Find information on thousands of medical conditions and prescription drugs.

Progressive multifocal leukoencephalopathy

more...

Home
Diseases
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Arthritis
Arthritis
Bubonic plague
Hypokalemia
Pachydermoperiostosis
Pachygyria
Pacman syndrome
Paget's disease of bone
Paget's disease of the...
Palmoplantar Keratoderma
Pancreas divisum
Pancreatic cancer
Panhypopituitarism
Panic disorder
Panniculitis
Panophobia
Panthophobia
Papilledema
Paraganglioma
Paramyotonia congenita
Paraphilia
Paraplegia
Parapsoriasis
Parasitophobia
Parkinson's disease
Parkinson's disease
Parkinsonism
Paroxysmal nocturnal...
Patau syndrome
Patent ductus arteriosus
Pathophobia
Patterson...
Pediculosis
Pelizaeus-Merzbacher disease
Pelvic inflammatory disease
Pelvic lipomatosis
Pemphigus
Pemphigus
Pemphigus
Pendred syndrome
Periarteritis nodosa
Perinatal infections
Periodontal disease
Peripartum cardiomyopathy
Peripheral neuropathy
Peritonitis
Periventricular leukomalacia
Pernicious anemia
Perniosis
Persistent sexual arousal...
Pertussis
Pes planus
Peutz-Jeghers syndrome
Peyronie disease
Pfeiffer syndrome
Pharmacophobia
Phenylketonuria
Pheochromocytoma
Photosensitive epilepsy
Pica (disorder)
Pickardt syndrome
Pili multigemini
Pilonidal cyst
Pinta
PIRA
Pityriasis lichenoides...
Pityriasis lichenoides et...
Pityriasis rubra pilaris
Placental abruption
Pleural effusion
Pleurisy
Pleuritis
Plummer-Vinson syndrome
Pneumoconiosis
Pneumocystis jiroveci...
Pneumocystosis
Pneumonia, eosinophilic
Pneumothorax
POEMS syndrome
Poland syndrome
Poliomyelitis
Polyarteritis nodosa
Polyarthritis
Polychondritis
Polycystic kidney disease
Polycystic ovarian syndrome
Polycythemia vera
Polydactyly
Polymyalgia rheumatica
Polymyositis
Polyostotic fibrous...
Pompe's disease
Popliteal pterygium syndrome
Porencephaly
Porphyria
Porphyria cutanea tarda
Portal hypertension
Portal vein thrombosis
Post Polio syndrome
Post-traumatic stress...
Postural hypotension
Potophobia
Poxviridae disease
Prader-Willi syndrome
Precocious puberty
Preeclampsia
Premature aging
Premenstrual dysphoric...
Presbycusis
Primary biliary cirrhosis
Primary ciliary dyskinesia
Primary hyperparathyroidism
Primary lateral sclerosis
Primary progressive aphasia
Primary pulmonary...
Primary sclerosing...
Prinzmetal's variant angina
Proconvertin deficiency,...
Proctitis
Progeria
Progressive external...
Progressive multifocal...
Progressive supranuclear...
Prostatitis
Protein S deficiency
Protein-energy malnutrition
Proteus syndrome
Prune belly syndrome
Pseudocholinesterase...
Pseudogout
Pseudohermaphroditism
Pseudohypoparathyroidism
Pseudomyxoma peritonei
Pseudotumor cerebri
Pseudovaginal...
Pseudoxanthoma elasticum
Psittacosis
Psoriasis
Psychogenic polydipsia
Psychophysiologic Disorders
Pterygium
Ptosis
Pubic lice
Puerperal fever
Pulmonary alveolar...
Pulmonary hypertension
Pulmonary sequestration
Pulmonary valve stenosis
Pulmonic stenosis
Pure red cell aplasia
Purpura
Purpura, Schoenlein-Henoch
Purpura, thrombotic...
Pyelonephritis
Pyoderma gangrenosum
Pyomyositis
Pyrexiophobia
Pyrophobia
Pyropoikilocytosis
Pyrosis
Pyruvate kinase deficiency
Uveitis
Q
R
S
T
U
V
W
X
Y
Z
Medicines

Progressive multifocal leukoencephalopathy (PML), also known as progressive multifocal leukoencephalitis, is a rare and usually fatal viral disease that is characterized by progressive damage (-pathy) or inflammation (-itis) of the white matter (leuko-) of the brain (-encephalo-) at multiple locations (multifocal). It occurs almost exclusively in people with severe immune deficiency, e.g. transplant patients on immunosuppressive medications, or AIDS patients.

Cause and epidemiology

The cause of PML is a type of polyomavirus called the JC virus (JCV), after the initials of the patient in whom it was first discovered. The virus is widespread, found in at least 70 percent of the general population by some estimates, but usually remains latent, causing disease only when the immune system has been severely weakened.

