NURS519PP.ppt

Hi!

Please find attached our post!

Tammy, Merissa and Heather

Hi,

His mental status is flat and depressed. He has had numerous psych evaluations with no real insight. I am not sure if the depression came before or after his weakness and dysfunction. His TSH is normal. Thanks for the great ideas!

Thanks, Megan

• Can arise from primary tumors of spinal cord or metastatic disease
• Intramedullary tumors: arise within the cord
• Extramedullary-intradural: develop within the dural layers; examples - astrocytoma, meningioma
• Metastases is classified as:
  
• Intramedullary: within spinal
• Leptomeningeal: within lining of spinal cord
• Epidural: outside the lining of the spinal cord

• Compression of the epidural venous plexus is an early occurence of SCC
• Compression of venous plexus or direct mechanical injury cause:

1. Edema to the cord
2. Decreased capillary blood flow

• The effects of edema & decreased blood flow cause: ischemia, conduction block, & demyelination of (mostly) white matter.
• There is evidence that the compression of neural tissue releases serotonin, prostaglandin, and vascular endothelial growth factor (VEGF)which in turn cause neurochemical changes resulting in further tissue damage and neurological changes.
• 70% of SCC occur at the level of the thoracic spine
• 1/3 patients will have multple sites
  
• The manifestations of SCC depend on the level of lesion on spinal cord and the extent of compression

• Initial symptom BACK PAIN, accompanied/followed by MOTOR weakness, and DECREASED SENSATION, further progression results in:
• loss of PROPRIOCEPTION, VIBRATORY SENSE, BOWEL AND BLADDER function

• 95% of patients with SCC present with BACK PAIN
• 1/3 of these patients can have significant compression with a normal neurological exam
• the presenting back pain is usually located within one or two verebrae of the compression site, but remember can occur at multiple sites
• Impending cord compression can be present from a few days to months.
• Pain similar to degenerative disease or herniated disk
• Pain Elicited with: movement, valsalva, cough, straight leg raise or neck flexion.
• PAIN INCREASES WHEN LYING FLAT (due to venous congestion and edema)
• Patients more comfortable with upright positioning
  
• RADICULOPATHY: very common to see in SCC
• Caused by tumor irritaion of the nerve roots and the pain then follows the distribution of the nerve root
• EXAMPLES:
• Cervical and Lumbosacral compression: usually unilateral pain that can radiate to a limb. Radicular pain is most commonly associated with these sites.
  
• Thoracic compression: associated with bilateral pain and patients will often describe "constrictive-band-like" pain.
• MOTOR WEAKNESS:
• usually described as HEAVINESS or STIFFNESS
• involves PROXIMAL MUSCLES
• patients state:***DIFFICULT TO GET UP FROM CHAIR or CLIMB STAIRS
• test musle strength by watching patient get up from chair, walk a few steps and push extremety against resisting force
• muscle tone: check for spasticity and elasticity

• with Cervical compression: tendon reflexes may by hyperactive
• with Thoracic & lumbosacral compression: reflexes may be decreased or absent
• SENSORY CHANGES
• less common than motor weakness
• can see parasthesia & numbness
• sensory loss usually ascends from toes to level of compression
• with a cauda equina lesion, sensory loss involves the perianal area, lateral or posterior thighs and is usually bilateral (follows dermatome).
• progression of compression: loss of proprioception, loss of position sense and vibration, loss of temperature sense and deep pressure
• loss of vibration - posterior spinocerebellar pathwy
• loss of pain and temperature - spinal thalmic pathway, lateral colum, white matter
  
• deep tendon reflexes: decreased at level of lesion; hyperactive below level of lesion
• AUTONOMIC CHANGES
• disruption of lower motor neuron function
• bowel and bladder function (incontenince or retention)
• poor sphincter tone - poor prognosis
  
• late sign of cord compression
• usually not ambulatory, often paraplegia results
  

• Uremic neuropathy is a mixed motor and sensory polyneuropathy that is distal, symmetrical, and has greater lower limb than upper limb invovlement. It is a progressive and insidious disease.
• It is estimated to be present in some degree in 60-100% of patients on dialysis. It is associated with glomerular filtration rates less than 12 ml/min.
  
• Attributed to toxins that are not usually dialyzed out, even with regular hemo or peritoneal dialysis. Essentially, metabolic failure at the distal parts of the nerves leads to distal axonal degeneration.
• Researchers don't know exactly how the toxins usually filtered out by healthy kidneys are neurotoxic. It may be that certain toxins disable the axonal Na+/K+ pumps, thus iterrupting Ca+ release and nerve excitability (Krishnan & Keirnan, 2007)
• Another theory is that neurotoxic compounds deplete the energy supplies by inhibiting nerve fibre enzymes that are required to maintain energy production (Pan, 2006).
  
• Uremic neuropathy is complicated by the fact that potassium (K+) builds up in between dialysis periods. This puts the nerves into a chronically depolarized state and leads to nerve dysfunction. So, the patient may see some improvement in his condition immediately post-dialysis when K+ levels are normalized. It can also be complicated by diabetes.
  
