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Presentation on theme: "TIA/CVA & NEUROLOGICAL ASSESSMENT 2015"— Presentation transcript:

Ida Shepherd . Many neurological disorders occur for reasons beyond our control, but some can be prevented or minimised.

2 Learning Outcomes Define various neurological conditions
Identify risk factors for stroke Describe the functions of each of the 4 brain lobes List the mechanisms of ischaemic cell injury Differentiate between subarachnoid and intracerebral haemorrhagic strokes Describe the pathology of TIA’s Compare & contrast 5 types of CVA Identify the physiological/cognitive effects of a CVA Describe the nursing interventions for patients experiencing a CVA or post-CVA Describe the basic principles of nursing care of a patient with IICP. Identify how to care for a seizure patient. Demonstrate the principles of a basic neuro assessment To appreciate the significant changes that take place with aging, a brief review of the neurologic system is required.

3 Significant changes in aging nervous system
The central nervous system (CNS) is divided into three major functional components: higher level brain or cerebral cortex, lower level brain (basal ganglia, thalamus, hypothalamus, brainstem, and cerebellum), and spinal cord. The brain is divided into three major areas, which include the cerebrum, brainstem, and cerebellum.

4 Definitions Cerebrovascular disease refers to any pathological processes involving the blood vessels of the brain. Cerebrovascular accident (CVA) – a focal neurological dysfunction whose symptoms last over 24 hours. Brain Attack – a term for CVA/Stroke. Transient Ischaemic Attack (TIA) – a brief episode of neurological deficit that resolves without any residual effect. All conditions require immediate attention - time is of the essence

5 Defintions Reversible Ischemic Neurological deficit (RIND) – a neurological deficit persisting beyond 24 hours but resolving with no permanent deficit. Stroke – a generic term, lacking pathological meaning & laypersons term. Stroke in evolution- Progressive neurologic deterioration occurs; residual neurologic deficit present. Develops over 1-3 days Completed Stroke-Patient appears stable with neurologic deficit permanent and unchanging

6 Epidemiology Cerebrovascular disease was the third leading cause of death in the total population in 2006, after cancer and ischaemic heart disease. There were 2674 deaths from cerebrovascular disease in 2006 and the majority (62.6 percent) were female deaths. Māori females had the highest age-standardised mortality rate of the four groups in 2006, followed by Māori males. The calculated Māori male age- standardised rate was 6.6 percent higher than the non-Māori male rate in 2006, and the calculated Māori female rate was 34.3 percent higher than the non-Māori female rate.

7 Stroke Foundation Facts
Stroke is the third largest killer in New Zealand (about 2500 people every year). Around 10 percent of stroke deaths occur in people under 65. Every day about 24 New Zealanders have a stroke. A quarter occur in people under 65. To recognise a stroke click here. Stroke is the major cause of serious adult disability in New Zealand. Stroke is largely preventable, yet about 9000 New Zealanders every year have a stroke. For information about reducing your stroke risk click here. There are an estimated 60,000 stroke survivors in New Zealand. Many are disabled and need significant daily support. However, stroke recovery can continue throughout life. Most people can’t recognise the signs of a stroke occurring. Make sure you are aware of the signs to look for. For more information click here. High blood pressure is a major cause of strokes. One in five New Zealanders has high blood pressure, and a third of these don’t know it. Reducing your blood pressure can greatly reduce stroke risk. For more information click here. Stroke is a medical emergency but many New Zealanders do not have access to the best possible stroke hospital services. http// Stroke affects annually around 17 million people globally

8 Epidemiology Stroke is the second most common cause of death worldwide and a common cause of disability in adults in developed countries (Johnston et al, 2009; Rothwell, 2001). Stroke is a major public health challenge in New Zealand (MOH, 2000). It is the third greatest cause of death in New Zealand, after all cancers combined and heart disease (MOH, 2009), and has an enormous physical, psychological and financial impact on patients, families, the health care system and society (Strong et al, 2007; Caro et al, 2000). A systematic review of 56 stroke incidence studies (Feigin et al, 2009) showed that the age-adjusted stroke incidence rate in New Zealand is high compared with other developed countries. Approximately 6000 New Zealanders suffer from a stroke every year (Brown, 2009; Tobias et al, 2007) and approximately 2000 deaths each year are attributable to stroke

