MENTAL DISORDERS (see also diseases of the central nervous system) Table of contents : Show
Epidemiology : a national survey of US citizens has found that 6% of them have a debilitating mental illness. More startling, almost 50% of those surveyed were found to have had a mental disorder at some point during their lives; > 25% had had 1 in the year before the interview. Treatment is hard to get, and often not sufficient when available. Only about 33% of those in care receive "minimally adequate treatment", such as the appropriate drugs or a few hours of therapy
over a period of several monthsref1, ref2, ref3,
ref4. The statistics are nearly impossible to compare with previous studies, thanks to constantly changing definitions of mental illness, but in general things don't seem to have changed much over the past decade. > 9,000 US adults, chosen randomly, were visited in their homes as part of the
National Comorbidity Survey, which looks at the incidence of multiple mental disorders. An interview then probed to see whether they had mental difficulties as determined by the latest Diagnostic and Statistical Manual of Mental Disorders. The study also classified the severity of disorders, separating them into severe, moderate or mild conditions. The definition of disorders used by the study was quite broad. A few
instances of road rage, for example, might qualify as an intermittent explosive disorder. Such a wide net may not be any use in determining who needs medication or treatment, but the survey does provide some useful information. It reveals, for example, that 50% of those with a mental disorder encountered problems before their 14th birthday. This indicates that
watching for signs of mental distress in early years could help to avert larger problems in the future. Progress will be made in finding biological markers that can help distinguish children who are simply shy or have a quick temper from those whose difficulties are likely to degenerate into illness, perhaps through an analysis of genes or brain scans. Meanwhile, the first order of business is to improve the quality of treatment. The prevalence of mental disorders did not change during the
decade (29.4% between 1990 and 1992 and 30.5% between 2001 and 2003), but the rate of treatment increased. Among patients with a disorder, 20.3% received treatment between 1990 and 1992 and 32.9% received treatment between 2001 and 2003. Overall, 12.2% of the population 18 to 54 years of age received treatment for emotional disorders between 1990 and 1992 and 20.1% between 2001 and 2003. Only about half those who received treatment had disorders that met diagnostic criteria for a mental
disorder. Significant increases in the rate of treatment (49.0% between 1990 and 1992 and 49.9% between 2001 and 2003) were limited to the sectors of general medical services (2.59 times as high in 2001 to 2003 as in 1990 to 1992), psychiatry services (2.17 times as high), and other mental health services (1.59 times as high) and were independent of the severity of the disorder and of the sociodemographic characteristics of the respondents. Despite an increase in the rate of treatment, most
patients with a mental disorder did not receive treatment. Continued efforts are needed to obtain data on the effectiveness of treatment in order to increase the use of effective treatmentsref.
An inability to process language needn't stop you from doing maths : 3 men with severe aphasia, a linguistic impairment, can understand 'grammatical' rules in mathematics even though they cannot handle analogous rules in language. Aphasia leaves people unable to use or comprehend words, and is often triggered by stroke or other brain injuries. The discovery challenges a commonly held view that linguistic and mathematical mental processing draw on the same cognitive resources. According to the view of cognition developed by linguist Noam Chomsky, language processing is a fundamental skill that is used for related grammatical tasks in the brain, such as certain mathematical ones. Previous studies of the relationship between linguistic and mathematical ability have lent some support to this notion. For example, brain-imaging studies have shown that some areas of the brain involved in language processing also become active when people are performing mathematical tasks. But it has been unclear whether this use of neural language centres is essential for maths: there are also indications that the two mental functions can work independently. All 3 of their patients were aged between 50 and 60 and were well educated; one had been a university professor before incurring a brain lesion. The 3 men were almost entirely unable to communicate verbally or in writing, but they clearly retained much of their higher mental functioning and could communicate, for example, through "highly expressive" drawings. Their impairments left them unable to decode the grammatical relationships of simple sentences. For example, they had great difficulty distinguishing subject and object in the phrase "The boy chased the girl," which they were unable to differentiate from "The girl chased the boy." Analogous object-relation problems are posed by mathematical expressions such as 90 ÷ 30 and 30 ÷ 90. More complex expressions might involve problems of nesting, such as the use of brackets (90 - [(3 + 17) x 3]), which mirror linguistic sub-clauses and embedded relations, such as in the phrase "The man who killed the lion was angry." Although the patients were unable to decode such linguistic expressions, they were all able to perform the mathematical calculations accurately with pen and paper. They could interpret Arabic numerals correctly even though they struggled to understand number words such as 'three' or 'ninety', when spoken or written. It might be possible to use this capacity for mathematical grammar to help the patients find a way to interpret speech and the written word. Therapy : there are no controlled clinical trials investigating the therapeutic options for LKS. Only open-label data are available. Early diagnosis and initiation of prompt medical treatment appear to be important to achieving better long-term prognosis. Several antiepileptic drugs have been reported to be beneficial in treating this syndrome. These include valproic acid, diazepam, ethosuximide, clobazam, and clonazepam. Reports on the efficacy of