The ppt covers all aspects concerning organic brain disorder - Dementia and Delirium. It includes Alzheimer's, Parkinson's along with clinical features (according to ICD 10); cognitive, physical, neurobiological changes; treatment and assessment scales. Diagrams and charts are included wherever necessary for ease of understanding.

1. PSYCHOPATHOLOGY OF
NEUROLOGICAL CONDITIONS AND
ORGANIC BRAIN DISORDERS
By : Attreye Datta Mazumder
MSc. Clinical Psychology
Year – I

2.  Clinical Manifestations
 Dementia, Head Injury, Stroke, Delirium, Epilepsy, Alzheimer’s,
Parkinsonism
SYLLABUS

3. ORGANIC BRAIN DISORDERS

4. INTRODUCTION
There are broadly three types of psychiatric disorders:
1. Those due to a known organic cause.
2. Those in whose causation an organic factor has not yet been proven.
3. Those primarily due to psychosocial factors.
Disorders with a known organic cause are known as
organic mental disorders.

5. DEFINITION:
Organic disorders are behavioral or psychological disorders associated with
transient or permanent brain dysfunction and include only those mental and
behavioral disorders that are due to demonstrable and independently diagnosable
cerebral disease or disorder, either primary (primary brain pathology) or secondary
(brain dysfunction due to systemic diseases)
(Neeraj Ahuja, 2011)
The term “symptomatic” is used for those organic mental disorders in which cerebral
involvement is secondary to a systemic extracerebral disease or disorder. (ICD – 10)
In DSM-5, the term ‘Neurocognitive Disorders’ is used.

6. TOPICS OF DISCUSSION:
1. DELIRIUM
2. DEMENTIA
 Alzheimer’s
 Parkinson’s

7. DELIRIUM

8. Lipowski (1990) defines delirium as ‘a transient organic mental syndrome of acute
onset, characterized by global impairment of cognitive functions, a reduced level of
consciousness, attentional abnormalities, increased or decreased psychomotor
activity and a disordered sleep–wake cycle’.
Delirium, a transient disorder of brain function manifested by global cognitive
impairment and other behavioural phenomena (Kaplan)
Delirium is the commonest organic mental disorder seen in clinical practice.
(Ahuja)
5% – 15% of all pts in medical and surgical inpatient units are estimated to develop
delirium at some time in their life. The percentage is higher in postoperative pts.
Studies in India are mostly done on pts in ICU.

9. A study was conducted in 2012 to evaluate the incidence, prevalence, risk factors
and outcome of delirium in the respiratory intensive care unit of a tertiary care
hospital in India.
Scale administered: Delirium Rating Scale-Revised 98 version (DRS-R-98).
Results: Delirium is highly prevalent in the ICU setting and delirium is associated
with longer ICU stay and higher mortality.
Incidence rate of delirium: 24.4%
Prevalence rate of delirium: 53.6%

10. DEFINITION (ICD – 10)
An etiologically nonspecific syndrome characterized by :
• concurrent disturbances of consciousness and attention, perception, thinking,
memory,
• psychomotor behavior emotion, &
• sleep-wake cycle.
It may occur at any age but is most common after the age of 60 years. A delirious
state may be superimposed on, or progress into, dementia.

11. SYNDROMES DUE
TO BRAIN
DISORDERS
Acute
Delirium
Sub acute Delirium
Organic stupor or
torpor
Twilight State
Sub acute
Chronic
In acute organic syndromes the most common feature is :
alteration of consciousness, which can be dream-like,
depressed or restricted.

12. DELIRIUM SUB ACUTE DELIRIUM
In delirium there is a dream-like change in
consciousness so that the patient may also be
unable to distinguish between mental images
and perceptions, leading to hallucinations and
illusions.
Usually there is severe anxiety and agitation.
In subacute delirium, there is a general
lowering of awareness and marked
incoherence of psychic activity, so that the
patient is bewildered and perplexed.
Isolated hallucinations, illusions and delusions
may occur and the level of awareness varies
but is lower at night-time.
The subacute delirious state can be regarded
as a transitional state between delirium and
organic stupor.

13. Confusion of thinking can be described as occurring either when the individual
describes his own thinking as being confused or when the external observer
considers that the thought processes are disturbed and confused.
Phenomenologically, therefore, it is simply a description of the patient’s self-
experience or the doctor’s observation.
What is confusion of thinking?