About five percent of AIDS patients develop PML. It is unclear why PML occurs more frequently in AIDS than in other immunosuppressive conditions; some research suggests that the effects of HIV on brain tissue, or on JCV itself, make JCV more likely to become active in the brain and increase its damaging inflammatory effects (Berger, 2003).

Disease process

PML is a demyelinating disease, in which the myelin sheath covering the axons of nerve cells is gradually destroyed, impairing the transmission of nerve impulses. It affects the white matter, which is mostly composed of axons in the outermost parts of the brain (cortex). Symptoms include weakness or paralysis, vision loss, impaired speech, and cognitive deterioration. PML is similar to another demyelinating disease, multiple sclerosis, but since it destroys the cells that produce myelin (unlike MS, in which myelin itself is attacked but can be replaced), it progresses much more quickly. Most patients die within four months of onset.

Diagnosis

PML is diagnosed by testing for JC virus DNA in cerebrospinal fluid or in a brain biopsy specimen. Characteristic evidence of the damage caused by PML in the brain can also be detected on MRI images.

Treatment

There is no known cure. In some cases, the disease slows or stops if the patient's immune system improves; some AIDS patients with PML have been able to survive for several years, with the advent of highly active antiretroviral therapy (HAART).

AIDS patients who start HAART after being diagnosed with PML tend to have a slightly longer survival time than patients who were already on HAART and then develop PML (Wyen et al., 2004). A rare complication of effective HAART is immune reconstitution inflammatory syndrome (IRIS), in which increased immune system activity actually increases the damage caused by the infection; though IRIS is often manageable with other types of infections, it is extremely dangerous if it occurs in PML (Vendrely et al., 2005).

Read more at Wikipedia.org


[List your site here Free!]


Progressive multifocal leukoencephalopathy in a patient with AIDS
From PT Magazine, 2/1/99 by Drench, Meredith E

AIDS can have a number of complications resulting from secondary opportunistic infections of the CNS, with devastating effects on function.

OBJECTIVES

After reading "Progressive Multifocal Leukoencephalopathy in a Patient with AIDS," you should be able to:

List some of the neurological complications associated with acquired immune deficiency syndrome (AIDS).

Describe the pathology of AIDS-related progressive multifocal leukoencephalopathy (PML).

Describe elements of a comprehensive rehabilitation program for a patient with specific impairments associated with AIDS-related PML.

Describe the global psychosocial stressors of AIDS-related disability and those particularly unique to PML.

Discuss what aspects should be included in patient and caregiver education for a patient with PML.

Discuss the prognosis for patients with AIDS-related PML and how physical therapy can help improve quality of life.

On successful completion of the examination (page 70), .2 CEUs (=2 contact hours) and a certificate of completion will be awarded. Fee is $15 for APTA members, $21 for nonmembers. You can access CE articles and CEU tests online. For more information, visit http://www.apta.org/ceu.

This CE offering is written by Meredith E Drench, PhD, PT, Director of Adaptive Health Associates Inc, East Greenwich, RI. She is author of Red Ribbons Are Not Enough: Health Care,givers' Stories About AIDS and a contributing author to Issues in HIV Rehabilitation, a publication of the HIV Special Interest Group of APTA's Oncology Section. Acquired DS) results from ' ciency syndrome (AIDS) results from an infection caused by human immunodeficiency virus (HIV), which is aA retrovirus. Like viruses such as those that cause rubella, influenza, and polio, retroviruses have ribonucleic acid (RNA)- rather than deoxyribonucleic acid (DNA--as their genetic material. What makes retroviruses unique is their ability to use the enzyme reverse transcriptase to make DNA from viralencoded RNA. The HIV attacks white blood cells, taking over the production of DNA and RNA, so that when the white blood cells produce, the HIV's DNA is produced, thereby resulting in the reproduction of the retrovirus rather than the white blood cells1Retrovirus production increases, then, with a conconitant reduction in white blood cells2 In a healthy immune system, macrophages engulf and eliminate microorganisms; antigens stimulate B cells that divide and become plasma cells, which in turn produce antibodies that can identify the original stimulating antigen; T cells suppress or stimulate other parts of the immune response; and suppressor, or cytotoxic, T cells destroy infected cells, preventing microorganisms from multiplying and spreading. T-helper cells-lymphocytes that are one type of T cell-generally are stimulated by the antigen on the surface of macrophages. These T-helper cells function as "command central," coordinating the work of suppressor-cytotoxic cells, macrophages, and B cells.'

