Prakash B Neuro Delirium Depression Dementia

DELIRIOUS / DEMENTED / DEPRESSED ?
B.PRAKASH
CONSULTANT NEUROLOGIST
Kovai Medical Center and Hospital
Kasturi Neuro Diagnostic Centre
89-A, East Lokamanya Street
RS Puram, Coimbatore

Delirium, Dementia & Depression
 All the three illnesses present with Confusional state
 Three most common mental health conditions among ELDERLY
 Complex and multi-faceted (Unrecognized and untreated)
 There may be initial difficulties in diagnosing.
 Correct Diagnosis can be sorted out by experienced physician
 Once differentiated, the evaluation and Mx are easier
 Either One illness may overlap with other (Dementia may have Delirium)
 Or Initial presentation of one may be like another (Dem present like Dep)
 Or All the three may be present in the same patient

1. DELIRIUM
3. DEMENTIA2. DEPRESSION
6
D
e
m
+
D
e
p
1. Delirium
2. Depression
3. Dementia
4. Del + Dep
5. Del + Dem
6. Dep + Dem
7. Del + Dep + Dem

DELIRIUM – INTRODUCTIONAcute confusional state / Toxic-metabolic encephalopathy/ Organic brain syndrome / ICU or Post op psychosis
 Deficits in attention
 Acute Confusional State
 ↓Comprehension, Coherence & Capacity to reason
 Change in cognition
› Memory, Language, Orientation
 Disturbed level of consciousness
 Perceptual disturbance
› Hallucinations/ Delusions
 Visuo-spatial deficits / Apraxia
 Word-finding deficits
 Develops rapidly and fluctuates
 Usually caused by a medical illness
 Somnolence (Hepatic, Uremic, Drugs)
 Agitation (Alcohol withdrawal)

DELIRIUM - INCIDENCE
 Nursing homes : 25%
 Nursing home Elderly (>75Yrs) : 60%
 Ward In- patients : 18 to 64%
 Ward IP Elderly : 10 - 30%
 Post-operative : > 50%
 Elderly in ICU : 75 - 80 %
 Pts at end of life : 50 - 80%

DELERIUM - RISK FACTORS
AT HOME RISKS
 Old age ( > 65)
 Baseline cognitive dysfunction
 Sensory deprivation
› Hearing and visual impairment
 Poor overall health
 Immobility
 Malnutrition
 Underlying medical or neurologic illness.
HOSPITALISATION RISKS
 Catheterization
 Restraints
 Sleep deprivation
 Three or more new medications
 Inhalational anaesthetics
 Procedures CABG
 ↓/↑ Treatment of Post Op pain

DELIRIUM – CAUSES
 Medical Illnesses
 Metabolic / Electrolytic Causes
 Infection / Fever / Drugs
 Neurologic illness / Dementia
 Psychiatric/ Psychologic illness
 Discomfort : Pain / Physical
 Deprivation : Sleep / Alcohol

DELIRIUM - CAUSES
METABOLIC CAUSES
 Hyper - Natremia
 Hyper - Calcemia
 Hypo / Hyper - Glycemia
 Hyper osmolar state
 Uremia
 Liver failure
INFECTIOUS CAUSES
 Urinary tract infection
 Pneumonia
 Sepsis
 Delirium may be the first sign

CNS CAUSES OF DELIRIUM
 Dementia (Rapid worsening)
 Seizures / Post-ictal state
 Stroke / CVT
 Alcohol withdrawal (delirium tremens)
 Barbiturate/BZD withdrawal (rare)
 Increased intracranial pressure
 Head Injury
 Encephalitis / Meningitis
 Vaculitis

DRUGS - ANTICHOLINERGIC EFFECTS
USUAL
 Benztropine (Cogentin)
 Trihexyphenidyl (Pacitane)
 Tricyclic Antidep (Tryptomer)
 Thioridazine (Mellaril)
 Chlorpromazine (Largactil)
 Paroxetine(Paxil)
 Narcotics
 Antihistamines
COMMON
 Furosemide
 Digoxin
 Theophylline
 Ranitidine
 Cimetidine
 Isordil
 Nifedipine
 Cerebral cortex is widely innervated by cholinergic neurons
 Age / Anticholinergic drugs  ↓ Cholinergic transmission 
 Diminished ability to perform ADLs

MEDICATIONS WITH DEFINITE ANTICHOLINERGIC ACTIVITY (POTENT ANTICHOLINERGICS)
Class Specific Medications
Antidiarrheals Diphenoxylate/Atropine.
Antihistamines Cyproheptadine, Chlorpheniramine, Dexchlorpheniramine, Hydroxyzine, Clemastine, Diphenhydramine.
Antidepressants
Amitriptyline, Amitriptyline/Chlordiazepoxide, Amitriptyline/Perphenazine, Clomipramine, Doxepin, Imipramine,
Mirtazapine, Nortriptyline, Protriptyline, Trazodone, Paroxetine
Antipsychotics
Chlorpromazine, Clozapine, Fluphenazine, Haloperidol, Mesoridazine, Olanzapine, Thioridazine, Thiothixene,
Prochlorperazine, Promethazine.
Antiemetics Dimenhydrinate, Meclizine, Prochlorperazine, Promethazine, Trimethobenzamide.
Antiparkinson agents Amantadine, Benztropine, Biperiden, Trihexyphenidyl.
Antiarrhythmics Disopyramide, Quinidine, Procainamide.
Cardiovascular agents Dipyridamole
Antispasmotics
Belladonna Alkaloids, Clidinium/Chlordiazepoxide, Dicyclomine, Flavoxate, Hyoscyamine, Oxybutynin, Propantheline,
Tolterodine.
MEDICATIONS WITH POSSIBLE ANTICHOLINERGIC ACTIVITY (WEAK ANTICHOLINERGICS)
Antiulcerants Cimetidine, Ranitidine.
Bronchodilators Ipratropium Bromide, Theophylline, Homatropine, Tropicamide.
Cardiovascular agents Captopril, Furosemide, Isosorbide Dinitrate, Triamterene/Hydrochlorothiazide, Warfarin, Digoxin, Nifedipine.
Muscle relaxants Carisoprodol, Chlorzoxazone, Cyclobenzaprine, Metaxolone, Methocarbamol, Orphenadrine.

