Clinical depression is a state of intense sadness, melancholia or despair that has advanced to the point of being disruptive to an individual's social functioning and/or activities of daily living. A person suffering from depression may feel tired, sad, irritable, lazy, unmotivated, and apathetic. Clinical depression is generally acknowledged to be more serious than normal depressed feelings. It often leads to constant negative thinking and sometimes substance abuse. Extreme depression can culminate in its sufferers attempting or committing suicide.

Without careful assessment, delirium can easily be confused with depression and a number of other psychiatric disorders because many of the signs and symptoms are conditions present in depression, as well as other mental illnesses including dementia and psychosis.

 Types of depression:

Major clinical depression:

Major Depression, or, more properly, Major Depressive Disorder (MDD), is characterized by a severely depressed mood that persists for at least two weeks. Major Depressive Disorder is specified as either "a single episode" or "recurrent"; periods of depression may occur as discrete events or recur over the lifespan. Episodes of major or clinical depression may be further divided into mild, major or severe. Where the patient has already had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder (also called bipolar affective disorder) is usually made instead of MDD; depression without periods of elation or mania is therefore sometimes referred to as unipolar depression because the mood remains on one pole. The diagnosis also usually excludes cases where the symptoms are a normal result of bereavement. Diagnosticians recognize several possible subtypes of Major Depressive Disorder. ICD-10 does not specify a melancholic subtype, but does distinguish by presence or absence of psychosis.

Dysthymia is a long-term, mild depression that lasts for a minimum of two years. There must be persistent depressed mood continuously for at least two years. By definition the symptoms are not as severe as with Major Depression, although those with Dysthymia are vulnerable to co-occurring episodes of Major Depression. This disorder often begins in adolescence and crosses the lifespan. People who are diagnosed with major depressive episodes and dysthymic disorder are diagnosed with double depression. Dysthymic disorder develops first and then one or more major depressive episodes happen later.

Bipolar I Disorder is an episodic illness in which moods may cycle between mania and depression. In the United States, Bipolar Disorder was previously called Manic Depression. This term is no longer favored by the medical community, however, even though depression plays a much stronger (in terms of disability and potential for suicide) role in the disorder. "Manic Depression" is still often used in the non-medical community. Bipolar II Disorder is an episodic illness that is defined primarily by depression but evidences episodes of hypomania.

Postpartum Depression or Post-Natal Depression is clinical depression that occurs within two years of childbirth. Owing to physical, mental and emotional exhaustion combined with sleep-deprivation, motherhood can "set women up", so to speak, for clinical depression.(Kathy,2005)

Premenstrual dysphoria is a pattern of recurrent depressive symptoms tied to the menstrual cycle. The premenstrual decline in brain serotonin function is strongly correlated with the concomitant worsening of self-rated cardinal mood symptoms.(Eriksson et al , 2006) Of considerable clinical importance, the recent understanding of premenstrual dysphoria as depression points directly to effective treatment with Selective serotonin reuptake inhibitor (SSRI) antidepressants. Previously, disrupting ovarian cyclicity had been the only recognized treatment. A recent review of studies of a number of SSRIs has revealed that they can effectively ameliorate symptoms of premenstrual dysphoria and may actually work best when taken only during the part of the menstrual cycle when dysphoric symptoms are evident.

Recurrent brief depressive disorder (or recurrent brief depression) is in the ICD-10 classification. It is described as meeting the criteria for a mild, moderate or severe depressive episode; the depressive episodes have occurred about once per month over the last year; individual episodes last less than two weeks (typically less than 2-3 days), and they do not occur solely in relation to the menstrual cycle.  Some people are at risk of self-harm, as well as the disruption to everyday life, particularly work

Physiological causes

Genetic predisposition

The tendency to develop depression may be inherited: according to the National Institute of Mental Health there is some evidence that depression may run in families, though this familial trend probably includes both biological and environmental factors.

Neurological:

Many modern antidepressant drugs change levels of certain neurotransmitters, namely serotonin and norepinephrine (noradrenaline). However, the relationship between serotonin, SSRIs, and depression usually is typically greatly oversimplified when presented to the public, though this may be due to the lack of scientific knowledge regarding the mechanisms of action. Evidence has shown the involvement of neurogenesis in depression, though the role is not exactly known.(Castren,2005). Recent research has suggested that there may be a link between depression and neurogenesis of the hippocampus. This horseshoe-shaped structure is a center for both mood and memory. Loss of neurons in the hippocampus is found in depression and correlates with impaired memory and dysthemic mood. That is why treatment usually results in an increase of serotonin levels in the brain which would in turn stimulate neurogenesis and therefore increase the total mass of the Hippocampus and restores mood and memory, therefore assisting in the fight against the mood disorder.

In about one-third of individuals diagnosed with attention-deficit hyperactivity disorder (ADHD), a developmental neurological disorder, depression is recognized as comorbid Dysthymia,(Hallowell,Edward and Ratey,2005) a form of chronic, low-level depression, is particularly common in adults with undiagnosed ADHD who have encountered years of frustrating ADHD-related problems with education, employment, and interpersonal relationships

Medical conditions

Certain illnesses, including cardiovascular disease(Maney and Maney,2004) hepatitis, mononucleosis, hypothyroidism, and organic brain damage caused by degenerative conditions such as Parkinson disease, Multiple Sclerosis or by traumatic blunt force injury may contribute to depression, as may certain prescription drugs such as hormonal contraception methods and steroids.

Dietary

The increase in depression in industrialised societies has been linked to diet, particularly to reduced levels of omega-3 fatty acids in intensively farmed food and processed foods(Felicity,2004) This link has been at least partly validated by studies using dietary supplements in schools  and by a double-blind test in a prison. An excess of omega-6 fatty acids in the diet was shown to cause depression in rats.Depression can also be caused by a magnesium deficiency or lower magnesium levels.

Sleep quality

Poor sleep quality co-occurs with major depression. Major depression leads to alterations in the function of the hypothalamus and pituitary causing excessive release of cortisol which can lead to poor sleep quality. Individuals suffering from Major Depression have been found to have an abnormal sleep architecture, often entering REM sleep sooner than usual, along with highly emotionally-charged dreaming. Antidepressant drugs, which often function as REM sleep suppressants, may serve to dampen abnormal REM activity and thus allow for a more restorative sleep to occur.

Seasonal affective disorder

Seasonal affective disorder (SAD) is a type of depressive disorder that occurs in the winter when daylight hours are short. It is believed that the body's production of melatonin, which is produced at higher levels in the dark, plays a major part in the onset of SAD and that many sufferers respond well to bright light therapy, also known as phototherapy.

Psychological factors

Low self-esteem and self-defeating or distorted thinking are connected with depression. Although it is not clear which is the cause and which is the effect, it is known that depressed persons who are able to make corrections in their thinking patterns can show improved mood and self-esteem (Cognitive Behavioral Therapy). Psychological factors related to depression include the complex development of one's personality and how one has learned to cope with external environmental factors such as stress.

Early experiences

Events such as the death of a parent, issues with biological development, school related problems, abandonment or rejection, neglect, chronic illness, and physical, psychological, or sexual abuse can also increase the likelihood of depression later in life. Post-traumatic stress disorder (PTSD) includes depression as one of its major symptom.

