Gait disorder in older adults: Is it NPH - hydroassoc.org disorder in older adults: Is it NPH? The...

Gait disorder in older adults: Is it NPH?

14 The Nurse Practitioner • Vol. 36, No. 3 www.tnpj.com

n older gentleman enters a coffee shop on the up-per west side of Manhattan. He can barely lift his feet as he walks and has a wide gait with little knee

fl exion. His gait is slow and he is inattentive. He stops for a minute or so and gazes around the shop, down at the fl oor, and then back to the door he just entered. His posture is not straight. His body has a slight lean backward as he walks. He continues to walk, and as he turns his body slightly to the left, he almost loses his balance. The man’s arms look relaxed and they swing in a typical way while moving. It takes him about 10 minutes to walk from the door he entered to the counter of the coffee shop about 30 feet away. Once at the counter, he appears unsure of what to order and then orders his usual hazelnut coffee. Although his feet appear as if they are stuck

to the fl oor as he tries to walk, he manages to make it safely to a table nearby. He sits to enjoy his coffee over the next 30 minutes. Once done, it takes the gentleman about 10 minutes to exit the door and very slowly walk to his apartment, which is two doors down from the coffee shop.

The gentleman in the case study has the distinctive gait and other common signs and symptoms of possible normal pressure hydrocephalus (NPH) in older adults.

NPH is often the cause of hypokinetic gait in older adults.1 The triad of symptoms most commonly associated with NPH are a distinctive gait, cognitive impairment, and urinary continence problems.2 (See NPH triad of symptoms.)

Although the exact incidence of NPH is unknown, it is estimated that approximately 375,000 people in the United

By Cira Fraser, PhD, RN, ACNS-BC, and Sharon W. Stark, PhD, RN, APRN-BC

2.5CONTACT HOURS

A

Gait disorder in older adults:

Abstract: In normal pressure hydrocephalus (NPH), there is enlargement of the brain’s

ventricular system due to an excess of cerebrospinal fl uid. The triad of symptoms in NPH are

gait disorder, cognitive impairment, and urinary continence problems. NPs need to consider

the possibility of NPH in older adults with a hypokinetic gait.

Key words: cognitive impairment, gait disorder, hypokinetic gait, normal pressure hydrocephalus

Is it

NPH?

Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.


www.tnpj.com The Nurse Practitioner • March 2011 15

States, or 5% of the population may have NPH. The num-bers are expected to increase due to extended longevity.3 In 2005, an international study group developed and reported comprehensive guidelines for NPH.3

In NPH, there is an enlargement of the brain’s ventricular system due to an excess of cerebrospinal fl uid (CSF) thought to be related to decreased reabsorption of CSF by the arachnoid villi surrounding the exterior of the brain (see Normal fl ow of CSF). As the ventricles slowly enlarge from the accumulation of CSF, tissue compliance increases and further ventricular enlargement results.4 Subsequently, increased intracranial pressure is transient as the ventricles are able to accomodate more CSF. As the ventricles continue to enlarge, edema, and permanent changes in the shape of the ventricles may cause periventricular and vascular damage. Additionally, compres-sion of brain parenchyma and vessels and the accumulation of toxins due to slow refreshment of CSF and decreased clearance of metabolites increases CSF-fl ow obstruction and progres-sive ventriculomegaly. Signs and symptoms of NPH occur as various areas of the brain are compressed.4

The etiology of NPH is unclear. Chrysikopoulos4 states the perplexing feature of NPH is the progressive enlargement of the ventricles in the absence of mechanical obstruction of CSF, along with a normal mean intraventricular and mean intracranial pressure. NPH can be either idiopathic or secondary to head trauma, meningitis, or subarachnoid bleed. The author hypothesized that in NPH, alterations in the normal systolic-diastolic cycle of blood fl ow in the brain will disrupt the normal propulsion of CSF. Abnormal ventricular systole in the brain is thought to be caused by stiff and narrowed arteries due to atherosclerosis and hy-pertension.4 Poor circulation of CSF is proposed to result in toxic/osmotic effects that may include cellular and axonal dehydration. Chrysikopoulos4 states there is evidence linking NPH to diseases of the cerebral arteries.