CAUSES OF DELIRIUM
D Drugs
E Eyes, ears, and other sensory deficits
L Low O2 states (e.g. heart attack, stroke, and pulmonary embolism)
I Infection
R Retention (of urine or stool)
I Ictal state
U Under - hydration / Under - nutrition
M Metabolic causes (DM, Post-operative state, sodium abnormalities)

OTHER CAUSES OF DELIRIUM
Toxins
 Drugs with anticholinergic properties, narcotics, and BZD
 Drugs of abuse: Alcohol intoxication / withdrawal, opiates,
ecstasy, LSD, GHB, PCP, ketamine, cocaine, "bath salts;
marijuana
 Poisons: Inhalants, CO, ethylene glycol, pesticides
Metabolic conditions
 Electrolyte Abn: ↑/↓ Glycemia, ↑/↓Na+, ↑/↓ Ca, ↓Mg
 ↑/↓ Thermia
 Pulmonary Failure: Hypoxemia And Hypercarbia
 Liver Failure/ Hepatic Encephalopathy
 Renal Failure/ Uremia
 Cardiac Failure
 Vitamin Deficiencies: B12, Thiamine, Folate, Niacin
 Dehydration And Malnutrition
 Anemia
Infections
 Systemic : UTI, pneumonia, skin and soft tissue infections,
sepsis
 CNS infections: Meningitis, Encephalitis, Brain Abscess
Endocrine
 Hyperthyroidism, Hypothyroidism
 Hyperparathyroidism, Adrenal Insufficiency
Cerebrovascular Disorders
 Global Hypoperfusion States, HTNve Encephalopathy
 CVA / ICH
 Nondominant Parietal And Thalamic Lesions
Autoimmune Disorders
 CNS Vasculitis
 Cerebral Lupus
Seizure-related Disorders
 Nonconvulsive Status Epilepticus
 Intermittent Seizures With Prolonged Postictal States
Malignancies
 Gliomatosis Cerebri, Carcinomatous Meningitis
 CNS Lymphoma
 Diffuse Metastases To The Brain
 Neurologic Paraneoplastic Syndromes
Hospitalization
 Terminal End-of-life Delirium

DELIRIUM : SYMPTOMS
 Disorganized thinking
 Disorientation to time and place
 Reduced level of attention
(drowsiness)
› Pt may fall asleep during an interview
 ↑/ ↓Psychomotor activity
› Apathy may be mistaken for depression
› Increased agitation
 Disturbances in sleep cycle
 Perceptual disturbances
› Hallucinations / Delusions
 Mood & Affect changes
 Sun-downing (“late-day confusion”)
› Confusion / Agitation get worse in eve’g
 Autonomic disturbance

DELIRIUM - PATHOGENESIS
 Ach Deficiency / Dopamine Excess
 Widespread disturbances in cortical and subcortical structures
 Diffuse localization 
› Brainstem, Thalamus, Prefrontal Cortex, And Parietal Lobes
 Focal lesions 
› Right Parietal and Medial Dorsal Thalamic lesions

TYPES OF DELIRIUM
HYPERACTIVE :
 Psychomotor agitation, Increased arousal
 Hallucination, delusions, Severe Autonomic instability
HYPOACTIVE :
 Quiet, Withdrawal, Lethargy
 Reduced arousal, Apathy, psychomotor slowing
MIXED:
 Characteristics of both hyperactive and hypoactive delirium
The hypoactive form is frequently overlooked as pt present with less problematic behavioral symptoms

DELIRIUM- DIAGNOSTIC ALGORITHM
CONFUSION ASSESSMENT METHOD (CAM)
Feature 1. Acute onset and fluctuating course
a. Is there any ACUTE CHANGE in mental status?
b. Did the behavior FLUCTUATE during the day ?
(TIME)
c. Did it increase and decrease in severity ?
(SEVERITY)
Feature 2. Inattention
a. Difficulty in KEEPING TRACK of what was being
said ?
b. Is the pt being easily DISTRACTIBLE ? (ACTIVE)
Feature 3. Disorganized thinking
a. Is there any rambling or IRRELEVANT CONVERSATION ?
b. Does he have unclear or ILLOGICAL FLOW OF IDEAS ?
c. Is he UNPREDICTABLY SWITCHING the subject ?
Feature 4. Altered level of consciousness
Level of consciousness: apart from normal alertness
a. Vigilant ( Hyper-alert)
b. Lethargic (Drowsy / Easily aroused)
c. Stupor (Difficult to arouse)
d. Coma (Un-arousable)
1 + 2 + [3 (or) 4]

DELIRIUM- CLINICAL EVAL’N
CLINICAL HISTORY (ATTENDER)
 Baseline cognitive function
 Onset / Course of present illness
 Hallucn / Delution, HT/DM/COPD/↓↑Thy
 Symptoms of Organ failure / Infection
 History of illicit Drug use / Current Medn
 HI/ Seiz / Vomiting / Headache / LOC
 Dogbite / Vaccin / Rash / Fever / Trauma
 Addiction / Malignancy / EMC / HZ
 Covid contact / Infection / Fractures
 Family Hx Dementia / Psy illnesses
 Scorpion or other bites / Failed Suicide attpt
PHYSICAL EXAMINATION (POSSIBLE)
 GPE : PICCLE / Tender sites/ Nutrition
 Vitals : Pulse, BP, RR, SpO2, Wt,
 Organomegaly / Cirrhosis / Card Resp
 HMF (Imp : Attn, Orietn, Cogn, Memory)
 Neck stiffness / Muscle tone
 Papilledema / Lower Cr N deficit
 Limb weakness / Ataxia / Dehyd’n
 DTR /Plantar/ Curled posture/ Jaw clench
 Exam of Skull & Spine
 Tremors – Fine / WFT / Rest -Pill Rolling

DELIRIUM - INVESTIGATIONS
First-tier evaluation
 Urine/CBC/ESR /LFT/ RFT/ ELECT/ Ca,Mg,Ph
 CXR / ECG / ABG
 Systemic infection screening tests
 Urine & Blood cultures
 Serum and/or urine toxicology screen
 CT / CECT/ Abd-Lung CT/ MRI & Gd/ DWI
 LP after CT, Plt : Rout + Virology, Autoimm
 Suspected seizure : EEG
Second-tier evaluation
 Vitamin levels: B12, D, Folate, Thiamine
 Endocrine: T3,T4, TSH, Cortisol
 Serum Ammonia
 Autoimmune serologies:
› ANA, Complement , p-ANCA, c-ANCA.
 Paraneoplastic workup
 Infectious serologies:
› Rapid plasmin reagin (RPR); fungal and viral
serologies, HIV, VDRL, Covid
CLINICAL CLUES  SELECT THE TESTS

MANAGEMENT OF DELIRIUM
 Find the cause(s) & Appropriate treatment
 Usually multifactorial
 Look for medication toxicity & Antidote
 Re-orient patient (Clock , Calender)
 Quiet, unstimulating environment (Sleep cycle)
 Antipsychotic medications for agitation
 Benzodiazepines often makes delirium worse
 1:1 observation/restraints only when needed
 Freq Family member visit

