Schizophrenia

HISTORY AND FACTS 

n  Emil Kraepelin: First to differentiate schizophrenia (then, dementia praecox) from manic-depressive psychosis

n  Dementia: progressive deterioration

n  Praecox: “early harvest” to denote early onset

n  Eugene Bleuler: Changed name to schizophrenia to denote splitting of personality’s functions

n  NOT “split personality”

n  Pervasive impairment in a full range of functions, i.e., thoughts, feelings, perception and behavior

n  Medicated vs unmedicated patient may well give the impression of two different people

n  Worldwide prevalence rate of 1%

n  In the 80s, 50% of psychiatric hospital beds were occupied by persons with schizophrenic disorders (closer to 33% today)

n  About 1 in 3 of the homeless have a schizophrenic disorder

n  3% of the prison population; 6% of maximum security prisoners

n  1 in 4 attempt suicide, 1 in 10 are eventually successful

n  Equal gender distribution, but this is complex… early onset in males, better prognosis for females

n  Generally onset in males, 20-25, females 25-30

n  Females show another peek after age 45

n  Course is more severe for males and for females with late onset

n  Seen in all SES groups but more common in lower SES… this relationship is complex

n  Chicken-Egg problem

n  Kraepelin and Bleuler thought they were secondary, but today, hallucinations and/or delusions are recognized as primary symptoms and at the core of the diagnosis

n  Other characterizations: acute vs chronic, good premorbid vs bad premorbid, excesses vs deficits, positive vs negative symptoms

n  Importantly: Persons with schizophrenic disorders are often mischaracterized as dangerous because of Hollywood portrayals… truth is just the opposite

n  The core symptoms of schizophrenia are at the basis of what we call psychosis or psychotic, i.e., delusions and hallucinations (positive symptoms)

n  Delusion: a false belief, a misrepresentation of reality… some are bizarre, some are not

n  Hallucination: a sensory experience without any input from the surrounding environment

n  Almost always auditory in schizophrenia

n  Note depiction in “Beautiful Mind”

DIAGNOSTIC CRITERIA

n   Two or more of the following:

n  Delusions

n  Hallucinations

n  Disorganized speech

n  Grossly disorganized or catatonic behavior

n  Negative symptoms

n  Flat affect

n  Alogia or Avolition

n  Anhedonia

n  Major impairment in functioning

n  Persistent symptoms for six months with one month of primary symptoms (May include prodromal or residual phase of the illness)

n  Rule out schizoaffective disorder or mood disorder

n  Rule out effects of psychoactive substance use

n  Rule out medical or neurological condition

n  Rule in or out co-existing pervasive developmental disorder (autism, Asperger’s, etc.)

Subtypes of schizophrenia

n  Paranoid

n  Disorganized

n  Catatonic

n  Undifferentiated

n  Residual

n  Other Psychotic Disorder

Positive vs. Negative Distinctions

n  Positive (Type I)

n  Presence of positive (identifiable) symptoms

n  Good response to medication

n  Optimistic prognosis

n  Absence of intellectual impairment

n  Negative (Type II)

n  Presence of negative symptoms (absence of behaviors)

n  Poor response to medication

n  Pessimistic prognosis

n  Intellectual impairments obvious

Etiology of Schizophrenia

n  Evidence is clear that stress can precipitate the first appearance of schizophrenia and can precipitate a relapse during residual or recovery phase, but genetic vulnerability usually present

n  No support over the years for “schizophrenogenic mother” as cause (double bind, mixed messages, ambivalence)

n  Note research on “Expressed Emotions” in families, a kind of “generic henpecking”

 

Treatment for schizophrenia

n  Appearance of Chlorpromazine (Thorazine, Stelazine) in the 1950s helped empty hospitals

n  These are the neuroleptics, dopamine antagonists

n  Not all pts respond, and side effects can be devastating and irreversible (e.g., tardive dyskinesia)

n  New drugs (atypical antipsychotics) in the 1990s came from benzodiazapine family (clozapine and olanzapine) and helped many who were unresponsive to conventional antipsychotics, not without their side effects (agranulocytosis)

n  Rip Van Winkle phenomenon

n  Freud never advocated psychoanalysis for schizophrenia; when tried, usually failure

n  Despite dramatic tx effects in some, the outcome of psychopharmacological approaches to schizophrenia is still only marginally effective (around 50%)

n  Supportive psychotherapy may help sustaining adjustment but medication will always be necessary for persons with schizophrenia

n  Interesting findings from behavior modification; note work of Teodoro Ayllon and Nathan Azrin on Token Economy

