)
Table of contents :
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.
Web resources : Do
I Need Therapy online test
content in CSF and serum, with a return to normal concentrations between
attacks
intoxication
(0.25 mg i.v.)
,
cannabinoids),
schizophrenic
disorders, and
schizotypal
personality disorder. Some do not draw a distinction between depersonalization
and derealization, using depersonalization to include both.or
disease, usually with simplified sentence structure (telegraphic speech)
and errors in tense, number, and gender
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
or disease
detects abnormal pulses of activity in the right intraparietal sulcus)
but cannot speak independently.
)
or epileptic
attack. The patient is irrequiet and continuously repeats the same questions.
or delirium.
There may be disorientation, confabulation, and lack of insight into the
memory deficit
from chronic alcohol abuse (Wernicke-Korsakoff
syndrome);
now considered offensive
and SCN2A,
result in the seizure disorder GEFS+. The variant R1902C in SCN2A is located
in the calmodulin binding site and was found to reduce binding affinity
for calcium-bound calmodulin. R542Q in SCN1A was observed in one autism
family and had previously been identified in a patient with juvenile myoclonic
epilepsy,
which is poorly absorbed, may lead to significant improvement in these
children. Fecal flora of children with regressive autism was compared with
that of control children, and clostridial counts were higher. The number
of clostridial species found in the stools of children with autism was
greater than in the stools of control children. Children with autism had
9 Clostridium spp.
not found in controls, whereas controls yielded only 3 species not found
in children with autism. In all, there were 25 different clostridial species
found. In gastric and duodenal specimens, the most striking finding was
total absence of non-spore-forming anaerobes and microaerophilic bacteria
from control children and significant numbers of such bacteria from children
with autism. These studies demonstrate significant alterations in the upper
and lower intestinal flora of children with late-onset autism and may provide
insights into the nature of this disorderref
infection of the intestinal tract as the underlying cause for symptoms
of autism observed in some individuals. A significant percentage of individuals
with autism have a history of extensive antibiotic use. Oral antibiotics
significantly disrupt protective intestinal microbiota, creating a favorable
environment for colonization by opportunistic pathogens. C. tetani
is an ubiquitous anaerobic bacillus that produces a potent neurotoxin.
Intestinal colonization by C. tetani, and subsequent neurotoxin
release, have been demonstrated in laboratory animals which were fed vegetative
cells. The vagus nerve is capable of transporting tetanus neurotoxin (TeNT)
and provides a route of ascent from the intestinal tract to the CNS. This
route bypasses TeNT's normal preferential binding sites in the spinal cord,
and therefore the symptoms of a typical tetanus infection are not evident.
Once in the brain, TeNT disrupts the release of neurotransmitters by the
proteolytic cleavage of synaptobrevin, a synaptic vesicle membrane protein.
This inhibition of neurotransmitter release would explain a wide variety
of behavioral deficits apparent in autism. Lab animals injected in the
brain with TeNT have exhibited many of these behaviors. Some children with
autism have also shown a significant reduction in stereotyped behaviors
when treated with antimicrobials effective against intestinal clostridia.
When viewed as sequelae to a subacute, chronic tetanus infection, many
of the puzzling abnormalities of autism have a logical basisref.
(expecially in measles-mumps-rubella
(MMR) vaccine).
The UK government has been accused of blocking imports of measles and mumps
vaccines, sending prices soaring to force parents into using the controversial
measles, mumps, rubella (MMR) triple jab. Doctors in Edinburgh, Glasgow
and London are now charging more than £100 for a single measles or
mumps vaccine because it is increasingly difficult to get them in the UK.
In recent months, the government has cut supplies further, restricting
them to only 25 doses per day.
: it deposits 25 mg of ethyl mercury into a
child.)