Although HIV invades many types of cells, including macrophages, B cells, and central nervous system (CNS) cells, it most commonly infects the T-helper cells. In addition, in patients with AIDS, some B cells do a faulty job, resulting in the production of antibodies at the wrong time, the production of fewer antibodies than necessary, or a lack of response to new antibodies. The HIV dramatically compromises the immune svstem, then, by severely depleting the cells that play a primary role in coordinating the system's activity. The assault on these white blood cells is a terrible irony: The HIV attacks and debilitates the very cells responsible for its control or elimination. AIDS-Defining Illnesses

When the T-helper cell count is depleted, the body's defense against infectionswhich can be protozoan, fungal, yeast, bacterial, or viral-is weakened.3 Opportunities exist for microorganisms to establish a foothold and affect all systems of the body. These "opportunistic infections" are considered to be AIDSdefining illnesses. A protozoa causes Pneumocystis carinii pneumonia, the yeast-like fungi Cryptococcus causes a systemic infection, and the yeast Candida causes thrush. Bacterial infections may include those caused by Streptococcus pneumoniae and Hemophilus influenzae, which can result in pneumonia, and Mycobacterium avium-intracellulare, which results in a tuberculoid illness that can affect the lungs, the liver, the bone marrow, and the gastrointestinal tract. Cytomegalovirus, Epstein-Barr virus, herpes simplex virus I and II, and hepatitis B virus cause common AIDS-defining viral infections. Malignancies such as B-cell lymphomas and Kaposi sarcomas also may arise.

Neurological disorders. HIV-associated neurologic diseases are both primary (caused directly by the effects of HIV on the neuraxis) and secondary (resulting from HIV-induced immunosuppression).5 7 Primary illnesses include AIDS dementia complex (HIV encephalopathy), myelopathy, distal sensory polyneuropathy, and myopathy.68-10 Secondary CNS opportunistic infections include cerebral toxoplasmosis, primary CNS lymphoma, progressive multifocal leukoencephalopathy (PML), cytomegalovirus infection, and cryptococcal meningitis.' Neurologic disorders also may be caused by significant abnormalities of AIDS-associated cellular immunity, primary and metastatic neoplasms, drug toxicity, metabolic and nutritional imbalances, and cerebrovascular problems .A8I

Neurologic complications of HIV infection can be debilitating and often are associated with a high mortality rate. Some sources have reported that between 40% and 70% of all people with HIV infection develop neurologic disorders8,12,15; others have reported that the incidence of neurologic disorders discovered at autopsy is between 80% and 90%.16-21' Neurologic complications can involve any part of the neuraxis at any level of the CNS and peripheral nervous system.5 The range of these diseases is large, varied, and expanding. HIV-related neurologic complications may be the first sign of AIDS in 10% to 20% of patients..12-14

Cognitive changes and headaches are early symptoms of CNS disease. Impaired memory, problems with concentration, and changes in mental status may signal AIDS dementia complex.'o

In continuing education, attention typically is given to the primary illnesses related to HIV and AIDS; however, the manifestations and implications of secondary CNS opportunistic infections also have an important impact on rehabilitation. This article focuses on the hypothetical case example of a patient diagnosed with one such infection. A composite picture drawn from actual patient histories, the case of Ms D highlights clinical decision making in the physical therapist management of specific AIDS-related neurologic impairments and functional limitations.

EXAMINATION History and Systems Review

Following a 5-day stay at a local hospital, Ms D is transferred to an inpatient rehabilitation facility. On her first day at the facility, a physiatrist refers her to a physical therapist for examination, evaluation, and intervention for increasing left-sided weakness, incoordination, and visual disturbance. In accordance with facility policy. physical therapy begins the day following referral.

A marketing consultant for a large computer company, Ms D is a 31-year-old woman who lives with her 8-year-old daughter and 6-year-old son. Her marriage recently ended in divorce after years of domestic violence. As the physical therapist learns from the medical record, Ms D had good health, did not smoke or take medications, and walked with her children every day after work as a form of family exercise. Then her world suddenly began to change.

After having a seizure at work, Ms D was admitted to the hospital. A computerized tomography (CT) scan revealed multiple hypodense, nonenhancing white matter lesions that involved demyelination of the cerebral hemispheres (particularly the parieto-occipital area) and the cerebellum, find- ings that were suggestive of PML. A neurologist determined that the brain stem, graywhite matter border, and cortical gray matter were not yet involved.22,24

Cerebrospinal fluid analysis was normal for Ms D. Blood tests were positive for HIV but were other vise unremarkable. Her CD4 cell count was 195/mm^ sup 3^, congruent with the clinical category for AIDS-defining conditions of less than 200/mm^ sup 3^ in adults, as set by the Centers for Disease Control and Prevention.25

Magnetic resonance imaging (MRI) showed PML lesions more clearly. They were greater in number on T^ sub 2^-weighted spin-echo MR images.26,27 However, although MRI is the radiologic diagnostic tool of choice for PML, definitive diagnosis typically is made through pathological specimens obtained by stereotactic brain biopsy.28