DELERIUM - MORBIDITY AND MORTALITY
 Patients with an in-hospital episode of delirium
› Tend to go for longer length of stay
› More likely to be discharged to a nursing home
› More likely to have repeated episodes of delirium
› Fivefold higher mortality rate
› 1 year mortality rate is 35-40 percent

DELIRIUM IN COVID -Julie Helms et al.,
 140 Covid pts @ Strasbourg University Hospital (Median age 62 )
 118 (84.3%) developed a delirium with cognition disturbances.
 88 (69.3%) presented an unexpected state of agitation despite sedation
 17/28 (60.7%) showed abnormalities in MRI
 All 42 EEGs revealed unspecific diffuse, bifrontal, slow activity.
 18/28 CSF exam : inflam responses/ oligoclonal bands /elevated IL-6.
 CSF RT-PCR SARS-CoV-2 was positive in one patient
 The delirium /neu symtoms were responsible for longer ventilation
 Could be secondary to systemic inflammatory reaction to SARS-CoV-2.

DEPRESSION - INTRODUCTION
 Persistent feeling of sadness and hopelessness
 Loss interest in activities once enjoyed
 Dx is easy when present with sadness
 Can also present with
› Cognitive impairment
› Physical symptom ( chronic pain , digestive issues)
 May manifest as irritability in older adults
 Symptoms must be present for at least two weeks

DEPRESSION - EPIDEMIOLOGY
 Depression is one of the leading causes of disability
 1-year prevalence : 2.7% to 10.3%
 Lifetime cumulative incidence : 16.2% to 17.1%
 Suicide thought in depressed : 26.9%
 High risk : Women, singles, Low socio-economic status
 Higher prevalence rate : American Indians, Native Alaskans
 Lower prevalence rate : Asian, African Americans
 Co- Occurrence with other psychiatric disorders:
› Anxiety (59.2%), Substance abuse disorder (24%), Impulse control disorder (30%)
› Anorexia nervosa, Bulimia nervosa, Borderline personality disorder
Medical Illness and
↑aging (20%) lead to ↑
risks of depression

SADNESS VS DEPRESSION
SADNESS DEPRESSION
Trigger By a specific person or event No such trigger is needed
Situation related emotion
Usual emotion; loss of a job, end of a
relationship or death of a loved one
Reasons present to be happy; but
loses the ability to experience joy
Previously enjoyed: TV, food In spite of sadness they can enjoy No longer interesting or pleasurable
Motivation, sleep, desire to eat Normal Will not do
Something said or did early
Might feel regret : won’t experience
any permanent sense of worthlessness
Worthlessness or guilt self-
diminishing, negative thoughts
Self-harm and suicidal inclinations No
Self-harm, death, or suicide, or have
a suicide plan expressed.
Extreme sadness is not Depression

DEPRESSION – RISK FACTORS
 Adverse life events :
› Early childhood trauma
› Adverse or negative life events
› Personality traits
 Substance abuse
 Physical illness
 Prolonged grief
 Cultural differences in social
interaction styles
GENETIC RISKS
 Heritability : 37 %.
 First-degree relatives : 2-4 fold
 5-HTTLPR [SLC6A4] :
› Short allele variant of the
serotonin transporter gene

UNDERDIAGNOSIS
 Somatic rather than mood complaints
 Belief that depression is a natural reaction
 Stigma of psychiatric diagnosis
 Nonspecific symptoms
 Overlap with medical illness
 Time limitations in primary care
NEW SPECIFIERS DSM-5
 Present with Manic symptoms
 Present with Anxious state
› Affect Tt, Response to Tt & Prog

DEPRESSION DSM-5 DIAGNOSTIC CRITERIA
1. Depressed mood most of the day, nearly every day.
2. Diminished interest or pleasure in all activities most of the day, nearly every day.
3. Significant ↓/↑weight, or ↓/↑ in appetite nearly every day.
4. A slowing down of thought and a reduction of physical movement (objective)
5. Fatigue or loss of energy nearly every day.
6. Feelings of worthlessness or excessive or inappropriate guilt nearly every day.
7. Diminished ability to think or concentrate, or indecisiveness, nearly every day.
8. Recurrent thoughts of death, suicidal ideation ± a plan, or a suicide attempt
5 or > 5 symptoms during the same 2-weeks / One of the symptoms should be (1) or (2)

DEPRESSION: PHYSICAL SYMPTOMS
 Unusual appetite with weight loss or weight gain.
 Unusual sleep
› Difficulty falling asleep
› Frequent awakenings / Early morning awakening.
 Fatigue or loss of energy.
 Psychomotor retardation or agitation.
 Symptoms may be expressed as cultural metaphors such as:
› Heavy heart, Self esteem problems
› Lack of balance or harmony, Just a “normal part of life”

COGNITIVE / MEDICAL SYMPTOMS
COGNITIVE SYMPTOM
 Unusual self-reproach
 Inappropriate guilt
 Unusual poor concentration
 Thoughts of death or suicide
MEDICAL SYMPTOMS
 Prevalence in medical OP : 20%
 < 50% of depressed are ∆ ed
 Cushing’s / Addison’s
 Hypo / Hyper-thyroidism
 Huntington’s / Parkinson’s
 Must be distinguished from
› Dementia, Delirium, Subs Abuse

DEPRESSION - NATIVE AMERICANS
 DSM-IV criteria may not be applicable:
› Vast differences in tribal beliefs about mental illness
› Cultural labeling of emotions /Conceptual language differences
 Modifications to DSM-IV
› Shorten threshold for duration of sad mood (2 1 week)
› Assess the presence of chronic and major depression
› Clarify date of onset if associated with alcoholism
› Assess the content and impact of auditory hallucinations