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
(a dopamine agonist that blocks DAT,
significantly increasing extra cellular dopamine, so correcting the dopamine
deficiency in the frontal lobes and basal ganglia (expecially the striatum)
structures, regions associated with attention and behaviouri. This is strikingly
similar to the mechanism of action of cocaine, a primary stimulant drug
of abuse. When administered intravenously, MPH like cocaine has reinforcing
effects (euphoria) at doses that exceed a DAT blockade threshold of 60%
(therapeutic doses of MPH block > 50% of DAT). When administered orally
at clinical doses, the pharmacological effects of MPH also exceed this
threshold, but reinforcing effects rarely occur). ADHD is a controversial
problem in sport since participants with this disorder often require banned
stimulant medication while competing.
(atomoxetine),
a nonstimulant approved by the US Food and Drug Administration
or zinc deficiency)
severe enough to explain the feeding anomaly and not attributable to other
mental disorder (e.g. rumination disorder)
or lack of available food.
(lasting > 12 months)
(for babies with a mental age > 4 years))
(not due to a general medical condition)
or imperious micturition (e.g. untreated diabetes mellitus or diabetes
insipidus,
hypoxia,
hypoglycemia,
or hepatic or renal
failure..
as well as one or more of other abilities in subjects that have reached
normality (on the contrary of mental
retardation).,
being of insidious onset and gradually progressive course, with histopathological
changes characteristic of Alzheimer's disease and not due to other CNS,
systemic, or substance-induced conditions known to cause dementia. It is
subcategorized on the basis of accompanying features, including
but having a distinctive histopathology; cortical atrophy is symmetric
> asymmetric and is confined to the frontal and/or temporal lobes and
sometimes may involve the basal nuclei
),
impaired judgements and propriety sense, generally euphoric, hypocritical,
logorrheic, agitated, and with primitive reflexes.
dementia (DLBD) (15.4%, the second most common degenerative dementia;
DLBD is diagnosed only when they are not associated with Alzheimer's
disease
or idiopathic Parkinson's
disease)
is a neuropathological entity, characterized by abundant LBs not only in
the basal ganglia and brain-stem but in the cerebral cortex, combined with
senile changes. Juvenile onset DLBD is called pure form of DLBD
because of no or few senile changes. The LBs are present in the amygdala,
nucleus basalis of Meynert, hypothalamic nuclei, substantia nigra, nucleus
paranigralis, locus caeruleus, dorsal vagal nucleus and reticular nuclei.
The cerebral LBs are numerous in the parahippocampal gyrus, cingular gyrus,
and insular, frontal and temporal cortices. The LBs show immunoreactivity
to ubiquitin and the ubiquitin-immunoreactive neurites in the CA2-3 region
appear to be specific for DLBD. The clinical features of DLBD in the senium
are progressive dementia, psychotic state (delirium,
visual > auditory hallucinations), falls,
potentially
fatal hazard of neuroleptics and benzodiazepines,
parkinsonism and autonomic signs. In general, progressive dementia is an
initial symptom, followed by parkinsonism in the later stage. Some show
progressive autonomic failure. A few present respiratory failure or vocal
cord palsy resulting in sudden death in DLBD. DLBD is characterized neurochemically
by severe affection of multiple neurotransmitters networks. In DLBD an
impairment of the innominato-cortical cholinergic and mesocortical dopaminergic
system, differentiating from Alzheimer's
disease
and idiopathic Parkinson's
disease,
may play an important role in developing disease process.
It is estimated that dementia occurs in approximately 40% of people with
PD and that it may affect up to 80% of PD patients as the disease further
progresses. Previous studies suggest that patients with PD have up to a
6-fold increase in the risk of developing dementia compared to elderly
patients without PD
tartrateref
: a-synuclein is present in axonal spheroids,
Lewy-related
dystrophic neurites,
glial
cytoplasmic inclusions (GCI)
and neuronal
cytoplasmic inclusions (NCI)
metabolism ?