• The most prevalent clinical features have to do with large fibre involvement so we see symptoms like parasthesias, muscle wasting, weakness and impaired reflexes. There might also be autonomic symtpoms such as hypotension, impaired sweating, diarrhea, impotence and constipation (Krishnan & Kerinan, 2007).
  

• Renal transplantation has shown to almost cure the neuropathy
• Erythropoietin (EPO) can improve nerve conduction. There are EPO receptors present on Schwann cells and in dorsal root ganglions. With axonal injury, EPO receptors are up-regulated and then giving EPO can reduce limb weakness and pain (Krishnan & Keirnan, 2007).
• As mentioned previously, TCA's, anticonvulsants, a lidocaine patch, or gapabentin can be used to help control symptoms (Pan, 2006).
  

Thank you for your enlightening post!

I have a patient that has been a bit of a mystery to my coworker’s and I. He is about 80, and has a history of HTN, DM and renal failure. He complains of general weakness, heavy legs and appears to have a lack of motivation. When his creatinine is elevated he has trouble walking; which can be described as a Parkinson’s shuffle. Generally speaking the nursing staff and his physician find him difficult and frustrating. Most likely due to our doctor’s inability to provide him with a diagnosis and a cure, as well as, the nursing staffs inability to improve his quality of life. Peripheral neuropathy could possibly be contributing to this patient’s status. His symptoms seem to come and go, he has poor balance, and finds it harder and harder to walk. It seems progressive and debilitating at times.

“Peripheral neuropathy isn't a single disease, but rather a symptom with many potential causes. For that reason it can be difficult to diagnose” (Mayo Foundation, 2009). After a NP or Doctor completes a thorough history and physical Mayo Foundation (2009) suggests the following tests: “level of vitamin B-12, a urinalysis, thyroid function tests and, often, electromyography — a test that measures the electrical discharges produced in your muscles” and possibly a nerve conduction study “which measures how quickly your nerves carry electrical signals” (Mayo Foundation, 2009). After diagnosis, there are several treatment options: pain relievers, anti-seizure medications (ex: gabapentin for nerve pain), lidocaine patch (to relieve pain at site), and antidepressants (ex: amitriptyline interferes with chemical processes in your brain and spine that cause people to feel pain) (Mayo Foundation, 2009).

Reference

Mayo Foundation for Medical Education and Research. (2009). Peripheral Neuropathy. Retrieved January 30, 2009 from http://www.mayoclinic.com/health/peripheral-neuropathy

CVA.doc

Hi Everyone,

Please find attached our posting in response to this question.

...I tried to cut and paste, but the figure wouldn't paste into moodle.

Enjoy.

Tammy, Merissa and Heather

Hi Shelley,

Thanks for sharing the FAST accronym and the stroke protocol in place at your hospital.  It sounds like everyone from EMS, lab, and diagnostic imaging have worked together to try to optimize diagnosis and treatment for stroke victims.

Heather

The previous posts on educating our patients on the symptoms of stroke were very well done and I would just like to add a few things.

Symptom recognition and the believing of the symptoms is the most difficult thing for most people.  Admitting there might be something wrong I think delays treatment.  My friend's husband was recently diagnosed with hypertension and high cholesterol and he has a significant family history of stroke.  Being that she is a nurse she made up post it notes to stick in the bathroom, computer room, and by the phone for her husband and son to use as reminders of what they need to be aware of, it is the FAST pneumonic and it is as follows:

F facial weakness

A arm weakness

S speech difficulties or inablility to smile

T time to call 911

I think this a simple tool we could use to educate our patients on the classic signs of stroke in the hopes of getting them to ER quicker.

In terms of treatment, our hospital has a stroke protocol in place and if EMS has a pt with a suspected stroke they radio ahead and stroke alert is paged overhead in the hospital.  This alerts departments like CT (they are to ensure a table is free at the time of the page until the patient is CT'd).  The lab is present on patient on arrival as well as the doctor.  TPA is in the room ready to go.  This is effective alot of times but for obvious reasons, if the time factor is not sufficient (4 hours) or if it is a hemorrage type of stroke the medication is not given but surgical options are discussed much quicker. 

Shelley

Thank you Janice, Megan, and Sarah for your information and insight regarding early stroke intervention and treatment.  In the U.S., Primary Stroke Centers are designated facilities that have received credentialing and recognition by following recommended guidelines for timely stroke intervention and treatment (American Stroke Association, 2008). 

Among the criteria that Primary Stroke Centers must meet include the following:  24 hour access to CT/MRI and a physician to interpret results; onsite access to neurosurgery; rapid results of lab tests; a written t-PA protocol; established care pathways for stroke assessment and management; an acute stroke team on site; a stroke unit on site; and trained ER staff in acute stroke assessment and treatment (Vega, 2008). 

The Canadian Stroke Network and the Heart and Stroke Foundation of Canada (2006) have created The Canadian Stroke Strategy:  Canadian Best Practice Recommendations for Stroke Care 2006 which is a document outlining best practice recommendations.  The document includes recommendations for stroke prevention and education, acute stroke management, stroke rehabilitation, and community reintegration.  As mentioned in previous postings, enhancing education regarding stroke with the general population as well as with health care professionals and creating evidence based policies and procedures are crucial in decreasing the burden of stroke. 

