OT 10211 3S2L Neurocognitive Disorders PDF

Asst. Prof. Joselito Diaz, MD, MHA, FPNA, FPCPsych De Jesus, Gayeta, Oblea, Pineda A., Salas, Victoria / Burgos, Gan, Muncada, Ronquillo, Rosario, Torres 3S2L: NEUROCOGNITIVE DISORDERS...

Asst. Prof. Joselito Diaz, MD, MHA, FPNA, FPCPsych De Jesus, Gayeta, Oblea, Pineda A., Salas, Victoria / Burgos, Gan, Muncada, Ronquillo, Rosario, Torres 3S2L: NEUROCOGNITIVE DISORDERS R. Psychiatric And Cognitive Changes In Dementia: OUTLINE Sundown Syndrome 12 NEUROCOGNITIVE DISORDERS 1 S. Dementia: Treatment 12 A. Neurocognitive Domains 1 AMNESTIC DISORDER 12 1. Complex Attention 1 A. Amnesic Disorder: Major Causes 12 2. Executive Function 2 B. Amnesic Disorder: Anatomical Substrate 13 3. Learning and Memory 2 C. Amnesic Disorder: Clinical Features 13 4. Language 2 D. Amnesic Disorder: Course And Prognosis 13 5. Perceptual-Motor 3 6. Social Cognition 3 MILD COGNITIVE IMPAIRMENT (MINOR NEUROCOGNITIVE DISORDER) 13 NEUROCOGNITIVE DISORDERS A. DSM-5 Diagnostic Criteria For Mild Cognitive Impairment A. Delirium 13 B. Dementia (Major Neurocognitive Disorder) B. Mayo Clinic Alzheimer’s Disease Research Center C. Amnestic Disorder (MCADRC) MCI Criteria 13 D. Mild Neurocognitive Disorder C. MCI: Risk Factors 13 CLINICAL EVALUATION OF PATIENTS WITH D. Outcome of Clinical Phenotypes of MCI 14 NEUROCOGNITIVE DISORDERS 4 E. MCI: Course/Prognosis And Treatment 14 A. Medical History 4 B. Comprehensive Physical And Neurologic Examination MENTAL STATUS EXAMINATION NEUROCOGNITIVE DISORDERS A. Neuropsychiatric Mental Status Examination Commonly recognized as “those na nagkakaroon ng B. Mini Mental State Examination (Mmse) dementia.” But neurocognitive disorders do not mean dementia only. MONTREAL COGNITIVE ASSESSMENT – PHILIPPINES ○ There are milder cases of cognitive disorders– (MOCA-P) 3 mild cognitive impairments (MCI), delirium A. Screening Laboratory Tests Neuropsychiatric disorders B. EEG Individuals suffering from a neurocognitive disorder would C. Brain CT and MRI reflect a disruption in one or more cognitive domains: D. Neuropsychological Testing ○ Complex attention DELIRIUM 6 ○ Executive function A. Classic Presentation 6 ○ Learning and memory 1. DSM-5 Diagnostic Criteria For Delirium 7 ○ Language 2. Delirium: Epidemiology 7 ○ Perceptual-motor 3. Delirium: Predisposing Factors 7 ○ Social cognition 4. Delirium: Predisposing Factors 7 Disruption in the cognitive domains may be single, but is 5. Delirium: Etiology 7 usually multiple. 6. Dementia Vs Delirium 8 ○ It will be dependent on the different causes of the 7. Delirium: Course 8 cognitive decline that will tell us which of the 8. Delirium: Prognosis 8 9. Delirium: Treatment 8 following domains would be affected. 10. Delirium: Pharmacotherapy ○ Example 1: individuals with subcortical 11. Delirium In Parkinson’s Disease dementias, usually secondary to a vascular origin DEMENTIA (MAJOR NEUROCOGNITIVE DISORDER) 8 (e.g., stroke) may be presenting primarily with disruption in executive functioning A. Dementia Etiology 8 ○ Example 2: individuals with stroke, which would B. DSM-5 Diagnostic Criteria For Major Neurocognitive Disorder 9 involve the temporal lobe (hippocampus) may C. Dementia of the Alzheimer’s Type 9 present with problems in learning and memory D. Neuropathology In Alzheimer’s Disease 9 ○ Example 3: individuals with Alzheimer’s E. Neurotransmitters In Alzheimer’s Disease 9 Dementia (the most common) would initially F. MRI Brain: Normal Vs AD 9 present problems with memory. G. Vascular Dementia 10 ○ Example 4: individuals with Huntington’s chorea H. Binswanger’s Disease 10 or dementia, or those with Parkinson’s later on I. Pick’s Disease 10 developing dementia may have problems with J. Frontotemporal Dementia 10 K. Frontotemporal Dementia 10 executive functioning L. Clinical Criteria For Dementia With Lewy Bodies 11 Each of the different causes/ etiology of dementia may M. Huntington’s Disease 11 have different presentations. N. Parkinson’s Disease 11 O. HIV-Related Dementia 11 P. Head Trauma-Related Dementia 12 Q. Psychiatric And Cognitive Changes In Dementia: Catastrophic Reaction 12 1  NEUROCOGNITIVE DISORDERS NEUROCOGNITIVE DOMAINS ○ There could be loss of immediate or recent memory COMPLEX ATTENTION LANGUAGE Sustained attention, divided attention, selective attention, processing speed Expressive and receptive language ○ Has increased difficulty in environments with ○ Often uses general-use phrases such as “that multiple simultaneous stimuli (TV, radio, thing” and “you know what i mean,” and prefers conversation) general pronouns rather than names ○ Is easily distracted by competing events in the They cannot name objects or people environment (talking to somebody while the radio Anomic aphasia- instead of saying is on) “ballpen” tinatawag na “that thing” ○ Has difficulty holding new information in mind ○ May not even recall names of closer friends and (recalling phone number just given) family ○ Unable to perform mental calculations ○ Grammatical errors, idiosyncratic word usage, ○ All thinking takes longer than usual echolalia, economy of utterances, mutism Those individuals who have a problem in this domain would have difficulty in environments wherein there are several multiple stimuli simultaneously PERCEPTUAL-MOTOR ○ Difficulty sustaining attention in one stimulus or Visual perception, visuoconstructional, the other perceptual-motor, praxis, gnosis ○ They may be a little confused when there are too ○ Has significant difficulties with previously familiar many sensory stimuli activities (driving motor vehicle, using tools), In order to have a functioning working memory, having navigating in familiar environments attention is important so that there would be registration of ○ Is often confused at dusk, when shadows and information. lowering levels of light change perceptions ○ If attention is already impaired, you do not expect them to have intact immediate memory. SOCIAL COGNITION EXECUTIVE FUNCTION Recognition of emotions, theory