WEEK+7+Alterations+in+Neuro

4. Discuss the diagnostic evaluations (laboratory & radiological tests) and special procedures related to neurological function and examine the abnormalities.

5. Describe the incidence and etiology for cerebrovascular attack (CVA).

6. Discuss current statistics related to cerebrovascular disease.

__//**7. Describe the classifications of a cerebrovascular accident.**//__

The occluded artery leads to ischemia. Thrombotic brain attacks are often gradual. They often occur during periods of inactivity like during sleep because BP falls or w/ dehydration. The most common location for clot to form is in bifurcations of common carotid artery & Junction between vertebral & basilar arteries. A part of the Occurs suddenly; any time of day. It usually occurs in the middle cerebral artery because the internal carotid leads directly to it. S/S can be temporary as the emboli breaks up into smaller pieces and moves on. Then smaller pieces occlude smaller vessels. Body doesn’t usually have time to form collateral circulation. Causes are usually are r/t heart; atrial fib, Rheumatic Heart disease; common cause seen in younger-mid aged adults, mural thrombi that forms after an MI b/c ventrical not contracting as it should and blood stays longer, forming a clot, and prosthetic heart valve. The result is blood causing the adjacent brain tissue to be displaced and compressed and decreasing cerebral blood flow, which leads to ischemia and infarction. Initial s/s and warning signs are sudden and include severe headache, nausea and vomiting. S/S progress over minutes-hours as bleeding progresses. Vasospasms occur in subarachnoid hemorrhage but not in parenchymal hemmorhage. A ruptured vessel can cause a sudden, explosive headache, changes of LOC including loss of consciousness, n/v, and a dramatic rise in intracranial pressure.
 * a) Ischemic**; results from inadequate blood flow to the brain from partial or complete occlusion of an artery- account for 80% of strokes
 * -Thrombotic;** occurs from injury to a blood vessel wall in the brain and blood clot formation. R/t artherosclerosis, which causes plaque to build up and/or the inflammation in the artery. Increased platelets build up over the area forming a clot and occlude the artery. HTN and DM are risk factors for artherosclerosis and thrombotic CVAs. Also can be r/t coagulation disorders and drug abuse.
 * -Embolic;** involves fragments of plaque that break from a thrombus formed outside brain or in the heart, aorta, or common carotid that travel to the cerebral vasculature. When it reaches an artery in the brain that is too narrow to pass through, it lodges there and causes ischemia.
 * b) Hemorrhagic;** account for approx 15% of strokes
 * -Parenchymal; aka- intracerebral;** results from bleeding into the brain tissue itself. Caused by an interruption or rupture of a brain vessel. Poor prognosis. HTN is most important cause, b/c it weakens blood vessels.
 * -Subarachnoid;** occurs when there is intracranial bleeding in the cerebral fluid-filled space between arachnoid and pia matter membranes on surface of brain. Common causes are head trauma from falls, ect, aneurysms, and arteriovenous malformation.

__//**8. Describe a transient ischemic attack (TIA) and contrast it with a CVA (Brain Attack).Lewis 1504, Huether 382, Modules and power point p. 9;**//__

Because there is no way to tell whether symptoms are from a TIA or an acute stroke, a prompt evaluation (within 60 minutes) is necessary to identify the cause of the TIA and determine appropriate therapy. CT scan is an important initial diagnostic study. TIAs are often warning signs that a person is at risk for a more serious and debilitating stroke. About one-third of those who have a TIA will have an acute stroke some time in the future.
 * “Silent Stroke”** A transient ischemic attack (TIA) is a temporary focal loss of neurological function caused by ischemia, lasting <24 hour and often lasting <15 min. It’s probably a result of platelet clumping or microemboli that temporarily decreases brain blood flow. TIA symptoms, which usually occur suddenly, are similar to those of stroke but do not last as long. Most symptoms of a TIA disappear within 24 hours. Symptoms depend on area of brain that is ischemic and can include temporary changes in vision, speech, motor fx, dizziness or loss of consciousness


 * CVAs;** This is the real deal; CVA is defined as a sudden, nonconvulsive focal neurologic deficit and are clinical manifestations of Cerebrovascular Disorders; problems with the brain’s vascular system that can lead to ischemia or hemorrhage. The result is death of brain cells and occurs w/in minutes to hours. Both TIAs and CVAs have same risk factors (#5) but symptoms may be permanent and are the leading cause of disability in the US. The severity of the loss of fx varies according to location and extent of brain involved. In the mildest form pt may have no symptoms. In most severe state CVAs can cause hemiplegia, coma and death.


