Failed Back Surgery Syndrome (FBSS)

Failed back surgery syndrome (FBSS) is a syndrome characterised by continuing back and/or leg pain despite undergoing lower spinal surgery. FBSS is diagnosed when the outcome of such surgery does not meet the expectations of the patient or the surgeon that were outlined before the surgery.

FBSS occurs as a complication in 5–40% of patients undergoing lower spinal surgery.

It is thought that patients undergoing spinal surgery may be more likely to develop FBSS if they have:

Epidural fibrosis (development of hard connective tissue around one of the layers surrounding the spinal cord and part of the nerves coming from it)Recurrent disc herniationInstability of a segment of spineIncorrect initial diagnosis of the back problemIncomplete decompression (reduction in pressure on the nerve root)Decompression at the wrong levelPoor patient selection for surgeryArachnoiditis (inflammation of one of the layers surrounding the spinal cord and part of the nerves coming from it) Permanent nerve root damageFacet joint disease

The progression of FBSS varies between individuals. It is probably influenced by factors such as the underlying problem with the back before surgery, what kind of surgery was performed, why and when FBSS develops, and how it is managed.

Individuals with FBSS usually experience significant long term back or leg pain following surgery. This may occur in the early stages after surgery, or some time later. Often medication and physiotherapy do not fully relieve this pain, which may result in a reduced level of function.

FBSS is commonly associated with conditions such as depression, anxiety disorder and substance abuse. These conditions need to be identified and managed in order to best treat the pain associated with FBSS.

All chronic pain conditions are significantly impacted by, and have a large impact on, the state of mind of the person experiencing the pain. How the person feels about the pain and how they approach it psychologically plays a significant role in how they function.

The doctor will examine the patient's back, as they would for all patients presenting with back pain. This includes feeling for painful structures, testing range of movement, testing reflexes (by tapping places such as the knees and ankles), checking sensation (touch, hot/cold, pain), and checking leg strength.

There are many tests that may be carried out to determine the underlying cause of FBSS, though the diagnosis can usually be made on the basis of what the patient is feeling (their symptoms).

Possible tests that may be suggested include x-rays, MRI, CT scan, and injection of structures in the back (e.g. the discs and joints).

Unfortunately, FBSS is very difficult to treat effectively, and there is no one treatment known to effectively cure the pain that accompanies FBSS. The likelihood of reducing the pain depends on the underlying cause, and the methods used to treat that cause. 

No one treatment is effective for all people with FBSS. Treatment will vary according to the individual, and the underlying cause of FBSS.

Conservative management

Pharmacotherapy

Medication may be used in pain management. Opioid medication should be used with caution, as it can be habit-forming, and the long term outcome of its effectiveness in FBSS is not clear. GPs or specialists (surgeons, pain specialists, etc) will prescribe medication if it is appropriate.

Exercise/physiotherapy

Gentle exercise programs assist with return to function and psychological wellbeing. It is best if this exercise is tailored to the individual by a physiotherapist or exercise physiologist;

Counselling

Counselling may help with pain management and control strategies. The GP or specialist may arrange a referral to a clinical psychologist to provide this counselling.

Pain clinic

Each of the options outlined above may be combined and provided in the setting of a specialist pain clinic. A GP or specialist may arrange a referral to a pain clinic, which is usually based at a tertiary hospital.  

Spinal cord stimulation

Spinal cord stimulation (SCS) involves electrodes being implanted next to the spine, and an electric current applied. This current modifies the pain signals that are sent by damaged structures. This is an effective option for some individuals with FBSS, as it has been shown to improve health related quality of life in this group.

Injections

Injecting anaesthetic or steroids into the structures around the spine may provide short term relief. Injecting saline or other substances to physically break up scar tissue, a process called lumber percutaneous adhesiolysis, may be effective in some cases.

Further surgery

Some causes of FBSS may be treated with further surgery. For example, if a disc bulge has re-occurred following surgery, it may need to be repaired again. Cutting certain nerves from the spine (medial branch neurotomy) may occasionally be suggested.

For more information about spinal cord stimulation devices, click here.

Anderson VC, Israel Z. Failed back surgery syndrome. Curr Rev Pain. 2000; 4(2): 105-11.Van Goethem JW, Parizel PM, van den Hauwe L, De Schepper AM. Imaging findings in patients with failed back surgery syndrome. J Belge Radiol. 1997; 80(2): 81-4.Schofferman J, Reynolds J, Herzog R, Covington E, Dreyfuss P, O'Neill C. Failed back surgery: Etiology and diagnostic evaluation. Spine J. 2003; 3(5): 400-3.Fiume D, Sherkat S, Callovini G, Parziale G, Gazzeri G. Treatment of the failed back surgery syndrome due to lumbo-sacral epidural fibrosis. Acta Neurochir Suppl (Wien). 1995; 64: 116-8.Heithoff KB, Burton CV. CT evaluation of the failed back surgery syndrome. Orthop Clin North Am. 1985; 16(3): 417-44.North RB, Kidd DH, Campbell JN, Long DM. Dorsal root ganglionectomy for failed back surgery syndrome: A five-year follow-up study. J Neurosurg. 1993; 39: 301-311.Wilkinson H. The failed back syndrome: Etiology and therapy [2nd edition]. Philadelphia: Harper & Row; 1991.Long DM, Filtzer DL, BenDebba M, Hendler NH. Clinical features of the failed-back syndrome. J Neurosurg. 1988; 69(1): 61-71.North RB, Ewend MG, Lawton MT, Kidd DH, Piantadosi S. Failed back surgery syndrome: 5-year follow-up after spinal cord stimulator implantation. Neurosurgery. 1991; 28(5): 692-9.Fan YF, Chong VF. MRI findings in failed back surgery syndrome. Med J Malaysia. 1995; 50(1): 76-81.Talbot L. Failed back surgery syndrome. BMJ. 2003; 327: 985-6.Mavrocordatos P, Cahana A. Minimally invasive procedures for the treatment of failed back surgery syndrome. Adv Tech Stand Neurosurg. 2006; 31: 221-52. North RB, Kidd DH, Farrokhi F, Piantadosi SA. Spinal cord stimulation versus repeated lumbosacral spine surgery for chronic pain: A randomized, controlled trial. Neurosurgery. 2005; 56(1): 98-106.Skaf G, Bouclaous C, Alaraj A, Chamoun R. Clinical outcome of surgical treatment of failed back surgery syndrome. Surg Neurol. 2005; 64(6): 483-9.Polatin PB, Kinney RK, Gatchel RJ, Lillo E, Mayer TG. Psychiatric illness and chronic low-back pain. The mind and the spine-which goes first? Spine. 1993; 18(1): 66-71.Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N. Clinical features of patients with pain stemming from the lumbar zygapophysial joints. Is the lumbar facet syndrome a clinical entity? Spine. 1994; 19(10): 1132-7.Schwarzer AC, Wang SC, Bogduk N, McNaught PJ, Laurent R. Prevalence and clinical features of lumbar zygapophyseal joint pain: A study in an Australian population with chronic low pack pain. Ann Rheum Dis. 1995; 54(2): 100-6.van Akkerveeken PF. The diagnostic value of nerve root sheath infiltration. Acta Orthop Scand. 1993; 64(Suppl 251): 61-3.Slipman CW, Shin CH, Patel RK, Isaac Z, Huston CW, Lipetz JS, et al. Etiologies of failed back surgery syndrome. Pain Med. 2002; 3(3): 200-14.Derby R, Kine G, Saal JA, Reynolds J, Goldthwaite N, White AH, et al. Response to steroid and duration of radicular pain as predictors of surgical outcome. Spine. 1992; 6(Suppl): S176-83.Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine. 1995; 20(1): 31-7.Kumar K, Taylor RS, Jacques L, Eldabe S, Meglio M, Molet J, et al. Spinal cord stimulation versus conventional medical management for neuropathic pain: A multicentre randomised controlled trial in patients with failed back surgery syndrome. Pain. 2007; 132(1-2): 179-88. Hayden JA, van Tulder MW, Malmivaara A, Koes BW. Exercise therapy for treatment of non-specific low back pain. Cochrane Database Syst Rev. 2005; (3): CD000335.Bala MM, Riemsma RP, Nixon J, Kleijnen J. Systematic review of the (cost)effectiveness of spinal cord stimulation for people with failed back surgery syndrome. Clin J Pain. 2008; 24(9): 741-56. Manca A, Kumar K, Taylor RS, Jacques L, Eldabe S, Meglio M, et al. Quality of life, resource consumption and costs of spinal cord stimulation versus conventional medical management in neuropathic pain patients with failed back surgery syndrome (PROCESS trial). Eur J Pain. 2008; 12(8): 1047-58.