Krauss et al5 investigated vascular risk factors and ar-teriosclerotic disease in NPH in older adults. The sample included 65 participants who ranged in age from 50 to 87 with a mean age of 70.8 years. Forty-six percent were men, and 54% were women. Variables examined included systemic arterial hypertension, diabetes mellitus, smoking, hyperlipid-emia, hypercholesterolemia, obesity, and cardiac, cerebrovas-cular, and other arteriosclerotic disease. A highly signifi cant association was found between NPH and systemic arterial hypertension. A positive relationship was also found between the severity of clinical symptoms of NPH and the presence of systemic arterial hypertension, especially for severe gait disturbance. Diabetes mellitus was found to be associated with NPH; however, when the variables were examined using logistic regression, only systemic arterial hypertension was found to have a signifi cant association with NPH.

Since NPH typically is most common in individuals in their sixth and seventh decades, its characteristic triad of symptoms can be easily mistaken for other conditions attrib-uted to aging, thereby delaying its diagnosis.6 The diagnosis of NPH does not require the presence of all three symptoms. The fi rst symptom to be exhibited is usually a change in gait, while cognitive and urinary changes occur later. In fact, if cognitive impairment occurs before disturbances in gait then NPH is probably not present.7,8

■ Distinctive gait of NPHNPH is a diagnostic challenge with gait impairment as the cardinal sign.9 Gait disturbance is an early sign of NPH. The distinctive gait is described as having reduced veloc-ity, diminished stride length, broad-based, and reduced foot-to-floor clearance. There is an increased foot angle, with the feet rotated outward.10 Step height is greatly diminished, giving the appearance that the person’s feet are stuck to the floor.1

Older adults with NPH tend to hesitate when initiating ambulation or turning. They are unsteady and lose their balance easily. NPH is distinguished from a similar gait in Parkinson disease by the preservation of reciprocal arm swing when walking.11 Also, a levodopa challenge may be done to differentiate between NPH and Parkinson disease. Patients with NPH will not respond to levadopa.12

Those with NPH struggle to rise from a seated position and have diffi culty initiating the fi rst steps in walking. Climb-ing stairs may be problematic, as their step height is dimin-ished and their stride length is shortened. Some patients may only present with a history of frequent falls.7,13 Individuals with NPH may also appear to lean backwards slightly when standing and ambulating and have a larger sway area than healthy individuals.14

■ Cognitive impairmentCognitive impairments in NPH can range from minimally detected to profoundly severe. Over time, cognitive impair-ments may become more generalized and more diffi cult to manage.2 In NPH, cognitive impairment typically includes inattentiveness, lack of spontaneity, and latency in recall. The processing of information tends to be slow. A fact recalled by a person with NPH is most often accurate. The answers provided to questions are frequently correct. The dementia from NPH is distinct from that noted in a person with Al-zheimer disease (AD). The individual with NPH should not have diffi culty with word formation or carrying out simple tasks that do not require concentration.13

Differentiating between cortical and subcortical defi -cits is key to distinguishing NPH from other cognitive impairments and dementias. If cognitive impairment is




the predominant symptom, it is not likely that NPH is present.7,8 Symptoms such as memory loss and aphasia are the result of a dysfunction in the cortex and are not likely to be associated with NPH.7,13 AD in conjunction with NPH is common among the elderly with hypertension.15

■ Urinary continence problemsUrinary continence issues in NPH primarily involve uri-nary urgency and frequency. These early symptoms can later progress to urinary incontinence. Urinary continence problems may include episodic or persistent urinary in-continence and frequent perception of a pressing need to void. Urinary frequency in NPH is typically more than six voiding episodes in 12 hours despite limited fl uid intake. Also nocturia more than twice in an average night is com-mon in NPH.2 Underlying medical problems, such as benign prostatic hyperplasia, bladder cancer, neurogenic bladder, and cystitis should be considered before attributing urinary symptoms to NPH. Also the use of diuretics, anticholen-ergics, and other medications may be the cause of urinary urgency and frequency.7,13

