NeuroRehab Lecture Slides 2022 PDF

Introduction to NeuroRehab Nora Cullen, MD, MSc, FRCPC Specialist PM&R Professor, McMaster University Chief PM&R Hamilton Health Sciences and St Joseph’s Healthcare Hamilton November 26, 2021  Overview ◼ Who gets...

Introduction to NeuroRehab Nora Cullen, MD, MSc, FRCPC Specialist PM&R Professor, McMaster University Chief PM&R Hamilton Health Sciences and St Joseph’s Healthcare Hamilton November 26, 2021  Overview ◼ Who gets a Brain Injury? ◼ Predicting recovering ◼ Functional problems ◼ Team members ◼ Other Neurologic Insults ◼ Stroke ◼ Multiple Sclerosis ◼ Parkinson’s Disease  Objectives Participants will be able to: 1. Identify how injury affects basic brain function 2. Recognize signs and symptoms of mild, moderate and severe brain injury 3. Describe functional, physical and psychiatric issues faced by brain injured patients and make appropriate responses to treat and refer as required  Where is the lesion? ◼ Each function that the body performs can be traced back to a specific area of the brain Brain Map ◼ Physical ◼ Motor ◼ Sensory ◼ Autonomic ◼ Cognitive ◼ Behavioral  Epidemiology of TBI ◼ Annual incidence of TBI is 250/100,000 ◼ Males 15 – 24 years old, also peaks in >75 yrs ◼ male: female ratio 3:1 ratio ◼ 80% mild, 20% moderate to severe ◼ leading cause of death and disability in children and young adults  Epidemiology of TBI ◼ 53 % single, 13 % divorced, 5% separated, 3% widowed = 74% are not married ◼ 53% employed, student 10%, 9% homemaker/retired = mostly employed ◼ tend to be injured on Saturday or Sunday between 8 pm and 4 am ◼ 73% have associated fractures which may obscure or delay detection of TBI Traumatic Brain Injury Epidemiology TBI is often the result of substance abuse, crime, environmental hazards, driving safety and supervision of children and elderly  Acquired Brain Injury - Traumatic Traumatic Brain Injury ◼ Non-degenerative, non- congenital ◼ Mechanical force ◼ Permanent or temporary impairments of cognitive, physical, and psychosocial functions Traumatic Brain Injury Pathophysiology ◼ Classification ◼ Primary ◼ Occurs at the moment of trauma as a result of direct mechanical damage ◼ Closed ◼ Open ◼ Secondary ◼ Occurs after trauma as a result physiologic responses to initial injury  Open Brain Injuries ◼Missiles e.g. Gun shot wounds ◼High velocity missiles inflict the most damage ◼ Bullets often fragment, causing damage in multiple directions Skull Fractures ◼ Associated with increased risk of brain injury, hematoma, CN damage ◼ Vault fractures are closed or open, simple or compound, linear or stellate, non-depressed or depressed ◼ Basal skull fractures Basal Skull Fractures Closed Head Injuries Intracranial Hemorrhages ◼ Epidural ◼ Subdural ◼ Subarachnoid ◼ Intracerebral ◼ Intraventricular ◼ Diffuse Axonal Injuries Epidural Hematomas ◼ Relatively uncommon (11 weeks is inconsistent with independent living  Secondary Brain Injury ◼ Evolves over hours or days following traumatic insult ◼ Causes cerebral ischemia and tissue hypoxia leading to further neuron loss ◼ Mechanisms: ◼ Neurochemical and Cellular Events ◼ Cerebral Edema ◼ Hydrocephalus  Impairments Following TBI ◼ Cognitive/Behavioral ◼ Affective (mood) ◼ Physical – motor, sensory, autonomic ◼ Social  Emotional & Behavioural Changes ◼ Reduced Insight ◼ Lack of control ◼ Social Behaviour ◼ Loss of social skills, withdrawal from social interactions ◼ Apathy ◼ Lack of initiative, poor motivation ◼ Depressed & Anxious Mood ◼ 60% of all TBI survivors ◼ 1/5 contemplate suicide during first 5 years  Cognitive ◼ During & After Posttraumatic Amnesia ◼ Inappropriate responses to environment ◼ Discipline-specific goals ◼ Re-orient to the environment using calendars, schedules etc. ◼ Compensatory strategies ◼ Focus on specific areas of deficits ◼ Carry-over learning  Maximizing Cognition ◼ Rule out correctable biological etiologies ◼ Cognitive Rehabilitation ◼ Cognitive Enhancing Medications  Cognitive Rehabilitation ◼ Post-Acute Rehabilitation ◼ Structured settings - Challenged