Transcript document

Psychotic Disorders of Later
Life
Epidemiology,
Classification, Treatment
and Prognosis
Background
• Term ‘paranoid’ still in popular use, but
incorrectly applied
• Refers to symptoms, personality types or
syndromes
• Can be qualitatively or quantitatively different
from ‘normal’
• KRAEPILIN: Association of paranoid
symptoms with sensitive pre-morbid
personalities (Sensitive BeziehungswahnKrestchmer)
• Freud: Proposed that origin was unconscious
from defence mechanisms of denial and
projection
Paranoid states/Delusional disorders
• Psychotic disorders without PRIMARY
mood-related, schizophreniform or organic
basis
• Characterised by acute/chronic course with
self-referential delusions, frequently fixed,
elaborated and systematised
• ‘Delusional disorder’ replaces ‘paranoid
state’ in ICD-10
• Derived from concept of ‘paranoia’
(KAHLBAUM 1863)
‘A primary delusional system remaining
unchanged for years’
• Modern concepts of delusional disorder are
broadly in keeping with this
Paranoid personality disorder
• Equates with ‘sensitive’ personality
• DSMIII-R defines it as:
 Pervasive tendency to interpret actions of
others as
deliberately demeaning/threatening
 Expects to be exploited/harmed by others
 Questions loyalty of friends
 Reads threats/insults into neutral actions
 Bears grudges over altercations
 Reluctant to confide in others for fear of
being betrayed
 Easily offended/angered by slights
 Questions fidelity of spouse/sexual
partners
Late-onset psychotic disorders
• KRAEPILIN (1912): Chronic fantastic
delusions and hallucinations noted
preservation of personality, lack of thought
disorder and preservation of volition that
distinguished it from schizophrenia
• Originally thought to hold an intermediate
position between schizophrenia and
paranoia
• ROTH (1955): ‘Late paraphrenia’. Wellorganised system of paranoid delusions
with/without auditory hallucinations with
preservation of personality and affective
response
• FISH (1960): ‘Senile schizophrenia’
• POST (1966): ‘Persistent persecutory
states of the elderly’
• ICD-9 (1970s): Paraphrenia
• ICD-10 (1990 TO DATE): Persistent
delusional disorder
PROBLEMS WITH
CLASSIFICATION
• Important to distinguish late-onset
delusional disorders from people with
schizophrenia who have become older
• American classificatory systems have used
age cut-off as 45 compared with 60/65 in
British systems
• Earlier classifications included mood
disorder, personality disorder and
symptoms of schizophrenia in definitions
• Often difficult to establish clinical picture
such as age of onset because, by definition,
sufferers often less amenable to interview
• Approximately 15%. 7% and 5% of people
with a lifetime history of schizophrenia
will develop the disorder after the ages of
45, 60 and 65 respectively
Epidemiology
• Late-onset delusional disorders have a
prevalence of between 2 and 4% of
psychiatric disorders for over-65s in the
community
• Incidence studies rare, but one study found
incidence of between 17 and 26 per
100,000
• Aetiological associations encompass
personality characteristics, genetic factors,
physical impairment and organic brain
disease
Pre-morbid personality
• Greater likelihood of paranoid/schizoid
personality disorder
• Persistent delusional disorder may represent
an accentuation of pre-existing paranoid
personality disorder
• Schizoid personality disorder characterised
by:
PERVASIVE INDIFFERENCE TO
SOCIAL RELATIONS
DECREASED RANGE OF EMOTIONAL
EXPRESSION
‘ECCENTRIC’, ‘ALOOF’, ‘COLD’
INDIFFERENT TO
PRAISE/CRITICISM
LACK OF CLOSE
FRIENDS/CONFIDANTES
Genetic factors
• Some evidence for genetic loading (Kay
1972)
• However, methodological problems
include:
Variability in diagnostic criteria
Unreliable information on family
pedigree Overinclusiveness of psychotic
phenomena
• Late-onset makes genetic studies
problematic
• HLA sub-types show some heritability in
persistent delusional disorder (HLA B37)
[Naguib et al 1987]
Socio-demographic factors
• Early postulated associations with unmarried status and low fertility (Post
1966), subsequent studies have not
confirmed this (Kay and Roth 1961)
• Social isolation has a consistent association
with persistent delusional disorder,
suggested as a consequence of maladaptive
personality traits (Kay 1972), BUT social
isolation of onset in later life also
implicated (Almeida et al 1995)
• Excess of females with persistent
delusional disorder (Ranges from 3:1 to
45:2). Not simply a reflection of later onset
of psychotic disorder in women. Theories
include an excess of Dopamine receptors
in older women and delayed onset of
psychotic disorder through early use of
coping mechanisms
• Association with social class not
informative
Sensory impairment
• Experimental hearing loss associated with
paranoid symptoms and auditory hallucinations
• Hearing impairment present in upto 40% of
people with persistent delusional disorder
• Earlier onset may be related to social isolation
and suspiciousness
• Psychotic symptoms may be diminished after
improving hearing
• Some limited evidence for an association with
visual impairment
Organic brain disease
• Classically, late-onset psychotic disorders
have been associated with Organic Brain
Disease, but the majority of clinical
longitudinal studies provided little
evidence for a significant association
• Neuro-imaging studies HAVE found strong
associations between persistent delusional
disorder and cerebrovascular lesions,
cortical atrophy and ventricular
enlargement (Almeida et al 1995)
• A variety of neurological ‘soft signs’ have
been associated with persistent delusional
disorder (e.g. signs of extrapyramidal and
frontal lobe damage)
Clinical features
• Presence of elaborated/systematised delusions
is common in persistent delusional disorder
• Delusions of persecution/reference frequent.
