Week 4 Summary Neuro PDF

etiology and pathophysiology 4.1 stroke intro & clinical presentation cerebral vascular accident/stroke: damage after loss of blood flow to brain ischemic 80% are ischemic caused by thrombus: blood clot formed w/in cerebral arteries or thromboembolism: small piece of blood clots break off distal vei...

etiology and pathophysiology 4.1 stroke intro & clinical presentation cerebral vascular accident/stroke: damage after loss of blood flow to brain ischemic 80% are ischemic caused by thrombus: blood clot formed w/in cerebral arteries or thromboembolism: small piece of blood clots break off distal vein and goes into cerebral vessel once clot occludes a cerebral artery deprives brain of O2 due to blood flow results in infarction/tissue death common causeL cardiovascular disease ischemia sets off inflammatory cascadedisturbs normal homeostasis of brain hemorrhagic caused by rupturing of vessel in brain -blood pools in brain ^ rupture caysed by cerebral aneurysms or small out-pocketing of vessel -grow weak due to vasculature, either due to congenital abnormalities or CVD subarachnoid hemorrhages bleeds w/in subarachnoid space in brain due to primary vessel disease arteriovenous malformations congenital abnormality progressively dilate w aging- more prone to rupture on vessels by increasing ICP- may cause ruptures lead to increased ICP=more compression on cerebral vasculature herniation and midline shifting of brain -v damaging & severe clinical signs of increased ICP: decreased consciousness increased HR cheyenne-stokes respiration: irregular respiratory patterns-fast shallow breathing >heavier breathing and apneic breathing vomiting (frequent SE) CN 3 signs: decreased pupil reactivity when ICP is elevated TIA-transient ischemic attack (mini stroke) -only transient symptoms caused by temporary interruption of blood flow by emboli, hypertension ect clinical signs usually go away after 24 hours residual damage-not significant warning sign for other impending & more severe attacks (stroke or myocardial infarction) risk factors cardiovascular disease -hypertension -deficits w heart rhythm -other coronary/peripheral artery deficits: type 2 diabetes -presence of comorbid chronic disease -diet & smoking AHA ppl w BP less than 120/80 have 50% less risk of stroke educate pts of importance of a healthy, nutritious lifestyle that includes exercise to prevent warning signs FAST easy warning of stroke f-face: facial droop a-arm weakness: unable to sustain 90 degrees of shldr flex or attain position s-speech: garbled and not making sense, unable to repeat sentence back to you t-time: contact emergency if any warning signs *not all signs need to be present for it to be an emergency* -the faster we get pt to ER the better vascular syndromes anterior cerebral artery (ACA) 1st branch off internal carotid supplies medial aspect of frontal &. parietal lobes & BG, ant fornix and ant corpus callosum damage: CL hemiparesis & sensory loss w LE impact (more significant) than UE based on motor homunculus middle cerebral artery (MCA) most common site for lease on supplies: lat aspect of frontal, temporal and parietal lobes includes post internal capsule, corona radiata and part of BG damage: significant impairment associated w edema and increased ICP presentations: CL spasticity, hemiparesis, & sensory loss of UE & face more than LE lesions to left parieto-occipital cortex produce aphasia (broca’s and wernicke’s) lesions to R hemisphere: spatial and perceptual deficits internal carotid artery (ICA) supplies MCA and ACA often leads to death bc CL circulation not present posterior cerebral artery (PCA) supplies post aspects: upper brainstem, midbrain, post diencephalon & thalamus presentation: CL sensory loss or thalamic pain syndrome housed w/in occipital lobe: visual deficits-agnosia, homonymous hemianopsia or cortical blindness damage to temporal region: memory loss lacunar infarct caused by infarcts w/in smaller vessels of brain symptoms: dysarthric motor aspects, ataxia, dystonia or hemiballismus (if affecting more BG) vertebrobasilar artery supplies cerebellum, medulla, pons & inner ear depending in infarct will determine ipsi or cl clinical signs branches off basilar art: cerebellar arteries-perfuse cerebellum if one of these arteries are affected, for example, the symptoms of cerebellar ataxia will be ipsilateral to the lesion locked-in syndrome lesion to basilar artery & infarction of pains significant bc pts have preserved consciousness & sensation but cant move or speak associated conditions variable levels of consciousness - must be monitored injury to L lateral hemisphere may produce