lamotrigine, sultiame, felbamate, nicardipine, vigabatrin, levetiracetam, vagal nerve stimulation, and a ketogenic diet are few and more experience is needed. Carbamazepine and possibly phenobarbital and phenytoin have been reported to occasionally exacerbate the syndrome. As initial therapy, valproic acid or diazepam is often empirically chosen. Subsequently, other antiepileptic drugs, corticosteroids, or IVIG therapy are often used. GR agonists therapy should probably not be delayed > 1-2 months after the initial diagnosis. Various corticosteroid regimens including oral prednisone and, recently, high doses of intravenous pulse corticosteroids, as well as ACTH have been reported to be effective in LKS. Oral corticosteroids are used more often and usually need to be maintained for a long period of time to prevent relapses. The use of IVIG has been associated with an initial dramatic response in only a few patients. In our experience, a long-term worthwhile improvement has been noted in only 2 of 11 patients. These two patients had an immediate response to IVIG initially and after relapses before eventually achieving a long-term sustained remission.Surgical treatment by multiple subpial transection, which is reserved for patients who have not responded to multiple medical therapies, has been followed in selected cases by a marked improvement in language skills and behavior. However, a widely accepted consensus about suitable candidates for this surgery and about its efficacy is still lacking. Speech therapy, including sign language, and a number of classroom and behavioral interventions are helpful in managing LKS, and should be used in all patientsref Aetiology : Gerstmann's syndrome Aetiology : Turner's syndrome Laboratory examinations : Symptoms & signs : Dejerine-Lichtheim sign or phenomenon : in some types of motor aphasia the patient cannot speak but can indicate with fingers the number of syllables in a word being thought of Aetiology : Gerstmann's syndrome
Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis : Epidemiology : 5% of people in the USA at some time in their lives. Stuttering usually begins in the preschool years, and there is a higher incidence in males. Stuttering usually starts in the third and fourth years of life, after a period of apparently normal speech development. Around 5% of children begin to stutter (Bloodstein O. A handbook on stuttering. San Diego, CA: Singular Publishing Group, 1995). Although the recovery rate without professional intervention is 74%ref, the natural recovery rate of cases presenting to clinics has not been researched. To date, sex and family history of recovery are the major identified predictors of natural recovery. Girls are more likely to recover than boys, and children with a family history of recovery are more likely to recover than those without such a history. Natural recovery does not seem to be related to severity of stutteringref. Aetiology : a complex interaction among many factors, including genetic, language, motor and emotional. These findings will help reduce the stigma � such as the myth that the disorder is the result of poor parenting or a psychological problem � often associated with stuttering Pathogenesis : adults who stutter often have great language skills, meaning they don't have problems with rules of grammar or with the sounds we use to code the words of our language. When they speak, however, their motor output falters, so they pause or trip over words. The study of their brain activity when they were not stuttering and, in fact, when they were not having to engage their speech motor systems shows that individuals who stutter are using right hemisphere brain areas to a greater extent to accomplish the rhyming tasks than those who don't stutterref Symptoms & signs : a speech disorder involving 3 factors: Epidemiology : prevalence = 4-5 cases every 1,000 people Aetiology : Pathogenesis : mirror neurons are brain cells in the premotor cortex. First identified in macaque monkeys in the early 1990s, the neurons -- also known as "monkey-see, monkey-do cells" -- fire both when a monkey performs an action itself and when it observes another living creature perform that same action. Though it has been impossible to directly study the analogue of these neurons in people (since human subjects cannot be implanted with electrodes), several indirect brain-imaging measures, including EEG, have confirmed the presence of a mirror neuron system in humans. The human mirror neuron system is now thought to be involved not only in the execution and observation of movement, but also in higher cognitive processes -- language, for instance, or being able to imitate and learn from others' actions, or decode their intentions and empathize with their pain. Suppression of m rhythm (8�13 Hz) over sensorimotor cortex correlates with mirror neuron activity and is defective in subjects with autism spectrum disorders : one therapeutic possibility suggested by the study's findings is biofeedback. Another possible therapy would involve ordinary mirrorsref Symptoms & signs : affected individuals look normal at birth, and the symptoms manifest at the first 2-3 years of life (median : 13.8 months), with medical diagnosis at median 2.7-6.8 years (differential diagnosis with mental retardation or language disorders is stable if done before age 2, sure since month 18). The spectrum of clinical symptoms and the severity of the disorder are variable even among siblings. Qualitative impairment in reciprocal social interaction (e.g., lack of awareness of the existence of feelings of others, failure to seek comfort at times of distress, lack of imitation), in verbal and nonverbal communication, and in capacity for symbolic play, and by restricted and unusual repertoire of activities and interests. Other characteristics sometimes include cognitive impairment (> 66% have some degree of mental retardation), hyper- or hyporeactivity to certain stimuli, stereotypic behaviors, neurological abnormalities such as seizures or altered muscle tone, sleeping or eating pattern abnormalities, and severe behavioral problems. As adults they develop OCD and mental retardation (higher functioning PDD : high IQ in adulthood). Laboratory examinations : several screening instruments have been developed to quickly gather information about a child's social and communicative development within medical