PML is a demyelinating disease of the CNS and is caused by a neurotropic papovavirus, JC virus (JCV).22,29 JCV seropositivity normally exists in a majority of adults and seems to be "reactivated" in the immunocompromised population.30With its multiple areas of whitematter demyelination, PML may be directly caused by reactivation of the dormant JCV in the brain or indirectly when the virus travels to the CNS from other infected organs. Once rarely seen, PML today has a greater incidence that is associated with the immunodeficiency of HIV infection-the most common predisposing factor to PML.22,31- 34 It has been estimated that 4% to 5% of people with AIDS develop PML; in 29% of these patients, PML is the first manifestation of AIDS.3s The DNA of JCV has been discovered in peripheral blood lymphocytes in 70% to 90% of patients who have been diagnosed with AIDS and PML.36-40 Image-guided stereotactic brain biopsy showed that Ms D had foci of whitematter demyelination in addition to some eosinophilic inclusions in oligodendrocytes and abnormal giant astrocytes. JCV-like virions were nucleus inclusions and were also found in the cytoplasm of the oligodendrocytes, detected by electron microscopy.28,41 The diagnosis of PML therefore was confirmed by histopathologic examination, with the expectation that over a period of several weeks, repeat CT scans and MRI will show the rapid progression in size and number of lesions that is typical in PML.42

The interview. A seizure was identified as Ms D's presenting symptom of PML. PML is thought to be a possible cause of new-onset seizures in patients with HIV.43,44 In the case of Ms D, PML was identified as the AIDS-defining illness. During the initial physical therapy visit, she reports that, in retrospect, she had noticed clumsiness in her left hand and temporary episodes of double vision when working on the computer and occasional stumbling after catching her left foot on carpeting, gravel, and scatter rugs for as many as 3 weeks prior to the seizure. Ms D also reports that when she was tired, she was not speaking clearly and had to repeat herself. She had dismissed these symptoms, attributing them to stress. (The therapist notes that her dominant right hand and foot seem to be unaffected.) Physical impairments had appeared, therefore, before Ms D learned of her HIV seropositivity.

Ms D is the sole breadwinner for her children. She reports that after the divorce, her former husband "died from a stroke, which I just found out was AIDS-related...and left nothing for the children." After rehabilitation, she says, she plans to return home to her children-and to eventually return to work. Supportive parents live in the same town and help take care of her children; four sisters and one brother live out of state but are in frequent telephone contact with her.

College-educated (she holds a master's degree), Ms D has only a limited knowledge of AIDS. She tells the physical therapist, "I just thought that AIDS was a disease you died from," although she recently read that people with AIDS were living longer. She is relieved to have learned that with its increased survival rate, AIDS has been classified as a chronic rather than a terminal disease.45 The therapist notes, however, that Ms D does not seem to understand the anticipated outcome of PML.

Ms D reports that she requires help in self-care because of spasticity and incoordination. She also is disturbed by her fatigue. The result of both physical factors and psychological factors such as stress and depression, fatigue is one of the most common symptoms of AIDS and one of the most common obstacles to rehabilitation for people with AIDS.46

Ms D's current pharmacological regimen includes dilantin for seizures, cytosine arabinoside (intravenous cytarabine, known as Ara-C) for PML,47-49 and high doses of zidovudine (formerly azidothymidine, or AZT) for HIV infection.so-50-54

As the physical therapist considers the medical history and Ms D's interview responses, he knows that it will be critical for him to form a partnership with her-to manage the "whole patient." He will need to take into account her values, attitudes, beliefs, and preferences. The goal of this "therapeutic alliance" will be to (1) help educate Ms D about the PML disease process, seizures, and AIDS, especially as they relate to function, and (2) engage her in open communication about the physical therapist management of her condition, her expectations about outcomes, and her role in the therapeutic process.55 This partnership, which should facilitate dialogue and therapeutic adherence,56 is inherent in the five elements of patient/client management by physical therapists examination, evaluation, diagnosis, prognosis, and intervention-as put forth by APTA's Guide to Physical Therapist Practice (the Guide).57

The results of the therapist's systems review are essentially unremarkable for physiological and anatomic status of the cardiopulmonary, integumentary, and musculoskeletal areas. An overview of the neuromuscular system, however, reveals left-sided weakness with spasticity, incoordination, and difficulty with gait and functional activities. Ms D has double vision and dysarthric but intelligible speech. According to the Guide, Ms D's problems belong to neuromuscular pattern C, impaired motor function and sensory integrity associated with progressive disorders of the CNS in adulthood.57 Tests and Measures

As many as one third of patients with AIDS who are referred for rehabilitation may have impairments secondary to CNS disorders.58 Early diagnosis and medical therapy may prolong life*; the physical therapist believes that early physical therapy may enhance the quality of that life. Because multiple neurologic disorders may coexist and patients may have atypical patterns of symptoms,5 careful examination and evaluation are essential.

