Organic brain syndrome

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Organic brain syndrome

  1. 1. Organic brain syndromeTai Zu HuangTeoh Wee Loon
  2. 2. Introduction• Brain dysfunction caused by organic pathologyinside or outside of the brain• Can be classified by:– Global syndromes• Delirium• Dementia– Specific syndromes• Amnesic syndrome• Organic mood disorder• Organic delusional state• Organic personality disorder
  3. 3. DementiaDEFINITION:•An acquired, generalized and usuallyprogressive impairment of cognitivefunctions (iememory, recall, orientation, language, abstraction etc)•Content being affected but not level ofconsciousness
  4. 4. Epidemiology• Affect predominantly elderly people• Prevalence increases with age:– 15% >65y/o (different studies have different prevalence)– 25% >85y/o• F > M• A community survey (n=223) amongst Malays age 60 yearsand above in Selangor:24% were cognitively impaired• Another study found the prevalence of dementia in urbancommunities of Malays (>60y/o) in KL was 6%• Study of elderly in Malaysia yielded a prevalence of organicmental disorder (inconclusive of dementia) at 14.4%• Down syndrome is also associated with the development ofdementia
  5. 5. ClassificationPart ofbrainaffectedAetiology
  6. 6. Part of brain affected• Brain damage affects the brain cortexor upper layer• Cause problem withmemory, language, thinking & socialbehaviour• Eg: Alzheimer’s & Creutzfeld –Jakobdiseasecortical• Affects brain below the cortex• Changes in emotion & movement• Eg Huntington’sdisease, Parkinson’s disease & AIDSsubcortical
  7. 7. Aetiology•Alzheimer’s disease• Parkinson disease•Lewy body dementiaDegenerative•Pseudodementia of depression• Cognitive decline in late life scizophreniaPsychiatric•Multi infarct dementiaVascular• multiple sclerosisDemyelinating• Vitamin def (e.g vitB12,folate), endocrinopathies (eghypothyroidism), abnormality of cortisolmetabolismMetabolic
  8. 8. Aetiology• Prion disease ( Creutzfeld –Jakob disease)• AIDSInfection• Alcohol, heavymetals, irradition, pseudodementia d2medication (anticholinergics), carbon monoxideDrugs andtoxins• Huntington disease, trauma(dementia pugilisticain boxers), tumorOthers
  9. 9. VITAMIN D VEST• V – Vitamin Deficiency [B12, folate andthiamine(Wernicke-korsakoff)]• I – Intracranial masses (tumour, abscess)• T – Trauma (head injury, dementia pugilistica)• A – Anoxia• M- Metabolic (diabetes)• I – Infection (HIV, syphilis, Creutzfeldt-Jakod)• N- Normal pressure hydrocephalus
  10. 10. We must always think of treatable causes of dementia before we start to managethem although it is very rare (10%)• D – Degenerative(Alzheimer’s, Hungtington’s, CJD)• V – Vascular (multi-infarct dementia)• E – Endocrine (hypothyroid)• S – Space occupying lesion (subduralhematoma)• T – Toxic (alcohol)
  11. 11. Diagnosis of dementiaDementia is diagnosed based on:History (based on aetiology) Mental state examination including MMSEOther lab investigation depend on aetiologyMost type of dementia can be diagnosedbased on criteria in DSM –IV
  12. 12. Clinical features:• Personality changes: become more hostile, irritable and explosive• Hallucination and delusions– 20-30% pts have hallucinations– 30-40% have delusions (delusion of paranoid or persecutory)• Mood changes: depression and anxiety (40-50% of pts)• Cognitive changes• Thinking: slow and impoverished• Insight: poor• Catastrophic changes – when patient are taxed beyond theirrestricted abilities, there maybe sudden change to anger and tears• Sundowner syndrome – confusion, ataxia, drowsiness after“sundown”