Depression

People can become depressed through different routes, including genetics, traumatic experiences, hormonal problems, substance abuse, head injuries, brain tumors, and other illnesses. People with major depression feel sad and helpless every day for weeks at a time. They have little energy, fell worthless, contemplate suicide, have trouble sleeping, cannot concentrate, find little pleasure, and can hardly even imagine being happy again. Standards for diagnosis inevitably vary from place to place, and psychiatrists have no laboratory tests to confirm diagnosis. Defined by the presence and recurrent episodes of either depressed mood (Depression, Depressive Episode) or manic mood (Mania, Manic Episode). These are disturbances of mood more than thought, distinguishing them from “thought disorder” (most notably, schizophrenia)

This distinction is emphasis rather than exclusivity. Mood disorders are accompanied by thought disturbances. Thought disorders are accompanied by mood disturbances, defined by the presence, duration, and severity of either:

Depressive (Mood) Episodes

Manic (Mood) Episodes

Or Both

Episodes are clearly defined. Episodes define the Mood Disorder

Depressive Episode

Must be either Depressed Mood or Anhedonia, and five or more of…

Appetite/weight disturbance

Sleep disturbance

Psychomotor retardation/agitation

Fatigue or loss of energy

Feelings of worthlessness or guilt

Difficulties in concentration or indecisiveness

Recurrent thoughts of death or suicide

R/O effects of drugs or general medical condition

Importantly, R/O Bereavement

1/3 of bereaving continue to grieve one month later

2 months of grief is the beginning of a red flag

<20% continue to grieve one year later

Concern also when grief is extremely severe, has psychotic features, or includes suicidal ideation

Remember that vulnerability may last two years

Symptoms cause clinically significant distress

Sleep Disorders

Nightmares, night terrors, sleepwalking, sleep talking, head banging, wetting the bed and grinding your teeth are kinds of sleep problems called parasomnias. There are treatments for most sleep disorders. Sometimes just having regular sleep habits can help.

Insomnia (in-SOM-ne-ah) is a common sleep disorder. People who have insomnia have trouble falling asleep, staying asleep, or both. As a result, they may get too little sleep or have poor-quality sleep. They may not feel refreshed when they wake up.

Insomnia can cause daytime sleepiness and a lack of energy. It also can make you feel anxious, depressed, or irritable. You may have trouble focusing on tasks, paying attention, learning, and remembering. These problems can prevent you from doing your best at work or school.

Insomnia also can cause other serious problems. For example, you may feel drowsy while driving, which could lead to an accident.

One type of insomnia is sleep apnea, impaired ability to sleep breathe while sleeping. People with sleep apnea have breathless periods of a minute or so from which they awaken gasping for breath. Sleep apnea results from several causes, including genetics, hormones, and old-age deterioration of the brain mechanisms that regulate breathing. Another cause is obesity, especially in middle-aged men. 

Narcolepsy is a sleep disorder that causes excessive sleepiness and frequent daytime sleep attacks. Narcolepsy is a nervous system disorder. The exact cause is unknown. In some patients, narcolepsy is linked to reduced amounts of a protein called hypocretin, which is made in the brain. What causes the brain to produce less of this protein is unclear. There is a possibility that narcolepsy is an autoimmune disorder. An autoimmune disorder is when the body's immune system mistakenly attacks healthy tissue. Narcolepsy tends to run in families. Certain genes are linked to narcolepsy. Narcolepsy has four main symptoms; (1) gradual or sudden attacks of sleepiness during the day, (2) occasional cataplexy, (3) sleep paralysis, and (4) hypnagogic hallucinations. 

Currently, the most common treatment for Narcolepsy is stimulant drugs, such as methylphenidate (Ritalin), which enhance dopamine and norepinephrine activity. 

Another sleep disorder is periodic limb movement disorder, characterized by repeated involuntary movement of the legs and sometimes arms. Frequent or especially vigorous leg movements may awaken the person or his/her partner. In some cases, tranquilizers help suppress the movements. 

A night terror is a sleep disruption that seems similar to a nightmare, but with a far more dramatic presentation. Though night terrors can be alarming for parents who witness them, they're not usually cause for concern or a sign of a deeper medical issue. During a typical night, sleep occurs in several stages. Each is associated with particular brain activity, and it's during the rapid eye movement (REM) stage that most dreaming occurs. Night terrors happen during deep non-REM sleep. Unlike nightmares (which occur during REM sleep), a night terror is not technically a dream, but more like a sudden reaction of fear that happens during the transition from one sleep phase to another.

