Movement Disorders & Dementia Lecture Notes - PDF

Movement Disorders Introduction and Neuroanatomy Dr. Nora Darakjian, PT, DPT Board-Certified Neurologic Clinical Specialist  Lecture Objectives Gain a basic understanding of the features of some common movement disorders. Recognize the signs and symptoms of Parkinson disease (PD) a...

Movement Disorders Introduction and Neuroanatomy Dr. Nora Darakjian, PT, DPT Board-Certified Neurologic Clinical Specialist  Lecture Objectives Gain a basic understanding of the features of some common movement disorders. Recognize the signs and symptoms of Parkinson disease (PD) and atypical parkinsonian syndromes, through clinical findings. Understand the neuroanatomy involved in common movement disorders. Be able to distinguish between Parkinson disease and parkinsonian syndromes.  Neuroanatomy Neuroanatomy Pathogenesis General considerations Pathogenesis Step 1 General Disease course Clinical findings Clinical findings Disease course Red flags Step 2 Diagnosis Diagnosis/differential diagnosis Medical management Medical management Clinical management Prognosis Clinical management Step 3 Prognosis Neuroaxis: Look Where You Are Now? Cortex ALS, CVA, TBI, dementia, Basal ganglia Neoplasm, MS, Cerebellum PD, HA, CP, Vestibular Autism, vestibular Cranial nerve disorders Brainstem SCI, SB Spinal cord ALS Motor neuron GBS, CIDP, Peripheral nerve DM MG NMJ MD Muscle  CNS vs. PNS CNS PNS UMN Sensory Other LMN Sensory Autonomic Motor CN and Cranial nerves: Basal ganglia Neuroanatomy Cortical Cortical nuclei* sensory and special Cerebellum Anterior horn* Spinal peripheral Brainstem Brainstem nerve and nerve root Cortical Spinal nerve root association areas and peripheral Spinal Spinal nerve cord (e.g., cognition, cord behavior) NMJ Autonomic: hypothalamus, basal ganglia, Muscle limbic system, brainstem, spinal cord  Movement Disorders Movement disorders are Inputs to the motor system conditions that produce inadequate or excessive Neuroanatomy movement, usually involving basal ganglia pathology. Basal ganglia gates the proper initiation of movement; it also provides input to the motor cortex. Purves Figure 16.1 Purves: Neuroscience 5e Copyright 2012 to Sinauer Associates, Inc  Movement Disorders Movement disorders are often explained as an imbalance in the direct and indirect pathways in the basal ganglia. Neuroanatomy Indirect pathway Direct pathway Suppresses Supports movement movement Cortex Cortex D1 D2 Caudate/ Caudate/ SNpc GPe Putamen Putamen Strengthens Weakens indirect direct pathway pathway GPi GPi STN VL/VA VL/VA Neurotransmitters: Martin Figure 14.5 Glutamate GABA Purves Figure 18.8 Dopamine  Movement Disorders Hypokinesias: Hyperkinesias: inadequate excessive movement movement Neuroanatomy Akinesia Tremor Bradykinesia Chorea Rigidity Dystonia Myoclonus Tics Parkinson disease* Essential tremor Atypical parkinsonian Huntington’s disease syndromes Dystonia  Symptoms of Movement Disorders Hypokinesias (all can occur in Parkinson disease) Bradykinesia: slowness of movement Akinesia: loss or absence of movement Rigidity: stiffness of muscle tone with passive movement Hyperkinesias Neuroanatomy Tremor: oscillatory, usually rhythmical and regular movement affecting one or more body parts (limbs, neck, tongue, chin, vocal cords) Examples: Parkinson disease, essential tremor Chorea: random, quick, unsustained, purposeless movements that have an unpredictable, flowing pattern Examples: Huntington disease, cerebral palsy Dystonia: torsional movements that are partially sustained and produce twisting postures Myoclonus: sudden, brief, shock-like, involuntary movements usually caused by muscular contractions (can occur in CBD) Movement Disorders Parkinson Disease  Parkinsonism General Considerations Parkinsonism Primary idiopathic Atypical Secondary Parkinson Parkinson Parkinsonism disease (PD) Progressive Drug-induced Sporadic supranuclear palsy (PSP) Vascular Normal pressure Hydrocephalus Familial Trauma