  13. 13. Investigation:• Depend on suspected etiologies• CBC (note MCV), glucose, TSH, B12, folate• electrolytes, LFTs, renal function• CT head• MRI as indicated• as clinically indicated – VDRL(syphilis), HIV, ANA, anti-dsDNA(SLE), caeruloplasmin, copper (wilson’sdisease), cortisol, toxicology, heavy metals
  14. 14. Management of dementia:• Treat treatable causes• Treat the cause of superimposed delirium• Biological: medication• Psychosocial: home care, day care, inpatientcare, residential care, avoidance of driving
  15. 15. Management of dementia:Non-pharmacologicalPharmacological CaregiversInterventionCognition Behaviour MoodPromotingindependence:communication,ADL skilltraining,exercise,rehabilitation,combinationMaintainence ofcognition:reality therapy,Validation, lifereviewCholinesteraseinhibitors:donepezil•Mild, moderateand severe AD•Vasculardementia•Dementia withLewy Body(DLB)Atypicalantipsycotics:•can be usedagitation andpsychosis•Avoid in DLBAntidepressants Evaluatecaregiver needsMulticomponent intervention:•Psychotherapy•Psychoeducation•Supportivetherapy•Respite/daycare•training
  16. 16. Non-pharmacologicalPharmacological CaregiversinterventionCognition Behaviour MoodChallengingbehaviours•Behaviourmanagement•Music•ReminiscencetherapyReduction ofco-morbidemotionalproblem (egdepression andanxiety)Memantine(glutamateNMDAantagonist)•Severe ADCognitiveenhancers:•Cholinesterase inhibitors•Memantine(NMDAreceptorantagonist)Antidepressantin fronto-temporaldementia
  17. 17. Alzheimer disease• First described by Alois Alzheimer in 1907• Although cause remains unknown, progress had been made to tryto understand molecular basic of amyloid deposits• genetic factors– a minority (<7%) of AD cases are familial, autosomal dominant– 3 major genes for autosomal dominant AD have been identified:• amyloid precursor protein (chromosome 21)• presenilin 1 (chromosome 14)• presenilin 2 (chromosome 1)– the E4 polymorphism of apolipoprotein E is a susceptibility genotype (E2 isprotective• Biochemical factors– Neurotransmitter such as Ach and Norepinephrine become hypoactive– Neuroactive peptides somatostatin and corticotrophin also decreased in concentration
  18. 18. DSM-IV-TR diagnostic criteria for dementia ofAlzheimer’s type• A. Development of multiple cognitive deficitsmanifested by both:– 1) memory impairment– 2) ≥1 of the following cognitive disturbances:• Aphasia• Apraxia• Agnosia• Disturbances in executive functioning
  19. 19. • B. cognitive deficits in criteria A1 and A2 causesignificant impairment in social and occupationalfunctioning and represent a significant decline froma previous level of functioning• C. gradual onset and continuing cognitive decline• D. not due to any other– CNS conditions– Systemic conditions– Subtance-induced conditions• E. Deficits do not occur during the course ofdelirium• F. Disturbance is not better accounted by otherAxis-I disorder (MDD, Schizophrenia)
  20. 20. Risk factors• Aging (elderly people > 65 years of age)• Female• Family history-Defective genes on chromosomes 1,14,21• Hypothethical risk factor : aluminium toxicity• Having history of head injury• Low education level• Smoking• Down syndrome (y?)