settings. Among them are Differential diagnosis : Epidemiology : 1:10,000 individuals, occurring exclusively in females and present from birth Aetiology : dominant mutations in the MECP2 gene, a X-linked transcriptional repressor, or its controlled genes, including BDNF or UQCRC1. A severe early-onset Rett phenotype that often includes seizures or infantile spasms can be caused by mutation in the CDKL5 gene Pathogenesis : the timing of the period of regression in RTT--during ages 1 to 2 years--parallels the period of intense synaptic development. The effects of the MECP2 mutation also increases concomitantly with peak synaptogenesis. Neuropathological findings in Rett include the selective reduction of dendritric spines in the pyramidal cells of RTT brains; this feature has also been reported in autism. Studies have observed that MECP influences the expression of brain-derived neurotrophic factor and thus may influence synaptic plasticity. Abnormalities in synapse maintenance and modulation may contribute to regression in RTT and autism. A recent study observed abnormal expression of MeCP2 in RTT and other neurodevelopmental disorders such as autism. Although the genetic background and certain clinical features differ in RTT and autism, a similar mechanism involving MeCP2 regulation and expression may contribute to regressionref. Symptoms & signs : progressive and is characterized by autistic behavior (but a preserved speech variant exists), ataxia, dementia, seizures, and loss of purposeful use of the hands, with cerebral atrophy, mild hyperammonemia, and decreased levels of biogenic amines. During the regression stage, RTT girls display many autistic features, such as loss of communication and social skills, poor eye contact, and lack of interest, and initially may be given the diagnosis of autism. Differential diagnosis : Differential diagnosis : Laboratory examinations : during the last few years, screening instruments have been devised to screen for Asperger syndrome and higher functioning autism. The Autism Spectrum Screening Questionnaire (ASSQ)ref, the Australian Scale for Asperger's Syndromeref, and the most recent, the Childhood Asperger Syndrome Test (CAST)ref, are some of the instruments that are reliable for identification of school-age children with Asperger syndrome or higher functioning autism. These tools concentrate on social and behavioral impairments in children without significant language delay. Differential diagnosis : Epidemiology : prevalence = 3% to 10% of the pediatric population. Datamonitor estimates that 23 million children and adolescents across the 7 major pharmaceutical markets suffer from ADHD, a physician perceived prevalence rate of about 15%. However currently only 12% of those, or only 1.8% of children in the total population, are actually correctly diagnosed with ADHD. Despite the availability of numerous longer-acting therapies, currently only 20% of newly diagnosed patients receive such drugs as a first-line treatment, falling to 3% at second-line. Pathogenesis : the number and density of DATs and DAT binding sites are increased by up to 70 % Symptoms & signs : inattention (such as distractibility, forgetfulness, not finishing tasks, and not appearing to listen), by hyperactivity and impulsivity (such as fidgeting and squirming, difficulty in remaining seated, excessive running or climbing, feelings of restlessness, difficulty awaiting one's turn, interrupting others, and excessive talking) or by both types of behavior. The disorder is subtyped as Differential diagnosis : Differential diagnosis : Differential diagnosis :
Aetiology : conditions that result in derangement of cerebral metabolism, including Epidemiology : 24.3 million people have dementia today, with 4.6 million new cases of dementia every year (one new case every 7 seconds). The number of people affected will double every 20 years to 81.1 million by 2040. Most people with dementia live in developing countries (60% in 2001, rising to 71% by 2040). Rates of increase are not uniform; numbers in developed countries are forecast to increase by 100% between 2001 and 2040, but by more than 300% in India, China, and their south Asian and western Pacific neighboursref. Aetiology : Therapy : rivastigmine tartrateref Pathogenesis : dopamine-neuromelanine system ; disturbances of vitamin B5 metabolism ? Laboratory examinations : MRI shows bilaterally symmetrical hyperintense signal changes (due to gliosis, demyelination, neuronal loss, and axonal swelling) in the external segment of globus pallidus and substantia nigra, with surrounding hypointensity (caused by loss of signal secondary to iron deposition) on T2wi. These imaging features are fairly diagnostic and have been termed the "eye-of-the tiger sign" Course : Differential diagnosis :
Web resources :
Laboratory examinations : Redlich-Fisher miliary plaques (thickened, dark colored areas in the neuroglia reticulum of the brain, seen in cases of senile psychoses) Types : Experimental animal models : bulbocapnine experiment : the experimental injection of the alkaloid bulbocapnine into animals, which produces in them the motor phenomena typical of catatonia. Aetiology : double bind : a situation in which one person receives conflicting messages from another and in which response to either message, recognition of the conflict, or withdrawal is met with rejection or disapproval; thought to be a characteristic mode of interaction in some families of schizophrenics and in other dysfunctional families. Differential diagnosis : Differential diagnosis : Differential diagnosis :
