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| Epidemiology |
��" Oxford Textbook of psychiatry", 2 nd
edition ���_�a�ϸ����o�Ͳv����]�G
(1)differences in diagnositic criteria
(2)differences in migration: more able to tolerate extreme isolation
(3)differences in methods of case-finding
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| Acute syndrome |
��" Oxford Textbook of psychiatry", 2 nd
edition 1.Behavior: preoccupation, social withdraw, smile or laugh
without obvious reason
2.Thought disorder: vagueness, concrete thought
3.Stream of thought disorder: pressure of thought, poverty, blocking
4.Loosening of association: illogical, talking past the
point(Vorbeireden), verbigeration, paraphrases, neologism
5.Mood abnormalities:
(1)anxiety, depression, irritability, euphoria
(2)blunting of affect
(3)incongruity of affect
6.Auditory hallucinations: Gedankenlautwerden, écho
de la pensée
7.Delusional halluscinations
8.Delusions(characteristic): "Wahnstimmung"
(1)of persecution
(2)of reference
(3)of control
(4)about possession of thought
9.Orientation: normal, Attention: impaired
10.Insight: impaired
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| Chronic syndrome |
��" Oxford Textbook of psychiatry", 2 nd
edition 1.Schizophrenic defect state: negative features:
diminished volition
2.Disorders of movement:
(1)Catatonia: stupor, excitement
(2)Waxy flexibility(Catalepsy): symbolic significance
(3)Stereotypy(not goal-directed), Mannerism(goal-directed)
(4)Ambitendence(Ambivalence, Mitgehen, forced grasping , automatic
obedience)
3.Social behavior deterioration
4.Delusions with little emotion or "encapsulated"
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| Depressive symtoms |
��" Oxford Textbook of psychiatry", 2 nd
edition 1.Side effect of antipsychotics: not the full, motor
side-effects mistaken for depressive retardation
2.Response to recovery of insight
3.Intergral part of schizophrenia |
| Factors modifying the clinical features |
��" Oxford Textbook of psychiatry", 2 nd
edition 1.Social stimulation: Under-stimulation increases negative
symptoms....Over-stimulation precipitates positive symptoms
2.Social background: religious ��
3.Age
4.Low intelligence |
| History |
��" Oxford Textbook of psychiatry", 2 nd
edition 19c Einheitpsychose(Griesinger)����Classification(Morel)
1852 démence précoce(Morel):
withdrawl, odd mannerism, self-neglect, intellectual deterioration
1863 catatonia(Kahlbaum)
1871 hebephrenia(Hecker)
1893 dementia praecox(Kraepelin)
��It is commonly held that Kraepelin regarded dementia precox as
invariably progressing to chronic deterioration. However, he
reported that , in his series of cases, 13 percent recovered
completely, and 17 percent were ultimately able to live and work
without difficulty.
1911 schizophrenia(Bleuler)
��concerned less with prognosis and more with the mechanisms of
symptom formation
��Fundamental symptoms: associations, emotional reactions, autism
��Accessory symptoms: hallucinations, delusions, catatonia, abnormal
behaviors
1959 first rank symptoms(Schneider)
��not supposed to have any central psychopathological role, but
helping in diagnosis
��(1)auditory hallucinations:
hearing thoughts spoken aloud
hearing voices referring to himself / herself, made in the third
person
auditory hallucinations in the form of a commentary
(2)thought withdrawal, insertion and interruption
(3)thought broadcasting
(4)somatic hallucinations
(5)delusional perception
(6)feelings or actions experienced as made or influenced by external
agents
1960 Europe(Schneider's, narrower)����US(psychodynamic,
wider)
����the former:
high reliability in diagnosis, no apparent heritability, meet
criteria of mania
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| ��DSM-IV Diagnostic Criteria |
A. Characteristic symptoms: Two (or more) of the following, each present
for a significant portion of time during a 1-month period (or less if
successfully treated):
Delusions
Hallucinations
Disorganized speech (e.g., frequent derailment, incoherence)
Grossly disorganized or catatonic behavior
Negative symptoms (e.g., affective flattening, alogia, avolition)
Note: Only one Criterion A symptom is required if delusions are bizarre or
hallucinations consist of a voice keeping up a running commentary on the
person�s behavior or thoughts, or two or more voices conversing with each
other.