of mind ○ Behavior clearly out of acceptable social range Planning, decision making, working memory, (shows insensitivity to social standards of responding to feedback/ error correction, overriding modesty in dress or of political, religious or habits/ inhibition, mental flexibility sexual topics of conversation) ○ Abandons complex projects due to difficulty in They can be wearing inappropriate planning clothes to different occasions ○ Needs to focus on one task at time (cannot ○ Focuses excessively on a topic despite group’s multitask) disinterest or direct feedback ○ Needs to rely on others to plan instrumental Even if it is obvious na no one is activities of daily living or make decisions interested in the topic, tinutuloy niya pa Difficulty in executive functioning would denote problems ring pag-usapan because there is failure in the subcortical region, particularly in the basal ganglia to recognize the affect of people he is or prefrontal cortex. conversing with ○ Makes decisions without regard to safety Kahit na lasing, iniinsist pa rin niya na LEARNING AND MEMORY magdrive Immediate memory, recent memory, very long-term memory NEUROCOGNITIVE DISORDERS ○ Repeats self in conversation, often within the Frequently complicated by behavioral symptoms same conversation ○ Anxiety, depression, psychosis, sleep ○ Cannot keep track of short list of items when disturbance and aggression shopping or of plans of the day Interface between neurology, medicine and psychiatry ○ Requires frequent reminders to orient to task at ○ These professions will be collaborating in hand neurocognitive disorder cases Impaired immediate and recent memory would denote ○ Biological insults result in behavioral problems in the temporal lobe, particularly in the medial symptomatology temporal region, wherein the hippocampus is located. Delirium Immediate and recent memory: Stored in the ○ Major neurocognitive disorder hippocampus and limbic system Amnestic disorder Very long-term memory: Stored in the different association ○ Mild cognitive disorder cortices in the brain ○ Problems in long-term memory would denote DELIRIUM impairment of the whole brain, not only on the Marked by short-term confusion and changes in temporal lobe, but already a dysfunction in the cognition whole cerebral hemisphere, both right and left. ○ Remember that in individuals with delirium, Individuals with amnestic cognitive impairment would need there would be an impairment in the level of to write down everything so that they do not forget. consciousness wherein they’re not comatose Requires frequent reminders to orient to task at hand or stuporous but they are confused and due 2  NEUROCOGNITIVE DISORDERS to the confusion, there can be changes in the Causes: cognition. (1) Medical conditions (hypoxia) Usually transient and not progressive For example, they went into Once the underlying problem is resolved, they should cardiorespiratory arrest and they go back to their normal level of functioning. are revived, but there could be 4 subcategories based on causes: damage to the temporal lobe. (1) General medical condition (e.g., infection) (2) Toxins or medications (e.g., marijuana, This is the usual cause, especially diazepam) during the height of the pandemic. (3) Unknown causes Those with COVID-19 would have concomitant respiratory infection MILD NEUROCOGNITIVE DISORDER and would go into delirium. They Presence of mild cognitive decline not warranting the may be very aggressive or they diagnosis of dementia but with preserved basic could be hallucinating. activities of daily living Usually they are confused, would ○ How do we know that it’s not dementia? try to remove all the apparatuses Usually they have preserved basic and that are attached to them, may be instrumental activities of daily living violent, or shouting, and this is In the DSM-5 classified as mild neurocognitive secondary to a medical condition. disorder due to multiple etiologies or unspecified (2) Substance induced (e.g., cocaine, opioids, neurocognitive disorder phencyclidine [PCP]) The use of illicit drugs CLINICAL EVALUATION OF PATIENTS WITH (3) Multiple causes (e.g., head trauma and NEUROCOGNITIVE DISORDERS kidney disease) (4) Other or multiple etiologies (e.g., sleep deprivation, medication) MEDICAL HISTORY For example, those who will be Blood chemistries (including electrolytes, renal and taking antibiotics hepatic indexes, and glucose) Those who will be given Temporal development of the illness corticosteroids which may cause ○ Onset: delirium Sudden (acute) Can also be secondary to sleep Insidious (long term but progressive) deprivation ○ Course: Fluctuating (may be delirium or DEMENTIA (MAJOR NEUROCOGNITIVE DISORDER) something psychiatric, such as being Severe progressive impairment in cognition in caused by depression or anxiety) clear consciousness Progressive (neurodegenerative They are alert but when you do your evaluation, you disorder or medical disorder that is will see that there is progressive impairment in one or worsening such as liver or kidney several cognitive domains. problem. They are already uremic and Subcategories: this causes the progressive decline in (1) Dementia of the Alzheimer's type cognitive functioning) Usual onset is ≥ 65 years of age Static (such as in vascular dementia (2) Vascular dementia (vessel thrombosis or wherein there is an insult to the brain hemorrhage) and then their level of functioning will Because of stroke remain the same, and then if they have (3) Human immunodeficiency virus (HIV) a stroke, there would be a decline. Like disease a step ladder.) (4) Head trauma Occupational and social functioning (if there are (5) Pick’s disease or frontotemporal lobar disruptions in their ADLs, it might be dementia and not degeneration mild neurocognitive disorder) (6) Prion disease such as Creutzfeldt-Jakob ○ Appraise impact of illness disease Whether the patient would still be Another example is Kuru disease independent in their ADLs (basic, (mostly