  21. 21. Pathology• Macroscopic appearance of brain : diffuseatrophy, esp frontal, parietal and temporallobes, flattened sulci & enlarged cerebralventricles• Microscopic findings : senile plaques (amyloidplaques – amount indicatesseverity), neurofibrillary tangles (composed ofcytoplasmic skeleton, mainly phosphorylated tauprotein), neuronal loss(in cortex &hippocampus), synaptic loss ( 50 % in cortex) &granulovascular degeneration of neurons
  22. 22. Course, prognosis & treatment• Slowly progress memory impairment• Aphasia, apraxia and agnosia also present• May later develop motor & gait disturbances;may become bedridden• Mean survival is 7 years from onset• Treatment : cholinesterase inhibitor (eg:galantamine, rivastigmine, donepezil)
  23. 23. • There is a new case of dementia every 7seconds in our world• Alzheimer is the most common cause ofdementia and is not part of aging process• There are currently no prevention and curefor it
  24. 24. Vascular dementia• Caused by blockage of in brain’s blood supply• Leading to progressive decline in memory &cognitive functioning• > ,affects people between the ages of 60 and75, HTN or CV dss• Approximately 10-15% have coexisting vasculardementia and dementia of Alzheimer’s type• Pathology : a/w multiple infarcts coz bythromboembolism fr extracranial arteriesarteriosclerosis in main vessels
  25. 25. Vascular dementia• Clinical features:-sx are fluctuating & episodes of confusion are common esp atnight-Neurological signs is common-in some cases emotional & personality changes may beapparent b4 impairment of memory & intelect• Diagnosis, other signs and symptoms are as according to DSM-IV diagnostic criteria• Prognosis-lifespan averages is 4-5 years from time of diagnosis
  26. 26. Deliriumacute generalized impairment ofmental disorderHallmark symptoms :impairmentof consiousness, in association withglobal impairment of cognitivefunctionsCommon psychiatric symptoms:abnormalities ofperception, mood, behaviourCommon neurological symptoms:tremor, nystagmus, incoordination, urinary incontinence, asterixis.
  27. 27. Epidemiology:• general population: 1.1%• medically ill patient who are hospitalized: 10-30%• surgical intensive unit: 30%• cardiac intensive care unit: 40-50%• AIDS: 30-40%
  28. 28. Risk factor• Hospitalization• Nursing home resident• Childhood (example: febrile illness)• Old age especially male• Severe illnesses like cancer, AIDS• Pre-existing cognitive impairment or brain pahtology• Recent anesthesia• Substance abuse
  29. 29. Etiology:• Common pathway to any brain insult.• Is thought to involve dysfunction of the reticularformation & acetylcholine transmission.• Reticular formation→attention & arousal• Study shown decrease in acetylcholinergic activity• Other neurotransmitter: serotonin & glutamate
  30. 30. INTRACRANIAL CAUSES• Epilepsy and postictal states• Brain trauma (especially concussion)• Infections• Meningitis• Encephalitis• Neoplasms• Vascular disorders
  31. 31. EXTRACRANIAL CAUSES• Drugs (ingestion or withdrawal) and poisons(Anticholinergic, anticonvulsants, antihypertensives, antiparkinsonians, antipsychotics, cardiacglycosides, insulin, opiates, sedatives andhypnotics, steroids, alcohol)• Endocrine dysfunction (hypofunction or hyperfunction)(Pituitary, Pancreas, Adrenal, Parathyroid, Thyroid)• Diseases of nonendocrine organs(Hepatic encephalopathy, Uremic encephalopathy, Carbondioxide narcosis, Hypoxia, Cardiacfailure, Arrhythmias, Hypotension )
  32. 32. • Deficiency diseases(Thiamine, nicotinic acid, B12, or folic acid deficiencies)• Systemic infections with fever and sepsis• Electrolyte imbalance of any cause• Postoperative states(postoperative pain, insomnia, pain medication, electrolyteimbalance, infection, fever, blood loss)• Trauma (head or general body)
  33. 33. Impaired delivery (of brain substrate eg. vascularinsufficiency due to stroke)MetabolicDrugsEndocrinopathyLiver diseaseInfrastructure (structural disease of corticalneurons)Renal failureInfectionOxygenUrinary tract infectionSensory deprivation
  34. 34. CLINICAL FEATURES OF DELIRIUM• Impairment of consciousness – disorientation & poorconcentration, fluctuating course & often worse in the evening.• Behavior – overactive or underactive, sleep is often disturbed.• Thinking – slow, muddled, ideas of reference & delusions aretransient and poorly elaborated.• Mood – anxious, irritable or depressed, often labile.• Perception – is distorted, misinterpretations ofillusions, hallucination (mainly visual). Tactile and auditoryhallucination can occur but less frequent.• Memory – impaired.• Insight – impaired
  35. 35. Diagnosis• DSM-IV diagnostic criteria for delirium due to a generalmedical conditionA. Disturbance of consciousness (i.e. reduced clarity of awarenessof the environment) with reduced ability to focus, sustain or shiftattention.B. A change in cognition (such as memorydeficit, disorientation, language disturbance) or the developmentof perceptual disturbance that is not better accounted for by apreexisting, established or evolving dementia.C. The disturbance develop over a short period of time (usuallyhours to days) & tends to fluctuate during the course of the day.D. There is evidence from the history, PE or laboratory findingsthat the disturbance is caused by the direct physiologicconsequences of a general medical condition.