During a night terror, a child might suddenly sit upright in bed and shout out or scream in distress. The child's breathing and heartbeat might be faster, he or she might sweat, thrash around, and act upset and scared. After a few minutes, or sometimes longer, a child simply calms down and returns to sleep.

Here are some steps recommended by the Mayo Clinic in order to sleep better 

No. 1: Stick to a sleep schedule

Go to bed and get up at the same time every day, even on weekends, holidays and days off. Being consistent reinforces your body's sleep-wake cycle and helps promote better sleep at night. There's a caveat, though. If you don't fall asleep within about 15 minutes, get up and do something relaxing. Go back to bed when you're tired. If you agonize over falling asleep, you might find it even tougher to nod off.

No. 2: Pay attention to what you eat and drink

Don't go to bed either hungry or stuffed. Your discomfort might keep you up. Also limit how much you drink before bed, to prevent disruptive middle-of-the-night trips to the toilet.

Nicotine, caffeine and alcohol deserve caution, too. The stimulating effects of nicotine and caffeine — which take hours to wear off — can wreak havoc with quality sleep. And even though alcohol might make you feel sleepy at first, it can disrupt sleep later in the night.

No. 3: Create a bedtime ritual

Do the same things each night to tell your body it's time to wind down. This might include taking a warm bath or shower, reading a book, or listening to soothing music — preferably with the lights dimmed. Relaxing activities can promote better sleep by easing the transition between wakefulness and drowsiness.

Be wary of using the TV or other electronic devices as part of your bedtime ritual. Some research suggests that screen time or other media use before bedtime interferes with sleep.

No. 4: Get comfortable

Create a room that's ideal for sleeping. Often, this means cool, dark and quiet. Consider using room-darkening shades, earplugs, a fan or other devices to create an environment that suits your needs.

Your mattress and pillow can contribute to better sleep, too. Since the features of good bedding are subjective, choose what feels most comfortable to you. If you share your bed, make sure there's enough room for two. If you have children or pets, set limits on how often they sleep with you — or insist on separate sleeping quarters.

No. 5: Limit daytime naps

Long daytime naps can interfere with nighttime sleep — especially if you're struggling with insomnia or poor sleep quality at night. If you choose to nap during the day, limit yourself to about 10 to 30 minutes and make it during the mid-afternoon.

If you work nights, you'll need to make an exception to the rules about daytime sleeping. In this case, keep your window coverings closed so that sunlight — which adjusts your internal clock — doesn't interrupt your daytime sleep.

No. 6: Include physical activity in your daily routine

Regular physical activity can promote better sleep, helping you to fall asleep faster and to enjoy deeper sleep. Timing is important, though. If you exercise too close to bedtime, you might be too energized to fall asleep. If this seems to be an issue for you, exercise earlier in the day.

No. 7: Manage stress

When you have too much to do — and too much to think about — your sleep is likely to suffer. To help restore peace to your life, consider healthy ways to manage stress. Start with the basics, such as getting organized, setting priorities and delegating tasks. Give yourself permission to take a break when you need one. Share a good laugh with an old friend. Before bed, jot down what's on your mind and then set it aside for tomorrow.

Know when to contact your doctor

Social Pain

Social pain is the experience of pain as a result of interpersonal rejection or loss, such as rejection from a social group, bullying, or the loss of a loved one. Research now shows that social pain results from the activation of certain components in physical pain systems. Although social, clinical, health, and developmental psychologists have each explored aspects of social pain, recent work from the neurosciences provides a coherent, unifying framework for integrative research.

Most doctors don’t recommend Tylenol for a broken heart or a supportive friend for a headache. But an article published by Janet Taylor Spence Award recipient Naomi I. Eisenberger in the February 2012 edition of Current Directions in Psychological Science shows there is a growing body of evidence that social pain shares some of the neural circuitry that underlies physical pain.

Eisenberg explains that physical pain has two components — sensory and affective — each of which is associated with different parts of the brain. Psychological scientists who study social pain have shown that the dorsal anterior cingulated cortex (dACC) and anterior insula, which are crucial to the affective or unpleasant component of pain, are also involved in the experience of social pain. One recent study even indicated that separate regions of the brain associated with the sensory experience of pain were also activated when participants were asked to remember a difficult breakup.