Diff.Dx OF MAJOR DEPRESSIVE DISORDER
Psychiatric Disorders
Adjustment disorder
Bipolar dis type 1 / type 2
Persistent depressive disorder
Schizoaff dis/ Schizophrenia
Neurologic Disorders
Brain tumors / CFS
Limbic /autoimmune enceph’s
Multiple sclerosis
Neurodegenerative disorders
Alz/ Lewy body / FT dementia
PD / NPH / SDH
Postconcussion syndrome
Pseudobulbar affect
Seizure / Stroke/ TIA
Sleep Disorders
Circ rhythm sleep disorders
Insomnia
Obstructive sleep apnea
Restless leg syndrome
Metabolic Disorders
Addison / Cushing
Diabetes mellitus
Graves / Hashimoto thy
↑/ ↓ thyroidism
Hypoglycemia
Hyperparathyroidism
Pituitary tumors
Nutritional Deficiencies
Fe/ FA / B12 / B3 (N) def
Infections
Encephal/ Meningitis
HIV/AIDS/ Syphilis
Neoplasia
CNS tumors
Paraneoplastic syndromes
Subs Abuse/Dependence
Alcohol
Cocaine
Marijuana
Medications
Methyldopa / Amantadine
Amphetamines / steroids
ACE inhibitors
AED / Beta-blockers
Interferons
Bromocriptine
Clonidine/ steroids
Digoxin/ Diltiazem
Estrogens/ Hydralazine
Isotretinoin / Levodopa
Metoclopramide
Progestins/ Reserpine
Sedatives/hypnotics
Statins/ Thiazides
Toxins
Aluminum
Arsenic
Mercury
Pregnancy
Cardiovascular Disorders
Arrhythmias / Cardiac
failure
CMP / CAD
Respiratory Disorders
Hypercapnia
Hypoxia
Blood Disorders
IDA / Sic Cell A
Pernicious anemia
GI Disorders
CLD / IBS
Fructose malabsorption
Lactose intolerance
Inflammatory Disorders
Autoimmune dis
Connective tissue dis
Heritable CTD
osteogenesis imperf
EDS
Electrolyte Abnormalities
↑Ca, ↓Na

RATING SCALES IN EVALUATION OF DEPRESSION
Self-Report Scales
Beck Depression Inventory-II (BDI-II) Beck Hopelessness Scale (BHS)
Zung Self-Rating Depression Scale Patient Health Questionnaire-9 (PHQ-9)
Patient Health Questionnaire-2 (PHQ-2) Center for Epidem Studies Depression Scale (CESD-R)
Major Depression Inventory (MDI) Inventory of Depressive Symptoms (IDS)
Hospital Anxiety and Depression Scale (HADS) Quick Inventory of Depressive Symptoms (QIDS-16)
Clinically Useful Depression Outcome Scale (CUDOS)
Researcher-Rated and Clinician-Rated Scales
Hamilton Depression Rating Scale (HAM-D) Montgomery-)sberg Depression Rating Scale (MADRS)
Raskin Depression Rating Scale Inventory of Depressive Symptoms (IDS)
Specific Population Scales
Geriatric Depression Scale (GDS) Kutcher Adolescent Depression Scale (KADS)
Edinburgh Postnatal Depression Scale (EPDS)

CLINICAL FEATURES OF DEPRESSION
 Depressed mood
 Diminished interest
 Decreased pleasure (anhedonia)
 Significant weight loss / gain
 Insomnia / hypersomnia
 Irritability
 Brooding (engaged in deep thought)
 Obsessive rumination (rptd thought)
 Psychomotor retardation or agitation
 Anxiety / Phobias
 Worry / Pain
 Fatigue, loss of energy
 Feelings of worthlessness, guilt
 Diminished concentration
 Indecisiveness ( lack of firmness)
 Suicidal ideation

ILLNESSES CONTRIBUTING TO DEPRESSION
MEDICAL FACTORS
 Anorexia : GI illness, cancer, chemo
 Weight loss : ↑Thy, DM, Malabsp’n
 Insomnia : OSA, Sleep MC
 Early morning awakening
 Delirium / Anxiety / Mania / CFS
 Pain / ↑Parathy / Cushing
PSYCHOLOGICAL FACTORS
 Death and dying
 Disfigurement / Disability
 Loss of role
 Family conflict
 Lifelong issues
CANCER
 50% of cancer pts
 Uncontrolled pain
 Brain metastases
 Death and Dying Young
 Disability and independence
 Disfigurement
 Chemotherapy
 Steroids / Interferon
CARDIAC ILLNESS
 20% of CAD / post MI

ILLNESSES CONTRIBUTING TO DEPRESSION
STROKE
 Not merely 2° to Neu disability
 30-50% of CVA / Half - Major dep
 High-risk period :1st 2 years
 Common with left anterior lesions
 Assd higher morbidity
 Antidepressant helps
NEU DISEASES
 Parkinson’s
 Huntington’s
 Multiple sclerosis
 ALS
 Epilepsy
 AIDS
DRUGS
 Reserpine/
Methyldopa
 Inderal
 OCP
 Corticosteroids
 BZD /Alcohol
 Opioids /Opiate
 Cocaine withdrawal

NEUROIMAGING IN DEPRESSION
 Reduced brain volume
› Frontal , orbitofrontal cortex, cingulate cortex, hippocampus, and striatum
 Pituitary enlargement
 White matter hyperintensities
 Decreased PET, and SPECT activity Left prefrontal cortex

MANAGEMENT OF MAJOR DEPRESSION
 Medications
› TCA / MAOI
› SSRI / SNRI
› Mood stabilizer
› Mood stimulant
› Anti psychotics
 Psychotherapy
 Alternative treatments
 Somatic treatment modalities
› Electroconvulsive therapy (ECT)
 Severe Depressive Disorder With
 Psychotic Features / Catatonia /
 Suicide Risk /6 Food Refusal /
 Drug-resistant / Pregnancy /
 Rapid Antidepressant Response NEEDS
› Transcranial magnetic stimulation (TMS)
› Vagal nerve stimulation (VNS)
› Deep brain stimulation (DBS) : Targets
 Subgenual cingulate gyrus,
 Nucleus accumbens,
 Ventral capsule, Ventral striatum
 Inferiorthalamic peduncle
 Lateral habenula

PSYCHOTHERAPY
 As mono-therapy in
› Mild to moderate depressive disorder
 Psycho-therapy + Pharmaco -therapy
› More beneficial
 Others
› Cognitive- behavioural Therapy Interpersonal Psychotherapy
› Psychodynamic Psychotherapy Problem-solving Therapy
› Marital And Family Therapy Group Therapy

PSYCHOSOCIAL TREATMENTS
 Supportive psychotherapy
 Clarification
 Fight stigma
 Family issues
 Substance abuse rehab
 Optimize level of care
 Home health aides
 Meals on wheels
 Adult Day Health Care
 Partial Hospitalization

ALTERNATIVE TREATMENTS
 BECOMING POPULAR
 Folate, Ω-3 FA, s-adenosyl-l-methionine, St john’s wort, Light therapy and Acupuncture
› Modest evidence for antidepressant efficacy
› Require further study
 Novel hormone and peptide treatment strategies
› Hypothalamic-pituitary-adrenal axis augmentation
› Tri-iodo thyronine/ Testosterone/ Gonadal hormones

DEPRESSION : OUTCOME
 Lead to Social isolation, Malnutrition, Slowed recovery from medical conditions
 Depression with co-morbids / in elderly can lead to increased mortality
 The most troubling outcomes of depression is suicide
 Single, white, elderly males have the highest rate of suicide
 Elderly > 85 : Higher Suicide (21/10,000 people)
 Males more likely to succeed than female

MORBIDITY AND MORTALITY
 Depression signficantly increases morbidity and mortality
 Increased risk of MI, angioplasty, and death following cardiac cath
 Independent risk factor for mortality post-MI
 Increased mortality post-CVA
 Similar results in dialysis, cancer, and general acute illness
 Possible neuroendocrine mind-body connection

DEPRESSION AND COVID
 Am I depressed or Covid fatigued?
 Covid causes Depression
 Lonliness of Covid aggravates depression
 Suicidal ideations if a depressed pts get quarantined
 Depression Symptoms 3 Times Higher during Covid
› 8.5 percent before COVID to 27.8 percent during Covid.