deficits in speech, language, and swallowing aphasia disorder of language comprehension, formulation & use and can occur in 30 to 36% of ppl w stroke. (she said #s seem low from what shes seen clinically) aphasia types: fluent, nonfluent and global broca’s area: L frontal l one brocas aphasia-expressive or nonfluent aphasia pt will be able to comprehend info but speech not fluent ^^ pts tend to recognize deficits and get frustrated wernicke’s area: fluent aphasia aka receptive aphasia pts unable to comprehend info but able to produce speech fluently pts dont know what youre asking and cant follow demands ex: asking for name and DOB and they say something random or couldn’t comply for MMT at first global aphasia: both areas affected to some degree comprehension comes back fairly quickly depending on prog struggle w expressive aspect most dysarthria causes slurred speech display both types of language disorders at same time (dysarthria and aphasia) dysphasia swallowing disorder happens frequently post stroke CN 5,7,11,12 may be affected risk factor: aspiration pneumonia- where food, liquid or saliva falls down wrong tube (down airway) could lead to death if untreated -why speech pathologists are important: tells us what pt can and cannot eat !! dont offer a post stroke pt water if you dont see speech evalv on their chart until speaking with healthcare colleagues!! pts require thickened liquids if unable to take things by mouth pts required to be NPO-nothing by mouth; use NG tube (nasogastric tube) or a percutaneous endoscopic gastrostomy tube (PEG tube) directly into stomach cognitive deficits disorientation-varying levels of attention & memory, perseveration, confabulation executive fxn also impaired hemispheric differences R hemispheric lesions difficulty w abstract reasoning and safety awareness a lot of hemineglect or bruising in hospital pts more impulsive & do things w/o thinking L hemispheric lesions & subsequent R hemiparesis trouble w communication “left-language” individuals more cautious w behavior, more insight to deficits & more realistic expectations & prog perseveration tasks & are distractable 3 main deficits regardless of hemispheric region: cognitive limitations emotional deficits visual deficits : homonymous hemianopsia perceptual deficits pusher syndrome: graviceptional deficits perceptual deficit where pts feel they’re falling toward less involved (stronger) side use less involved side to push ipsi toward more involved side prognosis-good 3.6 weeks longer to attain fxnal goals 10% of ppl post stroke unilateral (hemi)-neglect perceptual deficit lack awareness -body or environment pts w R hemispheric involvement generally dont recognize body/stimuli on L side of body agnosias inability to recognize visual cues being seen (even though visual system is NOT compromised) -consult with PT and ST to assist in treating these disorders comorbid factors seizures mainly happen in acute stages B & B dysfxn w MS pts too neurogenic bladders post stroke: spastic or flaccid or both timed routine will help w this compounding cardiopulmonary dysfxn occur due to directly from stroke or after period of time (2nd complication) due to decreased mobility & exercise DVT & PE loss of mobility to hemiparesis side =dvt to distal vasculature > lower leg or lower arm (could be prox) use compression devices or SCDs in acute settings- prevention PE signs and symptoms : chest pain, attack cardio, anxiety, apprehension, diaphoresis & restlessness pharmacological management: anticoagulants or IVC filters-withheld til pt has interventions in order to prevent thromboemboli osteoporosis & fractures due to decrease of mvmnt old pts - normal sarcopenia processes cause degradation of bone mass fall risk summary stroke - ischemic vs. hemorrhagic - modifiable risk factors - FAST warning signs - associated conditions - R vs. L hemispheric involvement - comorbid conditions r.i.p to me after this lecture 4.2 stroke medical management general approaches increase cerebral perfusion: by reestablishing circulation where necessary O2 given via nasal cannula or ext mechanical ventilary support (intubation) tissue plasminogen activator: ischemic stroke pts aka clot buster maintain BP and CO2- antihypertensive pharm agents & decrease unnecessary stress -permissive HTN: physician holds off on or decreases meds immediately after stroke 2013 guidelines of AHA- BP depends on pts circumstances -TPA: systolic BP should be less than 185 mm mercury bc risk of hemorrhage diastolic lower than 110 mm mercury before initiating thrombolytic administer meds if systolic bp: greater than 220 mm mercury and diastolic bp greater than 120 mm