wiped), usually seen in instrumental) Papua New Guinea where tribes Impact on the caregiver practice cannibalism Behavioral and personality changes Another example is Mad cow ○ Define the etiology and help in the treatment disease (7) Substance induced, caused by toxin or medication (e.g., gasoline fumes, atropine) COMPREHENSIVE PHYSICAL AND NEUROLOGIC (8) Multiple etiologies EXAMINATION (9) Not specified (if cause is unknown) To determine the etiology (cognitive/neurological) of the AMNESTIC DISORDER cognitive decline Classified in DSM-5 as major neurocognitive disorders caused by other medical conditions MENTAL STATUS EXAMINATION Present primarily by memory impairment in addition to Psychiatric point of view other cognitive symptoms A means of surveying functions and abilities to allow a definition of personal strength and weakness 3  NEUROCOGNITIVE DISORDERS A repeatable, structured assessment of symptoms and MINI MENTAL STATE EXAMINATION (MMSE) signs that promotes: ○ Establish baseline functioning Baseline or screening test for individuals complaining of Determine any improvement or cognitive decline, especially memory progressive decline Orientation ○ Establishes the basis for future comparison Registration ○ Documenting therapeutic effectiveness ○ Giving 3 objects to remember Pharmaceutical non/pharmacological ○ Ex: Filipino MMSE: mangga, lamesa, pera. ○ Effective communication between clinicians Tandaan po, mamaya itatanong ko ulit. May be read by other professionals (OT, (recall) psychologists, psychiatrists) Pakiulit po ano yung tatlong bagay ○ Comparison between patients ○ Would also examine language and attention There may be same diagnosis, age, No attention = no registration medications, but the progression of Attention and calculation disorder or presentation of effect of ○ Pakibaybay na lang po ang salitang “mundo” medications may vary pabaligtad ○ If English is not their first language, use Tagalog, or serial sevens NEUROPSYCHIATRIC MENTAL STATUS 100-7-7-7 (mental calculation) EXAMINATION Language ○ Understanding is important General description ○ Praxis and attention are also examined Language and speech ○ Read and obey a written command on a piece of Thought paper “Close your eyes” – no need to say it out Mood and affect aloud → checking reading ability Insight and judgment ○ Write a sentence – check for writing and Cognition language, ability to comprehend complex tasks ○ Memory Copying ○ Visuospatial skills ○ Checking for visuoconstructional praxis ○ Constructional ability ○ Ability to comprehend the command ○ Mathematics ○ Writing Table No 1. Categories in MMSE ○ Reading PARAMETER POSSIBLE PARAMETER ○ Fine sensory function (stereognosis, POINTS graphesthesia, two-point discrimination) Orientation to 5 From broadest to most ○ Finger gnosis time narrow. ○ Right-left orientation ○ Executive function Correlated with future ○ Abstraction decline. Orientation to 5 From broadest to narrow. place Sometimes narrowed down to streets, and sometimes to floor. Registration 5 Repeating named prompts Checking for immediate or short-term memory Attention and 5 Serial sevens or spelling calculation “world” backwards. It has been suggested that serial sevens may be more appropriate in a population where English is not the first language. Recall 3 Registration recall Language 2 Naming a pencil and a watch Repetition 1 Speaking back a phrase Complex 6 Varies. commands Can involve drawing figure shown. 4  NEUROCOGNITIVE DISORDERS MONTREAL COGNITIVE ASSESSMENT – ○ May be secondary to infection PHILIPPINES (MOCA-P) Thyroid function tests ○ Hypothyroidism can manifest in slowness in thinking Urinalysis ○ Check for infection Electrocardiogram ○ Cardiac or pulmonary condition Chest radiograph Blood and urine drug screens Pregnancy test ○ Especially, if you are going to give medication ○ Rule out pseudodementia Serum protein ○ Hypoalbuminemia may cause confusion ANCILLARY LABORATORY TESTS Blood cultures, HIV testing, rapid plasma reagin test, heavy metals, serum B12, folate levels ○ To rule out HIV, malnutrition, exposure to toxins, etc. ○ Rapid plasma reagin test: to check for syphilis EEG Brain CT, MRI, PET, SPECT (neuroimaging) Brain biopsy CSF analysis ○ Rule out infection More detailed examination Neuropsychological testing Visuospatial / Executive ○ Formal neurocognitive assessment especially to ○ Connect succeeding numbers and letters know the person’s capacity to make decisions ○ Copy the cube (legal problems) ○ Draw a clock test (Sampungminuto makalipas ○ Maybe they are lending or withdrawing money to ang alas onse) family members ○ Can test planning and visuospatial ○ Contention with the will Naming ○ Name particular animals EEG Memory ○ Three terms to remember in MMSE Toxic-metabolic states (diffuse slowing of brain activity) ○ In the MOCA-P, there is 5 (mukha, asul, ○ Secondary to drug, infection, metabolic state like simbahan, rosas, seda) renal or liver failure Attention Rule out nonconvulsive status epilepticus ○ Repeating 5 numbers forward and 3 numbers Rule out factitious disorders, depression or psychotic backward disorders ○ Serial of 7 ○ EEG should be normal ○ Tap table everytime they hear the letter “A” Language BRAIN CT AND MRI ○ Read specific statements ○ In one minute, give filipino words starting with the Brain atrophy characteristic of Alzheimer’s or letter “B” frontotemporal dementia Abstraction WM changes in MS, HIV infection, vascular dementia ○ Similarities and differences ○ You can see a particular lesion in the MRI Delayed Recall Most important is what it can exclude rather than what it ○ Recall items mentioned during memory test can demonstrate specifically Orientation ○ To see that it is not because of stroke, trauma to Maximum score: 30 head, or tumor in the brain ○ Normal: 26 and above ○ If they have an education less than 12 years, add 1 point NEUROPSYCHOLOGICAL TESTING Standardized, quantitative, reproducible evaluation of a patient's cognitive abilities SCREENING LABORATORY TESTS