■ Additional problems associated with NPHIn addition to the triad of symptoms most often associ-ated with NPH, there are a number of additional prob-lems that may occur in NPH. Affected neuropsychologic and cognitive functions may include, but are not limited to, short-term memory, numeracy (math skills needed to cope with everyday life), abstract thought, concentration, dexterity, and writing skills. In addition, behavioral and psychiatric changes observed in NPH may include awaken-ing fl uctuations, fantastic confabulation, reduced alertness, easily fatigued, apathy, bipolar disorder, depression, and obsessive-compulsive disorder.10

■ Health history and assessmentA thorough health history and physical exam are essential to effi ciently and accurately diagnose NPH so that treatment can begin quickly. Delayed diagnosis and treatment have negative effects on the patient’s prognosis.6,16

A thorough patient history of symptom onset and progression, medical history of both the patient and the family, and past and present medications are important components of the evaluation.8,16,17 A detailed gait history should be obtained from the patient and family about the onset of walking problems and whether the gait problems had a sudden onset or a gradual decline. A gradual decline is consistent with NPH.7 Many other diseases present with similar symptoms as NPH and must be considered in the differential diagnoses. Headache, visual disturbances, and nausea may be present as a result of the increased intra-cranial pressure.8,16,17

Gait should be assessed for reduced velocity, diminished stride length, broad-based stance, and reduced foot-to-fl oor clearance. Also assess for an increased foot angle, with the feet rotated outward.10 A greatly diminished step height gives the appearance that the person’s feet are stuck to the fl oor.1 Hesitation when the individual initiates ambulation and when turning, unsteadiness, and loss of balance are consistent with NPH.11 The gait of NPH is distinguished from that of Par-kinson through observation of posturing and arm swing.11,14

A cognitive evaluation will typically reveal mild cog-nitive impairments presenting as inattentiveness, lack of spontaneity, and latency in recall.13 Although the processing of information tends to be slow, memory recall is accurate and answers to questions are mostly correct. Unlike those with Alzheimer disease, individuals with NPH can carry out simple tasks and do not experience diffi culty with word formation and understanding.7,13 Cognitive evaluation using standardized neuropsychologic evaluation tools are useful in identifying cognitive impairments and dementias.6

Urinary continence issues are identifi ed during history taking and can be further evaluated through urodynamic

NPH triad of symptoms1,2,10,11,13

Gait disturbance

• Appears before cognitive or urinary symptoms• Reduced velocity• Diminished stride length• Broad based• Reduced fl oor-to-foot clearance • Diminished step height• Increased foot angle• Feet rotated outward• Feet appear to be stuck to the fl oor• Hesitates when initiating ambulation• Hesitates when turning• Unsteady• Loses balance easily• Normal reciprocal arm swing when walking

Cognitive impairment

• Inattentiveness• Lack of spontaneity• Latency in recall• Slowed processing of information• Fact recall most often accurate• Answers provided to questions frequently correct• No diffi culty with word formation• Can carry out simple tasks

Urinary continence problems

• Perception of pressing need to void• Urinary frequency more than six voiding episodes in

12 hours • Nocturia more than twice in an average night• Episodic incontinence• Persistent incontinence (later sign)




evaluation. It is a late sign in NPH patients and patients will initially relate that they experience uri-nary urgency, frequency, and noc-turia. Other underlying medical issues and/medications need to be ruled out before attributing incontinence to NPH.2,7,13

■ Diagnostic testsStandardized neuropsychologic tests are useful for identifying cognitive impairment and to dis-tinquish subcortical from corti-cal dementias.6 There are several screening instruments useful to determine cognitive deficits in those with NPH. The Mini-Cog and Short Portable Mental Sta-tus Questionnaire are useful to identify cognitive impairment, and the Folstein Mini-Mental State Examination can identify the severity of cognitive impair-ment. Visuospatial skills and ex-ecutive function are assessed with the Clock Drawing Test.7 Finally, the Geriatric Depression Scale identifi es depression that may present as cognitive defi ciencies. These tests are helpful in determining not only whether a person is a candidate for shunting, but also how successful the shunting is when completed.6,7