DEMENTIA - DEFINITION
 Dementia is an acquired loss of multiple cognitive domains which is chronic
and progressive, sufficiently severe to affect social or occupational function
FEATURES OF DEMENTIA
 Memory dysfunction + One additional cognitive deficit
 Aphasia, Apraxia, Agnosia, or Executive Dysfunction
 Difficulty in abstract thinking, Loss of judgment
 Decline from prior level of function
 Impaired ADL

DEMENTIA - RISK FACTORS
 Aging
› 10% of > 65 years and 50% of > 85 years.
 Non-modifiable risk factors
› Female sex, Black race, Hispanic ethnicity,
 Genetic factors
› Apolipoprotein e (apo-e) gene
 Modifiable risk factors
› Hypertension, Diabetes, Diet, Limited cognitive, physical, social activities

DEMENTIA AND MILD COGNITIVE IMPAIRMENT
DEMENTIA
The loss of cognitive abilities
Several cognitive domains
Memory + 1 other
Language, Visuospatial, Executive
+
Decline from the prior level of function
+
Impaired daily functional abilities
- Social, Occupational, Self-care
MILD COGNITIVE IMPAIRMENT
The loss of cognitive abilities
Demonstrable on cognitive testing
Amnestic or Non- amnestic MCI
Single or Multi-domain MCI
+
Not sufficient to impair
Functional abilities or
Independence
Criteria for dementia are not met

10 WARNING SIGNS OF DEMENTIA
1. Misplacing things
2. Diff in performing familiar tasks
3. Disorientation to time and place
4. Memory loss
5. Poor judgment / Calculation
6. Mood or behavior Changes
7. Loss of initiative
8. Problems with abstract thinking
9. Personality Changes
10. Language Problems

COMMON CAUSES OF DEMENTIA
 Treatable Dementia
› Drug related dementias
› Depression
› CNS infection
› Trauma / SDH
› Hydrocephalus / NPH
› Vit Deficiencies
› Tumor related
› Metabolic disorders
 Progressive Dementia
› Alzhiemer Disease > 65%
› Vascular Dementia >17%
› Pick’s disease
› Lewy Body Disease
› Parkinsons Disease / PSP
› Huntington’s disease
› AIDS
› Combination of Alz & Vas

DEMENTIA – CLINICAL EVALUATION
 History:
› Cognitive decline (>2) and impairment in daily activities
› Interview caregiver and patient together and separately
› Clinical course / ADL / Premorbid level of function
 MMSE: to show impairments in
› Screening questionnaire  Neuro Psychological testing
 HMF Evaluation
› Memory, Language, Attention, Visuospatial Cognition, Executive Function, and Mood
 Neurological and Physical examination
› Etiology

MMSE FOR QUICK & RE EVALUATION
 Orientation to time
 Orientation to place
 Registration
 Attention & Calculation
 Recall
 Language
 5 points
 5 points
 3 points
 5 points
 3 points
 9 points

LABORATORY TESTS
 BLOOD TESTS
› CBC, ESR
› Sugar, Urea Creatine
› LFT, TFT, Electrolyte
› Vit B12, Folic acid, Vit D
› VDRL, HIV, COVID
 ECG
 Chest x-ray
 Urinalysis
 BRAIN SCAN – CT / MRI
 Functional Brain Imaging
› (SPECT, PET)
 EEG, Evoked potentials (P 300)
 CSF analysis
› Routine studies
› Elevated tau
› Decreased Amyloid
 Heavy metal screen
 Genotyping
› Apo-lipoprotein-E (supportive dx)

TREATMENT OF AGITATION
Behavioral measures
 Calm consistent environment
 Reminding and Cuing
 Emphasize cognitive strengths
 Music & Light therapy
 Safe environment for wandering
 Daytime exercise, minimize naps
Medications
 Antipsychotics (Typical/ Atypical)
› Improve agitation and violence
 Antidepressants
 Benzodiazepines (Avoid)

DIFFERENTIAL DIAGNOSES OF DEMENTIA
1. Alzheimer Disease
2. Vascular Disease
3. Drugs, Depression, Delirium
4. Ethanol
5. Medical / Metabolic abnormalities
6. Endocrine (thyroid, diabetes), Ears, Eyes, Environ.
7. Neurologic (Other degen, Fronto-temp, DLBD, Parks)
8. Tumor, Toxin, Trauma
9. Infection, Idiopathic, Immunologic
10. Amnesia, Autoimmune, Apnea (mnemonics: AV-DEMENTIA)

CORTICAL VS SUBCORTICAL
DEMENTIACHARACTERISTICS CORTICAL SUBCORTICAL
MEMORY Severe, Recall and recogn’n
affected
Forgetfulness, Recognition better
than recall
LANGUAGE Aphasia N/ mild dysarthria
VISUOSPATIAL PERCEPTUAL ABILITY Impaired Impaired
COGNITIVE PROCESSING Normal Slowed / Bradyphrenia
FRONTAL EXECUTIVE ABILITY Preserved in early stages Impaired from onset
PERSONALITY Preserved till late Apathetic, Inert
MOTOR SPEED Normal Slowed
POSTURE AND GAIT Normal Abnormal

VASCULAR DEMENTIA
 Risk factors:
› HTN, DM, Dyslip, smoking
 Stepwise deterioration
 Preserved personality
 Multiple or single large infarct
 Lacunar state: BG, Thal, IC
 Psychomotor slowing (Subcortical)
 Binswanger’s Disease:
› Ischemia frontal white matter
› Preserved visuospatial functions
 No specific treatment
› Quit smoking
› Control BP
 Anti- Platelets

FRONTOTEMPORAL DEMENTIA
 Degeneration
› Frontal & temporal lobes
 Prior to cognitive dysfn
› Apathy, Disinhibited personality
 Selective Impairment of
› Executive functions and Naming
 Preserved
› Visuo-spatial skills
 Misdiagnosed as
› Depression, Mania
 Subtypes
› Pick’s disease, dementia of ALS.
 Decreased metabolism
› Frontal and temporal lobes
 Decreased serotonin
 Familial type
› Mutations in tau gene on chr 17

ALCOHOL RELATED DEMENTIA
 Prevalence : 6-25% (elderly alcoholics)
 Termed Korsakoff’s dementia
 Overlaps with AD
 Associated with peripheral neuropathy
 Speech functions often preserved
 Confabulatory
 Relatively subtle to diagnose

 Progressive deterioration of previously acquired intellectsImpairment in
› Thinking / Remembering / Reasoning / Social and occupational functioning
› Gradual onset, variable rate of progression
 Described by German Psychiatrist Alois Alzhiemer on 3/11/1906 (114Yrs)
 Symptoms:
› Forget recent events / difficulty performing familiar tasks
› Confusion / Personality and behavioral changes
› Communication difficulties / Impaired judgment
› In late stages, pt unable to care for him or herself.
WHAT IS ALZHEIMER’S DISEASE ?

