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Postnatal depression

Posted on March 24, 2014 by JmaC

About 1 in 10 mothers develop postnatal depression. Support and understanding from family, friends, and sometimes from a professional such as a health visitor can help you to recover. Other treatment options include psychological treatments such as cognitive behavioural therapy or antidepressant medicines.

What is meant by postnatal depression?

Having a baby is a very emotional experience. You may feel tearful and your mood may feel low. There are three causes of low mood after childbirth:
•Baby blues. This is very common and almost considered normal. Symptoms include being weepy, irritability, anxiety and feeling low. It usually starts around the 3rd day, but usually goes by the 10th day after childbirth. It does not usually need any medical treatment. Baby blues is not discussed further in this leaflet.
•Postnatal depression. This occurs in about 1 in 10 mothers. It usually develops within the first four weeks after childbirth. However, it can start several months following childbirth. Symptoms, including low mood, last for much longer than with baby blues. Treatment is advised. Most of this leaflet is about this common form of depression.
•Postnatal (puerperal) psychosis. This is an uncommon, but severe form of depression. It develops in about 1 in 1000 mothers. It is discussed briefly at the end of this leaflet.

The baby’s father may also develop postnatal depression.

Tricyclic Anti-Depressants

Posted on March 24, 2014 by JmaC

Tricyclic antidepressants are used to treat depression and some other conditions. They often take 2-4 weeks to work fully. A normal course of antidepressants lasts at least six months after symptoms have eased. Side-effects may occur, but are often minor and may ease off. At the end of a course of treatment, you should gradually reduce the dose before stopping completely.

Tricyclic antidepressants are not just for depression

Tricyclic antidepressants are used to treat depression. They are also used to treat some other conditions such as migraine, panic disorder, obsessive-compulsive disorder, recurrent headaches, and some forms of pain. The word tricyclic refers to the chemical structure of the medicine.

SAD

Posted on March 24, 2014 by JmaC

Low mood during winter months has been noted as far back as 1845; however, it was not formally recognised as a disorder until the 1980s.

Seasonal affective disorder (SAD) is now classified as a variant of depression, characterised by depressive episodes that recur annually at the same time each year, usually during the winter months. It can be very disabling for patients, and 6-35% of patients require hospitalisation for SAD at some point.

SAD patients spend over 40% of the year struggling with substantial depressive symptoms during most years, beginning in young adulthood.

Epidemiology
•2% of the population in Northern Europe have severe depression resulting from SAD.
•In the UK, up to 6% of adults have ‘recurrent major depressive episodes with seasonal pattern’.[1]
•The mean age at presentation of SAD is 27 years.
•During the reproductive years, it is four times more common in women than in men.
•Children can also be affected and rates in boys and girls are similar.
•The prevalence rates reduce in older age and the genders are affected equally.
•Vulnerability to SAD is increased the further away you live from the equator.
•There is also a genetic component in that you are more likely to suffer from SAD if a close relative is affected.
•A seasonal pattern has been observed in 15% of patients with recurrent mood disorders, including unipolar and bipolar forms.

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How does light affect mood and behaviour?[2][3]

Light and darkness are thought to affect mood and behaviour via the complex interaction between circadian rhythms and the biological clocks which control them.

Circadian rhythms are innate physiological, mental and behavioural changes which follow a roughly 24- to 25-hour cycle. Biological clocks are groups of interacting molecules in cells throughout the body. A master biological clock is located in the supra-chiasmic nucleus (SCN) which sits within the hypothalamus. This co-ordinates all the body clocks so that they are synchronised.

The master clock in the SCN is affected by light and darkness via the retino-hypothalamic tract. The retino-hypothalamic tract is a neurological pathway connecting the retinal ganglion cells (RGCs) of the retinae to the SCN in the hypothalamus. This connects with the pineal gland via the superior cervical ganglion (SCG).

RGCs → melanopsin → SCN → SCG → pineal gland → supression of melatonin

Sunlight (or light at 480 nm) stimulates the RGCs to produce the photoreceptor melanopsin. Melanopsin ‘signals’ daytime to the SCN which in turn induces the pineal gland to suppress melatonin production.

Melatonin is produced by the pineal gland. Its primary function is to signal day length to the SCN, acting as a cue for innate nighttime behaviour. Via the activation of melatonin receptors, it affects sleep propensity and the sleep/wake rhythm, circadian rhythms; it induces heat loss, reduces arousal, and delays cortisone production. Melatonin is synthesised from serotonin, which is in turn synthesised from L-tryptophan. Large increases in melatonin production at night are due to a concomitant increase in the activity of the penultimate enzyme in melatonin synthesis, arylalkylamine N-acetyltransferase (serotonin N-acetyltransferase, AANAT). Serotonin levels have a major role in mood modulation.

Light can also affect mood by affecting ‘alertness’. Light can affect alertness via non-circadian pathways.[4]

Causes[5][6]

Despite ardent research, the cause of SAD is not yet fully understood. One prevailing theory is that patients with SAD are phase-delayed.[7] This suggests that most patients with SAD become depressed in the winter, at least in part because of a phase delay in circadian rhythms relative to the sleep/wake cycle. The cause of this ‘phase delay’ and why it has such a pronounced effect on mood and behaviour, is likely to be multifactorial, involving abnormalities at various levels along the retino-hypothalamic tract, its links with the pineal gland, and the metabolism of melatonin and serotonin. Familial studies suggest a higher incidence of SAD among first-degree relatives, with genetic factors accounting for between 29-69% of variance in seasonal mood symptoms.[2] This suggests that genetic aberrations may underlie the various abnormalities which cause SAD symptoms.

Melatonin secretion occurs later in the night, and for longer periods during the early morning compared to healthy individuals.