Life experiences

Job loss, poverty, financial difficulties, gambling addiction, long periods of unemployment, the loss of a spouse or other family member, rape, divorce or the end of a committed relationship, involuntary celibacy, inability to have proper sex or premature ejaculation or other traumatic events may trigger depression. Long-term stress at home, work, or school can also be involved.

Evolution: Potential adaptive advantages of clinical depression:

Evolutionary analyses examine the ways in which depression as a response to certain environmental stimuli may act as an adaptive advantage and increase genetic fitness, either of the individual or the society as a whole.

Treatment

Treatment of depression varies broadly among individuals. The level, type, and methods of intervention vary dramatically. There are two primary modes of treatment that are typically used in conjunction; medication and psychotherapy. A significant number of recent studies have indicated that changes in lifestyle such as regular exercise and dietary supplements have beneficial effects.(Castren,2005)

In most cases, one particular medication or combination of medications can provide significant change, although, in some cases, the condition does not respond well. Treatment-resistant depression warrants a full assessment, which may lead to the introduction of psychotherapy, a focus on lifestyle change, an increase of medication, or a change in medication.

In emergencies, hospitalization is an intervention employed to keep at-risk individuals safe until they cease to be a danger to themselves or others. An alternative treatment program is partial hospitalization, in which the patient sleeps at home but spends most of the day in a psychiatric hospital setting. This intensive treatment usually involves group therapy, individual therapy, medication management, and often in the case of children and adolescents, academics.

Medication

Medication that relieves the symptoms of depression has been available for several decades. Typical first-line therapy for depression is the use of a selective serotonin reuptake inhibitor, such as citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft). Under some circumstances, medication and psychotherapy may be more effective than either treatment separately(Thase,1999). Selective serotonin reuptake inhibitors (SSRIs) 

Selective serotonin reuptake inhibitors (SSRIs) are a family of antidepressants considered to be the current standard of drug treatment. It is thought that one cause of depression is an inadequate amount of serotonin, a chemical used in the brain to transmit signals between neurons. SSRIs are said to work by preventing the reuptake of serotonin by the presynaptic nerve, thus maintaining higher levels of 5-HT in the synapse. Recently, however, work by two researchers has called into question the link between serotonin deficiency and symptoms of depression, noting that the efficacy of SSRIs as treatment does not in itself prove the link.(Lacasse and Leo,2005). Recent research indicates that these drugs may interact with transcription factors known as "clock genes", which may be important for the addictive properties of drugs of abuse and possibly in obesity.(Yuferov et al., 2005)

Recent randomized controlled trials in Archives of General Psychiatry showed that up to one-third of effects of SSRI Treatment can be seen in first week. Early effects also shown to have secondary effect of reducing absolute reduction in HDRS score by 50 percent. Even more recent studies, published by the Archives of General Psychiatry note that 25% of so-called clinical depression does not meet a disease criteria and should be considered to be ordinary sadness and adjustment to the difficulties in life.

This family of drugs includes fluoxetine (Prozac), paroxetine (Paxil), escitalopram (Lexapro), citalopram (Celexa), and sertraline (Zoloft). These antidepressants typically have fewer adverse side effects than the tricyclics or the MAOIs, although such effects as drowsiness, dry mouth, nervousness, anxiety, insomnia, decreased appetite, and decreased ability to function sexually may occur. Some side effects may decrease as a person adjusts to the drug, but other side effects may be persistent. Though safer than first generation antidepressants, SSRI's may not work as often, suggesting the role of norepinephrine. However, it should be noted that all psycho-active medications extend the reaction time, thus increasing the likelihood of falls and road crashes.  

Psychotherapy

In psychotherapy, or counseling, one receives assistance in understanding and resolving habits or problems that may be contributing to or the cause of the depression. This may be done individually or with a group and is conducted by mental health professionals such as psychiatrists, psychologists, clinical social workers, or psychiatric nurses.

Effective psychotherapy may result in different habitual thinking and action which leads to a lower relapse rate than antidepressant drugs alone. Medication, however, may yield quicker results and be strongly indicated in a crisis. Medication and psychotherapy are generally complementary, and both may be used at the same time.

Transcranial magnetic stimulation

Repetitive transcranial magnetic stimulation (rTMS) is under study as a possible treatment for depression. Initially designed as a tool for physiological studies of the brain, this technique shows promise as a means of alleviating depression. In this therapy, a powerful magnetic field is used to stimulate the left prefrontal cortex, an area of the brain that typically shows abnormal activity in depressed people.

Recent work  in Poland suggested that weak, variable magnetic fields may offer relief from depression in those who have not responded to medication. However, some of the existing work has been questioned, with claims that the effect is not as significant once environmental conditions are controlled.

Vagus nerve stimulation

Vagus nerve stimulation therapy is a treatment used since 1997 to control seizures in epileptic patients and has recently been approved for treating resistant cases of treatment-resistant depression (TRD). The VNS Therapy device is implanted in a patient's chest with wires that connect it to the vagus nerve, which it stimulates to reach a region of the brain associated with moods. The device delivers controlled electrical currents to the vagus nerve at regular intervals.

Electroconvulsive therapy

Electroconvulsive therapy (ECT), also known as electroshock or electroshock treatment, uses short bursts of a controlled current of electricity (typically fixed at 0.9 ampere) into the brain to induce a brief, artificial seizure while the patient is under general anesthesia.

In contrast to direct electroshock of years ago, most countries now allow ECT to be administered only under anaesthesia. In a typical regimen of treatment, a patient receives three treatments per week over three or four weeks. Repeat sessions may be needed. Short-term memory loss, disorientation, and headache are very common side effects. Detailed neuropsychological testing in clinical studies has not been able to prove permanent effects on memory. ECT offers the benefit of a very fast response; however, this response has been shown not to last unless maintenance electroshock or maintenance medication is used. Whereas antidepressants usually take around a month to take effect, the results of ECT have been shown to be much faster. For this reason, it is the treatment of choice in emergencies (e.g., in catatonic depression in which the patient has ceased oral intake of fluid or nutrients).

There remains much controversy over electroshock. Advocacy groups and scientific critics, such as Dr Peter Breggin, call for restrictions on its use or complete abolishment. Like all forms of psychiatric treatment, electroshock can be given without a patient's consent, but this is subject to legal conditions dependent on the jurisdiction. In Oregon patient consent is necessary by statute.

Light therapy

Bright light (both sunlight and artificial light) is shown to be effective in seasonal affective disorder, and sometimes may be effective in other types of depression, especially atypical depression or depression with "seasonal phenotype" (overeating, oversleeping, weight gain, apathy).

Exercise

It is widely believed that physical activity and exercise help depressed patients and promote quicker and better relief from depression. They are also thought to help antidepressants and psychotherapy work better and faster. It can be difficult to find the motivation to exercise if the depression is severe, but sufferers should be encouraged to take part in some form of regularly scheduled physical activity. A workout need not be strenuous; many find walking, for example, to be of great help. Exercise produces higher levels of chemicals in the brain, notably dopamine, serotonin, and norepinephrine. In general this leads to improvements in mood, which is effective in countering depression.