Cystoscopic and urodynamic testing are useful in deter-mining stress and/or overfl ow incontinence, as well as other causes of urinary symptoms such as benign prostatic hyper-plasia, bladder cancer, neurogenic bladder, and cystitis.18,19 A urodynamic evaluation will show hyperactivity of the bladder.8

Radiographic imaging is used to support the diagnosis of NPH, as well as ruling out other causes of symptom presentation. In NPH, computed tomography (CT) scans reveal ventricular enlargement. Magnetic resonance imag-ing (MRI) results reveal signifi cantly increased CSF in the ventricles of the brain. There is also decreased CSF in the medial subarachnoid spaces when those with NPH are com-pared with those with vascular dementia or with Alzheimer disease.20 The following imaging criteria may be helpful to ascertain ideal candidates for shunt placement: ventricu-lomegaly, improvement of symptoms after CSF drainage, normal-sized or occluded sylvian fi ssures and cortical sulci, absent or moderate white matter lesions.12

In NPH, single-photon emission computed tomography (SPECT) will reveal diminished cerebral blood fl ow that is

common in NPH. Radionuclide cisternogram differentiates communicating from obstructive hydrocephalus and deter-mines CSF fl ow after radioactive material is infused into the CSF and tracer activity identifi es CSF outfl ow obstructions.6,17,19

Tests that involve lumbar puncture show the most po-tential in diagnosing NPH and also identify appropriate candidates for shunt placement. A lumbar puncture reveals normal CSF pressure and normal levels of protein, glucose, and cell counts.15 McGirt et al21 conducted a 10-year retro-spective study and found that NPH can be diagnosed accu-rately using a 3-day CSF drainage trial via spinal catheter or CSF pressure monitoring. The withdrawal of 50 mL of CSF is also used for the prognostic evaluation. There is varying specifi city and sensitivity evident in the medical literature. The removal of CSF reveals transient improvement in gait and cognition.22 A CSF infusion test involves infusion of fl uid into the lumbar subarachnoid space to determine a patient’s capacity to absorb CSF (CSF absorptive capacity) and shows improvement in symptoms. Symptom improve-ment in any of these tests indicates that ventricular shunting is an appropriate intervention (See NPH diagnostic tests).15

■ TreatmentsNPH is often treated with a ventriculoperitoneal shunt (VP Shunt) to divert excess CSF away from the brain. A ventricu-

Normal fl ow of CSF

The illustration below represents the normal fl ow of CSF from its formation from blood in the choroid plexuses until its return to the blood in the superior sagittal sinus.

Choroidal plexusfourth ventricle

Foramen of Magendie

Choroidalplexus thirdventricle

Arachnoid villiSuperiorsagittal

sinus

Subarachnoidspace

Lateral ventricle

Interventricularforamen

Pons

Source: Porth CM, Matfi n, G. Pathophysiology Concepts of Altered Health States. 8th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2009.




lar catheter is inserted into the brain, and CSF exits through a valve and is connected to a catheter that is tunneled under the skin down to the peritoneal cavity.6,8,19

Following the insertion of a VP shunt, care should in-clude positioning the individual supine 12 to 24 hours and elevating the head of the bed gradually, following the neurosurgeon’s protocol. This gradual elevation helps to prevent overshunting of CSF.23 Overshunting can result in collapse of the ventricles of the brain and cause bleeding. Acute intracranial hemorrhage is the primary risk following the insertion of a VP shunt and tends to be underreported.23 A new laparoscopic technique is being used by some neu-rosurgeons to insert the peritoneal portion of the VP shunt catheter. This new approach has a number of benefi ts when compared with the traditional approach. The length of time for surgery is shorter, less trauma for the patient, and fewer complications, especially shunt obstruction.24