 * //__9. Analyze the pathophysiology and clinical significance of increased intracranial pressure and decreased cerebral perfusion pressure.(1468-69 Lewis) (349-350 Heuther)__//**

Cerebral vascular resistance is generated by the arterioles within the cranium. When Cerebral vascular resistance is high, blood flow to the brain tissue is impaired, which decreases CPP. Elevated ICP is clinically significant because it decreases CPP, which increases risk of brain ischemia and infarction.
 * Patho:** The mean arterial pressure (MAP) must be 60 for auto-regulation to be effective. The upper limit of systemic pressure for auto-regulation is 150.
 * Cerebral perfusion pressure (CPP)** -is the pressure need to ensure blood flow to the brain.

//__Patho-__// caused by destruction of motor neurons in the pyramidal pathway
 * //__10. Examine the pathophysiology and the following clinical manifestations related to the client with a cerebrovascular accident:__//**
 * a. motor deficits-**

//__Manifestations__//:Impaired mobility, respiratory function, swallowing and speech, gag reflex, self-care abilities, loss of skilled voluntary movement, hemiplasia/plagia, flaccidity & spasticity, Hypo/hyper reflexia, Akinesia.

//__Patho__//: Occur initially and are temporary, when one hemisphere is effective the prognosis is good. Control of urination altered r/t cognitive deficits
 * b. bowel and bladder deficits**

//__Manifestations:__// incontinence, urgency, frequency, constipation due to immobility

//__Patho-__// the left hemisphere is dominant for language skills, Damage to this side may cause these communication deficits
 * c. communication deficits**

//__Manifestations-__// Aphasia, dysphasia, agraphia

//__Patho-__// Stroke on the right side more likely to cause spatial issues
 * d. sensory-perceptual deficits**

//__Manifestations-__//incorrect perception of self & illness, may deny their illness or body parts, erroneous perception of space, may neglect all input from affected side. Homonymous hemianopsia, agnosia, apraxia, pain, cold, pressure, taste, smell, hearing ,equalibrium, Anosognsia

//__Patho-__// due to frustration on not being able to perform ADL’s, Left sided brain stroke is more likely to result in memory loss& cautious Right sided more impulsive
 * e. cognitive-emotional deficits**

//__Manifestations:__// -difficulty controlling emotions, may be exaggerated, depression. Labile emotions, decreased tolerance for stress, confusion


 * Akinesia-** loss of skilled voluntary movement
 * Hyporelexia-** depressed reflexes
 * Hyperreflexia-** hyperactive reflexes
 * Aphasia-** total loss of comprehension and use of language
 * **Global aphasia-** and communication and receptive function loss
 * **Receptive (Wernicke’s)-**neither sounds or meaning is understood
 * **Expressive(Broca’s)**-difficulty in speaking and writing
 * Dysphasia-** difficulty related to the comprehension or use of language
 * **Fluent-** speech is present but meaningless
 * **Nonfluent-** minimal and slow speech that requires effort
 * Dysarthria-** disturbances in the muscular control of speech
 * Homonymous hemianopsia-** blindness occurs in the same half a visual field in both eyes
 * Agnosia-** inability to recognize an object by sight, touch or hearing
 * Apraxia-** inability to carry out learned sequential movements on command
 * Agraphia:** loss of abilty to right
 * Ipsilateral:** same side
 * Contrallateral:** opposite side
 * Hemiparesis:** one sided weakness
 * Hemipalegia**: one sided paralysis
 * Anosognosia:** unaware of nuerological deficit