Meditation

Meditation is increasingly seen as a useful treatment for some cases of depression. The current professional opinion on meditation is that it represents at least a complementary method of treating depression, a view that has been endorsed by the Mayo Clinic. Since the late 1990s, much research has been carried out to determine how meditation affects the brain (see the main article on meditation). Although the effects on the mind are complex, they are often quite positive, encouraging a calm, reflective, and rational state of mind that can be of great help against depression.

Deep brain stimulation

Though still experimental, a new form of treatment called deep brain stimulation offers some hope in the relief of treatment resistant clinical depression. Published in the journal Neuron (2005), Helen Mayberg described the implanting of electrodes in a region of the brain known as Area 25 The electrodes act in an inhibitory fashion, on an otherwise overactive region of the brain. Further research is required before it becomes available as a method of treatment, but it offers hope for those suffering from treatment resistant depression.

Dr Smita Pandey Bhat, Cinical Psychologist

Alzheimer's disease (AD), also known simply as Alzheimer's, is a neurodegenerative disease. Characterized by progressive cognitive deterioration, together with declining activities of daily living and by neuropsychiatry symptoms or behavioral changes, it is the most common type of dementia.

Stages and symptoms

• Mild — At the early stage of the disease, patients have a tendency to become less energetic or spontaneous, though changes in their behavior often go unnoticed even by the patients' immediate family. This stage of the disease has also been termed Mild Cognitive Impairment (MCI) although this term remains somewhat controversial.
• Moderate — As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities.
• Severe — As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need constant supervision. They become incontinent of bladder and then incontinent of bowel. They will eventually lose the ability to walk and eat without assistance. Language becomes severely disorganized, and then is lost altogether. They may eventually lose the ability to swallow food and fluid and this can ultimately lead to death.

Diagnosis

The diagnosis is made primarily on the basis of history, clinical observation, memory tests and intellectual functioning over a series of weeks or months, with various physical tests (blood tests and neuroimaging) being performed to rule out alternative diagnoses. No medical tests are available to diagnose Alzheimer's disease conclusively pre-mortem. Expert clinicians who specialize in memory disorders can now diagnose AD with an accuracy of 85–90%, but a definitive diagnosis of Alzheimer's disease must await microscopic examination of brain tissue, generally at autopsy. Functional neuroimaging studies such as PET and SPECT scans can provide a supporting role where dementia is clearly present, but the type of dementia is questioned. Recent studies suggest that SPECT neuroimaging approaches clinical exam in diagnostic accuracy and may outperform exam at differentiating types of dementia (Alzheimer's disease vs. vascular dementia). However, Alzheimer's disease remains a primarily clinical diagnosis based on the presence of characteristic neurological features and the absence of alternative diagnoses, with possible neuroimaging assistance. Interviews with family members and/or caregivers are extremely important in the initial assessment, as the sufferer him/herself may tend to minimize his symptomatology or may undergo evaluation at a time when his/her symptoms are less apparent, as quotidian fluctuations ("good days and bad days") are a fairly common feature. Such interviews also provide important information on the affected individual's functional abilities, which are a key indicator of the significance of the symptoms and the stage of dementia.

Initial suspicion of dementia may be strengthened by performing the mini mental state examination, after excluding clinical depression. Psychological testing generally focuses on memory, attention, abstract thinking, the ability to name objects, visuospatial abilities, and other cognitive functions. Results of psychological tests may not readily distinguish Alzheimer's disease from other types of dementia, but can be helpful in establishing the presence of and severity of dementia. They can also be useful in distinguishing true dementia from temporary (and more treatable) cognitive impairment due to depression or psychosis, which has sometimes been termed "pseudodementia". In addition, a 2004 study by Cervilla and colleagues showed that tests of cognitive ability provide useful predictive information up to a decade before the onset of dementia. However, when diagnosing individuals with a higher level of cognitive ability, in this study those with IQs of 120 or more, patients should not be diagnosed from the standard norm but from an adjusted high-I.Q norm that measured changes against the individual's higher ability level.

Neuropathology

Both amyloid plaques and neurofibrillary tangles are clearly visible by microscopy in AD brains. At an anatomical level, AD is characterized by gross diffuse atrophy of the brain and loss of neurons, neuronal processes and synapses in the cerebral cortex and certain subcortical regions. This results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus.Levels of the neurotransmitter acetylcholine are reduced. Levels of the neurotransmitters serotonin, norepinephrine, and somatostatin are also often reduced. Glutamate levels are usually elevated.

Epidemiology

Alzheimer's disease is the most frequent type of dementia in the elderly and affects almost half of all patients with dementia. Correspondingly, advancing age is the primary risk factor for Alzheimer's. Among people aged 65, 2-3% show signs of the disease, while 25–50% of people aged 85 have symptoms of Alzheimer's and an even greater number have some of the pathological hallmarks of the disease without the characteristic symptoms. Every five years after the age of 65, the probability of having the disease doubles.[46] The share of Alzheimer's patients over the age of 85 is the fastest growing segment of the Alzheimer's disease population in the US, although current estimates suggest the 75-84 population has about the same number of patients as the over 85 population.[47]

Prevention

Ageing itself can not be prevented, but the senescence of it can be mitigated. However, the evidence relating certain behaviors, dietary intakes, environmental exposures, and diseases to the likelihood of developing Alzhemier's varies in quality and its acceptance by the medical community.[48] It is important to understand that interventions that reduce the risk of developing disease in the first place may not alter disease progression after symptoms become apparent. Due to their observational design, studies examining disease risk factors are often at risk from confounding variables. Several recent large, randomized controlled trials—in particular the Women's Health Initiative—have called into question preventive measures based on cross-sectional studies. Some proposed preventive measures are even based on studies conducted solely in animals or in cell cultures but are not listed here.

Risk reducers

• Intellectual stimulation (e.g., playing chess or doing crosswords)
• Regular physical exercise
• Regular social interaction
• A Mediterranean diet with fruits and vegetables and low in saturated fat, supplemented in particular with:
  • B vitamins
  • Omega-3 fatty acids
  • Fruit and vegetable juice
  • High doses of the antioxidant Vitamin E (in combination with vitamin C) seem to reduce Alzheimer's risk in cross sectional studies but not in a randomized trial and so are not currently a recommended preventive measure because of observed increases in overall mortality
  • The moderate consumption of alcohol (beer, wine or distilled spirits)
• Cholesterol-lowering drugs (statins) reduce Alzheimer's risk in observational studies but so far not in randomized controlled trials
• Female Hormone replacement therapy is no longer thought to prevent dementia based on data from the Women's Health Initiative
• Long-term usage of non-steroidal anti-inflammatory drugs (NSAIDs), used to reduce joint inflammation and pain, are associated with a reduced likelihood of developing AD, according to some observational studies. The risks appear to outweigh the drugs' benefit as a method of primary prevention.[

Risk factors

• Advancing age
• ApoE epsilon 4 genotype (in some populations)
• Head injury
• Poor cardiovascular health (including smoking, diabetes, hypertension, high cholesterol and strokes)

Psychosocial interventions

Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacologic treatment, especially in the early to moderately advanced stages of disease. Treatment modalities include counseling, psychotherapy (if cognitive functioning is adequate), reminiscent therapy, reality orientation therapy, and behavioral reinforcements as well as cognitive rehabilitation training.

