Cognitive disorders.

1. Mr. Ngoma
PSY
COGNITIVE DISORDERS

2. DELIRIUM

3.  Delirium is a syndrome not a disease, characterized
by an impairment of consciousness along with global
impairment of cognitive function
 It may be associated with various neurological and
psychiatric symptoms such as tremors, nystagmus,
hallucinations, mood changes.
EPIDEMIOLOGY
 Delirium is a common bt underdiagnosed disorder.
 About 10-15% of pts in surgical wards, 15-25% in
medical wards.
 40-50% of pts recovering frm of hip # develop
delirium.

4. ETIOLOGY
 Disturbance in acetylcholine and reticular formation
is responsible.
Risk factors:
 Advanced age
 Very young age
 Pre-existing brain damage
 H/o delirium, cancer, sensory impairment
 Malnutrion
 Fractures
 Systemic infection

5. causes
Intracranial causes Extracranial cuases
 Meningitis
 Encephalitis
 Epilepsy
 Post ictal state
 Brain injury
 Endocrine dysfunction
 Cardiac failure
 Hepatic encephalopathy
 Uremic encephalopathy
 Anticholinergic agents
 Sedatives and hypnotics
 Steroids
 Insulin
 Anticonvulsants
 Carbon monoxide
 Heavy metals
 Vitamin deficiency
 Septicemia
 Electrolyte imbalance
 Post op state

6. Clinical features
 Cardinal feature is impaired consciousness with reduced
ability to focus, sustain or shift attention.
 Onset is sudden with a brief and fluctuating coarse with
lucid periods alternating with symptomatic peroids.
 Orientation to time, place and person is impaired.
 Level of arousal varies frm hypoactive to hyperactive and
hyperalert.
 Immediate and recent memory may be impaired with
preserved remote memory.
 Thought process may show alterations of
incoherence/irrelevant speech.
 Mood changes vary frm marked irritability, fear, anger
and apathy.
 Sleep-wake cycle may be reserved, with freq naps and
fragmented short sleep cycles.
 At times pt may show excerbation of symptoms in the
evening, commonly knw as sundowning

7. evaluation
 The diagnosis is usually clear frm hx
Standard work up:
 Blood tests- FBC/DC/ESR, U&E+Cr, LFTs, RBS
 Urinalysis, urine m/c/s
 T3, T4 and TSH
 Serology for syphilis
 HIV test
Additional tests:
 CSF studied
 Vitamin levels
 CT scan or MRI
 EEG

8. Differential diagnosis
 Demintia
 Psychoactive sub intoxication
 Schizophrenia
 Acute manic state
COURSE AND PROGNOSIS
 Delirium has a flacuating and brief course
 Symptoms last as long as the underlying cause
is present. Usually resolves in 3-7 days.

9. treatment
 Identify and treat/correct underlying cause
 Prevent physical injuries and accidents
 Optimize sensory input-enviroment should not be
over/under stimulating.
 Make the surrounding familiar by the presence of a
familiar person, picture, clock, calendar.
 Reorient the patient as often as possible
 Minimize use of medications, if possible.
 Tx insomia with short acting benzodiazepines e.g.
lorazepam.
 Use atypical antipsychotics to control psychotic and
behavioral problems to lessen side effects.

10. DEMENTIA

11. dementia
 This is a heterogeneous group characterized by
multiple impairments in cognitive functions in
clear consciousness along with impairment in
social and occupational function and represents a
definitive decline from a previous level of
functioning.
Epidemiology
 Dementia is common in the elderly.
 5% of all persons who reach 65yrs suffer from
dementia
 15% of cases are mild and 5% are severe cases

12. Dementia
 Two Types:
 Reversible
 Irreversible
 Individuals must have intensive medical physical
to rule out reversible types of dementia.

13. Etiology
→50-60% is due to Alzheimer's dementia & 15-30% is
vascular dementia
 Alzheimer's disease
 Vascular dementia:
infarcts, stroke
 Intracranial masses:
tumors, subdural
hematoma
 Head injury
 Neurodegenerative
disorders:
Parkinson's, Wilson's
disease
 Drugs and toxins
 Infections: AIDS,
neurosyphilis,
encephalitis
 Nutritional disorders:
vitamin deficiency
 Metabolic disorders:
dialysis dementia,
hypo/hyper thyroidism
 Chronic inflammatory
disease: SLE,
vasculitis

14. Etiology
treatable causes of dementia
 Head injury
 Subdural hematoma
 Meningitis
 Encephalitis
 Normal pressure
hydrocephalus
 Chronic psychoactive
substance abuse
 Hypothyroidism
 Hypoglycemia
 Hypercalcemia
 Vit B12 deficiency
 Thiamine deficiency
 Renal failure
 Hepatic failure
 Medication induced

15. Clinical features
 Dementia is characterized by multiple cognitive deficits.
 Essential to the diagnosis is impairment of memory.
 Immediate and recent memory are impaired with sparing
of remote, until later.
 Pts may confabulate to cover up deficits in memory.
 Aphasia maybe seen in vascular dementia involving the
dominant hemisphere.
 Pts may develop agnosia, apraxia and may have
impairment of abstract thinking, planning and completion
of complex.
 Poor judgment and insight ca cause pts to make
unrealistic plans and engage in dangerous activities.
 Socially disinhibited behavior and emotional liability can
be a source of frustration and embarrassment for the
family.

