdomen and joints. Gastrointestinal symptoms are usually present; these can include bloating, nausea and diarrhoea. Neurological symptoms, such as difficulty swallowing and sexual symptoms, for example heavy menstrual bleeding, are also common. Somatisation disorder is more common in females, with a prevalence of 0.2-2%, while in males it is likely to be less than 0.2%.1 The DSM-5 classification differs to ICD-10 as it has now placed somatisation disorder under the umbrella term of “somatic symptom disorder”, which includes other diagnoses such as hypochondriasis and pain disorder.3


1 Maii F. Canadian Journal of Psychiatry 2004;49(10):652-662.
2. WHO ICD-10 Version:2015 2015 http://apps.who.int/classifications/icd10/browse/2015/en#/F45 (accessed 02/03/17).
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-5). 5th ed. Arlington, VA: American Psychiatric Publishing, 2013.


7. Capgras delusion

Lucy Button

Capgras is a delusion of misidentification, therefore a belief that someone emotionally close to them, such as a partner or child, is an identical looking imposter. The delusion is characteristically associated with underlying psychiatric disorders such as paranoid schizophrenia, but it has also been seen in neurodegenerative disorders such as Alzheimer’s disease and Lewy body dementia.1

The delusion has also been associated with more systemic, organic and metabolic aetiologies; notable examples include cases associated with diabetes mellitus and hypothyroidism. Hence a thorough investigation of the presenting patient is important to exclude secondary causes.2, 3 It is important to note that the delusion is not simply misidentification, but the patient recognises that the imposter has the identical physical appearance of the true person.1


1. Riggs S, Perry T, Dowben J, Burson R. Perspect Psychiatr Care. 2016.
2. Hines A, Stewart JT, Catalano G. J Psychiatr Pract. 2015;21(6):445-8.
3. Collins MN, Hawthorne ME, Gribbin N, Jacobson R. Postgrad Med J. 1990;66(782):1064-7.