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"
in brains of 83% of VaD patients vs. 34% of age-matched normal people;
it may last from a few months to years
in the brain : humans with chronically high cortisol levels have smaller
hippocampi
and folic acid
improves by 10% mental functioning in healthy elderly men and cognitively
impaired type-2 diabetic patients by lowering levels of cortisol in the
brainref.))|
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psychotogens |
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physical dependence : continued administration of the drug is required to maintain normal function => temporarywithdrawal syndrome when administration is terminated (symptoms tend to be opposite to the original effects produced by the drug before tolerance developed) | => DA
in the "shell" of nucleus accumbens
=> positive reinforcing effect (e.g. conditioned place preference)
=> psychological dependence
: psychic abstinence syndrome
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social substance dependence |
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| amphetamines
(neurotoxicity : autooxidation of DA to 6-hydroxyDA or hyperactivity
of Glu-ergic circuits => DA-ergic neurons) |
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| LSD |
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| cocaine |
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| heroin |
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| psilocybin |
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| cannabinoids |
seen clinically only in persons who use marijuana on a daily basis and then suddenly stop |
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| mescaline |
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| inhalants |
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| nicotine |
irritability, impatience, hostility, anxiety,
dysphoric or depressed mood, difficulty concentrating, restlessness, bradycardia,
hyperphagy or weight gain |
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although > 80% of smokers express a desire to quit, only 35% try to stop each year, and < 5% are successful in unaided attempts to quit | |||||
| caffeine
/ teine |
fatigue, sedation, headache, nausea
and vomiting |
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| PCP |
somnolence, tremor, seizures, diarrhea,
piloerection, bruxism,
and vocalizations |
schizophrenia | ||||||
| opioids |
regular withdrawal : mydriasis,
restlessness, irritability, hyperalgesia, sweating, piloerection,
tachycardia, nausea and vomiting,
gastritis, colic, diarrhea,
myalgia, systemic
arterial hypertension,
dysphoria,
yawning, insomnia,
anxiety,
fever,
strabismus,
rhinorrhoea, crying, cough ;
protracted withdrawal (up to 6 months): anxiety, insomnia, cyclic changes in weight, pupil size, respiratory center sensitivity |
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| chloral hydrate |
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| paraldehyde |
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| glutethimide |
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| BDZ |
seizures, delirium |
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| meprobamate |
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| barbiturates |
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| ethanol |
,
sleep disturbance, tachycardia, systemic
arterial hypertension,
sweating, perceptual distortion, seizures (12-48 hrs after last drink);
in conjunction with infection, trauma, malnutrition, or electrolyte imbalance
=> delirium
tremens |
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| SSRI |
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,
gastrointestinal disturbances;
a coarse, irregular tremor, and delusions, vivid
hallucinations;
wild, agitated behavior, fever,
diarrhea,
and mydriasis. The onset is usually 2 or 3 days
after cessation of drinking; the delirium and other withdrawal symptoms
usually resolve in 3 or 4 days
(Wernicke-Korsakoff syndrome or psychosis
/ alcoholic dementia) : a syndrome of anterograde
amnesia
and retrograde amnesia
with confabulation associated with alcoholic or nonalcoholic polyneuritis
described as “cerebropathia psychica toxemica” by Korsakoff; currently
used synonymously with the term amnestic syndrome or, more narrowly,
to refer to the amnestic component of the Wernicke-Korsakoff syndrome,
i.e., an amnestic syndrome resulting from thiamine
deficiency
are twice as likely to develop schizophrenia as those whose blood levels
were below this threshold. If the finding holds up in other groups, as
many as 25% of all schizophrenia cases in this same age group might be
explained by leadref.
In the 1950s and 60s, lead exposure in California was relatively high because
of the use of leaded gasoline
mothers are twice as likely to develop schizophrenia. Most agree it is
likely to have both genetic and environmental triggers. Researchers first
saw a link between schizophrenia and hunger when investigating the Dutch
'hunger winter' of 1944-45, when the Nazis blocked food supplies to much
of the Netherlands. Babies born that year were twice as likely to become
schizophrenic, according to a 1992 studyref.