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Chronic Pain Syndrome

Chronic pain syndrome encompasses any pain that persists longer than the reasonable expected healing time for the involved tissues. The duration of pain is often arbitrarily set at 3 months duration. In contrast to acute pain, which is a vital protective mechanism, chronic pain serves no physiological role.

It is not a symptom, but rather a disease state. Some conditions that lead to chronic pain syndrome include:

Low back pain (e.g. lumbar radiculopathy, spinal stenosis, facet syndrome, myofascial pain); Neck/shoulder pain (e.g. whiplash, cervical radiculopathy, fibromyalgia); Headache (e.g migraine, cluster, tension type, cervicogenic); Musculoskeletal pain (e.g. soft tissue injury, myofascial pain syndrome, fibromyalgia, arthritis);Neuropathic pain (e.g. post-herpetic neuralgia, chronic regional pain syndrome I and II, phantom limb pain, diabetic neuropathy); Chronic postoperative pain (e.g. post-thoracotomy pain, neuroma formation, neuropraxia).

Chronic pain syndrome has been reported to effect up to 54% of the population at some stage.

Chronic pain syndromes are more common in womens health than men health. People with depression or anxiety are also more likely to develop chronic pain syndromes. Some people who have chronic pain syndrome later develop anxiety or depression as a result of their illness.

Chronic pain syndromes often develop after an acute pain, such as an injury, but they may develop with no recognised preceding injury. Chronic pain is defined as pain that lasts for longer than the expected time for recovery of injured tissues, nominally 3 months.

The history of the pain varies greatly according to the type of pain, but can include

Headaches;Pain;Back pain;Muscle pain;Neuropathic pain;Chronic postoperative pain.

Your doctor will ask you questions about how long the pain has been a problem, how it started, what treatments you have tried and which treatments were effective, what makes the pain better and what makes it worse as well as a general history on other body systems.

Results of the clinical (physical) examination is variable according to the cause of the pain.

Your doctor may order some investigations when determining the cause of your pain, however investigations are not useful once a chronic pain syndrome has been diagnosed.

The prognosis for chronic pain syndromes is extremely variable.

Treatment for chronic pain syndrome can involve several different approaches. It is not always possible to get rid of chronic pain completely. When thinking about managing your pain, the goal may not be to be entirely pain free, but rather to be able to complete more of your daily activities than before (for example, be able to play golf or tennis again).

 

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Domestic Violence

Domestic violence is when an individual is in some way hurt by a person that he or she knows. Domestic violence is not limited to physical harm: a person also can be sexually abused or psychologically abused. Often a victim is hurt in more than one of these ways. Domestic violence usually continues over a long period of time and gets more frequent and more severe over time.

In 2000, the National Violence Against Women Survey (US) reported, in a study of 8000 women and 8000 men, that nearly 25% of women and 7.9% of men indicated that a current or former spouse, cohabitating partner, or date victimized them at some time in their life. Rape was reported by 7.7% of women and 0.3% of men. Physical assault affected 22.1% of women and 7.4% of men. Within the previous 12 months, 0.2% of women reported having been raped, which would equate nationally to 201,394 women. Physical assault was reported by 1.3% of women and 0.9% of men, resulting in national estimates of 1,309,061 women and 834,732 men so victimized. Victimization often occurs repeatedly.

Data from the survey revealed that women averaged 6.9 physical assaults by the same partner, with men averaging 4.4 assaults. Given the data on multiple attacks per victim, it is estimated that every year approximately 4.8 million intimate partner rapes and physical assaults are perpetrated against women, and approximately 2.9 million are committed against men. Almost 5% of women and 0.6% of men in the survey indicated that an intimate had stalked them, with an annual rate of 0.5% of surveyed women and 0.2% of surveyed men. Extrapolation from these data indicates that 503,485 women and 185,496 men were stalked by an intimate partner within the previous 12 months. High-profile news may affect willingness to report domestic violence. Following the Simpson and Goldman murders, the Los Angeles County Sheriff's Department noted a significant increase in domestic violence dispatches. Estimates indicate that at least 2 million women are assaulted by their partners each year. The true incidence may be twice that. Exact figures for males are hard to come by.

Certain groups of women may be at higher risk for abuse. These include women who: Are single, separated or divorced (or planning separation or divorce). Are between the ages of 17 and 28. Abuse alcohol or other drugs or whose partners do. Are pregnant. Have partners who are excessively jealous or possessive.

Characteristic injuries: Bilateral injuries, especially to the extremities. Injuries at multiple sites. Fingernail scratches, cigarette burns, rope burns. Abrasions, minor lacerations, welts. Subconjunctival hemorrhage suggests a vigorous struggle between victim and assailant. Fingernail markings

Three types of fingernail markings may occur, either singly or in combination as follows:

Impression marks: These result from fingernails cutting into the skin. They may be shaped like commas or semicircles. Scratch marks: These are superficial and long and may be narrow or as wide as the fingernail. Scratches caused by the longer fingernails of women are frequently more severe than those from a male assailant. Claw marks: These occur when the skin is undermined, thus they appear to be more dramatic and vicious. While claw marks may be grouped parallel markings down the front of the neck, they often are randomly scattered.

Domestic violence typically recurs and progressively escalates both in frequency and severity. Of persons first injured by domestic violence, 75% continue to experience abuse. Half of battered women who attempt suicide try again. Brookoff reported a study of 62 episodes of domestic assault, in which 68% involved the use or display of weapons (5 handguns, 1 shotgun, 17 knives, and 19 blunt instruments such as hammers or baseball bats), and 15% resulted in serious injury. Eighty-nine percent of victims reported previous assaults by their current assailants, with 35% experiencing violence on a daily basis. The ultimate result of domestic violence may be death from suicide or homicide.

It may seem obvious that a victim of domestic violence should leave the abuser, but it's not always that simple. Some victims of abuse were raised in violent households as children and are caught in a cycle of abuse. Sometimes years of psychological abuse cause victims to believe they deserve to be treated this way. They may feel defeated from repeated abuse and unable to see a way out, or they may desperately hope that the situation will change. They may fear what the abuser will do if they try to leave. Other reasons women do not leave their abusers include having no place to go, no money or no place that will accept her children; fear of losing custody of children; concerns about immigration status (being reported); and religious or cultural beliefs that make abuse seem acceptable.

Abbott J: Injuries and illnesses of domestic violence. Ann Emerg Med 1997; 29: 781-785. Bachman R, Saltzman LE: Violence against women: Estimates from the redesigned survey August 1995. NCJ-154348 Special Report. US Department of Justice. Heilig S, Rodriguez M, Martin S, Louie D, eds: Domestic violence: A practical approach for clinicians. San Francisco Medical Society: 1995.


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Female Sexual Dysfunction (FSD)

Watch a video on Sex

 

The World Health Organisation defines female sexual dysfunction (FSD) as “the various ways in which an individual is unable to participate in a sexual relationship…she would wish.” FSD is classified into a range of disorders depending on the specific nature of the sexual difficulties a woman encounters. They are:

Women suffering from FSD become anxious or distressed about being unable to engage in or experience sexual activity as they wish. However, other women may experience sexual difficulties (e.g. inability to orgasm) which do not cause them distress. These women do not have FSD.  Amongst women with FSD, hypoactive sexual desire and orgasmic disorders are the most commonly reported.

There are many physical causes of FSD and these are mainly related to hormone levels and changes. However, FSD is most commonly the result of psychological factors (e.g. relationship satisfaction, depression).  Even when FSD is the result of physical factors, psychological factors often contribute to the problem (e.g. women who have difficulty achieving adequate vaginal lubrication or find sex painful may become anxious about approaching sexual encounters, and find it even more difficult to lubricate).

Research suggests that the majority of women experience sexual dysfunction at some point in their lives, and for many it is an ongoing or recurring issue. A large survey of Australian women reported that 70% had experienced sexual difficulties (including inability to orgasm and not feeling like sex) in the year before the survey. Women over 50 were most likely to experience sexual difficulties, although they were common in all age groups (over 60% of women aged over 50 reported lack of interest in sex, and more than half of women aged 16-49 also reported this difficulty).

Survivors of sexual assault often experience difficulties in future sexual relationships, which may bring back difficult memories of incidents of assault. Women who are pregnant, have recently given birth or are breastfeeding are more likely to experience sexual dysfunction than those who are not. Hormonal imbalances and psychological factors both play a role for these women. 

Women also often experience sexual dysfunction following menopause, which is mainly a result of hormonal imbalances.