mercury (permissive hypertension let stay there) organ damage- may be lowered restore homeostasis -fluids: electrolytes & other prophylactics via IV blood glucose needs to remain appropriate edema & ICP need to be stablized - crucial bc detriment to recovery prevention of midline herniation & shifting actively performed -VP shunt: artificial opening bw cerebral ventricals to drain fluid and avoid pressure in cerebral structures control associated med factors: infections or seizures in acute stage post-stroke maintain integumentary system: pressure injuries preserve muscle mass improve cardiovascular responses encourage alertness decrease incidence of pressure injury maintain B & B fxn: mvmnt will help allows gravity to work on excretory system B & B programs used decrease complications DVT PE aspiration pneumonia prothrombin time international normalized ratio (PT/INR) measures time it takes for blood to clot in blood sample ex: pt as low pt/inr in chart: means it takes them less time for clot to happen high pt/inr: more time for clot to occur depends on stroke type pharmacological management 1.thrombolytics; tissue plasminogen activator or TPA tpa-naturally occurring fibronolytic med-beneficial bw 3-4 hrs post stroke: dissolve clot used for ischemic strokes risk of bleeding and neurotoxicity 2.anticoagulants: warfin aka coumadin or heparin used to decrease risk of blood clots & prevent growth med prescribed to mitigate DVT & PEs need during therapy to prevent risk of bleeding 3.antiplatelet therapy: aspirin and plavix decrease adherence of blood cells prevent thrombus formation can use w anticoagulants why was all this 1 mf slide 4.antihypertensive agents: ACE inhibitors, beta blockers, diuretics used to control high BP beta blockers all end in O-L-O-L ex: atenolol, metoprolol, propanolol: all antihypertensive meds or beta blockers 5.angiotensin II receptor antagonists reduce BP 6. anticholesterol agents/statins-anything w statin at end lower cholesterol- cause plaque formation if too high 7.antispasmodics/spasmolytics: flexeril & valium decrease muscle spasms more secondary medication treating adverse symptoms 8.antispastics: baclofen decrease spasticity 9. GABA receptor antagonists: baclofen decrease spasticity 10.anticonvulsants: tegretol, klonopin & luminal used in acute stage post stroke if seizure activity is present 11.antidepressants: prozac & zoloft 12. neurotoxins: botox decrease spasticity more localized antiplatelet therapy 2021 guidelines to prevent stroke & TIA from AHA and ASA who and who dont get antiplatelet therapy which class of med should be used- single or dual medication therapy based upon evidence based outcome measures one is based on NIH stroke scale or NIHSS neurosurgical management thrombectomy-removal or large blood clots performed w/in 6 hours of stroke & only after TPA has been received aneurysm coiling aka endovascular embolization: pts w hemorrhagic stroke: images performed- may result in location of an aneurysm imagining could find aneurysm thats at risk for rupture require surgical intervention surgeon may tie off aneurysm if ruptured wire thru femoral art then up to internal carotid then to side of aneurysm where they coil it to fill it and prevent excess pressure from building and rupturing w/in aneurysm itself = effectively blocks blood flow to area carotid endarterectomy: remove fatty tissue from stenotic carotid arteries performed w/in chronic stage after stroke at least 6 months post stroke hopes to decrease risk of another stroke or TIA AVM resection may have high risk for future rupture summary general approaches - restore/improve, control, maintain pharmacological interventions - direct or indirect surgical procedures - vary based on circumstance 4.3 Stroke: Examination ‘ Examination process post Stroke patient interview observation systems reviews tests and measures National Institutes of Health Stroke Scale (NIHSS) a scale to measure severity of symptoms baseline, 2 hrs post med intervention, 24hrs post onset, 7-10 days , 3 months Timeline development of symptoms STROKE IMPACT SCALE (self Assessment for NIHSS perceived changes) level of consciousness VIsions Physical problems Facial Palsy Memory/thinking Motor of arms and legs Changes in mood and Ataxia emotion Sensation Communication Speech and Language ADLs Extinction and inattention Home and community mobility SCORE 0-42 Hand ability very severe is >25 Participation Mild (1-5) Recovery Postural Control and Balance Asymmetrical Alignment Hemiparesis, decreased proprioception, decreased perceptual abilities, sensation deficits Lateral Trunk FLX Paretic shoulder subluxation Weightbearing towards