in novel environments ◼ Adaptive strategies and cognitive techniques on an outpatient basis ◼ Community Integration ◼ Address adjustment issues  Case 1 ◼ 19 year old male involved in single vehicle collision when rock thrown onto car from overpass ◼ Traumatic Brain Injury ◼ GCS 3/15 ◼ ICU admission ◼ Coma for 2 months ◼ Several facial surgeries, blind, damaged frontal lobes, seizures, hemiplegic, pituitary gland non functioning  Case 1 ◼ Patient emerged from coma ◼ Went on to have partial recovery ◼ Became partially independent in ADL’s over 2 years ◼ Neuropsychology testing revealed profound memory and attentional deficits with frontal lobe symptoms ◼ unable to resume previous hobbies, driving or schooling, but engages in an array of activities including college courses Agitation in TBI Stages of Recovery post TBI Ranchos Los Amigos Scale I No Response II Generalized response III Localized response IV Confused and agitated V Confused and non-agitated VI Confused and appropriate VII Appropriate and automatic VIII Appropriate Agitation in TBI Rule out other causes Drugs Alcohol withdrawl Pain Infection Metabolic derangement Seizures - temporal or occipital Sleep disturbance Vasospasm Space occupying lesion Agitation in TBI Attempt to de-escalate the situation Use simple directions Avoid scolding Control your voice Consider the short-term memory deficits Redirect attention Agitation in TBI - Physical Interventions Quiet, private, safe, structured room Observation of triggers Video camera Alarms Sleep log Restraints - Use only when other measures fail  Depression post TBI ◼ Interferes with recovery ◼ May produce further cerebral damage ◼ Antidepressants reduce depression ◼ may also protect against further cell death  Medical Considerations Systems Approach: ◼ Cardiovascular ◼ Gastrointestinal ◼ Genitourinary ◼ Integumentary ◼ Respiratory ◼ Metabolic ◼ Neurological ◼ Musculoskeletal  Hydocephalus ◼ The dilation of the cerebral ventricular system ◼ Occurs when normal CSF flow is impaired, leading to fluid accumulation ◼ Limits blood flow to the brain.  Medical Considerations Neurological ◼ Hydrocephalus ◼ communicating - h/a, n&v, lethargy, decreased mental status, ◼ non-communicating - obstructed, CSF backs up ◼ normal pressure - weird, wet ,wobbly = gait ataxia, dementia, incontinence  Fatigue post TBI 21% at one year post injury Decreased amount of sleep Increased sleep interruptions Reduction or absence of deep sleep Sleep wake reversal Decreased growth hormone, testosterone  Treatment Education - prioritizing, pacing, delegating, scheduling, structured routines, one activity at a time, scheduled rest times Exercise - regular, graded physical activity, adaptive devices, social activities, biofeedback, relaxation techniques, meditation, music, pet/ horticulture therapy consider stimulant  Reintegrate to Community ◼ Accessible Environment ( home & work) ◼ Attendant Care ◼ Transportation ◼ Sexuality ◼ Vocational/avocational Goals ◼ Parenting  Reintegrate to Community ◼ Injury prevention counseling ◼ Driver’s license suspension ◼ Avoid alcohol use for one year at least ◼ Wear helmet for sports ◼ No ladders/bicycles for patients with poor balance  Resources ◼ Ontario Neurotrauma Foundation: onf.org ◼ Brain Injury Canada braininjurycanada.ca ◼ Evidence Based Review of Acquired Brain Injury ◼ abiebr.com/ ◼ Centre for Outcome Measurement in Brain Injury- good outcome measures ◼ tbims.org/combi ◼ Emedicine- good medical explanations ◼ emedicine.com/pmr/contents.htm ◼ Center for Disease Control (US) ◼ cdc.gov ◼ Ontario Brain Injury Association ◼ obia.on.ca Stroke and Its Management  Objectives ◼ What is stroke? ◼ Etiology, pathophysiology ◼ Presentation according to location ◼ Secondary prevention ◼ Intracerebral hemorrhage ◼ Etiology ◼ Prognostic Factors ◼ Rehabilitation ◼ Factors affecting stroke prognosis ◼ Time course of clinical improvement  How Common is Stroke? ◼ Every 45 seconds someone has a stroke ◼ Every 3-4 minutes someone dies from a stroke ◼ A stroke survivor has a 20% chance of having