In this case, the physical therapist decides to use the HIV Evaluation Form59 to help assess impairments and functional limitations. Designed for the rehabilitation setting, this form includes items for strength, range of motion, coordination, spasticity, sensation, endurance, and cognition and items for activities of daily living (ADL), such as hygiene, dressing, food preparation, and ability to use transportation. The therapist uses the form in identifying specific HIV-related neuromuscular deficits, level of functional abilities, and the need for assistive devices. First, however, the therapist uses the Guide tests and measures categories to organize the examination findings:

Aerobic capacity and endurance. The physical therapist determines that Ms D's baseline heart rate is 80 bpm and that her baseline blood pressure is 130/80. These values are slightly elevated but are still considered to be within the "normal" range. Arousal, attention, and cognition. Ms D reports that she is occasionally forgetful and says that is unusual for her. She is oriented to person, place, and time.

Sensory integrity and reflex integrity Sensation to light touch, pinprick, and proprioception is intact. The physical therapist notes hyperreflexia in both lower extremities, greater in the left than in the right, with a positive Babinski sign and a 4- to 5-beat clonus on the left. Diplopia is evident.

Motor function. There are moderate deficits in finger-to-nose and rapid alternating movement testing in the left upper extremity, and severe deficits in heel-to-shin and rapid toe-tapping tests in the left lower extremity.

Range of motion and muscle performance. The physical therapist notes that passive range of motion, using inhibitory techniques to help minimize the effect of spasticity on joint 60is within functional limits. According to the results of manual muscle testing as described by Kendall et al,61 muscle strength is 4/5 in the right upper and lower extremities. Strength is not tested in the left extremities due to spasticity. A left footdrop is present.

Gait, locomotion, and balance. Sitting balance is good without support. Ms D is able to transfer from the sitting position to the standing position independently. Standing balance, with and without the Rhomberg test, requires minimal assistance of the physical therapist's hand for steadying support. Because footdrop is present, the therapist decides not to use such tests as tandem walking and walking on toes and heels. Ms D's gait has a slow cadence, and she has left hip external rotation and abduction and hip hiking that affects left leg clearance through the swing phase of gait. There is left forefoot and toe drag. The physical therapist determines that Ms D lacks left ankle dorsiflexion and is unable to attain left heel strike.

Ms D is able to walk 10 feet on a level surface with minimal assistance for support. As the therapist expects, her chief reason for stopping is fatigue.

Self-care and home management. Ms D scores 91 points on the Functional Independence Measure (FIM),62 indicating modified dependence in self-care, transfers, walking, communication, and social cognition. She is completely independent in bowel and bladder management. Environmental, home, and work barriers. Before Ms D was transferred to the rehabilitation facility, Ms D's father had been asked to photograph her home so that an analysis could be done and recommendations could be made.

The entire living space is on one level. Two steps with a right-sided railing are at the main entrance. Doorways are sufficiently wide for wheelchair access, and the master bathroom has a stall shower with a door. Scatter rugs are in several rooms, and there is thick carpeting in the living room. Given the anticipated course of PML, the therapist decides not to consider work barriers.

In addition to using the above tests and measures, the physical therapist decides to measure Ms D's perceptions of her condition. He chooses the General Health SelfAssessment,63 a self-administered modular questionnaire of quality of life that was used in a clinical trial to measure quality of life for patients with HIV. Reliability and construct and discriminant validity were established for the following domains: physical, psychological, role/social functioning, health care utilization, and symptom distress.63 However, the physical therapist keeps in mind that validation of this instrument is clearest for patients who were enrolled in a particular clinical trial and for patients with early HIV infection-and that the instrument therefore may have limitations when used to measure Ms D's perceptions.

Ms D's responses on the questionnaire indicate that she has a low quality-of-life rating, which the therapist judges to be unsurprising, considering her recent hospitalization and symptoms. EVALUATION, DIAGNOSIS, AND PROGNOSIS

According to the physical therapist's examination findings as recorded on the HIV Evaluation Form, Ms D has evolving visual, speech, motor, and mental dysfunction, which is typical of PML.5,6 Visual disturbances, which can include cortical blindness, may be secondary to field loss, oculomotor disorders, or visual agnosias; for Ms D, they take the form of diplopia. She also demonstrates progressive left hemiparesis, some right-sided weakness, ataxia, disdiadokinesia, gait abnormalities, and dysarthria. Aphasia, however, is not present with left-sided weakness and bilateral cerebral damage.

Ms D's cognitive impairments include changes in memory but not in judgment, reasoning, language, calculations, attention, and reading, which can be concomitant problems.5,31 Although the initial manifestation of PML was a seizure, Ms D reports no vertigo, altered sensation, or headaches. Personality changes have not been observed by the physical therapist, other health care professionals, or family members, with the exception of occasional lability.

