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585-13
Community Rehab/ ALS & myasthenia gravis
| Term | Definition |
|---|---|
| community rehab | Complex process Depends on multidisciplinary team Uses biopsychosocial model of illness Collaborative approach towards goals |
| wade asks | What's effective rehab? Who benefits? Location? Common features? What interventions used? |
| location considerations | Access Generalizability Safety Population it serves |
| outpatient rehab & specialized services | Services that support people in community Builds capacity Prevents & deters illness & disability Enhances function for meaningful activity |
| TBI timeline | ABI Acute care (ER & ICU) Inpatient rehab (optional, timing & intensity) Outpatient rehab |
| outpatient duration | 2-3x/ week Based on insurance and other financial stuff No to minimal assistance at home |
| why community rehab | Least costly programs to run Cost effective OT needs to advocate for it's need in healthcare |
| access & wayfinding | Pt & families know how to find services Can also guide referral sources to access points |
| patient, family, & community outcomes | Pt & families participate in all aspects of their own care Encouraged to be active participants through shared decisions and goal setting Measure meaningful progress Consistently use standardized tools & outcome measures |
| collaborative goal setting | Shared decision making- what can they work on now Client & family centered Documented Goal driven intervention |
| transitions | Pt & families experience optimal transitions Planned from start of care based on needs Good transition relies on initial visit & collaborative planning |
| service options | Pt & families get appropriate services Optimize match of specific needs Use variety of evidence informed rehab services Standardize rehab services to promote safety, experience, outcomes, efficacy Give different options of type, level, freq, duration |
| service types | Prevention Health promotion Education Intervention Case management |
| professional practice | Pt & families work w/ providers who have supports Professional practice is used OT competencies |
| myasthenia gravis pathology | Autoimmune disease Presence of auto-antibody attached to receptor sites on post-synaptic membrane |
| myasthenia gravis | Worsens w/ sustained activity Fatigue/ muscle weakness gets worse at end of day Does not affect involuntary muscles More in women |
| myasthenia gravis muscle symptoms 1. ocular 2. bulbar 3. neck | 1. double vision 2. difficulty in chewing, swallowing, talking 3. difficulty in lifting head up from lying position |
| myasthenia gravis muscle symptoms 1. trunk 2. proximal limb 3.distal limb | 1. breathing problems & difficulty in sitting from side lying position 2. difficulty in lifting arms above shoulder level, standing from low chairs, getting out of bath 3. weak hand grip, ankles, feet |
| myasthenia gravis management | Immunosuppression Surgery- remove thymus that helps immune system develop Plasma exchange Watch for fatigue & take exercise precautions |
| myasthenia gravis precautions | Aware of type of exercise, intensity, duration of workload Ax physical limitations Avoid exercising outside during hottest time of day Pre-cooling Gentle exercises Don't over do |
| motor neuron disease | Loss of lower mn (pons, medulla, SC) &/or upper mn (motor cortex) Bulbar (medulla oblongata), upper limb, trunk, lower limbs Sensory & autonomic functions intact Resp muscles may lead to chest infection Only striated muscles affected |
| upper motor neuron involvement characteristics | Muscle wasting unlikely Increased tone of clasp-knife type- resistance and then a give Weakness most evident in anti-gravity muscles |
| lower motor neuron involvement characteristics | Muscle wasting Twitching due to spontaneous depolarization of LMN which has spontaneous contraction Decreased tone Weakness Decreased or no reflexes |
| ALS (or Lou Gehrig's Disease) | Muscle wasting, Involves UMN & LMN Fatal disease Familial onset 45-52 years, sporadic onset 55-62 years 3x more in men Nerves hit first, then demyelinate |
| etiology of ALS | Fatal, progressive, degenerative Massive loss of anterior horn cells & motor nerve nuclei Demyelination & gliosis of CST & corticobulbar tract |
| possible causes of ALS | Mitochondrial pathways dysfunction results in protein buildup that leads to motor neuron death Inflammation Glutamate insufficiency, metal toxicity, autoimmune, genetics, virus |