Multiple system atrophy (MSA) Metabolic Tumors Corticobasal Toxins degeneration (CBD)  Parkinson Disease General Considerations Prevalence 160 cases per 100,000 people At age 70, increases to 550 cases per 100,000 people 6–7 million cases worldwide 1–2 million in the U.S. Incidence 20 cases per 100,000 people, per year At age 70, increases to 120 cases per 100,000 people 2:1 male-to-female ratio Mean age of symptom onset is 56 years  Parkinson Disease Genetic load + Environmental triggers PD Pathogenesis Etiology Most cases are sporadic–unknown cause, also known as idiopathic PD Genetic contributions in 5–40% of cases Environmental contributions  Parkinson Disease Degeneration of dopamine-producing neurons within the substantia nigra pars compacta (SNpc) and the locus ceruleus in the brainstem Accumulation of the misfolded protein alpha-synuclein Pathogenesis spreads through the brain areas forming Lewy bodies Lewy Body Unstained: SNpc—see loss of DA-producing neurons  Parkinson Disease When symptoms become clinically evident… 60% of dopaminergic neurons of the substantia nigra have been lost Dopamine level has decreased by 80% Pathogenesis Pathophysiology of Cortex Parkinson Disease Caudate nucleus Basal Putamen Thalamus ganglia Globus pallidus Loss of dopaminergic input to striatum Midbrain Degeneration of neurons in substantia nigra pars compacta Adapted from: Picture credit: slideplayer.com/slide/11926855/  Parkinson Disease Typical progression Insidious onset Typical age of onset: about 55–60 years old Young onset: < 40 years old Late > 78 years old Progressive, degenerative over years (20-plus) Disease Course Death of Nonmotor Progression of all Bed symptoms symptoms leading to dopamine > motor Dx problems with bound; cells symptoms mobility dementia Hoehn and 1 2 3 4 5 Yahr stages Bilateral Impaired Severe Needs Sx one side disability; able to Wheelchair of the body sx; no postural or imbalance reflexes stand or walk bedridden  Typical Progression Mild PD: about 5–7 years post-dx Movement symptoms inconvenient, but do not affect daily activities Changes in posture, walking ability, or facial expression Parkinson medications effective Disease Course Regular exercise important Moderate PD: about 7–15 years post-dx Motor fluctuations and dyskinesias “Freezing” episodes occasional Regular exercise and skilled physical therapy very important for good mobility and balance Goal to keep them moving as often and as safely as possible Balance and gait dual-task difficulty  Typical Progression Advanced PD: about 15–20 years post-dx Cognitive problems may be prominent Balance and gait dual-task difficulty Medication less effective Disease Course May have frequent freezing or falls Swallowing—dysphagia Autonomic Severe orthostatic hypotension Severe constipation causing impaction Weight loss  Parkinson Disease: Six Cardinal Motor Symptoms Resting Cogwheel Bradykinesia Tremor rigidity Clinical Findings Loss of Flexed Freezing postural posture of gait reflexes Other associated motor features: Hypophonia (soft voice) Hypomimia (masked face) Micrographia (small writing)  Parkinson Disease: Non-Motor Symptoms Cognitive Sleep disorders Anosmia Bradyphrenia Vivid dreams Loss of smell (slowness in thinking) REM behavioral sleep Dementia (late in disorder Clinical Findings disease course) Neuropsychiatric Autonomic Anxiety Fatigue Depression dysfunction Hallucinations  Parkinson Disease Parkinson disease is a clinical diagnosis Asymmetric onset Gradual onset and progression Six cardinal signs: 1. Bradykinesia 2. Rest Tremor 3. Rigidity Diagnosis 4. Flexed posture 5. Freezing 6. Loss of postural responses Parkinsonism = Bradykinesia plus rest tremor or rigidity (two of the six cardinal motor signs) Clinical Findings Bradykinesia Clinical Findings Rest Tremor  Postural Instability/Retropulsion Clinical Findings  Freezing and Festinating Gait Clinical Findings  Parkinson Disease Parkinson disease is a clinical diagnosis: 1. MDS-UPDRS (clinical examination) 2. Symptomatic improvement with levodopa helps to confirm idiopathic PD 3. Absence of red flags Imaging MRI is performed to rule out other diagnoses DaTScan is mostly used for Diagnosis research Picture credit: www.apdaparkinson.org Skin biopsy To detect presence of phosphorylated alpha-synuclein (marker of neurodegeneration) Postuma RB, Berg D, Stern M, et al. MDS clinical diagnostic criteria for Parkinson’s disease: MDS-PD Clinical Diagnostic Criteria. Movement disorders. 