The survival rate is increasing for people with HIV and AIDS,45 resulting in a greater number of referrals to rehabilitation to assess, manage-and, when possible, prevent-impairments, functional limitations, and disability. However, opportunistic diseases tend to diminish the survival rates of patients with HIV, independent of the CD4 cell count.64 In AIDS-associated PML, symptoms progress over weeks, and patients have a median survival of 2 to 6 months.31,35.54,65 Although PML usually is a fatal neurological disease, survival has exceeded 1 year in 8% to 10% of patients, and spontaneous improvement and recovery have been reported.31,66 Factors that may reduce the likelihood of improvement include a diagnosis of PML as the AIDSdefining illness, CD4 counts of less than 200 cells/mm3, contrast enhancement on MRI, and histopathological inflammatory infiltrates.3l67,68, Unfortunately, all of these factors apply to Ms D.

Functional status and physical disability are important to quality of life,69 and the physical therapist believes that he can work with Ms D to maximize her outcomes within the constraints of her prognosis. Discharge to home is both the patient's goal and the therapist's plan.

Based on the prognosis, the broad goals of rehabilitation for Ms D include:

To enhance her sense of well-being and her quality of life.

To minimize her disability and dependence and maximize her independent function.

To promote her adherence to the therapeutic regimen.

Anticipated goals are to increase strength and endurance, improve standing and walking balance, decrease spasticity, enhance self-care, conserve energy, and achieve safe and independent home and community mobility. Therapeutic goals and interventions must be established carefully, with the realization that the course of PML usually includes progressively diminished function and independence. Special attention must be paid to planning for and ordering equipment.

A Team Approach to the Plan of Care

A comprehensive interdisciplinary team approach will be critical in the case of Ms D. A speech and language pathologist will manage Ms D's dysarthria to improve her communication. A neuropsychologist will evaluate and manage attention, concentration, visual spatial deficits, and higher cognitive function.46 Occupational therapy M ill be directed toward improving ADL and instrumental ADL skills, and, as changes in patient status necessitate, fabrication of a splint.

To facilitate Ms D's adjustment to disability and the disease process, a social worker will provide patient and family counseling. It is estimated that by the year 2000, the number of children who lose their mothers to AIDS may reach as many as 82,000.46 Ms D's children will need special psychological support as they deal not only with their mother's AIDS but with specific problems related to her PML. In addition, Ms D will need counseling to help her develop custody plans, because the children's father has predeceased her. (Fortunately, the children's HIV test results have been negative.)

To promote the healing process, all team members will need to engage in a continuing dialogue with Ms D about psychosocial issues.'70,71, Confidentiality is essential for all patients and especially for those with the diagnosis of HIV/AIDS. Societal bias can become apparent among family and friends, coworkers, and community members.

The AIDS "Roller Coaster"

Many disease processes have a linear progression, whereas AIDS often is characterized by a roller-coaster effect, with ups and downs in strength and function. PML also may have fluctuations; however, a generally deteriorating course with a poor life expectancy is typical.

Clinicians often deliberate over how much information to share with patients. Fearing an adverse reaction, some may censor details. Others may walk a tightrope between being "problem-centered" and "person-centered." How much information does Ms D need to make rational decisions? How much information would negatively affect her participation in the rehabilitation process? Ms D has a limited knowledge of AIDS. She only recently learned about increased survival rates, the shifting paradigm of AIDS from terminal to chronic status, and the death of her ex-husband from an AIDS-related stroke. She seems to be unaware of-or unable to grasp-the anticipated outcome of PML. Although some patients with PML have had improvement and spontaneous remissions, that is not the typical course. Should the physical therapist discuss this "better news/bad news" balanced scenario with Ms D?

In collaboration with other team members, the physical therapist further assesses Ms D's understanding of her condition, how much she wants to know, and how much information will be useful to her. He carefully applies the therapeutic skills of listening, probing, reflective communication, and empathy. Asking open-ended questions, he explores Ms D's world, helps clarify her message, and probes for more information. The team determines that although Ms D has not fully grasped the probable course of PML, the AIDS-related death of her former husband has given her reason to fear for her life. She is desperately concerned with the welfare of her children, who, she says, "might become orphans because of their lousy father."