B. Social/occupational dysfunction: For a significant portion of the time
since the onset of the disturbance, one or more major areas of functioning
such as work, interpersonal relations, or self-care are markedly below the
level achieved prior to the onset (or when the onset is in childhood or
adolescence, failure to achieve expected level of interpersonal, academic,
or occupational achievement).
C. Duration: Continuous signs of the disturbance persist for at least 6
months. This 6-month period must include at least 1 month of symptoms (or
less if successfully treated) that meet Criterion A (i.e., active-phase
symptoms) and may include periods of prodromal or residual symptoms.
During these prodromal or residual periods, the signs of the disturbance
may be manifested by only negative symptoms or two or more symptoms listed
in Criterion A present in an attenuated form (e.g., odd beliefs, unusual
perceptual experiences).
D. Schizoaffective and Mood Disorder exclusion:
Schizoaffective Disorder
and Mood Disorder With Psychotic Features have been ruled out because
either (1) no Major Depressive, Manic, or Mixed Episodes have occurred
concurrently with the active-phase symptoms; or (2) if mood episodes have
occurred during active-phase symptoms, their total duration has been
brief, relative to the duration of the active and residual periods.
E. Substance /general medical condition exclusion:
The disturbance is not
due to the direct physiological effects of a substance (e.g., a drug of
abuse, a medication) or a general medical condition.
F. Relationship to a Pervasive Developmental Disorder: If there is a
history of Autistic Disorder or another Pervasive Developmental Disorder,
the additional diagnosis of Schizophrenia is made only if prominent
delusions or hallucinations are also present for at least a month (or less
if successfully treated).
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| ��ICD-10 Diagnostic Criteria |
The disturbance involves the most basic
functions that give the normal person a feeling of individuality,
uniqueness, and self-direction. The most intimate thoughts,
feelings, and acts are often felt to be known to or shared by
others, and explanatory delusions may develop, to the effect that
natural or supernatural forces are at work to influence the
afflicted individual's thoughts and actions in ways that are often
bizarre.
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| Although no strictly pathognomonic
symptoms can be identified, for practical purposes
it is useful to divide the above symptoms into
groups that have special importance for the
diagnosis and often occur together, such as:
(a) thought echo, thought insertion or
withdrawal, and thought broadcasting;
(b) delusions of control, influence, or passivity,
clearly referred to body or limb movements or
specific thoughts, actions, or sensations;
delusional perception;
(c) hallucinatory voices giving a running commentary
on the patient's behaviour, or discussing the
patient among themselves, or other types of
hallucinatory voices coming from some part of the
body;
(d) persistent delusions of other kinds that are
culturally inappropriate and completely impossible,
such as religious or political identity, or
superhuman powers and abilities (e.g. being able to
control the weather, or being in communication with
aliens from another world);
(e) persistent hallucinations in any modality, when
accompanied either by fleeting or half-formed
delusions without clear affective content, or by
persistent over-valued ideas, or when occurring
every day for weeks or months on end;
(f) breaks or interpolations in the train of
thought, resulting in incoherence or irrelevant
speech, or neologisms;
(g) catatonic behaviour, such as excitement,
posturing, or waxy flexibility, negativism, mutism,
and stupor;
(h) "negative" symptoms such as marked apathy,
paucity of speech, and blunting or incongruity of
emotional responses, usually resulting in social
withdrawal and lowering of social performance; it
must be clear that these are not due to depression
or to neuroleptic medication;
(i) a significant and consistent change in the
overall quality of some aspects of personal
behaviour, manifest as loss of interest,
aimlessness, idleness, a self-absorbed attitude, and
social withdrawal. |
|
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| Type I and Type II |
��Crow, T.J. (1980). Molecular pathology
of schizophrenia: More than one disease process? British Medical
Journal, 280, 66-68.
1.Acute schizophrenia, also known as Type I syndrome, is
characterized by the presence of positive symptoms (delusions,
hallucinations, and thought disorder) that are associated with an
increase in dopaminergic transmission. Type I symptoms tend to
respond well to neuroleptic treatment because these drugs are
dopamine antagonists, and therefore, may be reversible. Individuals
with the Type I syndrome also have a better prognosis than
individuals with the
2.Type II syndrome, which Crow argues is a more chronic form of
schizophrenia that is characterized by the presence of negative
symptoms. Because these symptoms are apparently unrelated to
dopaminergic transmission, and are instead thought to be associated
with structural brain abnormalities, such as enlarged ventricles,
neuroleptic treatment is often unsuccessful, and has actually been
found to exacerbate the negative symptoms.
