GERIATRIC PSYCHIATRY

According to Ukrainian and foreign

authors, from 10 to 25 % of all the
people older 60-65 suffer from mental
disorders with various severity
Etiology and pathogenesis
•1. neuroendocrine shifts caused by climacteric;
•2. various functional and structural changes in all the
systems and organs caused by aging;
•3. accumulation of somatic diseases and age-specific
ailments;
•4. a peculiar social-psychological situation in which an
aging person finds himself (discontinuation of his
occupational activity, narrowing of social relations,
isolation because of death of his relatives, impossibility to
satisfy most of his interests and requirements, difficulties
in self-service);
•5. psychological aging, changes in the character occurring
in the process of involution (a decrease of the emotional
background, scantier interests and their shift to the sphere
of material welfare and physical well-being, anxious over-
anxiousness about one’s health, conservatism,
suspiciousness, inertia of mental processes).
• The above peculiarities in mental
disorders of the presenile and senile age
contributed to isolation of a specific
branch of psychiatry, gerontological
psychiatry, as well as to organization of
specialized psychiatric aid to old
patients: gerontological departments,
hospices in mental hospitals, boarding-
houses for old people suffering from
mental disorders.
Classification
In psychiatry, the age of 45-60 years is regarded as
presenile, and after 60 senile. Mental disorders of
the old age are classified in the following way:
1. Nonpsychotic mental disorders of involutional
genesis
2. Functional psychoses of the old age:
- involutional depression (melancholia)
- involutional paranoid
•3. Atrophic (degenerative) cerebral diseases:
- Alzheimer’s disease
- Pick’s atrophy
- Senile dementia
Nonpsychotic mental disorders of involutional genesis

•Menopause may be considered, at the same

time, both as a physiological, normal state and as a
morbid one.
The climacteric syndrome develops in 20-30 % of
women.
•The physiological character of climacteric is
determined by its regularity, while morbidity by
persistent abnormalities in the systems which
control vital activity with a resultant reduction in
the adaptive abilities of the organism.
In the physiological climacteric, a reconstruction of
the organism caused by discontinuation of the
hormonal function of the gonads takes place
gradually and is accompanied by adaptation of the
soma and mind to new life conditions.
Pathological climacteric
•In the pathological climacteric, neuroendocrine
shifts are rougher, the activity of diencephalic
formations is affected and accompanied by a
hyperfunction of the thyroid gland.
•The rate and expressiveness of climacteric
symptoms depend upon biological, cultural and
socioeconomic factors, such as significance of
menses for some ethnic groups, a social position of
the female, an attitude to her as a sex partner, a
degree of a change in the role of the female in the
climacteric period and her ability to perform new
functions in the family and society.
•The dysharmonious climacteric most frequently
manifests itself by psychopathological, autonomic
and endocrine syndromes.
The climacteric syndrome most
frequently manifests by neurotic
symptoms:

• -asthenic
• - senesthopathic-hypochondriacal
• - anxious-depressive
• - hysteroform.
Asthenic Syndrome
• Hypersthenic stage Asthenic stage
Autonomic disturbances.
•- autonomovascular paroxysms like hot flushes,
skin hyperaemia, sensations of fever or chill,
palpitation, dizziness, fluctuations of blood
pressure and pulse recur often during a day and
are very unpleasant for the patients.
•- there are faints and sleep disturbances: the
period of falling asleep becomes prolonged and
poignant, the sleep is superficial, with frequent
episodes of waking up and unpleasant dreams.
•- There are libido changes (it increases or oftener
decreases) and
•- a loss of appetite, sometimes a liking for a
certain kind of food develops.
The senestho-hypochondriacal syndrome
Senesthopathies are characterized by unpleasant
and unusual feelings in the body: the brain grows
soft, the muscles come off the bones, vesicles in
the lungs burst, etc. Particularly unpleasant are
various painful feelings in the region of external
sex organs. Senesthopathies, which often change
their localization, result in the appearance of
overvalued hypochondriacal ideas with increased
apprehension for one’s own health. Such women
would often visit out-patients clinics, take medical
advice of different doctors and sometimes cannot
believe that these hardly tolerable feelings are
caused by climacteric.
 The hysteroform syndrome
•Women with the hysteroform syndrome have an augmentation
of their emotional sensitivity and lability. Extremely typical are
complaints about the feeling of “a lump in the throat”, reduced
skin sensitivity of the “stocking”, “sock”, “waistcoat” type, they
“lose the use” of their legs. In the state of nervousness it is
difficult for them to speak, they develop stammering which is
uncommon for them.
•Some women have already had hysteroid streaks in their
character before, they are: an aspiration for being in the centre of
attention, egocentrism, increased autosuggestion,
ostentatiousness, theatricality of their behaviour. In this case it is
possible to say about some decompensation of hysteroid
psychopathy caused by climacteric.
•Clinical manifestations of neurotic disorders caused by
climacteric are characterized by polymorphism and changeability,
and often even the same woman develops the signs of 2 or even 3
syndromes.
•The prognosis of climacteric neurotic disorders
is favourable. The majority of patients make a
full recovery without any signs of disorders of
their psychic activity. In some women,
protracted neurosis-like disorders lead to a
pathological development of the personality.
•The treatment of climacteric neurotic
disorders is usually outpatient. General health
improving vitamin therapy is administered.
Sedatives and light stimulating phytodrugs are
recommended.
•Psychotherapy should take an important place
in the treatment of neurotic disorders.
Functional psychoses of presenile age
• Functional psychoses of the presenile age are
psychotic states which develop for the first time
at the presenile or old age, are supposedly
caused by a complex of factors (pathological
climacteric, the extreme type of the higher
nervous activity, a psychic trauma), directly or
indirectly related to aging, and do not result in
an expressed organic decrease in the level of the
personality or dementia
Etiology and pathogenesis
• Presenile psychoses result from an interaction of
biological, individual-psychological and social-
psychological age-specific factors.
• 75 % of the cases reveal heredity.
• Usually presenile psychoses develop at the age
of 45-55 years, some time after the beginning of
climacteric, in the majority of patients after the
beginning of menopause, in people with the
extreme type of higher nervous activity and
often following psychic traumas
Clinical picture
•Usually presenile psychoses develop slowly, little
by little, rarer subacutely. Sometimes acute
psychotraumatizing or somatogenic factors are
followed by an acute onset of the disease.
•The initial period of presenile psychoses is
characterized by neurotic symptoms or
aggravation of the personality peculiarities.
•Gradually there is development of psychotic
symptoms, the depressive and paranoid forms
being the most typical for presenile psychoses.
There is a certain relationship between premorbid
peculiarities of the personality and clinical
manifestations of presenile psychoses.