ALZHEIMER’S - EPIDEMIOLOGY
 Not a normal part of aging
› Prevalence increases with age.
 Risk doubles every 5 years after age 65
› 65-74: 2% / 75-84: 19% / > 85yrs: 47%
 6th leading cause of death (One Alz / 71 sec)
 The costs > $148 billion each year.

ALZ DISEASE : PREVALENCE INCRESES WITH AGE

RISK FACTORS
 Age related NOT age determined
› Many people > 80,90 have no cog deficits
› Accd aging (progeria) do not develop AD
 Family History
› 1st degree relative  4 fold risk
› Early onset AD (< 60 yrs)  1° rel with AD
 Females
› Due to hormones, Environments, Education
› Not to the proportion
 Infection
 Lower educational state
› Not creating mental threshold
› Not very significant
 Head Injury
› Probably not a risk
› Dementia pugilistica
 Inflammation
› Use of NSAID
› Astrocyte/ Microglia -IL1
› Soluble βAP Insoluble amyloid
(Neurotoxic)
 Chromosome 14 & 1
 Aluminum Toxicity

LOWER RISK OF AD
 Higher levels of education
 Moderate levels of daily wine consumption
 Higher levels of fish in the diet
 Differences in the prevalence of AD among population groups worldwide suggest
› yet undisclosed genetic or environmental effects

ALZHEIMER’S Vs AGING MEMORY DECLINE
Activity Alzheimer’s Disease
Age-associated Memory
Problems
Forgets Whole experiences Parts of an experience
Remembers later Rarely Often
Can follow written or
spoken directions
Gradually unable Usually able
Can use notes Gradually unable Usually able
Can care for self Gradually unable Usually able

PSYCHIATRIC ASPECTS OF DEMENTIA
 Agitation
 Wandering
 Pacing (Walking to and fro)
 Insomnia
 Hoarding (distress at the thought of getting rid of the items)
 Catastrophic reactions
 Capgras’ syndrome (a close person has been replaced by a
duplicate)
 Psychosis
 Depression
 Anxiety
 Aphasia
 Agnosia
 Apraxia
 Deficits in abstract thinking

• The brain has 100 billion neurons, and 100 trillion
synapses.
• To stay healthy,
• Neurons must communicate
• Carry out metabolism
• Repair themselves
• Alzheimer’s Disease disrupts all three of these
essential functions
INSIDE THE HUMAN BRAIN
75

ALZHEIMER’S - NEUROSCIENCE
 Amyloid plaques (Extraneuronal)
 Neurofibrillary tangles and tau protein (Intraneuronal)
 Loss of cholinergic innervation (Nucleus Basalis of Meynert)
 Cerebral atrophy (nonspeciific)
 Decreased perfusion and metabolism in temporoparietal cortex and hippocampus
 Deficits may predate cognitive impairment
 Abnormal extraneuronal processing of b-amyloid precursor protein
› (b-APP) to 42- a.a. instead of 40-a.a. fragment
 Familial AD - single-point mutations in b-APP
 Presenilins (chromosome 14 and 1) may be b-APP secretases
 Apolipoprotein E4 - risk factor for sporadic AD.
 Subtle deficits in younger life - decreased “idea density”

ALZHEIMER’S: ASSESSMENT
 Tools for staging of Alzheimers dementia:
› Global Deterioration Scale
› Brief Cognitive Rating Scale
› Functional Assessment Staging Tool
 Tool cognitive strength
› Mini Mental Status Exam (MMSE)
 Other cognitive tests:
› Clock test, SLUMS exam, Brief Portable Mental Status Questionnaire.
 Clinical diagnosis by ruling out other causes
 Absolute method for diagnosis : autopsy

RULE OUTS FOR ALZHEIMER’S DEMENTIA
TESTS RATIONALE – rule out…
Urinalysis
Kidney dysfunction, toxic
encephalopathy
CBC, ESR, ELECTROLYTE Anemia, electrolyte imbalance
RFT, LFT Liver dysfunction
TFT Thyroid dysfunction
Serum B12 Vitamin deficiency
Syphilis serology Syphilis
HIV test AIDS dementia
Neuroimaging studies: CT or MRI
Tumor, SDH, abscess, stroke, or
hydrocephalus

STAGES OF ALZHEIMER’S
Alzheimer’s disease has recognizable stages:
1. No cognitive impairment
2. Very mild decline
3. Mild cognitive decline
4. Moderate cognitive decline
5. Moderately severe cognitive decline
6. Severe cognitive decline
7. Very severe cognitive decline

ALZHEIMER’S - TREATMENT
Cholinergic
 Donepezil 5 mg  10 mg
› Modest but consistent effect
› Useful in all stages of AD
› No effect on MMSE
› ADLs, memory, attention &
neuropsychiatric symptoms improve
 Rivastigmine is similar drug
 Memantine
Neuro- protective
 Antioxidants (Vitamin E, L-Deprenyl)
 Anti-inflammatories
 Inhibitors of secretases
 Vaccines against b-amyloid

CLINICAL FEATURES
 Impairment of delayed recall
 Inability to retrieve information
acquired in the past
 Gradual impairment of short &
long term memory
› Misidentifying family member
 Later
› Apraxia (Inability to perform learned
movements on command )
› Visuo spatial disorientation
› Aphasia
› Anosognosia (Deny having any
abnormalities)
› Depression
› May become aggressive
81

TYPICAL CLINICAL SYNDROME OF AD
1. Amnestic type of memory defect
› Difficulty learning and recalling new
information
2. Progressive language disorder
› Beginning with anomia and progressing to
fluent aphasia
3. Disturbances of visuospatial skills
› Manifested by environmental disorientation
and
› Difficulty copying figures in the course of
mental status examination
4. There are usually deficits in executive
function
› Planning
› Insight
› Judgment
5. The patient is typically unaware of
memory or cognitive compromise.
6. All cognitive deficits progressively
worsen.