9 Epidemiology Significant disparities exist between Māori and non-Māori in the prevalence of stroke risk factors, stroke incidence and mortality rates, access to stroke care and stroke outcomes.  Māori are also younger on average at first stroke onset than New Zealand Europeans (mean age 61 years compared with 76 years).

10 Epidemiology Pacific peoples, along with Māori, experience strokes at high rates compared with other New Zealanders. Pacific stroke mortality rate for 2001 to 2004 was over two times the mortality rate of European/Other New Zealanders for the same period (Blakely et al, 2007). In 2001 to 2004, age-standardised stroke mortality rates were 27.3 per 100,000 for Pacific males and 19.9 per 100,000 for Pacific females. There was no significant difference in these stroke mortality rates between males and females (Blakely et al, 2007). Studies on the incidence of stroke show onset occurring at younger ages among Pacific people (Anderson et al, 2005; Bonita et al, 1997b; Carter et al, 2006; Feigin et al, 2007; Fink, 2006) and on average, 10 to 15 years earlier compared with New Zealand Europeans (Carter et al, 2006). This higher incidence of stroke among Pacific people is associated with the presence of more risk factors for stroke including diabetes, obesity, smoking and hypertension (Carter et al, 2006; Fink, 2006; Feigin et al, 2006), and may also reflect lower use of primary and secondary preventive care (eg, lower use of cholesterol- lowering and blood pressure control medications) (Fink, 2006). In addition Pacific peoples, along with Māori and Asian/Other New Zealanders, experience more severe strokes than New Zealand Europeans (CTRU, 2010).

11 Risk factors Age Oral contraceptive use (especially if a smoker) Male
Heart Disease & AF Diabetes ↑ hematocrit or other hypercoagulability states Earlier stroke or TIA Asymptomatic carotid artery stenosis Hypertension Oral contraceptive use (especially if a smoker) Family history Excessive ETOH intake Drug abuse Obesity Sedentary lifestyle Elevated serum cholesterol & triglycerides Migraines Cigarette smoking Sickle cell disease

12 Revision- Physiology of the brain Major arteries supplying the brain
Carotids supply anterior portion of brain. Vertebral - basilar artery and supplies the posterior portions of the brain.

13 The Circle of Willis - In theory allows blood to circulate from one hemisphere to other - Functionally, two hemispheres usually remain separate Picture 43-2 p. 1365 The circle of Willis is the region of the brain in which the branches of the basilar and internal carotid arteries join, creating a circular network, which in theory allows blood to circulate from one hemisphere to the other and from the anterior to the posterior portions of the brain. The Circle of Willis has a downside, however. Cerebral aneurysms tend to occur at the junctions between the arteries that make up the Circle Collateral circulation - an alternative route

14 Cerebral Cortex and Functions
Revise all own notes from Patho & A & P Texts: Lewis & Jarvis

15 CPP is measured by monitoring ICP
Optimal Cerebral Perfusion Pressure (CPP) has a MAP of 50mmHg which is maintained with mL of blood /min, using 20% of the CO. When perfusion falls below 50mmHg, cerebral ischaemia begins (syncope/ blurred vision) & cerebral vessels dilate & constrict in response to changes in BP & CO2 retention. A complex cascade of biochemical changes occur in response to the ischemia