Other studies have suggested that these overlaps in brain activity can affect how people experience social or physical pain. For example, when Eisenberg and her colleagues asked female study participants to rate the pain caused by heat stimuli, the women reported less pain when they were looking at pictures of their romantic partners or holding their romantic partners’ hands. In another experiment, Eisenberg’s team asked participants to take a pill daily and self-report their “hurt feeling” every evening for three weeks. Participants who took acetaminophen (aka Tylenol) daily experienced a decrease in hurt feelings that was not duplicated in the control group, which received a placebo.

There may be an evolutionary explanation for the painful sting of social rejection. Just like physical pain teaches us to avoid dangerous situations, Eisenberg suggests that “over the course of evolutionary history, social pain may have helped us to avoid social rejection, increasing our connections with others, our inclusion in the social group, and ultimately our chances of survival.”

In conclusion, they say, accumulating evidence is revealing that physical and social pain are similar in experience, function, and underlying neural structure. Continuing to explore the commonalities between physical and social pain may provide us with new ways of treating physical pain and new techniques for managing social pain. Having a better understanding of the physical-social pain overlap may help to grant social pain the same status that physical pain has achieved in the medical and clinical communities, as evidenced by the amount of time and attention dedicated to its treatment and prevention.

Alzheimer's Disease

Alzheimer's Disease

Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, or neurons, resulting in loss of memory, thinking and language skills, and behavioral changes. 


           

These neurons, which produce the brain chemical, or neurotransmitter,

acetylcholine, break connections with other nerve cells and ultimately die.

For example, short-term memory fails when Alzheimer's disease first

destroys nerve cells in the hippocampus, and language skills and judgment

decline when neurons die in the cerebral cortex. 


           

Two types of abnormal lesions clog the brains of individuals with 

Alzheimer's disease: Beta-amyloid plaques—sticky clumps of protein fragments and cellular material that form outside and around neurons; and neurofibrillary tangles—insoluble twisted fibers composed largely of the protein tau that build up inside nerve cells. Although these structures are hallmarks of the disease, scientists are unclear whether they cause it or a byproduct of it. 


           

Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older. Alzheimer's disease is not a normal part of aging. 


           

Origin of the term Alzheimer's disease dates back to 1906 when Dr. Alois Alzheimer, a German physician, presented a case history before a medical meeting of a 51-year-old woman who suffered from a rare brain disorder. A brain autopsy identified the plaques and tangles that today characterize Alzheimer's disease. Her symptoms included memory loss, language problems, and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary tangles).

Plaques and tangles in the brain are two of the main features of Alzheimer’s disease. The third is the loss of connections between nerve cells (neurons) in the brain.

Although we still don’t know how the Alzheimer’s disease process begins, it seems likely that damage to the brain starts a decade or more before problems become evident. During the preclinical stage of Alzheimer’s disease, people are free of symptoms but toxic changes are taking place in the brain. Abnormal deposits of proteins form amyloid plaques and tau tangles throughout the brain, and once-healthy neurons begin to work less efficiently.

Over time, neurons lose their ability to function and communicate with each other, and eventually they die. Before long, the damage spreads to a nearby structure in the brain called the hippocampus, which is essential in forming memories. As more neurons die, affected brain regions begin to shrink. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly.

Scientists don’t yet fully understand what causes Alzheimer’s disease, but it has become increasingly clear that it develops because of a complex series of events that take place in the brain over a long period of time. It is likely that the causes include some mix of genetic, environmental, and lifestyle factors. Because people differ in their genetic make-up and lifestyle, the importance of any one of these factors in increasing or decreasing the risk of developing Alzheimer’s may differ from person to person.

Most people with Alzheimer’s disease have “late-onset” Alzheimer’s, which usually develops after age 60. Many studies have linked the apolipoprotein E (APOE) gene to late-onset Alzheimer’s. This gene has several forms. One of them, APOE ε4, seems to increase a person’s risk of getting the disease. However, carrying the APOE ε4 form of the gene does not necessarily mean that a person will develop Alzheimer’s disease, and people carrying no APOE ε4 can also develop the disease.

Research suggests that a host of factors beyond basic genetics may play a role in the development and course of Alzheimer’s disease. There is a great deal of interest, for example, in associations between cognitive decline and vascular and metabolic conditions such as heart disease, stroke, high blood pressure, diabetes, and obesity. Understanding these relationships and testing them in clinical trials will help us understand whether reducing risk factors for these conditions may help with Alzheimer’s as well.

Further, a nutritious diet, physical activity, social engagement, and mentally stimulating pursuits can all help people stay healthy as they age. New research suggests the possibility that these and other factors also might help to reduce the risk of cognitive decline and Alzheimer’s disease.