Pt 351 Pt In Neurology (1) PDF

11/5/2024 PT 351 PT IN NEUROLOGY (1) Cerebro Vascular Accident (CVA)- Stroke PART 1 Ali Bani Ahmed PT, MS/DPT, CPT, CKTP, CES, CDNP, PhD 1 What is stroke?...

11/5/2024 PT 351 PT IN NEUROLOGY (1) Cerebro Vascular Accident (CVA)- Stroke PART 1 Ali Bani Ahmed PT, MS/DPT, CPT, CKTP, CES, CDNP, PhD 1 What is stroke? Sudden impairment in brain function. Sudden focal and acute neurologic signs and symptoms that result from diseases involving blood vessels and last for more than 24 hours. 2 1  11/5/2024 http://t1.gstatic.com/images?q=tbn:ANd9GcSSSxYzsPPxy4Mf8Ucp-zI0Vva5Ns8J9KegP9bh3ByjpdM7VBMbUD4Bz9s Stroke Definition “Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular origin” – Tumors, poisoning and trauma are excluded 3 Epidemiology Forth leading cause of death (30% die in first year ) Most common cause of disability among adults ▪ 700.000 cases per year in US; 500.000 new strokes and 200.000 recurrent strokes ▪ About 7 million stroke survivors/ around 3% of the population ▪ 26% in US are in nursing homes Incidence is greater in males than females (2:1) until the age of 75 when risk becomes higher in females Risk increase with age ; 20%of cases below 65 years Up to 80% of strokes are preventable through risk factors management 4 2  11/5/2024 Stroke Incidence About 795,000/yr (new/recurrent stroke) Every 40 seconds, someone in the United States has a stroke. Every 3.5 minutes, someone dies of stroke The leading cause of long-term disability worldwide 6.4 million stroke survivors (Heart Disease and Stroke Statistics – AHA, 2020) 5 6 3  11/5/2024 Stroke & Aging - Pathology The small vessels of the brain appear to be highly susceptible to the effect of aging (vessels are fragile) Lipohyalinosis : arteriolar wall disorganization (i.e. thickening) Amyloid angiopathy: accumulation of abnormal proteins- stiffness 7 Stroke Prevalence by Age 8 4  11/5/2024 Stroke Etiology Atherosclerosis – most common. Heart disease – Atrial fibrillation/ Myocardial Infarction/ Valvular Disease/ Heart failure Embolization of intracardiac thrombi 9 Risk factors Major modifiable risk factors: Non-modifiable: ▪ Hypertension ▪Age ▪ Heart disease ▪Gender ▪ Diabetes ▪Race Other modifiable risk factors: ▪Genetics ▪ Smoking ▪ Sedentary life style (lack of exercise) ▪ Obesity ▪ High alcohol consumption ▪ High blood cholesterol 10 5  11/5/2024 Stroke Pathophysiology Stroke is a disease that affects the arteries leading to and within the brain Occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts. When that happens, part of the brain cannot get the blood (and oxygen) it needs, so it starts to die. 11 Stroke Symptoms/Complications Trouble walking Circumduction gait Loss of balance/coordination Trouble speaking (Mainly in Left CVA / Right hemiplegia) Expressive/ Broca’s / Non-fluent aphasia → difficulties in articulating (Talking) Receptive/ Wernick’s/ Fluent aphasia → difficulties in verbal comprehension (Understanding) Muscle weakness in the face, arm, or leg (Contralateral hemiplegia) Change in alertness (including sleepiness, unconsciousness, and coma) Changes that affect sensation (touch, pain, pressure and/or temperatures Dizziness or abnormal feeling of movement (vertigo) Lack of control over the bladder or bowels (acute cerebral shock phase) Numbness or tingling on one side of the body Personality, mood, or emotional changes Problems with eyesight, including decreased vision, double vision, or total loss of vision http://www.aasthahealthcare.in/neuro/stroke.html 12 6  11/5/2024 Stroke Symptoms/Complications Following a stroke, there is no “Intact” side (i.e. both are affected) Stroke-affected side compared to the less-affected side http://www.asbweb.org/conferences/2012/abstracts/39.pdf http://pal.colostate.edu/documents/Massie_Cont_Reach_J_Motor_Beh_2012.pdf 13 Know the Signs Stroke victims may not realize that they are having a stroke. However, They have the best chance if a bystander recognizes the symptoms and acts quickly. What are the symptoms of a stroke? Sudden numbness or weakness of the face, arm, or leg (especially on one side of the body) Sudden confusion, trouble speaking or understanding speech Sudden trouble seeing in one or both eyes Sudden trouble