16 Ischaemic Cell Injury Interruption of oxygenated blood flow to an area of the tissue (heart, brain, limb) (cerebral blood flow falls to less than 25mL/100g/min) Oxygen tension within cell decreases leading to decreased ATP Local acidosis build-up, pH levels change Failure of sodium pump, decreased potassium Influx of sodium and water into cell causing swelling Progressive loss of glycogen and protein synthesis Morphologic deterioration (cell structure begins to degenerate) Mitochondria begin to swell, EPR dilates Glutamate released causing further cell damage Reversible to this point with reperfusion of tissues Do some more reading around this partic after irreversibility The brain is very sensitive to a decrease in blood supply. As a result, when cerebral blood flow is reduced to a level insufficient to maintain neuronal viability, it causes a state of hypoxia. This hypoxic state leads to tissue ischemia and injury. Short-term ischemias result in TIAs. Long-term ischemia leads to permanent infarction (death of cerebral cells). (Meiner, Sue E.. Gerontologic Nursing, 3rd Edition. Mosby, ).

17 Brain Infarction

18 CT scan taken some time after a large stroke
CT scan taken some time after a large stroke. The black area is where the stroke was and now the brain tissue has died and left a large hole.

19 Transient Ischaemic Attacks (TIA’s)
Results from temporary impairment of blood flow to a specific region of the brain due to atherosclerosis, obstruction of cerebral microcirculation by a microembolus, a decrease in CPP (N=50mmHg) or cardiac arrhythmias. TIA’s can’t be distinguished from a stroke, but before diagnosing TIA consider other cases of transient neurological dysfunction – migraine, partial seizures, hyper/hypoglycaemia, hypotension, syncope Post TIA, 5-10% of patients will develop infarction if left untreated. Risk greatest in the first 7 weeks. Not all patients who develop cerebral infarction have had a warning TIA. ABCD 7 Day Stroke Risk Scorecard If flow is restored within the critical period, ischaemic symptoms will reverse themselves. The ABCD score can be used in routine clinical practice to identify high-risk individuals who need emergency investigation and treatment.

20 Aetiology - CVA Ischemic stroke results from complete or partial occlusion of one or more cerebral blood vessels secondary to thrombus formation (site of stenosis as seen in atherosclerosis) or embolisation (resulting from an embolus commonly originating in the heart, may be due to AF). Cerebral oedema develops within minutes of the insult to the neuronal cells, peaks within 2 to 4 days, and contributes to neurolgic deficits.

21 Ischaemic Strokes-80-85% Large artery thrombotic strokes:
Due to atherosclerotic plaques in the large blood vessels of the brain. Thrombus formation and occlusion at the site of the atherosclerosis result in ischaemia and infarction. Small penetrating artery thrombotic strokes: Affect one or more vessels and are the most common type of ischaemic stoke. These are also called lacunar strokes because of the cavity that is created once the infarcted brain tissue disintegrates. Cardiogenic embolic strokes: Are associated with cardiac arrhythmias, usually atrial fibrillation. Emboli originate from the heart and circulate to the cerebral vasculature, most commonly the left middle cerebral artery, resulting in a stroke. Embolic strokes may be prevented by the use of anticoagulation therapy in patient with atrial fibrillation. Cryptogenic Strokes: Have no known cause; idiopathic. Other strokes: From causes such as cocaine use, coagulopathies, migraine, and spontaneous dissection of the carotid or vertebral arteries. Information from: Farrell (2004), p. 1896Percentages from: The University Hospital, Newark, New Jersey

22 Haemorrhagic Strokes- 15-20% Typically classified by location of bleeding
Subarachnoid haemorrhagic stroke - bleeding into subarachnoid space. - usually rupture of cerebral aneurysm or arteriovenous malformation Intracerebral haemorrhagic stroke - occurs from bleeding into brain tissue itself. - rupture of a small artery – often deep penetrating vessel, & often related to poorly controlled hypertension. Abrupt increase in intracranial pressure (ICP) which may cause cerebral oedema (With intra cerebral bleeding blood is forced into the adjacent brain tissue then extends the ischaemic damage – can result in brain tissue displacement or herniation) Subarachnoid haemorrhage causes: Sacular (Berry aneurysm) Fusiform Intracerebral haemorrhage causes: High blood pressure (hypertension) is the most common cause of this type of stroke. Blood Vessel Abnormalities: Blood vessel abnormalities in the brain include arteriovenous malformations (AVMs) and arteriovenous fistulas (AVFs).