another stroke within 2 years American Heart Association 2007  What is the Outcome of Stroke? ◼ For every 10 stroke patients… ◼ 2 will die ◼ 2 will recover ◼ 6 will be left with disability ICES data, 2001 Stroke is a Leading Cause of ◼ Physical disability ◼ Death ◼ Cognitive Impairment ◼ Depression ◼ Epilepsy ◼ Falls ◼ Long Hospital Stays ◼ Institutionalization Stroke Definition Rapid development of symptoms and/or signs of focal loss of cerebral function due to vascular malfunction  Five Warning Sings Weakness - Sudden loss of strength or sudden numbness in the face, arm or leg, even if temporary. Trouble speaking - Sudden difficulty speaking or understanding or sudden confusion, even if temporary. Vision problems - Sudden trouble with vision, even if temporary. Headache - Sudden severe and unusual headache. Dizziness - Sudden loss of balance, especially with any of the above signs. Stroke Non Modifiable Risk Factors Age Gender M>F Prior Stroke History Family History  Modifiable Stroke Risk Factors ◼ Carotid artery disease ◼ Dietary factors ◼ Hypertension ◼ Physical inactivity ◼ Hypercholesterolemia ◼ Obesity ◼ Diabetes mellitis ◼ HRT and oral ◼ Cigarette smoking contraceptive pill ◼ Atrial fibrillation ◼ Sickle cell disease ◼ Other cardiac causes ◼ Valvular heart disease ◼ Cardiomyopathy AHA/ASA Primary Stroke Prevention Guidelines Stroke. 2006;37:1583-1633 Stroke Types Stroke Types Differentiation Between Ischemic versus Hemorrhagic Strokes Ischemic Stroke Syndromes: Middle Cerebral Artery Occlusion  Middle Cerebral Artery ◼ Contralateral hemiparesis (face, arm>leg) ◼ Contralateral hemisensory impairment ◼ Contralateral homonymous hemianopsia ◼ Gaze deviation away from the hemiparetic side ◼ Specific hemispheric signs: ◼ Left (dominant hemisphere) ◼ Aphasia (expressive, receptive, global) ◼ Right ◼ Dysarthria ◼ Neglect  Anterior Cerebral Artery ◼ Contralateral weakness of leg >> arm ◼ Contralateral hemisensory impairment in the same distribution ◼ Mood and cognition disturbance: ◼ Depression ◼ Agitated confusion ◼ Emotional lability  Symptoms associated with Posterior Circulation Strokes ◼ Slurred speech ◼ Trouble swallowing ◼ Double vision ◼ Vertigo ◼ Contralateral weakness ◼ Crossed sensory signs ◼ Cranial nerve palsies ◼ Ipsilateral incoordination ◼ Unsteady gait ◼ Fluctuating LOC ◼ Hearing loss  Ischemic Stroke Syndromes Posterior Cerebral Artery ◼ Contralateral hemianopia  Lacunar Syndromes ◼ Small vessel ischemic disease ◼ 5 main clinical syndromes ◼ Pure motor ◼ Pure sensory ◼ Ataxic hemiparesis ◼ Clumsy hand-dysarthria ◼ Mixed motor-sensory  Transient Ischemic Attack ◼ Sudden onset focal neurological symptoms of vascular etiology that resolve within 24 hours ◼ Caused by a sudden, usually temporary, interruption of blood flow to the brain or to the eye ◼ Most TIAs last between 10-60 mins ◼ TIA is a stroke warning event ◼ 15-20% of stroke patients have had a preceding TIA  Hypertension ◼ Most important modifiable risk factor (increases stroke risk 2-5 x) ◼ Ischemic stroke ◼ Intracerebral hemorrhage ◼ “Silent strokes” ◼ Overall, 30-40% relative risk reduction in stroke with a BP reduction of 10/5mmHg ◼ BP control is important in both primary and secondary stroke prevention  Impact of Lifestyle Therapies on Blood Pressure in Hypertensive Adults Intervention Change SBP/DBP Sodium intake - 100 mmol/day -5.8 / -2.5 Weight - 4.5 kg -7.2 / -5.9 Alcohol intake - 2.7 drinks/day -4.6 / -2.3 Exercise* 3 times/week -7.4 / -5.8 Dietary patterns DASH diet -11.4 / -5.5 DASH Eating Plan: http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf * 1- Exercise and Hypertension. Medicine & Science in Sports & Exercise. 36(3):533-553, March 2004. 2- Result of aggregate and metaanalyses of short term trials. Miller ER et al. J Clin Hyper 1999: Nov/Dec:191-8.  