Baseline and periodic assessment Blood chemistries (including electrolytes, renal and ○ To determine if improving or worsening hepatic indexes, and glucose) ○ Advisable for legal implications ○ Check for kidney and liver functions, blood sugar (might be hypoglycemic which is the cause of DELIRIUM confusion) Characterized by an acute decline in both the level of ○ Electrolytes: sodium and potassium consciousness and cognition with particular impairment in Complete blood count with white cell differential attention 5  NEUROCOGNITIVE DISORDERS ○ Involves perceptual disturbances, abnormal attention and awareness are disturbed. Also psychomotor activity (agitated / violent), mood includes individuals whose activity rapidly disturbance (irritable) and sleep cycle impairment fluctuates (awake most of the time) Other Names of Delirium ○ Common neurological symptoms: nystagmus, ○ Intensive care unit psychosis tremors, incoordination, dysarthria and myoclonic They are in the ICU for several days. jerks There could be some behavioral Life threatening, yet potentially reversible disorder of the changes that could occur because of CNS this setting and seeing the same people ○ Brain is not functioning normally but reversible and just staring at those 4 walls. depending on the underlying etiology They become agitated and may have Hyperactive: most common type of delirium behavioral or psychological symptoms ○ Acute confusional state ○ Acute brain failure CLASSIC PRESENTATION ○ Encephalitis Sudden onset (hours or days) ○ Encephalopathy ○ Biglang nagkaroon ng behavioral problem ○ Toxic metabolic state A brief and fluctuating course ○ Central nervous system toxicity ○ In the morning, okay. In the afternoon, a little bit ○ Paraneoplastic limbic encephalitis agitated. In the late afternoon, okay again. At ○ Sundowning night, shouting and don’t want to sleep ○ Cerebral insufficiency Rapid improvement when the causative factor is identified ○ Organic brain syndrome and eliminated For all: Secondary to delirium ○ Secondary to underlying infection, metabolic problem, medication DELIRIUM: EPIDEMIOLOGY If corrected, then there will be Common especially among the elderly population improvement ○ ER: 5-10% Depends on what is the cause of why DSM-5 DIAGNOSTIC CRITERIA FOR DELIRIUM they are brought to the emergency room A. A disturbance in attention (i.e. reduced ability to ○ Time of admission to ward: 15-21% direct, focus, sustain, and shift attention) and Would have delirium at this time awareness (reduced orientation to the environment). ○ During hospitalization: 5-30% Problem with attention and awareness is Highest one. The longer that they are in only at the level of confusion the hospital. ○ Not because of coma This can be because of the severity of B. The disturbance develops over a short period of the underlying medical illness or the time (usually hours to a few days), represents a medication given to them change from baseline attention and awareness, and Reported prevalence rates: tends to fluctuate in severity during the course of the ○ General surgical patients: 10-15% day Not only restricted to the elderly patients C. An additional disturbance in cognition (e.g. ○ Open heart surgery patients: 30% memory deficit, disorientation, language, visuospatial ○ Hip fracture patients: >50% ability or perception). Usually elderly, immobile, and given D. The disturbance in Criteria A and C are not better pain medication explained by another preexisting, established or ○ ICU setting: 70-87% evolving neurocognitive disorder and do not occur in ○ End of life care: up to 83% the context or a severely reduced level of arousal, Causes of postoperative delirium: such as coma. ○ stress of surgery, E. There is evidence from the history, physical ○ postoperative pain, examination or laboratory findings that the ○ insomnia, pain medication, disturbance is a direct physiological consequence ○ electrolyte imbalances, of another medical condition, substance intoxication ○ Infection, or withdrawal (i.e. due to a drug of abuse or to a ○ fever, and medication), or exposure to a toxin, or is due to ○ blood loss multiple etiologies. Specify if: DELIRIUM: PREDISPOSING FACTORS ○ Hyperactive: the individual has a hyperactive Numerous factors increase the risk for delirium level of psychomotor activity that may be ○ Advanced age: major risk factor (30-40 % > 65 accompanied by mood lability, agitation and/or y/o) refusal to cooperate with medical care. MAJOR risk factors ○ Hypoactive: the individual has a hypoactive level ○ Cognitive and functional status of psychomotor activity that may be accompanied Only increase the chance of having by sluggishness and lethargy that approach delirium stupor. Suddenly the px will prefer to sleep all Ex: dementia, mild cognitive impairment the time. May poverty na sa language. It then nagka infection tapos elderly. should have a fluctuating course pa rin. ○ Medications/drugs taken ○ Mixed level of activity: the individual has a ○ Sensory impairment (hearing, visual) normal level of psychomotor activity even though Hearing aids, or visual impairments 6  NEUROCOGNITIVE DISORDERS ○ Male gender The older the patient and the longer the patient has been ○ Decreased oral intake delirious, the longer the delirium takes to resolve Dehydration or malnutrition ○ The longer the delirium, the longer it would take to resolve ○ Coexisting medical conditions Recall of what transpired during a delirium is vague DELIRIUM: PREDISPOSING FACTORS DELIRIUM: PROGNOSIS Major causes of delirium Poor prognostic sign ○ Drugs 3-fold increased institutionalization rate for > 65 y/o Narcotics, sedative-hypnotics, 3-month mortality rate: 23-33% antibiotics, anticholinergic drugs, alcohol 1-year mortality rate: up to 50% or drug withdrawal Elderly inpatients mortality rate during hospitalization: ○ Primary neurological disease 21-75%; after discharge, up to 15% die within 1-month, Secondary Stroke, intracranial bleed, 25% die within 6 months meningoencephalitis (infection), ○ Due to serious nature of the associated medical ○ Intercurrent illnesses conditions that lead to delirium Infections (UTI), hypoxia, dehydration, metabolic derangements, seizures, DELIRIUM: TREATMENT anemia, poor nutritional status, fever or Primary goal is to treat underlying cause If due to hypothermia anticholinergic toxicity ○ Surgery ○ Physostigmine salicylate Especially in those who underwent hip Provide physical, sensory, and environmental support fracture surgery or open heart surgery ○ Neither sensory deprived nor overly stimulated by ○ Environmental the environment ICU admission, physical restraints, ○ Sensory treatment is usually done for those with bladder catheter, feeding tube, psychosis emotional stress, sleep deprivation When all px can hear are the beeping of the monitors, the visitors, and the four DELIRIUM: PHARMACOTHERAPY corners of the room, that may facilitate a Psychosis delirium ○ Antipsychotic: preferably typical, atypical ○ Agitated, actively hallucinating DELIRIUM: ETIOLOGY ○ Preferably atypical antipsychotic Major neurotransmitter involved: acetylcholine Insomnia Major neuroanatomical area involved: reticular formation ○ Benzodiazepine with short or intermediate half ○ Principal area regulating attention and arousal lives Major pathway implicated: dorsal tegmental pathway ○ Includes alprazolam ○ Projects from the mesencephalic reticular ○ Not diazepam which has a long halflife formation to the tectum and thalamus Delirium associated with alcohol withdrawal associated with hyperactivity of the locus coeruleus → norepinephrine DELIRIUM IN PARKINSON’S DISEASE d/t hyperactivity of locus coeruleus Antiparkinsonian agents may cause delirium Other neurotransmitters: serotonin and glutamate Increased likelihood with associated dementia Treatment: ○ Decreasing antiparkinsonian agent dosage DEMENTIA VS DELIRIUM ○ Clozapine or quetiapine (atypical antipsychotic) Table No 2. Dementia vs Delirium DEMENTIA (MAJOR NEUROCOGNITIVE DISORDER) Feature Dementia Delirium Components: Onset Slow Rapid ○ Progressive cognitive impairment, involving Duration Months to years Hours to weeks multiple domains, in clear consciousness Attention Preserved Fluctutates ○ Decline from a previous level of functioning Memory Impaired remote Impaired recent ○ Result in significant impairment in social and and immediate occupational functioning memory Identify the syndrome and clinical workup of its cause are Speech Word-finding Incoherent (slow or essential rapid) ○ Don’t just do all examinations and wait what is Sleep-Wake Fragmented Sleep Frequent disruption positive Cycle (day-night reversal) ○ Since all examinations we gave them are out of Thoughts Impoverished Disorganized pocket Awareness Unchanges Reduced Temporal profile depends on etiology *Hallmark of 15% have reversible causes if treatment is initiated early delirium Alertness Usually normal Hypervigilant or DEMENTIA ETIOLOGIES reduced vigilance I. Degenerative dementias (Alzheimer’s dementia, Frontotemporal dementia, Parkinson’s dementia, DELIRIUM: COURSE LBD) Upon resolution of primary problem, recedes over 3-7 II. Miscellaneous (Wilson’s disease, Huntington’s days chorea) Some symptoms may take up to 2 weeks to resolve III. Psychiatric (pseudodementia of depression, late life completely schizophrenia) 7  NEUROCOGNITIVE DISORDERS A. Normal course for patients with C. The cognitive deficits do not occur exclusively in the schizophrenia to develop dementia later in context of a delirium. life when not treated D. The cognitive deficits are not better explained by IV. Physiologic (NPH/ Normal Pressure Hydrocephalus) another medical disorder (e.g., major depressive V. Metabolic (vitamin deficiency [B12], endocrinopathies/ disorder, schizophrenia). hypothyroidism, chronic metabolic disturbances) Specify whether due to: VI. Tumor (primary or metastatic) ○ Alzheimer’s disease VII. Traumatic (dementia pugilistica, posttraumatic ○ Frontotemporal lobar degeneration dementia, subdural hematoma) ○ Lewy body disease A. dementia pugilistica - seen in athletes ○ Vascular disease (boxers, football players) with frequent head ○ Substance/medication use injuries ○ HIV infection VIII. Infection (HIV, neurosyphilis, prion diseases) ○ Prion disease IX. Cardiac, vascular, anoxia (Binswanger’s disease, ○ Parkinson’s disease cerebral infarctions, cerebral hypoperfusion or ○ Huntington’s disease hypoxia) ○ Another medical condition A. Secondary to stroke/ hypoxia/ anemia/ blood ○ Multiple etiologies loss ○ Unspecified X. Drugs and toxins (alcohol, heavy metals, irradiation, Specify: CO) ○ Without behavioral disturbance: if the cognitive XI. Demyelinating Diseases (MS) disturbance is not accompanied by any clinically significant behavioral disturbance DEMENTIA ETIOLOGY ○ With behavioral disturbance: if the cognitive Alzheimer’s Disease disturbance is accompanied by clinically ○ Most common: 50-60% significant behavioral disturbance (e.g., psychotic ○ Prevalence increases with age symptoms, mood disturbance, agitation, apathy, When you reach 70, double the chance or other behavioral symptoms.) for dementia Specify (characterize the severity): ○ Neurodegenerative disorder ○ Mild: difficulties with instrumental activities of Vascular Dementia daily living (e.g., money management, ○ Second most common: 15-30% housework) ○ More common in men ○ Moderate: difficulties with basic activities of daily ○ Secondary to stroke living (e.g., feeding, dressing). Mixed Dementia ○ Severe: fully dependent ○ Have both Vascular dementia and Alzheimer’s disease DEMENTIA OF THE ALZHEIMER’S TYPE ○ d/t old age develops stroke Pathways for the generation of amyloid plaques and neurofibrillary tangles DSM-5 DIAGNOSTIC CRITERIA FOR MAJOR NEUROCOGNITIVE DISORDER A. Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on: a. Concern of the individual, a knowledgeable informant, or the clinician that there has been a significant decline in cognitive function; and b. A substantial impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another qualified clinical There could be accumulation of neurofibrillary tangles assessment. that are located within the neurons that toxic to the i. Doc’s experience: a former neurons causing neuronal death of neurofibrillary caregiver and relative borrowed half tangles then there would be accumulation of amyloid a million in the name of the pt. Who plaques extracellularly that are again toxic to the had dementia. How will they return neuron causing brain atrophy half a million? This will become a legal case. ii. Have a formal neuropsychological test done because they are going to court B. The cognitive deficits interfere with independence in everyday activities (i.e., at a minimum, requiring assistance in complex instrumental activities of daily living such as paying bills or managing medications). a. Requiring assistance in their IADLs 8  NEUROCOGNITIVE DISORDERS NEUROPATHOLOGY IN ALZHEIMER’S DISEASE ○ Reason why one of the medications given is directed to glutamate SEA MRI BRAIN: NORMAL VS AD Brain of alzheimer’s has atrophy of the medial temporal lobe where the hippocampus will be residing General atrophy of the brain Initially what would be affected in patients with ANSMITTERS IN ALZHEIMER’S DISEA alzheimer’s would be more of the temporal lobes VASCULAR DEMENTIA That is why initially they would have memory impairment and it would eventually affect the inferior frontal lobes and eventually cause impairment of the whole brain Looking at the amyloid plaques, what would be affected would be the medial temporal lobe that is why the presentation is amnestic then the problem would be on short term memory Later on when the whole brain is affected even the Vascular dementia remote memory would be affected Second most common Frontal lobe affected: problems in personality, Formerly referred to as multi-infarct dementia executive functioning, and behavioral problems would Cognitive decline is due to multiple areas of cerebral already occur. vascular disease of small and medium sized cerebral If you look a the brain of a person with alzheimer’s vessels there is marked atrophy of the whole brain which More common in men with cardiovascular risk factors could be in the severe alzheimer's especially hypertension NEUROTRANSMITTERS IN ALZHEIMER’S DISEASE Exhibit a decremental, stepwise deterioration Second image: shows normal level of functioning then there would be a decline in their functioning and then it would be static If they have another stroke it would worsen and another one would worsen it Unlike the neurodegenerative disorder such as alzheimer’s there will be a progressive decline not stepwise If you treat them and there are no further stroke then it would plateau and be static Similar to the delirium, the neurotransmitter that would be implicated would be the acetylcholine Cholinergic hypothesis ○ Secondary to the degeneration of nucleus basalis of Meynert which would be the source of acetylcholine to the brain or ○ There could be reduction choline acetyltransferase activity and acetylcholine ○ Progressive loss of nicotinic receptors in the Presentation would not be motor or sensory deficit but brain they may present with cognitive impairment Why is this particular hypothesis? The TERS IN ALZHEIMER’S DISEA medication being given for dementia is anticholinergic agents as we see later on ○ Worsening of symptoms with cholinergic antagonists can cause improvement with agonist Norepinephrine, somatostatin and corticotropin are decreased Excessive stimulation by glutamate 9  NEUROCOGNITIVE DISORDERS BINSWANGER’S DISEASE Frontal lobe affected: behavioral and personality changes Temporal lobe: may also present with weak aphasia. FRONTOTEMPORAL DEMENTIA Another vascular disorder that can cause memory decline Also known as subcortical arteriosclerotic encephalopathy Characterized by multiple small infarctions of the white Often characterized by hallucinations, parkinsonian matter that spare the cortical regions features and extrapyramidal signs MRI: white matter of the brain shows vascular changes ○ Though hallucinations are present, antipsychotic that would be located in the white matter that spares the medications are NOT recommended as this can cortical region. worsen their condition. S IN ALZHEIMER’S Lewy inclusion bodies are found in the cerebral cortex PICK’S DISEASE Neuroleptic sensitivity of patients Lewy Body in Midbrain: presents with Parkinson’s Lewy Body in Cortex: dementia of Lewy body CLINICAL CRITERIA FOR DEMENTIA WITH LEWY BODIES The patient must have sufficient cognitive decline to interfere with social and occupational functioning. Of note early in the illness, memory symptoms may not be as prominent as attention, fronto-subcortical skills, and Preponderance of atrophy in the frontotemporal regions visuospatial ability. Probable DLB requires two or more ○ Neuronal loss, gliosis, neuronal Pick's bodies core symptoms, whereas possible DLB only requires one Picture on the right is called the “Pick’s core symptom. bodies”. Core features Cause is unknown ○ Fluctuating levels of attention and alertness Early stages more often characterized by personality and ○ Recurrent visual hallucinations behavioral changes, with relative preservation of other Not threatening cognitive functions Ex) Within the room there are ○ Initial presentation would be aphasia with relative several people preservation of other cognitive function ○ Parkinsonian features (cogwheeling, ○ As the symptoms progresses, other cognitive bradykinesia and resting tremors) remains are also affected Supporting features More common in men ○ Repeated falls Typically begins before 75 years of age ○ Syncope ○ Familial cases have an earlier onset ○ Sensitivity to neuroleptics Features of Kluver-Bucy syndrome (e.g., hypersexuality, ○ Systematized delusions placidity and hyperorality) ○ Hallucinations in other modalities (e.g. auditory, S DI tactile) FRONTOTEMPORAL DEMENTIA HUNTINGTON’S DISEASE Subcortical type of dementia