Therapy : CCBs : Epidemiology : prevalence = 3-5% Aetiology : mutations in SLITRK1ref Symptoms & signs : noticeable hair loss or patches of baldness, often accompanied by other psychiatric conditions, such as anxiety, depression, obsessive compulsive disorder or Tourette syndrome Prognosis : Epidemiology : 2-10% of fertile females are severely affected, 30-80% mildly Aetiology : unknown cause, conditioned by maternal imprinting and axpiration to emancipation; chances of having symptoms are more likely for heavier women with a higher BMI and less likely for women using hormonal contraception Pathogenesis : reduced luteal development => Symptoms & signs (typically occurring in the period between ovulation and the onset of menstruation, lasting up to 2 weeks; occurring anamnestically for most of menstrual cycles for many years and confirmed in the 2 following cycles) : feelings of depression, hopelessness, aggressiveness, increased fatigue or lethargy, anxiety, or anger, emotional lability (tendence to crying and social isolation, decreased libido), bloating, diffuse edema with increased body weight and sense of tenderness, pelvic pains and headache, mammary tenderness or mastodynia, heat flushes, intestinal alterations, acne, seborrhea, foruncles, changes in appetite or cravings for selected foods, breast swelling and tenderness, constipation, and decreased ability to concentrate. Rarely hyperthymic disorder. Laboratory examinations : Aetiology : Pathogenesis : decrease in activity of CNS noradrenergic and serotoninergic systems => decrease in BDNF synthesis => decreased trophism of limbic system. Experimentally induced by reserpine. Symptoms & signs usually last 4-6 months and can chronicize when lasting > 2 years. They range from normal feelings of �the blues� through dysthymic disorder to major depressive disorder. It in many ways resembles the grief and mourning that follow bereavement; there are often feelings of low self-esteem, guilt, and self-reproach, withdrawal from interpersonal contact, and somatic symptoms such as eating and sleep disturbances. There is only mild social or workplace impairment. Grading : Differential diagnosis : Aetiology : SNPs in BDNF, GRK3 Pathogenesis : up to 40% less grey matter than normal in brain regions associated with mood Mood Disorder Questionnaire (MDQ) by AstraZeneca Therapy : Prognosis : without some form of therapy, up to 20% of sufferers will commit suicide. But up to 80% of sufferers have a positive reaction to lithium, and the suicide rate is reduced by a factor of 8 Aetiology : Associated diseases : Differential diagnosis : Therapy : after 2 sessions of behavioural therapy, patients reported a 10% decrease in anxiety levels. When the sessions were supplemented with D-cycloserine (DCS), their anxiety dropped 50% Aetiology : primitive fear of lack of O2 during life into caves : Symptoms & signs : antisocial behaviour (delays at work, dismissals, brawls, ) Laboratory examinations : Aetiology : deficiency of socializing hormone(s) (oxytocin, ADH (e.g. high in montane vole (Microtus montanus : asocial, minimally parental, low separation distress), low in prairie vole (Microtus ochrogaster : highly social, biparental, high separation distress, high bonds)), opiates, peptides, , ACTH, PRL, melatonin, noradrenalin, and serotonin). Mating increases ADH in males and oxytocin in females. Kinds of separation anxiety : Comorbidity : sometimes accompanied by depression and/or bipolar disorder. In adulthood patients may develop partner separation anticipatory anxiety disorder, inhability to separate from object the patient would like to go away, or panic disorder. Differential diagnosis : Differential diagnosis : Laboratory examinations : Mosloch burnout inventory (MBI) A bout of PTSD may do damage to the brain that kick-starts memory problems, scientists have discovered. Even patients who had recovered from a period of stress started to get age-related memory difficulties about a decade earlier than non-traumatized people. Post-traumatic stress, a condition that can cause patients to feel physical pain on remembering a traumatic event, is known to have a number of effects on the mind and body. One of the side effects is that patients tend to be forgetful, unable to remember a story or a list of words after they've heard it, for example. This problem, which could come from emotional distraction and an inability to concentrate, can interfere with everyday tasks. The link between PTSD and memory problems was investigated by looking at what happens to 3 groups of people as they age (Yehuda R., et al. Biol. Psychiatry, (in the press) (2006)) : Holocaust survivors with continued PTSD, survivors who had recovered from their trauma, and a control group who had not lived through the Holocaust and had never had PTSD. The researchers looked at the study participants' ability to remember associations between common words such as 'desk and chair', a task that is known to become more difficult as we age. They tested their participants at the age of 67, and again at 72. Those who had PTSD, even if they had subsequently recovered, could only come up with answers for half of the questions by the age of 72, a score that's usually expected from those over 80 years old. And they had showed a marked deterioration in scores from when they were 67. Those who had not had a trauma consistently got most, or all, of the questions right at both ages. Having PTSD early in life seems to set up future problems. It's like getting sunburnt at 15 and developing melanoma later. Researchers aren't sure how this might happen. Some think that stress hormones called glucocorticoids, which erupt in the body after a traumatic event such as fighting in a war, attack the hippocampus, a brain area that is key for memory. Some studies have shown the hippocampus of PTSD patients being unusually small, perhaps because it has been eaten away by stress hormones. Others think that people with a naturally small hippocampus may be predisposed to both memory problems and PTSD. Perhaps it isn't trauma that shrinks this part of the brain, but a small hippocampus that increases the likelihood of a stress disorder after a trauma. There's another possible explanation: perhaps some other factor, such as diet, was very different between the Holocaust survivors and the control group. The study didn't look at nutrition or weight loss in the Holocaust survivors, and this could be linked to their memory problems now. But it is stress that's to blame. Not all of the cognitive functions were worse in the Holocaust survivors. The ability to learn and repeat back a list of words, for example, a skill linked to the pre-frontal cortex, was actually better in patients who had recovered from PTSD, as though their brain was compensating for difficulties in the hippocampus. Ageing and trauma will nibble away at memory performance but the brain will be able to compensate to a point. The team's next steps are to look at soldiers who fought in wars to see whether they show the same pattern of decline. They are also going to look at young people who have been through trauma and follow them up later in life Onset of symptoms : Therapy : Web