Treatments in clinical development

A large number of potential treatments for Alzheimer's disease are currently under investigation, including four compounds being studied in phase 3 clinical trials. Xaliproden had been shown to reduce neurodegeneration in animal studies. Tramiprosate (3APS or Alzhemed) is a GAG-mimetic molecule that is believed to act by binding to soluble amyloid beta to prevent the accumulation of the toxic plaques. Tarenflurbil (MPC-7869, formerly R-flubiprofen) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide. Leuprolide has also been studied for Alzheimer’s. It is hypothesized to work by reducing leutenizing hormone levels which may be causing damage in the brain as one ages.

• Vaccines or immunotherapy for Alzheimer's, unlike typical vaccines, would be used to treat diagnosed patients rather than for disease prevention. Ongoing efforts are based on the idea that, by training the immune system to recognize and attack beta-amyloid, the immune system might reverse deposition of amyloid and thus stop the disease. Initial results using this approach in animals were promising, and clinical trials of the drug candidate AN-1792 showed results in 20% of patients. However, in 2002 it was reported that 6% of multi-dosed participants (18 of 300) developed symptoms resembling meningoencephalitis, and the trials were stopped. Participants in the halted trials continued to be followed, and 20% "developed high levels of antibodies to beta-amyloid" and some showed slower progression of the disease, maintaining memory-test levels while placebo-patients worsened. Microcerebral haemorrhages with passive immunisation and meningoencephalitis with active immunisation still remains to be potent threats to this strategy Work is continuing on less toxic Aβ vaccines, such as a DNA-based therapy that recently showed promise in mice. Researchers from University of South Florida announced a patch version of the drug was shown to be safe and effective when tested on mice.

• Proposed alternative treatments for Alzheimer's include a range of herbal compounds and dietary supplements. In the AAGP review from 2006, Vitamin E in doses below 400 IU was mentioned as having conflicting evidence in efficacy to prevent AD. Higher doses were discouraged as these may be linked with higher mortality related to cardiac events.

Occupational and lifestyle therapies

Modifications to the living environment and lifestyle of the Alzheimer's patient can improve functional performance and ease caretaker burden. Assessment by an occupational therapist is often indicated. Adherence to simplified routines and labeling of household items to cue the patient can aid with activities of daily living, while placing safety locks on cabinets, doors, and gates and securing hazardous chemicals and guns can prevent accidents and wandering. Changes in routine or environment can trigger or exacerbate agitation, whereas well-lit rooms, adequate rest, and avoidance of excess stimulation all help prevent such episodes. Appropriate social and visual stimulation, however, can improve function by increasing awareness and orientation. For instance, boldly colored tableware aids those with severe AD, helping people overcome a diminished sensitivity to visual contrast to increase food and beverage intake.

 

Dr Smita Pandey Bhat, Clinical Psychologist

Chronic pain was originally defined as pain that has lasted 6 months or longer. It is now defined as pain that persists longer than the normal course of time associated with a particular type of injury. This constant or intermittent pain has often outlived its purpose, as it does not help the body to prevent injury.

Causes

Chronic pain is essentially caused by the bombardment of the central nervous system (CNS) with nociceptive impulses, which causes changes in the neural response. The pain subsequently provokes changes in the behavior of the patient, and the development of fear-avoidance strategies. As a result, the patient may also become physically atrophied and deconditioned. However, it is important to remember that chronic pain is multifactorial, with the underlying biological changes affecting physical and psychosocial factors.

Pain is usually elicited by the activation of specific nociceptors ('nociceptive pain'). However, it may also result from injury to sensory fibres, or from damage to the CNS itself ('neuropathic pain'). Although acute and subchronic, nociceptive pain fulfils a warning role, chronic and/or severe nociceptive and neuropathic pain is maladaptive.

Types

It  discusses chronic pain in two categories: malignant and non-malignant.

• Pain associated with malignancy can be caused by the cancer itself or by treatment.
• Non-malignant pain includes a variety of causes: arthritis, neuropathy/neuralgia, back pain from injury or disorders (cervical stenosis, degenerative disc disease, other disc disorders, etc), migraines and other types of headaches, abdominal pain from chronic pancreatitis, bowel disorders, etc; pelvic pain from various conditions (endometriosis, interstitial cystitis, etc); and also diffuse conditions such as fibromyalgia, reflex sympathetic dystrophy, lupus and other systemic autoimmune/connective tissue conditions, multiple sclerosis and some other neuromuscular conditions.

Chronic pain can occur anywhere in the body; this list includes only a few examples of conditions that can cause chronic pain.

The most common symptoms are a tingling sensation near or around the area where the operation was performed, sharp shooting pains, severe aches after much movement, constant 'low ache' all day and sometimes a general 'weak' feeling.

Contrary to popular belief, all pain is real. This may seem like an obvious statement, but people with chronic pain are sometimes treated as if their chronic pain is either imaginary or exaggerated. In some cases, they feel like they have to prove their chronic pain to their friends, family and doctors. Some patients are told by their doctor that there is no reason for the chronic pain and therefore “it cannot be that bad”.

Chronic pain  is a personal experience and cannot be measured like other problems in medicine, such as a broken leg or an infection. For instance, a broken leg can be confirmed by an X-ray and an infection by a blood test measuring white blood cell count. Unfortunately, there is no medical test to measure chronic pain levels.

To make matters more challenging for the patient, for many chronic pain problems there is no objective evidence or physical findings to explain the pain. Thus, many chronic pain sufferers go from one doctor to the next searching for explanations. This process can lead to unnecessary evaluations and treatments, in addition to putting the patient at risk for actually being harmed or made worse by the healthcare profession.

Everyone experiences and expresses pain differently. Two people with the exact same injury will feel and show their pain in unique ways depending on a number of things such as:

• The situation in which the pain occurs
• Thoughts about the chronic pain, such as “this is nothing serious” versus “this pain could kill me”
• Emotions associated with the chronic pain, such as depression and anxiety versus hopefulness and optimism
• Cultural influences determining whether a person is to be more stoic or more dramatic in showing pain to others

The newest theories of chronic pain can now explain, on a physiological level, how and why people experience pain differently.

( Azad and Zieglagansberger, 2003)

 

 

 

Dr Smita Pandey Bhat, Clinical Psychologist 

 

http://child-psychologist.blogspot.com

Chronic pain was originally defined as pain that has lasted 6 months or longer. It is now defined as pain that persists longer than the normal course of time associated with a particular type of injury. This constant or intermittent pain has often outlived its purpose, as it does not help the body to prevent injury.

Causes

Chronic pain is essentially caused by the bombardment of the central nervous system (CNS) with nociceptive impulses, which causes changes in the neural response. The pain subsequently provokes changes in the behavior of the patient, and the development of fear-avoidance strategies. As a result, the patient may also become physically atrophied and deconditioned. However, it is important to remember that chronic pain is multifactorial, with the underlying biological changes affecting physical and psychosocial factors.

Pain is usually elicited by the activation of specific nociceptors ('nociceptive pain'). However, it may also result from injury to sensory fibres, or from damage to the CNS itself ('neuropathic pain'). Although acute and subchronic, nociceptive pain fulfils a warning role, chronic and/or severe nociceptive and neuropathic pain is maladaptive.