Individuals with a shorter duration of NPH symptoms and the presence of gait impairment are likely to improve fol-lowing the insertion of a VP shunt.21 In a review of the litera-ture back to 1966, Klinge, Marmarou, Bergsneider, Relkin, and Black25 found that gait improvement following the insertion

of a VP shunt ranged from 30% to 95%. Improvement is not sudden, but occurs slowly over the weeks and months that follow the insertion of the shunt. Improvement will persist as long as the shunt is working properly.7

Unlike other dementias, cognitive impairment in NPH can, in some cases, be reversed. Patients with multiple medi-cal problems should be thoroughly evaluated so that success-ful reversal of NPH is not delayed. Surgical shunting provides the most benefi t when performed early in the disease pro-cess. Shprecher, Schwalb, and Kurlan15 reported that AD, in combination with NPH, is common among the elderly with hypertension. Although shunting may improve gait dysfunc-tion, severe dementia does not improve. Therefore, shunting in patients with severe dementia is discouraged.

■ Complications Shunt complication are estimated to be as follows: intrace-rebral hematoma 3%, infection 6%, seizure activity 3% to 11%, subdural hematoma 2% to 17%, and shunt malfunc-tion 20%.23 Malfunction includes obstruction and over- and underdrainage of CSF. Shunt obstruction is the most common complication and should be suspected when there is no improvement in symptoms or if symptoms recur.8,12

■ Implications for practiceNPs and other healthcare professionals are likely to recognize the symptoms of NPH in older adults and make a difference in the quality of life of older adults and their family members. Fraser and Fraser26 state that all healthcare professionals need to become familiar with the gait in NPH. The gait is the car-dinal sign of NPH. The ability to recognize the NPH gait can be sharpened by observing those recently diagnosed, those who just had a shunt inserted, or by reviewing a video of the distinctive gait.27 When a patient presents with the distinc-tive gait of NPH alone, or with cognitive impairment and/or urinary continence problems, a comprehensive history and physical exam is indicated to differentiate NPH from other diseases. Family-focused care is essential in obtaining an ac-curate history of the patient’s symptoms, behaviors, walking characteristics and pattern over time, history of falls, and activities of daily living. Family-focused care is also essential during the ongoing care of the older adult with NPH.26

Evaluation of gait, changes in cognition over time and present cognitive state, and present urinary symptoms and progression of symptoms provide important indicators for diagnosing NPH. If NPH is suspected, imaging studies should be performed to identify ventriculomegaly. If ven-triculomegaly is confi rmed, prompt referral for neurologic or neurosurgical evaluation is essential.

Following shunt placement, improvement may develop over weeks and months.7 Education provides the knowl-

NPH diagnostic tests

Neurologic

• CT scan reveals ventricular enlargement 20

• MRI reveals increased CSF in the ventricles 12

• SPECT reveals diminished cerebral blood fl ow 6, 17, 19

• Radionuclide cisternogram with radioactive tracer differentiates communicating from obstructive hydro-cephalus, CSF fl ow, and outfl ow obstructions 6, 17, 19

• Lumbar puncture reveals CSF pressure, protein, glucose, and cell counts 17

• 3-day CSF drainage trial via spinal catheter or CSF pressure monitoring reveals transient improvement in gait and cognition 21, 22

• CSF infusion test determines CSF absorptive capacity and improvement in symptoms15

Cognitive

• The Mini-Cog evaluates level of cognitive ability6, 7

• Short Portable Mental Status Questionnaire evaluates level of cognitive ability6, 7