But as only 25 people in the sample were diagnosed with the illness, the
result could have been a statistical fluke. Now another famine, halfway
across the world, has lent support to the link between famine and schizophrenia.
In China around 1960, a combination of bad weather and Mao Zedong's Great
Leap Forward - in which farmland became industrial, and ineffective new
agriculture was tried - plunged the country into famine. One of the hardest-hit
areas was Anhui province in 1959-61. The researchers selected one area
in that province and gathered data from the local psychiatric hospital.
Just as in the Netherlands, the risk of children developing schizophrenia
doubled during the famine years: hundreds of children per year were later
diagnosed with the disease, putting their risk at 2%, compared to 1% for
children born in easier timesref.
The finding is unlikely to much affect the total number of schizophrenics,
as fewer babies overall survive during famines. Although the link between
malnurishment in the womb and schizophrenia is clear, the mechanism by
which they are related is still unknown. Nobody knows what is going on,
but we are beginning to think of it as a gene-environment interaction.
One popular idea is that a deficiency of folic acid is to blame. Lack of
this nutrient, found in leafy greens and some vitamin supplements, is also
implicated in developmental defects in the baby's spinal cord. Researchers
are looking at genes for folic acid metabolism and how these might relate
to mental illness. It is difficult to find natural experiments in which
to conduct such studies, as the famines must be at least 40 years old in
order to give schizophrenia a chance to develop. Epidemiologists and medical
researchers can take satisfaction in the fact that they can take something
so catastrophic and wring from it scientific knowledge that would otherwise
be unavailable. Wonderful as that is, lets none of us forget that we should
be active in the present to prevent further catastrophes.
(John M. Eagles hypothesis)
antagonists are effective after 7-15 days
=> deafness),
which was associated with the witch trials at Salem, Massachusetts, USA,
because of its psychoactive properties,
which occurs when there is an inadequate dietary intake of thiamine
is administered to place the patient in a deep hypoglycemic
coma,
which is reversed in an hour or less by administration of glucagon, usually
for 20 to 60 such treatments.
: the relative effectiveness of second-generation (atypical) antipsychotic
drugs as compared with that of older agents has been incompletely addressed,
though newer agents are currently used far more commonly. Olanzapine was
the most effective in terms of the rates of discontinuation, and the efficacy
of the conventional antipsychotic agent perphenazine appeared similar to
that of quetiapine, risperidone, and ziprasidone. Olanzapine was associated
with greater weight gain and increases in measures of glucose and lipid
metabolismref
:
: 120-360 mg/day
: 30-180 mg/day
4-16 mg/day
: 10-30 mg/day
: 4-16 mg/day
30 mg IV + haloperidol
2-4 mg i.m. + chlorpromazine
50-100 mg i.m. (eventually repeat after 1 hr)
600-900 mg/day in acute phase => maintenance with plasma levels = 0.8-1.2
mEq/L (toxicity when > 2.0 mEq/L)
: carbamazepine, valproate or dipropylacetamide 600-1200 mg/day
: 20-30 mg/day
: 200-600 mg/day
: 50-600 mg/day:
40-120 mg/day
: 50-400 mg/day
: 50-150 mg/day
: 2-6 mg/day,
hyperphagia and carbohydrate craving => weight gain, substance abuse; hypersensitivity
to denial; reactivity of mood,
daily or seasonal alternance (usually worse at morning, better at evening)
and less likely for women using hormonal
contraception
,
prostaglandins, serotonin, GABA, vitamin
B6,
and intracellular magnesium,
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.
for > 4 months
or progestins
(triphasic combinations may worsen mood disorders and headache)
for perimenstrual headache
2.5 mg/day in luteal phase, danazol
200 mg/day for 3 months, enantone or decapeptyl for mastodynia
in last 4-5 days for water retention
0.25 mg/bid for anxiety (intermittent usage in luteal phase only may cause
anxiety at suspension)
for depression,
increased need for sleep, hyperphagia, and carbohydrate craving; it intensifies
in one or more specific seasons, most commonly the winter months, and is
hypothesized to be related to melatonin
levels
and serotoninergic
systems => decrease in BDNF
synthesis => decreased trophism of limbic system. Experimentally induced
by reserpine.