Diabetes Mellitis ◼ Diabetes affects 8% of the population ◼ 15-33% of stroke patients are diabetic ◼ Diabetes is a clear risk factor for stroke ◼ Higher incidence of atherosclerosis ◼ Higher prevalence of HT, hyperlipidemia, obesity ◼ 1.8-6 fold increased relative risk of stroke  Hyperlipidemia ◼ Statin treatment provides 25% relative risk reduction  Cigarette Smoking ◼ 1.5-4x increased risk ◼ 33% risk reduction ◼ risk normalizes 5 yrs after quitting ◼ independent of age  Antiplatelet Therapy: Best Practice Recommendations ASA 81-325 mg/day in patients with TIA/stroke  Atrial Fibrillation ◼ 2-year stroke risk – 20% with no therapy – 16% with ASA – 7% with warfarin  Treatment Strategies ◼ Multidisciplinary Team approach – PT, OT, SLP, SW, psychology, psychiatry, nursing, physiatry, family doc ◼ Medications ◼ Targeting Symptoms ◼ Spasticity management ◼ Fatigue ◼ Depression ◼ Ataxia ◼ Neurogenic bladder and bowel management  Multiple Sclerosis 11/30/2022  Background ◼ The most common acquired neurological disease ◼ 50 - 100 per 100,000 (0.1%) ◼ F:M ratio is 2:1 ◼ Onset 15-45 years old, mean 30 ◼ Higher socio economic status ◼ Life expectancy is about 40 years from onset Pathophysiology ◼ Autoimmune ◼ antibodies to myelin are formed ◼ results in demyelination with axon sparing 11/30/2022 Pathophysiology ◼ periventricular white matter of cerebellum, brainstem and spinal cord ◼ patient is susceptible to microenvironmental changes resulting in conduction blocks 11/30/2022  Types ◼ Benign ◼ Relapsing remitting ◼ Secondary Chronic Progressive ◼ Primary Progressive ◼ Malignant 11/30/2022  Course of Illness ◼ Symptoms at onset can be physical or cognitive/ behavioural Physical ◼ E.g. weakness, altered sensation, gait difficulty, visual disturbances, vertigo, spasticity, bladder problems, seizures, poor coordination ◼ Lhermitte’s sign, Uhtoff’s phenomenon 11/30/2022 Course of Illness ◼ most start with relapsing remitting course progressing to second attack within 5 - 10 years, then decreasing frequency of attacks ◼ May stabilize or progress slowly (esp if > 40 y.o.) ◼ Highly variable exacerbation rate (0.1-1.15 per year) 11/30/2022  Course of illness ◼ 30% start with chronic progressive course (worse prognosis) ◼ 5% die within 5 years ◼ 10% have severe disability within 5 years, 25% within 10 years, 50% within 18 years ◼ 20% have no disability within 15 years ◼ Exacerbations associated with: ◼ Infections, pregnancy, fatigue, heat, stress, trauma, heavy metals, diet, other autoimmune diseases  Medications ◼ Disease modifying agents ◼ Chronic Progressive ◼ Immune suppression ◼ Acute attacks ◼ Severe relapse: High dose Steroids ◼ Moderate relapse: Low dose Steroids  Treatment Strategies ◼ Multidisciplinary Team approach – PT, OT, SLP, SW, psychology, psychiatry, nursing, physiatry, family doc ◼ Medications ◼ Targeting Symptoms ◼ Spasticity management ◼ Fatigue ◼ Depression ◼ Ataxia ◼ Neurogenic bladder and bowel management  Parkinson’s Disease ◼ progressive neurodegenerative illness due to deficiency of dopamine in the substantia nigra  Parkinson’s Disease ◼ Dopamine allows nerve cells to transmit messages between each other and then to muscles to allow normal movement to take place. ◼ Characterized by TRAP ◼ Tremor ◼ Rigidity ◼ Akathesia ◼ Postural instability  Parkinson’s Disease ◼ 16/1000 aged >65, increases with age ◼ Prevalence: 100,000 people in Canada ◼ M=F ◼ Drug therapy replaces dopamine in the brain ◼ Rehabilitation efforts towards maintaining function for as long as possible  Approach to Rehabilitation ◼ Goal is to maximize function ◼ Multidisciplinary approach ◼ Communication between team members ◼ Concise rehab goals generated by patient and family  Team Members ◼ Physio ◼ Occupational ◼ Speech ◼ Social Work ◼ NeuroPsychology ◼ Medicine ◼ Support Workers  Others ◼ Nursing ◼ Recreational Therapist ◼ Psychologists ◼ Dietician ◼ Pharmacist ◼ Kinesiologist  Reintegrate to Community ◼ Accessible Environment ( home & work) ◼ Attendant Care ◼ Transportation ◼ Vocational Goals ◼ Sexuality ◼ Parenting ◼ Injury prevention ◼ Pacing  Summary ◼ Neurologic impairment is common and can be life altering ◼ Location of damage results in a pattern of impairment ◼ Severity can be classified by outcome measures ◼ Team approach to treatment is essential