Sexual dysfunction associated with cancer

Between 10 and 88% of patients diagnosed with cancer experience sexual problems following diagnosis and treatment. The prevalence varies according to the location and type of cancer, and the treatment modalities used. Sexuality may be affected by chemotherapy, alterations in body image due to weight change, hair loss or surgical disfigurement, hormonal changes, and cancer treatments that directly affect the pelvic region.

Sexual problems are reported in many patients with breast and gynaecological (e.g. cervical or vulval) cancer. They are also reported in patients with cancer that does not directly effect sexual organs, including lung cancer (48% of patients), Hodgkin's disease (50%), and laryngeal (60%) and head and neck cancers (39-74%). 

For more information, see Sexual Difficulties Associated with Cancer in Women.

While sexual dysfunction is wide spread in Australia, it is more common in particular groups of women.  Factors associated with sexual dysfunction in women include:

It is uncertain how they influence sexual function, but you may also have an increased risk if FSD if you have:

Hormonal changes, which are the most common physical cause of FSD, tend to occur during and after childbirth and following menopause. Certain medications (e.g. antidepressants, hypertension medication) can also alter hormone levels. FSD is more common in women who take these medications.

Unlike in men, sexual dysfunction in women is most commonly the result of psychological factors which can arise throughout life. There is an immense amount of pressure on women in their roles as employees, wives and mothers. This can lead to stress, anxiety and fatigue, which are all more common in women who suffer from FSD than in those who do not. Women who are not satisfied with their relationships more commonly report FSD, as do those who are depressed.

FSD impacts on women’s sexual functioning and on their overall sense of wellbeing. It is associated with depression and relationship satisfaction. Although it is not clear whether FSD causes depression and relationship satisfaction or vice versa, it is likely that, at least in some cases, FSD leads to depression and dissatisfaction with relationships. If you suffer from FSD it is also likely to affect your sexual partner, so you may both want to talk to about professional.

The effects on the partner can have important implications. For example while studies are limited, it has been shown that female sexual function can be negatively impacted on by male sexual dysfunction. A study comparing the sexual function of women with partners with erectile dysfunction to those without showed that sexual arousal, lubrication, orgasm, satisfaction, pain and total score were significantly lower in those who had partners with erectile dysfunction. Later in that study, a large proportion of the men with erectile dysfunction underwent treatment. Following treatment, sexual arousal, lubrication, orgasm, satisfaction and pain were all significantly increased. It was concluded that female sexual function is impacted by male erection status, which may improve following treatment of male sexual dysfunction.

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Lewy Body Dementia (LBD)

Dementia with Lewy bodies (DLB) is a neurodegenerative disorder associated with abnormal structures (Lewy bodies) found in certain areas of the brain. In addition to dementia, patients with dementia with Lewy bodies experience hallucinations, motor impairment, and fluctuating alertness.

Dementia with Lewy bodies is the third most frequent cause of dementia in older adults, and accounts for 15–35% of all dementias. Dementia with Lewy bodies is also the most common dementia syndrome associated with Parkinsonism. It is primarily a disease affecting the elderly population. Men may be at higher risk of developing Lewy body dementia than women.

The cause of dementia with Lewy bodies is still unknown. A very few cases of familial (inherited) dementia with Lewy bodies have been reported, but this is rare.

As with other forms of dementia, the patient will experience a steady decline in their cognitive ability. This may include loss of recent memory, poor awareness of location and the development of inappropriate behaviours. This occurs in a similar fashion to Alzheimer's disease.

In some cases of Lewy Body dementia, patients may also develop increased muscle activity resulting in muscle stiffness and the development of a tremor. The severity of the physical and psychological symptoms may fluctuate greatly, making some days more difficult than others. Patients with this disease may also be unusually sensitive to certain medications such as anti-psychotics and sedatives, which must be used carefully to avoid an increase in the severity of symptoms.

People with dementia with Lewy bodies may present with classical symptoms of any dementia: the subtle development of defects in thinking, reasoning, remembering, imagining, or learning words.

In particular, people with dementia with Lewy bodies will have the following:

Motor symptoms such as rigidity and tremor (similar to the symptoms of Parkinson's disease).Fluctuations in alertness and consciousness.Frequent visual hallucinations.Increased sensitivity to some drugs which act on the brain.

As with other forms of dementia, the aim of investigation is to exclude other causes of the altered mental state. A large number of blood tests and imaging procedures will be carried out to exclude infection, electrolyte imbalance, anaemia, thyroid and liver disease. A CT and MRI scan of the patient's head may be required to improve the accuracy of diagnosis and exclude certain brain conditions that may result in an altered mental state.

The prognosis of dementia with Lewy bodies is generally poor, as there is no specific treatment to reverse the progression of disease. Many patients with this form of dementia respond well to medications that may improve psychological and physical symptoms over a limited period of time. This condition, however, will inevitably progress over time.

Any secondary causes of DLB should be treated if found - these are infrequent (10%), but must be excluded as some causes are potentially reversible. There is currently no treatment to cure Lewy body dementia, or to slow its progression. As such, medical treatment aims to control the symptoms of the dementia, such as the muscle stiffness, tremor and psychiatric disturbances.

Medications can be divided into the following groups:

Acetylchlinesterase inhibitors (e.g. galantamine or donepezil): these may be used to treat agitation and hallucinations, or to reduce confusion and symptom fluctuation. They do not worsen motor symptoms of disease.Anti-Parkinson's medications (e.g. levodopa/carbidopa, dopamine agonists): these are used to treat the motor symptoms (muscle stiffness and tremor) of Parkinson's disease, which are similar to the motor symptoms of Lewy body dementia. However, patients with DLB are often very sensitive to these medications, with little change to motor symptoms but worsening hallucinations and confusion. Because of this, anti-Parkinson's medications are used very carefully in DLB, and only in patients with severe motor symptoms.Antidepressants: these may be used to treat symptoms of depression, common in patients with DLB.
For more information on dementia, including Alzheimer's disease and other types of dementia, information for carers of dementia patients and supportive care, as well as some useful tools and videos, see Dementia.
Collerton D, Burn D, McKeith I, O'Brien J. Systematic review and meta-analysis show that dementia with Lewy bodies is a visual-perceptual and attentional-executive dementia. Dement Geriatr Cogn Disord. 2003; 16(4): 229-37. [Abstract]Fernandez HH, Wu CK, Ott BR. Pharmacotherapy of dementia with Lewy bodies. Expert Opin Pharmacother. 2003; 4(11): 2027-37. [Abstract]Galvin JE. Dementia with Lewy bodies. Arch Neurol. 2003; 60(9): 1332-5. [Abstract]Braunwald E, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine (16th edition). New York: McGraw-Hill Publishing; 2005. [Book]NINDS Dementia With Lewy Bodies Information Page [online]. National Institute of Neurological Disorders and Stroke; 2005 [cited 12 January 2006]. [URL link]McKeith IG, Galasko D, Kosaka K, et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the consortium on DLB international workshop. Neurology. 1996; 47(5): 1113-24. [Abstract]Small GW. Neuroimaging as a diagnostic tool in dementia with Lewy bodies. Dement Geriatr Cogn Disord. 2004; 17(Suppl 1): 25-31. [Abstract]Kaufer DI. Pharmacologic treatment expectations in the management of dementia with Lewy bodies. Dement Geriatr Cogn Disord. 2004; 17(Suppl 1): 32-9. [Abstract]Duda JE. Pathology and neurotransmitter abnormalities of dementia with Lewy bodies. Dement Geriatr Cogn Disord. 2004; 17(Suppl 1): 3-14. [Abstract]Kumar P, Clark M (eds). Clinical Medicine (5th edition). Edinburgh: WB Saunders Company; 2002. [Book]


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Spasmodic Dysphonia (Laryngeal Dystonia)

Dystonia encompasses a broad and complex spectrum of clinical presentations that occur as a result of opposite muscles contracting (muscle co-contraction), involuntarily causing the muscle to spasm. Spasmodic dysphonia (SD) is a rare form of dystonia that affects the laryngeal muscles (vocal cords). It is also known as laryngeal dystonia.

The term spasmodic describes sudden and intermittent jerking movements of muscles and, as such, SD is characterised by poor vocal motor control during speech due to intermittent and involuntary spasms of the laryngeal muscles. SD is a task-specific disorder, which means that symptoms are only experienced while performing a specific task – in this case, speech. Emotive expressions such as screaming, crying and laughing are not affected and so SD is purely a speech disorder. Speech while whispering, shouting or singing appears to be less affected by the muscle contractions, and people may use one or more of these sensory "tricks" to try to alleviate the problem (e.g. speaking with a sing-song intonation or adopting an accent).

People with SD exert significant effort and strain to speak. There are two types of SD which display markedly different vocal symptoms. Very rarely, a person may experience both forms of SD.

