1. Ataxia in the Stroke Patient Kelli Kulpa BSN, RN Alverno College MSN Student Neurosciences Department Froedtert Hospital

2. Objectives Describe pathophysiology of cerebellum as it relates to smooth muscle movements Describe how ischemia to cerebellum causes ataxia in stroke patient Identify presence of ataxia in stroke patient Identify appropriate nursing interventions and outcomes

3. TOPICS TO REVIEW STROKE CEREBELLUM ATAXIA NIH STROKE SCALE CARE OF THE PATIENT WITH ATAXIA

4. Stroke “Syndrome of acute focal neurologic deficit from a vascular disorder that injures brain tissue” Porth (2005, p. 1245) US leading cause of mortality & morbidity About 700,000 Americans afflicted with stroke Many survivors left with some degree of deficit Image from Microsoft Clipart (Porth, 2005)

5. Risk Factors for Stroke Controllable Hypertension (HTN) Atrial Fibrillation High Cholesterol Diabetes Tobacco Use & Smoking Alcohol Use Physical Inactivity Obesity Uncontrollable Age Race Gender Family History Previous Stroke or TIA Fibromuscular Dysplasia Patent Foramen Ovale (National Stoke Association, 2009) Image from Microsoft Clipart

6. Uncontrollable Risk Factor AGE: Risk of stroke increases with age After age 55, risk doubles for every decade that passes Increased prevalence of controllable risk factors as age increases Hypertension High Cholesterol Diabetes RACE: AFRICAN- AMERICAN Most impacted race in US Twice as likely to die from stroke than Caucasians Occur earlier in life Reasons not fully understood, but have a higher rate of risk factors ex: 41% have HTN (National Stoke Association, 2009) Image from Microsoft Clipart

7. Uncontrollable Risk Factor GENDER: WOMEN 55,000 more women than men experience stroke each year Unique risk factors: Oral Contraceptives Pregnancy Hormone replacement therapy Post-menopausal with thick waist and high triglyceride levels Suffer more migraines, increase risk 3-6 times (National Stoke Association, 2009) Image from Microsoft Clipart

8. Uncontrollable Risk Factor FAMILY HISTORY Evidence suggests genes influence vulnerability to HTN & stroke A region on: Chromosome 13 in Caucasians Chromosome 19 in African-Americans Carotid intimalmedial wall thickness (IMT) Surrogate measure of subclinical atherosclerosis Strong predictor of future ischemic strokes Homozygous for 6A genotype Genetically predisposed to produce less stromelysin 1 High carotid artery wall thickness & greater risk of stroke Image from Microsoft Clipart (Morrison, Brown, Kardia, Turner, & Boerwinkle, 2003) (Humphries & Morgan, 2004)

9. Controllable Risk Factor & Inflammation Inflammation can influence the development of atherosclerosis Causes endothelial dysfunction One of the earliest manifestations of atherosclerosis Inflammatory markers associated: Coronary disease development Disease severity Occurrence of coronary events Progression of atherosclerosis may be associated with high concentrations of inflammatory markers (Humphries & Morgan, 2004)

10. GREAT! SORRY! Cannot control if you have a history of stroke OPPS! Cannot control age GOOD JOB! TEST YOUR KNOWLEDGE Select the controllable risk factors for stroke (Multiple answers) Hypertension Age Previous Stroke Hyperlipidemia

11. Yes! Women are at higher risk of stroke & also have increased mortality. Sorry! Women are at higher risk of stroke & also have increased mortality. TEST YOUR KNOWLEDGE Men are at higher risk of stroke TRUE FALSE

12. Types of Stroke ISCHEMIC Interruption of blood flow in a cerebral vessel Most common type Account for 70-80% of strokes HEMORRHAGIC Bleeding into the brain tissue, from blood vessel rupture Caused by: HTN Aneurysms AVM Head injury Much higher fatality rate 37-38% of occurrence results in death (American Heart Association, 2010) (Porth, 2005) Image from Microsoft Clipart

13. Cell Ischemia Reduced or absent blood flow deprives cell of needed nutrients Effects occur quickly No stored glucose in brain Incapable of anaerobic metabolism (Porth, 2005)

14. Neuronal Injury: Excitotoxicity Ischemia depletes neuronal energy stores causing energy dependent membrane ion pumps to fail Results in increased extracellular glutamate concentration Release of excitotoxic glutamate & aspartate open up calcium channels Influx of calcium, sodium and chloride Intracellular calcium responsible for activation of a series of destructive enzymes Out flux of potassium Resulting in irreversible neuronal damage Results in release of cytokines and other mediators (Porth, 2005)

