Lecture no.

5
Organic, including symptomatic,
mental disorders
 Content
Organic, including symptomatic, mental disorders
1. Dementia
1.2 Dementia in Alzheimer disease
1.3 Vascular dementia
1.4 Mixed dementia
1.5 Degenerative dementia
1.6 Infectious dementia
1.7 Dementia in other somatic ilnesses
2. Organic amnesic syndrome, not induced by alcohol and other psychoactive
substances
3.Delirium, not induced by alcohol and other psychoactive substances
4. Other mental disorders due to brain damage and dysfunction and to physical
disease
4.1 Organic hallucinosis
4.2 Organic mood (affective) disorder
4.3 Mild cognitive disorder
5. Personality and behavioural disorders due to brain disease, damage and
dysfunction
5.1Organic personality disorder
5.2Postencephalitic syndrome
5.3 Postconcussional syndrome
 Organic, including symptomatic,
mental disorders
• Neurocognitive disorders:
– Memory impairment, especially recent memory;
– Aphasia (failure of language function);
– Apraxia (failure of ability to execute complex
motor behavior);
– Agnosia (failure to recognize or identify people or
objects);
– Disturbances in executive function: impairment in
the ability to think abstractly and plan such
activities as organizing, shopping and maintaining
a home.
 1. Dementia
Definition and highlights: Dementia is a syndrome due to
disease of the brain, usually of a chronic or progressive
nature, in which there is disturbance of multiple higher
cortical functions, including:
– Memory
– Thinking
– orientation
– Comprehension
– Calculation
– learning capacity
– Language
– Judgement.
• Consciousness is not clouded.
• The impairments of cognitive function are commonly
accompanied, and occasionally preceded, by deterioration
in emotional control, social behaviour, or motivation.
 1. Dementia
• This syndrome occurs in Alzheimer disease, in
cerebrovascular disease, and in other conditions
primarily or secondarily affecting the brain:
1.2 Dementia in Alzheimer disease
1.3 Vascular dementia
1.4 Mixed dementia
1.5 Degenerative dementia
1.6 Infectious dementia
1.7 Dementia in other somatic ilnesses
1.2 Dementia in Alzheimer disease
• Epidemiology:
– Occupy more than 50% of nursing-home beds;
– Found in 50-60% of patients with neurocognitive
disorder;
• Risk factors: female, family history, head trauma,
Down syndrome;
• Neuroanatomic findings: cortical atrophy,
flattened sulci, enlarged ventricles;
• Histopathology: senile plaques (amyloid
deposits), neurofibrillary tangles, neuronal loss,
synaptic loss, granulovacuolar degeneration of
neurons;
1.2 Dementia in Alzheimer disease
• Genetics: Associated with chromozome 21
(gene for the amyloid precursor protein);
• Neurotransmitters: Decreased Ach
(acetylcholine) and NE (norepinephrine);
• Course: Deterioration is generally gradual,
with average duration from onset to death
being about 8 years;
• Associated symptoms: Focal neurologic
symptoms are rare.
 Alzheimer’s Disease (9 min)
https://www.youtube.com/watch?v=PZu51MnqfF4
 1.3 Vascular dementia (multi-infarct
neurocognitive disorder)
• Epidemiology: Found in 15-30% of patients with
neurocognitive disorder;
• Risk factors: male, advanced age, hypertension
or other cardiovascular disorders;
• Affects small and medium-sized vessels;
• Examination may reveal carotid bruits, enlarged
cardiac chambers, fundoscopic abnormalities;
• MRI may reveal hyperintensities and focal
atrophy suggestive of old infarctions;
 1.3 Vascular dementia (multi-infarct
neurocognitive disorder)
• Course: Deterioration may be stepwise or
gradual, depending on underlying pathology;
• Focal neurologic symptoms (pseudobulbar
palsy, dysarthria, dysphagia);
• Associated symptoms: Abnormal reflexes and
gait disturbance are often present;
• Control of risk factors such as hypertension,
smoking, diabetes, hypercholesterolemia,
hyperlipidemia is useful.
 Mixed dementia
• Mixed cortical and subcortical vascular
dementia
• Unequal distribution of deficits in higher
cognitive functions, with some affected and
others relatively spared.
• Thus memory may be quite markedly affected
while thinking, reasoning and information
processing may show only mild decline.
• There is clinical evidence of focal brain damage.
• There is evidence from the history, examination,
or tests, of a significant cerebrovascular disease,
which may reasonably be judged to be
etiologically related to the dementia (e.g. a
history of stroke; evidence of cerebral infarction).
 Mixed dementia
• Mixed cortical and subcortical components of the
vascular dementia may be suspected from the clinical
features, the results of investigations (including
autopsy), or both.
• Dementia in Alzheimer's disease, atypical or mixed
type
• Use this term and code for dementias that have
important atypical features or that fulfil criteria for both
early (< 65 years old) and late (>65 years old) onset type
of Alzheimer's disease. Mixed Alzheimer's and vascular
dementia is also included here.
Alzheimer vs Vascular
(Kaplan)
 1.5 Degenerative dementia
• The following types of dementia meet the
general criteria of this disorder and can be
distinguished by their characteristic features:
– Dementia in Pick’s disease
– Dementia in Creutzfeldt-Jakob disease
– Dementia in Huntington’s disease
– Dementia in Parkinson’s disease
 Dementia in Pick’s disease
• Slow onset with steady deterioration.
• Predominance of frontal lobe involvement
evidenced by two or more of the following:
(1) emotional blunting;
(2) coarsening of social behaviour;
(3) disinhibition;
(4) apathy or restlessness;
(5) aphasia.
• Relative preservation, in the early stages, of
memory and parietal lobe functions.
 Dementia in Creutzfeldt-Jakob disease