Presenile (involutive) depression
Usually develops slowly. The above neurosis-like
disorders are joined by exaggerated apprehension
for one’s own health, the health of her children,
husband, material welfare of the family. There is a
gradual increase of anxiety, accompanied by
asthenia in some patients, hypochondriacal
symptoms in others, or developing into the state
of agitation. Owing to polymorphism in clinical
manifestations of presenile depression, 3 main
syndromes typical for this form of presenile
psychosis are distinguished: astheno-depressive
and astheno-hypochondrical syndromes and
agitated depression.
Presenile (involutive) paranoid
•begins slowly, gradually with neurosis-like symptoms,
passing to the subpsychotic and psychotic level.
•Sometimes their relatives do not notice an inadequacy
in the patients’ behaviour for years and attribute some
singularities to age-specific changes, unsociability, over-
anxiousness about one’s health.
•In the process of the development of the disease the
patients begin to bear grudges against their neighbours
or relatives because of a loss of their belongings and
foodstuffs. The suspiciousness and mistrustfulness
increase.
•The most typical ones are delusions of persecution and
damage
Course and prognosis
•begins slowly, gradually with neurosis-like symptoms,
passing to the subpsychotic and psychotic level.
•Sometimes their relatives do not notice an inadequacy
in the patients’ behaviour for years and attribute some
singularities to age-specific changes, unsociability, over-
anxiousness about one’s health.
•In the process of the development of the disease the
patients begin to bear grudges against their neighbours
or relatives because of a loss of their belongings and
foodstuffs. The suspiciousness and mistrustfulness
increase.
•The most typical ones are delusions of persecution and
damage
Treatment
• Complex
• To treat psychotic syndrome – antypchotic
therapy
• To treat comorbid somatic (arterial
hypertension, atherosclerosis, heart rhythm
disturbances and gastrointestinal tract)
 ALZHEIMER DISEASE = AD
It was first described by, and later named after,
German psychiatrist and pathologist Alois
Alzheimer in 1906. In 2015, there were
approximately 29.8 million people worldwide with
AD.
Two types:
- Early –onset AD
- Later –onset AD = senile dementia
It most often begins in people over 65 years of
age, although 4% to 5% of cases are early-onset
Alzheimer's which begin before this. It affects
about 6% of people 65 years and older. In 2015,
dementia resulted in about 1.9 million deaths.
Causes
1. The genetic heritability of AD, based on
reviews of twin and family studies, ranges from
49% to 79%. Around 0.1% of the cases are
familial forms autosomal dominant inheritance
early-onset AD. Most cases of Alzheimer's
disease do not exhibit autosomal-dominant
inheritance and are termed sporadic AD, in
which environmental and genetic differences
may act as risk factors. The best known genetic
risk factor is the inheritance of the ε4 allele of
the apolipoprotein E (APOE).
2. The oldest, on which most currently available
drug therapies are based, is
the cholinergic hypothesis, which proposes that
AD is caused by reduced synthesis of
the neurotransmitter acetylcholine.
3. In 1991, the amyloid hypothesis postulated that
extracellular amyloid beta (Aβ) deposits are the
fundamental cause of the disease. The theory
holds that an amyloid-related mechanism that
prunes neuronal connections in the brain in the
fast-growth phase of early life may be triggered by
ageing-related processes in later life to cause the
neuronal withering of AD.
4. Tau protein abnormalities initiate the disease
cascade. It forms neurofibrillary tangles inside
nerve cell bodies. When this occurs,
the microtubules disintegrate, destroying the
structure of the cell's cytoskeleton which collapses
the neuron's transport system. This may result first
in malfunctions in biochemical communication
between neurons and later in the death of the
cells
5. The cellular homeostasis of biometals such as
ionic copper, iron, and zinc is disrupted in AD,
though it remains unclear whether this is
produced by or causes the changes in proteins.
6. An infection with Spirochetes in gum
disease may cause dementia and may be involved
in the pathogenesis of Alzheimer's disease
Clinical types of AD
Clinical Features Presenile = early onset AD Senile = later –onset AD