Types

It  discusses chronic pain in two categories: malignant and non-malignant.

• Pain associated with malignancy can be caused by the cancer itself or by treatment.
• Non-malignant pain includes a variety of causes: arthritis, neuropathy/neuralgia, back pain from injury or disorders (cervical stenosis, degenerative disc disease, other disc disorders, etc), migraines and other types of headaches, abdominal pain from chronic pancreatitis, bowel disorders, etc; pelvic pain from various conditions (endometriosis, interstitial cystitis, etc); and also diffuse conditions such as fibromyalgia, reflex sympathetic dystrophy, lupus and other systemic autoimmune/connective tissue conditions, multiple sclerosis and some other neuromuscular conditions.

Chronic pain can occur anywhere in the body; this list includes only a few examples of conditions that can cause chronic pain.

The most common symptoms are a tingling sensation near or around the area where the operation was performed, sharp shooting pains, severe aches after much movement, constant 'low ache' all day and sometimes a general 'weak' feeling.

Contrary to popular belief, all pain is real. This may seem like an obvious statement, but people with chronic pain are sometimes treated as if their chronic pain is either imaginary or exaggerated. In some cases, they feel like they have to prove their chronic pain to their friends, family and doctors. Some patients are told by their doctor that there is no reason for the chronic pain and therefore “it cannot be that bad”.

Chronic pain  is a personal experience and cannot be measured like other problems in medicine, such as a broken leg or an infection. For instance, a broken leg can be confirmed by an X-ray and an infection by a blood test measuring white blood cell count. Unfortunately, there is no medical test to measure chronic pain levels.

To make matters more challenging for the patient, for many chronic pain problems there is no objective evidence or physical findings to explain the pain. Thus, many chronic pain sufferers go from one doctor to the next searching for explanations. This process can lead to unnecessary evaluations and treatments, in addition to putting the patient at risk for actually being harmed or made worse by the healthcare profession.

Everyone experiences and expresses pain differently. Two people with the exact same injury will feel and show their pain in unique ways depending on a number of things such as:

• The situation in which the pain occurs
• Thoughts about the chronic pain, such as “this is nothing serious” versus “this pain could kill me”
• Emotions associated with the chronic pain, such as depression and anxiety versus hopefulness and optimism
• Cultural influences determining whether a person is to be more stoic or more dramatic in showing pain to others

Factors determining how the spinal nerve gates will manage pain

Many factors determine how the spinal nerve gates will manage the pain signal. These factors include the intensity of the pain message, competition from other incoming nerve messages (such as touch, vibration, heat, etc), and signals from the brain telling the spinal cord to increase or decrease the priority of the pain signal. Depending on how the gate processes the signal, the message can be handled in any of the following ways:

• Allowed to pass directly to the brain
• Altered prior to being forwarded to the brain (for instance, influenced by expectations)
• Prevented from reaching the brain (for instance, by hypnosis-induced anesthesia)

Once a pain signal reaches the brain, a number of things can happen. Certain parts of the brain stem (which connects the brain to the spinal cord) can inhibit or muffle incoming pain signals by the production of endorphins, which are morphine-like substances that occur naturally in the human body. Stress, excitement, and vigorous exercise are among the factors that may stimulate the production of endorphins. The impact of endorphins is why athletes may not notice the pain of a fairly serious injury until the “big” game is over. It is also why regular low-impact aerobic exercise (e.g. a riding stationary bike) can be an excellent method to help control chronic back pain.

Pain prevalence and impaired cognition:

Pain prevalence did not differ between the communicative resident with normal cognition (48.7%), mildly impaired cognition (46.5%), or severely impaired cognition (42.9%). However, the latter 2 groups reported more acute pain than those with normal cognition (7.9% to 14.1% vs. 2.5%). Those with impaired cognition reported constant pain more often, reported fewer total sites of pain, and had more frequent and more severe pain. Regardless of cognitive status, 73.3% to 100% of residents had significant scores on depression or anxiety measures when they reported pain-related mood disturbance. Pain-related reduction in activity was associated with a lower Human Activities Profile score. Sixteen of 36 uncommunicative residents had pain on the Pain Assessment in Advanced Dementia and at least 12 of them had significant mood disturbance.  They found that  Cognitive status does not affect pain prevalence; however, it affects the chronicity and characteristics of reported pain. Self-report of pain-related mood involvement is associated with significant mood scores.( Leong and Nuo ,2007)

Older adults with chronic low back pain demonstrated impaired neuropsycholgical performance as compared with pain-free older adults. Further, pain severity was inversely correlated with Neuropsycholgical performance, and Neuropsychological performance mediated the relationship between pain and physical performance ( Weiner et al.,2006).

Conclusion

Chronic pain syndromes are characterized by altered neuronal excitability in the pain matrix. The ability to rapidly acquire and store memory of aversive events is one of the basic principles of nervous systems throughout the animal kingdom. These neuroplastic changes take place e. g. in the spinal cord, in thalamic nuclei and cortical and subcortical (limbic) areas integrating pain threshold, intensity and affective components. Chronic inflammation or injury of peripheral nerves evokes the reorganisation of cortical sensory maps. Neurons conveying nociceptive information are controlled by various sets of inhibitory interneurons. The discharge activity of these interneurons counteracts long-term changes in the pain matrix following nociceptor activation, i. e. it prevents the transition of acute pain signaling to chronic pain states. The  most recent research suggests that pain states may be sensitive to novel families of agents and therapeutic measures not predicted by traditional preclinical pain models as well as human pain states. The endogenous cannabinoid system plays a central role in the extinction of aversive memories. It is proposed  that endocannabinoids facilitate extinction of aversive memories via their selective inhibitory effects on GABAergic networks in the amygdala.

 

 

 

Dr Smita Pandey Bhat, Clinical Psychologist, Gurgaon, Delhi - NCR, INDIA

dr.smitapandey@gmail.com 

 

http://child-psychologist.blogspot.com  

Communicating with someone who has delusions

A delusion is a fixed false belief that can't be swayed by reasoning. Paranoid, grandiose, and religious delusions are most common. A paranoid delusion is very frightening: The person thinks someone is out to harm him. Acknowledge what he says but don't agree. For example, if your patient tells you that the FBI is after him, hone in on his feelings: "Sensing that you're being watched all the time must be very frightening."

Keep your patient's environment as safe as you can. Try to have the same staff assigned to his care each day and prepare him for any changes without providing too many details; for example, "Mr. Jones, we're getting some new patients today so we have to move you to a different room." If he responds negatively, reassure him that he'll be safe and you'll protect him.

Grandiose and religious delusions are typically less frightening. A person having a grandiose delusion, for example, thinks he's someone very powerful or important. Someone with a religious delusion may claim to be a religious figure.

Follow these guidelines to maintain a therapeutic relationship with your patient:

• Accept him as he is. His mental illness is causing his abnormal perceptions.
• Monitor for hallucinations and delusions to assess his response to psychotropic medications.
• Assess his safety and monitor for warning signs such as withdrawal and depression.
• Give him appropriate feedback on how you interpret his communications and try to help him focus on the realities around him.
• Encourage him to learn about his medical illness and help with his care; involve him with diversions such as reading, writing, or solving puzzles. These activities can diminish irrational thinking and help him feel comfortable and safe.