  36. 36. Course & prognosis• Onset usually sudden.• Symptoms persist as long as the causative factors arepresent, although delirium generally lasts less than aweek.• After removal of the causative factors, the symptomsof delirium usually recede over a 3- to 7-dayperiod, although some symptoms may take up to 2weeks to resolve completely.• The older a patient and the longer the patient has beendelirious, the longer the delirium takes to resolve.
  37. 37. Differential diagnosis:• Dementia• Schizophrenia & mania– No rapidly fluctuating course, do not impair the level ofconsciousness or significantly impair cognition• Acute amnesic syndrome• Depression
  38. 38. Investigation:First line Other useful testBlood test FBC, ESR,Urea and electrolyte (BUSE)Calcium, MagnesiumLiver function testThyroid function testCardiac enzymeVitamin B12Anti-nuclear antibodyTumour markerAnti-thyroid antibodyCopper studiesCNS investigation Head imaging ( CT, MRI) Lumbar punctureEEGOthers ABGECGInfection screening (bloodculture, urine culture)Viral screen
  39. 39. Amnesic syndromeCharacterized by a prominent disorder of recent memoryin the absence of generalized intellectual impairment(dementia) or impaired of consciousness (delirium)Clinical features:• Recent memory severely impaired• Remote memory spared• Disorientation in time• Confabulation• Other cognitive function preservedOrganic Brain syndrome
  40. 40. Korsakoff syndrome• Amnesic syndrome accompany with acute neurologicalsymptoms caused by neuronal damage that results fromthiamine deficiency in association with chronic alcoholabuse.• It usually is preceded by an episode of Wernickeencephalitis (eg, ataxia, confusion, oculomotor palsy),typically precipitated by administration of glucose to amalnourished alcoholic without concomitant parenteralthiamine.• Confabulation is a hallmark finding of Korsakoffsyndrome (also called Korsakoff psychosis).• Treatment: IV thiamineOrganic Brain syndrome
  41. 41. Organic personality disorder• Frontal lobe damage• Clinical features:- behaviour is disinhibited- overfamiliar- overtalkative- inappropriate jokes- euphoria- concentration and attention will be reduced- insight impairedOrganic Brain syndrome
  42. 42. Head injurymajor head injury has both immediate and long-termneuropsychiatric consequences.Acute psycholoqical effects of head injury:• Impairment of consciousness• Delirium• Post-traumatic amnesia: transient amnesia with retrograde(events prior to injury) and anterograde (events followinginjury) features.Long-term consequences:• Personality changes• Emotional symptomsOrganic Brain syndrome
  43. 43. Dementia Delirium Pseudodementia ofdepressionOnset gradual/step-wisedeclineacute(hours-days) subacuteDuration months-years days-weeks variableNatural History Progressive , usuallyirreversiblefluctuating,Reversible, highmorbidity/mortalityin very oldrecurrent,usuallyreversibleLevel ofconsciousnessnormal fluctuating(over24hours)normalOrientation intact initially impaired(usuallytime and place)intactMood and Affect labile but no usuallyanxiousanxious, irritable,fluctuatingdepressed,stable
  44. 44. Thank you!

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