stronger pelvis LE flexor synergy patterning hip abduction and external rotation of paretic side Balance Impairments reactive control and abnormal timing Balance Examination and Postural Control Static Balance Eyes open Eye Closed Pertubations Dynamic Balance Multidirectional reaching Postural Assessment Scale for Stroke. (PASS) (Outcome measure) Used for STROKE REHAB Sitting without SUpport Standing with Support Standing without SUpport Standing on Nonparetic Leg Standing on Paretic Leg Examination for Perception PUSHER SYNDROME (prognosis is quite good) Slight push to weaker side Tilt 20 degrees towards weaker side Vestibular and visual orientation to vertical are found to be intact Clinical Scale for Contraversive Pushing is a Outcome measure scale for this Gait and Functional Mobility Observational Gait Analysis (OGA) Spatiotemporal Gait parameters step length and width Distance Gait Speed/velocity Cadence Functional Mobility Functional Independence Measure CARE ITEM SET Barthel Index (performance of feeding ,bathing, bladder control, chair transfers, ambulation, stair climbing, grooming dressing) Stroke Specific Assessments of Motor Recovery FUGL MEYER Assessment UE after stroke. acute sub acute and chronic BRUNNSTROM STAGES OF MOTOR RECOVERY used to categorize stages of post stroke recovery UE Assessment Outcome measure scales ARAT Action Research Arm Test fine motor and gross, grasping, gripping, pinching Floor and ceiling effects are present MAL Motor Activity Log self perceived quality in UE movement object manipulation, gross motor activities, and ROM Body Functions and Structures Exam MMT, ROM, Joint Mobility, Muscle tone(Modified Ashworth), Sensation, Pain(WOngBaker, McGill Questionnaire) Cognition (MMSE, MoCA) 4.4 Brunnstrom stages of stroke recovery synergy: muscles activated/coordinated together synergy w/ stroke: inability of motor system to perform mvmts outside of pattern no fractionated mvmts UE Synergy: Flexion dominates flexion scap retract/elevation shldr abd/ER elbow flexion forearm sup wrist flexion fingers/thumb flexion & add Extension scap protraction/depression shldr add/IR elbow ext forearm pro wrist either flex/ext finger & thumb flexion & add LE - extensor dominates flexor extensor pelvic elevation/retract hip ext/add/IR hip flex, abd, ER knee ext knee flex ankle PF/inv ankle DF/inv toes PF toe DF occurs when trying to extend at knee, difficultly flexing hip and keeping knee straight brunnstrom grading - ability to move into and out of patterns, ability to break out of patterns, characterize stage of motor recovery post stroke stage 1 flaccid/significant hypotonic no active voluntary mvmt limb hang loose protect from subluxation/cant support individual in standing stage 2 (cont recovery) increase signs of spasticity evidence of voluntary mvmt in weak synergistic patterns - begins prox at shldr or hip and progress down distally the limb limbs move in one direction (clothing in wind) stage 3 more spastic/rigid movements PEAK spasticity move in basic synergies no isolate mvmts like startched clothes stage 4 decreasing spasticity beginning of early isolated motor control minimal active mvmt outside of synergies but is possible UE: hand toward sacral region, lift arm to shldr flex while maintaining elbow ext, sup/pro elbow while in flexion LE: flex knee greater than 90 while seated, DF ankle greater than neutral w/o lifting foot off ground stage 5 AAHH C-3PO spasticity still present but significantly decreased increased isolated motor control more complex mvmts UE: abd shldr to 90 w/ elbow extended, flex shld past 90 w/ elbow ext, pro/sup forearm in elbow ext LE: flex knee w/ hip extended while standing, DF ankle in standing in step stance position stage 6 no spasticity at rest full/near full motor control stressed =. increased tone/spasticity (like using quick or force) lack coordination w/ task standing: abd leg fully stage 7 fxn normally regardless of force/speed may not always start at stage 1 and may not always progress different body parts progress faster sometimes Summary stages of motor recovery post stroke based on presence of spasticity and isolated, controlled mvmts synergy patterns characterized by flexion vs ext in extremities 4.5 Stroke Rehab Management Evaluation Take environment, ADLs, Personal, Participation factors into consideration Individual Factors is the goal Motor Learning? Or Motor Performance? Determine patient’s stage of motor learning Task Salient interventions Does patient have the capacity to learn the whole task? Or must it be broken down? Environment Gentiles Taxonomy Set patient up in a environment that leads to success Interventions