• Very rapid progression of the dementia, with

disintegration of virtually all higher cerebral functions.
• The emergence, usually after or simultaneously with
the dementia, of one or more of the following types of
neurological symptoms and signs:
(1) pyramidal symptoms;
(2) extrapyramidal symptoms;
(3) cerebellar symptoms;
(4) aphasia;
(5) visual impairment.
 Dementia in Huntington’s disease
• Subcortical functions are affected first and dominate
the picture of dementia throughout; manifest as
slowness of thinking or movement and personality
alteration with apathy or depression.
• Presence of involuntary choreiform movements,
typically of the face, hands or shoulders, or in the gait.
The patient may attempt to conceal them by
converting them into a voluntary action.
• A history of Huntington's disease in one parent or a
sibling; or a family history which suggests the disorder.
• The absence of clinical features otherwise accounting
for the abnormal movements.
 Dementia in Parkinson’s disease
• Diagnosis of Parkinson's disease.
• Absence of cognitive impairment attributable to
anti-parkinsonian medication.
• There is no evidence from the history, physical
examination or special investigations for any
other possible cause of dementia, including:
– other forms of brain disease
– damage or dysfunction (e.g. cerebrovascular disease,
HIV disease, Huntington's disease, normal pressure
hydrocephalis)
– a systemic disorder (e.g. hypothyroidism, vit. B12 or
folic acid deficiency, hypercalcaemia)
– alcohol or drug abuse.
 1.6 Infectious dementia
• Dementia in human immunodeficiency (HIV)
disease
– The general criteria for dementia must be met.
– Diagnosis of HIV infection.
– There is no evidence from the history, physical
examination or special investigations for any other
possible cause of dementia, including:
• other forms of brain disease
• damage or dysfunction (e.g. Alzheimer's disease,
cerebrovascular disease, Parkinson's disease, Huntington's
disease, normal pressure hydrocephalis)
• a systemic disorder (e.g. hypothyroidism, vit. B12 or folic
acid deficiency, hypercalcaemia)
• alcohol or drug abuse.
 1.6 Infectious dementia
• Dementia in progressive supranuclear palsy (PSP)
• Cognitive dysfunction and personality change are
common in patients with PSP, but they are generally
milder in degree than those seen in patients with
primary dementing illnesses such as Alzheimer disease.
• Slowed cognitive processing, sequencing and planning
difficulties, mild memory difficulty, and apathy are
typical.
• These are generally more prominent later in the
course of the disease.