2015;30(12):1591-1601. doi:10.1002/mds.26424  Parkinson Disease Early falls Autonomic dysfunction Early cognitive symptoms UMN signs Cerebellar signs Red Flags  Parkinson Disease Normal pressure hydrocephalus (NPH) Differential Diagnosis Drug-induced parkinsonism Vascular parkinsonism Essential tremor: action tremor Wilson’s disease Atypical parkinsonian syndromes  Parkinson Disease 1. Exercise Preventative Restorative Medical Management Symptomatic 2. Medications Dopaminergics: levodopa Non-dopaminergics 3. Surgical Deep Brain Stimulation (DBS)  Levodopa Gold standard Converts to dopamine once it enters the brain Dopamine alone does not cross Medical Management blood brain barrier Carbidopa/levodopa (Sinemet) Prevents peripheral conversion of L-Dopa to dopamine Most effective drug to treat Levodopa symptoms replaces dopamine However, new symptoms (called motor fluctuations) emerge over time  Parkinson Disease Life span is a few years less than normal Disease progression can be for 20 years or more Death from other causes such as heart disease, cancer, secondary complications like pneumonia PIGD: postural instability—gait difficulty Prognosis Arch Neurol. 2001;58(10):1611-1615  Clinical Management Identify Intervene Flexed posture Meaningful exercises that Gait difficulties (shuffling, encourage power, extensor freezing, turns) strengthening, body awareness, timing, coordination, agility Clinical Management Balance Dual-task training Functional mobility Functional training with Dexterity repetition, progression, and Bradykinesia variability Tremor Vigorous aerobic exercise Fatigue Skill-specific practice Difficulty dual-tasking Stress reduction Pain Falls Movement Disorders Atypical Parkinsonian Syndromes  Parkinsonism General Considerations Parkinsonism Primary idiopathic Atypical Secondary Parkinson Parkinson Parkinsonism disease (PD) Progressive Drug-induced Sporadic supranuclear palsy (PSP) Vascular Normal pressure Hydrocephalus Familial Trauma Multiple system atrophy (MSA) Metabolic Tumors Corticobasal Toxins degeneration (CBD)  Atypical Parkinsonian Syndromes General Considerations Can be known as atypical parkinsonism or Parkinson-plus syndromes Has parkinsonian symptoms with additional features Three major syndromes 1. Progressive supranuclear palsy (PSP) 2. Multiple system atrophy (MSA) 3. Corticobasal degeneration (CBD)  Progressive Supranuclear Palsy (PSP) General Considerations Prevalence: 1.39 cases per 100,000 people Incidence More frequent in men Mean age of onset is 65 years Most frequent atypical parkinsonian syndrome  Progressive Supranuclear Palsy (PSP) Neuronal degeneration of basal ganglia neurons Pathogenesis Loss of postsynaptic dopamine receptors Neurofibrillary tangles and tau-positive astrocytes in basal ganglia and brainstem structures  Progressive Supranuclear Palsy (PSP) Insidious, progressive, and more rapid than PD Death in 5–10 years, often due to aspiration Disease Course Freezing, Progressive Progressive Parkinsonian sx, cog supranuclear dementia, gaze palsy, wide- dysphagia, motor and involvement, early falls, cognitive axial rigidity, absence of based gait, dysarthria, affected speech, emotional lability, decline until tremor death facial dystonia volatile mood  Progressive Supranuclear Palsy (PSP) Key features: Progressive parkinsonism Vertical supranuclear ocular palsy or slow vertical saccades Clinical Findings Early onset of falling Axial rigidity Facial dystonia Usually no tremor  Progressive Supranuclear Palsy (PSP): Eye movements Clinical Findings  Progressive Supranuclear Palsy (PSP): Imbalance/Posterior Loss of Balance Clinical Findings  Clinical Management for PSP Identify Intervene Vision impairment Balance training Axial rigidity Functional training with Early falls repetition, progression, and Clinical Management variability Postural instability Vigorous aerobic exercise Early cognitive involvement and strengthening Equipment ordering Compensatory strategies Patient/family education Speech Therapy  Multiple System Atrophy (MSA) General Considerations Prevalence Less than 10% of patients with parkinsonism have MSA Incidence Onset is usually at 30–50 years of age More males are affected than females Sporadic, rapidly progressing with undetermined etiology  Multiple System Atrophy (MSA) General Considerations Patients eventually develop symptoms of Parkinson disease (e.g., slowed movement, rigidity), autonomic dysfunction, and cerebellar signs N Engl J Med 2015; 372:249-263  Multiple System Atrophy (MSA) Marked neuronal degeneration in multiple pathways Pathogenesis Poor therapeutic response Cerebellar ataxia Symptomatic orthostatic to levodopa Dysphagia and hypotension Early postural instability dysarthria Impotence May not have tremor Urinary incontinence Increased DTR Bowel/bladder dysfunction  Multiple System Atrophy (MSA) Progressive and more rapid than PD Patients are often using wheelchairs or are markedly disabled within five years Mean survival rate about 8–9 years after Disease Course the onset of symptoms Prominent autonomic dysfunction— worse prognosis Progressive Parkinsonian sx, cog Postural Progressive motor and involvement, autonomic instability, UMN dementia, cognitive dysfunction, cerebellar signs, bowel dysphagia, decline until ataxia and bladder dysarthria death  Clinical Management for MSA Identify Intervene Orthostatic Abdominal binders, hypotension/autonomic compression stockings involvement Equipment ordering Axial rigidity Functional training with Clinical Management Early falls repetition, progression, and Vision impairment variability Postural instability Vigorous aerobic exercise and strengthening Early cognitive involvement Multiple Health Providers Patient/family education  Corticobasal Degeneration (CBD) General Considerations Incidence and prevalence unknown Estimated 0.62–0.92 per 100,000 people Age of onset often in the 60s, but can range 45–77 years  Corticobasal Degeneration (CBD) Nerve cell loss and atrophy of multiple areas of the brain including cortex and basal ganglia Significant parietal atrophy—asymmetric Pathogenesis AM Tokumaru, T O’uchi, Y et al. Corticobasal degeneration: MR with histopathologic comparison. AJNR Am J Neuroradiol 1996. 17 (10) 1849-1852. http://www.ajnr/org/content/17/10/1849.  Corticobasal Degeneration (CBD) Typically begins at or around the age of 60 May first appear on one side of the body (unilateral), but eventually affect both sides Progresses over the course of 6–8 years Disease Course Death is generally caused by pneumonia or other complications of severe debility such as sepsis or pulmonary embolism Early falls, UMN Progression to Inability to walk, Parkinsonian sx, unilateral signs, apraxia, bilateral and progressive axial dementia, arm or leg dystonia or progressive rigidity, cortical sensory mobility decline, involvement, bradyphrenia, dysphagia, loss decline until deficits death motor blocks of mobility  Corticobasal Degeneration (CBD) Key features: Parkinsonism Unilateral arm rigidity and dystonia Cortical sensory deficits Clinical Findings Other possible symptoms: UMN features—hyperreflexia, (+) Babinski sign Apraxia Dementia Rigidity Dysphagia Myoclonus Alien limb phenomenon  Dystonia in CBD Dystonia: torsional movements that are partially sustained and produce twisting postures In CBD: unilateral rigidity and dystonia in the arm Clinical Findings  Clinical Management for CBD Identify Intervene Arm or leg rigidity or dystonia Splints, manual therapy Early