DEMENTIA Acquired deterioration in cognitive abilities that impair the successful performance of activities of daily living Episodic memory is the cognitive function most commonly involved In addition to memory other components of cognition ID: 1045319
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1. Dr Gouri Krishnan M GAPPROACH TO DEMENTIA
2. DEMENTIAAcquired deterioration in cognitive abilities that impair the successful performance of activities of daily living.Episodic memory, is the cognitive function most commonly involved.In addition to memory, other components of cognition i.e language , visuospatial, praxis, calculation, problem solving abilities may be affected
3. CLINICAL DIAGNOSISAccording to DSM 5:AMNESIA + 2 out of 4 1.Apraxia 2.Agnosia 3.Aphasia 4.loss of executive functionsDuration :6 monthsClear sensorium
4. THE NEURAL NETWORKLeft presylvian for languageParieto frontal for spatial orientationOccipitotemporal for face and object recognitionLimbic for memory Prefrontal for executive functions
5. CAUSES OF DEMENTIAMost common causes include:Alzheimers diseaseVascular dementia:Multi infarct Diffuse white matter disease(Binswangers disease)PDD/LBD spectrumAlcoholismDrug/medication intoxication
6. Other less common causes include:Vitamin deficiencies: Thiamine:Wernicke’s EncephalopathyB12:subacute combined degeneration of spinal cordNicotinic acid:PellagraEndocrine causes:HypothyroidismHypo or HyperparathyroidismRenal failureLiver failureChronic infectionsHIVNeurosyphilis
7. Head traumaNPHIntracranial neoplasmsDrugs and heavy metal intoxicationsPsychiatric diseases like depression,schizophreniaDegenerative disorders: Huntington’s disease MSA
8. APPROACH TO A PATIENT WITH DEMENTIAIs it Reversible or not?REVERSIBLEIRREVERSIBLE OR DEGENERATIVEPSYCHIATRIC DISORDERSHYPOTHROIDISMALZHEIMERSDEPRESSIONTHIAMINE DEFICIENCYFTDSCHIZOPHRENIAVIT.B12 DEFICIENCYHUNTINGTON’SCONVERSION REACTIONNPHDLBSUBDURAL HEMATOMAVASCULARCHRONIC INFECTIONSLEUCOENCEPHALOPATHIESBRAIN TUMORSPARKINSONSDRUG INTOXICATIONAUTOIMMUNE ENCEPHALOPATHY
9. CLINICAL DIFFERENTITION OF MAJOR DEMENTIASDISEASEHISTORY/FIRST SYMPTOMMENTAL STATUSNEUROPSYCHIATRYNEUROLOGYIMAGING1.ADMemory lossEpisodic memory lossIrritability, anxiety and depressionSpares motor system until later in the course.Entorhinal cortex and hippocampal atrophy2.FTDApathy,poor judgement,/insight, hyperoralityFrontal /executive and / or language ; spares drawingPersonality changes, apathy disinhibition, overeatingVertical gaze palsy, axial rigidity,dystonia, MNDs.Frontal, insular, and/ or temporal atrophy;usually spares posterior parietal lobe3.DLBVisual hallucination,REM sleep behavioral disorder,delirium,sensitivity to psychoactive medicationsDrawing frontal and executives ;spares memoryVisual hallucinations,depression,sleep disorder,delusionsParkinsonsim Posterior parietal atrophy
10. DISEASEHISTORY/FIRST SYMPTOMMENTAL STATUSNEUROPSYCHIATRYNEUROLOGYIMAGING4.CJDDementia, mood, anxiety, movt disordersVariable; frontal/executive,focal cortical,memoryDepression ,anxiety ,psychosisRapid progression with myoclonus, rigidity, parkinsonismCortical ribboning,basal ganglia or thalamus hyperintensity on FLAIR/diffusion images5.VASCULARHistory of stroke,with irregular stepwise progresionFrontal,executive,cognitive slowing;can spare memory.Apathy,delusions,anxietyMotor slowing ,spasticity but can be normalCortical & or /subcortical infarcts,confluent white matter disease.
11. DISEASEHISTORY /CLINICAL FEATURES5.CNS INFECTIONSHigh risk sexual behavior /IV drug abuse6.CHRONIC SUBDURAL HEMATOMA,CHRONIC TRAUMATIC ENCEPHALOPATHYRecurrent head trauma7.CORTICOBASILAR SYNDROMEAssymetric akinesia,rigidity,dystonia,myoclonus,alien limb phenomenon,pyramidal signs and prefrontal deficits-non fluent aphasia with or without motor speech deficit,executive dysfunction ,apraxia or a behavioral disorder.8.PROGRESSIVE SUPRANUCLEAR PALSYUnexplained falls,axial rigidity,dysphagia and vertical gaze deficits.9.CJDDiffuse rigidity, akinetic mutism, startle sensitive myclonus10.VITAMIN B12 DEFICIENCYVeganism,h/o bowel irradiation,autoimmune diathesis,a remote history gastric surgery,chronic anti-histamine therapy for dyspepsia/GERD11.NPHEarly ataxia,gait abnormalities,dementia and urinary incontinence
12. COGNITIVE AND NEUROPSYCHIATRIC EXAMINATIONScreening tools include:MMSEMOCACONGNISTAT
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14. LABORATORY TESTSThyroid function testsVit B12 levelsCBCElectrolytesCT/MRILumbar punctureEEG
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19. TREATMENTMajor goal –treatment of underlying causes.Hypothyroidism : thyroid replacementThiamine/b12 deficiency: vitamin therapy Opportunistic infections: antimicrobialsHIV :AntiretroviralsNPH: ventricular shunting CNS neoplasms: radiation and chemotherapyRemoval of cognition impairing drugs
20. Provide support and comfort to care givers and patients.Patients with degenerative disorders may be depressed or anxious, SSRIs or SNRIs can be given(low dose of ssri, eg:escitalopram starting dose 5mg daily,target dose 5-10 mg daily)In patients with agitation or aggression or psychosis,second generation antipsychotics such as Quetiapine(12.5-25 mg daily) can be given.Treatment of AD: Cholinesterase inhibitors-Donepezil, Rivastigmine, galantamine can be used. NMDA Antagonists: Memantine
21. Non drug behavioral therapy-preparing lists,schedules,calenders and labels can be helpful in early stagesStress on familiar routines ,walks and simple physical exercises.
22. THANK YOU..