11. Examine the multidisciplinary approach to the management of the client with a cerebrovascular accident. The goals during the acute phase are the preservation of life, preventing further brain damage and reducing disability. Table 58-5 Lewis 1511 Emergency management for stroke. Acute care begins with ABC’s (airway, breathing, circulation) Baseline neurologic assessment is done. Treat for increased cranial pressure (ICP) if present. As a last resort a bone flap may be removed to allow edema without increased ICP Drugs Recombinant tissue plasminogen activator (tPA) produces localized fibrinolysis by binding to fibrin in the thrombin. Careful screening to rule out hemorrhagic stroke, coagulation disorders, GI bleeding, and recent surgery. After patient is stabilized can be treated with platelet inhibitor and anticoagulants to prevent further clots. Contraindicated for hemorrhagic stroke. Surgical Therapy Aneurysms and hemorrhage Immediate evacuation of aneurysm-induced hematomas or cerebellar hematomas larger than 3cm. Clipping, wrapping or coiling the aneurysm to prevent rebleeding.

12. Relate the characteristics of a cerebrovascular accident with the involved vasculature. Transient Ischemic Attack A temporary focal loss of neurologic function caused by ischemia of one of the vascular territories. Due to microemboli that temporarily block the blood flow. If the carotid system is involved patient may have temporary loss of vision in one eye, transient hemiparesis, numbness or loss of sensation, or sudden inability to speak. Signs of a TIA involving the vertebrobasilar system may include tinnitus, vertigo, darkened or blurred vision, diplopia, ptosis, dysarthria, dysphagia, ataxia, and unilateral or bilateral numbness or weakness. (Lewis 1504-1505) Ischemic Stoke Thrombotic Stroke Occurs from injury to blood vessal wall and formation of a blood clot. The Lumen of the blood vessel becomes narrowed and if it becomes occluded, infarction occurs. (Lewis 1505) Lacunar stroke Occlusion of a small penetrating artery with development of a cavity in the place of the infracted brain (Lewis 1505) Embolic Stroke When an embolism lodges in and occludes a cerebral artery. Resulting in infarction and edema of the area supplied by the involved artery. Embolisms travel upward to the cerebral circulation and lodge where vassals narrow and bifurcate. (Lewis 1506) Hemorrhagic Stroke Intracerebral Hemorrhage Approximately half of intracerebral hemorrhages occur in the putamen and internal capsule, central white matter, thalamus, cerebelluar hemisphere and pons. (Lewis 1506) Subarachnoid Hemorrhage Intracraninal bleeding into the cerebrospinal fluid-filled space between the arachnoid and pia mater membranes on the serface of the brain. Commonly caued by rupture of a cerebral aneurysm. The Majority of aneurysms are in the circle of Willis. (Lewis 1507)

13. Differentiate between left hemisphere cerebrovascular accident and right hemisphere cerebrovascular accident. Lewis page 1508 Fig 58-5 Right side brain damage • Paralyzed left side: Hemiplegia • Left-side Neglect • Spatial-perception deficits • Tends to deny or minimize problems • Rapid performance, short attention span • Impulsive, safety problems • Impaired judgment • Impaired time concept Left side brain damage • Paralyzed right side hemiplegia • Impaired speech/language aphasias • Impaired right/left discrimination • Slow performance, cautios • Aware of deficits: depression, anxiety • Impaired comprehension related to language, math

14. Analyze the physiologic mechanisms that maintain intracranial pressure/cerebral blood flow. ICP is the hydrostatic force measured in the brain CSF compartment. Normal ICP is the total pressure exerted by these 3 components: Brain tissue, Blood, and Cerebrospinal fluid (CSF). Under normal conditions, intracranial pressure consists of approximately: Brain tissue: 80% Blood: 10% CSF: 10% In the rigid skull, these remain fairly constant and the balance maintains the ICP. If the volume of any one of these components increases AND the volume of another component is displaced, __total intracranial pressure does not change__ (modified Monro-Kellie doctrine) **__ Compliance: __** ability to accommodate changes in volume w/out significant increase in pressure.  Normal Compensatory Adaptations: 1) Changes in the CSF volume- achieved by altering CSF production or absorption & by displacement into the spinal subarachnoid space. 2) Brain tissue volume compensates through distention of the dura or compression of brain tissue. 3) Autoregulation of Cerebral Blood Flow- automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow-ensures consistent CBF to provide for the metabolic needs of brain tissue & to maintain CPP within normal limits. (CPP- //cerebral perfusion pressure//- the pressure needed to maintain blood flow to the brain)  15. Examine the etiology, types, mechanisms, clinical manifestations, and collaborative management of increased intracranial pressure. **(Lewis pg 1469-1472) see table 57-2 for causes of cerebral edema, and table 57-3 for diagnostic & collaborative care for ICP.**  Cerebral edema (increased accumulation of fluid in extravascular spaces of brain tissue) results in increase of tissue volume & carries potential to increase ICP.
 * __-See Lewis pg 1468*__**.