Adductor SD (ADSD)

ADSD involves sudden, involuntary spasmodic hyperadduction of the laryngeal muscles during vowel production, resulting in closure of the vocal cords. This causes strangled-sounding "breaks" during speech.

Abductor SD (ABSD)

ABSD involves hyperabduction of the laryngeal muscles during speech production, which results in opening of the vocal cords. ABSD is the less common form of SD. It is characterised by breathiness with aphonic whispered speech segments or breathy breaks.

SD is a rare disorder which is difficult to diagnose, and for this reason the prevalence is largely unknown. It is estimated that 1 in 100,000 people will develop the condition.

ADSD is nine times more common than ABSD. One third of all people with SD will also experience tremor of the voice, although it is possible to have vocal tremor without SD.

Women make up around 60–80% of both subtypes of people with SD. The process can occur in a wide age range, but the averageage that the condition is diagnosed is 39 years.

Unlike other dystonias, there have been no genes identified for SD, although this may be because the condition is so rare that family studies are difficult to conduct.

SD occurs due to irregular inhibition (obstruction) of the laryngeal muscles. The mechanism for this inhibition is not clear. Post-mortem studies have determined that people with SD show decreased axonal and myelin density and increased numbers of inflammatory cells in areas of the brain that control laryngeal behaviour.

The following have not been confirmed as risk factors for SD, but have been associated with the condition at the time of diagnosis:

Like other dystonias, stress and fatigue appear to make SD symptoms worse and could be a trigger for contracting the condition, but whether they are causes is still unknown.

SD is a difficult condition to diagnose and is often confused with other voice disorders, which is why a number of specialists are required to make the diagnosis. Speech pathologists, neurologists and ear, nose and throat specialists work together with the information they have from their separate assessments.

Initially, the general practitioner will discuss the symptoms with their patient in order to understand the problem and then refer them to the specialist or a specialised voice clinic. After all the symptoms have been identified and discussed, a clinical and nasolaryngoscopy examination will confirm the diagnosis. Aside from these, usually no other tests are required.

Assessing the response to certain treatments will also provide an indication of whether the voice disorder is in fact SD. For example, SD does not improve with voice therapy, which can be assessed by a speech therapist. Once this has been concluded, a neurologist will test the response to botulinum toxin (BoNT; Botox) injections, as SD usually improves after this treatment.

SD is a chronic disorder that develops suddenly and often in the third decade. Once developed, people tend to experience a gradual worsening of symptoms. If left untreated, the intensity of spasms is reduced over time in some people, indicating that eventually a change does occur in the muscles.  However, very little is known in this area and it is not recommended to leave the condition untreated for this reason.

Firstly, it is important to develop coping and management skills, as SD symptoms worsen during stress and fatigue. Therefore people are taught ways to relax and respond to stress in a more positive manner, which may decrease the intensity of the laryngeal spasms.

In terms of physical treatments, destroying the nerve endings (denervation) in laryngeal muscles is the most successful treatment for SD. This is most commonly achieved temporarily with botulinum toxin. 

Botulinum toxin (BoNT; Botox)

BoNT injections into the adductor laryngeal muscles (thyroarytenoid) are the most effective treatment for 90% of ADSD patients. Injections can be given into one or both adductors of the vocal folds. BoNT blocks the release of acetylcholine at the neuromuscular junction, and hence reduces contractions in the injected muscles. The mechanism of action may be more complex than just producing weakness in this muscle. The procedure needs to be repeated after 3–6 months.

Different people will respond differently to the treatment. It will work better for some people than others, and some people will require repeat injections sooner than others.

Side effects associated with BoNT use for SD include breathiness, stridor, aspiration and difficulty swallowing. People with ABSD do not tend to respond as well to BoNT injections.

Surgical treatment

Surgical treatment provides permanent structural changes to the larynx, and should only be considered for people who respond well to BoNT and desire longer term management for their condition.

The aim of the procedure is to denervate the larynx to better control the muscle spasms. There is a risk of producing aphonia (an inability to speak), breathiness and swallowing difficulties after denervation. The risk of these adverse events must be weighed against the potential benefits.

Radiofrequency (RF) ablation

Radiofrequency ablation involves the use of a high frequency alternating current to destroy damaged or dysfunctional tissue. In the case of SD, the tissue destroyed is the dystonic laryngeal muscles. This is an advantageous procedure, as it is less invasive than surgery and does not require anaesthesia.

RF ablation has been found to improve scores in acoustics and voice handicap two months after the operation. RF also does not leave a scar on the neck. Some people will require further ablation or BoNT one year after RF ablation. 

Article kindly reviewed by:

Dr Karl Ng MB BS (Hons 1) FRCP FRACP CCT Clinical Neurophysiology (UK)
Consultant Neurologist, Voice Clinic, Dept of Speech Pathology, Royal North Shore Hospital
Sydney North Neurology & Neurophysiology (download referral form and map)
Conjoint Senior Lecturer, University of Sydney and Editorial Advisory Board Member of the Virtual Neuro Centre

Blitzer A, Brin MF, Stewart CF. Botulinum toxin management of spasmodic dysphonia (laryngeal dystonia): A 12-year experience in more than 900 patients. Laryngoscope. 1998;108(10):1435-41. [Abstract]Ludlow C. Research priorities in spasmodic dysphonia [online]. Itasca, Illinois: National Spasmodic Dysphonia Association; 2009 [cited 14 February 2010]. Available from: URL linkLudlow CL. Treatment for spasmodic dysphonia: Limitations of current approaches. Curr Opin Otolaryngol Head Neck Surg. 2009;17(3):160-5. [Abstract]Simonyan K, Tovar-Moll F, Ostuni J, et al. Focal white matter changes in spasmodic dysphonia: A combined diffusion tensor imaging and neuropathological study. Brain. 2008;131(Pt 2):447-59. [Abstract | Full text]Sazgar AA, Akrami K, Akrmi S, et al. Evaluation of brainstem function in patients with spasmodic dysphonia using vestibular evoked myogenic potentials and auditory brainstem responses. Acta Otolaryngol. 2008;128(2):177-80. [Abstract]Brain Foundation. Spasmodic dysphonia [online]. Crows Nest, News South Wales: Brain Foundation; 2010 [cited 14 February 2010]. Available from: URL linkPaniello RC, Barlow J, Serna JS. Longitudinal follow-up of adductor spasmodic dysphonia patients after botulinum toxin injection: quality of life results. Laryngoscope. 2008;118(3):564-8. [Abstract]Kim HS, Choi HS, Lim JY, et al. Radiofrequency thyroarytenoid myothermy for treatment of adductor spasmodic dysphonia: How we do it. Clin Otolaryngol. 2008;33(6):621-5. [Abstract]Allergan Australia. Product Information: Botox. Gordon, New South Wales: Allergan Australia Pty Ltd; 6 August 2009.


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Post-Traumatic Stress Disorder (PTSD)

Post-traumatic stress disorder (PTSD) is a psychological disease. This condition is commonly associated with an extraordinarily stressful event which is re-lived by the person who experienced it in an episodic manner throughout life, causing them to re-experience the stress and anxiety associated with their first encounter.

The incidence of this condition is normally related to the occurrence major traumatic events that are most often political in nature. Following any military conflict, many soldiers suffer PTSD from their witness of fellow soldiers being killed in active service. Because of this association, there remains an incidence of 1-3% in general population, rising up to 30% in Vietnam war veterans.

PTSD is most related to the personal intensity of the experience, if the experience during occurred during childhood or if the patient has suffered previous psychiatric ilness.

The condition may occur at any age, the onset related to the experience of a traumatic event. Such an event may include the witness of traumatic death, serious accidents, natural disasters or being the victim of violent crime, rape, torture or terrorism. Symptoms will usually begin within 6 months of experiencing the traumatic event.

Typical clinical features include:

Flashbacks: repeated vivid reliving of the trauma in the form of intrusive memories, often triggered by a reminder of the trauma; Insomnia usually accompanied by nightmares, the nocturnal equivalent of flashbacks; Emotional blunting, emptiness or numbness, alternating with: Intense anxiety at exposure to events that resemble an aspect fo the traumatic event, including anniversaries of the trauma;Avoidance of activities and situations reminiscent of the trauma;Emotional detachment from other people;Hypervigilance with autonomic hyperarousal and an enhanced startle reaction.

There are no relevant investigations for this condition. The diagnosis is made on clinical history alone.

The best prognosis, or outcome, depends on how soon the symptoms develop after the trauma, and on early diagnosis and treatment. Prognosis depends on how soon symptoms are recognised and the disorder is correctly diagnosed therefore allowing for immediated treatment.