Age 45-60 years More then 60

Beginning Depression, because patients Cognitive deficit, intensification

understand there cognitive deficit of the negative personal
features

Clinically Cognitive disturbances like agnosia, Memory disturbances

apraxia, aphasia

Course Quick development of marasmus Slow development of marasmus

 Clinical manifestations of later-onset AD
usually develops at the age of 65-85 years.
The onset is almost always slow, insidious, with characterological changes.
•The latter resemble personality shifts which are typical for the natural aging but differ from
them with expressiveness, exaggeration, a more rapid progressing. At the initial stage,
individual psychological peculiarities become sharper, and later smooth down. Grotesque
egocentrism, hard-heartedness, miserliness, collecting of old unnecessary things are peculiar
to such patients. They lose former interests and passions, with a simultaneous disinhibition
of elementary biological needs.
•Their appetite becomes voracious.
•A peculiar hypersexuality develops in the form of an increased interest to young people of
the opposite sex, a disposition to talks on erotic subjects, and sometimes attempts of lewd
acts with juveniles.
•On the whole, the emotional life becomes still more and more primitive, monotonous.
•Even the initial stage of the illness develops signs of cognitive deficite
•The mood at earlier stages is characterized by sullenness, constant dissatisfaction and
querulousness which later give place to dull carelessness and euphoria.
•Typically, the sleep formula is distorted: continuous daytime sleep is combined with night
insomnia accompanied by fussiness, aimless walking.
•The patients’ behaviour in the beginning of the development of the cerebral-atrophic
process of mental deficiency is relatively organized. Gradually they become more and more
fussy, confused, helpless in their everyday life, slovenly and unable for self-service.
Thinking
•begin with difficulties in abstracting, generalizing and revealing
casual relations, increase and reach to the lack of understanding
the simplest questions, an inability to comprehend the
surrounding situation.
•For a comparatively long period of time the speech remains
regular, but with time it is roughly impaired too, turning into a
meaningless garrulity.
•The perception gradually becomes still more defective, diffuse.
Memory
•fixation amnesia, first leading to disorientation in time, and then
in the surroundings . With time, the memory is devastated to
such an extent that the patients do not know where they live,
how many children they have got, do not remember their names,
are not able to say how old they are and what their occupation
is. Spotty memory defects are often filled with false recollections
(pseudoreminiscences), and later with substituting
confabulations.
•Subsequent memory disturbances develop according to
regularities of progressive amnesia.
Psychotic symptoms of senile
dementia
•In the majority of patients with senile dementia no
psychotic disorders are observed .
• Some 10 % of the patients develop psychoses (the
psychotic form of senile dementia), usually at relatively early
stages of the illness.
•More common are small-scaled delusions of damage,
persecution, robbery, poisoning. In rarer cases, there are
hallucinations, hallucinatory-delirious states, paraphrenic
states with delusions and confabulations having some
fantastic content.
•With progressing of the dementia, the productive psychotic
symptoms become scantier, fragmentary and finally
disappear.
 Early-onset AD
I STAGE - Pre-dementia
The first symptoms are often mistakenly attributed to ageing or stress . Detailed neuropsychological
testing can reveal mild cognitive difficulties up to eight years before a person fulfils the clinical criteria
for diagnosis of AD. These early symptoms can affect the most complex activities of daily living. The
most noticeable deficit is short term memory loss, which shows up as difficulty in remembering
recently learned facts and inability to acquire new information. Subtle problems with the executive
functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic
memory (memory of meanings, and concept relationships) can also be symptomatic of the early stages
of AD. Apathy can be observed at this stage, and remains the most
persistent neuropsychiatric symptom throughout the course of the disease. Depressive symptoms,
irritability and reduced awareness of subtle memory difficulties are also common. The preclinical stage
of the disease has also been termed mild cognitive impairment (MCI). This is often found to be a
transitional stage between normal ageing and dementia. MCI can present with a variety of symptoms,
and when memory loss is the predominant symptom, it is termed "amnestic MCI" and is frequently
seen as a prodromal stage of AD.
II STAGE Early AD
In people with AD, the increasing impairment of learning and memory eventually leads to a definitive
diagnosis. In a small percentage, difficulties with language, executive functions, perception (agnosia), or
execution of movements (apraxia) are more prominent than memory problems.[ AD does not affect all
memory capacities equally. Older memories of the person's life (episodic memory), facts learned
(semantic memory), and implicit memory (the memory of the body on how to do things, such as using a
fork to eat or how to drink from a glass) are affected to a lesser degree than new facts or memories.