resources : Therapy : escitalopram oxalate Aetiology : SNPs in SLC6A5 / SERT Symptoms & signs : doubtful facing new situations or situations implying an even minimal risk of failure Differential diagnosis : Laboratory examinations : Experimental animal models : Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis : Aetiology : women who have had bilateral oophorectomy typically experience a 50% drop in circulating testosterone, which is associated with HSDD Having too little sexual desire is the most common sexual issue among women, reported by 10 to 51% of women surveyed in various countriesref1, ref2 (Matthiesen S, Hauch M. Wenn sexuelle erfahrungen zum problem warden. Familiendynamik 2004;29:136-60). Data from these surveys, as well as from other sources, indicate that a low level of desire is usually accompanied by low levels of arousal and sexual excitement and infrequent orgasms and is frequently associated with sexual dissatisfactionref1, ref2, ref3, ref4 (Davis SR, van der Mooren MJ, van Lunsen RHW, et al. The efficacy and safety of a testosterone patch for the treatment of hypoactive sexual desire disorder in surgically menopausal women: a randomized, placebo controlled-trial. Menopause). Current definitions of sexual dysfunction in women reflect a change in our understanding of normal sexual responseref. Rather than the traditional view of a sexual response progressing through discrete phases in sequence (desire, arousal, orgasm, and resolution), it is now recognized that these phases overlap and that the sequence can vary. Also recognized is the importance to sexual satisfaction of the subjective experience and of an environment and stimuli that are conducive to sexual feelingsref. Women have many motivations and reasons for engaging in sex, including a desire for emotional closeness, whereas sexual desire is an infrequent reason for women in established relationshipsref. Among the 2400 multiethnic women (Hispanic, white non-Hispanic, African American, Chinese, and Japanese) in six U.S. cities in midlife who completed baseline questionnaires in the prospective Study of Women's Health across the Nation (SWAN), 40% reported that they never or infrequently felt sexual desireref. Nevertheless, the majority reported being capable of arousal, and only 13% expressed discontent with their sexual experiences. The prevalence of the sexual desire/interest disorder, diagnosed when a woman fails to feel desire at any stage during the sexual experience, is uncertain. Studies have focused on a lack of desire at the initiation of and between sexual experiences, as well as on a lack of sexual thoughts. However, sexual thoughts are infrequent in many women without apparent sexual dissatisfactionref, and the frequency of sexual fantasies or sexual thoughts has little correlation with sexual satisfaction in womenref1, ref2. Arousal disorders are categorized according to whether there is a lack of subjective arousal alone or a lack of both subjective arousal and awareness of genital congestion. No objective measurements are used to establish diagnoses. Arousal disorders also have an uncertain prevalence; most studies focus only on vaginal lubrication. In a survey of 979 British women who were 18 to 70 years of age, 17% identified problems with arousal (defined as distinct from vaginal dryness)ref; 5% of women in SWAN did as wellref Definitions of sexual dysfunction :
Therapy : the management of sexual dysfunction in women is guided by the history. Data from randomized trials that support the use of any particular intervention are limited.
Sexual dysfunction associated with antidepressants : the prevalence of sexual disorders that are associated with the use of antidepressants in women is estimated at 22 to 58%, with higher rates reported for selective serotonin-reuptake inhibitors and lower rates reported for bupropion than for other drugsref. A recent Cochrane review of strategies to ameliorate
dysfunction associated with antidepressants did not recommend any particular drug, although the potential advantages of adding bupropion were notedref. A drug holiday (e.g., halting the use of shorter-acting selective serotonin-reuptake inhibitors over the weekend) seems to be a logical strategy but is not recommended, owing to withdrawal symptoms and compromise of compliance.
Differential diagnosis : Web resources : Therapy : Side effects :
Epidemiology : mostly females aged 12-25 years
Epidemiology : occurring predominantly in females with high economical level, with onset usually at age 12-35; prevalence = 1-2% of general population, 5-9% of universitary or high-school population Aetiology : autoimmune disease Symptoms & signs : episodic subjective or objective (20,000-30,000 cal) binge eating > 2 times a week for > 3 months, followed by binge behaviors designed to prevent weight gain, including purging, vomiting, fasting, diuretics (very dangerous !) and/or excessive exercise. Episodes of binge eating involve intake of quantifiably or subjectively excessive quantities of food alone within a short, discrete period (more times a day) as well as a sense of loss of control over food intake during these periods. The person with bulimia nervosa has a preoccupying pathological fear of becoming overweight, feels an unusually strong tie between self-worth and local body shape and size (hips, buttocks, thighs, ...), is aware that the eating pattern is abnormal, and frequently experiences feelings of self-recrimination. In contrast to persons with anorexia nervosa, patients with bulimia nervosa tend to be somewhat older, more socially inclined, have less obsessive characteristics (cyclothymic disorder), dress appariscent when happy and do not exhibit extreme weight loss; it is not diagnosed in the presence of anorexia nervosa. 50% have transient amenorrhea Prognosis : mortality due to hyperkalemia, suicide, self-lesionism, substance abuse Differential diagnosis :
Aetiology : high-risk job (models) and sports (dancers) Symptoms & signs Prognosis : mortality = 5-20% (33% due to cardiac complications : prolongation of the QT interval and cases of sudden death) Differential diagnosis :