need to focus on rehab and recovery, and compensation OPTIMAL INTERVENTIONS It DEPENDS based on patient presentations Allow for motivation Better for carryover effect Evidence PNF? Neurofacilitation? Task oriented training Participation Interventions hard to facilitate Simulate activities in the clinic Outings Community re-integration Virtual reality Activities postural control challenging dynamic balance challenging forearm WB weightshifting Increase degrees of freedom overtime Progress to standing Progress to reaching activities to challenge movements outside BOS Incorporate LE movement Modify Environment Body Fxns and Structures Strengthening (weights, bands, within in the task) ROM ( stretching and joint mobilizations ) Proprioceptive training (weightbearing) Compensatory Interventions Orthotics/Splints/Braces Ankle Foot orthoses, hand splints, ACE wrap Wheelchairs Hemi-height Assistive Devices Walkers, Canes 4.6 TBI General Presentation, Pathophysiology Traumatic Brain Injury- result of external force. gunshot wound, motor vehicle accidents, falls to head Geriatric population sustains TBI’s mostly from falls Consequenceslong standing disability, Personality and Behavior change, decreased mobility, swallowing Financial Burdens Changing Family Dynamics Premature Death Primary or Secondary ? Primary - Direct result of external force contusions in area of contact Localized to site of injury Coup Contrecoup injury- brain bouncing inside the skull coup-front. Contra- posterior Additional shearing and compressive forces in the brain create DAI- diffuse axonal injury DAI- moderate to severe , may not be detected due to microtrauma Blast- overpressure from blast wave happens in military increases CSF and subsequent cerebral edema Secondary- inflammatory response - histamine and other nutrients to flood the area for healing cerebral edema, leads to intracranial pressure, hypoxemia, and hypotension Release of excitatory neurotransmitters like glutamate causes further edema, leads to more intracranial pressure NORMAL ICP is 5-20 mmHg Cognitive Impairments- arousal, attention, concentration, learning and memory, executive functioning, initiation, planning, self generation, response inhibition and sequencing Coma No Arousal Vegetative State Unaware of surroundings may be weaned off ventilator Sleep wake cycles are present No conscious understanding or awareness Minimally conscious state Mild awareness Stupor Arousal with vigorous stimuli Obtunded Sleepiness/delayed reaction Neurobehavioral Impairments Communication Dysarthria Seizure Activity overreactive response to stimuli elevated HR, RR, and BP and diaphoresis Decorticate and Decerebrate posturing Cort- closed hands, legs IR, Feet turned Inward, arms flexed rostral injuries to the cerebrum, lesions to forebrain, dienchephalon or rostral mid brain Cere- arms straight EXT, legs straight, toes pointed downward Head neck arched Animal studies that deCEREBRATE happens only from noxious stimuli Associated with severe cerebral lesion Posturing can present asymmetrically. can be decorticate one side and decerebrate another Anatomical difference between these two postures Intercollicular line at the red nucleus lesions ABOVE- decorticate lesions BELOW- decerebrate EMERGENCY SERVICES IMMEDIATELY. 37% who demonstrate decorticate posturing survive 10% who demonstrate decerebrate posturing survive Secondary Impairments GI Genitourinary Respiratory Cardiovascular Integumentary DVT (deep vein thrombosis) HO (Heterotopic ossification) Contractures Associated Fractures Participation Restrictions Walking UE handling ADL Return to work Return to family Caregiver Roles 4.7 Brain Injury Medical Management interdisciplinary collaboration!! Nursing continuous management of pt med status meds b&b programs vitals/integumentary monitor tin turning, positioning, splinting most info bc see all day social work support to pt/family coordinate counseling/support groups neuropsychologist RT/OT/SLP case manager insurance (DME,transfers) recreational therapists test pt baseline cognitive fxn evaluation/tx of mobility limitations/ADLs speech, swallowing, cognition learning & mem care (SLP) assist pt doing things they enjoyed before, music, sports, games respiratory care more severe TBU monitor airways during tx Early Medical Management 1. stabilize 2. minimize secondary complications - restoring cerebral blood flow 3. identify injuries 1. monitor continuously systolic bp = above 90mmHg O2 = above 90% some may need to be intubated/supplemental o2 stabilize in collar = 30 degrees to maintain ICP More Diagnostic Criteria GCS assess severity GOAT of injury amnesia test less severe