Heather

References:

American Stroke Association (2008).  Certified primary stroke centers.  Retrieved online January 30, 2009 from http://www.strokeassociation.org/presenter.jhtml?identifier=3030093

The Canadian Stroke Network and the Heart and Stroke Foundation of Canada (2006).  The Canadian stroke strategy:  Canadian best practice recommendations for stroke care 2006.  Retrieved online January 30, 2009 from

http://www.strokecenter.org/prof/CSSManualENG_WEB_Sept07.pdf

Vega, J. (2008).  Primary stroke centers provide superior care for stroke patients.  Retrieved online January 30, 2009 from

http://stroke.about.com/od/caregiverresources/a/StrokeUnit.htm

Prevention and education is key. NP’s must complete thorough history and physical exams while encouraging changes toward a healthy lifestyle. NP’s must provide patients’s with the tools to help themselves overcome unhealthy lifestyles like smoking, alcohol abuse, high cholesterol, and excessive weight. As noted by Group B, intensive post stroke rehab can improve a stroke survivor’s functional and cognitive status, but dose not undo damage already sustained to the brain.

Rehabilitation commences within 24 hours of the patient’s diagnosis (National Institute, 2009). “The types and degrees of disability that follow a stroke depend upon which area of the brain is damaged. Generally, stroke can cause five types of disabilities: paralysis or problems controlling movement; sensory disturbances including pain; problems using or understanding language; problems with thinking and memory; and emotional disturbances” (National Institute, 2009). Rehabilitation begins with turning patients regularly and encouraging patients to complete ADL’s. Of course, a patient who has sustained a stroke requires a multidisciplinary approach to their rehabilitation. Depending on the deficits that the patient sustained, this involves nurses, physicians, rehabilitation nurses; physical, occupational, recreational, speech-language, and vocational therapists; and mental health professionals (National Institute, 2009). Also, I think that it is important to note that rehab may promote a feeling of hope for our patients. As healthcare professionals we have to remember how devastating the effects of a stroke can be. Our stroke patients are going through immense, devastating loss. They may also want to speak with their spiritual leader to find hope and reasoning.

Reference

National Institute of Neurological Disorders and Stroke. (2009). Stroke Rehabilitation. Retrieved January 30, 2009 from http://www.ninds.nih.gov/disorders/stroke/poststrokerehab.htm

Hello All,

Group B, you have done a great job of explaining the different types of strokes, the illustrations really helped to put things into better light. Responding to your question I agree with comments that others have made but I really think there needs to be more education placed around the issue of strokes .Intense efforts   need to take place in order to educate the public and health care professionals that stroke is an emergency and that acute stroke symptoms should be treated with the same urgency as a gunshot wound to the head.

When I worked ER we still followed the three hour window so it is good to see that research has been done and the treatment time expanded to 4 1/2 hours. My experience is that people sit home too long waiting for the symptoms to pass. Once they reach ER they need to have many tests done prior to treatment. Rapid treatment with “clot-busting agents,” such as tissue plasminogen activator (tPA) has reduced the effects of CVA in some individuals, but initial screening to rule out hemorrhage or other contraindications for anticoagulant drugs is essential. Surgical intervention may be possible to relieve carotid artery obstruction. (Gould, 2006)

The term stroke is generally used specifically to mean cerebral infarction. An older, still frequently used, term is cerebrovascular accident (CVA). However, this term is no longer defensible scientifically, because the underlying pathology is usually well established or easily identifiable or both. As a result, the processes by which many pathologic disorders (e.g., hypertension) lead to stroke are predictable, reproducible, and even modifiable. Therefore the occurrence of stroke is not an "accident" in any sense of the word.(Price,2003)

 As you stated TPA continues to be the standard of care for acute stroke within the first three hours after symptom onset (National Institutes of Health [NIH], 1995). However, only 1% to 2% of patients currently receive therapy, usually because they present to emergency care too late to be treated within the recommended 3-hour time window. The greatest risk of using thrombolytic treatment is intracerebral hemorrhage. Therefore the therapy must be used only on patients who have been carefully screened and who meet criteria.

Janice

                                         Reference

 Gould, B., (2006). Pathophysiology for the Health Profession (3^rd ed). Philadelphia: Elsevier Inc.

Price, S, A.,(2003) Pathophysiology: Clinical Concepts of Disease Processes(6th ed),Mosby

Hi group B,

I just wanted to comment on your question about what NP’s can do about improving stroke care and why so many people don’t get appropriate treatment. I’m focusing on the hyperacute stroke stage… there’s a lot more to talk about in terms of the acute hospitalization, rehab, and prevention stages as well so hopefully other class members will address these areas. I just wanted to add a little sidenote too: the Heart and Stroke Foundations’ most recent guidelines suggest that patients with disabling ischemic stroke have a treatment window (with tPA) that is up to 4.5 hours. That’s increased from the previous three hour window (Lindsay, Bayley, Hellings, Hill, Woodbury & Phillips, 2008).