15. Inflammation Following Ischemia Rapid production of inflammatory mediators White blood cell (WBC) recruitment to ischemic area as early as 30 minutes Capillary endothelium produces adhesive proteins causing WBCs to adhere to capillary lining WBCs move into injured tissue Phagocytize injured cells Extent of inflammation can be determined by C-reactive protein levels Image used with permission from http://images.wellcome.ac.uk/ (Porth, 2005)

16. Try again There are increased levels of glutamate. GOOD JOB! No energy is getting to the cell. Try again Phosphorus is not directly related to this process Try again If the cell is not getting adequate blood flow, there is not enough energy available. TEST YOUR KNOWLEDGE Neural cell ischemia is caused from: Too much energy available to the cell Lack of phosphorus available Energy dependent membrane ion pumps fail Decreased levels of glutamate

17. Cerebellum Stores learned sequences of movements Fine tuning & coordination of movement produced elsewhere in brain Integrates all information to produce fluid movements (Dubuc, 2002) Image used with permission from http://thebrain.mcgill.ca/flash/i/i_06/i_06_cr/i_0 6_cr_mou/i_06_cr_mou.html#3

18. Movement Motor cortex: Sends signals to cerebellum Communicates movement to make Cerebellum: Makes continuous adjustments Final result: Smooth movement, key with delicate maneuvers (Porth, 2005) Image used with permission from http://thebrain.mcgill.ca/flash/i/i_06/i_06_ cr/i_06_cr_mou/i_06_cr_mou.html Cerebellum Hover over the highlighted words for definition

19. Cerebellum Involvement Receives proprioceptor input from vestibular systemproprioceptor input vestibular system Feedback from muscles, tendons, & joints Indirect signals from somesthetic, visual, & auditory systems to provide background info for ongoing movement somesthetic (Porth, 2005) Can continuously assess status of each body part Position Rate of movement Forces, such as gravity, opposing it (McGill University, 2002)

20. Cerebellum Involvement Can continuously assess status of each body part Position Rate of movement Forces, such as gravity, opposing it Image used with permission from http://thebrain.mcgill.ca/flash/i/i_06/i_06_ cr/i_06_cr_mou/i_06_cr_mou.html (McGill University, 2002)

21. Dampening Muscle Movement All body movements are pendularpendular Intact cerebellum analyzes proprioceptive information to predict:proprioceptive information Future position of moving parts Speed of movement Projected time course of movement As movement approaches target, Cerebellum will: Inhibit agonist musclesagonist muscles Excite antagonist musclesantagonist muscles (Porth, 2005) Image from Microsoft Clipart (Porth, 2005)

22. “Require a burst of energy from an agonist muscle group; the movement is programmed from the start, so the movement proceeds from start to finish without modification” Type of Movement Simple Movement Self-terminating Movement: require smooth muscle sequence of coordinated agonist & antagonist movements programmed by higher brain centers to start, then are modified as the movement proceeds Complex Movement Click for Explanation Porth (2005, p. 1194) Image from Microsoft Clipart

23. Try again; This is part of the somesthetic system. GOOD JOB! OPPS! Vestibular apparatus, try again. Try again; This is part of the somesthetic system. TEST YOUR KNOWLEDGE Proprioreceptor input is: Meaningfulness of integrated sensory information from various sensory systems The inner ear structures that are associated with balance and position sense Any sensory nerve ending responding to stimuli from within body related to movement & spatial position Concerning perceptions of ‘where’ the stimulus is in space and in relation to body parts

24. Opps! Think this through again. Movement is pendulous. Yes! Movement is pendulous, so muscles have to be stopped. TEST YOUR KNOWLEDGE As movement approaches a target, the cerebellum will: Inhibit agonist muscles & Excite antagonist muscles Excite agonist muscles & Inhibit antagonist muscles

25. Ataxia People with ataxia experience Failure of muscle control in arms and legs Results in: Lack of balance & coordination Disturbance in gait Image from Microsoft Clipart (National Institute Of Neurological Disorders And Stroke, 2010)

26. Acquired (non-genetic) Ataxia Conditions that can cause acquired ataxia Stroke Multiple Sclerosis Tumors Alcoholism Peripheral neuropathy Metabolic disorders Vitamin deficiencies (National Institute Of Neurological Disorders And Stroke, 2010) Image from Microsoft Clipart