14. 1. A relatively acute onset.
2. Clouding of consciousness, characterized by a decreased awareness of
surroundings and a decreased ability to respond to environmental stimuli.
3. Disorientation (most commonly in time then in place and usually later in
person), associated with a decreased attention span and distractibility.
CLINICAL FEATURES OF DELIRIUM
DISORIENTATION IN TIME
Disorientation for time is demonstrated by the inability to correctly tell the time without recourse
to a clock, to indicate the date, day and season. The second abnormality is impairment of the
ability to assess the duration of time, and this is also disturbed in organic states. (Sim’s)

15. (Clinical features contd.)
• Marked perceptual disturbances such as – Illusions, Misinterpretations
Hallucinations also occur. These are most commonly visual though other
perceptual domains can also be involved.
• There is often a disturbance in the sleep-wake cycle most commonly insomnia
at night with daytime drowsiness with worsening of symptoms in the evening
and night (sun downing)

16. (Clinical features contd.)
• Psychomotor disturbance usually in form of agitation an occasionally
retardation, is present.
• Generalized autonomic dysfunction, speech and thought disturbances (such as
slurring of speech, incoherence, dysarthria and fleeting delusions) are often
present.
• Hypoacusis (decreased sensitivity to noise) occurs in delirium, where the
threshold for all sensations is raised. The defect of attention found in delirium
further reduces sensory acuity.

17. The motor symptoms in delirium can include:
1. Asterixis (flapping tremor)
2. Multifocal myoclonus
3. Carphologia or floccillation (picking movements at cover-sheets and clothes)
4. Occupational delirium (elaborate pantomimes as if continuing their usual occupation in the
hospital bed)
5. Tone and reflex abnormalities
Lability of affect is usually present.
Motor and verbal perseveration, dysnomia, agraphia and impaired comprehension can also be seen.

18. DIAGNOSIS
According to ICD – 10, for a definitive diagnosis of delirium, symptoms (mild or severe)
should be present in each one of the five areas described:
1. Impairment of consciousness and attention
2. Global disturbance of cognition
3. Psychomotor disturbances
4. Disturbance of sleep-wake cycle
5. Emotional disturbances

19. It is important to differentiate delirium from the following:
1. Twilight State
2. Mania à Potu (Pathological Intoxication)
3. Automatism
4. Dream like (Oneiroid) state
5. Stupor
6. Sleep disorders
RELATED SYNDROMES

20. TWILIGHT STATE
A twilight state is a well-defined interruption of the continuity of consciousness (Sims et
al.,2000). It is usually an organic condition and occurs in the context of epilepsy, alcoholism
(mania à potu), brain trauma and general paresis; it may also occur with dissociative states.
MANIA A POTU (PATHOLOGICAL INTOXICATION)
This is one type of twilight state specifically associated with alcoholism. It is important to
distinguish this syndrome of acute pathological intoxication with alcohol from delirium
tremens, which is a symptom of withdrawal.

21. AUTOMATISM
Automatism implies action taking place in the absence of consciousness.
It has been defined by Fenwick (1990) as follows:
An automatism is an involuntary piece of behavior over which an individual has no control. The
behavior itself is usually inappropriate to the circumstances, and may be out of character for
the individual. It can be complex, coordinated, and apparently purposeful and directed, though
lacking in judgement. Afterwards, the individual may have no recollection, or only partial and
confused memory, of his actions.

22. DREAM LIKE (ONEIROID) STATE
This is an unsatisfactory term not clearly differentiated from twilight state or delirium. The
patient is disorientated, confused and experiences elaborate hallucinations, usually visual. There
is impairment of consciousness and marked emotional change, which may be terror or
enjoyment of the hallucinatory experiences; there may also be auditory or tactile hallucinations.
The patient may appear to be living in a dream world, and so-called occupational delirium
could be mentioned in this context:
For eg., the ship’s petty officer, admitted to hospital after a head injury at sea (associated with
excess alcohol intake), who kept shouting ‘Man the boats’.