falls Pain management Postural instability Functional training with Clinical Management Early cognitive involvement repetition, progression, and variability Vision impairment Vigorous aerobic exercise and strengthening Balance training Equipment ordering Stress reduction Patient/family education  Atypical Parkinsonian Syndromes Often patients are initially diagnosed with PD Clinical findings and the fast rate of progression MRI and PET can be performed but not diagnostic Neuropsychiatric testing for cognitive involvement Clinical diagnosis Diagnosis  Differential Dx of Parkinsonism Differential Diagnosis  Atypical Parkinsonian Syndromes Symptomatic Medications Secondary impairment management Medical Management Botox injections for dystonia Often not responsive to levodopa Deep brain stimulation (DBS) often not helpful  Functional independence Clinical Management Clinical Management and quality of life Time/disease progression Safety Capacity Natural progression With intervention Movement Disorders Summary PD Atypical parkinsonian syndromes (PSP, MSA, CBD) Etiology Unknown Unknown Genetic and environmental factors Signs/symptoms Bradykinesia, rigidity, Early falls, gaze resting tremor, postural abnormalities, instability autonomic dysfunction, early dementia Diagnosis Clinical: (motor) Clinical, nonresponsive to signs/symptoms + asymmetric levodopa. onset, gradual Possible findings on imaging Responsive to levodopa Progression Gradual progression 20-plus More rapid progression years Treatment Medication (levodopa), DBS, Medication less effective exercise Symptomatic Exercise Dementia Introduction and Neuroanatomy Dr. Nora Darakjian, PT, DPT Board-Certified Neurologic Clinical Specialist  Objectives for Students Understand what dementia is, from a medical perspective Identify cortical regions involved in cognition Have a working knowledge of Alzheimer’s disease diagnosis Recognize role of screening, including importance of MCI Know other conditions that cause dementia or change in cognition Focus on Normal Pressure Hydrocephalus Have some understanding about how dementia may be managed medically  Neuroanatomy Neuroanatomy Pathogenesis General considerations Pathogenesis Step 1 General Disease course Clinical findings Clinical findings Disease course Red flags Step 2 Diagnosis Diagnosis/differential diagnosis Medical management Medical management Clinical management Prognosis Clinical management Step 3 Prognosis  CNS vs. PNS CNS PNS UMN Sensory Other LMN Sensory Autonomic Motor CN and Cranial nerves: Cortical Cortical Basal ganglia nuclei* sensory and special Cerebellum Anterior horn* Spinal peripheral Brainstem Brainstem nerve and nerve root Cortical Spinal nerve root association areas and peripheral Spinal Spinal (e.g. cognition, nerve cord cord behavior) NMJ Autonomic: hypothalamus, basal ganglia, Muscle limbic system, brainstem, spinal cord  Cognitive Function The mental functions involved in attention, thinking, understanding, learning, remembering, solving problems, and making decisions. Memory Neuroanatomy Reasoning Personality (executive function) Domains Language Visuospatial  Cognitive Functions Localized Neuroanatomy  Limbic Association Areas Neuroanatomy Hippocampus Limbic cortex Memory Personality Behavior Mood Motivation  Dementia: Overview General Considerations A progressive deterioration in mental function that interferes with activities of daily living appropriate for one’s age and background Dementia (from Latin) de, “undoing” and mentis, “of the mind” Most common cause: Alzheimer’s disease (AD) PTs play an important role in recognition and management  Incidence and Prevalence General Considerations Widely varying estimates Challenges related to classification and estimation Most conservative estimates 3.7 million individuals with dementia in US over 2.5 million of these have Alzheimer’s disease Some estimates are double this 13.9 percent of people age 71 and older in the US have dementia Recent studies suggest