Aetiology : approximately 50% of the variation in sleeping disorder symptoms can be pinned on genetic factors. For disruptive snoring it is 42%, daytime sleepiness 45%, restless legs 54% and legs jerking 60%. Aetiology : nocturnal frontal epilepsy, narcolepsy, psychiatric disorders, neurological diseases, drugs, obesity, SNPs in T-type calcium channel (genetically altered rodents showed a loss of delta waves and exhibited a higher incidence of brief awakening) which selects painful stimuli from each part of the body and relays them to the cortices of the brain Duration : Web resources : Narcolepsy and Overwhelming Daytime Sleep Society of Australia (NODSS) Aetiology : shorter PER3 gene (75%) or mutations in arylalkylamine N-acetyltransferase (AANAT) Pathogenesis : natural cycle is thought to be much longer than 24 hours Symptoms & signs : people sleep late into the day and feel alert only when burning the midnight oil Therapy : melatonin Aetiology : mutations in PER2 and CKId Symptoms & signs : sleep for the same length of time as non-sufferers but typically are wide awake and raring to go long before everyone else is up and about Differential diagnosis : epilepsy Aetiology : autoimmune somnambulism Aetiology : autoimmune ? Epidemiology : prevalence : 0.5% Symptoms & signs : chronic excessive sleepiness during night work and insomnia when attempting to sleep during the day Therapy : 200 mg of modafinilref Adolescents and young adults are often excessively sleepy. This excessive sleepiness can have a profound negative effect on school performance, cognitive function, and mood and has been associated with other serious consequences such as increased incidence of automobile crashesref. Sleep research data indicate that adolescents and even young adults under 21 still require 9-10 hours' sleep a night. But since the 1980s, the average sack time for both college and high school students has diminished to 6-7 hours nightly. Youngsters who are aged 9-10 years tend to sleep, on average, for about 10 hours on school nights and usually not more (and many times a lot less!) on weekends. But teenagers typically begin to enjoy sleeping in on the weekends. This trend increases during the high school years. As teens also develop a yen for late-night activities, their sleep debt increases daily. Developmental changes in circadian rhythms, endocrine and neurobehavioral systems, not to mention busier schedules, earlier start times for school, and parental supervision, also contribute to the problem of a teenager's getting less sleep. Regardless of the causes, however, this scenario often proves far more serious than a mere yawn or a brief encounter in slumber land. Current high school start times contribute to sleep deprivation among adolescents. Consistent with a delay in circadian sleep phase, students performed better later in the day than in the early morning. However, exposure to bright light in the morning did not change the sleep/wake cycle or improve daytime performance during weekdays. Both short-term and long-term strategies that address the epidemic of sleep deprivation among adolescents will be necessary to improve health and maximize school performanceref. In USA the percentage of people who typically sleep < 6 hours was : 12% in 1998; 13% in 2001; 15% in 2002; 16% in 2005. People who sleep > 10 hours per night have an average BMI = 26.4 kg/mBSA2, while people sleeping 2-4 hours per night have a BMI = 30.1 kg/mBSA2ref Therapy : chronotherapy : treatment of certain sleep disorders by capitalizing on the natural phase delay in adults; the bedtime is successively advanced by one to several hours each day until the individual can retire, sleep, and arise at appropriate times.
Differential diagnosis : Differential diagnosis : Differential diagnosis : Differential diagnosis :
Epidemiology : aas of February 2006, more than 2,000 reports of the disease have been reported on the Foundation's website. Reports come from all 50 U.S. states and 15 nations, including Canada, the UK, Australia and The Netherlands. The majority of reports have come from Texas, California and Florida. Interest in the disease was recently rekindled after afflicted Texas teenager Travis Wilson committed suicide in April 2006ref. Symptoms & signs : feelings of insects or parasites scuttling beneath their skin and open lesions that heal slowly and which ooze out blue and white fibers, some as thick as spaghetti strands. Attempts to remove the fibers are said to elicit shooting pains radiating from the site. The lesions range from minor to disfiguring in appearance and fibers appear either as single strands or as bundles. Patients also sometimes report the presence of fibers or black granular specks on their skin even in the absence of lesions. Some patients even report symptoms of the disease in their pets�dogs mostly, but also cats and horses. About 95% of patients also report suffering from disabling fatigue, or "brain fog," that hinders their ability to pay attention. Other reported symptoms include joint pain, sleep disorders, hair loss, decline in vision, and even the "disintegration" of perfectly healthy teeth. It appears that once patients contract the disease, they have it for life. To date, there have been no reports of spontaneous remissions. A preliminary analysis of the fibers suggests they are more than just lint from household materials such as clothing, carpets or bedding. The fibers are not common textiles, nor are they black specks of pepper, as several dermatologists have proposed. Further deepening the mystery, some analyses suggest the fibers might be made of cellulose, a molecule generally found in plants. They're basically fibers that you wouldn't expect to see in humans. The disease is named after a medical condition described in 1674 by the British author Thomas Browne. Known as "Morgellons," the disorder caused children to "critically break out with harsh hairs on their backs�" It is doubtful that the 17th century disease is related in any way to modern day Morgellons. The "matchbox sign" of delusional parasitosis, when patients bring in hair, skin or clothing lint, sometimes in matchboxes, that they claim contain the insects or parasites responsible for their torment. However, when examined, the samples reveal no such thing. The lesions and scratches sometimes seen on patients with delusional parasitosis are usually self-inflicted. Laboratory examinations : skin biopsies to rule out infections Therapy : anti-psychotic or anti-anxiety medicines Web resources : Morgellons Research Foundation, a non-profit organization devoted to raising public awareness about the disease.