27. Ataxia after Stroke Right side of cerebellum controls coordination on right side of body, left side controls left When nerve cells are lost or damaged: Provide less control to muscles Resulting in: loss of coordination During a stroke: Blood supply is interrupted or severely reduced Deprivation of oxygen and nutrients to brain tissue Brain cells begin to die (Mayo Clinic Staff, 2009) Image from Microsoft Clipart

28. Recent Findings 15% of all cerebral strokes involve the cerebellum (Timmann et al., 2009) Anterior lobe of cerebellum is involved in motor control Concluded from a study containing 34 patients with cerebellar infarcts (Schmahmann, Macmore, & Vangel, 2009) Image from Microsoft Clipart

29. Cerebellar Ataxia How does alcohol relate? Select the beer for the answer! Decomposition of movement Each component of the movement occurs separately instead of being blended into a smooth action (Porth, 2005) “Ethanol specifically affects cerebellar function, persons who are inebriated often walk with a staggering and unsteady gait” Porth (2005, p. 1213) Image from Microsoft Clipart (Porth, 2005)

30. Ataxia Rapid alternating movements are performed slowly and jerky Such as pronation-supination- pronation of hands Touching a target : Movements broken down into small steps Each movement goes too far, then overcompensated DYSMETRIA SELECT THE TARGET TO SEE AN ANIMATION OF DYSMETRIA Image from Microsoft Clipart (Porth, 2005)

31. Clinical Pearl Read the CT or MRI reports to identify where the infarct is located in the brain. If the cerebellum is involved, chances are ATAXIA will be exhibited in the patient Image from Microsoft Clipart

32. Try again GOOD JOB! OPPS! Try again TEST YOUR KNOWLEDGE Ataxia is: Weakness Impaired speech Lack of coordination No need to pay taxes

33. Almost there… look closer at the options. Think again, motor cortex is involved in movement, but not directly related to ataxia. Try again; not related to movement AWESOME! TEST YOUR KNOWLEDGE What part of the brain was infarcted if the patient has ataxia? Cerebellum Parietal Lobe Motor Cortex Cerebrum

34. Opps! Ataxia after a stroke is not a genetic cause of ataxia. Genetic ataxia is caused from mutations in genes. Yes! Acquired ataxia is non-genetic. TEST YOUR KNOWLEDGE Ataxia in stroke is acquired ataxia. True False

35. National Institute of Health Stroke Scale (NIHSS) Stroke scale functions: Document and communicate Baseline deficits Changes over time First used in 1989 Administered in mean time of 6.6 minutes Interrater and intrarater agreement is good Image from Microsoft Clipart (Jensen & Lyden, 2006)

36. National Institute of Health Stroke Scale (NIHSS) Strongly predicts the likelihood of recovery after stroke Total score > 16 high probability of death or severe disability <6 predicts a good recovery Image from Microsoft Clipart (Duncan et al., 2005)

37. National Institute of Health Stroke Scale (NIHSS) 15 Item Clinical Deficit Scale Assess: Level of Consciousness Gaze Vision Facial Palsy Arm & Leg Strength Limb Ataxia Neglect Dysarthria Aphasia REMEMBER: MUST BE ASSESSED IN ORDER LISTED Image from Microsoft Clipart (Jensen & Lyden, 2006)

38. NIHSS Limb Ataxia “A few items consistently show poor agreement, notably ataxia, dysarthria, and facial weakness” Jensen & Lyden (2006, p. 2) YOU’RE NOT THE ONLY ONE WHO MAY MAKE AN ERROR SCORING ATAXIA!!!

39. NIHSS Limb Ataxia Assesses evidence of a unilateral cerebellar lesion Assesses incoordination from weakness Test with eyes open, in intact visual field Test on bilateral extremities (NIH Stroke Scale International, 2001) (National Institute Of Neurological Disorders And Stroke, 2001)

40. Evaluating Limb Ataxia Scored if present out of proportion to weakness Two instances when ataxia would not be assessed Absent in patients who do not understand or are paralyzed Untestable (UN) if amputation or joint fusion present (NIH Stroke Scale International, 2001) (National Institute Of Neurological Disorders And Stroke, 2001)