23 10 percent of stroke survivors recover almost completely
25 percent recover with minor impairments 40 percent experience moderate to severe impairments requiring special care 10 percent require care in a nursing home or other long-term care facility 15 percent die shortly after the stroke

24 Subarachnoid haemorrhage & Intracerebral haemorrhagic

25 Massive hypertensive haemorrhage rupturing into a lateral ventricle.


27 Herniation of the brain & Intracranial Pressure
When the intracranial pressure increases enough it will cause particular regions of the brain to herniate into adjacent compartments, resulting in mechanical and secondary vascular damage. Cushing’s response is seen when cerebral blood flow decreases significantly: elevated SBP, widening pulse pressure and decreased HR Following this, the patient will exhibit significant changes in mental status and vital signs and Cushing’s triad appears: bradycardia, hypertension and bradypnoea. As ICP continues to rise, restlessness, confusion or increasing drowsiness may appear followed by the patient becoming stuperous.

28 Care of the patient with IICP
Alteration in LOC ranging from irritability, restlessness, and confusion to lethargy Possible onset or worsening of headache Beginning pupillary dysfunction, such as sluggishness; visual disturbances, such as diplopia or blurred vision Onset of or increase in sensorimotor changes or deficits, such as weaknes; Onset or worsening of nausea. Continued deterioration of LOC leading to stupor and coma; projectile vomiting Hemiplegia; posturing Alterations in VS (typically increased SBP, widening pulse pressure, decreased pulse rate); respiratory irregularities, such as Cheyne-Stokes breathing; pupillary changes, such as inequality, dilation, and non-reactivity to light; papilledema Impaired brainstem reflexes (corneal, gag, swallowing). Early indicators of IICP Late indicators of IICP

29 Increased intracranial pressure can be due to a rise in cerebrospinal fluid pressure. It can also be due to increased pressure within the brain matter caused by a mass (such as a tumor), bleeding into the brain or fluid around the brain, or swelling within the brain matter itself. Brain herniation: Occurs when IICP causes displacement of brain tissue from one intracranial compartment to another, resulting in compression, destruction, and laceration of brain tissue. In the presence of actual brain herniation, patient is in a deep coma, pupils become fixed and dilated bilaterally, posturing may progress to bilateral flaccidity, brainstem reflexes generally are lost, and respirations and VS deteriorate and may cease.

30 The single most important early indicator of IICP is a change in LOC
The single most important early indicator of IICP is a change in LOC. Late indicators of IICP usually signal impending or occurring brainstem herniation. Signs generally are related to brainstem compression and disruption of cranial nerves and vital centres. Hypotension and tachycardia in the absence of explainable causes, such as hypovolemia, usually are seen as a terminal event in TBI. IICP usually peaks around 72 hr after initial insult and then gradually subsides over 2–3 wk.

31 Cushing’s Triad Bradycardia Hypertension Bradypnoea
Cushing's triad is a clinical triad variably defined as having: Irregular respirations (caused by impaired brainstem function) Bradycardia. Hypertension (Widening Pulse Pressure) Subarachnoid hemorrhage as shown on a CT scan. It is denoted by the arrow. This type of injury may result in damage to the brainstem

32 Subarachnoid hemorrhage
Ninety percent of primary subarachnoid hemorrhages arise from congenitally derived arterial outpouchings (berry aneurysms) that lie at bifurcations of the major components of the circle of Willis. The most common sites are the carotid-posterior communicating and the anterior cerebral-anterior communicating artery junctions

33 Major Stroke Syndromes (C.O.W.)
Middle Cerebral Artery (MCA) Syndrome Anterior Cerebral Artery (ACA) Syndrome Posterior Cerebral Artery (PCA) Syndrome Vertebrobasilar Artery (VBA) Syndrome Internal Carotid Artery (ICA) Syndrome Lacunar Strokes