The symptoms of this condition will usually begin within six months of the traumatic event and resolve within 12 months in the greater majority of cases. The symptoms may persist for a longer period of time in some cases.

There are two main forms of therapy for this condition: psychotherapy and medication.

Psychotherapy

This is the main form of treatment for PTSD. The patient is encouraged to share their fears and difficulties with their condition on regular intervals, tailored to the individual. The psychotherapy is mainly supportive, providing an outlet for the patient to release their frustrations. This form of therapy may be less successful on long-term cases of PTSD. There have been suggestions that debriefing people after the experiencing of a traumatic event may reduce the risk of developing this condition, but these claims have been largely unproven.

Medication

In patients who cannot be managed by psychotherapy alone, the use of antidepressant medications has been proven to improve the outcome of counselling in such patients. Commonly used drugs include the SSRIs, including nefazodone and the SNRIs such as venlafaxine.

 

 

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Rett Syndrome (Pervasive Developmental Disorder)

Rett syndrome (RS) is a neurological disorder which also affects many other systems in the body. In 1965 Andreas Rett, an Australian physician identified a syndrome in 22 girls who, after 6 months of apparently normal development, deteriorated in a devastating fashion.

The incidence of RS varies widely in different studies from 1 in 10 000 to 1 in 45 000, on average it is 1 in 23 000. It affects females almost exclusively.

Most cases (99.5%) are due to spontaneous mutations, rather than being inherited. However, the incidence of familial cases is higher than would be expected by chance, so there may be involvement of a genetic factor.

Children with this condition have problems with physical and social development. They generally suffer the loss of many motor, or movement, skills - such as walking and use of their hands - and develop poor coordination. In addition, there is loss of language skills previously acquired. RS generally becomes evident when the patient 2-4 years of age; however, the underlying developmental problems may starts in infants as young as 6 months. The patient goes through a period where development remains static followed by a period of developmental regression. Disease progression stabilizes in many patients once they reach adolescence and although they may regain some function they never fully recover. Death in RS patients can occur suddenly and is often secondary to pneumonia.Many patients with RS also have scoliosis. With the progression of disease, muscle tone seems to change from hypotonia to spasticity to rigidity and subsequent wasting, resulting in many patients being wheelchair bound after 10 years.

Genetic testing looking for mutations in the MECP2 gene. Tests that will exclude other possible causes of the patients symptoms and signs include; serum lactate, ammonia, pyruvate, and amino acids, urine organic acids and chromosomal analysis. MRI can also exclude other diagnosis. Findings in RS include decreased size of the cerebral cortex size and cerebellar atrophy. ECG abnormalities may be present. Barium swallow or overnight pH probe to diagnose GOR. EEG for assessing seizures. Psychometric testing which generally indicates severe intellectual impairment.

Patients with RS generally survive into their fifth or sixth decade of life and there have been reports of women surviving into their seventies.Risk factors that decrease life expectancy include epilepsy, loss of mobility, and swallowing difficulties. It is difficult to predict the neurodevelopmental outcomes in patients with RS. Some patients retain some functional ability and 60% of patients with RS will continue to walk, however others will have severe disabilities.With appropriate medical care, physiotherapy, occupational therapy and good nutrition life expectancy is dramatically increased.

There is currently no cure for RS so treatment is supportive. A plan of therapy must be developed with the child's specific needs in mind. This aims to address the child's needs at home and at school. This requires significant cooperation between the parents, healthcare providers, teachers and others who may be needed to provide services, such as counselors, social workers and occupational, physical or speech therapists. Such a plan aims to improve socialising and communication skills, as well as improving ability to function.Some of the different interventions used might include:

Physiotherapy to prevent contractures of the hands. Behavioural therapy to help improve self-harming behaviours. Epilepsy: antiepileptic medications may be used to treat seizure activity. Gastroesophageal reflux treatment; Metoclopramide, thickened feeding solutions, and semi upright positioning at bedtime may all help to reduce reflux. If these fail surgery may be necessary. Scoliosis: Bracing may be needed and surgery is an option in patients with pain or loss of function. Constipation: High fibre diet, stool softeners and exercise should help.

[1] eMedicine[2] Medline Plus[3] Amir RE, Van den Veyver IB, Wan M, et al: Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl- CpG-binding protein 2. Nat Genet 1999 Oct; 23(2): 185-8[4] Hagberg B, Berg M, Steffenburg U: Rett Syndrome - an odd handicap affecting girls. A current 25-year follow-up in western Sweden. Lakartidningen 1999; 96(49): 5488-90[5] Kaplan and Sadock's Synopsis of Psychiatry, 9th ed.

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Personality disorders

Personality disorder is a psychological disease. A personality can be described as a pervasive "characteristic configuration of behavioural response patterns apparent in everyday life," that is both stable and predictable in many diverse situations. A personality disorder is said to exist when the response patterns exceed those limits set by social opinion. The personality disorder will consequently lead to social rejection and occupational dysfunction throughout life.

The prevalence of all personality disorders is estimated at 6-9%, but some authorities believe the true prevalence is up to 15% of the general population. These disorders affect men and women equally. The personality disorder will always begin in childhood, with the beginning of personality development.

The most important predisposing factor is a family history of psychiatric illness. Other predisposing factors may include: 1. Previous head injury. 2. Previous brain infection including meningitis or encephalitis. 3. Birth injury. 4. Emotionally and/or physically abusive childhood.

Personality disorders comprise deeply ingrained and enduring patterns of behaviour which manifest themselves as inflexible responses to a broad range or personal and social situations. Personality disorders are developmental conditions that appear in childhood or adolescence and continue in adult life. Personality disorders are not secondary to another psychiatric disorder or brain disease, although they may precede or coexist with other disorders. In contrast, personality change is acquired, usually in adult life, following severe or prolonged stress, extreme environmental deprivation, serious psychiatric disorder or brain injury or disease. The personality disorder is normally present at an early age and persists throughout life, as the character traits are part of the patient's personality. The course is variable, but most patients tend to remain stable, with few improving over time. These patients are also more likely to develop major psychiatric conditions such as depression with increasing duration of the disease.

A number of investigations may be performed to ensure that the condition does not have an organic origin. This may include a series of blood tests and brain imaging by MRI and CT scan.

The prognosis of personality disorders is relatively poor. As a personality is essentially a fixed system of behavioural responses, patients will sustain an abnormal personality throughout their lives. Some patients may improve but the majority remain stable or even deteriorate throughout the course of disease. The risk of major psychiatric disorders such as depression is increased, and may occur at later stages of the illness.

The treatment of personality disorders requires long-term psychotherapy and possibly medications. The patient is usually not motivated, making psychotherapy difficult for the involved therapist. Psychotherapy remains the main form of therapy for these patients, taking the form of psychoanalysis, supportive counselling, group therapy, family therapy and occasional hospitalisation for more frequent intensive treatment during episodes of increased symptoms. Certain medications may also be useful in the management of this condition including antipsychotics, (usually olanzapine) antidepressants (usually SSRI's such as Zoloft or Prozac) and anti-anxiety therapy (usually benzodiazepines such as valium.) The patient will normally require long-term treatment for personality disorder is a lifelong disorder in the majority of cases.

Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 2002. Sadock BJ, Sadock VA. Kaplan and Sadock's Pocket Handbook of Clinical Psychiatry 3rd Edition. Lippincott Williams and Wilkins, Philadelphia USA.


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Anorexia Nervosa (Self-Starvation, Malnutrition, Severe Weight Loss, Extreme Weight Loss)

Anorexia nervosa is a psychological disease.

This condition is hallmarked by an extreme reluctance to consume food as a result of a psychological disturbed body image. This may lead to extreme malnutrition and weight loss. Anorexia nervosa is potentially life-threatening.

The incidence of anorexia nervosa is 1-10 per 100,000 females aged between 15 and 34 years. There is a prevalence rate of 1-2% among schoolgirls and university students. Anorexia nervosa is much less common among men with a 1:10 ratio of boys:girls.

The onset of anorexia nervosa disease usually occurs between the ages of 10 and 30 years, initiated by a stressful life event. Anorexia nervosa occurs mostly in those individuals striving for success in industries that demand a slim body image such as modelling and dancing. There is also a higher prevalence of anorexia nervosa in higher social classes.

Several theories have been put forward to explain the origin of anorexia nervosa, but none have stood the test of time.

The following are important important associations of anorexia nervosa:

Stressful life events: The condition most commonly follows a stressful situation or event in the patient's life. Genetic: There is a higher rate of anorexia nervosa in those with a family history of this anorexia. An increased occurrence has beenshown to exist in full-blood sisters.Turbulent family relationships: Overprotective parents, and a pattern of conflict avoidance is shown to increase the risk of developing anorexia in children. Children are thought to use anorexia nervosa as a kind of hunger strike. The child then gains power in the family dynamic for it is the child who recieves the attention and decides the outcome of a family dilemma.