.
Still indicated for elderly patients with durg-resistant depression or
malignant hyperthermia
:
: 100-300 mg/day:
20-60 mg/day
: 50-100 mg/day
: 20-60 mg/day
: 20-60 mg/day
: 75-375 mg/day
: 150-600 mg/day
: 15-45 mg/day
: 8-12 mg/day
: cognitive therapy, when provided by an experienced therapist, may be
as effective as antidepressant medications in the initial treatment of
moderate to severe major depressionref,
GRK3
(300 mg 3 times a day, monitoring lithemia in the range = 0.5-0.8 mEq/L),
atypical
antipsychotics
(clozapine,
olanzapine)
: valproate (500 mg 3 times a day), carbamazepine, gabapentin, lamotrigine,
topiramate), CCB
(verapamil,
diltiazem)
(60%))
detection ([CO2]air > 9,000 ppm : a single inhalation
of 35% CO2 activates the hypothalamic-pituitary-adrenocortical
(HPA) axis, increases blood pressure (BP) and increases subjective fear
responses in healthy volunteers)
(RR = 4), severe headache
(RR = 2), mitral
valve prolapse (MVP)
(20-30%; RR = 2; selection bias due to hypochondriasis
?), and thyroid conditions
(patients use to switch radiators off)
receptors in the anterior cingulate cortex, the posterior cingulate cortex
and the raphe nucleus
=> trycyclic antidepressants
(TCA)
=> SSRI (imipramine
(10-300 mg 3 times a day) => trimipramine
(25-200 mg 3 times a day; side effects : sleepiness and weight gain, diarrhea,
tachycardia due to anticholinergic effects); nowadays the drugs of choice
are paroxetine
> sertraline.
Fluoxetine
has disinhibiting effects). Cholinergic blockers are associated (sulpirides
cause decreased libido and limit erection and ejaculation
: once side effects were treated with testosterone
and gonadotropins,
but that caused increased PRL => gynecomastia and galactorrhea)
for anticipatory anxiety (educational, existential, psychoanalytic, group,
cognitive psychotherapy, meditation, relaxation, biofeedback, behavioural)
+ trycyclic antidepressants
(TCA),
their anxiety dropped 50%
,
caused by pain from spasms of the pharynx or larynx)
addiction (> 20%; used as autotherapy)
: phenelzine and tranylcypromine (unusual worsening of anxiety). Moclobemide
is not effective
: paroxetine
gives responses in 70%
(side effect : sedation and depression)
40-80 mg or atenolol
50-150 mg) 1-2 hours before social performances : they decrease anxiogenic
vegetative symptoms (tachycardia, tremors), but are not effective on generalized
social phobia and worse depression
: contrasting findings
are not effective !,
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.
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| opiates |
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| oxytocin |
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| ADH |
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| noradrenalin |
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| cortisol |
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| estrogens |
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| progestins |
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| PRL |
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| oxytocin |
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for aspects of the event.
Longer engagements made PTSD more common. A soldier would be hunkered down
in a trench, hearing explosions day after day, with little hope. After
30 days new guys would come in. But nobody put it together until after
World War I, when it was dubbed "battle shock". By World War II
it had become "battle fatigue", then later "post-Vietnam syndrome"
before PTSD. Vietnam was a milestone. No nation had rigorously conducted
an epidemiological survey of males and females in the theater, but scrutiny
was delayed. It was done in the mid-1980s, but the conflict raged in the
1960s and 1970s. For the first Gulf War, PTSD research began 5 years later.