• Folstein Mini-Mental State Examination evaluates level of cognitive ability 7

• Clock Drawing Test identifi es visuospatial skills and executive function7

• Geriatric Depression Scale identifi es depression6, 7

Urologic

• Cystoscopic and urodynamic testing determines causes of urinary symptoms 18,19

• A urodynamic evaluation identifi es bladder hyperactivity8




edge necessary for patients and families to have realistic expectations and recognize shunt complications early. They should be taught to be attentive to the return of preopera-tive symptoms, headaches, visual disturbances, fatigue, sleep diffi culties, personality changes, and paralysis and reporting them promptly to the neurosurgeon.6,7,19 The patient and family need to be aware that headache that is relieved when the person reclines may possibly be due to overshunting and should be reported promptly to the neurosurgeon. A CT scan may reveal the presence of collapsed ventricles. Infec-tion near the implanted shunt itself may result in meningitis or CSF infection that may result in peritonitis. The patient and family should be taught the general signs and symptoms of infection, as well as those for meningitis and peritonitis. Any problems or concerns should be reported immediately to the neurosurgeon. Also, the patient should receive regular follow-up care with the neurosurgeon.25

As older adults live longer, stress and burden will in-crease among families and individuals who take on the role of family caregiver for the older adult. As such burden and stress will be experienced in increasing levels, NPs can as-sist caregivers. Therefore, NPs must advocate for patients’ families and caregivers by referring them for support services through local support groups, social services, and NPH or-ganizations. Support and knowledge can improve the quality of life for both those affected by NPH and those responsible for their care. (See NPH websites and Case study of a delayed diagnosis and recovery from NPH).

Lastly, it is important that patients and families be in-formed about the treatment options and prognoses when deciding on shunting intervention. NPs have an opportu-nity to provide unbiased information about NPH signs, symptoms, diagnosis, treatment, surgical risks, benefi ts, and

prognosis and to educate patients and families so they can make educated decisions and best care for themselves and their dependent elders.

REFERENCES 1. Stolze H, Kuhtz-Buschbeck JP, Drücke H, et al. Gait analysis in idiopathic

normal pressure hydrocephalus- which parameters respond to the CSF tap test? Clin Neurophysiol. 2000;111(9):1678-1686.

2. Relkin N, Marmarou A, Klinge P, Bergsneider M, Black PM. Diagnosing idiopathic normal-pressure hydrocephalus. Neurosurg. 2005;57(3 suppl):S4-S16.

3. Marmarou A. Foreward to INPH guidelines. Neurosurg. 2005;57(3):S2:1.

4. Chrysikopoulos H. Idiopathic normal pressure hydrocephalus: Thoughts on etiology and pathophysiology. Med Hypoth. 2009;73(5):718-724.

NPH websites

Life NPH: Hope for People with Normal Pressure

Hydrocephalus

http://www.lifenph.com/

Chicago Institute of Neurosurgery and Neuroresearch

CINN NPH Program http://www.cinn.org/other/nph-home.html

Medtronic: Normal Pressure Hydrocephalus

http://www.medtronic.com/hydrocephalus/nph/index.html

National Institute of Neurological Disorders and Stroke

Normal Pressure Hydrocephalus Information Page

http://www.ninds.nih.gov/disorders/normal_pressure_ hydrocephalus/normal_pressure_hydrocephalus.htm

Hydrocephalus Association

http://www.hydroassoc.org/tag/normal-pressure- hydrocephalus/

Case study of a delayed diagnosis and

recovery from NPH26

SF was 74 when his daughter realized that he was having some new problems. SF had a 10-year history of type 2 diabetes and hypertension, but started to have a problem with his walking and frequent falls. His gait was extremely slow and his feet looked as though they were glued to the fl oor. His stance was wide-based with little knee fl exion. SF tended to lean backward a bit as he stood in place or walked. Because he had inattentiveness and the slow gait, it took him about 10 minutes to walk from one room to another in his apartment. He seemed forge tful and slower in thought, yet he was able to carry out simple tasks independently. SF had been very good with his math for most of his life and started to have diffi culty managing his checkbook. He was getting forgetful and had diffi culty tak-ing his medication properly. He had urgency, frequency, nocturia, and bladder incontinence at least once a day. His daughter was concerned about his health and took him to his long-time primary care provider every 3 months and also to a geriatric specialist. Both stated there was nothing that could be done about his recent health issues and that his dementia would gradually get worse. This went on for 4 years, but he only had mild cognitive decline during this time and continued problems with walking, occasional falls, and the urinary symptoms.