16. All dementias exhibit the same core clinical features, a
distinction however is made between dementias with
primary cortical and those with sub cortical pathology.
Cortical dementia Sub cortical dementia
Conditions:
 Alzheimer's type
 Frontotemporal dementia(e.g.
picks dz)
 Dementia due to CJD
Clinical features include:
 Prominent memory
impairment
 Apraxia (inability to perform
purposive actions)
 Agnosia (inability to recognize
things)
 Language deficits
Conditions:
 Parkinson's disease
 HIV dementia
 Huntington's disease
 Multiple sclerosis
Clinical features include:
 Greater deficit in recall memory
 Slowed thinking
 Apathy
 Laconic speech
 Mood changes
some dementias are characterized by both cortical and subcortical features e.g.
vascular dementia and Lewy body dementia

17. evaluation
 A comprehensive workup must be done when
evaluating a case of dementia to detect the
reversible causes.
 CT scan and MRI brain scans can help to
differentiate betwn difficult cases.
Differential diagnosis
 Delirium
 Depressive disorder
 Normal aging

18. Course and prognosis
 Disorder begins with subtle sympts which become
conspicuous sa the dementia progresses.
 Dz runs a slow course with gradual deterioration
over 5-10 yrs.
 However pts with early onset and +ve family Hx
of dementia tend to have a rapid course.
 In terminal stages, pt is markedly disoriented,
incoherent, amnestic and doubly incontinent.

19. treatment
 Follows the bio psychosocial approach
1. Psychopharmacological
 Symptomatic Rx of associated features such as
insomnia, anxiety, depression and psychotic
features with appropriate psychotropic drugs.
 Correcting the underlying cause that can Rx
reversible dementias.
 Dz specific Rx: cholinesterase inhibitors such as
donepezil, rivastigmine; ACE inhibitors and recpt
modulators such as galatamine; NMDA
antagonists such as memantine can halt the
progress of the disease process.

20. 2. Psychological intervention
 Psycho-education regarding the illness, the
impact and disabilities caused by the illness and
various Rx options available.
 Nature and course of illness should be explained
to pt in simple terms.
 other interventions include, handling of emotional
rxn, supportive psychotherapy and memory
enhancing aids.

21. 3. Family therapy
 Educating the family regarding the nature, possible
cause and course of illness and its impact on a day –
day life of pt as well as family.
 Psychological support to handle the emotions of the
caregivers.
 Providing information regarding various helps
available, e.g. day care centre, weekend helper,
holiday homes

22. 4. Environmental manipulation
 Keep pts room well lighted specially at dusk and
dawn.
 To use bold letter calenders and a time piece to
help pt stay oriented.
 Not to test the pts memory by repeatedly asking
questions regarding his memory.
 Making simple schedules to help structure daily
activities.
 Noting down the works to be carried out rather
than relying on memeory.

23. AMNESTIC DISORDERS

24. defination
 These are disorders characterized by the only sympt
of memory disturbance that interferes with social and
occupational fxn.
 Disorder appears in clear consciousness and
represents a significant decline frm a previous level
of fxning
EPIDEMIOLOGY
 Exact prevalence and incidence are unkwn
 However incidence seems to be declining possible
dur to early Rx of responsible diseases.

25. etiology
 Epilepsy
 Head injury
 Brain tumours
 Brain surgery
 Encephalitis
 Hypoxia
 CO poisoning
 Electroconvulsive
therapy
 Korsakoff syndrome
 Hypoglycemia
 Alcohol disorders
 Chronic use of
sedatives and
hypnotics

26. Clinical features
 Pt shows impaired ability to learn new
information- antrograde amnesia
 Inability to recall previously learned material-
retrograde amnesia.
 Remote memory is generally intact.
 Pt has no insight
 Confabulation is seen in early stage dz and is
characterized by unrealistic and inaccurate
responses to questions.
 Orientation is intact.

27. evaluation
 A thorough Hx, detailed physical exam and
appropriate Ix in accordance with the suspected
cause will help to make the diagnosis and point to
the cause.

28. Differentia diagnosis
 Delirium
 Dementia
 Malingering
 Psychogenic amnesia

29. Course and prognosis
 Underlying cause determines course and
prognosis.
 Onset may be acute as in head injury or gradual
as in nutritional deficiencies.
 symptons may be transient or persistent.

30. treatment
 The primary goal is to treat the underlying cause.
 Supportive prompts regarding time, place and
person help to reorient the person and reduce the
anxiety.
 Family counseling and individual psychotherapy
may help

31. THE END