The two major roles I see for NP’s include advocating and educating.

ADVOCATE

There are not enough neurosurgical services in our province and almost none available in the LIHN where I live. As it turns out, we send a lot of our patients to other centers, out of province or even across the border to the USA for neurosurgical consultation and intervention. This is valuable penumbra time…

EDUCATE

The Canadian best practices for stroke care were updated in 2008 by the Heart and Stroke Foundation (HSF) and Canadian Stroke Strategy (CSS). These suggest that all members of the public should know what a stroke looks like and that it is absolutely a medical emergency. I wonder if it is part of provincial educational curriculum? It is also vital to educate our patients and families with risk factors such as hypertension, high lipids, coronary artery disease, diabetes and smoking habits.

In terms of why so many people don’t get treatment, I didn’t really know… so I did some research. I started by talking to my husband. He is very much outside of health care so he qualifies as a lay person. I asked him to tell me about the top five signs of a stroke and what to do if you thought someone was having one. He said that a person having a stroke would have symptoms such as “lightheadedness, headache and shortness of breath.” Oooops, 2 out of 5 is not so bad but he’s young and educated and has seen the commercials so I’m not sure where he missed the bus. I often find it difficult as a medical professional to remember that other people don’t know information that we consider as so basic.

The more formal research indicates some barriers to people receiving treatment. There are numerous reasons including:

• Poor patient education- its rushed
• Physician’s perceived risk of legal liability from negative patient outcomes (Bambauer, Johnston, Bambauer & Zivin, 2006).
• Patient or family not recognizing signs of acute stroke or not seeking urgent help
• Patient or family called general practitioner first (rather than 911)
• There were delays in neuroimaging and laboratory services
  
• Difficulties in obtaining consent for thrombolysis
• Uncertainty about delivering thrombolytic meds- I see this one in my own unit. Its always a huge deal to give tPA and there is a lot of waxing and waning about it (Kwan, Hand & Sandercock, 2004)
• Co-morbidites and contraindications to receiving thrombolysis
• Rural and underserviced areas

References

Bambaueer, K.Z., Johnston, S.C., Bambauer, D.E., & Zivin, J.A. (2006). Reasons why few patients with acute stroke receive tissue plasminogen activator. Archives of Neurology 63: 661-664.

Kwan, J., Hand, P., & Sandercock, P. (2004). A systematic review of barriers to delivery of thrombolysis for acute stroke. Age and Ageing, 33: 116-121.

Lindsay, P., Bayley, M., Hellings, C., Hill, M., Woodbury, E., & Philips, S. (2008). Canadian best practice recommendations for stroke care (updated 2008). Canadian Medical Association Journal, 179(12): S1-S25.

Group_E_Neurologic_case_study_1.ppt

Hello All,

Please   see  attached pp.

Thanks group E

Hi Shelley,

Interesting story and good question, I have to wonder if the wife knew....

I think this really drives home the moral of not assuming anything...you know what they say about assuming...

Thanks a bunch,

Tammy

Absolutely, testing blood sugar should be a first line assessment when anyone has a change in LOC.

Thanks,

Tammy

Janice

Another thing I have seen is make sure you do a drug screen before you diagnosis someone with stroke.  I was involved with a case where a physician who had received a kidney transplant a few years ago had become uncompliant with his treatment, he was in a funk lets just say.  He presented to ER with weakness drooling and semiconsciousness, the ER doc diagnosed him with stroke ( he had one prior) and his wife made him CTC.  Well after a few hours he seemed to improve and it wasn't until days later when he was on the ward he admitted to taking an attempted overdose of his benzodiazepines no one bothered to do a CT or drug screen partly because of his presentation and that his wife said he wouldn't want anything heroic done because he was tired of being sick.  Did she know?  I'm not sure,  but just something else to consider.

Moral of the story is don't jump to conclusions with your diagnosis, do all appropriate testing first regardless of the story.

Shelley

Thanks Tammy,

Great information the other thing i learned the hard way as an ER nurse was that you should always ''check a clients sugar first''before you try to dx them with a stroke.

Janice

Hi,

Thanks so much for all the great information.  Everything is so thorough; it is difficult to find other things to add!

Nevertheless, I just wanted to share my thoughts about subdural hematomas and their presentation.  As an ER nurse, I have learned to always suspect a subdural hematoma when patients come in (usually accompanied by a family member who has insisted they come to the hospital) with any of the signs and symptoms you have described in your PP.  I have heard family members say things like, “he just isn’t himself” or “he has never been confused before.”  Once we perform a thorough history, we find out that he fell or bumped his head at some time during the previous week to several weeks. 

Karnath (2004) speaks to an example where a subdural hematoma occurred in a woman (68-years-old), who fell on her buttocks in the weeks prior to presentation.  She did not sustain any injury to here head, but she was on anticoagulants for atrial fibrillation.  This is a very salient example of recognizing the potential causes of a subdural hematoma.  Sometimes, it’s not so obvious.