SF’s daughter felt that something could be done for her father and arranged for him to be evaluated by a multidisciplinary team. The diagnosis of NPH was made when he was 78 years old. He had a neurologic assess-ment; a CT scan revealed dilated lateral ventricles in the brain. The withdrawal of 50 mL CSF via lumbar puncture resulted in transient improvement in his gait for about 18 hours. The ventriculoperitoneal shunt insertion into the lateral ventricle on the nondominant side of his brain resulted in gradual improvement over a 1-year period. During the fi rst month, his social interactions improved and he was more attentive. He walked with a quad cane to avoid falling and received physical therapy three times a week at home for 1 month.

At 3 months, his gait was steady and he could walk slowly and safely in his apartment without a cane. At 6 months, his memory had improved. He was once again able to calculate simple math problems and manage his own checkbook. He walked at a normal pace without fall-ing. One year after surgery he was able to write better, was more attentive, and had improved memory.




5. Krauss JK, Regal JP, Vach W, Droste DW, Borremans JJ, Mergner T. Vascular risk factors and arteriosclerotic disease in idiopathic normal-pressure hydrocephalus of the elderly. Stroke. 1996;27(1):24-29.

6. Thynne K. Normal pressure hydrocephalus. J Neurosci Nurs. 2007;39(1),27-32.

7. Factora R, Luciano M. When to consider normal pressure hydrocephalus in the patient with gait disturbance. Geriatrics. 2008;63(2):32-37.

8. Gallia GL, Rigamonti D, Williams MA. The diagnosis and treatment of idiopathic normal pressure hydrocephalus. Nat Clin Pract Neurol. 2006;2(7):375-381.

9. Vanneste JA. Diagnosis and management of normal-pressure hydrocephalus. J Neurol. 2000;247(1):5-14.

10. Jones HC, Klinge PM. Hydrocephalus. 17-20th September, Hannover Germany: A conference report. Cerebrosp Fluid Resear. 2008;5:19. doi:10.1186/1743-8454-5-19.

11. Kuba H, Inamura T, Ikezaki K, et al. Gait disturbance in patients with low pressure hydrocephalus. J Clin Neurosci. 2002;9(1): 33-36.

12. Dalvi AI, Premkumar AP. Normal pressure hydrocephalus. EMedicine. 2010. http://emedicine.medscape.com/article/1150924.

13. Verrees M, Selman WR. Management of normal pressure hydrocephalus. American Family Physician. 2004;70(6):1071-1078.

14. Blomsterwall E, Svantesson U, Carlsson U, Tullberg M, Wikkelsö C. Postural disturbance in patients with normal pressure hydrocephalus. Acta Neurol Scand. 2000;102(5):284-291.

15. Shprecher D, Schwalb J, Kurlan R. Normal pressure hydrocephalus: Diagnosis and treatment. Curr Neurol Neurosci Rep. 2008;8(5):371-376.

16. Siedlecki SL. Normal pressure hydrocephalus: Are you missing the signs? J Gerontol Nurs. 2008;34(2):27-33.

17. Wilson JA, Islam O. Normal pressure hydrocephalus. 2004. http://www.emedicine.com/radio/topic479.htm.

18. Bejjani GK, Hammer MD. Normal-pressure hydrocephalus. Another treatable dementia. Part I. Contemp Neurosurg. 2005;27(1):2-4.

19. Johnson M, Graham K. Diagnosis and surgical treatment of normal-pressure hydrocephalus. J AAPA. 2010;23(5):51-56.

20. Kitagaki H, Mori E, Ishii K, Yamaji S, Hirono N, Imamura T. CSF spaces in idiopathic normal pressure hydrocephalus: Morphology and volumetry. AJNR Am J Neuroradiol. 1998;19(7):1277-1284.

21. McGirt MJ, Woodworth G, Coon AL, Thomas G, Williams MA, Rigamonti D. Diagnosis, treatment, and analysis of long-term outcomes in idiopathic normal-pressure hydrocephalus. Neurosurgery. 2005;57(4):699-705.