Sensitivity to light and melanopsin in SAD patients
•Recent studies have shown that the retinal sensitivity to light is decreased in SAD patients compared to controls, and that this reduced sensitivity is more frequent among those with a mutated variant of the melanopsin gene.[8] .
•Preliminary investigations have found that individuals with a mutated variant of the melanopsin gene (TT) were 5.6 times more likely to have SAD than those without this variant.[2]
•Sleep onset among those with the TT genotype was later in the day when individuals were assessed on longer days and earlier in the day on shorter days, whereas individuals in the other genotype groups (ie CC and CT) did not show this interaction effect.[9]

Light and melatonin[10]

•Light therapy clearly improves depressive symptoms.
•Melatonin levels rise later in the night in those with SAD compared with those who do not have SAD.
•SAD patients have a longer duration of nocturnal melatonin secretion in winter than in summer months, while healthy controls do not.

Serotonin and SAD[11]
•It is well established that serotonin has a major role in suppressing various aspects of feeding behaviour. SAD patients report distinct subjective responses to high-carbohydrate meals, which can enhance serotonin turnover via increased tryptophan uptake into the brain.
•Serotonin levels in human postmortem samples are found to be at minimum levels during the winter months.
•Depletion of L-tryptophan, which is a precursor of serotonin, is associated with a relapse of depressive symptoms in patients who are in remission due to light therapy.
•Although treatment with melatonin itself is not helpful for people with SAD, the novel drug agomelatine, which acts as a melatonin receptor agonist, but also as a 5HT2C antagonist (and so increases serotonin availability at the synapse), has been found to have good results in treating SAD.
•Exercise, which activates the serotoninergic system potentiates light-induced delays of circadian rhythms.

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Classification and seasonal affective disorder variants

SAD with autumn- or winter-onset depression, with symptoms remitting or hypomanic or manic symptoms during the spring or summer, is the most common.

Sub-syndromal SAD is characterised by seasonal mood disruptions with milder functional impairments. Symptom changes may not be as severe. Patients may not meet Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition Text Revision (DSM-IV-TR) or International Classification of Diseases Tenth Revision (ICD-10) criteria for a clinical mood disorder. However, the mood disruption and impairments may still be significant.

SAD with summer onset of depressive symptoms, with remission or hypomanic or manic symptoms during the winter months (less common than autumn- or winter-onset depression).

Presentation

Patients may develop the following symptoms in a step-wise fashion, beginning in September and culminating with depression and anxiety in December. SAD symptoms persist until springtime in April.
•Difficulty waking
•Decreased energy/lethargy
•Carbohydrate craving
•Increased appetite
•Increased sleep
•Weight gain
•Difficulty concentrating
•Decreased libido
•Withdrawal from family and friends
•Depression/anxiety/irritability

Other symptoms include
•Family problems
•Tearfulness
•Physical symptoms – eg, headache, palpitations, and generalised aches and pains

Differential diagnosis

The patient should be assessed for other psychological conditions including:
•Major depressive disorder.
•Bipolar I and ll disorders (all patients with autumn- or winter-onset depression should be screened for spring or summer hypomania or mania symptoms. An estimated 20% of people with SAD may present with a bipolar disorder).
•Dysthymic disorder.
•Cyclothymic disorder.
•Premenstrual dysphoric disorder (associated with bloating and breast tenderness with onset during the later part of the luteal phase of the menstrual cycle and remission of symptoms during the follicular phase).
•Chronic fatigue syndrome.
•Hypothyroidism.
•Substance misuse.
•Alcohol misuse.

Many of these disorders do not have a seasonal pattern. The seasonality of symptoms may be determined by asking the patient to record symptoms in a diary or using the seasonal pattern assessment questionnaire (SPAQ).[12]

Investigations

TFTs and urine and blood tests for illicit substances and alcohol will help to rule out some of the above conditions.

Diagnosis

SAD is categorised as a form of depressive disorder in the DSM-IV. The gold standard for diagnosis is a structured interview to determine whether patients fulfil the DSM-IV criteria. The SIGH-SAD clinical assessment tool is commonly used.[13]

Using this tool, the diagnosis of SAD is based on:
•Depression cycles on a regular basis during autumn/winter.
•Full remission of symptoms in spring/summer.
•Seasonal symptoms for at least two consecutive years.
•Atypical features, which may or may not be present.

During the psychological examination, it is also important to assess:
•Suicidal ideation.
•Abnormal mechanisms of coping – eg, social isolation, alcohol use.

Associated disorders[10]
•Eating disorders – eg, bulimia
•Panic attacks
•Anxiety disorder
•Attention deficit hyperactivity disorder

Treatment[1]

The most current National Institute for Health and Care Excellence (NICE) guidelines for depression state that depression in SAD patients should be managed in the same way as non-seasonal depression.[14]

Cognitive behavioural therapy (CBT), light therapy and prescribed medications have all been found to help to induce remission of SAD symptoms during winter months. In patients with SAD, or symptoms that are highly suspicious of it, it is important not to wait until they are showing signs of depression, but to start nondrug treatment while they have early symptoms such as lethargy and carbohydrate cravings around September.

Social anxiety disorder

Posted on March 24, 2014 by JmaC

Social anxiety disorder was recognised as a psychiatric entity in 1980. It is persistent fear and anxiety about one or more social or performance situations.

We all have some degree of social anxiety. It may be regarding an interview or a public performance such as public speaking, acting, singing or playing a musical instrument. A certain amount of adrenaline (epinephrine) can enhance the performance but we are all aware of how too much can also ruin it. A fairly normal trait may become a disease when the severity interferes with normal everyday life.

Epidemiology

Social anxiety disorder is one of the most common anxiety disorders. It has been estimated that 12% of adults in the USA will have social anxiety disorder at some point in their lives. This compares to 6% for generalised anxiety disorder, 5% for panic disorder and 2% for obsessive-compulsive disorder.[1] Like most other phobias, social phobias are more common in women.[2] They are more common in young people; however, there is a shortage of surveys in children and the elderly.[3]

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Features of the disorder
•Social anxiety is a fear of being around people and having to interact with them. Sufferers fear being watched and criticised. Normal activities such as working, shopping, or speaking on the telephone are marked by persistent feelings of anxiety and self-consciousness. They feel dread as a situation approaches and afterwards they analyse or ruminate on how they could have done better. Hence, it may be seen as a fundamentally normal response but exaggerated to the point of being pathological.
•Physical symptoms include trembling, blushing, sweating and palpitations.
•They often experience chronic insecurity about their relationships with others, excessive sensitivity to criticism, and profound fears of being judged negatively, mocked, or rejected by others.
•There are two forms of the condition: •Generalised social anxiety which affects most, if not all areas of life. This is the more common type and affects around 70% of sufferers.
•Performance social anxiety, where these feelings only occur in a few specific situations such as public speaking, eating in public or dealing with figures of authority.