| early markers of ALS | Weakness of hand & feet muscles Asym foot drop Twitching Muscle cramps- calf Weakness from distal to proximal Atrophy Fatigue, loss of balance |
| ALS motor regression patterns | LE onset more common Distal to proximal Flexor muscles weaker Bulbar symptoms in later disease stage- small muscles, speaking/swallowing, to resp failure |
| symptoms of ALS | Drop things, slurred speech, abnormal fatigue, emotional liability Focal muscle weakness- arm leg, bulbar Marked muscle atrophy Weight loss Spasticity Twitching |
| prognosis of ALS | Onset 16-77 Progressive, rapid deterioration Avg survival 1-5 years Younge people have more mild symptoms, have functional improvements, and live longer (10-16%) Death from resp failure |
| better ALS prognosis if | Young age of onset Deficits in either UMN or LMN, not both Absent/ slow changes in resp Few twitches |
| corticospinal tract vs. corticobulbar tract | Motor cortex to LMN in ant horn. Fine voluntary motor control of limbs. Voluntary control of posture vs. Motor cortex to pons and medulla oblongata. Facial and jaw muscles, swallow, tongue movements. |
| progressive bulbar palsy | Corticobulbar tracts & brainstem nuclei Variant ALS, may develop into ALS UMN involvement Loss of muscles by cranial nerves- 9, 10, 12 Dysarthria, dysphagia, face & tongue weakness/ wasting |
| progressive muscular atrophy | Only LMN Weakness & atrophy Twitch in limbs, trunk, bulbar Cramps in thighs, fall risk From hand muscles, upper arm, shoulder. Lower limbs have limited mobility Better prognosis |
| primary lateral sclerosis | Benign Only UMN CST & CBT Progressive spastic paraplegia In any age, slower progression, non-fatal Progression varies- managed with minimal devices typically for energy conservation |
| LMN symptoms | Focal & multifocal weakness Atrophy Muscle cramping & twitching Reduced ROM Fatigue |
| UMN symptoms vs. CBT symptoms | Spasticity Hyperreactivity Dysphagia Dysarthria vs. Dysphagia Dysarthria Dyspnea |
| diagnosis for ALS | Clinical symptoms EMG- denervation & twitching MRI, CT scan to rule out other causes Blood tests normal CSF normal w/ raised protein |
| medical management of ALS | Control symptoms or inflammation Non-invasive positive pressure ventilation, increased lifespan Low radiation or botox into salivary glands Palliative care New drugs Stem cell tx |
| OT ax for ALS | MMT, ROM, balance, coordination Swallow & eating Psychosocial Depression & cognition Productivity Leisure activities Roe checklists- self report |
| functional autonomy measuring system vs. occupational performance history interview | ADLs, mobility, communication, mental function, IADLs. Administered by interviewing or observations vs. 45-60 min, semi-structured/ narrative interview. Look at roles, routines, activity, choices, critical life events |
| ALS stage 1-2 | Mild/ mod weakness, clumsy Can do normal ADLs Minor limitation & pain may appear Reduced endurance Engage in work & employment |
| OT intervention for ALS stage 1-2 | Energy conservation ROM & stretching Work simplification Adaptive equipment Orthotics Consider safety |
| stage 3 ALS vs. interventions for ALS stage 3 | Severe, selective weakness in ankles, hands, wrists Fatigue w/ ambulation, still ambulatory vs. WC prescriptions Universal cuffs Discuss need for home modifications |
| ALS stage 4 vs. 5 | Hanging arm syndrome w/ shoulder pain & edema Need w/c for ambulation LE weakness vs. Severe LE weakness, moderate- severe UE weakness |
| ALS stage 4-5 intervention | Arm sling Explore environmental control systems Family training for transfers, positioning, turning, ADL assistance Control devices Adapt w/c Psychosocial intervention |
| stage 6 ALS vs. intervention for stage 6 | Totally dependent- confined to bed/ chair vs. Evaluate dysphagia & provide w/ speech devices Continue PROM, massage |
| ALS therapeutic activity & exercise | Gentle exercise maintains ROM, strength, endurance. Don't overwork Mild progressive resistance exercise for pt w/ good muscle strength- but watch for fatigue & pain Important to maintain ADL independence as much as possible |
| ALS exercise program | 1/day To resistance & hold for 30 sec Slowly start exercise, gradually build up Aim for full ROM Don't force movement Support limbs Watch pt reaction for response |
| ALS exercise precautions | Muscle strengthening is not part of tx program, can't alter disease course & may cause cramping/ fatigue Watch for decreased resp function Avoid fatigue Consider cost, appearance, acceptability to person & family |
Created by:
craftycats_
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