that prevalence might be decreasing (Langa et al, JAMA Internal Med, 2016)  Criteria for Diagnosis of Dementia When cognitive or behavioral symptoms: 1. Interfere with function and usual activities 2. Represent a progressive decline from previous levels of function Not acute Not explained by delirium or major psychiatric disorder Clinical Findings 3. Involve at least two of the following domains: Impaired memory─deficits in acquiring and remembering new information Impaired reasoning, poor judgment, and deficits in ability to carry out complex tasks Impaired visuospatial abilities Impaired language functions Changes in personality, behavior, comportment  Most Common Causes of Dementia Mild cognitive impairment Dementia Pathogenesis AD Vascular Alcoholism PD related Drug/medication Alzheimer’s disease (AD): about 2/3 Vascular dementia Alcoholism* Parkinson-related dementias Drug/medication intoxication* *Potentially reversible  Differential Diagnosis Alzheimer disease (app. 2/3 of all dementias) Differential Diagnosis Vascular dementias Parkinson-related dementias (e.g., PSP) Dementia with Lewy bodies Delusions, hallucinations Frontotemporal dementia Normal pressure hydrocephalus Dementia Normal Pressure Hydrocephalus (NPH)  Normal Pressure Hydrocephalus Excessive fluid accumulation in brain Usually develops over a period of months Not caused by obstruction, but rather by inadequate resorption of CSF Intracranial pressure is not elevated Contrast with acute hydrocephalus, caused by obstruction Characteristic triad of signs Wide-based ‘magnetic’ gait (G) Pathology Urinary incontinence (I) Impaired cognition (Foggy) (F) Causes Prior subarachnoid hemorrhage, meningitis, tumor, surgery May simply result from aging Often idiopathic  Normal Circulation of CSF Neuroanatomy  Cerebral cortical atrophy Diagnosis Normal pressure hydrocephalus Picture: https://docplayer.gr/82028894-Aaistoriko-tis-paroysas-nosoy-kefalaio-1-v-zali-v-entopisi- ton-symptomaton-g-adynamia-g-poreia-sto-hrono-d-tromos-e-aimodies-st.html  Normal Pressure Hydrocephalus General Considerations Diagnostic CT or MRI─enlarged ventricles without other signs of cortical atrophy Spinal tap─improvement of symptoms after large volume of CSF removed Can be treated with shunting Ventriculoperitoneal, ventriculoatrial, or lumboperitoneal 40-50% show sustained improvement after shunting Prognosis favorable with shunting and proper management But concomitant AD may be present Usually best prognosis when initial symptoms involve gait Favorable response to spinal tap is also a good indicator  Normal Pressure Hydrocephalus General Considerations Classic NPH Gait Pre-Shunt Surgery - YouTube  Normal Pressure Hydrocephalus General Considerations Classic NPH Gait Improvement Post Successful Shunt Surgery - YouTube  Clinical Management: NPH Assess and monitor functional measures: gait speed, balance Assess and monitor pre- and post- shunt placement Dual task training Clinical Management Aerobic Exercise Functional training Balance training Fall recovery training Dementia Alzheimer’s Disease  Alzheimer’s Disease (AD) General Considerations Most common cause of dementia Usually in people of age greater than 65, but rare cases of early-onset AD (less than 40) Gradual, progressive decline Insidious onset, usually beginning with memory deficits (amnestic type) Sporadic and autosomal dominant forms Cause unknown, but appears to involve abnormal production of certain proteins that make up neurons Folding of membrane protein (amyloid precursor protein) Deposition of neuritic (amyloid) plaques Neurofibrillary tangles (tau proteins involved in structure of microtubules─‘tauopathies’) End result: degeneration and death of neurons leading to cerebral atrophy  Amyloid Plaques and Neurofibrillary Tangles in Alzheimer’s Disease Pathogenesis  Distribution of Pathologic Changes in Alzheimer Disease (AD) Pathogenesis Association cortex in the parietal, temporal, and frontal lobes is particularly affected Brust: Current Diagnosis and Treatment Neuroanatomy 2 nd Ed Copyright 2011 by McGraw-Hill Education  Cerebral Atrophy in Alzheimer Disease Pathogenesis  Diagnosis of Alzheimer Disease Definitive diagnosis only possible with histological confirmation by postmortem or brain biopsy During life, two possible diagnoses 1. Probable AD Meets criteria for diagnosis of dementia Insidious decline (months and years) Clear-cut history of worsening of cognition (ideally by repeated testing) Other causes of dementia ruled out Diagnosis 2. Possible AD Atypical course, or Mixed etiology Testing Lab studies, lumbar puncture, imaging to rule out other causes  Risk Factors in Alzheimer Disease Risk factors Increasing age Vascular disease (esp. stroke, hypertension) Diabetes Family history Female greater than male (related to more females living longer) History of multiple head injuries? “Genetically heterogeneous” Diagnosis Abnormal proteins may arise from genetic and/or acquired factors Some genes are causative (only 5% of AD) Some genes have been identified that may influence risk for AD Esp. APOE4 Familial history of AD is common, but not determinative  Disease Course Stages of Alzheimer Disease Mild AD Mod AD Severe AD Death usual from Disease Course MCI (?) Still Some Constant secondary independent supervision supervision causes Typical time course is 7-10 years (range 3-20)  Treatment of Alzheimer Disease There are no cures or disease-modifying treatments Drug therapies Cholinesterase inhibitors and NMDA receptor Medical Management antagonists Primarily aimed at cognitive symptoms with significant but usually modest benefit Vit E, B, DHA? Some potential therapies in early stages of testing Some promising indications that exercise may be preventive and also potentially disease-modifying Four pillars of Dementia care  Four Pillars of Dementia Care 1. Treat the disease If possible… 2. Treat the symptoms Drug therapies to boost cognitive capacities Medical Management Neuropsychiatric symptoms (e.g., depression) 3. Support the patient Management to maximize independence, safety, overall health 4. Support the caregivers Education, counseling, support groups  Lifestyle Factors: Prevention and Maintenance Control BP, DM, CVD Management of weight/BMI Dietary recommendations: Eat veggies, fruit, and fish (decrease dairy, meat, saturated fats) Medical Management Perform cognitive activities Smoking cessation Sleep! Treat depression, manage stress Avoid head trauma Regular physical activity! (minimum aerobic; three times a week for 40 minutes) Sandra et al 2003. Will a Healthy Lifestyle Help Prevent Alzheimer’s Disease? Yu et al 2020. Evidence-based prevention of Alzheimer's disease: systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials  Clinical Management: AD Assess and monitor functional measures: gait speed, balance Fall recovery training Dual task training Aerobic Exercise Clinical Management Fall prevention strategies Equipment management Caregiver education/training  Dementia Summary AD NPH Etiology/ Abnormalities of proteins in cortical Excessive accumulation of CSF pathophysiology areas, esp. temporal, parietal, frontal without obstruction; causes lobes damage to cortical and subcortical regions Signs/symptoms Cognitive decline over years, usually Wide based magnetic gait, starting with memory, orientation and impaired cognition, urinary language incontinence Dx tests MOCA and neuropsych testing MRI/CT No definitive test except histological Spinal tap exam of brain tissue post-mortem. CT/MRI to rule out other causes Prognosis Progressive decline over 7−10 years. 50% respond well to shunting Death from secondary conditions Treatment Four pillars of dementia care Shunting is only treatment  Key points Domains of cognition and which areas of the brain are responsible for each Key signs and symptoms of NPH Pathologic findings and risk factors in AD Potential benefit of exercise in prevention and management of AD Differential Diagnosis of Dementia