The US military has already questioned 2,530 soldiers in Iraq and 3,671
in Afghanistan about PTSD symptoms pre- and postdeployment. The most telling
finding is that only 23% to 40% of those affected sought help, fearing
stigmatizationref.
Since in the past symptoms typically peaked 2 years postengagement, current
figures may be an underestimate.,
peptic
ulcer,
ulcerative
colitis,
systemic
arterial hypertension,
hypoglycemia,
hyperinsulinism, hyperthyroidism,
hypothyroidism,
Cushing
disease
antagonists
(carbamazepine and valproate) reduce number of flashbacks
oxalate
,
dermatopathies)
or mental disorder (stuttering, anorexia
nervosa, body dysmorphic disorder
)
(diazepam and imipramine)
(hysterical chorea),
hysterical
anesthesia,
blindness, or aphonia) having no demonstrable physiological basis and whose
psychological basis is suggested by (1) exacerbation of symptoms at times
of psychological stress, (2) relief from tension or inner conflicts (primary
gain) provided by the symptoms, or (3) secondary gains (support, attention,
avoidance of unpleasant responsibilities) provided by the symptoms. Many
patients exhibit “la belle indifférence” [Fr. “beautiful
indifference”], an inappropriately complacent attitude (lack of concern)
toward their condition and impairment caused by the symptoms ; histrionic
personality traits are also common. Symptoms are neither intentionally
produced nor feigned, and are not limited to pain or sexual dysfunction.
typically experience a 50% drop in circulating testosterone,
which is associated with HSDD
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| hypoactive sexual desire disorder : persistent or recurrent deficiency or absence of sexual fantasies and desire for sexual activity. Judgement of deficiency is made by the physician, taking into account factors that affect sexual functioning (such as age and context of the person's life) | sexual desire/interest disorder : absent or diminished feelings of sexual interest or desire, absent sexual thoughts or fantasies, and a lack of responsive desire. Motivations for attempting to become sexually aroused are scarce or absent. Lack of interest goes beyond a normal lessening with increasing age and relationship duration | minimal spontaneous sexual thinking or minimal desiring of sex ahead of sexual experiences does not necessarily constitute a disorder (according on data on women in sexually satisfactory, established relationships). Lack of desire triggered during the sexual encounter (i.e., responsive desire) is integral in the AUA Foundation diagnosis |
| lack of subjective arousal : no DSM-IV definition addresses the lack of subjective arousal | combined arousal disorder : absent of markedly reduced feelings of sexual arousal (sexual excitement and sexual pleasure) from any type of stimulation, and absent or impaired genital sexual arousal (vulval swelling and lubrication) | there is no sexual excitement in the mind and no awareness of reflexive genital vasocongestion |
| lack of subjective arousal : no DSM-IV definition addresses the lack of subjective arousal | subjective arousal disorder : absent of markedly reduced feelings of sexual arousal (sexual excitement and sexual pleasure) from any type of stimulation. Vaginal lubrication and other signs of physical response still occur | there is no sexual excitement in the mind, but there is awareness of adequate lubrication |
| female sexual arousal disorder : persistent or recurrent inability to attain, or to maintain until completion of sexual activity, adequate lubrication and swelling response to sexual excitement | genital arousal disorder : absent or impaired genital sexual arousal (minimal vulval swelling or vaginal lubrification from any type of sexual stimulation, and reduced sexual sensations when genitalia are caressed). Subjective sexual excitement still occurs from nongenital sexual stimuli. | the presence of subjective arousal (sexual excitement) from nongenital stimuli (e.g. erotica, stimulation of the partner, receiving breast stimulation, kissing) is key to receiving the AUA Foundation diagnosis |