The age of onset of anorexia in women is usually between 10 and 30 years of age, seldom occurring after the age of 30 years.

The onset of anorexia nervosa usually goes unnoticed until a significant amount of weight has been lost. Weight loss is achieve with severe diet restriction and excessive amounts of exercise. Weight loss may be also occur with self-stimulation of vomiting and excessive use of laxatives. With further weight loss, a woman's period may cease, and the patient may develop low blood pressure, slow heart rate, and become very sensitive to the cold. Throughout any stage of the disease, the patient may exhibit psychological symptoms of depression and anxiety, related to their distorted body image of being "fat."

Fecal occult blood may be indicative of esophagitis, gastritis, or repetitive colonic trauma from laxative abuse as well as a bleeding disorder or severe protein malnutrition.

Anorexia nervosa runs a fluctuating course, with exacerbations and partial remissions. Long-term follow up suggests that about two-thirds of patients maintain normal weight and that the remaining one-third are split between those who are moderately underweight and those who are seriously underweight.

Indicators of a poor anorexia nervosa outcome include:

A long initial illness; Severe weight loss; Older age at onset; Bulimia, vomiting or purging; Personality difficulties; and Difficulties in relationships.

Suicide has been reported in 2-5% of patients with chronic anorexia nervosa. The mortality rate per year is 0.5% from all causes. More than one-third have recurrent affective illness, and various family, genetic and endocrine studies have found associations between eating disorders and depression.

50% of patients make a full recovery, 30% a partial recovery and 20% none.

Anorexia nervosa treatment can be conducted on an outpatient basis unless the weight loss is severe and accompanied by marked physical symptoms such as dizziness, weakness and/or electrolyte and vitamin disturbances. Hospital admission may then be unavoidable and may need to be on a medical ward initially. Rarely the patient's weight loss may be so severe as to be life-threatening. If the patient cannot be persuaded to enter hospital, compulsary admission may have to be used.

Inpatient treatment goals include:

Establishing a good relationship with the patient; Restoring the weight to a level between the ideal bodyweight and the patient's ideal weight; The provision of a balanced diet, building up to 12.6MJ (3000 calories) in 3 to 4 meals per day; The elimination of purgaitve and/or laxative use and vomiting.

Outpatient treatment can be conducted on either or both of cognitive behavioural psychotherapeutic lines or dynamic psychotherapeutive lines. It is vital to set up a therapeutic alliance. Individual psychotherapy is better than family therapy if the patient has left home and vice versa.

Motivational enhancement techniques have been used with some success.

Drug treatment has met with limited success, except to symptomatically treat insomnia and depressive illness.

 

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Postnatal Depression (Postpartum Depression)

Postnatal depression is also known as puerperal depression, postpartum depression, baby blues, and puerperal psychosis.

The first month after the delivery of a newborn baby (the postpartum period) is a time of major changes for women. Female hormones and weight are rapidly readjusting. There may be new and stressful changes in relationships with other children, the father of the baby, parents and in-laws, colleagues at work, and friends. Of course, the new baby needs almost constant attention and feeding every two hours, resulting in the feeding mother's sleep deprivation. All of these factors can contribute to postnatal depression and mood swings.

If the moodiness only lasts 2-3 weeks and then goes away, it is commonly called the "baby blues". This natural reaction to stress is experienced by more than half of new mothers.

However, if the feelings of depression or anxiety continue for more than three weeks, a more serious condition called postpartum depression may exist.

For most women, symptoms are transient and relatively mild (i.e. postpartum blues). However, 10-15% of women experience a more disabling and persistent form of mood disturbance (e.g. postpartum depression, postpartum psychosis).

Postpartum psychiatric illness was initially conceptualized as a group of disorders specifically linked to pregnancy and childbirth, and thus was considered diagnostically distinct from other types of psychiatric illness. More recent evidence suggests that postpartum psychiatric illness is virtually indistinguishable from psychiatric disorders that occur at other times during a woman's life.

During the postpartum period, up to 85% of women suffer from some type of mood disturbance. About 10% of women experience significant depression after a pregnancy.

You have a higher chance of postnatal depression if:

You experienced mood disorders prior to pregnancy, including depression with a prior pregnancy. You have a close family member who has had depression or anxiety. Anything particularly stressful happened to you during the pregnancy (e.g. illness, death or illness of a loved one, a difficult or emergency delivery, premature delivery, illness or child abnormailty). You are in your teens or over 40 years of age. The pregnancy in question is unwanted or unplanned. You are currently substance abusing.

There is no single test to diagnose postpartum depression. Sometimes depression following pregnancy can be related to other medical conditions. Hypothyroidism, for example, causes symptoms such as fatigue, irritability, and depression. Women with postpartum depression should have a blood test to screen for low thyroid hormones. This condition is easily treated with supplemental hormone. Another clue to this condition can be weight gain or failure to lose weight after pregnancy, despite breastfeeding the baby.

Because postpartum depression is so common, questionnaire screening tests are available. Women with any of the risk factors, or with symptoms of depression, should consider taking such a test to determine if they need treatment.

Medication for postnatal depression and psychotherapy are effective in reducing or eliminating symptoms of depression in new mothers.

If left untreated, postpartum depression can last for months or years. The potential long-term complications are the same as in major depression.

The treatment for depression after birth often includes medication, psychotherapy, or a combination of both. Fortunately, several antidepressant medications may be given to breastfeeding mothers.

Once postnatal depression is diagnosed, the mother will need to be followed closely for at least six months.

Appleby L, Warner R, Whitton A. A controlled study of fluoxetine and cognitive-behavioural counselling in the treatment of postnatal depression [see comments]. BMJ 1997; 314(7085): 932-6. Davidson J, Robertson E. A follow-up study of post partum illness, 1946-1978. Acta Psychiatr Scand 1985; 71(5): 451-7. eMEDICINE. Medline Plus.


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Tourettes Syndrome (Gilles de la Tourette Syndrome; Tics)

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Phobic disorders

A phobia is the irrational fear of an object or situation. The patient is often aware that their fear is irrational but remains powerless to control their reaction.Anxiety disorders are classified according to whether the anxiety is persistent (general anxiety) or episodic, with the episodic conditions classified according to whether the episodes are regularly triggered by the same cue (phobia) or not (panic disorder).

This is the most common form of anxiety disorder. The prevalence of all phobias is 8%, with many patients having more than one. Phobias are most likely to begin in late childhood and continue into adulthood if left untreated. Women have twice the prevalence of most phobias than men.

As with most anxiety disorders, the only known risk factor is a family history of anxiety disorder. Many types of phobia run in families, expecially those relating to blood injection and certain types of injury.

Phobias generally arise from a bad experience with a previously benign stimulus. For example, a person who has been previously trapped in an elevator runs a greater risk of devloping a phobia of elevators. In children, however, phobias usually arise from imagined threats to their personal safety (e.g. stories of ghosts told in the playground).Most phobias will last indefinitely until the patient decided to overcome their specific fear of an object or social situation. Certain phobias such as the fear of spiders (arachnophobia) is quite easily managed by the complete avoidance of spiders. Patients with such as specific phobia need not suffer social or occupational dysfunction to avoid the stimulus. Patients who fear social ridicule (social phobia) are more likely to suffer social and occupational harm, for the phobia prevents their participation in activities of everyday life.

There are no specific investigations for phobic illness. If the patient appears to suffer from generalised anxiety which is exacerbated by certain phobias, a limited number of tests are performed to exclude medical conditions that bring about feelings of anxiety. These may include a number of different blood tests for hormone balance and a blood sugar level. An ECG is also typically performed to exclude any heart problem that may be causing a patient's palpitations.

Most phobias will tend to develop in late childhood and continue through adult life unless the patient seeks appropriate therapy. If the phobia stimulus is easy to avoid, the patient may live their entire life by avoiding the object or situation. If the phobia is less easy to avoid, the patient is more likely to seek help to resolve their apparent fears. The prognosis with therapy is excellent for most forms of phobic illness. The prognosis is less promising for the condition of agoraphobia, which is most resistant to behavioural therapy and psychotherapy.