34 Clinical manifestations- differ or are similar for each syndrome
Clinical manifestations- differ or are similar for each syndrome. Some are listed below: Contralateral Hemiparesis/hemiplegia Homonymous Hemanopia Receptive/expressive aphasia Drowsiness, stupor Agnosia Neglect, inattention of double simultaneous stimulation Sensory deficits Impaired gait Flat affect, disinhibition, personality change, loss of decision making Urinary incontinence Speech preseveration Dizziness Nystagmus & diplopia Dysphagia & dysarthria Pain Ipsilateral numbness & weakness Clumsiness Staggering gait & ataxia Syncope Apraxia Paralysis of the contralteral face, arm & leg

35 Lacunar Strokes Include, but not limited to:
Contralateral paresis or plegia of face, arm, or leg Contralateral decreased sensation of face, arm, or leg Slurred speech, and weakness and ataxia of the arm Numbness Called lacunar strokes because of the cavity that is created once the infarcted brain tissue disintegrates.

36 Locked-In Syndrome Brainstem infarct or Pontine haemorrhage leaving the patient paralysed but with intact cortical function. Breathes spontaneously. Paralysis of horizontal eye movements but retains the ability to look up. Retained sensation in the limbs and hearing Check for this by attempting to establish communication with the patient using upward eye movements. For example: “Look up once for Yes, look up twice for No”. Then, “Can you hear me?”

37 Seizures Seizures are an abnormal, sudden, excessive discharge of electrical activity within the brain.

38 Dysphasia Diet Four (4) types of dysphagia diets.
Link: Four (4) types of dysphagia diets. NDD Level 1: Dysphagia-Pureed (homogenous, very cohesive, pudding-like, requiring very little chewing ability). NDD Level 2: Dysphagia-Mechanical Altered (cohesive, moist, semisolid foods, requiring some chewing). NDD Level 3: Dysphagia-Advanced (soft foods that require more chewing ability). Regular (all foods allowed). National Dysphagia Diet – NDD – (What to swallow)

39 Aspiration Pneumonia General Guidelines for Aspiration Pneumonia prevention Patient should sit upright (45 degrees) for eating Each bolus should be less than one teaspoon Place food well into mouth Encourage patient to gently cough after each swallow Patient should swallow several times after each bolus

40 Bladder & bowel Deficits
Frequency, urgency and incontinence Potential for bladder retraining if cognitively intact Avoid catheterization Bowel – constipation (related more to immobility)

41 Communication Deficits
Motor Aphasia – Broca’s area- speak very little or not at all, no activation of muscles to produce speech, but can comprehend spoken or written language. Expressive aphasia: aka: non- fluent aphasia; unable to form words that are understandable; may be able to speak in single-word responses (Broca’s, frontal lobe) Sensory Aphasia- Wernicke's area- can speak but cannot understand spoken or written language. Speech is effortless but is garbled and incomprehensible. Receptive aphasia: aka: fluent aphasia; unable to comprehend the spoken word; can speak but may not make sense (Wernicke's, parietal lobe) Global (mixed) aphasia: Combination of both receptive and expressive aphasia Communication Deficits

Timing is paramount when dealing with brain conditions

43 Carotid Endarterectomy

44 Interventions: Neuroprotectants Control of fever Glycaemic control
DVT prevention Aspiration precautions Avoidance of IDC’s Bowel (&bladder) regimen Early mobilisation

45 Other Interventions Prevent joint deformities
Establish an exercise program Prevent pain Enhance self-care Manage sensory-perceptual difficulties Manage dysphagia Improve thought processes Improve communication Maintain skin integrity Improve family coping Assist patient & partner with sexual dysfunction

46 Nursing Assessment Neurologically the patient will primarily be assessed thoroughly covering all anatomical systems, including neurologically ( e.g. Seidel’s Neuro assessment) PMH, 5 dimensions of health, medications and ADLS, IADL’s using a functional assessment (e.g. Barthels assessment).