| female orgasmic disorder : persistent or recurrent delay or absence of orgasm after a normal sexual excitement phase | orgasmic disorder : lack of orgasm, markedly diminished intensity of orgasmic sensations, or marked delay or orgasm from any kind of stimulation, despite self-reported high sexual arousal or excitement | women with arousal disorders rarely or never experience orgasm and are frequently given a misdiagnosis of orgasmic disorder |
| type of sexual dysfunction | drug | comments |
| sexual desire/interest disorder, subjective and combined arousal disorders | bupropion (a dopamine and norepinephrine agonist) | in one small, four-months study, nondepressed, premenopausal women showed increased arousability and sexual response but not initial desireref |
| testosterone
(plus estrogen) |
in 6-months randomized trialsref1,
ref2,
ref3
(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), women had improved "total satisfying sexual activity" and improved
measures of desire and responses, as reported on questionnaires. No long-term
safety data on women lacking estrogen are available
a transdermal patch that delivers the equivalent to 300 mg of testosterone. At the end of 24 weeks, there was a 74% increase in total satisfying sexual activity scores in the testosterone group compared with 33% in the placebo group. Sexual desire scores improved by 56% and 29%, respectively, and personal distress scores decreased by 65% and 40%, respectively. Improvements were seen after at least 4 weeks of starting therapy and all were highly significant. Around 70% of women had at least some adverse reaction related to treatment, including site irritation (30%), as well as acne and hirsutism, observed in approximately 6% of the treated women. Deepening of the voice was reported in slightly > 2%. About 8% of treated women found the adverse events serious enough to drop out of the study. These adverse events were seen early in the study |
|
| dehydroepiandrosterone (a precursor of estradiol and testosterone) | data from trials involving women with adrenal insufficiency are conflictingref1, ref2, ref3. A study of perimenopausal women with reduced feelings of well-being and low level of desire showed no benefitref | |
| tibolone (an estrogenic, progestogenic, androgenic steroid) | data from small trials of postmenopausal women show improved sexual function, as compared with those receiving placebo or a regimen of 17b-estradiol (1 mg daily) plus norethindrone (1 mg daily). The drug has not been studied in women with diagnosed sexual dysfunction and is associated with a possible increased risk of breast cancerref | |
| phosphodiesterase inhibitors (sildenafil, tadalafil, vardenafil) | in large multicenter trials involving pre- and postmenopausal women, no benefit from sildenafil was reportedref | |
| yohimbine (a centrally acting noradrenergic agent) plus arginine (a precursor of nitric oxide) | in one randomized, controlled crossover laboratory study of 24 women, yohimbine (6 mg) plus arginine (6 g) increased vaginal congestion, but not subjective arousal, in response to an erotic filmref. | |
| ephedrine (agonist of a- and b-adrenergic receptors) | in one randomized, controlled crossover laboratory study of 20 women, yohimbine (50 mg) increased vaginal congestion, but not subjective arousal, in response to an erotic filmref. | |
| genital arousal disorder despite estrogen-replete status | phosphodiesterase inhibitors (sildenafil, tadalafil, vardenafil) | in one laboratory randomized trial, it was shown that only some women given a diagnosis of genital arousal disorder have demonstrably reduced genital congestion, and they alone showed evidence of benefit. It was not possible clinically to distinguish this subgroupref. In one randomized study of neurogenic genital arousal disorder from multiple sclerosis, treatment with sildenafil led to increased lubricationref. |
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.
Areas of uncertainty : a better understanding is needed of the endogenous
and environmental factors that mediate sexual desire and arousal. Randomized
clinical trials are also needed to assess the effects of psychological
and pharmacologic therapies alone and in combination. The risks and benefits
of long-term testosterone therapy require further study, including studies
of women with a complete loss of arousal and desire.