Subdural hematoma can be confused with several other diagnoses, including Alzheimer’s dementia, stroke, TIA, normal pressure hydrocephalus and intracranial neoplasm (Karnath, 2004).  Differentiating between them is summed up as follows:

Alzheimer’s Dementia: Confusion and altered mental state progresses over months to     

years as opposed to subdural hematoma which progresses over days to weeks.

Stroke:                        Symptoms usually occur within hours.

Neoplasms:                 Difficult to differentiate.  Neuroimaging is diagnostic (MRI    

preferably).

Normal Pressure Hydrocephalus:  Urinary incontinence is usually a late sign of normal

pressure hydrocephalus; but usually not present in subdural hematoma.  Difficult to differentiate, neuroimaging is diagnostic (Karnath, 2004).

 I hope this is helpful.

Tammy

Karnath, B. (2004, July). Subdural hematoma: presentation and management in older

adults. Geriatrics, (59)7. 18-23.

Thanks for the information on post concussion syndrome, I experienced this after falling while trying to race my son on skates (not the brightest thing I have done).  I was diagnosed with concussion and was sent home.  I experienced headaches and transient dizziness for 2 weeks after.  Thankfully I work in an Intensive Care with neurosurgeons who I can access as I had never heard of this prior to myself experiencing it and they had explained it to me but it was nice to have the information again. 

Shelley

Hi Dianne and everyone,

Thank you for the great summary on concussion and TBI.  I appreciated the visuals, and especially the quiz. 

Here is some information on Post Concussion Syndrome.

•  Post Concussion Syndrome  is a complex disorder in which concussion symptoms (headaches and dizziness)  can last from week to months; up to 15 % of people have symptoms for >1 year

• Prevalence: Between 30-80% of people with mild to moderate brain injury will also experience at least some of the symptoms of post-concussion syndrome

• Symptoms: headaches (tension/migraine or mixed), dizziness, fatigue, irritability, anxiety, insomnia, loss of concentration and memory, noise and light sensitivity, behavioral or emotional changes (family may notice that the person has become more irritable, argumentative, stubborn, opinionated or suspicious)

• Causes: structural damage or disrupted neurotransmitter systems d/t impact.  Psychological factors: b/c the most common symptoms of post concussion syndrome (headache, dizziness, sleep problems) are often experienced by people who have been diagnosed with depression, anxiety, or PTSD.

• Risk Factors: risk increase with age, greater prevalence in women (attributed to women been more likely to seek treatment), occurs more often following, MVC, falls, or assaults, less likely following sports related injuries (attributed to athletes concealing injury so as to not be removed from play)

• Test & Diagnosis:  no definitive test, MRI more sensitive than CT (MRI can detect brain abnormalities in about 30% of people who have had a normal CT);  profound dizziness: ENT referral; psychologist/psychiatrist  if symptoms include anxiety or depression

Thanks, Erica

Post Concussion Syndrome (2008). Mayo Foundation for Medical Education and Research. Retrieved February 1, 2009 from http://www.mayoclinic.com/health/post-concussion-syndrome/DS01020

                    Group D You have submitted a great overview on concussions and brain injury. I have two teenage boys who both play rep hockey. The younger one had a bike accident a few years back and ended up with a mild diffuse axonal injury; he recovered well but continues to have headaches often. We are nervous when he plays hockey and he has had a concussion or two in the past.

It's funny because most people think that a concussion is often benign event, but, in reality, it can have significant life-long sequelae. Patients with a history of head injury and a GCS score of 15 are frequently under diagnosed (Price, 2003). Concussion should be   suspected when the mechanism of injury involves a blow to the head, acceleration-deceleration injury or a shaking incident, which are common following a sports or playground injury.

Thanks Jan

                                                  Reference

Price, S, A.,(2003) Pathophysiology: Clinical Concepts of Disease Processes(6th ed),ST.Louise,Missourie

Unit 4

What is a stroke and what can cause a stroke?

A stroke is defined as “the rapidly developing loss of brain functions due to a disturbance in the blood vessels supplying blood to the brain” (Wikipedia, 2009). This is caused by thrombosis or embolism or hemorrhage causing ischemia. The “affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech or inability to see one side of the visual field” (Wikipedia, 2009). The signs and symptoms of a stroke are dizziness, vision changes, weakness, trouble speaking and headache. “Typically, a clot forms in a small blood vessel within the brain that has been previously narrowed due to a variety of risk factors including: high blood pressure (hypertension), high cholesterol, diabetes and smoking” (MedicineNet, Inc., 2009).

Approximately 80% of stokes are ischemic, which means a blood clot is interrupting blood flow to the brain; thrombotic or embolic (Heart and Stroke Foundation, 2009). The build up of plaque (fatty materials, calcium and scar tissue) causes artery narrowing and hardening referred to as atherosclerosis. A piece of this plaque can break off and clog the artery. Thrombotic stokes are caused by a blood clot that forms in an artery directly leading to the brain (Heart and Stroke Foundation, 2009). On the other hand, embolic strokes are caused by clots that develop somewhere in the body and then travel through the blood stream to the brain (Heart and Stroke Foundation). For example, “a blood clot might originally form in the heart chamber as a result of an irregular heart rhythm, such as occurs in atrial fibrillation. Usually, these clots remain attached to the inner lining of the heart, but occasionally they can break off, travel through the blood stream, form a plug (embolism) in a brain artery, and cause a stroke” (MedicineNet, Inc., 2009).