23. ‘Stupor names a symptom complex whose central feature is a reduction in, or absence
of, relational functions: that is, action and speech’(Berrios, 1996).
This term should be reserved for the syndrome in which mutism and akinesis occur;
that is, the inability to initiate speech or action in a patient who appears awake and
even alert. It usually occurs with some degree of clouding of consciousness but does
not refer solely to a diminished level. The patient may look ahead or his eyes may
wander, but he appears to take nothing in.
STUPOR

24. 1. Pre-existing brain damage
2. Extremes of age (very old or very young)
3. Previous history of delirium
4. Alcohol or drug dependence
5. Generalized or focal cerebral lesion
6. Chronic medical illness
7. Surgical procedure and post-operative period
8. Severe psychological symptoms (such as fear)
9. Treatment with psychotropic medicines
10. Present or past history of head injury
11. Individual susceptibility to delirium
PREDISPOSING FACTORS IN DELIRIUM

25. ETIOLOGY
• Hypoxia, Hypoglycemia, Cardiac failure/arrest, Water and electrolyte imbalance
• Hypo- and Hyperpituitarism, Hypo- and Hyperthyroidism
• Alcohol, Sedatives, Hypnotics (especially barbiturates), Tricyclic antidepressants, Antipsychotics, Anticholinergics, Disulfiram
• Nutritional deficiencies - Thiamine, Niacin, Pyridoxine, Folic acid, B12
• Epilepsy (including post-ictal states)
• Head injury - Subarachnoid hemorrhage, Subdural hematoma
• Intracranial infections, e.g. Meningitis, Encephalitis, Cerebral malaria
• Migraine
• Stroke (acute phase)
• Hypertensive encephalopathy
• Focal lesions, e.g. right parietal lesions (such as abscess, neoplasm)
• Postoperative states (including ICU delirium)
• Sleep deprivation

26. `
MANAGEMENT
1. In case where cause is not obvious, a battery of investigations should be done which can
include complete blood count, urinalysis, blood glucose, blood urea, serum electrolytes,
liver and renal function tests, thyroid function tests, brain imaging, chest X ray, ECG etc.
2. Identification of the cause and its immediate correction e.g., 50 mg of 50% dextrose IV
for hypoglycemia, O2 for hypoxia, IV fluids for electrolyte imbalance.
3. Symptomatic measures: As many pts are agitated, emergency psychiatric treatment may
be needed.
Small doses of benzodiazepines (lorazepam or diazepam) or antipsychotics (haloperidol or
risperidone) may be given orally or parenterally.
4. Supportive medical and nursing care.

27. TREATMENT
 The primary treatment of delirium is to identify and ameliorate any causal or contributing
medical conditions.
 As part of that effort, the dosages of all sedatives and other CNS-active medications
should be minimized as much as possible. (The exception is sedative-hypnotic or alcohol
withdrawal delirium, in which treatment of the underlying problem requires the
administration of a cross-tolerant agent such as a benzodiazepine.)
 Delirious patients may need extra supportive physical care; maintenance of basic
functions such as food and fluid intake is crucial to rapid recovery.
 Keeping the patient in an environment that is quiet and free of unnecessary stimulation
may help reduce agitation.

28. Treatment (contd)
The primary treatment of delirium is to identify and ameliorate any causal
unnecessary stimulation may help reduce agitation.
Frequent cues to orientation may also be helpful.
Supportive contacts with the patient, family, and sometimes staff members are
necessary to reassure the patient that the new, often frightening behavioural state
reflects physical illness and that the patient is not going crazy.
Attention may need to be paid to the patient's legal capacity to participate in
informed clinical care decisions.

29. 1. Delirium Rating Scale Revised Version (DRS-R-98)
2. Confusion Assessment Method (CAM), CAM for intensive care unit
(CAM-ICU)
3. Paediatric Anaesthesia Emergence Delirium Scale and Paediatric CAM-ICU
ASSESSMENT SCALES FOR DELIRIUM

30. DEMENTIA

32. 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, and judgement.
 Consciousness is not clouded.
Impairments of cognitive function are commonly accompanied, and occasionally
preceded, by deterioration in emotional control, social behaviour, or motivation.
This syndrome occurs in Alzheimer's disease, in cerebrovascular disease, and in
other conditions primarily or secondarily affecting the brain.
DEFINITION (ICD – 10)

34. 1. Impairment of intellectual functions,
2. Impairment of memory (predominantly of recent memory, especially in early
stages)
3. Deterioration of personality with lack of personal care
CLINICAL FEATURES OF DEMENTIA
Dementia is a chronic organic mental disorder, characterised by the following
main clinical features:

35.  Impairment of all these functions occurs globally, causing interference with
day-to-day activities and interpersonal relationships.
 There is impairment of judgement and impulse control, and also
impairment of abstract thinking.
 There is however usually no impairment of consciousness (unlike in
delirium).
 The course of dementia is usually progressive though some forms of
dementia can be reversible.
(Clinical features contd.)