Now that the physical therapist knows more about Ms D's understanding of her condition, he is better prepared to help Ms D accomplish her goals within the parameters of her diagnosis. His evaluation of the examination findings indicates that Ms D may benefit from traditional rehabilitation interventions, such as the use of assistive devices and orthoses, instruction in work simplification and energy conservation, moderate strengthening exercises, and gait training.58,72,76 He considers the use of treatment principles and neurophysiologic techniques proposed by Knott and Voss,77 the Bobaths,60 Rood,78 and Brunnstrom79 to add sensory input and address facilitation, inhibition, and reflexive patterns of movement. Ms D's deficits in strength and coordination and her spasticity hamper her movements; functional restoration will be the aim of intervention. The therapist believes that an assistive device will help Ms D compensate for her balance and coordination challenges and provide greater safety and more judicious energy expenditure, a left lower-extremity orthosis will facilitate functional ambulation, and adaptive equipment for her bathroom will enhance safety and ease.

INTERVENTION

The physical therapist designs interventions that include weight-bearing activities in preparation for functional ambulation-with co-contraction around the shoulders, hips, knees, and ankles-and mat exercises that incorporate developmental sequence and proprioceptive neuromuscular facilitation techniques, such as rhythmic stabilization to enhance pelvic stability and coordination, with a focus on balance.77 He finds that manual contact at the key control points of the hips and shoulders is effective stimulation. Visual and auditory cues are included for sensory input and feedback. An eyepatch is rotated daily between the eyes to maintain eye muscle strength while curtailing diplopia.

The physical therapist also designs a submaximal strength-training program, using progressive resistance exercises, to be performed three times per week.80,81,el As indicated by Aitkens et al,80 bilateral upper-extremity exercises in the same motor pattern may help achieve greater symmetry of motion and help stimulate the weaker left arm.

An inhibitive ankle-foot orthosis is fitted on the left to maintain a neutral ankle position while decreasing clonus and toe-curling when weight-bearing. A protruding metatarsal notch, incorporated into the bottom of the orthosis, provides uniform contact on the foot and holds the foot in proper alignment. When wearing the orthosis in sneakers with adhesive fasteners, Ms D no longer drags the forefoot or has a steppage gait. Functional gait training begins with a hemiwalker, with contact guarding on the left, manual cueing, and verbal postural correction. Sidestepping and braiding, with manual support, are integrated into the program.

The physical therapist expects that by the end of week 2, Ms D's strength and control will be improved and that she will progress to walking a distance of approximately 100 feet on a level surface, under supervision, using a wide-based, 4-pronged ("quad") cane. Once that goal is met, the goal will be for Ms D to negotiate five stairs, using a railing on her right side, with contact guarding. Ms D also may begin to ride a stationary bicycle during week 2, with the left arm secured and supported by a platform mounted on the handlebar. The therapist will note when Ms D perceives that she is fatigued enough to stop, monitoring how long it takes for her heart rate to return to the previously established baseline (80 bpm). Once baseline is achieved, Ms D will be expected to resume exercise.

At week 3, the therapist plans on having Ms D use both upper extremities for functional activities in kneeling, half-kneeling, and standing positions and practice weight shifting in all planes of motion. He also plans to evaluate caregiver support at this time. During rehabilitation, both Ms D and her parents will receive instruction in seizure precautions, universal precautions, AIDS education, and safety awareness (eg, removing the scatter rugs, supervised ambulation). During Ms D's inpatient stay, the family also will be practicing a "home program" that emphasizes safety in functional activities.

REEXAMINATION AND GOAL MODIFICATION

As noted earlier, patients with AIDS typically experience a roller coaster of symptoms, and PML can progress at a rapid rate. At some point during her rehabilitation, Ms D's condition is likely to deteriorate, with repeat CT scans confirming progression of PML.'2 Her spasticity may increase, her energy level may decrease, and she may have occasional confusion and episodes of lability. A flexor synergy in the left upper extremity also may become evident but may be controllable during weight-bearing activities. Ms D would use a platform walker instead of a quad cane to provide stability and proprioceptive stimulation to her upper extremity. Ms D's program also might be modified to include a focus on maintaining range of motion and preventing skin compromise, such as positioning, monitoring, consistent passive and active exercise, and stretching. Baclofen, at a dose of 10 mg three times daily, may be prescribed by the neurologist to decrease spasticity, resulting in a mild functional improvement. The physical therapist will monitor the impact of this medication on physical activity and communicate these observations to the neurologist. At this time, the protease inhibitor ritonavir (600 mg taken orally, twice daily) also might be added to help slow the HIV and to assist the immune system. This drug may increase Ms D's fatigue and may require modification of anticipated goals.

Occupational therapists on the health care team may decide to fabricate a resting splint for the left wrist and fingers to maintain range of motion and help decrease spasticity. They also would help Ms D use compensatory strategies for dressing, grooming, and other ADL.

EXPECTED OUTCOMES

Even if there are setbacks, the physical therapist expects that by week 6 Ms D will be self-sufficient with self-care (washing, dressing, eating, toileting, taking medications, donning and doffing assistive equipment) with minimal setup and supervision. She would likely resume use of the quad cane on level surfaces with supervision and climb up and down one flight of stairs with contact guarding. Stationary bicycle riding and moderate resistance exercise would be continued, with monitoring for increases in spasticity Because fatigue has a "clinical and functional" impact on rehabilitation,58,72,76,82 energy conservation and work simplification techniques must be emphasized to ensure maximal independence with the smallest energy expenditure possible. For Ms D, a memory book and stress management would be helpful at this time.