characterized by more motor abnormalities and fewer language abnormalities Psychomotor slowing and difficulty with complex tasks, but memory, language, and insight remain relatively intact in the early and stages of the illness As the disease progresses, dementia becomes Complete ○ High incidence of depression and psychosis Degeneration of the caudate nucleus presenting with behavioral and psychological problems ○ Later on, presenting with chorea and memory decline Usually runs in the family There is a preponderance of the atrophy of the frontal PARKINSON’S DISEASE and temporal lobes: frontotemporal dementia Disease of the basal ganglia, commonly associated with Problem here is not initially the memory decline BUT dementia and depression a behavioral problem ○ May later on develop with depression then dementia 10  NEUROCOGNITIVE DISORDERS 20-30 % have dementia HEAD TRAUMA-RELATED DEMENTIA ○ Most especially in advanced stages Additional 30-40% have measurable cognitive impairment Slowed movement are paralleled with bradyphrenia or “slowed thinking” HIV-RELATED DEMENTIA Encephalopathy in HIV infection is associated with Chronic traumatic encephalopathy dementia Punch-drunk dementia or dementia pugilistica occurs ○ Also called AIDS dementia complex in boxers after repeated head trauma over many years ○ Annual incidence of ~14% ○ Emotional lability, dysarthria and impulsivity Declining of the availability of putting ○ Seen in professional boxer, football players after anti-retroviral drugs repeated concussions over many years ○ Parallel by appearance of parenchymal In the brain of CTE, in the septum pellucidum there is a abnormalities in MRI scans cavum; it is open but the septum pellucidum must close White matter changes in the brain, needing for an MRI PSYCHIATRIC AND COGNITIVE CHANGES IN Diagnosis requires laboratory evidence for systemic HIV, DEMENTIA: CATASTROPHIC REACTION at least two cognitive deficits and presence of motor Agitation secondary to the subjective awareness of abnormalities or personality changes (AIDS Task Force intellectual deficits under stressful circumstances Criteria for AIDS dementia complex) ○ Compensates for defects by using strategies to ○ Two cognitive sign and symptoms and/or one avoid demonstrating failures in intellectual motor or one behavioral performance If you look at the brain of HIV- Related Dementia you can Change the subject, make jokes or see that there is a white matter changes that is similar to divert the interviewer Binswanger Disease ○ If the individual recognize nanangkakroon na ng memory na problem they may present anxiety or Table No 3. Clinical Signs and Symptoms of HIV Dementia agitation SYMPTOMS SIGNS Lack of judgment and impulse control Cognitive Poor Slowness of thought ○ Coarse language, inappropriate jokes, neglect of Concentration personal appearance and hygiene and general Forgetfulness Executive cognitive disregard for the conventional rules of social dysfunction conduct Motor Gait instability Saccadic ocular Problem in their social cognition pursuit Urinary Slowing of repetitive PSYCHIATRIC AND COGNITIVE CHNGES IN urgency/hesitati movements DEMENTIA: SUNDOWN SYNDROME on Characterized by drowsiness, confusion, ataxia, and Behaviors Loss of interest Apathy accidental falls in friends, ○ Occurs in older people who are overly sedated hobbies and in patients with dementia who react adversely to even a small dose of a psychoactive drug or benzodiazepine ○ Occurs in demented patients when external stimuli, such as light and interpersonal orienting cues, are diminished DEMENTIA: TREATMENT Psychosocial therapies ○ – Supportive and educational psychotherapy ○ – Psychodynamic interventions with family members Pharmacotherapy ○ Alzheimer’s Disease Acetylcholinesterase inhibitors (donepezil, rivastigmine) 11  NEUROCOGNITIVE DISORDERS There could be degeneration of ○ Confabulation and apathy nucleus dorsalis of maynard Usually it would be the temporal lobe that is affected which source of cholinergic pathway AMNESIC DISORDER: CLINICAL FEATURES If you give them medication to Central symptom: anterograde amnesia and retrograde increase acetylcholine then amnesia that can improve their memory Cause significant problem in social or occupational NMDA receptor antagonists functioning (memantine) Amnesia can begin directly at the point of trauma or If there is to much activity of include a period before the trauma (retrograde amnesia) glutamate then we give them Onset can be sudden [e.g., trauma, cerebrovascular glutamate antagonist events (stroke), and neurotoxic chemical assaults] or ○ Vascular Dementia gradual [e.g., nutritional deficiency (Vitamin B12 deficiency Stroke prevention or Thiamine Deficiency) and cerebral tumors] Acetylcholinesterase inhibitors May be transient, lasting for hours or days or chronic ○ Parkinson’s Disease Dementia and DLB lasting weeks or months Acetylcholinesterase inhibitors ○ Depending on the etiology ○ – Other medications: Short-term and recent memory usually impaired Antidepressants for depression ○ Remote and immediate memory usually good Especially in the early stage of Behavioral symptoms may be present dementia ○ Apathy, lack initiative, unprovoked episodes of Antipsychotic drugs for delusions and agitation or overly friendly or agreeable hallucinations Cover their confusion with confabulatory answers to Prefer non sedating questions Benzodiazepines for insomnia and Characteristically, with poor insight to their condition anxiety We try not to give so much of Table No 4. Alzheimer’s Dementia vs Amnestic Disorder this drugs to prevent agitation FEATURE ALZHEIMER’S AMNESTIC DEMENTIA DISORDER AMNESTIC DISORDER Onset Insidious Can be abrupt Coded in DSM-5 as Major or Minor Neurocognitive Course Progressive Static or Disorder Due to Another Medical Condition deterioration improvement Results from a variety of diseases and conditions that Anterograde Impaired Impaired have amnesia as the major complaint memory ○ Impairment in the ability to