36. Additional features that may be present:
 Emotional lability (marked variation in emotional expression).
 Catastrophic reaction (when confronted with an assignment which is
beyond the residual intellectual capacity, patient may go into a sudden
rage).
 Thought abnormalities, e.g. perseveration, delusions.

37.  Urinary and faecal incontinence may develop in later stages.
 Disorientation in time;
Disorientation in place and person may also develop in later stages.
 Neurological signs may or may not be present, depending on the
underlying cause.

38. FEATURES DELIRIUM DEMENTIA
1. Onset Usually acute Usually insidious
2. Course Usually recover in 1 week; may take up to 1 month Usually protracted, although may be reversible in some
cases
3. Clinical features
a) CONSCIOUSNESS Clouded Usually normal
b) ORIENTATION Grossly disturbed Usually normal; disturbed only in late stages
c) MEMORY Immediate retention and recall disturbed
Recent memory disturbed
Immediate retention and recall normal
Recent memory disturbed
Remote memory disturbed only in late stages
d) COMPREHENSION Impaired Impaired only in late stages
e) SLEEP WAKE CYCLE Grossly disturbed Usually normal
f) ATTENTION &
CONCENTRATION
Grossly disturbed Usually normal
g) DIURNAL VARIATION Marked; sun downing may
be present
Usually absent
h) PERCEPTION Visual illusions and hallucinations very common Hallucinations may occur
i) OTHER FEATURES Asterixis; multifocal myoclonus Catastrophic reaction; perseveration

39. Dementia produces an appreciable decline in intellectual functioning, and usually
some interference with personal activities of daily living such as –
washing, dressing, eating, personal hygiene, excretory and toilet activities.
How such a decline manifests itself will depend largely on the social and cultural
setting in which the patient lives.
Note: Changes in role performance, such as lowered ability to keep or find a job,
should not be used as criteria of dementia because of the large cross-cultural
differences that exist in what is appropriate, and because there may be frequent,
externally imposed changes in the availability of work within a particular
culture.

40. Evidence of decline in both memory and thinking, sufficient enough to impair
personal activities of daily living, memory impairment, typically affecting
registration, storage, and retrieval of new information though previously
learned material may also be lost particularly in later stages, impaired thinking,
presence of clear consciousness (consciousness can be impaired if delirium is
also present), and a duration of at least 6 months.
DIAGNOSIS
According to ICD-10, the following features are required for diagnosis:

41. The following conditions must be kept in mind in the differential diagnosis of dementia -
1. Normal aging process
Although impairment of memory and intellect are commoner in elderly, their mere presence
does not justify a diagnosis of dementia.
Dementia is diagnosed only when there is demonstrable evidence of memory and other
intellectual impairment which is of sufficient severity to interfere with social and/or
occupational functioning.
The normal memory impairment in old age is called as benign senescent forgetfulness.
DIFFERENTIAL DIAGNOSIS

42. 2. Delirium
The syndromes of delirium and dementia may overlap. Follow Table for the comparison of
clinical features.
3. Depressive pseudodementia
Depression in the elderly patients may mimic dementia clinically. It is called as depressive
pseudodementia. Identification of depression is very important as it is far more easily treatable
than dementia.
The depressed patients often complain of memory impairment, difficulty in sustaining
attention and concentration, and reduced intellectual capacity. In contrast, patients with
dementia do not often complain of these disturbances. In fact, when confronted with evidence
of memory impairment, they often confabulate.
As depression may often be superimposed on dementia, it is at times necessary to undertake a
therapeutic trial with antidepressants, if the clinical picture is unclear.

43. DEMENTIA PSEUDODEMENTIA
(Depressive)
Patient rarely complains of cognitive impairment Patient usually always complains about memory impairment
Patient often emphasises achievements Patient often emphasises disability
Patient often appears unconcerned Patient very often communicates distress
Usually labile affect Severe depression on examination
Patient makes errors on cognitive examination ‘Do not know’ answers are more frequent
Recent memory impairment found on examination Recent memory impairment rarely found on examination
Confabulation may be present Confabulation very rare
Consistently poor performance on similar tests Marked variability in performance on similar tests
History of depression less common Past history of manic and/or depressive episodes may be
present