3 types of cerebral edema are (patients can have 1 or more): 1) vasogenic- most common; mainly in white matter; changes in endothelial lining of cerebral capillaries allow leakage to extracellular space- osmotic gradient then favors fluid flow from intravascular to extracellular space. Possible causes: brain tumor, abscesses, ingested toxins. Speed & extent influenced by systemic BP, site of injury, extent of blood-brain barrier defect. 2) cytotoxic- results from local disruption of functional or morphologic integrity of cell membranes; most often in gray matter; develops from destructive lesions or brain trauma resulting in hypoxia or anoxia, sodium depletion, & SIADH; edema results as fluid and protein shift from extracellular space directly into the cells causing swelling. 3) interstitial- result of periventricular diffusion of ventricular CSF in patients with uncontrolled hydrocephalus; also caused by enlarged extracellular space- a result of systemic water excess (water intoxication, hyponatremia); fluid moves into cells to equilibrate with the hypoosmotic interstitial fluid. <span style="font-family: Arial,Helvetica,sans-serif;"> <span style="font-family: Arial,Helvetica,sans-serif;"> Manifestations: 1) Change in LOC 2) Change in Vitals 3) Ocular signs 4) Decrease in motor function 5) Headache 6) Vomiting <span style="font-family: Arial,Helvetica,sans-serif;">The major complications of uncontrolled ICP are inadequate cerebral perfusion and cerebral herniation.

16. Differentiate between the following potential complications associated with trauma to the brain: **(Huether, pg 76 & pg 371, 372)**

a. Epidural hematoma- (Extradural hematoma) blood collection between the inner surface of the skull and the dura. Caused by a torn artery & almost always associated with a skull fracture. Most common in 20-40 yr olds; temporal fossa is most common site for this type

b. Subdural hematoma- blood collection (clot or pool) between the inner surface of the dura mater and the (arachnoid membrane) surface of the brain- a result of shearing of small veins that bridge the subdural space. Develop rapidly (within hours) & usually located at top of skull. Can result from falls, blows, or sudden acceleration/deceleration of the head- shaken baby syndrome. Also seen in vehicular accidents, and is common in the elderly or those with chronic alcohol syndrome.

c. Intracerebral hematoma- associated w/contusions- caused by forceful impact, usually vehicular accidents or falls from a distance; may be single or multiple; commonly found in frontal or temporal lobes; caused by penetrating injury or shearing forces that traumatize small blood vessels; the hematoma then acts as an expanding mass- increases ICP- compresses brain tissue- causes edema/ischemia. Delayed Intracerebral hematoma can show up 3-10 days after injury. The //reticular formation// is located between the lower end of the brainstem and the thalamus. It contains the **//reticular activating system// (RAS)**, which sends impulses contributing to alertness to the limbic system and to the cerebral cortex. When the RAS is stimulated, it increases its output of impulses, leading to wakefulness. Stress usually increases the degree of wakefulness and can lead to sleep disturbances.
 * __17. Describe the role of the reticular activating system as it applies to cognitive function__**. (patho p278, MS p113, PPT p7#1)
 * ~Maintains wakefulnees **

Rinaldi mentioned this when talking about the stages of ICP. She said change in LOC is a reliable indicator of neural function. Decrease blood flow and O2 to the RAS affects wakefulness and you start to see this in stage 3 (beginning decompensation) of ICP. (patho 349)