walking, dizziness, loss of balance or coordination Sudden severe headache with no known cause 14 7  11/5/2024 Why is there a need to act fast? 15 (1) The Ischemic Penumbra In Ischemic stroke, there are two major zones of injury: (1) The core ischemic zone (dead tissue) CBF < 10% to 25% (2) The ischemic penumbra (tissue at risk) CBF between 25% to 50% Identified with a Perfusion CT Irreversibly affected or dead tissue in black and tissue at risk or penumbra in red. scan based on changes in CBF Perfusion CT Diffusion image indicating the area with irreversible changes (dead tissue). Perfusion Image indicating a large area with hypoperfusion the diffusion-perfusion mismatch indicating the tissues at risk (Penumbra). → The brain tissue that maybe can be saved with emergency therapy 16 8  11/5/2024 http://www.auntminnie.com/index.asp?sec=ser&sub=def&pag=dis&ItemID=60465 In the penumbra, tissue will be metabolically impaired, but may be rescued for a longer time period of up to six hours (3-6 hrs). Brain Perfusion Computed Tomography for the Management of Acute Stroke Patients before and after intravenous thrombolysis 17 (2) Excitotoxcicty following a stroke Excitotoxicity Cell death caused by overexcitation of neurons Excitotoxicity is a key mechanism of cell and tissue destruction in cerebral ischemia ❖ Oxygen deprivation typically affects certain parts of the brain more severely than others Especially susceptible to injury structures include the hippocampus, the GLU cerebellum Purkinje cells, and the pyramidal cortical cells The increased vulnerability of these neurons is due to the abundance of neurotransmitter glutamate in these neurons Glutamate is the Regulates brain Has to be present in the Glutamate must be major excitatory development and right concentrations in kept inside the cells transmitter in the information which the right places for the (intracellularly) brain determines cellular right time. survival 18 9  11/5/2024 Excito-toxcicty following a stroke hypoxic- ischemic neuronal injury is greatly influenced by “overreaction” of certain neurotransmitters, primarily glutamate that also migrates to extracellular space It may extend into the region of the penumbra by means of neuron-glial cell units and synapses via excitotoxic mechanisms Glutamate becomes toxic Over-excitation of neurons in deoxygenated environment Anaerobic Glycolysis Increase Lactic Acid and free radicals Cell injury and death 19 Excitotoxicity Management Thrombolytic agents Targets the thrombus within the blood vessel The only approved medical therapy for acute ischemic stroke is tissue plasminogen activator (tPA) Neuroprotective Agents NMDA receptor antagonists Modulate neuronal receptors to reduce release of excitatory neurotransmitters Yet to be approved in the US because of Uncontrollable side effects and Interrupting normal Glutamatergic (excitatory) functions in other areas Medically Induced Coma ??? Environmental modification Low- stimulation Precautions Early rehabilitation is key to improved recovery (Teasell et al, 2005) However, Excessively vigorous rehabilitation too soon after the injury can be counterproductive Enhances Excitotoxcicty 20 10  11/5/2024 Excitotoxicity Management – Role of Sleep The success of a rehabilitation plan is heavily dependent on sleep especially in early stages following stroke → The most important aspect of recovery is simply sleep → two-thirds (2/3) of stroke survivors have sleeping disorders Sleep strengthens/recovers the brain sleep decreases risk of another stroke 21 What causes stroke? Stroke occur when a blood vessel that supplies oxygen and nutrients to the brain is blocked by a clot or disrupt 22 11  11/5/2024 23 The Human Brain Three inter-connected layers 24 12  11/5/2024 Central Core 5 regions Thalamus Pons Medulla Cerebellum Reticular information 25 Limbic System 3 regions Hippocampus Amygdala Hypothalamus 26 13  11/5/2024 Cerebral Cortex 4 lobes Frontal Parietal Occipital Temporal 27 Cerebral Cortex 28 14  11/5/2024 Cerebral Cortex Brain cortex defined into regions based on its cytoarchitecture (i.e. structure and organization of cells) Referred to by numbers from 1 to 52 – Brodmann Areas http://www.mrc-cbu.cam.ac.uk/people/jessica.grahn/neuroanatomy.html 