44. DEMENTIA
CORTICAL
SUB
CORTICAL

46. FEATURES CORTICAL DEMENTIA SUB CORTICAL DEMENTIA
1. Site of lesion Cortex (frontal and temporoparieto-occipital
association areas, and hippocamps)
Subcortical grey matter (thalamus, basal ganglia, and
rostral brain stem)
2. Examples Alzheimer’s disease, Pick’s disease Huntington’ chorea, Parkinson’s disease,
Progressive supranuclear palsy, Wilson’s disease
3. Severity Severe Mild to moderate
4. Motor system Usually normal Dysarthria, flexed/extended posture, tremors,
dystonia, chorea, ataxia, rigidity
5. Other features Simple delusions; depression uncommon;
severe aphasia, amnesia, agnosia, apraxia, acalculia,
slowed cognitive speed (bradyphrenia)
Complex delusions; depression common;
rarely mania
6. Memory deficit
(Short term)
Recall helped very little by cues Recall partially helped by cues and recognition tasks

47. • Alzheimer’s disease
• Pick’s disease
• Huntington’s chorea
• Lewy body dementia
• Toxic dementia: alcohol, drugs, psychotropic drugs, benzodiazepines
• Endocrine causes – Thyroid, parathyroid, pituitary, adrenal dysfunction
Anemia, folic acid deficiency, thiamine deficiency
• Infections: Creutzfeldt-Jacob disease, AIDS dementia, other HIV-related
disorders,
• Traumatic dementias: Chronic subdural haematoma, head injury
ETIOLOGY

48. ALZHEIMER’S DISEASE

49. Originally described by Alzheimer's in 1906, it detailed most of the familiar
clinical and neuropathological features
This is the commonest cause of dementia, seen in about 70% of all cases of
dementia in USA. (Ahuja, 2011)
It is more commonly seen in women.
There is some evidence to suggest that Alzheimer’s disease may have a genetic
basis.
ALZHEIMER’S

51. ALZHEIMER DISEASE

53.  Alzheimer's disease is a primary degenerative cerebral disease of unknown
etiology, with characteristic neuropathological and neurochemical features.
 It is usually insidious in onset and develops slowly but steadily over a period
of years.
 This period can be as short as 2 or 3 years, but can occasionally be
considerably longer.
 The onset can be in middle adult life or even earlier (Alzheimer's disease
with early onset), but the incidence is higher in later life (Alzheimer's
disease with late onset).
DEFINITION (ICD – 10)

54. The cardinal neuropathological sign of AD is the:
• presence of senile plaques,
• neurofibrillary tangles, and
• amyloid angiopathy.
Plaques are caused by neuronal degeneration and can be found in all areas of the
cerebral cortex but are often most common in the parietal lobe and hippocampal and
amygdaloid regions.
Neurofibrillary tangles are tangled bundles of fine fibers within the cell bodies of
neurons that occur throughout the brain but particularly around the hippocampus.
Neurochemically, there is a marked decrease in brain choline acetyltransferase (CAT)
with a similar decrease in brain acetylcholinesterase (AchE).

58. NORMAL BRAIN ALZHEIMER’S BRAIN

59. Alzheimer’s has a slowly progressive decline. The medicines can slow
the progression, NOT halt it.
FUNCTION
TIME

60. The following features are essential for a definite diagnosis:
Presence of a dementia as described.
Insidious onset with slow deterioration.
Absence of clinical evidence, or findings from special investigations, to suggest that
the mental state may be due to other systemic or brain disease which can induce a
dementia (e.g. hypothyroidism, hypercalcaemia, vitamin B12 deficiency)
Absence of a sudden, apoplectic onset, or of neurological signs of focal damage such
as hemiparesis, sensory loss, visual field defects, and incoordination occurring early in
the illness (although these phenomena may be superimposed later).
DIAGNOSIS

61. TREATMENT
• At present, Alzheimer’s dementia is not considered a treatable disorder.
• However, Cholinesterase Inhibitors such as Rivastigmine, Donepezil, and
Galantamine have been used in the recent past for treatment of moderate
dementia with Alzheimer’s disease.
• These elevate acetylcholine (Ach) concentrations in cerebral cortex by
slowing the degradation of acetylcholine released by still intact cholinergic
neurons in Alzheimer’s disease.
• Memantine, an N-methyl-D- aspartate antagonist, is also available for the
treatment of moderately severe to severe Alzheimer’s disease.

62. PARKINSON’S DISEASE

63. PARKINSON’S
 Described by James Parkinson in 1817, Parkinson's disease is a prototype of a subcortical
degenerative disease. It is idiopathic.
 Parkinson’s disease (PD) is a movement disorder that can, and often does, lead to
prominent changes in cognitive function and psychological status.
 It has been estimated that from 20–40% of all patients with PD eventually develop a
dementia syndrome (Brown & Mardsen, 1984; Lerner et al., 1997; Mayeux et al., 1988;
Rajput, 1992).
 The likelihood of intellectual and psychological deterioration increases as the illness
progresses (Lerner et al., 1997).