Pathology
 Atrophic brain
 Cerebrum
 Hippocampus
 Histology
 Senile plaques (Amyloid)
 Neuro fibrillary tangles
 Neuro transmitter abn
 Cholinergic transmission
 NA
 5HT
 Glutamate
 Sub P
83

The Hallmarks of AD : Plaques and Tangles
Brain with AD have an abundance of these two abnormal structures
An actual AD plaque An actual AD tangle
1. Beta-amyloid plaques, which are dense deposits of protein and cellular material that
accumulate outside and around nerve cells
2. Neurofibrillary tangles, which are twisted fibers that build up inside the nerve cell
ALZEIMER’S DISEASE AND THE BRAIN

85/3
0
 Neurofibrillary tangles
 Senile plaque
 Accumuln of β-Amyloid P
 Selective neuronal & synaptic loss
 Hirano Bodies
 Gen. Astrocytosis
 Neuropil threads
 Granulovasc. Degn.
 Assn area & limbic structure
involvement
 Degn. of subcort N & projc’ns
› Basal FB cholinergic Nuclei
› Locus cerulius
› Raphe Nuclei
› Thalamus & Amygdala
PATHOLOGY

PATHOLOGY
 Cerebral cortical atrophy
› Early onset (< 50 yrs): Cortical atrophy
› Late onset (> 65 yrs): Limbic atrophy
 Coronal sections:
› Accentuated sylvian & inter hemi spherical fissure
› Thinning of cortical mantle
› Ventriculo megaly
› Olfactory bulb atrophy
› Severe shrinkage of Hippocampus
› Enlargement of temporal horn
 Unaffected structures
› BG, Thalamus, BS, Cerebellum, Caudate N.,Sub.Nigra
› Parasaggital sec of cerebral hemispheres – N
› Pons and Locus cerulius are depigmented and pale

SENILE PLAQUES
 Extra cellular
 Composed of
› dystrophic axons and dendrites
› βAP
 42,43 AA Peptide
 Fragment of Amy Prec Pro (AAP)
 Gene for APP is at Chr 21
› Astrocytes
› Microglia
 Present in
› F,T&P Asssn areas
› Amygdala
› Hippocampus
› Pyriform cortex
› Cortical leptomeng’ Bl Vessal wall

NEUROFIRILLARY TANGLES
 NFT: Intraneuronal cytoplasmic structures
› Paired filments of helical periodicity
 Present in
› Neocortx, Hipp’s,NB of Maynert,Dorsal Raphe N
 NFT remain behind after the death of Neuron
› Sometimes seen in normal old people’s brain
 NFT are composed of ‘tau’ protein
› Hyperphoporylated microtubule asstd prot
 Normal neuronal cytoskeleton
› Microfil + Neurofil + tau assd helical microtubule
› For axonal transport &, Structural integrity
› tau Dissoc’n hyper phos’ln  aggrg’n  NFT

HIRANO BODIES
 Rod shaped Eosinophilic structures
 Excess in CA1 of HC in AD
 Present inside Dendrites
 Stain immuno chemically
 Also in elderly brain / other deg dis
 Intra cytoplasmic vacuoles
 Contain hyper eosinophilic granule
 Also present in normal elderly / more in AD
91/3
0
GRANULOVASCULAR DEGENERATION

OTHER PATHOLOGIES
 Cerebral amyloid angiopathy
› Involve small & medium sized bld vessels
 Of the leptomeninges and cortex
 In the parietal and frontal lobes
› Thickening and hyalinization of vessels
› Compromise the vessel integrity
 Hemorrhage (sub-cortical / Multi-centric)
 Multi neurotransmitter deficiency
› Loss of cholinergic markers
 ↓ Choline acetyl transferase
 ↓ Ach synthesis / ↓ Choline uptake
 ↓ Acetyl cholinesterase
› Pre-synaptic noradrenergic deficit
› Depletion of Serotonin, Somatostatin,
Corticotrophin releasing factor, &
Glutamate

Preclinical AD
•Signs of AD are first noticed in the ento-
rhinal cortex, then proceed to the
hippocampus.
•Affected regions begin to shrink as nerve
cells die.
•Changes can begin 10-20 years before
AD and the Brain

• AD spreads through the brain.
• The cerebral cortex shrinks as more neurons are affected
• Mild AD signs appears
• Memory loss, confusion, trouble handling money, poor judgment,
mood changes, and increased anxiety.
• Moderate AD signs follows
• Increased memory loss and confusion, problems recognizing people,
difficulty with language and thoughts, restlessness, agitation,
wandering, and repetitive statements.
Mild to Moderate AD
AD and the Brain
94

Severe AD •In severe AD, extreme shrinkage occurs in
the brain.
•Patients are completely dependent on
others for care.
•Symptoms can include weight loss, seizures,
skin infections, groaning, moaning, or
grunting, increased sleeping, loss of bladder
and bowel control.
•Death usually occurs from aspiration
AD and the Brain

ALZHEIMER’S DISEASE - TREATMENT
 Cholinesterase inhibition is the 1st successful line of Mx
› Improves (Modestly): Cognition, behaviour, ADL
 To be started early
› Donepezil /Galantamine
› Memantidine / Rivastigmine
 Supportive Therapy
› Life style modification / Family
› Environment / Anti depressants

ALZ DISEASE - SUMMARY
 Alzheimer’s is a progressive disease
 Age is the main risk factor
 Stable level of consciousness
 Insidious onset, not fluctuating
 Deficit is in short-term recall & at least in 3 cognitive areas
 No definitive treatment Exist
 We can temporarily slow it’s progression
 Treatment is largely for psychiatric complications
 Caregivers and support groups are very important

COVID AND DEMENTIA
 Several case reports : Cofusion as presentation of covid
 Like DDD, Covid also will be addl risk to elderly
 Regular SMS will be difficult to perform for Covid pts
 Covid health risk has raised the dementia caregiver burden
 If pt with dementia gets Covid  IP / ICU stay will be more complicated , mostly they
require sedation more morbidity and mortality
 People with dementia must not feel isolated
 loneliness and isolation are risk factors for both depression and dementia, 
lockdowns may worsen
 Alzheimer’s and Related Disorders Society of India (ARDSI), which, in partnership with
government institute, are
 If feasible, a family can shift temporarily with the elder one to a place where the
required supports can be provided easilyhelping in mobilization of support

DETAILED HX IN ACUTE CONFUSIONAL STATE
 Medical, Psychiatric, and Family history
 Onset and duration of symptoms
 Recent stressful or traumatic events
 Surgery or death in the family
 Changes in environment
 New drugs, including OTC drugs
 Diet history
 Personal or family history of
› Alcohol, Substance Abuse, Dementia, Depression, Suicide Attempts, Thyroid Disease