•Social phobias often start in adolescence and are centred around a fear of scrutiny by other people in comparatively small groups, often peer groups, rather than crowds, leading to avoidance of social situations. It can start in childhood and any assessment must take account of what is appropriate for age.
•There may be specific problems such as eating in public, public speaking, or encounters with the opposite sex; or, they may be diffuse, involving almost all social situations outside the family circle. A fear of vomiting in public is not uncommon. This is called emetophobia. Direct eye-to-eye contact may be avoided – but in some cultures it is inappropriate to look one’s superiors in the eye, so ethnic and cultural norms need to be differentiated from the abnormal.
•There is usually low self-esteem and fear of criticism. They may present to the doctor complaining of flushing, tremor, nausea, or urgency of micturition. They may be convinced that these physical manifestations of anxiety are the primary problem. It may progress to panic attacks. Avoidance may be marked or extreme, resulting in almost complete social isolation.
•Social anxiety disorder has a median age of onset of 13 years; however, it is often persistent and only about 50% with the problem will seek treatment. Commonly they only seek treatment after 15-20 years of symptoms.[1]

Identification and assessment

Identification

The National Institute for Health and Care Excellence (NICE) recommends the use of identification questions for anxiety disorders, in line with their guidelines. These ask about feelings of anxiety and their ability to control worry using the two-item Generalised Anxiety Disorder scale (GAD-2). However, if social anxiety disorder is suspected then they recommend:
•Use of the 3-item Mini-Social Phobia Inventory (Mini-SPIN); or
•Considering asking two questions: •Do you find yourself avoiding social situations or activities?
•Are you fearful or embarrassed in social situations?

Scoring 6 or more on the Mini-SPIN (see below), or answering ‘yes’ to either of the two questions, suggests further assessment for social anxiety disorder is warranted.

The Mini-SPIN is generally used as a screening instrument for social anxiety disorder.[4] It contains three items that should be asked and are about avoidance and fear of embarrassment rated on experience in the previous week. The items are rated using a 5-point Likert scale: 0 = not at all, 1 = a little bit, 2 = somewhat, 3 = very much, 4 = extremely.
Ask the person to answer whether:
1.Fear of embarrassment causes me to avoid doing things or speaking to people.
2.I avoid activities in which I am the centre of attention.
3.Being embarrassed or looking stupid are among my worst fears.

It is also worth being alert to the possibility of depression and NICE recommends the use of two questions:
•During the last month, have you often been bothered by feeling down, depressed or hopeless?
•During the last month, have you often been bothered by having little interest or pleasure in doing things?

Answering yes to either of these would point towards the need for further assessment.

Assessment

Some people may find attending the surgery distressing and an initial contact may have to be made via telephone. However, face-to-face contact will be needed for ongoing assessment and treatment.

The initial assessment will need to consider fear, avoidance, distress and functional impairment while considering the possibility of comorbid disorders. The following factors should be considered in assessing the person’s current social anxiety and associated problems:
•Feared and avoided social situations – as well as what they are afraid will happen to them in those situations (eg, blushing, sweating, trembling, etc)
•Anxiety symptoms
•View of self and content of self-image
•Safety-seeking behaviours
•Focus of attention in social situations
•Anticipatory and post-event processing
•Occupational, educational, financial and social circumstances
•Current and past medication, alcohol and recreational drug use

It is possible that a person may not return after initial contact or assessment. This is in the nature of the disorder, so efforts should be made to contact them (by their preferred method) and reduce barriers to further assessment and treatment.

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Differential diagnosis

A degree of depression or another diagnosis may be present but the final diagnosis needs to be made on the basis of the most important features. The following conditions may need to be considered when coming to a diagnosis:
•Panic disorder with agoraphobia or agoraphobia without panic disorder.
•Separation anxiety disorder. This is really a behavioural pattern of small children that presents at an inappropriate age, as in adolescence.
•Generalised anxiety disorder, also known as anxiety neurosis.
•Specific phobias may need distinguishing from social anxiety disorder.
•Schizoid personality disorder – which is not the same as schizophrenia. They tend to be emotionally rather cold and isolated but it excludes Asperger’s syndrome and autism.
•Avoidant personality disorder is a continuum, even perhaps a more severe form of social anxiety disorder. The European definition requires at least three of the following: •Persistent and pervasive feelings of tension and apprehension
•Belief that one is socially inept, personally unappealing, or inferior to others
•Excessive preoccupation with being criticised or rejected in social situations
•Unwillingness to become involved with people unless certain of being liked
•Restrictions in lifestyle because of the need to have physical security
•Avoidance of social or occupational activities that involve significant interpersonal contact because of fear of criticism, disapproval, or rejection

•There is considerable association between social avoidance and alcohol-related problems. A level of suspicion is required, as the potential for problematic or hazardous drinking may need exploration and the direction of causation may also be unclear.[5]
•Performance anxiety, stage fright, and shyness are more personality traits than diseases.

Management[1]

After diagnosis, NICE recommends that information be provided about the disorder and its treatment. Goals for treatment can be set. Treatment may be psychological, pharmacological or both.

If there are also symptoms of depression it is necessary to establish, if possible, which came first. If it is apparent that the depression preceded the significant social anxiety then the depression should be treated. Otherwise, it is reasonable to treat the social anxiety disorder first, depending on the preference of the patient.

ADHD

Posted on March 21, 2014 by JmaC

Attention deficit hyperactivity disorder (ADHD) is a common condition that mainly affects behaviour. It is usually diagnosed in children but can affect adults. Symptoms include persistent restlessness, impulsiveness and/or inattention. The diagnosis is made after a detailed assessment. Treatment includes parent training programmes and sometimes medication. Diet may be a factor and may be worth considering.