Language problems are mainly characterised by a shrinking vocabulary and decreased word fluency,
leading to a general impoverishment of oral and written language.[29][32] In this stage, the person with
Alzheimer's is usually capable of communicating basic ideas adequately. While performing fine motor
tasks such as writing, drawing or dressing, certain movement coordination and planning difficulties
(apraxia) may be present, but they are commonly unnoticed.[ As the disease progresses, people with AD
can often continue to perform many tasks independently, but may need assistance or supervision with
the most cognitively demanding activities.
III STAGE Moderate
progressive deterioration eventually hinders independence, with subjects being
unable to perform most common activities of daily living. Speech difficulties
become evident due to an inability to recall vocabulary, which leads to frequent
incorrect word substitutions (paraphasias). Reading and writing skills are also
progressively lost. Complex motor sequences become less coordinated as time
passes and AD progresses, so the risk of falling increases. During this phase,
memory problems worsen, and the person may fail to recognise close relatives.
Long-term memory, which was previously intact, becomes impaired. Behavioural
and neuropsychiatric changes become more prevalent. Common manifestations
are wandering, irritability and labile affect, leading to crying, outbursts of
unpremeditated aggression, or resistance to caregiving. Sundowning can also
appear. Approximately 30% of people with AD develop illusionary
misidentifications and other delusional symptoms. Subjects also lose insight of
their disease process and limitations (anosognosia).[Urinary incontinence can
develop. These symptoms create stress for relatives and carers, which can be
reduced by moving the person from home care to other long-term care facilities
IV – STAGE Advanced
During the final stages, the patient is completely dependent upon
caregivers. Language is reduced to simple phrases or even single words, eventually
leading to complete loss of speech. Despite the loss of verbal language abilities,
people can often understand and return emotional signals. Although
aggressiveness can still be present, extreme apathy and exhaustion are much more
common symptoms. People with Alzheimer's disease will ultimately not be able to
perform even the simplest tasks independently; muscle mass and mobility
deteriorates to the point where they are bedridden and unable to feed
themselves. The cause of death is usually an external factor, such as infection
of pressure ulcers or pneumonia, not the disease itself
Diagnosis
Alzheimer's disease is usually diagnosed based on the person's medical history,
history from relatives, and behavioural observations. The presence of
characteristic neurological and neuropsychological features and the absence of
alternative conditions is supportive.Advanced medical imaging with computed
tomography (CT) or magnetic resonance imaging (MRI), and with single-photon
emission computed tomography (SPECT) or positron emission tomography (PET)
can be used to help exclude other cerebral pathology or subtypes of
dementia. Moreover, it may predict conversion from prodromal stages (mild
cognitive impairment) to AD
Assessment of intellectual functioning including memory testing can further
characterise the state of the disease. Medical organisations have created
diagnostic criteria to ease and standardise the diagnostic process for practising
physicians. The diagnosis can be confirmed with very high accuracy post-
mortem when brain material is available and can be examined histologically
Pick's disease
is a for a group of neurodegenerative diseases with
symptoms attributable to frontal and temporal lobe
dysfunction. Common symptoms that are noticed early
are personality and emotional changes, as well as
deterioration of language. A defining characteristic of
the disease is build-up of tau proteins in neurons,
accumulating into silver-staining, spherical aggregations
known as "Pick bodies".
•was described by A. Pick in the end of the 19th century.
•Usually it begins at the age of 40-65 years. Particularly
often its first manifestations appear at 55-60. It is
characterized clinically by changes in personality early in
the course, deterioration of social skills, emotional
blunting, behavioral disinhibition, and prominent
language abnormalities.
•The initial stage of Pick’s atrophy, unlike AD, is characterized by
prevalence of emotional-volitional disturbances, rather than those of the
intellectual-mnestic sphere. Particularly typical is lack of
spontaneousness: indifference, passiveness, absence of any inner drives
for activity with preservation of a capacity for actions under the influence
of external stimuli. Rarer is a syndrome clinically resembling the picture of
progressive paralysis in the form of a reduced moral-ethic level of the
personality, carelessness, euphoria, disinhibited drives, uncritical attitude
to one’s own behaviour (the pseudoparalytic syndrome).
•One of the differences of Pick’s atrophy from Alzheimer’s disease is the
prevalence of an increasing intellectual insufficiency (weakening of
abilities to generalize and abstract, form adequate judgements and
conclusions, reveal causal relationships) over memory disturbances.
Expressed abnormalities of the memory appear late, amnestic