DEPRESSION + DEMENTIA
Delirium
Depression
Dementia

DEPRESSION IN DEMENTIA
 H/O depression doubles the risk of
dementia (Ownby et al.,)
 Mechanisms
› Depression is a prodrome of dementia
› Depression ↓ threshold for dementia
› Depression damages neural systems
(hippocampus)  ↑ Cortisol
 CVD, HTN, DM & vascular risks are common
 Tt of depression in dementia
› TCA, SSRI, MAOI (Not authenticated)
› Donepezil delays progression to AD
 Incidence: 20-40 % / IP : 65% (JAMA 2002)
 ↑Morbidity /Mortality /Stress to caregivers
 75% dementia had recent H/O N.Psy symp
› 55% had > 2 symptoms
› 44% had > 3 symptoms
 Dementia may mimic depression
› Apathy 36%
› Agitation 30%
› Loss of interest 32%
 Cognitive ↓  Poor expression of sadness

DEPRESSION AND DEMENTIA
 Cognitive impairment in late-life depression
› Important risk of dementia
 To do robust Cognitive screening
› For multiple domains
 Depression in Mid & Late life  ↑ risk of dementia
 As dementia progresses, his depression may become less noticeable
 Dx of depression may be confirmed if antidepressants reduce the symptoms

DELIRIUM AND DEPRESSION
Delirium
Depression
Dementia

DELIRIUM AND DEPRESSION
 Several studies:
 Delirium may be misdiagnosed as depression : 6-52%
 Present in both : weight loss, fatigue, reduced energy, reduced appetite
and psychomotor retardation
 Risk for Delirium in depressed : 1.9 – 9 fold
 Mechanism :
› In both dopaminergic-cholinergic imbalance as a common final neural pathway
› Aberrant interactions between inflammatory mechanisms
› Limbic-hypothalamic-pituitary-adrenocortical axis (LHPA)
› Disturbed melatonergic activity has been reported in delirium
› High levels of plasma cortisol, and dexamethasone non-suppressionhave been
reported in delirium

DELIRIUM AND DEMENTIA
Delirium
Depression
Dementia

DELIRIUM AND DEMENTIA
 Pts with both deliriumand dementia can be the most challenging
 Recent data suggest that delirium and dementia may reside more
on a continuum rather than as two separate disease entities.
Patients with either diagnosis have a higher risk of succumbing to
the other
 Both disorders seem to have acetylcholine deficiencies. Whereas
anticholinergic medications can make both dementia and delirium
patients worse, cholinesterase inhibitors can make them better.
 Patients can also have delirium superimposed on dementia [6],
making diagnosis and management more challenging.

CASE REPORT
 Mr KM, 79/M, Omalur
 HT/DM/CAD 6yrs, on Tt
 School HM / Well behaved
 Acute beh change 1 wk
 Disorientation/ Irritability
 ↓Sleep / ↑Talk
 Anger to wife
 III r episode 4yrs ago - ↓Na
 Vitals : N
 Mood/Perception : N
 Disorientation to time
 Poor attention span
 Judgment/Speech : N
 Insight: 1/6
 Mem: (Imm/ Recent): impaired
 MMSE : 21/30

CASE Contd..,
 Poor initiative
 Cannot draw sq-Triangle
 Dressing apraxia
 Mistakes in Calculation
 Clock : wrong No: / No arms
 Prosopagnosia : +
 Acute confusion with fluctuation
 Angry and Beh Changes
 Fron+Temp+Par+occ involvement
 Diag: Alzheimer’s Disease onset with
Delirium
 All Blood : N
 USG/ MRI/ CSF : N
 PET : Hypomet in FT lobes
 ? FT /Early Alz Dementia
 Donep  Aggressive  Stopped
 Qutipin and Beh Therapy
 1 month Review 
 No Delirium but MCI

DELIRIUM DEMENTIA
Onset
Rapid (hours/days); rapid decrease in
MMSE score.
Slow (months, years); slow decline
of 2 to 3 MMSE points over a
period of years.
Symptoms Fluctuate over the course of the day. Relatively stable.
Duration Days to weeks. Months to Years.
Orientation
Disorientation and disturbed thinking
are intermittent.
Persistent disorientation.
Level of
consciousness
Fluctuates, with inability to
concentrate.
Alert, stable.
Sleep/wake cycle Sleep/wake cycle may be reversed. Sleep may be fragmented.
IS IT DELIRIUM OR DEMENTIA ?

DELIRIUM IN DEMENTIA
 In dementia, if sudden mental agitation
› Assess for delirium
› Assess for Medical illness
› Assess for underlying distress
 Constipation, fever, pain, or infection.
 Communicating problems in Dementia
› Observation
› Physical exam
› Lab test
› Repeat history
 Prevalence of delirium in dementia : 22 - 89%
 Delirium may be under- recog’d in dementia
› Hypoactive form of delirium
› K/C/O Dementia / Age > 80
› Impairment of Vision
 Untreated delirium (in dementia) 
› Long-term cognitive and functional decline
› Hospitalization & Re-hospitalization
› Increased mortality

DELIRIUM, DEPRESSION, DEMENTIA
 Older adults (>65) are the faster growing segment
 Three most common mental health conditions among ELDERLY
 However these are not normal manifestations of aging
 Elderly may experience more than one at the same time
 They ay occur simultaneously or subsequently
 Complex and multi-faceted (Unrecognized and untreated)
 Difficult to distinguish when one overlaps another
 Negatively impact health, well-being, and quality of life
Number of Person over 65+
0
10
20
30
40
50
60
70
80
1900 1920 1940 1960 1980 1998 2000 2010 2020 2030
Year (as of July 1)
numbersinmillions

Weng et al., (2019)
 Prospective Cohort study
 2012-13 @ Taiwan
 Earlier admitted pts of age > 65
 Called and assessed ACS admn
 GDS / MMSE / CAM done
 Func status assessed by BI @
› Adm / Dis / 30d / 90d / 180d
 149 pts assessed and followed 6m
› Depression : 27 (18.1%)
› Dementia : 37 (24.8%)
› Delirium : 85 (57.0%)
 All func decline  Grad recovery
 Delirium &Dementia :Low Barthel Inx
 No func’l decline noted in Depression

Prakash B Neuro Delirium Depression Dementia

Recommandé

Recommandé

Contenu connexe

Similaire à Prakash B Neuro Delirium Depression Dementia

Similaire à Prakash B Neuro Delirium Depression Dementia (20)

Dernier

Dernier (20)

Prakash B Neuro Delirium Depression Dementia