What is attention deficit hyperactivity disorder?

Attention deficit hyperactivity disorder (ADHD) is also known as attention deficit disorder (ADD) and hyperkinetic disorder. It is a fairly common condition that mainly affects a child’s behaviour. There may also be problems with the child’s intellectual, social and psychological development as a result of the behaviour.

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What are the symptoms of attention deficit hyperactivity disorder?

Children with ADHD show persistent restlessness, impulsiveness and/or inattention. These features are seen in more than one setting. For example, at school and at home. They are also seen in more than one activity. For example, in schoolwork and in relationships. They occur at a level greater than expected for their age and cause significant disruption to the child’s daily life.

There are three subtypes of ADHD:
•Hyperactive-impulsive subtype. Some features of this type of ADHD are that a child may fidget a lot, run around in inappropriate situations, have difficulty playing quietly and may talk excessively. They may interrupt others and have trouble waiting their turn in games, in conversations and also in queues.
•Inattention subtype. In this subtype, a child may have trouble concentrating and paying attention, may make careless mistakes, may not listen or follow through on instructions and may be easily distracted. They may also be forgetful in daily activities, lose essential items such as school books or toys, and have trouble organising activities.
•Combined subtype. If a child has this subtype, they have features of both of the other subtypes.

Children with ADHD are also more likely than average to have other problems such as anxiety and depression, conduct disorders and co-ordination difficulties. Some children with ADHD also have reading difficulties and dyslexia.

Note: many children, especially those under the age of five, are inattentive and restless. This does not necessarily mean that they have ADHD.

What causes attention deficit hyperactivity disorder?

The cause of ADHD is not known. It is thought that there may be subtle changes in parts of the brain which control impulses and concentration. Although the main cause of ADHD is not known, various factors are thought to increase the risk of a child developing ADHD. These include:
•Genetics. Genes are passed on to a child from each parent. Our genes determine how our body functions, what we look like and sometimes what diseases we will get. Some studies have shown that certain genes are related to ADHD. A child may therefore be more likely to have ADHD if there is another family member such as mother, father, brother or sister with ADHD.
•Antenatal problems. If a mother drinks alcohol, smokes or takes heroin while she is pregnant, this may increase the risk of her child developing ADHD.
•Obstetric problems. This means problems that occur when a baby is born, such as a difficult labour causing lack of oxygen to the brain. Babies with very low birthweight have an increased risk of developing ADHD.
•Severe deprivation. If a child is severely neglected early in life, this may increase their risk of developing ADHD.

Factors in a child’s upbringing such as poor parenting, watching a lot of TV or DVDs, family stress, etc, do not cause ADHD. However, such factors may make the behaviour of a child with ADHD worse. Diet may be a factor (discussed further later).

How common is attention deficit hyperactivity disorder?

ADHD affects around 5 in 100 school-aged children in the UK. It is around three times more common in boys than in girls. Although ADHD is usually diagnosed in children aged 3-7 years, it may not be recognised until much later in life. Sometimes it is not diagnosed until adulthood.

How is attention deficit hyperactivity disorder diagnosed?

There is no simple test to diagnose ADHD. If your child’s teacher or doctor suspect that your child may have ADHD, it is likely that your child will be referred to a specialist who will be able to confirm the diagnosis by doing an assessment, and start any treatment. This specialist may be a specialist paediatrician (children’s doctor), a child psychiatrist, a member of your local Child and Adolescent Mental Health Service, or an adult psychiatrist. The type of specialist depends on the age of your child and also the availability of services in your local area.

The assessment may involve a discussion with you and your child as well as a physical examination. The specialist may ask for a report from the school and may even want to observe your child doing certain tasks. You and your child may also see a nurse or other healthcare professionals for further testing and assessment.

There are a few aims of this assessment. These include:
•To confirm whether your child definitely has ADHD.
•To make sure that there are no other reasons that explain your child’s behaviour. For example, a hearing difficulty, epilepsy or thyroid problem.
•To identify any other problems your child may have. For example, anxiety, low self-esteem or a learning difficulty.

For a doctor to make a firm diagnosis of ADHD, there are strict criteria that need to be fulfilled. For example, the symptoms of inattention and/or hyperactivity and impulsivity need to be present for at least six months. They also need to be causing problems in your child’s life as well as being different from what would be expected for their age. They also must have started to occur before the age of seven, and be present in more than one setting. For example, at home and at school. In addition, other causes for your child’s symptoms may need to be ruled out. For example, depression or anxiety.

What are the treatment options?

The treatments recommended depend on how severe the condition is as well as the age of your child. Ideally, treatment should involve a team of professionals, experienced and trained in ADHD. The team may include a doctor, teacher, nurse, social worker, occupational therapist, mental healthcare professional or psychologist. Treatments include drug and nondrug treatments.

Nondrug treatments for attention deficit hyperactivity disorder

Generally, for preschool children or for older children with mild-to-moderate ADHD, the first step is usually for you (parent or guardian) to be referred to a parent training programme. Sometimes your child will also be referred for a group treatment programme aimed at improving behaviour. The parent programme may include such things as:
•Learning skills to manage and reduce problem behaviour.
•Learning more effective ways to communicate with your child.
•Helping you to understand your child’s emotions and behaviours.

Your child’s schoolteacher may be invited to be involved in the treatment process. They may be able to use certain techniques in the classroom to help your child learn and function better. Family therapy may also be helpful.

In more severe ADHD, or where the above treatments have not succeeded, medication is usually recommended.

Drug treatments for attention deficit hyperactivity disorder

There are three main drugs licensed for the treatment of ADHD in the UK. Methylphenidate (trade name of Ritalin®) is the most commonly used drug. Atomoxetine and dexamfetamine are other drugs that may also be used. Drug treatments are not usually given to children aged under six years. Drug treatment is done under the supervision of a specialist in childhood behavioural disorders.

How effective is drug treatment?