Guidelines : recommendations for the evaluation and management of sexual
dysfunction in women have been put forth by the American College of Obstetricians
and Gynecologists (Basson R. Sexuality and sexual disorders in women. Clinical
updates in women's health care monograph. Vol. 2. No. 2. Washington, D.C.:
American College of Obstetricians and Gynecologists, 2003:1-94), the Society
of Obstetricians and Gynaecologists of Canada (Blake J, Belisle S, Basson
R, et al. Canadian Consensus Conference on Menopause 2006 update. J Obstet
Gynecol Can 2006;28:Suppl:1-92), the North American Menopause Societyref,
and the members of the 2003 International Consensus on Sexual Medicine
(organized by the International Consultation on Urological Disease, the
International Society for Urology, and the International Society for Sexual
Medicine) (Basson R, Althof S, Davis S, et al. Summary of the recommendations
on sexual dysfunctions in women. J Sex Med 2004;1:24-34). These organizations
advocate attention to mental and overall health and to both interpersonal
and personal psychological issues. Local estrogen therapy is recommended
for dyspareunia that is associated with vulval atrophy that results in
reduced sexual motivation. The Society of Obstetricians and Gynaecologists
of Canada notes that testosterone therapy should be viewed as investigational
and should be prescribed only by clinicians who are knowledgeable about
sexual dysfunction in women (Blake J, Belisle S, Basson R, et al. Canadian
Consensus Conference on Menopause 2006 update. J Obstet Gynecol Can 2006;28:Suppl:1-92).
The recent position statement of the North American Menopause Society provides
cautious support for the use of testosterone "in appropriate post-menopausal
women via transdermal patches or topical gels or creams administered at
the lowest dose for the shortest time that meets treatment goals"ref.
Counseling about the potential risks and benefits of testosterone use is
also advocated, as is evaluation for causes of low levels of desire (including
physical and psychosocial factors and medications) before treatment.
Conclusions and Recommendations : for women with desire and arousal
disorders, such as the woman described in the vignette, the evaluation
involves taking a detailed history of sexual difficulties from both partners,
preferably seen individually as well as together. Also included are an
assessment of the woman's mental health (including self-image), feelings
about the relationship, medical history, and her thoughts and emotions
during sexual activity. On the basis of clinical experience and limited
data on outcomes, I would recommend a combination of cognitive behavioral
therapy and sex therapy (typically three to six sessions). Sessions should
be focused on altering maladaptive thoughts, unreasonable expectations,
and misinformation about women's sexuality, as well as on discussing strategies
for improving the couple's emotional closeness and communication and enhancing
erotic stimulation. If the couple is excessively focused on intercourse
(as is common if there is a history of infertility), they should be advised
to emphasize nongenital stimulation first. Any apparent interpersonal problems
should be addressed before further sexual therapy is pursued. At the present
time, I would not recommend any pharmacologic therapy, pending the availability
of more (and longer-term) data in support of such treatment.
antidepressants. There is no specific therapy at present, although electroconvulsive
therapy (ECT)
has resulted in clinical improvement in cases where there was concomitant
severe depressionref1,
ref2,
ref3.
typically dampens sex drive and patients with the greater amount of amygdala
left intact after surgery have a larger sex drive. It is intimately linked
to other brain regions, including the hypothalamus, which sets off physical
responses to arousal, such as erectionsref.
(in females) not due to a general medical condition.
due to ...
due to ...,
endometriosis,
uterine
prolapse,
PID,
neoplasms)).
The relatively easily achieved orgasm induced by the mechanism of asphyxia
is hypothesized to be the common reason for repetitive deviant asphyxiophilic
behavior. Moreover, in women of the ejaculatory type (female ejaculators),
the desire to induce ejaculatory orgasm by asphyxia may also come into
play as this kind of orgasm is usually assessed as sensation of greater
delight than orgasm without ejaculationref.
,
Treponema
pallidum subsp. pallidum,
Chlamydia
trachomatis,
Haemophilus
ducreyi,
and Neisseria meningitidis.
Other respiratory organisms such as streptococci, Haemophilus
influenzae,
and Mycoplasma
pneumoniae
could also be transmitted by this route. A link between oro-genital sex
and bacterial vaginosis is currently being studied. In view of the increased
practice of oral sex this has become a more important potential route of
transmission for oral, respiratory, and genital pathogensref.
through an ascending infectious route.