Sexual themes not uncommon. Passivity
phenomena in up to 40%
• Relative preservation of personality/absence of
‘negative symptoms
• Auditory hallucinations can be conspicuous,
but not essential for diagnosis (2nd/3rd
person/olfactory/tactile)
• Depressive symptoms do not predominate
clinical picture
• Some evidence for mild cognitive impairment
associated with persistent delusional disorder.
One study has found that greater number of
psychotic symptoms associated with less
severe cognitive impairment
• Influence of pre-occupation with psychotic
symptoms, poor cooperation and side-effects
of neuroleptic drugs have to be taken into
account
Differential Diagnosis
(What else could it be?)
• Severe depressive disorder: Delusions
often have different content, e.g. nihilistic,
worthlessness, guilt. Also, presence of
other depressive symptoms and other clues
in history/mental state examination
• Dementia: Delusions and hallucinations
occur in up to 15% of sufferers, but
cognitive impairment progressive and
delusions more fleeting/fragmented
• Schizo-affective disorder: Presence of
symptoms typical of both mood disorder
and schizophrenia but core elaborated
delusional system more prominent than
mood-related symptoms
• Transient paranoid
reactions/personality disorder/organic
psychoses /drug-induced psychoses
Management
• More helpful to assess in person’s home,
since delusions may be situation-specific
• Sufferers often known to neighbours,
police, social services, other public bodies
• Rapport difficult to achieve initially
• Remediable factors such as hearing
impairment may bring about significant
reduction in severity of psychosis
• Social interventions may not be successful,
particularly if life-long solitariness
• Hospital admission may result in
‘honeymoon period’
Drug Treatment
• Placebo-controlled trials are rare
• Most studies of traditional neuroleptics
have found improvement in psychotic
symptoms (27% to 66%)
• Successful remission/partial remission
more difficult to achieve than in patients
with schizophrenia who have grown older
• Presence of accompanying physical illness,
altered metabolism/receptor sensitivity,
polypharmacy, variable compliance and
cognitive impairment are all complicating
factors
• Oral neuroleptics at 10 to 25% of
conventional dose used
• Low dose depot neuroleptics beneficial
(esp. compliance)
• Atypical neuroleptics minimise risk of
extrapyramidal side-effects
Outcome
• Most people follow a chronic course;
complete remission rare
• Marked reductions in psychotic symptoms,
however, can be achieved
• Progression of cognitive impairment not as
fast as in dementia
• Risk of tardive dyskinesia kept lower by
smaller doses of neuroleptics/use of atypical
antipychotics
• Most people kept on caseloads of community
teams for considerable lengths of time in
view of poor integration into community
(i.e. problems with neighbours etc)
Reading List
•Articles
•Almeida, O.P., Howard, R.J., Levy, R., David, A.S.
(1995) Psychotic states arising in later life.
Psychopathology and nosology and The role of risk
factors. British Journal of Psychiatry 166, 205-228
• Hymas, N., Naguib, B., Levy, R. (1989) Late
paraphrenia: a follow-up study. International Journal of
Geriatric Psychiatry 4, 23-29
•Howard, R., Almeida, O.P, Levy, R. (1994)
Phenomenology, demography and diagnosis in
late
paraphrenia. Psychological Medicine 24, 397-410
BOOKS
•Naguib, M, & Levy, R. (1995) Paranoid states in the
elderly and late paraphrenia. In Jacoby, R. &
Oppenheimer, C. (Eds) Psychiatry in the elderly. Oxford
University Press, Oxford
•Howard, R (1997) Drug treatments in paranoid states of
the elderly. In: C Holmes and R Howard (Eds), Advances
in Old Age Psychiatry: Chromosomes to Community Care.
Wrightson Biomedical Publishing, London.