The drugs used for ADHD have been used for many years and in many children with good effect. A number of studies have shown that drug treatment with or without intensive behavioural training programmes is more effective than behavioural training programmes alone.

How does the methylphenidate work?

Methylphenidate is a type of stimulant drug. It works by increasing the amount of a brain chemical called dopamine in certain parts of the brain. The parts that it works on are responsible for self-control and attention. Increasing the amount of dopamine in these areas of the brain stimulates them to work better. This then helps to focus your child’s attention and improve concentration.

How do I give methylphenidate to my child?

Usually, your child will start on a low dose such as 5 mg three times a day and will be carefully monitored for side-effects. This dose is often increased gradually, usually over 4-6 weeks, to a maximum of 20 mg three times daily according to how well it is working and whether side-effects occur. The most common side-effects to look out for with methylphenidate are insomnia (difficulty with sleep), loss of appetite and weight loss.

Once the total daily dose has been determined, it may be possible for your child to switch to a once-daily long-acting version of methylphenidate.

When your child is on medication, they should be reviewed regularly to check that the dose is working and that there are minimal side-effects. Your child will also have their height, weight, pulse and blood pressure measured at regular intervals.

It is good for this review to include feedback from those who are in regular contact with your child, such as teachers, family members and other carers.

How quickly does methylphenidate work?

The short-acting methylphenidate begins working within about 20 minutes and lasts for 3-4 hours. The longer-acting version takes longer to start working but lasts for about 12 hours and gives a more stable level of drug in the bloodstream throughout the day. It may take several weeks to see the full benefit of medication.

It is common to continue medication for several years. Once children become teenagers, it is recommended to trial off the medication each year. This is to make sure that medication is still necessary.

Sometimes methylphenidate causes unacceptable side-effects or is not effective. In this situation one of the two other drugs mentioned above may be used. Dexamfetamine is another type of stimulant. Atomoxetine is a different type of drug that works on a chemical called noradrenaline in the brain.

There are other drugs that may be used for ADHD but these are usually only recommended if the above drugs are not effective.

Are the drugs safe?

The use of drugs to treat ADHD is controversial. This is mostly because some people are worried about their effectiveness as well as the possibility of side-effects. Also, there is the possibility of the drugs being misused or abused. However, guidelines from the National Institute for Health and Clinical Excellence (NICE) advise that they are still useful and important in the treatment of severe ADHD and in milder forms when other treatments have not been effective. The benefits of drugs usually outweigh any risks in children with ADHD, aged over six years and in adolescents.

The drugs do not seem to have an addictive potential when used in children. There are reports of the drugs being abused in teenagers and adults. However, it is likely that the risk of substance abuse with street drugs such as cocaine in someone with untreated ADHD is greater than the risk of abuse of the prescribed drugs.

This controversy is largely unfounded because both scientific studies and years of experience have shown that these drugs are generally safe and effective.

What about diet?

Dietary changes for the treatment of ADHD have been widely used for many years. They take the form of:
•Supplements with substances thought to be lacking. For example, supplements of fatty acids such as omega 3 and omega 6, and/or:
•Cutting out foods thought to be harmful. For example, cutting out foods containing artificial colouring and other additives.

An authoritative guideline on ADHD was published by NICE in 2008. The guideline came to the conclusion that there is no good evidence that dietary changes can help children with ADHD. However, NICE advised that “assessment of ADHD should include asking about foods or drinks that appear to influence their hyperactive behaviour. If there is a clear link, healthcare professionals should advise parents or carers to keep a diary of food and drinks taken and ADHD behaviour. If the diary supports a relationship between specific foods and drinks and behaviour, then referral to a dietitian should be offered.”

Since the NICE guideline was issued, some interesting new research has been published . A study (cited at the end) followed 100 children with ADHD over several weeks. The researchers compared a group of children with ADHD who were given a strict restricted diet with those who were not. Of those in the restricted diet group over half showed a marked improvement in their symptoms. Not many foods were included in the restricted diet. The foods allowed consisted of those thought least likely to cause symptoms and allergies, such as rice, turkey, lamb, a few vegetables, pears and water. However, it is thought that if symptoms improved with a strict diet, new foods can then be gradually introduced over time to see which food or foods may trigger worsening symptoms.

This new study is encouraging. However, further research is needed to confirm the findings and to establish the place of dietary changes in the treatment of ADHD.

So, in short, diet probably does not cause ADHD, but a change in diet may help in some cases, but not in all cases. It may be that some children are negatively affected by certain foods or additives. If you notice that a particular ingredient or food makes your child’s symptoms worse, then take a note of it and discuss this further with your doctor or a dietician. And also, it has to be stressed – do not try a strict restrictive diet for your child by yourself. If you think that diet may be a factor, it is strongly advised that you ask your GP to refer you to a qualified dietician. A dietician can advise, and make sure that any limited diet contains the full range of nutrients that a growing child requires.

It is, however, recommended that all people with ADHD have at least a normal healthy balanced diet, and also do some regular exercise.

Is there anything else available for older children or adults?

In older children, there may be some benefit gained from psychological treatment such as cognitive behavioural therapy (CBT) or social skills’ training. These techniques aim to teach your child more about why they act and react the way that they do. They also give them strategies to use to help them to improve their behaviour and daily functioning.

In adults, medication is recommended as part of a comprehensive treatment programme. This should also include psychological treatment, advice on behavioural management and assistance with education and employment.

What is the prognosis (outlook)?

Up to 8 in 10 children with ADHD will continue to experience symptoms into their teenage years. This decreases to about 5 in 10 who continue to have some symptoms into adulthood. With age, the symptoms may alter. For example, a child who was always restless may feel a lot of inner tension as an adult. It is also likely that the symptoms will reduce in severity and cause less disruption over time. As mentioned, treatment can often improve symptoms.

Children with ADHD are more likely than average to have other problems as adults, such as unemployment, relationship difficulties, substance misuse and crime. However, treatment aimed at improving behaviour at an early age aims to reduce the long-term impact of the condition.