disorientation is absent.
Language and neurological changes, such as:
• reduced writing or reading skills
• echoing, or repeating what’s been said to you
• inability to speak, difficulty speaking, or trouble understanding speech
• shrinking vocabulary
• accelerated memory loss
• physical weakness
Treatment
•The principles of treating senile dementia, Alzheimer’s disease and Pick’s
atrophy practically do not differ. No methods of treatment capable of
arresting the process of mental deficiency have been found yet.
•In the brain, neurons connect and communicate at synapses, where tiny
bursts of chemicals called neurotransmitters carry information from one cell
to another. Alzheimer's disrupts this process, and eventually destroys
synapses and kills neurons, damaging the brain's communication network.
•The main groups medications to treat the symptoms of Alzheimer's
disease:
•- Cholinesterase inhibitors work by slowing down the process that breaks
down a key neurotransmitter. Donepezil, galantamine and rivastigmine are
cholinesterase inhibitors.
•- Memantine is an NMDA (N-methyl-D-aspartate) receptor antagonist,
which works by regulating the activity of glutamate, an important
neurotransmitter in the brain involved in learning and memory. Attachment
of glutamate to cell surface "docking sites" called NMDA receptors permits
calcium to enter the cell. This process is important for cell signaling, as well
as learning and memory. In Alzheimer’s disease, however, excess glutamate
can be released from damaged cells, leading to chronic overexposure to
calcium, which can speed up cell damage. Memantine helps prevent this
destructive chain of events by partially blocking the NMDA receptors.
•Medications to treat the symptoms of Alzheimer's disease are donepezil,
galantamine, memantine, rivastigmine
 Parkinson's disease (PD)
is a long-term degenerative disorder of the CNS that mainly affects the motor
system. The cause of Parkinson's disease is generally unknown, but believed to
involve both genetic and environmental factors. Those with a family member
affected are more likely to get the disease themselves. There is also an increased
risk in people exposed to certain pesticides and among those who have had
prior head injuries, while there is a reduced risk in tobacco smokers and those
who drink coffee or tea.
The motor symptoms of the disease result from the death of cells in
the substantia nigra, a region of the midbrain. This results in not
enough dopamine in these areas. The reason for this cell death is poorly
understood, but involves the build-up of proteins into Lewy bodies in
the neurons. Diagnosis of typical cases is mainly based on symptoms, with tests
such as neuroimaging being used to rule out other diseases.
The symptoms generally come on slowly over time. Early in the disease, the
most obvious are shaking, rigidity, slowness of movement, and difficulty with
walking.
Behavior and mood alterations are more common in PD without cognitive
impairment than in the general population, and are usually present in PD with
dementia. The most frequent mood difficulties are depression, apathy,
and anxiety.
The most common cognitive deficit in PD is executive dysfunction, which can include
problems with planning, cognitive flexibility, abstract thinking, rule acquisition, inhibiting
inappropriate actions, initiating appropriate actions, working memory, and control of
attention.]Other cognitive difficulties include slowed cognitive processing speed,
impaired recall and impaired perception and estimation of time. Nevertheless, improvement
appears when recall is aided by cues. Visuospatial difficulties are also part of the disease,
seen for example when the individual is asked to perform tests of facial recognition and
perception of the orientation of drawn lines. A person with PD has two to six times the risk of
dementia compared to the general population.
Punding in which complicated repetitive aimless stereotyped behaviors occur for many hours
is another disturbance caused by anti-Parkinson medication.
Hallucinations or delusions occur in approximately 50% of people with PD over the course of
the illness, and may herald the emergence of dementia. These range from minor
hallucinations – "sense of passage" (something quickly passing beside the person) or "sense
of presence" (the perception of something/someone standing just to the side or behind the
person) – to full blown vivid, formed visual hallucinations and paranoid ideation. Auditory
hallucinations are uncommon in PD, and are rarely described as voices. It is now believed that
psychosis is an integral part of the disease. A psychosis with delusions and
associated delirium is a recognized complication of anti-Parkinson drug treatment and may
also be caused by urinary tract infections (as frequently occurs in the fragile elderly), but
drugs and infection are not the only factors, and underlying brain pathology or changes in
neurotransmitters or their receptors (e.g., acetylcholine, serotonin) are also thought to play a
role in psychosis in PD.
Treatment

The main families of drugs useful for treating

motor symptoms are levodopa (always combined
with a dopa decarboxylase inhibitor and
sometimes also with a COMT inhibitor), dopamine
agonists (pramipexole) and MAO-B inhibitors
(seleginin).
• Also, quetiapine for psychosis,
• cholinesterase inhibitors for dementia
• modafinil for daytime sleepiness