Laboratory examinations :
Glossary :
Among elderly people hospitalization of a spouse is associated with an increased risk of death, and the effect of the illness of a spouse varies among diagnoses. Such interpersonal health effects have clinical and policy implications for the care of patients and their families. Overall, 383,480 husbands (74%) and 347,269 wives (67%) were hospitalized at least once, and 252,557 husbands (49%) and 156,004 wives (30%) died. Mortality after the hospitalization of a spouse varied according to the spouse's diagnosis. Among men, 6.4% died within 1 year after a spouse's hospitalization for colon cancer , 6.9% after a spouse's hospitalization for stroke, 7.5% after a spouse's hospitalization for psychiatric disease, and 8.6% after a spouse's hospitalization for dementia. Among women, 3.0% died within 1 year after a spouse's hospitalization for colon cancer, 3.7% after a spouse's hospitalization for stroke, 5.7% after a spouse's hospitalization for psychiatric disease, and 5.0% after a spouse's hospitalization for dementia. After adjustment for measured covariates, the risk of death for men was not significantly higher after a spouse's hospitalization for colon cancer (hazard ratio, 1.02; 95% confidence interval, 0.95 to 1.09) but was higher after hospitalization for stroke (hazard ratio, 1.06; 95% confidence interval, 1.03 to 1.09), congestive heart failure (hazard ratio, 1.12; 95% confidence interval, 1.07 to 1.16), hip fracture (hazard ratio, 1.15; 95% confidence interval, 1.11 to 1.18), psychiatric disease (hazard ratio, 1.19; 95% confidence interval, 1.12 to 1.26), or dementia (hazard ratio, 1.22; 95% confidence interval, 1.12 to 1.32). For women, the various risks of death after a spouse's hospitalization were similar. Overall, for men, the risk of death associated with a spouse's hospitalization was 22% of that associated with a spouse's death (95% confidence interval, 17 to 27%); for women, the risk was 16% of that associated with death (95% confidence interval, 8 to 24%)ref.According to the National Crime Victimization Survey for 1993 to 1999, conducted by the Department of Justice, the annual rate of nonfatal, job-related, violent crime was 12.6 per 1000 workers in all occupations. Among physicians, the rate was 16.2 per 1000, and among nurses, 21.9 per 1000. But for psychiatrists and mental health professionals, the rate was 68.2 per 1000, and for mental health custodial workers, 69.0 per 1000. For Tim Exworthy, a forensic psychiatrist at Redford Lodge Hospital in London who was recently assaulted by a patient, the risk of job-related violence is no longer a dry statistic. He was beaten unconscious by a 19-year-old psychotic man whom he had been treating in the hospital for 5 months. I was talking with him in a room and telling him why he couldn't leave, when I was suddenly aware of a few blows to my head. The next thing I knew, I was at the nursing station wiping the blood off my face. I never saw this coming and hadn't anticipated that he would react like that. Such attacks by psychotic patients highlight a larger question: Are people with mental illness really more likely than others to engage in violent behavior? If so, which psychiatric illnesses are associated with violence, and what is the magnitude of the increase in risk? Posing these questions is itself not without risk: being perceived as dangerous can have a devastating effect on a person's prospects for relationships, employment, housing, and social functioning. People with mental illness already bear the burden of much social stigma, and I am loath to add to it. But without a realistic understanding of this risk, medical practitioners can neither provide the best care for their patients nor ensure their own safety when the clinical situation warrants it. Until recently, most studies have focused on the rates of violence among inpatients with mental illness or, conversely, the rates of mental illness among people who have been arrested, convicted, or incarcerated for violent crimesref. For example, one national survey showed that the lifetime risk of schizophrenia was 5% among people convicted of homicide � a prevalence that is much higher than any published rate of schizophrenia in the general population � suggesting an association between schizophrenia and homicide convictionref.2 These studies, however, tend to be limited by selection bias: subjects who are arrested, incarcerated, or hospitalized are by definition more likely to be violent or very ill and thus are not representative of psychiatric patients in the general population. A more accurate and less biased assessment of the risk of violence perpetrated by the mentally ill comes from epidemiologic studies of community samples. The best known is the NIMH's Epidemiologic Catchment Area (ECA) study, which examined the rates of various psychiatric disorders in a representative sample of 17,803 subjects in five U.S. communities. Although this study was not initially designed to assess the prevalence of violent behavior, data on violence were collected for about 7000 of the subjects. "Violence" was defined as having used a weapon such as a knife or gun in a fight and having become involved, with a person other than a partner or spouse, in more than one fight that came to blows � behavior that is likely to frighten most people. Lifetime Prevalence of Violent Behavior among Persons with or without Major Psychiatric Disorders and Substance Abuse. The criteria for violent behavior were use of a weapon in a fight and engaging, with someone other than one's partner or spouse, in a fight that came to blows. Persons were considered to have a relevant psychiatric disorder if they met the lifetime criteria delineated in the Diagnostic and Statistical Manual of Mental Disorders (third edition) for schizophrenia, bipolar disorder, or major depression and had had active symptoms of that disorder within the previous 12 months (Swanson JW. Mental disorder, substance abuse, and community violence: an epidemiological approach. In: Monahan J, Steadman HJ, eds. Violence and mental disorder: developments in risk assessment. Chicago: University of Chicago Press, 1994:101-36) The study showed that patients with serious mental illness � those with schizophrenia, major depression, or bipolar disorder � were two to three times as likely as people without such an illness to be assaultive. In absolute terms, the lifetime prevalence of violence among people with serious mental illness was 16%, as