29 Left vs Right hemispheres Past & Future Present http://www.younme.com.my/useruploads/images/left-brain-right-brain.jpg 30 30 15  11/5/2024 Blood circulation of the brain 31 Requirement: knowledge of functional anatomy 32 16  11/5/2024 Functional anatomy 33 Requirement: knowledge of brain’s circulation 34 17  11/5/2024 Stroke Categories/Types Transient, evolving & completed. Ischemic / hemorrhagic Location & size and how they relate to severity Global / Focal 35 Stroke Types: Clinical Transient Ischemic Attack –resolves completely 75 known syndromes 55 Common Focal Stroke Visual cortex 56 28  11/5/2024 Common Focal Stroke 57 Common Focal Stroke 58 29  11/5/2024 Common Focal Stroke > 75 known syndromes 59 New York Times Bestsellers http://www.ted.com/talks/jill_bolte_taylor_s_powerful_stroke_of_insight.html 60 30  11/5/2024 Cerebral vascular supply – Ischemic Stroke Ischemic Stroke – Clinical Classification Cortical lesion SubCortical lesion Large vessel Diseases Small vessel Diseases ▪ Involve brain surface → MCA, ▪ Involve Basal ganglia, Internal capsule & ACA, PCA Thalamus ▪ +ve cortical signs ▪ Is called lacunar infarction (5 types) o Apahasia 1. Pure motor hemiparesis o Neglect 2. Pure sensory stroke (thalamic o Homonymous hemianopia lacuna) 3. Sensorimotor stroke (thalmocapsular lacuna) 4. Ataxic hemiparesis 5. Basal ganglia lacuna This classification is not 100% differentiate the lesion site, but its still helpful 61 62 31  11/5/2024 Cerebral vascular supply – Ischemic Stroke Ischemic Stroke – Clinical Classification This classification is not 100% differentiate the lesion site, but its still helpful Thalamic lacuna → Pure sensory loss Cortical infarction → Apahsia & cortical sensory loss 63 Cerebral vascular supply – simplified related deficits 64 32  11/5/2024 Cerebral vascular supply – related deficits 65 Cerebral vascular supply – related deficits 66 33  11/5/2024 MCA stroke R MCA (non dominant) L MCA (dominant) L hemiplegia, UL>LL R hemiplegia, UL>LL L hemisensory loss R hemisensory loss L homonymous hemianopia R homonymous hemianopia Motor/sensory/visual Dysphasia/aphasia neglect Spatial/perceptual Apraxia dysfunction 67 68 34  11/5/2024 Other stroke presentations Cerebellar infarct ACA infarct Ipsilateral ataxia Contralateral paresis LL dysarthria Contralateral sensory loss LL Vertigo/dizziness incontinence nystagmus Frontal lobe damage---- memory and behavioral impairments NO sensory loss 69 Hemiplegic stroke presentation 70 35  11/5/2024 Clinical picture Dependent on the area of the brain affected Can be a combination of: Motor and/or sensory impairments which include gait and balance dysfunction Visual disturbances Speech and language impairments Swallowing dysfunction Cognitive and perceptual dysfunction Incontinence Respiratory issues other 71 Clinical manifestations in CVA 72 36  11/5/2024 73 Post-stroke Motor Recovery 74 37  11/5/2024 75 76 38  11/5/2024 Clinical manifestation Sensory Loss Motor Loss Speech, Language, and Swallowing Loss Perceptual Disturbances Cognitive Impairment and Psychological Note Bladder, bowel and sexual dysfunctions are not a problem in most patients 77 Sensation Usually impaired but not lost Depend on the site and size of the lesion crossed symptoms indicates brain stem lesion: Ipsilateral facial impairment with contralateral trunk and limb involvement 78 39  11/5/2024 Sensation Somatic sensation: ✓pain and temperature, pressure (exteroception) ✓Proprioception ✓ cortical sensation ▪ Two point discrimination: is the ability to discern that two nearby objects touching the skin are truly two distinct points ▪ Tactile Recognition (Stereognosis): is the ability to recognize what the hand grasps in the absence of any auditory or visual clue ▪ Graphesthesia: is the ability to recognize writing on the skin purely by the sensation 79 Motor Symptoms Hemi- Paralysis or paresis: this involve one side of the body. 80-90 patients with CVA have paresis, the main reason for disability. Patients are unable to generate the force necessary for initiating and controlling the movement. Distal muscle affected more than the proximal muscles Progravity muscle > antigravity muscles Thus: - UE: extensors are weaker than flexors - LE: flexors are weaker than extensors 80 40  11/5/2024 Disturbances of muscle tone Patient usually starts with complete paralysis and flaccidity (loss of tone) which may last 2-6 weeks due to the stage of neural shock – Acute and subacute stages After this the tone gradually return and progress to spasticity (hypertonia) – Chronic Stage The spasticity affect the antigravity muscles more than progravity Spasticity decline, in some patients may completely disappear allowing smooth coordinated joint movement. 