41. Click on picture of face to view example of finger- nose-finger test with ataxia present Finger-Nose-Finger Test Ask patient to touch your index finger with his index finger and then back to his nose Repeat enough times to fully assess for ataxia, moving your index finger each time to make a new target Then repeat using other extremity (NIH Stroke Scale International, 2001) Image from Microsoft Clipart

42. Heel-Shin Test Ask patient to move right heel up and down the left shin Repeat enough times fully assess for ataxia Then repeat using other extremity (NIH Stroke Scale International, 2001) Image from Microsoft Clipart Click on picture to view example of heel-shin test with ataxia present

43. Limb Ataxia SCALE DEFINITION 0Absent (Not present or paralyzed) 1Present in 1 limb (an arm or a leg) 2Present in 2 limbs (both arms, both legs, or arm and leg on same side of body) UNAmputation or joint fusion (explain) The link below will take you to the National Institute of Health Stroke Scale Training Video Assessment #7 Limb Ataxia http://www.youtube.com/watch?v=8AXtl3QPH7Y&feature=related http://www.youtube.com/watch?v=8AXtl3QPH7Y&feature=related (NIH Stroke Scale International, 2001) Video used with permission from NIHSS English Training Campus

44. NIHSS ATAXIA INSTRUCTIONAL The link below will take you to the National Institute of Health Stroke Scale Training Video Assessment #7 Limb Ataxia http://www.youtube.com/watch?v=8AXtl3QPH7Y &feature=related http://www.youtube.com/watch?v=8AXtl3QPH7Y &feature=related (NIH Stroke Scale International, 2001) Video used with permission from NIHSS English Training Campus

45. Great job! Ataxia is incoordination, not weakness! False: Ataxia is incoordination, not weakness! TEST YOUR KNOWLEDGE Ataxia occurs because of muscle weakness after a stroke. True False

46. Great job! Ataxia is assessed after weakness! Think about the order of the exam. Ataxia is assessed after weakness! TEST YOUR KNOWLEDGE Ataxia needs to be assessed prior to weakness in the NIH Stroke Scale. True False

47. Great job! Ataxia is not present because the patient is unable to perform the test. The score would be absent due to paralysis. No, ataxia is not present because the patient is unable to perform the test. The score would be absent or 0 due to paralysis. TEST YOUR KNOWLEDGE If the patient has weakness in the right arm and is unable to lift the arm off the bed, would ataxia be present? Yes No

48. Try again! Only score UN if amputation or joint fusion present. GREAT JOB! Try again! Ataxia is only present in the R arm. Try again! Ataxia is present in R arm. TEST YOUR KNOWLEDGE The patient exhibits some weakness in the right arm and is able to perform the finger-nose-finger test. The patient misses the assessors finger. The patient completes test on left arm without difficulty. What score would be given for the upper extremity test? 0 2 1 UN

49. Treatment There is no current cure of ataxia following a cerebellar stroke Physical & Occupational Therapy Strengthen muscles Assistive devices Assist in walking and other activities of daily living (ADLs) (National Institute Of Neurological Disorders And Stroke, 2010) Image from Microsoft Clipart

50. Nurse Sensitive Outcomes Impaired Mobility Mobilize early to prevent complications Active & Passive range of motion (ROM) Participate in self-care & activities frequently Teach safe use of assistive devices Educate & Facilitate adaptation of home/work environment for maximal independence Teach safety precautions Expected outcomes: Optimal independence with ADLs & mobility Maintain safety precautions (Bader & Littlejohns, 2004)

51. Nurse Sensitive Outcomes Self-Care Deficit Evaluate ability to perform ADLs Consult occupational therapy (OT) Assess for risk of falls Expected outcomes: Functional abilities recognized & advanced (Bader & Littlejohns, 2004)

52. Nurse Sensitive Outcomes Safety Identify Fall Risk Implement fall prevention strategies Universal Fall Risk Interventions Fall Precautions due to activity impairment Expected outcome: Effective in decreasing vulnerability to falls and related injury (Summers et al., 2009)

53. Nurse Sensitive Outcomes Anticipatory grieving related to loss of functional abilities Facilitate discussions to allow patient/family to voice concerns Neuropsychiatry consult to evaluate cognitive vs. depressive issues Rehabilitation consult to evaluate needs Support Groups Expected outcomes: Supported & given resources to assist with coping (Bader & Littlejohns, 2004)