64. Parkinsonism and Parkinson’s Disease
Parkinsonism is a generic term used to describe a cluster of motor symptoms that includes
difficulty in initiating movement and bradykinesia (slowness of movement), in addition to
tremor, rigidity, gait disturbance (e.g., shuffling gait with many rapid, small steps), and postural
changes (i.e., stooped posture). These symptoms and signs can result from a variety of specific
illnesses (e.g., viral encephalitis) and/or toxin exposure (e.g., manganese poisoning) and are
often seen as side effects of long-term use of antipsychotic medications (La Rue, 1992).
Parkinson’s Disease (PD) is the occurrence of this constellation of symptoms with a gradual
onset and progressive course with- out a specific cause or etiology. Lezak (1995) has suggested
that approximately 80% of all cases that involve prominent Parkinsonism are idiopathic.

65. Parkinsonism
Parkinsonism may be produced by degenerative disorders (Parkinson's disease, progressive supranuclear palsy),
multiple small strokes (lacunar state), metabolic disorders (hypothyroidism, hypoparathyroidism), head trauma,
CNS infections (Creutzfeldt-Jakob disease, HIV encephalopathy), CNS tumours, hydrocephalus, and drug
treatment.
Medications most likely to induce parkinsonism include dopamine receptor antagonists.
The parkinsonian syndrome features:
1. Bradykinesia and
2. Plastic rigidity with or without a rest tremor.
Manifestations of bradykinesia include:
• a masked face,
• reduced spontaneous blinking,
• diminished spontaneous swallowing with sialorrhea,
• start hesitation when initiating movement,
• shuffling gait (combination of reduced stride length and
decreased step height),
• decreased arm swing when walking,
• en bloc turns, slowed movement, and
• reduced spontaneous gesturing.

66. • No particular distinguishing clinical features have yet been demonstrated.
• The dementia may be different from that in either Alzheimer's disease or
vascular dementia; however, there is also evidence that it may be the
manifestation of a co-occurrence of one of these conditions with Parkinson's
disease. This justifies the identification of cases of Parkinson's disease with
dementia for research until the issue is resolved.
ICD – 10
Diagnostic Guidelines: A dementia developing in the course of established
Parkinson's disease (especially its severe forms).

67. Consider:
 Other secondary dementias;
 Multi-infarct dementia associated with hypertensive or diabetic vascular disease;
 Brain tumour;
 Normal pressure hydrocephalus.
DIFFERENTIAL DIAGNOSIS

68. 1. Neuron loss in the substantia nigra and other pigmented brain-stem nuclei
2. The substantia nigra is a principal site of dopaminergic neurons, and cell
death in this region produces a deficiency in dopamine in associated brain
regions, including the striatum and prefrontal regions.
3. This dopaminergic disruption, it is thought, is responsible for the motor
disturbances seen in PD.
NEUROPATHOLOGICAL FEATURES

69. 1. Slowed cognition (bradyphrenia) is the most common cognitive change.
2. Forgetfulness and executive dysfunction, such as difficulty in planning, sequencing, and
problem solving are also relatively common in PD.
3. The motor signs of PD are typically easily identified and include the posture and gait
abnormalities mentioned before, resting tremor, and speech irregularities such as
hypophonia (reduced voice volume) and dysarthria (difficulty producing speech).
COGNITIVE & MOTOR CHANGES
Classic motor symptom triad in Parkinson’s: (Jankovic, 1987)
 Resting tremor,
 Rigidity, and
 Bradykinesia

70. Levodopa (L-dopa), the most effective Parkinson's disease medication. It's also
the best at controlling the symptoms of the condition, particularly slow
movements and stiff, rigid body parts.
It is a natural chemical that passes into your brain and is converted to dopamine.
Levodopa is combined with carbidopa (Lodosyn), which protects levodopa from
early conversion to dopamine outside your brain.
This prevents or lessens side effects such as nausea.
TREATMENT

73. 1. Dementia Severity Rating Scale (DSRS)
2. Alzheimer’s Disease Assessment Scale (ADAS-cog)
3. Unified Parkinson’s Disease Rating Scale
ASSESSMENT SCALES FOR DEMENTIA

74. Neeraj Ahuja
Kaplan CTP
Handbook of Psychopathology
REFERENCES