As with most psychiatric illness, panic disorder is best treated with both psychotherapy and anti-anxiety medications. There are a number of types of psychotherapy suitable for the treatment of panic disorder. These include relaxation therapy, behaviour therapy and cognitive behavioural therapy.Medications are used to assist psychotherapy as a primary form of treatment. Medications such as sedatives and antidepressants are used in this setting to reduce the frequency and severity of panic attacks. The most commonly used sedatives are the benzodiazepines such as diazepam, however their use beyond 4-6 weeks is discouraged with the emergence of dependence beyond this duration. The most commonly used antidepressant for this condition are the SSRI's such as flluoxetine and sertraline. Antidepressant medications will usually require three months of therapy to achieve adequate effect, but have the advantage that they do not induce patient dependency. Another class of drugs commonly used for panic disorder are the beta-blockers. These drugs block the body's response to anxiety, preventing the occurrence of palpitations, sweating and tremor in the event of a panic attack. They can also be taken in anticipation of stressful situations to reduce the effect of anxiety on the body.

[1] American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association Press; 1994. [2] eMedicine.[3] Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 2002.[4] Medline Plus.[5] Sadock BJ., Sadock VA. Kaplan and Sadock's Pocket Handbook of Clinical Psychiatry 3rd edition. Lippincott Williams and Wilkins 1996.

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Pathological gambling

Pathological gambling is a inpulse-control disorder. This means that a person acts on certain impulse that is potentially harmful but they cannot resist the action. This is not the same as problem gambling.In pathological gambling (disorder), there is a chronic inability to resist the impulse of gambling in a person. This is to the extent when gambling is so serious that it damages a person's financial, functional, social and vocational life.

Although comprehensive studies worldwide have not been compiled, there are local studies that all point to a 3-5% rate of problem gamblers in the general population, and approximately 1% rate of pathological gamblers.Australia has a long history of gambling, and the highest per capita expenditure on gambling of all Western nation. Hence it is no surprise that pathological gambling is on the rise in Australia.

There are several predisposing factors that are seen in pathological gamblers. Aside from early exposure to peer pressure, the following are the risk factors: Risk-taking behaviour: those who have morbid risk-taking behaviour are more likely to be pathological gambler, since gambling is a type of risk-taking. These people can have high attempted suicide rates as well. Mental disorder: pathological gambling may occur in any mental disorder, however it is most commonly associated with depression. Alcohol misuse/dependence and substance misuse/dependence are also common. Genetics/Hereditary: Studies have shown that childhood experiences and influences in early life can increase the risk of pathological gambling.

The typical pathological gambler is in the age group of 30-40s. The disorder often starts off like described below. In the settings of a big win or life stresses (as detailed below), the gambler starts to spend more time and money to engage in multiple gaming opportunities. Over the time frame from months to years, he or she begins to fall behind and hence repeating the spiral down again, instead of cutting and stopping loses. When all the options of obtaining money failed, men tend to resort to scams and credit card fraud; while women may go into prostitution.Generally, the pathological gamblers have a fluctuating course of disease. Depending on social situations and life events (e.g. stresses in life, relationship problems, financial crises, pregnancy, etc), pathological gambling can recur after some time of remission. Remission means that the person have the features of pathological gambling (as described below in clinical history).Some pathological gamlers will seek help and quit, yet many will run the vicious cycle as described above until serious complications occur.

Because this is a psychiatric disorder, no routine laboratory investigations are useful for the diagnosis of pathological gambling. Yet, as in clinical examination, some basic tests may show features of other disorders, such as alcoholism. Urine screen might show recreational drugs in the urine.

The prognosis of pathological gambling can be varied, depending on the underlying disorders or personality. Also it depends on the severity of life stresses or any triggering factors that initiated the cycle of pathological gambling.

Management of pathological gambling involves changing the lifestyle of the patient. For optimal outcome, it is important to involve a whole team of mental health workers, including psychiatrist, psychologist, social worker, counsellor, general practitioner and others.The following treatment options are most likely to be used in combination:

counselling: this need to assess the financial situation, marriage, relationship with spouse/partner, and other social issues that are affected by pathological gambling. self-help group: e.g Gamblers Anonymous Australia to provide social support for the individual and the family. psychological treatment: good outcome has been reported using cognitive-behavioural therapy. This is a psychological therapy first requiring the patient to recognise the disorder, then using step-by-step methods to treat pathological gambling. If complete stoppage cannot be achieved, sometimes controlled gambling can have good outcomes as well. psychiatric treatment: if there are any other mental disorders undelying pathological gambling, the patient need to have psychiatric assessment for further treatment.

[1] Dickerson M, Baxter P, Boreham P, Harley W, Williams J. Report of the First Year of the Study into the Social Impact of the Introduction of Gaming Machines to Queensland Clubs and Hotels, The State of Queensland (Department of Families, Youth and Community Care), 1995.[2] Gelder M, Lopez-Ibor JJ, Andreasen N. New Oxford Textbook of Psychiatry. Oxford University Press. 2003.[3] JAMA Patient Page: WHen Gambling Becomes a Bad Bet [online]. 2001. [Cited 2005 September 22nd]. Available from: URL:http://www.hmc.psu.edu/healthinfo/articles/gambling.pdf[4] Sadock BJ, Sadock VA. Kaplan and Sadock's Comprehensive Textbook of Psychiatry. 8th ed. Lippincott Williams & Wilkins. 2005.

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Generalised Anxiety Disorder (GAD)

Generalised Anxiety Disorder (GAD) is a psychological disease. This condition is characterised by excessive worry about actual circumstances, events or conflicts that occur in everyday life. Anxiety disorders are classified according to whether the anxiety is persistent (general anxiety) or episodic, with the episodic conditions classified according to whether the episodes are regularly triggered by the same cue (phobia) or not (panic disorder).

General anxiety disorder occurs in 3-8% of the population. The disorder may start at any time in life, including childhood. The majority of patients presenting with the disorder report that they have been anxious for as long as they can remember. GAD occurs somewhat more often among women than among men.

The most important risk factor for the development of any anxiety disorder is a family history of anxiety disorder. It is estimated that this condition affects 25% of first degree relatives of a person with GAD. Behavioral inhibition1, an early temperament associated with aversion to novel situations, has been found to be associated with later development of anxiety disorders.

This condition begins at variable ages, most commonly in early childhood. The course is usually long-term with the severity of symptoms decreasing as the patient gets older. As the duration of illness increases, the patient becomes more likely to develop depression, especially if the condition remains untreated.

Investigation of anxiety disorders is largely inappropriate as the test itself may become a source of anxiety for the patient. The condition is only investigated if there is strong suspicion of a medical cause of anxiety following history and physical examination. Investigat6ion may involve performing an ECG and blood tests for thyroid disease, adrenal disease and blood sugar levels.

If the condition remains untreated, the prognosis is poor. Most patients will develop secondary depression, requiring medical and psychological therapy for the management of depression. With treatment the prognosis is good, as the risk of developing secondary depression is reduced.

As with most psychiatric illness, generalised anxiety disorder is best treated with both psychotherapy and anti-anxiety medications. There are a number of types of psychotherapy suitable for the treatment of panic disorder. These include relaxation therapy, behaviour therapy and cognitive behavioural therapy. Medications are used to assist psychotherapy as a primary form of treatment. Medications such as sedatives and antidepressants are used in this setting to reduce the frequency and severity of panic attacks. The most commonly used sedatives are the benzodiazepines such as diazepam, however their use beyond 4-6 weeks is discouraged with the emergence of dependence beyond this duration. The most commonly used antidepressant for this condition are the SSRI's such as flluoxetine and sertraline. Antidepressant medications will usually require three months of therapy to achieve adequate effect, but have the advantage that they do not induce patient dependency. Another class of drugs commonly used for generalised anxiety disorder are the beta-blockers. These drugs block the body's response to anxiety, preventing the occurrence of palpitations, sweating and tremor in the event of a panic attack. They can also be taken in anticipation of a stressful situations to reduce the effect of anxiety on the body.

[1] Kagan J: Temperamental contributions to social behavior. American Psychologist 1989;44:668-674.[2] Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 2002.[3] Sadock BJ., Sadock VA. Kaplan and Sadock's Pocket Handbook of Clinical Psychiatry 3rd edition. Lippincott Williams and Wilkins 1996.

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Male Sexual Dysfunction (Erectile Dysfunction, Impotence)

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Erectile dysfunction is the inability to develop or maintain an erection that is rigid enough to allow penetration of the vagina, and therefore functional sexual intercourse. Generally, the term erectile dysfunction is applied if this occurs frequently (75% of the time) over a significant period if time (several weeks to months). If this is the case, the term impotence may also be used.

Erectile dysfunction may present in different ways. Some men are completely unable to develop an erection. Some may develop an erection that does not remain rigid enough to allow satisfactory intercourse.

There are several causes of erectile dysfunction, including certain drugs (prescription and non prescription), psychological causes, and problems with the hormones, nerves or blood vessels that supply the penis.

Other problems with male sexual function include a lack of sexual drive or desire (libido), problems with ejaculation (ejaculatory dysfunction), and lack of pleasurable sensation (orgasm) during sex. These problems will not be discussed in detail.