While episodes of Type I symptoms may be followed by the
development of the Type II syndrome, explains Crow, Type II symptoms
may occur in the absence of the Type I syndrome.
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| Differential diagnosis |
Medical: Delirium
Neural: Dementia, Epilepsy(Temporal lobe)
Opioid: Medication, Alcohol, Drug
(����clouding of consciousness, disorientation)
Psychy:
1.Personality disorder
2.Mood disorder, esp. mania
(����degree and persistence, relation , previous episodes, family hx)
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| Psychopathology |
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1.���\��P�{�걡�ҵL�k�t�X�A�����һ�ê(Bleuler)�B�k�Q�P��ı���]���ʡ^�g���C
2.�y�z�f�z�Gdeficit/ non-deficit
3.���g�߲z�G�`�N�O�B�O�СB��������A�H�Ρu�]��(gating)��ê�v�A�ϸ��L��ĵı
4.���g�ѭ�G�����X�j�B����´��֡Bprefrontal lobe��y�q���
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6.���M�L�P��i��s�G��Ǧ]��70�H
7.���Ϭy��f�ǡG���]�{�N�ƦӼW�[
8.�P�f��]�G�h��]�e�f�ASNP(single nucleotide polymorphism)�@fine
mapping�A�ؼЦbearly intervention
9.Dopamine/Serotonin system, N-methyl-D-aspartate system
10.�����믫�f�z��s��Paradigm:
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�]�a�`����s�^�@ |
| Etiology |
��" Oxford Textbook of psychiatry", 2 nd
edition 1.Predisposing causes:
genetic
environmental
neurological
interpersonal and social
psychodynamic
2.Precipitating:
life eventts
3.Perpetuating:
social and family influences
"Neurodevelopmental hypothesis"
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| 1.Genetics |
1.Family studiies: 5% lifetime risk
2.Twin studies
��Concordance rate: 50% in MZ, 10% in DZ
(1)environmental factors
(2)genetic susceptibility, the same, but not expressed
(3)differential gene expression3.Adoption studies: supports the
genetic hypothesis
4.Modes of inheritance
5.Molecular genetic studies (linkage analysis, candidate gene) |
| 2.Neuroanatomy |
1.enlargement of lateral ventricles, esp.
anterior, temporal horns
2.reduction of medial temporal structures, esp. hippocampus,
parahippocampal gyrus
3.more evident in left side of brain
4.cytoarchitectural disturbances in the hippocampus, frontal cortex,
cingulate gyrus, entorhinal cortex, not associated with gliosis
����disturbances in late migration/differentiation of neurons,
lateralization
5.reductions in the volume of temporal lobe(MRI) |
| 3.Clinical Neurology |
1.Soft signs: in stereognosis,
graphaeshesia, balance, propioception
2.Movement disorder
3.Temporal lobe epilepsy, Huntington's chorea |
| 4.Neurophysiology |
EEG:
����theta activity, fast activity, paroxymal activity
����P300 reponseFunctional imaging: Hypovascularity in PET& SPET
1.Hypofrontality, impaired WCST
2.Left dorsolateral prefrontal cortex, psychomotor poverty syndrome
3.MZ: all affected have decreased prefontal flow and reduced
hippocampal volume
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| 5.Neuropsychology |
1.Attension deficit
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| 6.Biochemistry |
The dopamine hypothesis 1.Amphetamine
releases dopamine at central synapses
2.Antipsychotic drugs share dopamine receptor blocking effects |
| 7.Neurodevelopmental |
1.Perinatal factors
(1)obsteric complications:
pre-existing brain dysfunction may predispose to the development of
obsteric complications.
(2)season of birth:
8 % excess in winter birth, perhaps viral in origin2.Childhood
development and antecedents
��passive as a baby, short attention span as a child, fast recovery
of galvanic skin reponses
3.Personality factors
��schizoid/schizotypal personality
��difficult to distinguish between premorbid/prodromal symptoms
��more common among schizo p't and 1 deg relatives
4.Sex and age of onset
��earlier in men than in women, determining prognosis |
| 8.Psychoynamic factors |
1.Freud: "On narcissism" ��libido was
withdrawn from external objects and attached to the ego. The result
was exaggerated self-importance.