81 Pattern of spasticity Upper extremity: ▪ Scapular: retractor ▪ Shoulder: adductors, depressors, and internal rotators ▪ Elbow: flexors ▪ Forearm: pronators ▪ Wrist and finger: flexors. spasticity may cause increased lateral flexion to the hemiplegic side. Lower extremity: ▪ Pelvic: retractors ▪ hip: adductors and internal rotators, ▪ Knee: extensors ▪ Ankle: plantarflexors and invertors ▪ Toe: flexors. 82 41  11/5/2024 83 Pattern of spasticity Upper extremity: MASS FLEXION ▪ Scapular: retractor ▪ Shoulder: adductors, depressors, and internal rotators ▪ Elbow: flexors ▪ Forearm: pronators ▪ Wrist and finger: flexors. 84 42  11/5/2024 Pattern of spasticity Lower extremity: MASS EXTENSION ▪ Pelvic: retractors ▪ hip: adductors and internal rotators, ▪ Knee: extensors ▪ Ankle: plantarflexors and invertors ▪ Toe: flexors. 85 Gait Circumduction Gait The leg is stiff, without flexion at knee and ankle, and with each step is rotated away from the body, then towards it, forming a semicircle. 86 43  11/5/2024 Deep Reflexes ▪Deep reflex are lost during the stage of neural shock this followed by hyper-reflexia Loss of superficial reflexes such as abdominal reflex Pathological reflexes: Clonus, frequently in the ankle and less frequently in the knee ( patella) and wrist Positive Babinski sign 87 88 44  11/5/2024 Pathological primitive reflexes Grip reflex: normally starts at birth and disappear at the age of 3 months Symmetric tonic neck reflex (STNR) ▪ Neck flexion arm flexion & leg extension. ▪ Neck extension opposite effects. Asymmetric tonic neck reflex (ATNR) ▪ Head rotation to the left extension of left arm & leg and flexion of the right arm & leg. ▪ Head rotation to the right leads to the reverse pattern These reflexes normally start at birth and disappear at the age of 6 month 89 Synergy pattern ❖ Stereotyped, primitive movement patterns associated with spasticity ❖ Patient is unable to perform an isolated movement of a limb segment without producing movements in the remainder of the limb ❖ There are two abnormal combination of movement for upper and lower limbs; one for flexion (flexor synergy) and one for extension (extension synergy) ❖ These synergies are considered the only way for the hemiplegic patient to move his upper and lower limbs. 90 45  11/5/2024 Synergy pattern 91 Muscles not involved: - latissimus dorsi - teres minor - serratus anterior - finger extension - ankle evertors 92 46  11/5/2024 93 94 47  11/5/2024 95 96 48  11/5/2024 97 Brunnstrom's Stages of Stroke Recovery 98 49  11/5/2024 99 100 50  11/5/2024 101 Muscles not involved: - Latissimus dorsi - Teres minor - Serratus anterior - Finger extension - Ankle evertors. 102 51  11/5/2024 103 104 52  11/5/2024 Video section (upper extremity flexion synergy in stroke) https://www.youtube.com/watch?v=uxHAYAmKy4U https://www.youtube.com/watch?v=9zWh-aed4KY&t=6s 105 Postural Control and Balance Balance is disturbed following stroke with impairments in steadiness, symmetry, and dynamic stability common. Problems may exist when reacting to a destabilizing external force (reactive postural control) or during self-initiated movements (anticipatory postural control). Reactive: ability to recover postural control after an unexpected perturbation Proactive (anticipatory): ability to modify postural control prior to a potentially destabilizing movement in order to avoid instability 106 53  11/5/2024 Postural Control and Balance Patients with stroke typically demonstrate asymmetry with most of the weight in sitting or standing shifted toward the stronger side. They also demonstrate increased postural sway in standing Compensatory responses typically include excessive hip and knee movement Patients with hemiplegia typically fall in the direction of weakness. 