The other 20% of strokes are hemorrhagic, which means “they are caused by uncontrolled bleeding in the brain” (Heart and Stroke Foundation, 2009). This interrupts normal blood flow in the brain resulting in dead brain cells. There are two main types of hemorrhagic stroke: subarachnoid hemorrhage and intracerebral hemorrhage. Subarachnoid hemorrhage is defined as uncontrolled bleeding on the surface of the brain, in the area between the brain and the skull (Heart and Stroke Foundation, 2009). Intracerebral hemorrhage occurs when an artery deep within the brain ruptures (Heart and Stroke Foundation, 2009). These can be caused by an aneurysm or ateriovenous malformation (Heart and Stroke Foundation, 2009). An aneurysm is defined as a weakened area in the blood vessel wall that fills with blood and bulges, which can be ruptured by high blood pressure or trauma causing uncontrolled bleeding in the brain (Heart and Stroke Foundation, 2009). An ateriovenous malformation is a “malformation of the brains blood vessels usually present at birth, that causes the artery walls to be weak and increases the risk of hemorrhagic stroke” (Heart and Stroke Foundation, 2009).

There is also a “mini-stroke” called a TIA or transient ischemic attack. This is defined as a temporary interruption of blood flow to the brain. The symptoms are similar to an ischemic stroke, although they resolve within 24 hours. A “TIA is an important warning sign that puts you at increased risk of a full-blown stroke” (Heart and Stroke Foundation, 2009). The cause of a TIA is plaque build up (atherosclerosis) or a blood clot formed in another part of the body that traveled to the brain (Heart and Stroke Foundation, 2009). Risk Factors for a TIA are: atherosclerosis, atrial fibrillation, problems with heart valves, foramen ovale, and a weakened heart muscle (Heart and Stroke Foundation, 2009).

Risk Factors

Family history

Increasing Age

Gender

Obesity

Diet

Diabetes

Smoking

High blood pressure

High cholesterol

Hear disease atrial fibrillation

Excessive alcohol consumption

Physical inactivity

Stress

History of previous stroke or TIA

Illicit drug use (cocaine or amphetamines)

Reference

Heart and Stroke Foundation. (2009). Stroke. Retrieved January 26, 2009 from

http://www.heartandstroke.com/site/c.ikIQLcMWJtE/b.3484151/k.A50E/Ischemic_stroke.htm

MedicineNet, Inc.(2009). Stroke. Retrieved January 27, 2009 from

http://www.medicinenet.com/stroke/page2.htm

Wikipedia. (2009). Stroke. Retrieved January 26, 2009 from

http://en.wikipedia.org/wiki/Stroke

What types of neuropathy are there and how do they differ?

Neuropathies can be classified into three different types:

1. Generalized symmetric polyneuropathies- These are characterized by the symmetric involvement of sensory, motor, or autonomic fibers. This type further divides into:

a) Distal axonal polyneuropathy which is the generalized peripheral neuropathy that we most commonly see. It involves the longest nerve in the body, those going to the feet. Sensory impairment with this type is greater than the motor impairment. Symptoms include burning pain, tingling, and numbness of the feet. The small nerve fiber damage causes decreased pain and temperature sensation and the large nerve fiber damage causes decrease light touch, vibration, and position sense. The most common causes of this type of neuropathy are diabetes and alcohol abuse, and occasionally neurotoxic therapeutic agents. Another group of distal axonal polyneuropathy’s is autonomic neuropathy. This group can involve virtually any sympathetic or parasympathetic nerve fiber. These neuropathies have a progressive course and are usually reversible.

b) Demelinating polyneuropathy occurs less frequently and affects the myelin or Schwann cells. Weakness is the predominant symptom with less sensory impairment. This group involves acute and chronic inflammatory neuropathies in which Guillain-Barre syndrome is the most widely recognized.

2. Generalized neuropathies- In this type the cell body of only one type of peripheral neuron are affected. In sensory neuropathies, the dorsal root ganglion cell is affected which produces numbness that may begin in a focal or asymmetric distribution or in a distal symmetric pattern. These are often seen in leprosy, some industrial solvent poisonings, some hereditary disorders, and chloramphenicol toxicity. In motor neuropathies, the anterior horn is affected which causes weakness that may be symmetric or asymmetric. They are caused by anterior horn cell diseases, such as amyotrophic lateral sclerosis (ALS) or paralytic poliomyelitis.

3. Focal or multifocal neuropathies - In this type, sensory and motor fibers are affected in one or more nerves. The most common are compression neuropathies such as carpal tunnel syndrome (median nerve compression), ulnar nerve compression (at the elbow) peroneal nerve compression, or sciatic nerve compression. They can involve one or more cranial nerves. Plexus injuries and radiculopathies also fall into this category.