22. Marmarou A, Bergsneider M, Klinge P, Relkin N, Black PM. The value of supplemental prognostic tests for the preoperative assessment of idiopathic normal-pressure hydrocephalus. Neurosurgery. 2005;57(3 suppl):S17-S28.

23. Bergsneider M, Black PM, Klinge P, Marmarou A, Relkin N. Surgical management of idiopathic normal-pressure hydrocephalus. Neurosurgery. 2005; 57(3 suppl):S29-S39.

24. Li B, Zhang Q, Liu J, Yu H, Hu S. Clinical application of a laparoscope in ventri-peritoneal shunting. Minim Invasive Ther Allied Technol. 2007;16(6):367-369.

25. Klinge P, Marmarou A, Bergsneider M, Relkin N, Black P. Outcome of shunting in idiopathic normal-pressure hydrocephalus and the value of outcome assessment in shunted patients. Neurosurgery. 2005;57(3 Suppl):S40-S52.

26. Fraser JJ, Fraser C. Gait disorder is the cardinal sign of normal pressure hydrocephalus: A case study. J Neurosci Nurs. 2007;39(3):132-134, 192.

27. Life NPH: Hope for people with normal pressure hydrocephalus. 2010. http://www.lifenph.com.

The authors have disclosed that they have no fi nancial relationships related to this article.

Cira Fraser is an associate professor and graduate faculty and Sharon W. Stark is associate dean and graduate faculty at Marjorie K. Unterberg School of Nursing and Health Studies, Monmouth University, West Long Branch, New Jersey, N.J.

DOI-10.1097/01.NPR.0000393969.13812.2e

DISCOUNTS and CUSTOMER SERVICE

• Send two or more tests in any nursing journal published by Lippincott Williams & Wilkins together and deduct $0.95 from the price of each test.• We also offer CE accounts for hospitals and other healthcare facilities on nursingcenter.com. Call 1-800-787-8985 for details. PROVIDER ACCREDITATION

Lippincott Williams & Wilkins, publisher of The Nurse Practitioner journal, will award 2.5 contact hours for this continuing nursing education activity. Lippincott Williams & Wilkins is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. This activity is also provider approved by the California Board of Registered Nursing, Provider Number CEP 11749 for 2.5 contact hours. Lippincott Williams & Wilkins is also an approved provider of continuing nursing education by the District of Columbia and Florida #FBN2454. Your certifi cate is valid in all states. The ANCC’s accreditation status of Lippincott Williams & Wilkins Department of Continuing Education refers only to its continuing nursing educational activities and does not imply Commission on Accreditation approval or endorsement of any commercial product.

TEST INSTRUCTIONS

• To take the test online, go to our secure website at http://www.nursingcenter.com/ce/NP.• On the print form, record your answers in the test answer section of the CE enrollment form on page 21. Each question has only one correct answer. You may make copies of these forms.• Complete the registration information and course evaluation. Mail the completed form and registration fee of $24.95 to: Lippincott Williams & Wilkins, CE Group, 2710 Yorktowne Blvd., Brick, NJ 08723. We will mail your certifi cate in 4 to 6 weeks. For faster service, include a fax number and we will fax your certifi cate within 2 business days of receiving your enrollment form.• You will receive your CE certifi cate of earned contact hours and an answer key to review your results.There is no minimum passing grade.• Registration deadline is March 31, 2013.

INSTRUCTIONSGait disorder in older adults: Is it NPH?

For more than 80 additional continuing education articles related to

Advanced Practice Nursing topics, go to NursingCenter.com/CE.

Earn CE credit online: Go to http://www.nursingcenter.com/CE/NP and

receive a certifi cate within minutes.


Gait disorder in older adults: Is it NPH - hydroassoc.org disorder in older adults: Is it NPH? The...

Documents

Transcript of Gait disorder in older adults: Is it NPH - hydroassoc.org disorder in older adults: Is it NPH? The...