107 ❖ Left hemisphere dominant for language skills in the right-handed person & most left-handed persons ❖ Aphasia/Dysphasia: is the general term used to describe a acquired communication disorder caused by brain damage and is characterized by an impairment of language comprehension, formulation, and use. ❖ Involvement Expression & Comprehension ❖ Receptive Aphasia (Wernicke’s area): People with receptive aphasia are unable to understand language in its written or spoken form. They can speak with normal grammar, syntax, rate, and intonation, they cannot express themselves meaningfully using language. (left temporal lobe) ❖ Expressive Aphasia (Broca’s area): (non-fluent aphasia) is characterized by the loss of the ability to produce language (spoken or written). (premotor area of the left frontal lobe) ❖ Global Aphasia: Sever aphasia characterized by marked impairments of both production and comprehension of language. It is often an indication of extensive brain damage. ❖ Severe problems in communication may limit the patient’s ability to learn and often impedes successful outcomes in rehabilitation 108 54  11/5/2024 Clinical Manifestation Speech, Language, Swallowing ❖Dysarthria: Affects the mechanics of speech due to muscle control disturbances –pronunciation, articulation, and phonation The lesion can be located in the primary motor cortex in the frontal lobe, the primary sensory cortex in the parietal lobe, or the cerebellum. Automatic actions such as chewing and swallowing and movement of the jaw and tongue are impaired resulting in slurred speech ❖Dysphagia: Swallowing difficulty ➔ Aspiration !!! ❖ Poor jaw and lip closure 109 114 55  11/5/2024 115 116 56  11/5/2024 Video section Observe a patient with stroke walking Identify 6 gait abnormalities https://www.youtube.com/watch?v=ihz74Zv6D84&t=43s 117 Complications and indirect Impairments: Musculoskeletal: ❖loss of range of movement (ROM) and contractures: loss of voluntary movement and immobility ❖Contractures can develop anywhere but are particularly apparent in the paretic limbs. ❖ As contractures progress, edema and pain may develop and further restrict mobility. ❖In the UE, limitations in the shoulder motions of flexion, abduction, and external rotation are common. Contractures are likely in the elbow flexors, wrist and finger flexors, forearm pronators. ❖In the LE, plantarflexion contractures are common. 118 57  11/5/2024 Complications and indirect Impairments: Musculoskeletal: Shoulder subluxation and pain: 70-84% of stroke patients have shoulder pain. Normally the scapula is held at an angle of 40o. In flaccid stage: due to paralysis of muscular attachment of the scapula, it is rotated downward by gravity. The downward rotation occurs due to: 1. low tone of the rotator cuff and serratus anterior muscles 2. spinal curvature that occurs with unilateral weight bearing to the sound side. ➔ downward rotation of the scapula orients the glenoid fossa vertically and the humerus will sublux inferiorly. In spastic stage: the strong downward pull of the latissimus dorsi and the active use of shoulder elevators cause the glenoid fossa to be vertically oriented, as the humerus postures or moves into hyperextension and internal rotation, the humeral head will sublux anteriorly 119 Complications and indirect Impairments: Musculoskeletal: ❖Disuse atrophy and muscle weakness ❖Osteoporosis ❖Fall ❖Fracture ❖Early mobilization stressing out-of bed upright postures and weight bearing activities along with forced use of the involved extremities are effective strategies in counteracting these effects 120 58  11/5/2024 Complications and indirect Impairments Cardiac problems: careful when planning exercise program/ endurance. other complications: respiratory problems postural hypotension pressure sores 121 Pressure sores 122 59  11/5/2024 Prognostic indicators 123 Prognostic indicators Good outcome Poor outcome Younger age Urinary incontinence Conscious at onset Previous strokes Lesser paralysis Lack of social support Sitting balance (early) Disorientation time/place Higher admission ADL Duration of coma score (prev independent) Living with partner Kwakkel et al 1996, Henley et al 1985 124 60  11/5/2024 125 61