Responding to disorganized speech

Classic verbal disturbances that might occur with schizophrenia include associative looseness, neologisms, clang association, word salad, and echolalia.

Associative looseness means one thought isn't connected to the next. When you tell your patient you've brought his medication, he might reply, "Blue lights and gold. I go round and round. The grass is green." These phrases seem disconnected but could shed light on his thoughts. If you suspect that the colors are significant, ask, "Are you asking what different medications you're getting here?" If you can't make a connection, tell him you don't understand but you'll keep trying.

 

 

Dr Smita Pandey Bhat, Clinical Psychologist, Gurgaon, Delhi - NCR, INDIA

dr.smitapandey@gmail.com 

 

http://child-psychologist.blogspot.com

Cognition is the ability to think, perceive, know and understand the world. In psychology the cognition refers to mental functions, mental processes and states of intelligent entities. The particular focus is on comprehension, inferencing, decision- making, planning and learning. The term cognition is broadly the act of knowing that ends up in thought and action.

 

Introduction of Fibromyalgia:

 

Fibromyalgia is a chronic syndrome characterized by tiredness , pain in muscles, bones, joints and tender points.( Tender points are places  in the neck, shoulders, back, hips , arms and legs that hurt when touched)[2,3]. Fibromyalgia is taken from the Latin words (fibra+ myo+ algos).Fibra means fibre or fibrous tissues, myo means muscles and algos means pain. The term was coined in 1976.[4]It more affects females than males with a ration of 9:1. by ACR (American College of Rheumatology) criteria [5].Fibromyalgia can occur in 3 to 6% of population. The age of  onset is between 20 and 50, though it may occur in childhood as well.

 

Symptoms:

 

The major symptoms of fibromyalgia are  widespread pain, tenderness to light touch, moderate to severe fatigue, heightened sensitivity to skin, tingling sensation achiness in the muscle tissues, prolonged muscle spasms, weakness in the limbs, and nerve pain and also chronic sleep disturbances. Other symptoms include headaches and facial pains,  depression, anxiety, mood changes, dizziness and difficulty concentrating etc.In addition to above symtoms the patients may experience cognitive dysfunctions as well.

 

Causes:

 

The causes of this disease are unknown. There are several theories which state the causes of pain. One such theory is “central sensitization” which states that the people with fibromyalgia have lower threshold of pain because of the increased sensitivity that causes pain. Other theories state that the sleep disturbances, injuries, infections abnormalities of autonomic nervous systems( sympathetic nervous system dysfunction) and changes in muscle metabolism (reduced blood flow to muscles) etc can cause fibromyalgia. Also , psychological stress. and hormonal changes may cause fibromyalgia.The increased psychosocial stress, excessive physical exertion, and lack of slow- wave sleep and changes in humidity and barometric pressure  may exacerbate the symptoms.

 

Risk factors:

 

The risk factors include the female sex , early and middle adulthood, disturbed sleep patterns, family history and rheumatic disease.

 

Treatments:

The drug treatment include analgesics, antidpressants, anti-seizure drug and muscle relaxants. The non drug treatment includes physical exercises, massage treatment , stress management, cognitive behavior therapy and neurofeedback  or biofeedback. Holistic treatment include management of sleep, diet, stress, pain , managing blood sugar levels and  avoiding known triggers etc.

 

Fibromyalgia and Cognition:

 

 The patient may experience cognitive dysfunction ( known as “brain fog” or “fibro fog”) which may be characterized by impaired concentration, unclear thinking and short-term memory consolidation, impaired speed of performance, inability to multi-task, and cognitive overload.Fibro fog is the term descibed by Stuart Donaldson as "decreased ability to concentrate, decreased immediate recall, and an inability to multi-task". Other symptoms include confusion and forget fullness, inability to recall simple words and  transposing words and numbers. Sometimes cognitive functions are so impaired that they get lost in familiar places and they have difficulty in communication. Sometimes they lose their jobs or pediatric patients drop out of school . Also , there is difficulty in finding the right word for the conversation and they have trouble retaining new information.

 

Causes Of Cognitive Dysfunction In Fibromyalgia:

The patients with were studied on CT(SPECT) to visualize their brain. It was found that there was decreased blood flow in the right and left caudate nuclei and thalami.

 

Abnormal levels of neurotransmitters such as substance P, serotonin, dopamine, norepinephrine, and epinephrine may be cause cognitive dysfunction. Neuroendocrine imbalance of the HPA axis may play a role in fibro-fog.

 

The distracting quality of pain may be another possible cause of the cognitive dysfunction. Cognitive performance of patients with fibromyalgia is correlated with their reported level of pain.

 

Researchers are looking at tissue volumes in areas of the brain (hippocampus) that may be damaged by the effects of stress hormones.

The results of a study  by Elvin et al (2006) support the suggestion that muscle ischemia can contribute to pain in FM, possibly by maintaining the central nervous changes such as central sensitisation/disinhibition.[

 

Others studies have implicated yeast overload, water retention, and glial-cell abnormalities as causes of cognitive dysfunction in fibromyalgia.

 

Fibromyalgia, Sleep And Cognition:

 

Cote and Moldofsky (1997) studied 10 female patients with fibromyalgia   and a matched non compalinative comparison group. They spent two nights in the sleep laboratory. The subjects completed self assessment of a computerized battery and performance tests at hourly intervals from 7.0h to 20h.  The results indicated that fibromyalgia patients spent more time on stage 1 sleep. They reported greater sleepiness, more fatigue, more pain, more negative mood, and lower accuracy on performance tasks across a 14 h day. The Fibromyalgia group was slower in speed, but not impaired in accuracy, on performance of complex tasks, i.e., grammatical reasoning, serial addition/subtraction, and a simulated multi-task office procedure.

 

 

Dr Smita Pandey Bhat, Clinical Psychologist

Email: dr.smitapandey@gmail.com 

Url: http://child-psychologist.blogspot.com

Since we all are here to reflect your thoughts with our great creative and scientific bent of mind, I would just like to ask all of us a question: Have you ever heard of a term called "High Functioning Mental Retardation?".

To those  who are not aware of Mental Retardation I would like to explain them that Mental retardation is a developmental disability that is marked by lower-than-normal intelligence and limited daily living skills. Mental retardation is normally present at birth or develops early in life. And usually mental retardation is more or less genetic and by birth but sometimes it develops in early childhood. Certainly, it is different from mental illness. Mentally retarded could be suffering from mental illness at the same time. But Mentally ill are never categorized as mentally retarded because before the period of the illness they were considered to be  “normal” individuals.  Moreover, mental illness could be treated with Drugs (Psychotherapeutic medications), counseling and psychotherapy and the person can reach to its premorbid or previous condition when the individual functioned normally but mentally retarded individuals though  could enhance  its skills with the help of several professionals  but could never have a so called “normal” condition  or functioning.
So it is thought provoking. Just think before making any such diagnoses as it may affect the patient's treatment as well your own career.