create new memories Retrograde Impaired Temporal gradient Possible etiologies: memory ○ Amnestic disorder caused by a general medical Episodic Impaired Impaired condition (e.g., head trauma) memory Most common that we would see: Head Semantic Impaired Intact Trauma memory ○ Substance-induced persisting amnestic disorder (e.g. CO poisoning or chronic alcohol Language Impaired Intact consumption) Praxis Impaired Intact ○ Amnestic disorder not otherwise specified AMNESIC DISORDER: COURSE AND PROGNOSIS AMNESIC DISORDER: MAJOR CAUSES Depends on etiology and institution of acute treatment Thiamine deficiency (Korsakoff’s syndrome) Usually has a static course ○ Caused by chronic alcohol consumption ○ Secondary to stroke, tumors, infections Hypoglycemia Little improvement, no progression Primary brain conditions In transient global amnesia, resolves entirely over hours to ○ Seizures, head trauma, cerebral tumors and days and amnesia associated with head trauma, stroke in temporal lobes and thalami, herpes improvement is seen gradually in the subsequent months simplex encephalitis, hypoxia, transient global amnesia, ECT, MS Substance-related causes MILD COGNITIVE IMPAIRMENT (MINOR ○ Neurotoxins, alcohol use disorders, NEUROCOGNITIVE DISORDER) benzodiazepines and other sedative-hypnotics Mild cognitive decline not warranting the diagnosis of dementia AMNESIC DISORDER: ANATOMICAL SUBSTRATE Preserved activities of daily living Major neuroanatomical structures involved: (Areas of the Gap between cognitive changes associated with aging Limbic Lobe) and cognitive impairment suggestive of dementia ○ Diencephalic structures (dorsomedial and midline In the DSM-5, classified as mild neurocognitive disorder nuclei of the thalamus ) due to multiple etiologies or unspecified neurocognitive ○ Midtemporal lobe structures (hippocampus, disorder mamillary bodies and amygdala) ○ Usually bilateral damage to these structures DSM-5 DIAGNOSTIC CRITERIA FOR MILD ○ If unilateral damage exists, left hemisphere COGNITIVE IMPAIRMENT usually implicated A. Evidence of significant cognitive decline from a Frontal lobe involvement previous level of performance in one or more 12  NEUROCOGNITIVE DISORDERS cognitive domains (complex attention, executive OUTCOME OF CLINICAL PHENOTYPES OF MCI function, learning and memory, language, perceptual-motor, or social cognition) based on: a. Concern of the individual, a knowledgeable informant, or the clinician that there has been a significant decline in cognitive function; and b. A substantial impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another qualified clinical assessment. B. The cognitive deficits do not interfere with capacity for independence in everyday activities (i.e., complex instrumental activities of daily living such as paying bills or managing medications are preserved, but greater effort, compensatory strategies, or accommodation may be required). If they have Amnestic MCI C. The cognitive deficits do not occur exclusively in the ○ In the domains, the problem would be on memory context of a delirium. ○ Single Domain: later on, they may develop AD D. The cognitive deficits are not better explained by (Alzheimer’s Dementia) another medical disorder (e.g., major depressive ○ If multiple domains, aside from the memory, the disorder, schizophrenia). patient may develop AD (Alzheimer’s Dementia) Specify whether due to: and VaD (Vascular Dementia) ○ Alzheimer’s disease If the patient is functional, it would be ○ Frontotemporal lobar degeneration secondary to Depression ○ Lewy body disease Non-Amnestic MCI ○ Vascular disease ○ Cognitive domain is not on memory ○ Substance/medication use ○ If affected is language and social cognition: ○ HIV infection FTD (Frontotemporal Dementia) ○ Prion disease ○ If multiple domains: ○ Parkinson’s disease DLB (Dementia with Lewy Bodies) and ○ Huntington’s disease VaD (Vascular Dementia) ○ Another medical condition ○ Multiple etiologies MCI: COURSE/PROGNOSIS AND TREATMENT ○ Unspecified Rate of progression to Alzheimer’s disease is 10-15% per year MAYO CLINIC ALZHEIMER’S DISEASE RESEARCH ○ Not all that would develop MCI would develop CENTER (MCADRC) MCI CRITERIA Alzheimer’s easily 1. Memory complaint, preferably qualified by an Diagnosis is not stable in both directions informant ○ Patients can either convert to Alzheimer’s 2. Objective memory impairment for age and education disease or revert back to normal Neuropsychological testing No FDA-approved treatments for MCI at this time 3. Preserved general cognitive function ○ Not required to be given medication Consciousness is not impaired Though some neurologists or 4. Intact activities of daily living psychiatrists may be giving medications 5. Not demented ○ They would be given non-pharmacological management MCI: RISK FACTORS APOε4 allele status, cerebrovascular events, chronic exposure to high levels of cortisol (depression) REFERENCES Brain Reserve ○ Brain size and neuron density may be protective Notes from the Discussion and University of Santo against dementia despite neurodegeneration Tomas PowerPoint Presentation by Dr. Joselito Diaz ○ Highly educated people have lesser risk of Sadock, B.J, Sadock, V.A & Ruiz, P. (2015). Kaplan developing MCI or Dementia and Sadock’s Synopsis of Psychiatry, Behavioral Science/Clinical Psychiatry (11th Ed.). Wolters Kluwer. 13  NEUROCOGNITIVE DISORDERS QUICK QUIZ IDENTIFICATION 1. Reported prevalence rates of delirium in end of life care 2. Major neurotransmitter involved in delirium: 3. Preferred pharmacotherapy in delirium with psychosis 4. Most common type of dementia 5. Characterized by multiple small infarctions of the white matter that spare the cortical regions TRUE OR FALSE 6. Antiparkinsonian agents may cause delirium 7. Dementia always has irreversible causes even if treatment is initiated early 8. Drugs and toxins do not cause dementia 9. Encephalopathy in HIV infection is associated with dementia 10. Amnesic disorder usually has a static course FREEDOM WALL 14