Men

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Mentruation and disorders

Posted on March 21, 2014 by JmaC

The female reproductive system consists of the ovaries, Fallopian tubes, uterus, vagina and the vulva. At birth all the woman’s immature follicles lie dormant in the ovaries. No more are produced. This is an important consideration – eg, in childhood leukaemias and chemotherapy, as they may need to be preserved to safeguard future fertility potential of the child.

Puberty/menarche
•Puberty is a process of maturation of the sexual and secondary sexual characteristics, with menarche (onset of menstrual bleeding) as a step within that process.
•The ovarian follicles lie dormant from birth until puberty arrives and the rising hormones lead to the maturation of several ovarian follicles per month; usually only one matures and is released.
•Normal menstruation is the monthly cycle of blood loss per vagina, resulting from the breakdown of the uterine lining when implantation of a fertilised ovum does not occur. Menstruation is not a sign of ovulation, but of the fact that the hormonal controls and the reproductive tract’s responses to it work.
•Normal menstrual loss is about 25 ml per day for 4-5 days per month. The amount of blood loss varies between individuals but tends to get heavier with age.
•Menarche is the start of the first menstrual period. Menarche has occurred at a younger age during the last century. This may be due to improved nutrition (and subsequent weight) in the population.
•The average age of menarche is 13 years, but it can be as early as 8 years and as late as 18 years and still be normal. Premature or delayed menarche should be investigated – ie before 8 years or after 16 years.[1]
•Normal menstruation then occurs in a monthly cycle until menopause, unless interrupted by pregnancy. A cycle may last between 21-35 days.

Hormonal control

MENSTRUAL CYCLE DIAGRAM
The menstrual cycle is under the control of three sets of hormones:
•Gonadotrophin-releasing hormones – leutinising hormone-releasing hormone (LHRH) and follicle-stimulating hormone-releasing hormone (FSHRH).
•Gonadotrophins – luteinising hormone (LH) and follicle-stimulating hormone (FSH).
•Ovarian hormones – oestrogen and progesterone.

The gonadotrophin hormone-releasing factors from the hypothalamus control the release of the pituitary hormones; the gonadotrophins – FSH and LH. They are produced by the anterior pituitary and control the ovarian hormones oestrogen and progesterone.
•During the follicular phase a rise in FSH from the pituitary stimulates the development of several follicles on the surface of the ovary. Each follicle contains an egg. Later, as the FSH level decreases, only one follicle continues to develop. This follicle also produces oestrogen.
•The LH peaks mid-cycle, triggering the release of the ovum – ovulation, which usually occurs 16-32 hours after the surge begins. The LH level falls a couple of days later.
•The oestrogen level from the ovaries increases gradually towards ovulation and peaks during the LH surge.
•The progesterone level starts to rise towards follicle release, preparing the endometrial lining of the uterus for implantation.
•Post-ovulation – the luteal phase – levels of LH and FSH decrease. The ruptured follicle closes (after releasing the egg) and forms a corpus luteum, which produces progesterone. If the ovum is fertilised, the progesterone levels are maintained by the corpus luteum and the endometrium is maintained.
•If the ovum is not fertilised the corpus luteum starts to degenerate and progesterone and oestrogen levels start to fall. The endometrial blood vessels constrict and the endometrial lining breaks down and is shed.
•The hormonal swings may be associated with changes in mood and libido, and with headaches in some women. However, some studies have not demonstrated good evidence for premenstrual mood symptoms.[2]
•The first day of the cycle is counted as the first day of the bleed – Day 1. The cycle runs from the first day of menstruation to the next first day.
•The typical changes of the menstrual cycle may allow natural family planning, if a woman wishes. Several methods are available, including calendar, temperature and cervical mucus observation, or palpating the cervix.[3]

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Range of problems

Abnormalities in menstruation may include:
•Quantity: usually perceived as too great a loss – menorrhagia. This is usually defined as a loss above 80 mls per menses and may cause iron-deficiency anaemia.
•Timing: may be too frequent (polymenorrhoea – more than one period per calendar month) or infrequent (oligomenorrhoea or amenorrhoea).
•Duration of bleeding: normal range is 3-7 days.
•Time of onset: precocious puberty (before 8 years) or delayed puberty (after 16 years).

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Intermenstrual and Postcoital Bleeding
Menorrhagia
Genitourinary History and Examination (Female)
Premenstrual Syndrome

Aetiology of abnormal bleeding

Non-reproductive causes
•Systemic disease disorders of blood coagulation – eg, von Willebrand’s disease or prothrombin deficiency, leukaemia, idiopathic thrombocytopenic purpura and hypersplenism.
•Hypothyroidism – can sometimes be associated with menorrhagia or intermenstrual bleeding (IMB).
•Cirrhosis – associated with reduced ability of the liver to metabolise oestrogens, and hypoprothrombinaemia.

free affirmations Naturally start conversations

Posted on March 21, 2014 by JmaC

Present Tense Affirmations

I can effortlessly come up with conversation topics
I am able to approach others and begin a conversation
I am at ease in social situations
I am able to overcome awkward situations when they arise
I am confident enough to be able to start a conversation
I am good at finding things I have in common with others
I do not care what other people think
I am happy to be myself in a conversation
I can advance my career by starting more conversations
I do not worry about making small talk

Future Tense Affirmations

I will be able to speak to anybody I like
Every day I become more confident
I will not worry about what others think of me
I will not be intimidated by others
I will be able to effortlessly approach people
I will improve my topics for starting conversations
I will be able to make more friends
Every day I become more relaxed in social situations
Starting conversations will begin to feel more natural
I will be more likely to find a soul mate by starting a conversation

Natural Affirmations

Starting a conversation is simple
I enjoy speaking to new people
Making more contacts will help me advance my career
Confidence is a key part of my life
Each time I start a conversation I broaden my horizons
Starting conversations comes naturally to me
People admire my communication skills
Making small talk is easy
I am confident in my personality
Other people have high opinions of my communication skills