In demylinating neuropathies the axon is spared and only the myelin degenerates. In axonal degeneration neuropathies, distal degeneration of the axon occurs first followed by degeneration of the myelin and the axis cylinder. One or more nerves may be involved in neuropathy.

When the axons are affected, muscle strength, muscle tone, and muscle bulk are also affected. Muscles of the feet are affected first and more severely because they are long large axons. The tone and deep tendon reflexes in the affected muscles are generally decreased in a neuropathy. Atrophy, fasciculation, mild fatigue, paralysis of limbs, trunk and neck may occur. Tenderness of the nerve trunks distinguish neuropathy from amyotrophy.

Neuropathies associated with autonomic disturbances are diabetes, alcoholism, nutritional, amyloidosis, porphyria, Guillain-Barre syndrome, Riley-Day syndrome, and familial sensory neuropathy. In chronic polyneuropathies, the feet, hands and spine become deformed.

Reference

McCance, K., Huether, S. (2006). Pathophysiology: The Biologic Basis for Disease in Adults and Children. Elsevier Mosby: St Louis Missouri.

Excellent presentation.  I used to work in a nursing home and cared for many patients who had strokes.  It was before I started nursing and I wihs I had more information because I think it would have helped me care for patients better. 

I find there is a lot more information available to the public now and strokes, there is a commercial in Ontario (I’m not sure about across Canada) for the signs and symptoms of a stroke. 

This made me think since the rate for stroke hospitalizations in 2004–2005 (127 per 100,000 population) was about 23% lower than five years before (Canadian Institute for Health Information, 2006). 

Do you think the lower rates of strokes is because people are more informed of the signs and symptoms and that has caused them to be more aware? Or because people have changed their lifestyles and risk factors for strokes?

Merissa

Reference

Hello All,

Group A, great overview of strokes. When I think of the risk factors associated with stroke I always go back to the ''family Dr''and feel that they play a large role in client education and really having a good look at all the co-morbidities there client has and treated them for same.ie high b/p, increased cholesterol, uncontrolled diabetes etc..I am sure it is difficult keeping up on the recent literature like hypertension guidelines, these are changing more frequently. As Np's I am certain that you will have more time to spend with clients especially in a supporting and educating role, perhaps as more NP's emerge the incidence of stroke will decrease. We can hope.

Janice

D_E_M_E_N_T_I_A.ppt

Hello

Happy reading,

Erica

Alzheimer’s disease can have a genetic component. Familial Autosomal Dominant Alzheimer’s Disease (FAD) is a rare form of Alzheimer’s disease that represents approximately 5-10% of all Alzheimer’s cases (Alzheimer’s Society of Canada, 2005). This form of the disease often has an early onset. FAD is a dominant trait associated with genetic mutations on chromosomes 1, 14 and 21 (National Institute of Aging, 2008). This means that if a parent develops this type of Alzheimer’s their children have a 50% chance of inheriting the disease gene.

References:

Alzheimer’s Society of Canada (2005). Genetics and Alzheimer’s disease. Retrieved January 31^st 2009 from: http://www.alzheimer.ca/english/care/ethics-genetictest.htm

National Institute of Aging (2008). Alzheimer’s disease genetic fact sheet. Retrieved January 31^st 2009

from:http://www.nia.nih.gov/nia.nih.gov/Templates/ADEARCommon/ADEARCommonPage.aspx?NRMODE=Published&NRNODEGUID=%7b3C4B634E-A2D8-4415-927F-4B79BEC47EA6%7d&NRORIGINALURL=%2fAlzheimers%2fPublications%2fgeneticsfs%2ehtm&NRCACHEHINT=Guest#gene

Great overview of dementias and alzheimers. I have to say that the more info I have on this the better, as kids don't often have this as a diagnosis

This will be especially great for studying and helped me to wrap my head around the different physiology of these diseases.

Did you happen to come across any stats regarding the genetic link for any of these diseases? If a immediate family member has one how likely are you to develop it?

Tanya

Unit4Neuro.docx

See Attached.

Melanie, Michele and Sarah

Thank you Group C for your posting on dementia and Alzheimer’s. 

Regarding Mr. C’s case, it is interesting to note the established link between diabetes and the development of vascular dementia and Alzheimer’s.  A recently published study found that “people with type 2 diabetes had moderately elevated risk for lacunes, hippocampal atrophy, and deep white matter lesions which supports the notion that the increased risk of cognitive decline and dementia in people with diabetes is probably due to dual pathological processes involving both cerebrovascular damage and neurgenerative changes” (Xu et al., 2009, p. 75).  Other related pathophysiological mechanisms of diabetes likely contributing to an increased risk of dementia include glycemia, insulin resistance, and inflammatory cytokines (Xu et al, 2009).  In the case study, it is reported that Mr. C’s blood sugars have been ‘out of control.’  Rasgon & Jarvik (2004) reported that poor glucose control may contribute to apoptosis and the formation of neurofibillary tangles, the lesions present in Alzheimer’s disease.  Mr. C’s diabetes, therefore, may be a contributing factor to his cognitive changes.