2.Klein:
��only late did the child realize that the same person could be
good at one time and bad at another. |
| 9.Family factor |
1.Deviant role relationships:
��"Schizophrenogenic mother"
��marital skew: complete yield to another
marital schism: contrary views
2.Disordered family communication
��"double blind": an instruction given overtly, but is
contradicted by a second more cover instruction.
��amorphous/fragmented communications
��an association between abnormal social communication in parents
and schizophrenic illness in children may, in fact, be a consequence
of a shared genetic inheritance. |
| 10.Social factors |
1.Culture
2.Occupation and social class: over-represented in lower social
class
3.Place of residence: over-represented in disadvantaged inner-city
areas
4.Migration
(1)Social selection: those unsettled people are becoming mentally
ill
(2)Social causation: the effects of new environment
5.Psychosocial stresses |
| Prognostic factors |
��Overall, 1/3 of patients achieve
significant and lasting improvement; 1/3 improve some but have
intermittent relapses and residual disability; and 1/3 are severely
and permanently incapacitated.
��Factors associated with a good prognosis include relatively good
premorbid functioning, late and/or sudden onset of illness, a family
history of mood disorders rather than schizophrenia, minimal
cognitive impairment, and paranoid or nondeficit subtype.
��Factors associated with a poor prognosis include early age of
onset, poor premorbid functioning, a family history of
schizophrenia, and disorganized or deficit subtype with many
negative symptoms. Men have poorer outcomes than women; women
respond better to treatment with antipsychotic drugs. |
| Social environment and course |
1.Cultural background 2.Life events
3.Social stimulation
��While an understimulating hospital environment is associated with
worsening of the so-called poverty syndrome, and overstimulating
environment can precipitate florid symptoms and lead to relapse.
4.Family life
��"high expressed emotion" (making critical comments, expressing
hostility, showing signs of emotional over-involvement) & relapse
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| ��Neuroleptic Malignant Syndrome: 5 criteria: |
1.Recent treatment with neuroleptics within past 1-4 weeks
2.Hyperthermia (above 38C)
3.Muscular rigidity
4.At least 5 of the following:
Change in mental status
Tachycardia
Hypertension or hypotension
Diaphoresis or sialorrhea
Tremor
Incontinence
Increased creatinine phosphokinase (CPK) or urinary myoglobin
Leukocytosis
Metabolic acidosis
5.Exclusion of other drug-induced, systemic, or neuropsychiatric illness
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| ��Neuroleptic Malignant Syndrome:Tx: |
��aggressive supportive care (rhabdomyolysis ��vigorous hydration and
alkalinize the urine with IV NaHCO3 to prevent renal failure)
��Dopamine agonists: Bromocriptine, Amantadine, Levodopa
��Skeletal muscle relaxant: Dantrolene |
| ��The rabbit syndrome |
��a neuroleptic induced extrapyramidal side effect with late onset,
consists of rapid fine rhythmic movements of the lips that mimic the
chewing movements of a rabbit.
��Unlike the buccolingual movements of the tardive dyskinesia, the rabbit
syndrome improves with antiparkinsonian medication. The condition is
reported to be rare.
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| ��restless legs syndrome (RLS) |
��Centrally acting dopamine receptor antagonists reactivate symptoms when
given to patients with the syndrome. Results of single-photon emission
computed tomography (SPECT) have suggested deficiency of dopamine D2
receptors. Sympathetic hyperactivity also has been implicated on the basis
of observations that sympathetic nerve blockade relieves periodic limb
movements of sleep and that alpha-adrenergic blockers improve symptoms of
RLS. Studies also have suggested possible underactivity of the serotonin
and gamma-aminobutyric acid (GABA) neurotransmitter systems.
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| ��restless legs syndrome (RLS): criteria |
��The criteria for diagnosis of RLS are based on those developed by the
International Legs Syndrome Study Group in 1995; 4 basic elements must be
present to make the diagnosis. They are as follows:
1. A compelling urge to move the limbs, usually associated with
paresthesias/dysesthesias
2. Motor restlessness, as seen in activities such as floor pacing, tossing
and turning in bed, and rubbing the legs
3. Symptoms worse or exclusively present at rest (ie, lying, sitting) with
variable and temporary relief on activity
Circadian variation of symptoms, which are present in the evening and at
night. Often, symptoms are relieved after 5:00 am. 4. In more severe
cases, symptoms can be present throughout the day without circadian
variation. |
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