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free affirmations charisma

Posted on March 21, 2014 by JmaC

Present Tense Affirmations

I am charismatic
I am positive and outgoing
Others are naturally attracted to my charisma
I always lead the conversation
I am full of positive energy
I make others feel good with my positive energy
I am always starting conversations and meeting new people
I am friendly, positive, and outgoing
I am a great conversationalist
I naturally attract others with my charisma

Future Tense Affirmations

I will unlock my natural charisma
I am turning into someone who others love to be around
I will confidently express my amazing pesonality
Others view me as a highly charismatic person
My natural charisma is growing
I will spread positive energy to others
I am starting to feel more outgoing and social
I am transforming into someone who loves meeting new people
Others are beginning to notice how charismatic I am
Everyday I become more and more outgoing

Natural Affirmations

Being charismatic is easy
I am just naturally charismatic
Being outgoing comes naturally to me
I have a magnetic personality
Being charismatic is just a normal part of my life
Others can’t help but be drawn to my positive energy
Making others feel happy is something I just naturally do
I enjoy sharing myself with others
I love being the center of attention at a party
People see me as someone who is always happy and positive

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Free affirmations win friends and influence people

Posted on March 21, 2014 by JmaC

Present Tense Affirmations

I am able to speak to new people
I enjoy starting conversations
I am good at persuading people
I am good at finding people I have common interests with
I can make new friends quickly and easily
People take my opinions seriously
I can inspire others with my words
I am improving my social skills every day
I am relaxed when beginning conversations
I can lead conversations in the direction I want them to go

Future Tense Affirmations

I will be able to make friends more easily
I will make more of an effort to begin conversations
My friends will listen to me more
I will find it easier to express my feelings
I will become more assertive and firm
Others will realise that I am easy to get along with
I will make my voice heard
Conversations will feel more natural to me
People will see me as outgoing and friendly
I will be able to show my personality more

Natural Affirmations

Others think I am confident and assertive
I enjoy meeting new people
My friends make me happy
Starting conversations is within my comfort zone
My social skills will help me excel in my career
People find me easy to get along with
I become better at making friends every day
Making friends comes naturally to me
Saying no is easy
My conversation skills allow me to help others

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Is this new treatment any good

Posted on March 21, 2014 by JmaC

When a new drug or treatment is launched, we have to ask if it is one that we should use. Does it represent a real advance? Be aware that with new drugs, a great deal of money has already been invested in the product, and the marketing team wishes to present it in the most favourable light to enhance sales.[1]

Amongst the questions to be answered are:
•Is it relevant to my patients?
•Is this drug a new concept, or a variation on a theme? Perhaps it is a “me too” drug in a lucrative but highly packed niche such as another angiotensin-converting (ACE) inhibitor.
•How much is known about its safety?
•Does it represent a significant advance on current options? Consider the following: •Is it more effective?
•Has it fewer adverse effects?
•Is it cheaper?
•Is the dosage or route of administration more manageable?

•How good is the evidence about it, and is any information missing?
•Do those promoting it have a conflict of interest?
•Are the benefits worth the risk of adverse effects (known and unknown)?
•Would I take this treatment myself?

Safety

The accepted principle is that clinicians should “trade a known risk for an unknown risk only when there is a reasonable expectation that the new therapy is better.”[2]

Drugs

New medicines in the UK require a licence from the Medicines and Healthcare products Regulatory Agency (MHRA).[3] They have undergone clinical trials, but this does not mean that the product is safe – for example, if the trials or follow-up are inadequate.[4] The number of patients tested in early trials is unlikely to be sufficient to ensure that all adverse effects are discovered. For example: the diabetes drug troglitazone was withdrawn 3 months after it was released because of hepatic side-effects.[2] Later, rosiglitazone was discovered to have important cardiovascular side-effects. Some argue that it was licensed too soon, and that the public is not well served by the current system of drug development.[5][2]

Safety monitoring

Licensing decisions take into account the seriousness of the condition being treated. For example, more uncertainties or adverse effects will be acceptable for an anticancer drug than for a painkiller used in minor illness.

New drugs carry a “black triangle”, indicating that they are “intensively monitored medicines”. Monitoring is continued until the MHRA is satisfied that the drug works safely in large numbers of people.[3]

For any black triangle medication, report ALL adverse reactions:[6] •Include non-serious reactions.
•Even if not certain whether they are due to the drug.

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Nondrug treatments
•Nondrug treatments, such as surgical procedures, psychological or social interventions, and complementary medicine, also require evaluation. However, with nondrug treatments it may not be feasible to use blinding in trial protocols.
•Some treatments may have a net harmful effect. For example, in post-traumatic stress disorder, negative outcomes were reported for some types of critical incident debriefing.[7]

Informed consent[8]

Good medical practice requires that doctors should tell patients about:
•Options for treatment, including the option not to treat and uncertainties.
•Details of the treatment.
•Adverse effects: •Common adverse effects.
•Serious adverse effects – even if rare.
This information should be shared in a way that the patient can understand.

Children, pregnancy and breast-feeding

Newly developed drugs and treatments have not usually been tested on pregnant or breast-feeding women or children, so there will be a lack of dosing and safety information for these groups, and indeed the treatment may not be licensed for them.[9] Older, more established treatments are the first choice. If a new treatment seems necessary, consult an expert, the National Teratology Information Service (for pregnancy)[10] or the British National Formulary for Children (BNFC) – for children and breast-feeding.[11]

Evaluating the evidence[1][12][13]

The authors and setting
•Who is presenting the evidence; do they have competing interests? Research suggests that industry sponsorship is widespread and is associated with pro-industry conclusions.[14][15]
•Is this a reputable journal or conference? Results from a recent study suggest that pharmaceutical advertising has an influence on the content of free medical publications (those that rely on advertising for revenue).[16]
•Is there peer review?
•Who are the authors? Bear in mind that “ghost writing” occurs,[17] and that “independent” research companies may also be vulnerable to commercial pressure.[18]

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Prescribing Issues and Concordance
Prescribing Analysis and Audit
Numbers Needed To Treat
Different Levels of Evidence

Study design

What type of study was done? The “gold standard” for measuring the effectiveness of a drug is the randomised controlled study (RCT).
This type of study may be:
•Single blind – the patient does not know which medication is being taken.
•Double blind – neither patient nor researcher knows which medication is being taken.
•Double blind, crossover – the patient will be taking active compound A and a placebo B, or new compound A and existing compound B, and then cross over to receive the other compound or placebo. Neither the patient nor the researcher will be aware which compound the patient is taking at any one time, and the subject is, in effect, his own control.