With  due regards to your sentiments, I would just like to ask  you a question then why do we then call it "Mental Retardation" , why cannot we discover of  some better term, when you already  that the individual is highly  functional.

I myself have met few  people which are  functioning as "highly  functional  people" like Prof. Ellen Sachs  diagnosed  as "high functioning Schizophrenia " and  the author of her book "The Center  Cannot Hold: My Journey Through Madness" and I  have  seen a  girl from Delhi, who was  highly scholastic and scored  almost 99% marks in her every class till then and very good in her knowledge in writing  but rarely she used  to speak  her feelings to her mother even with whom she had the best comfort level as she had  been diagnosed as "High functioning Autism".

My understanding is that these  people are  called as "High functioning" , because they are mentally ill but  at the same time  they  could  escape the  disabilities in intellectual and cognitive functioning because  many of the people with such kind of illnesses could become somewhat dysfunctional but  few  remain as functional as they  were earlier or even emerge  out to be a much more mentally healthy and highly intellectual and cognitively  functional than they were  earlier because of they are no longer imbalance in their  neuro-chemicals released in the brain.

I know that this would help in prognosis of any plan if the person is highly functional. But I  would like express my views  in the following manner:

The child I have seen the diagnoses  as "High functioning MR", (after which I raised  this issue)  has been changed the diagnosis at other  places  as well and all other mental  professionals negated the diagnoses of "Mental Retardation" itself, except the first diagnoses  which was made at this prestigious institute. (I would not like to name the  institute  at any cost as being one of the very good institutes of Mental  Health in  India, that may create a bias amongst the  professionals and my  debate is not against any institution  it is just against the "term", which has been discovered recently,  but I certainly could not  see any logical explanation in its favor  and nor any such research articles). Happening to be somebody related to me somehow he tried to clarify his doubts about the diagnoses. Also, it is sad that after  that he changed the name of his son because after confirmations of several other highly qualified professionals he could not digest the "term Mentally Retarded". I raised this issue because when his parents tried to get admission in some good school and being honest  they went with all his medical reports from that institute, he was denied admission  in that particular school and asked to take him to a school which  is meant for mentally retarded. Later he went to another school with a changed name and he is excelling in  studies has a very good inquisitiveness for mobile and computer technology. You can't imagine he could do  things himself  which I  and you can't even imagine at merely 8 years of  age. He  could play very high intellectual games  like "Soduku" and more over he is so inquisitive that he  would even ask you the highly philosophical but logical and intelligent questions "like what are the parts used in laptop", "how it has been developed"  and "how the internet connectivity functions”-seeing my husband  working on  the laptop. These questions  are  very normal for today's kids , but this raised a kind of alarm  in me about the particular  diagnoses and so  I raised  that question.  Now, my question to all the professional is that Should anyone still call the individual as Mentally Retarded?"

But at the same time I would  say that I am against  calling any person as "Mentally Retarded", when  we all know that individual is highly functional.
You and me as mental health professionals could understand the  meaning of diagnoses as being trained in those  professions but what about those people who are not at all informed about the  diagnoses  we make or very little informed.  I know we need to educate the masses also but at the same time we need to be having more  "social friendly" terms while making such kind of diagnoses.

I am happy that some people are passionate enough and have urge to help such kind of individuals by what they call as diluting the diagnoses but actually  we did not help this individual and this is an example, that before , many  more people like the individual stated above would be denied from mainstream education for the simple reason as stated above,  we need to correct ourselves

 

Dr Smita Pandey Bhat Clinical Psychologist

Email: dr.smitapandey@gmail.com 

 

Url :http://child-psychologist.blogspot.com  

Hallucinations, sensory experiences that occur without external stimuli. Hallucinations might  be  present in several mental  and neurological  disorders. Most common are auditory hallucinations-hearing voices or sounds that no one else hears. A visual hallucination is seeing someone or something that isn't there. Other hallucinations relate to touch (tactile), taste (gustatory), and smell (olfactory), but these are less common.

Hallucinations are usually unpleasant for the patient. Although he/she may not mention them, he/she may huddle under the covers, appear to be listening to someone, or talk to someone who isn't there. Confront such behavior: "Mr. Jones, you appear to be talking to somebody, but I don't see anyone."

The patient's reply might surprise you. Mr. Jones may tell you he's listening to the devil. Remain non-judgmental, empathize, and point out what's real: "I don't see anyone in the room, but this must be very frightening for you." Listen quietly to his response and try to make a connection. "You talk about devils, death, and hell. It sounds as though you're afraid of what might happen in the afterlife." He may be grateful that you're trying to understand.

A terrifying hallucination that can endanger you, your patient, and others is a command hallucination, which is usually auditory. If the patient reports, for example, that God is telling him to jump out the window, don't leave him. Summon help; he may need confinement for protection.

Dr Smita Pandey Bhat, Clinical Psychologist

Email  :  dr.smitapandey@gmail.com 

Url  : http://child-psychologist.blogspot.com  

 

 

INSOMNIA, CAUSES AND TREATMENT

 

WHAT IS INSOMNIA?

Insomnia is a condition in which there is the problem in initiation, and maintenance of sleep. Also, the duration of sleep may be reduced or the quality of sleep is hampered such that one has a disturbed sleep. Other consequences include the disturbances of mood, fatigue, problems in interpersonal relationships, occupational difficulties and reduced quality of life.

 

TYPES OF INSOMNIA

 

Transient insomnia occurs for less than a week, short term insomnia lasts for about one to four weeks and Chronic insomnia lasts for about a month.

 

Chronic insomnia occurs in about 10 -15% of the population. It occurs more frequently  in women, people with old age and patients with chronic mental and psychological disorders.

 

CAUSES OF INSOMNIA:

 

 Insomnia is primary or secondary. Primary insomnia is the one which might have been from childhood and may be due to heightened arousal during sleep. Sometimes the insomnia is paradoxical because there is a misperception of the state of sleep, such that the findings suggest that the person is sleeping but the person feels that he/she was not

 

Secondary insomnia occurs when there are psychosocial stressors causing adjustment problems, with inadequate sleep hygiene, or due to psychiatric disorders (depression, anxiety etc.) or due to medical problems or due to drug or substance abuse.

 

PSYCHOLOGICAL TREATMENT:

 

The technique to treat insomnia without medication includes a group of Cognitive Behavioral Techniques. These are described below:

 

1. STIMULUS CONTROL THERAPY:

 

          It assumes that insomnia is a maladaptive response to factors such as bedtime and bedroom environment. It includes the following points:

• Go to bed only when you are sleepy
• Use the bedroom only for sleep and sex.
• Go to another room when unable to sleep for 15-20 minutes.
• Then read or engage yourself in quiet activities and return to bed only when you are sleepy. Repeat the process if required.
• Have the regular wake time regardless of the duration of sleep.
• Avoid daytime napping.

 

2. SLEEP RESTRICTION THERAPY:

 

It assumes people can improve their sleep by temporary sleep deprivation through voluntarily reducing their time in bed.

Reduce time in bed to estimated total sleep (minimum by 5 hours).

Increase time in bed by 15 minutes every week, when estimated sleep efficiency (the ratio of time in bed) is at least 90%.