Pathophysiology, clinical manifestations__** (MS p1564, patho p347) The exact etiology of AD is unknown. Similar to other forms of dementia, age is the most important risk factor for developing AD. However, AD is a disease that destroys brain cells, which is not a normal part of aging. Only a small percentage of people younger than 60 years old will develop AD. When AD develops in someone less than the age of 60, it is referred to as //early-onset AD//. AD that becomes evident in individuals after the age of 60 is called //late-onset AD.// Persons in whom a clear pattern of inheritance within a family is established are said to have **familial Alzheimer's disease** (FAD)(Assos. with chromosome # 14 and 21). Other cases in persons in whom no familial connection can be made are termed //sporadic//. FAD is associated with earlier onset (before 60 years of age) and more rapid disease course. In both FAD and sporadic AD, the pathogenesis of AD is similar. **__ Patho __** Characteristic findings of AD relate to changes in the brain's structure and function: (1) amyloid plaques, (3) neurofibrillary tangles, and (3) loss of connections between cells and cell death.__ 9 __ __ Fig. 60-1 __ shows the pathologic changes in AD disease. As part of aging, people develop some plaques in their brain tissue, but in AD there are more plaques in certain parts of the brain. These **__plaques consist of__** clusters of insoluble deposits of a **__protein called //b//-//amyloid//__**//,// other proteins, remnants of neurons, non-nerve cells such as microglia (cells that surround and digest damaged cells or foreign substances), and other cells, such as astrocytes. β-Amyloid is cleaved from amyloid precursor protein (APP), which is associated with the cell membrane (__ Fig. 60-2 __). The normal function of APP is unknown. In AD, plaques develop first in areas of the brain used for memory and cognitive function, including the hippocampus (a structure that is important in forming and storing short-term memories). Eventually AD attacks the cerebral cortex, especially the areas responsible for language and reasoning. **__ Neurofibrillary tangles __** are abnormal collections of twisted protein threads inside nerve cells. The main component of these structures is a protein called //tau//. Tau proteins in the CNS are involved in providing support for intracellular structure through their support of microtubules. Tau proteins hold the microtubules together like railroad ties hold railroad tracks together. In AD the tau protein is altered, and as a result, the microtubules twist together in a helical fashion (see __ Fig. 60-2 __). This ultimately forms the neurofibrillary tangles observed in the neurons of persons with AD. Plaques and neurofibrillary tangles are not unique to patients with AD or dementia. They are also found in the brains of individuals without evidence of cognitive impairment. However, they are more plentiful in the brains of individuals with AD. The third feature of AD is the **__gradual loss of connections between neurons__**. This process leads to damage and then death of the neurons. Affected parts of the brain begin to shrink in a process called brain atrophy. By the final state of AD, brain tissue has shrunk significantly (__ Fig. 60-3 __). • Forgetfulness beyond what is seen in a normal person • Short-term memory impairment, especially for new learning • Difficulty recognizing what numbers mean • Loss of initiative and interests • Decreased judgment • Geographic disorientation • Impaired ability to recognize close family or friends • Agitation • Wandering, getting lost • Loss of remote memory • Confusion • Impaired comprehension • Forgets how to do simple tasks • Apraxia • Receptive aphasia • Expressive aphasia • Insomnia • Delusions • Illusions, hallucinations • Behavioral problems • Little memory, unable to process new information • Cannot understand words • Difficulty eating, swallowing • Repetitious words or sounds • Unable to perform self-care activities • Immobility • Incontinence
 * __18. Examine the data processing deficit of Alzheimer’s Disease, specific to its etiology,
 * __ Etiology __**
 * __ Clinical Manifestations __**
 * __ Early (Mild) __**
 * __ Middle (Moderate) __**
 * __ Late(Severe) __**


 * __19. Analyze the pathologic changes associated with Alzheimer’s Disease.__**


 * See patho above **

a. Amyloid plaques(MS p1565) b. Neurogibrillary tangles (patho p347, MS p1565) c. Loss of neuron connections(MS 1565)