Heather

References:

Rasgon, N., & Jarvik, L. (2004).  Insulin resistance, affective disorders, and Alzheimer’s disease:  Review and hypothesis.  The Journal of Gerontology, 59A (2). 178-183.  Retrieved January 28, 2009 from ProQuest Nursing & Allied Health Source database.

Xu., W., Qui, C., Gatz, M., Pedersen, N., Johansson, B., & Fratiglioni, L. (2009).  Mid-and late – life diabetes in relation to the risk of dementia:  A population-based twin study.  Diabetes, 58 (1), 71-77.  Retrieved January 28, 2009 from ProQuest Nursing & Allied Health Source database.

Great presentation Group C. I really like the chart comparing dementia and Alzheimers. I am a chart person!

When I was reading through Mr. C's issues this week the idea of brain mets from his colorectal cancer struck me as well, so I am happy you discussed the possibilty. Although it may not be at the top of the diagnostic list, I think that it definately is something that should be considered as a differential diagnosis.

I looked into this a little and did find a pretty good article about brain metastases and colorectal cancer. Here are a few highlights:

Metastatic brain tumors from colorectal cancer are rare, with a reported incidence of anywhere from 1.9% - 3.5%. The prognosis for people with resectable brain metastases is poor. Generally brain metastases are reported in patients with colorectal cancer in association with metastases to other organs, such as the liver and lungs. Mr. C did report being diagnosed with liver metastases. Since brain metastases are rare from colorectal cancer, this article stated there are not a lot of reports on this available in the literature. It seems from this article that surgery is the best option, with no real statistical difference seen in the patients in a study quoted by the Mayo Clinic (n=150) who received surgery alone, or had surgery and radiation treatment.

Cante, D., Girelli, G., La Porta, M.R., Sciacero, P., La Sala, S., & Ozzello, F. (2005). Late brain metastases from colorectal cancer: A case report and review of the literature. Tumori, 91, 280-282.

Thanks

Tanya

Thanks for the BBC story Jack. Autism spectrum disorders are definately a hot topic lately, and many more children are being diagnosed with this. I found a good article entitled Identification and Evaluation of Children with Autism Spectrum Disorders from the American Academy of Pediatrics. The article is written for primary care pediatricians but is very applicable for a pediatric NP interested in working in the community.

Here is the link:

http://www.aap.org/pressroom/issuekitfiles/IDandEvaluationofChildrenwithASD.pdf

Tanya

This week we will be looking at the Neurology System. It is a lot to pack into a week, but contains some important and frequently occurring presentations. For the unit discussions over this week:

Recall Mr. C. from the last unit. You haven't seen Mr. C. for some time: it has been 3 years since his colorectal cancer was "cured." At his appointment you find out he was discharged from hospital about 6 weeks ago. He had had a stroke and still has slight weakness on the left side. Mr. C.'s wife has come in with him because she is concerned his memory is not as it was before the stroke. He forgets where he puts things and forgets appointments. En route he will forget where they are going. Sometimes he is suspicious of her. Mrs. C. wants to know if his memory problems are due to his stroke. She also wants to know if his now-constant numbness of his feet is due to the stroke. Upon further review you find out that Mr. C. is now on medication for diabetes because his "sugars" have been "out of control." You also find out that Mr. C.'s cancer has "returned" and he may require further intervention for liver metastases.

There is a lot of pathophysiology involved in this case. For now, focus on the central and peripheral neurologic system, as you answer the following questions:

• What is a stroke and what can cause a stroke? You should identify 2 types of strokes and, from there, determine the common causes of each type. (Case 1 Group A)

• Is stroke damage reversible? (Case 1 Group B)

• Do you think Mr. C.'s memory problems are stroke related? If so, how would the pathophysiology be different for Alzheimer dementia? (Case 1 Group C)

• What other types of dementia are there? Do they have the same pathophysiology as Alzheimer dementia? (Case 1 Group D)

• Could Mr. C.'s foot numbness be related to his stroke? What other causes could there be for this pattern of numbness? (From the last unit, remember his history of alcohol intake, Type 2 diabetes and colorectal cancer.) (Case 1 Group E)

• What types of neuropathy are there and how do they differ? (Case 2 Group A)

• What is a radiculopathy and how would it present differently from a neuropathy? (Case 2 Group B)

• Mr. C. states that he had a least one seizure while in hospital. He wants to know why this happened and what happened in his brain to cause this. (Again, remember Mr. C.'s history with respect to common causes of seizures.) (Case 2 Group C)

• Finally, Mr. C. says that while in hospital he fell and hit his head on the floor. He was told he had a head injury. He doesn't remember any loss of consciousness but did have double/blurred vision for 1-2 hours after and a couple days of dizziness and nausea. What is the pathophysiology behind concussion/head injury? (Case 2 Group D)

• Given Mr. C.'s age (70) and multiple medical conditions, you wonder if he could have a subdural hematoma. Why would he now, when it is weeks after the head injury? (Case 2 Group E)

I will update the unit Cmaps and add some resources and PowerPoints. I look forward to a compelling week!

Jack