 

3. RELAXATION THERAPIES:

 

• It is based on the hypothesis that insomnia is associated with hyper arousal.
• It involves progressive muscular relaxation and biofeedback.
• It also involves mental imagery, meditation and hypnosis.

 

4. COGNITIVE THERAPIES:

 

It deals with the cognitive component of the therapy such that it involves educating the client about the sleep needs, the correction of unrealistic expectations and a discussion of anxiety and catastrophic thinking e.g. exaggerating oneself the poor consequences of sleep.

 

• Education to change the attitudes and belief about sleep
• Education to remove the catastrophic thinking
• Education to eliminate unrealistic expectations
• Changing the thinking style such that the person tries to get rid of mental worries.

 

5. SLEEP HYGIENE:

 

 It addressees the extrinsic factors like the noise in the room where one sleeps or the intake of caffeine etc.

 

• Correct the environmental disruptions such as noise or snoring partner.
• Keep the bedroom temperature comfortable
• Remove the bedside clock
• Do not use Alcohol, nicotine or caffeine few hours 4-6 hours before the bedtime
• Avoid the spicy, heavy or sugary food before the bedtime
• Do some exercises  but not before  2 hours of going to sleep

 

 With the above techniques, about 50% of patients show improvement.

 

 

Dr Smita Pandey Bhat, Clinical Psychologist 

 dr.smitapandey@gmail.com 

 

 http://child-psychologist.blogspot.com

 

 

 

 

 

Parkinson’s Definition:

Parkinson's disease is a degenerative disorder of the central nervous system that often impairs the sufferer's motor skills and speech.

Parkinson's disease belongs to a group of conditions called movement disorders. It is characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia) and, in extreme cases, a loss of physical movement (akinesia). The primary symptoms are the results of decreased stimulation of the motor cortex by the basal ganglia, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Secondary symptoms may include high level cognitive dysfunction and subtle language problems. PD is both chronic and progressive.

Symptoms

Motor symptoms

The cardinal symptoms are:

• tremor: normally 4-7 Hz tremor, maximal when the limb is at rest, and decreased with voluntary movement. It is typically unilateral at onset. This is the most apparent and well-known symptom, though an estimated 30% of patients have little perceptible tremor; these are classified as akinetic-rigid.
• Rigidity: stiffness; increased muscle tone. In combination with a resting tremor, this produces a ratchety, "cogwheel" rigidity when the limb is passively moved.
• bradykinesia/akinesia: respectively, slowness or absence of movement. Rapid, repetitive movements produce a dysrhythmic and decremental loss of amplitude. Also "dysdiadokinesia", which is the loss of ability to perform rapid alternating movements
• postural instability: failure of postural reflexes, which leads to impaired balance and falls.
• Gait and posture disturbances:
  • Shuffling: gait is characterized by short steps, with feet barely leaving the ground, producing an audible shuffling noise. Small obstacles tend to trip the patient
  • Decreased arm swing: a form of bradykinesia
  • Turning "en bloc": rather than the usual twisting of the neck and trunk and pivoting on the toes, PD patients keep their neck and trunk rigid, requiring multiple small steps to accomplish a turn.
  • Stooped, forward-flexed posture. In severe forms, the head and upper shoulders may be bent at a right angle relative to the trunk.
  • Festination: a combination of stooped posture, imbalance, and short steps. It leads to a gait that gets progressively faster and faster, often ending in a fall.
  • Gait freezing: "freezing" is another word for akinesia, the inability to move. Gait freezing is characterized by inability to move the feet, especially in tight, cluttered spaces or when initiating gait.
  • Dystonia (in about 20% of cases): abnormal, sustained, painful twisting muscle contractions, usually affecting the foot and ankle, characterized by toe flexion and foot inversion, interfering with gait. However, dystonia can be quite generalized, involving a majority of skeletal muscles; such episodes are acutely painful and completely disabling.
• Speech and swallowing disturbances
  • Hypophonia: soft speech. Speech quality tends to be soft, hoarse, and monotonous. Some people with Parkinson's disease claim that their tongue is "heavy".
  • Festinating speech: excessively rapid, soft, poorly-intelligible speech.
  • Drooling: most likely caused by a weak, infrequent swallow and stooped posture.
  • Non-motor causes of speech/language disturbance in both expressive and receptive language: these include decreased verbal fluency and cognitive disturbance especially related to comprehension of emotional content of speech and of facial expression
  • Dysphagia: impaired ability to swallow. Can lead to aspiration, pneumonia.
• Other motor symptoms:
  • fatigue (up to 50% of cases);
  • masked faces (a mask-like face also known as hypomimia), with infrequent blinking;
  • difficulty rolling in bed or rising from a seated position;
  • micrographia (small, cramped handwriting);
  • impaired fine motor dexterity and motor coordination;
  • impaired gross motor coordination;
  • Poverty of movement: overall loss of accessory movements, such as decreased arm swing when walking, as well as spontaneous movement.

Non-motor symptoms

Cognitive disturbances

• slowed reaction time; both voluntary and involuntary motor responses are significantly slowed.
• Executive dysfunction, characterized by difficulties in: differential allocation of attention, impulse control, set shifting, prioritizing, evaluating the salience of ambient data, interpreting social cues, and subjective time awareness. This complex is present to some degree in most Parkinson's patients; it may progress to:
• dementia: a later development in approximately 20-40% of all patients, typically starting with slowing of thought and progressing to difficulties with abstract thought, memory, and behavioral regulation. Hallucinations, delusions and paranoia may develop.
• short term memory loss; procedural memory is more impaired than declarative memory. Prompting elicits improved recall.
• medication effects: some of the above cognitive disturbances are improved by dopaminergic medications, while others are actually worsened.

Sleep disturbances

• Excessive daytime somnolence
• Initial, intermediate, and terminal insomnia
• Disturbances in REM sleep: disturbingly vivid dreams, and REM Sleep Disorder, characterized by acting out of dream content - can occur years prior to diagnosis

Sensation disturbances

• impaired visual contrast sensitivity, spatial reasoning, colour discrimination, convergence insufficiency (characterized by double vision) and oculomotor control
• dizziness and fainting; usually attributable orthostatic hypotension, a failure of the autonomous nervous system to adjust blood pressure in response to changes in body position
• impaired proprioception (the awareness of bodily position in three-dimensional space)
• reduction or loss of sense of smell (microsmia or anosmia) - can occur years prior to diagnosis,
• pain: neuropathic, muscle, joints, and tendons, attributable to tension, dystonia, rigidity, joint stiffness, and injuries associated with attempts at accommodation

Autonomic disturbances

• oily skin and seborrheic dermatitis
• urinary incontinence, typically in later disease progression
• nocturia (getting up in the night to pass urine) - up to 60% of cases
• constipation and gastric dysmotility that is severe enough to endanger comfort and even health
• altered sexual function: characterized by profound impairment of sexual arousal, behavior, orgasm, and drive is found in mid and late Parkinson disease. Current data addresses male sexual function almost exclusively
• weight loss, which is significant over a period of ten years - 8% of body weight lost compared with 1% in a control group

 

 

 

 

 

Dr Smita Pandey Bhat, Clinical Psychologist

 dr.smitapandey@gmail.com 

 http://child-psychologist.blogspot.com