47 Nursing Assessment SUBJECTIVE PMH Medications Health perception
Nutritional Elimination Activity Cognitive Review Neuro Assessment (Lewis & eds) OBJECTIVE General Respiratory Cardiovascular Gastrointestinal Urinary Neurological Lewis – 3rd & 4th editions

48 Cranial Nerves Jarvis (2004). Pocket companion.

49 Cranial Nerve (CN) Procedure CN I (olfactory) Test ability to identify familiar aromatic odors, one naris at a time with eyes closed. CN II (optic) Test vision with Snellen chart and Rosenbaum near vision chart. Perform ophthalmoscopic examination of fundi. CN III (oculomotor) Test visual fields by confrontation and extinction of vision. IV (trochlear) *** Inspect eyelids for drooping.*** VI (abducens)*** Inspect pupils' size for equality and their direct and consensual response to light and accommodation.*** Test extraocular eye movements. CN V (trigeminal)*** Inspect face for muscle atrophy and tremors.*** Palpate jaw muscles for tone and strength when patient clenches teeth.* Test superficial pain and touch sensation in each branch*** (test temperature sensation if there are unexpected findings to pain or touch). Test corneal reflex. CN VII (facial)*** Inspect symmetry of facial features with various expressions (e.g., smile, frown, puffed cheeks, wrinkled forehead).*** Test ability to identify sweet and salty tastes on each side of tongue. CN VIII (acoustic) Test sense of hearing with whisper screening tests or by audiometry. Compare bone and air conduction of sound. Test for lateralization of sound. CN IX (glossopharyngeal)*** Test ability to identify sour and bitter tastes. Test gag reflex and ability to swallow.*** CN X (vagus)*** Inspect palate and uvula for symmetry with speech sounds and gag reflex.*** Observe for swallowing difficulty.*** Evaluate quality of guttural speech sounds (presence of nasal or hoarse quality to voice). CN XI (spinal accessory)*** Test trapezius muscle strength (shrug shoulders against resistance).*** Test sternocleidomastoid muscle strength (turn head to each side against resistance).*** CN XII (hypoglossal)*** Inspect tongue in mouth and while protruded for symmetry, tremors, and atrophy.*** Inspect tongue movement toward nose and chin.*** Test tongue strength with index finger when tongue is pressed against cheek.*** Evaluate quality of lingual speech sounds (l, t, d, n).

50 Neurological Assessment
Test Selective Cranial Nerves (See previous slide and highlighted areas) Cerebellar Function and Proprioception 1. Evaluate coordination and fine motor skills by the following Rapid rhythmic alternating movements Accuracy of upper and lower extremity movements 2. Evaluate balance using the Romberg test & Heel-To-Toe test   3. Observe the patient's gait Posture Rhythm and sequence of stride and arm movements Sensory Function 1. Test primary sensory responses to the following    •    Superficial touch    •    Superficial pain Seidel (2006)

51 Neurological Assessment conti’d
2. Evaluate perception of position sense with movement of the great toes or a finger on each hand 3. Assess ability to identify familiar object by touch and manipulation (stereognosis) 4. Assess two-point discrimination -not taught 5. Assess ability to identify letter or number “drawn” on palm of hand (graphesthesia) 6. Assess ability to identify body area when touched Superficial and Deep Tendon Reflexes - not taught 1. Test abdominal reflexes 2. Test the cremasteric reflex in male patients 3. Test the plantar reflex 4. Test the following deep tendon reflexes • Biceps • • Triceps • Patellar • Achilles 5. Test for ankle clonus

52 4+ Very brisk; hyperactive with clonus, indicative of disease
Reflexes: 4+ Very brisk; hyperactive with clonus, indicative of disease 3+ Brisker than avg, may indicate disease 2+ Average, normal 1+ Diminished, low normal 0 No response Clonus = set of short jerking contractions of the same muscle.



55 Decorticate - Flexion Decerebrate - Extension

56 Changes to visual fields

57 Dr. Jill Bolte-Taylor


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