• Recommended site:
http://emedicine.medscape.com/article/1151430-clini
cal#b2
1.7 Dementia in other somatic ilnesses
• cerebral lipidosis
• epilepsy
• hepatolenticular degeneration
• hypercalcaemia
• hypothyroidism, acquired
• intoxications
• Lewy body (ies) (disease)
• multiple sclerosis
• neurosyphilis
• niacin deficiency [pellagra]
• polyarteritis nodosa
• systemic lupus erythematosus
• trypanosomiasis
• uraemia
• vitamin B12 deficiency
The Four Myths of Dementia (11 min)
https://www.youtube.com/watch?v=8a9AguRGmbE
 2. Organic amnesic syndrome, not
induced by alcohol and other
psychoactive substances
Definition and highlights: A syndrome of
prominent impairment of recent and remote
memory while immediate recall is preserved,
with reduced ability to learn new material and
disorientation in time.
• Confabulation may be a marked feature, but
perception and other cognitive functions,
including the intellect, are usually intact.
• The prognosis depends on the course of the
underlying lesion.
= Korsakov psychosis or syndrome, nonalcoholic
 2. Organic amnesic syndrome, not
induced by alcohol and other
psychoactive substances
• Memory impairment, manifest in both:
(1) a defect of recent memory (impaired learning of new material), to a
degree sufficient to interfere with daily living; and
(2) a reduced ability to recall past experiences.
• Absence of:
(1) a defect in immediate recall (as tested, for example, by the digit
span);
(2) clouding of consciousness and disturbance of attention;
(3) global intellectual decline (dementia).
• Objective evidence (physical & neurological examination,
laboratory tests) and/or history of an insult to or a disease of the
brain (especially involving bilaterally the diencephalic and medial
temporal structures but other than alcoholic encephalopathy) that
can reasonably be presumed to be responsible for the clinical
manifestations described above.
 3.Delirium, not induced by alcohol
and other psychoactive substances
Definition and highlights: An etiologically
nonspecific organic cerebral syndrome
characterized by concurrent disturbances of
consciousness and attention, perception,
thinking, memory, psychomotor behaviour,
emotion, and the sleep-wake schedule.
• The duration is variable and the degree of
severity ranges from mild to very severe.
Criteria:
• Clouding of consciousness, i.e. reduced clarity of
awareness of the environment, with reduced
ability to focus, sustain, or shift attention.
 3.Delirium, not induced by alcohol
and other psychoactive substances
• Disturbance of cognition, manifest by both:
(1) impairment of immediate recall and recent memory,
with relatively intact remote memory;
(2) disorientation in time, place or person.
• At least one of the following psychomotor
disturbances:
(1) rapid, unpredictable shifts from hypo-activity to
hyper-activity;
(2) increased reaction time;
(3) increased or decreased flow of speech;
(4) enhanced startle reaction.
 3.Delirium, not induced by alcohol
and other psychoactive substances
• Disturbance of sleep or the sleep-wake cycle,
manifest by at least one of the following:
(1) insomnia, which in severe cases may involve
total sleep loss, with or without daytime
drowsiness, or reversal of the sleep-wake
cycle;
(2) nocturnal worsening of symptoms;
 3.Delirium, not induced by alcohol and
other psychoactive substances
(3) disturbing dreams and nightmares which may
continue as hallucinations or illusions after
awakening.
• Rapid onset and fluctuations of the symptoms
over the course of the day.
• Objective evidence from history, physical and
neurological examination or laboratory tests of an
underlying cerebral or systemic disease (other
than psychoactive substance-related) that can be
presumed to be responsible for the clinical
manifestations.
 4. Other mental disorders due to
brain damage and dysfunction and to
physical disease
Criteria:
• Objective evidence (from physical and neurological
examination and laboratory tests) and/or history of
cerebral disease, damage or dysfunction, or of
systemic physical disorder known to cause cerebral
dysfunction, including hormonal disturbances (other
than alcohol or other psychoactive substance-related)
and non-psychoactive drug effects.
• A presumed relationship between the development (or
marked exacerbation) of the underlying disease,
damage or dysfunction, and the mental disorder, the
symptoms of which may have immediate onset or may
be delayed.
 4. Other mental disorders due to
brain damage and dysfunction and to
physical disease
• Recovery or significant improvement of the
mental disorder following removal or
improvement of the underlying presumed cause.
• Absence of sufficient or suggestive evidence for
an alternative causation of the mental disorder,
e.g. a highly loaded family history for a clinically
similar or related disorder.

4.1 Organic hallucinosis

4.2 Organic mood (affective) disorder
4.3 Mild cognitive disorder
4.1 Organic hallucinosis
• The above listed general criteria must be met.
• The clinical picture is dominated by persistent or
recurrent hallucinations (usually visual or
auditory).
• Occurrence of hallucinations in clear
consciousness.
• Comments: Delusional elaboration of the
hallucinations, as well as full or partial insight,
may or may not be present: these features are
not essential for the diagnosis.
4.2 Organic mood [affective] disorder
• The above listed general criteria must be met.
• The condition must meet the criteria for one of
the affective disorders (See Lecture no.8).
 Organic hallucinosis (21 min)
https://www.youtube.com/watch?v=0kbxM9wcYJU
 4.3 Mild cognitive disorder
• The above listed general criteria must be met.
• The presence of a disorder in cognitive function for
most of the time for at least two weeks, as reported by
the individual or a reliable informant. The disorder is
exemplified by difficulties in any of the following areas:
(1) New learning
(2) Memory (e.g. recall)
(3) Concentration
(4) Thinking (e.g. slowing)
(5) Language (e.g. comprehension, word finding, etc.)
• Abnormality or decline in performance on
neuropsychological tests (or quantified cognitive
assessments).
 5. Personality and behavioural
disorders due to brain disease,
damage and dysfunction
Criteria:
• Objective evidence (from physical and neurological
examination and laboratory tests) and/or history, of
cerebral disease, damage, or dysfunction.
• Absence of clouding of consciousness and of significant
memory deficit.
• Absence of sufficient or suggestive evidence for an
alternative causation of the personality or behaviour
disorder that would justify its placement in other section.