Look at the methods used section:
•Is the design biased in terms of patient selection, inclusion or withdrawal?
•Was there true randomisation of the patients?
•Is the study adequately powered? This means, is there a large enough number of subjects in the study? It is possible to calculate the number required before embarking on the study. The person reading the paper is unlikely to check such calculations but will simply ask the question, “Do the numbers look reasonable or are they rather small?”.
•What outcome (end point) is used? Be cautious about: •Surrogate outcome measures, eg the use of lipid values as an outcome, rather than actual clinical events such as myocardial infarction. If surrogate end points are used, there should be good evidence that they are valid for the condition being studied.
•Composite end points, eg combining non-fatal myocardial infarction and death. This can make a treatment appear more effective, but the two outcomes are clinically different and are best considered separately.

Validity of results

When assessing the validity of the results it is important to answer several questions:
•Were the groups made up of similar patients? Were the groups treated equally in all ways except the intervention?
•Follow-up – were all the patients entered into the trial accounted for at the end? NB: if many patients were “lost to follow-up”, be wary of the study’s results.[4] The “lost” patients may have had adverse effects or less benefit from the treatment.
•Have withdrawals and adverse events been recorded for both treatment groups?
•Were the patients analysed in the groups to which they were randomised? This is an important concept. For example, if a cancer trial puts patients who were too ill to receive the active intervention into the control group, this unfairly favours the intervention group.

Interpreting the results

Are the results clinically significant?
•It is important to consider what the new treatment was compared to – for example, to a placebo or to an existing treatment.[2] Is the comparison in the trial relevant to your patients?
•For example, a trial of a hypotensive agent may be able to demonstrate a statistically significant fall in blood pressure, but that fall may be so small that the clinical benefit is negligible.

Are the results expressed in a meaningful way?[19][20]

Results are often quoted as relative risk reduction, which makes the benefit of the new treatment appear more dramatic. However, absolute risk reduction and the number needed to treat (NNT) are more useful in clinical practice, because they take into account how common the outcomes are, and therefore the size of the treatment effect in practice.

The NNT is calculated as the reciprocal of the absolute risk reduction, i.e:
NNT = 1/absolute risk reduction as a fraction.

Similarly, adverse outcomes of a new treatment can be expressed as the number needed to harm (NNH). This can then be combined with the NNT to give the likelihood of being helped or harmed (LHH). The LHH is calculated as the ratio of NNT to NNH, ie LHH = 1/NNT:1/NNH.

Note that absolute risk measures, including the NNT, only apply to the population studied (or a population with similar baseline risks). And, as with all statistical estimates, the estimated values should be accompanied by a confidence interval.

Example

Here are the results of a hypothetical trial of a treatment (T) for a condition (C):

Example: trial of treatment T for condition C

Results of trial (% patients) Deaths from condition C Survival from condition C
No treatment 20% 80%
Given treatment T 10% 90%

These results can be expressed in various ways:
•Treatment T halved the rate of death from C (relative risk reduction).
•Treatment T reduced deaths from C by 10%, or increased the survival rate from 80% to 90% (absolute risk reduction).
•For 10 people treated with T, one death from C will be avoided (NNT).

Significance and confidence intervals

Statistical significance is often taken as P≤0.05, meaning there is a 1 in 20 probability that the difference between the two groups was due purely to chance.

Confidence intervals: these express the degree of uncertainly about the “true” result.

For example, suppose two trials appear, superficially, to have identical results. One is a small trial comparing A with B and the respective scores were 40% and 50%. Calculation of confidence intervals on the small sample show that there is a 95% probability that the “true” result lies somewhere between ±7% for each group. This means that there is a 95% chance that the “true” result for A is between 33% and 47% and the “true” result for B is between 43% and 57%. There is also a 5% chance that the actual figure lies further out. In this case, the result for A may be as high as 47% and the result for B may be as low as 43%. Hence, there is overlap between the confidence intervals and so the difference between A and B is unproven. Another trial has apparently similar results with A and B at 40% and 50% respectively but, being larger, the confidence interval is only ±3%. This means that there is a 95% chance that A lies between 37% and 43% while B lies between 47% and 53%. There is no overlap and so the difference between A and B has been demonstrated.

Example using risk values, NNT and cost

A hypothetical scenario: Mrs Z requests your help to encourage the PCT to fund a treatment for her cancer. She says that it halves her chance of dying and adds that £20,000 does not seem a high price to save a life. You find that the cost of treatment is actually £20,000 a year and the duration of treatment is usually 2 or 3 years. This makes the cost of a course of treatment £40,000 or £60,000. Let us call it £50,000. The risk of recurrence of her cancer is reduced from 20% to 10%. On this basis the NNT to prevent one recurrence is 10. This makes the cost of preventing one recurrence £500,000. Not everyone with a recurrence will die from it, but let us assume a poor outcome with a 50% mortality from recurrence. This means that two recurrences must be prevented to save one life. It would appear that the cost of saving a life is not £20,000 but nearer £1 million.

“New for old” drugs

New formulations of older drugs are often promoted by manufacturers, sometimes around the time that the patent on the older drug has expired. Bear in mind that some of these new drugs may benefit the manufacturer more than the patient.

“New for old” drugs include:
•”Me too” drugs which are similar to an existing product by another manufacturer.
•”Second-generation” products such as escitalopram or desloratadine. These are isomers or metabolites of an existing drug, and may be marketed as “more effective” (because a lower dose is required on a weight for weight basis). In practice there is seldom any clinical benefit.
•New formulations such as slow-release preparations – these may sound useful, but in practice the advantage may be minimal.

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The man and the idea – conceptual abstract illustration