54. Coping Challenges: Loss of independence May feel alone Lead to depression & anxiety Therapy or counseling may lessen sense of isolation and help cope Can lead to increased stress on the patient Habitual Stress The physiologic & behavioral changes induced by generalized stress response can threaten homeostasis (Porth, 2005) (Mayo Clinic Staff, 2009)

55. Generalized Stress Response Stroke is a life changing event people do not have time to prepare for Stress can impact controllable risk factors for stroke Hypertension High cholesterol Tobacco use Alcohol use Physical Inactivity Obesity

56. Generalized Stress Response (GSR) Sympathetic Nervous System (SNS) “Fight or Flight Response” Increased heart rate and strength of contraction Increased metabolic rate, stored fat released into circulation Bronchodilation in lungs Vasoconstriction of: Skin Gut  Decreased motility  Less insulin secreted Kidneys Pupils Dilate (Porth, 2005)

57. Renin-Angiotensin-Aldosterone Pathway Decreased blood flow to kidneys as response to SNS stimulation Renin releasedActivates angiotensinogenForms Angiotensin I Converted into Angiotensin II a strong vasoconstrictor Aldosterone released from adrenal cortex turns on Na/K ATPase in kidneys leads to increased blood volume and increased blood pressure, should increased blood flow to the kidneys (Porth, 2005)

58. Hormone Involvement in GSR Corticotropin-releasing Factor (CRF) Released by the hypothalamus Stimulates ACTH release Adrenocorticotropic hormone (ACTH) Released from the anterior pituitary gland Stimulates synthesis and release of cortisol Cortisol Released from adrenal cortex Affects many systems and processing in the body (Porth, 2005)

59. Effects of Cortisol Cardiovascular arterioles more responsive to sns increased contractility Liver stored glucose released into blood Pancreas decreased insulin release Adipose tissue lipids released from periphery, redeposited in trunk Skeletal decreased bone deposition Renal calcium lost in urine Na+/K+ pump reabsorbs Na+ and H2O into blood, secretes K+ into urine Muscular actin and myosin break down Immune production of prostaglandins blocked thymus atrophies neutrophils can't leave blood monocytes and macrophages less active (Porth, 2005)

60. Try again! Ataxia affects movement, not tissue perfusion. Try again; Ataxia does not affect breathing in the stroke patient. Great job! Very important to also consider fall risk! Try again; Ataxia does not affect breathing in the stroke patient. TEST YOUR KNOWLEDGE Identify the most appropriate nursing diagnosis in terms of special needs when ataxia is present. Impaired gas exchange Impaired physical mobility Ineffective breathing pattern Impaired tissue perfusion

61. GREAT! Currently no treatment available. PT & OT to help with function. Try again; Not used for treating ataxia. Try again; Movements are impaired because of communication error in the brain. Try again; Used for stroke treatment, but not for treating ataxia. TEST YOUR KNOWLEDGE Treatment for ataxia in the stroke patient is: TPA Muscle Relaxers Heparin No Treatment Available

62. Case Study A 67 year old male with a history of afib and prior stroke (with no deficits) was admitted from home with acute onset of nausea, generalized weakness, ataxia, and left sided weakness. Initial MRI noted a large acute ischemic infarct within the left cerebellum and smaller infarcted areas within the cerebellar vermis and right cerebellum with occlusion of the right internal carotid artery.

63. Try again; Be more specific Try again; Be more specific. GREAT!!! Case Study What is the anticipated medical diagnosis of the patient? Cerebellar Stroke Weakness Stroke

64. Try again; Ataxia is present in both upper extremities. GREAT! Score 2 if present in bilateral upper or lower extremities, or an arm and leg on the same side of the body. Opps! Ataxia is present, therefore, 0 cannot be the score. Case Study When tested for ataxia, it was present on the bilateral upper extremities. What score would be given according to the NIHSS? 0 2 1

65. Great! Think safety with patients experiencing ataxia! This patient has left sided weakness, plus BUE ataxia. This could make using mobility devices harder. Try again, This could be present in the patient, but does not relate to ataxia. Sorry, This would be appropriate, but not specific to the symptom of ataxia. Case Study What appropriate nursing diagnosis would be given to this patient related to the presences of ataxia? Impair tissue perfusion Impaired memory Risk for injury: falls

66. The End With the completion of the tutorial, you are now able to: Describe pathophysiology of cerebellum as it relates to smooth muscle movements Describe how ischemia to cerebellum causes ataxia in stroke patient Identify presence of ataxia in stroke patient Identify appropriate nursing interventions and outcomes

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