5.1 Organic personality disorder

5.2 Postencephalitic syndrome
5.3 Postconcussional syndrome
 5.1 Organic personality disorder
• The above listed general criteria must be met.
• At least three of the following features must be
present over a period of six or more months:
(1) Consistently reduced ability to persevere with goal-
directed activities, especially ones involving longer
periods of time and postponed gratification.
(2) One or more of the following emotional changes:
– Emotional lability (uncontrolled, unstable, and fluctuating
expression of emotions);
– Euphoria and shallow, inappropriate jocularity,
unwarranted by the circumstances;
– Irritability and/or outbursts of anger and aggression;
– Apathy.
 5.1 Organic personality disorder
(3) Disinhibited expression of needs or impulses without
consideration of consequences or of social conventions
(the subject may engage in antisocial acts such as
stealing, inappropriate sexual advances, ravenous
eating, or exhibit extreme disregard for personal
hygiene).
(4) Cognitive disturbances, typically in the form of:
– excessive suspiciousness and paranoid ideas;
– excessive preoccupation with a single theme such as
religion, or rigid categorization of other people's behaviour
in terms of "right" and "wrong".
(5) Marked alteration of the rate and flow of language
production, with features such as circumstantiality,
over-inclusiveness, viscosity, and hypergraphia.
(6) Altered sexual behaviour (hyposexuality or change in
sexual preference).
 5.2 Postencephalitic syndrome
• Residual neurological signs; manifest in at least one of the
following:
(1) paralysis;
(2) deafness;
(3) aphasia;
(4) constructional apraxia;
(5) acalculia.
• The syndrome is reversible, and its duration rarely exceeds
24 months.
• Residual symptoms and behavioural change following
either viral or bacterial encephalitis are non-specific and do
not provide a sufficient basis for a clinical diagnosis.
• They may include: general malaise, apathy or irritability;
some lowering of cognitive functioning (learning
difficulties); disturbances in the sleep-wake pattern; or
altered sexual behaviour.
 5.3 Postconcussional syndrome
• The above listed general criteria must be met
• History of head trauma with loss of
consciousness, preceding the onset of symptoms
by a period of up to four weeks (objective EEG,
brain imaging, or oculonystagmographic evidence
for brain damage may be lacking).
• At least three of the following:
(1) Complaints of unpleasant sensations and pains,
such as headache, dizziness (usually lacking the
features of true vertigo), general malaise and
excessive fatigue. or noise intolerance.
(2) Emotional changes, such as irritability,
emotional lability, both easily provoked or
exacerbated by emotional excitement or stress,
or some degree of depression and/or anxiety.
 5.3 Postconcussional syndrome
(3) Subjective complaints of difficulty in
concentration and in performing mental tasks, and
of memory complaints, without clear objective
evidence (e.g. psychological tests) of marked
impairment.
(4) Insomnia.
(5) Reduced tolerance to alcohol.
(6) Preoccupation with the above symptoms and fear
of permanent brain damage, to the extent of
hypochondriacal over-valued ideas and adoption
of a sick role.
 5.3 Postconcussional syndrome
• Posttraumatic epilepsy (PTE) is a recurrent
seizure disorder that apparently results from
injury to the brain. This injury may be due to
traumatic brain injury (TBI) or to an operation
on the brain.
• PTE must be differentiated from
posttraumatic seizures (PTS), which is a
broader-spectrum term and signifies seizures
that occur as a sequel to brain injury.
 5.3 Postconcussional syndrome
• Seizures that occur within 24 hours after brain
injury are called immediate PTS.
• PTS that occur within 1 week after injury are
termed early PTS, and seizures that occur more
than 1 week after injury are termed late PTS.
• About 20% of people who have a single late
posttraumatic seizure never have any further
seizures, and these people should not be
labeled as having PTE.