Erectile dysfunction is a common problem. It is important that men who experience erectile dysfunction discuss it with their doctor, because the condition can have a negative impact on relationships and self esteem; serious underlying causes need to be excluded; and effective treatment is available.

Erectile dysfunction: Could you have it?This questionnaire is based on the International Index of Erectile Function-5, and is used to assess a mans erectile function.

Erectile dysfunction is estimated to effect 150 million men worldwide, and more than one million men in Australia.

Overall, 25% of Australian men report erectile dysfunction and 8.5% report severe erectile dysfunction.

In one study, 9.6% reported 'occasional' erectile dysfunction, 8.9% reported erectile dysfunction occurring 'often', and 18.6% reported erectile dysfunction occurring 'all the time'. Of these, only 11.6% had received treatment. In another study, only 14.1% of men reported that they had received treatment, despite experiencing erectile dysfunction for longer than 12 months. 

Erectile dysfunction is never 'normal', however it does become more common and more severe as men age. One Australian study reported the rate of erectile dysfunction in different age groups:

20-29 years: 9.2% 30-39 years: 8.4% 40-49 years: 13.1% 50-59 years: 33.5% 60-69 years: 51.5% 70-79 years: 69.2% 80+ years: 76.2%

Due to the ageing Australian population, erectile dysfunction is expected to become more common.

There is no difference between the prevalence of erectile dysfunction between "white-collar" and "blue-collar" workers in Australia.

Sexual dysfunction associated with cancer

Between 10 and 88% of patients diagnosed with cancer experience sexual problems following diagnosis and treatment. The prevalence varies according to the location and type of cancer, and the treatment modalities used. Sexuality may be affected by chemotherapy, alterations in body image due to weight change, hair loss or surgical disfigurement, hormonal changes, and cancer treatments that directly affect the pelvic region.

Sexual problems are reported in many patients with prostate and testicular cancer. They are also reported in patients with cancer that does not directly effect sexual organs, including lung cancer (48% of patients), Hodgkin's disease (50%), and laryngeal (%60) and head and neck cancers (39-74%). 

For more information, see Sexual Difficulties Associated with Cancer in Men.

The predisposing factors for erectile dysfunction are as follows:

If a man has the risk factors for cardiovascular disease during middle age (smoking, obesity, high cholesterol), he is at an increased risk of developing erectile dysfunction.

Exercise has been shown to have a protective effect.

Around one third of men who experience erectile dysfunction find that, without treatment, it becomes worse over time. Around a third of men find that erectile dysfunction improves without treatment.

Around half of men with severe erectile dysfunction remain impotent in the long term without treatment.

These figures vary depending on the cause of the erectile dysfunction. Even if men choose not to pursue treatment for erectile dysfunction, it is important that they be investigated by a doctor, as erectile dysfunction may indicate an increased risk of cardiovascular disease.

Temporary failure of erection is very common and is likely to resolve. If ongoing erectile dysfunction develops, the impact on relationships and self-esteem can be devastating. Men who suffer from erectile dysfunction are known to experience significant psychological distress. It is believed that sexual self-consciousness leads to:

increased appearance related anxieties; interferes with attention, focus and concentration;impairs physical performance; and reduces awareness of our physiological arousals leading to sexual dysfunction.

This improves when erectile dysfunction is successfully treated.

While studies are limited, it has been shown that male sexual dysfunction can also negatively impact the sexual function of female partners. A study comparing the sexual function of women with partners with erectile dysfunction to those without showed that sexual arousal, lubrication, orgasm, satisfaction, pain and total score were significantly lower in those who had partners with erectile dysfunction. Later in that study, a large proportion of the men with erectile dysfunction underwent treatment. Following treatment, sexual arousal, lubrication, orgasm, satisfaction and pain were all significantly increased. It was concluded that female sexual function is impacted by male erection status, which may improve following treatment of male sexual dysfunction.

It is essential to discuss erectile dysfunction with your doctor, so any serious underlying causes can be excluded and treatment options can be discussed. Many men are embarrassed discussing this issue with their doctor, or even their partner. Open communication with your doctor, and in your relationship, is important for effectively managing this common problem.

Effective treatment for erectile dysfunction is available, and for most men will allow the return to a fulfilling sex life. The side effects of the treatment for erectile dysfunction vary depending on the treatment that is used. Some may interrupt the spontaneity of sexual activity. For example, PDE-5 inhibitors typically need to be taken one hour before sex. Side effects may include headaches, indigestion, vasodilation, diarrhoea and blue tinge to vision. Other treatments such as penile injections may cause pain at the injection site, or an erection that will not go down. Treatment options need to be carefully discussed with your doctor to determine which one is best suited to you.

Following a detailed discussion about the history of erectile dysfunction and its risk factors, your doctor will examine the testicles and penis to help determine the cause of erectile dysfunction. Your doctor will check reflexes and pulses in the area to see if problems with blood vessels or nerves are contributing to the erectile dysfunction. If necessary, your doctor will order tests to help diagnose erectile dysfunction.

Diagnosis is based on information provided to the doctor regarding the history of erectile dysfunction (how quickly it came on, how often it occurs, etc), the assessment of risk factors, and whether erections still occur overnight while a man is asleep. It is normal for a man to have 3-5 full erections overnight during REM sleep.

In order to establish whether normal erections are occurring overnight (nocturnal erections), the doctor may organise nocturnal penile tumescence (NPT) testing. This involves wearing a monitor overnight in your own home. The data from this monitor is then assessed to analyse how often erections occurred, how long they lasted, and how rigid and large the penis was during the erections. If NPT testing is normal, the cause of erectile dysfunction is usually psychological. If not, further testing of the blood flow in the genital area may be required to see if there is blockage or leakage. The doctor may also organise a blood test of levels of hormones such as testosterone, prolactin and thyroid stimulating hormone to see if these are contributing to the erectile dysfunction.

For the great majority of men, erectile dysfunction can be effectively treated.

It is essential that if you experience erectile dysfunction, you discuss it with your doctor. Serious underlying causes need to be excluded. Many treatment options are available, and your doctor can help you decide which one is most appropriate for you.

Some causes of erectile dysfunction such as hormonal problems or anxiety may be cured completely with treatment and/or therapy. Even if the underlying cause cannot be cured, medication may still allow a satisfactory erection. Ignoring the problem tends not to make it better, and can have a significant impact on relationships and self-esteem.

Before starting treatment for erectile dysfunction, a doctor needs to check there is no underlying cardiovascular disease, and do other checks to determine the cause of the erectile dysfunction.

The most common treatment for erectile dysfunction is drugs known as phosphodiesterase-5 (PDE-5) inhibitors. These include tadalafil (Cialis), vardenafil (Levitra), and sildenafil citrate (Viagra). These are effective for about 75% of men with erectile dysfunction. They are tablets that are taken around an hour before sex, and last between 4 and 36 hours. Sexual stimulation is required before an erection will occur. The PDE-5 inhibitors cause dilation of blood vessels in the penis to allow erection to occur, and help it to stay rigid. Men using nitrate medication (e.g. GTN spray or sublingual tablets for angina) should not use PDE-5 inhibitors.

If testosterone levels are found to be low, erectile dysfunction should initially be treated with testosterone replacement therapy.

If PDE-5 inhibitors are not suitable or don't work, other therapies include injections into the base of the penis, which cause flow of blood into the penis and a fairly immediate erection that lasts around an hour. The drugs injected are alprostadil (Caverject and Erectile dysfunctionex) and Invicorp (VIP and phentolamine). Alprostadil may also be inserted as a gel into the opening of the penis. This is not suitable if your partner is pregnant. 

Vacuum erection devices use a pump mechanism to create negative pressure around the penis, encouraging it to become erect. An elastic device is then placed around the base of the penis to help maintain the erection.

As a last resort, penile prostheses may be considered. Malleable rods and inflatable versions are available. This option involves surgery to insert the device, and so has more risks than the other treatments.

Surgery to correct blocked or leaking blood vessels used to be popular, but is not very effective for long term erectile function unless it is being done to correct traumatic vascular damage in young men.

Erectile dysfunction experienced by obese men has been shown to improve considerably with weight loss and exercise. Other lifestyle changes that improve erectile dysfunction include reducing the use of alcohol, recreational drugs and cigarettes.

If erectile dysfunction is found to be caused by anxiety or depression, psychotherapy may be an effective treatment on its own or in combination with certain drugs (e.g. antidepressants). Sexual therapy counsellors specialise in this field.

If men are found to be taking a medication that is known to cause erectile dysfunction, their doctor may prescribe an alternative, equally effective therapy.

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