compared with 7% among people without mental illness. Although not all types of psychiatric illness are associated with violence � anxiety disorders, for example, do not seem to increase the risk � and although most people with schizophrenia, major depression, or bipolar disorder do not commit assaultive acts, the presence of such a disorder is significantly associated with an increased risk of violence. Of course, because serious mental illness is quite rare, it actually contributes very little to the overall rate of violence in the general population; the attributable risk has been estimated to be 3 to 5% � much lower than that associated with substance abuse, for example. (People with no mental disorder who abuse alcohol or drugs are nearly seven times as likely as those without substance abuse to report violent behavior.) But substance abuse among the mentally ill compounds the increased risk of violence: one study involving 802 adults with a psychotic or major mood disorder showed that violence was independently correlated with several risk factors, including substance abuse, a history of having been a victim of violence, homelessness, and poor medical healthref. The 1-year rate of violent behavior for subjects with none or only one of these risk factors was 2% � a prevalence close to the ECA study's estimate for the general population. Thus, violence in people with serious mental illness probably results from multiple risk factors in several domains. Much can be done to diminish the risk of violence among the mentally ill. A study that compared the prevalence of violence in a group of psychiatric patients during the year after hospital discharge with the rate in the community in which the patients lived showed no difference in the risk of violence between treated patients and people without a psychiatric disorderref. Thus, symptoms of psychiatric illness, rather than the diagnosis itself, appear to confer the risk of violent behavior. So patients with schizophrenia who are free of the acute psychotic symptoms that increase this risk, such as having paranoid thoughts or hearing voices that command them to hurt others (called command auditory hallucinations), may be no more likely to be violent than people without a mental disorder. The study did not specifically monitor the treatments, but it seems possible that treating psychiatric illness does not just make patients feel better; it may also drastically reduce the risk of violent behavior. In the wake of Fenton's killing, there may be renewed efforts to expand the criteria or lower the clinical threshold for mandatory treatment of patients with psychosis � a movement that is sure to be controversial. We know that most such patients are not violent, but we also know that a patient with acute psychosis who is paranoid and has command auditory hallucinations or a history of being violent, being a victim of violence, or abusing alcohol or drugs is at high risk for violent behavior. Currently, in order to protect civil liberties, most states mandate treatment (whether hospitalization or medication) only if there is unambiguous evidence of an immediate danger to others, which is generally interpreted as overt threats or violent actions. Perhaps it makes sense to reset the threshold at the presence of known clinical risk factors � psychotic thoughts that are influencing behavior, a history of violence, and significant concurrent substance abuse. But expanding the criteria would require further substantiation that these factors can be accurately identified by clinicians and that their use in mandating treatment is warranted. The possibility that expanding the criteria might also discourage people with psychotic illnesses and substance abuse problems from voluntarily seeking treatment would also need to be considered. It is natural for psychiatrists and other medical professionals who treat psychiatric patients to deny, to some extent, the possible danger. After all, it is hard to have a therapeutic relationship with a patient we fear. Still, we need to remind ourselves that the risk of violence, though small, is real, and we must take necessary precautions. As Exworthy put it, "I guess I let down my guard and paid for it." Keeping up our guard means paying attention to our fear and anxiety about a patient; no physician should ever treat a patient whom he or she fears. It also means seeing patients with acute psychosis in locations where there is adequate assistance and security, such as hospitals and clinics, rather than in a private office setting. The challenge for medical practitioners is to remain aware that some of their psychiatric patients do in fact pose a small risk of violence, while not losing sight of the larger perspective � that most people who are violent are not mentally ill, and most people who are mentally ill are not violent. Web resources :
Copyright © 2001-2014 Daniele Focosi. All rights reserved | Terms of use | Legal notices About this site | Site map | Acknowledgements | Current link partners Abbreviations and acronyms | Medical terminology | Add a link | Translate | Softwares | Cite this page! for Which of the following is a rapid acting anesthetic that produces hallucinogenic effects?WHAT IS KETAMINE? Ketamine is a dissociative anesthetic that has some hallucinogenic effects. It distorts perceptions of sight and sound and makes the user feel disconnected and not in control. It is an injectable, short-acting anesthetic for use in humans and animals.
Which of the following is a popular biological treatment for erectile disorder?Oral drugs or pills known as phosphodiesterase type-5 inhibitors are most often prescribed in the U.S. for ED (Viagra, Cialis, Levitra, Stendra) Testosterone Therapy (when low testosterone is detected in blood testing) Penile Injections (ICI, intracavernosal Alprostadil)
Is by far the most heavily used stimulant quizlet?____ is by far the most heavily used stimulant. Caffeine - 75% of it is ingested through coffee. One cup has about 100 milligrams of caffeine. Caffeine users can develop a tolerance.
When people with narcolepsy waken they may experience brief periods when they can't move or speak referred to as?A person remains fully conscious during sleep paralysis, but is unable to speak or move. Periods of sleep paralysis can last for several minutes and, upon waking, people regain the ability to move and speak. About 25% of people with narcolepsy experience sleep paralysis7.
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