HIV infection and AIDS typically affect a younger population, usually people in the prime of life. In addition, family members or caregivers also may be ill. Despite promising treatments, AIDS is still a progressive disease with no known cure. And, unlike diseases with linear, predictable courses, patients with AIDS sometimes change dramatically from one physical therapy session to the next. The timetable for frequency, duration, and type of opportunistic infections is uncertain. Although patients with AIDS who have PML tend to have a downward spiraling journey with a briefer life expectancy, some patients improve and even have spontaneous remissions. Given the fluctuating course of the disease, Ms D may need repeated intervention by various team members. Additional equipment also may be necessary At the time of discharge, however, the physical therapist expects that functionally directed activities, traditional conditioning exercises, principles of therapeutic exercise, and a comprehensive team approach will have facilitated greater independence for Ms D. Increased adherence is associated with patients' participation in their own care.Ss Discharge

At discharge, Ms D probably will have a sadder but greater knowledge of her condition. Her verbal intelligibility will have improved. The physical therapist expects that she will be able to walk 115 feet on a level surface with a quad cane under supervision and climb up and down one flight of stairs with contact guarding, depending on level of spasticity and impaired coordination. Walking on ramps and uneven surfaces should require minimal assistance.

The therapist also expects that her selfcare will be improved, as indicated by a discharge FIM score above 100, with specific improvements observed in bathing, dressing, toileting, transfers, walking, communication, and problem-solving. The physical therapist also will administer the General Health SelfAssessment63 at this time to determine whether there is improvement in how Ms D rates her quality of life.

By this time, the baclofen should be reducing spasticity, and seizures should be controlled with medication. Both therapist and patient may be cautiously optimistic about the antiretroviral and protease inhibitor therapy

The Home Program The physical therapist expects that Ms D will return to her own home with nursing and home health aide services. Fortunately, the large company for which Ms D works has an insurance plan that will reimburse for these services. Her parents already have been taking turns staying at her home to provide child care during her hospitalization, and they want to continue that arrangement.

Equipment and services must be coordinated in preparation for Ms D's return to her home. Beneficial community services include Meals on Wheels, a support group, scheduled transportation for medical appointments, and an active role for the school counselor. Ms D will receive equipment such as a bath chair, a raised toilet seat with armrests, a bedside commode for night use, and a lightweight wheelchair for community locomotion. Both a hemiwalker and a quad cane will go home with her, and Ms D will continue to use the ankle-foot orthosis with adhesive-fastener sneakers and the wrist splint.

A home health physical therapist has been contacted to provide twice weekly visits to monitor Ms D's status and modify her exercise plan as may be necessary, given the possibility of continued fluctuations. The focus will be on moderate strengthening exercises, coordination activities in standing and locomotion, and gait training. The therapist will encourage her to continue participating in routine physical activities and exercise to tolerance.,838' People with HIV who participate in routine physical activity may obtain benefits (eg, an increase in cardiopulmonary fitness, improved muscle function, weight gain, increased number of CD4 cells, improved mood, more effective coping behaviors), suggesting a balance of the negative suppressor effects of stress on the immune system and CD4 count.85 Aggressive exercise protocols that cause fatigue, however, may have negative effects, such as overall exhaustion. Moderate exercises that avoid fatigue and maintain motor control therefore are preferred for Ms D.8' Ms D will have to be a "therapeutic partner" in using energy conservation techniques and managing her fatigue.

Because a patient may have multiple concurrent HIV-related manifestations,6 health care team members need to be alert to changes in Ms D's status. Major physical impairment can lead to greater functional loss. Rehabilitation staff therefore will continue to provide strategies to assist her, maximizing her independence, minimizing her disability, and enhancing her well-being. She has very complex issues to manage over the course of her disease, including the current and future welfare of her children. All care providers will need to help her develop coping strategies and manage stress.

AIDS causes physical and mental dysfunction and has far-reaching emotional and social ramifications. It is psychologically devastating to lose a job, a home, independence, dreams. There is only uncertainty about the future, and the natural order of life can be turned around as parents bury their children. Although people with AIDS may have stressors in common with others who are undergoing rehabilitation-experiencing similar feelings, such as shock, anger, loss, and grief-they also face a host of unique issues. Given the typical pattern of AIDS-related PML, Ms D has a limited scope of choices, but physical therapy can help her improve functional ability and may help facilitate a better quality of life. m

References

Connor S, Kingman S. The Search for the Virus The Scientific Discovery of AIDS and the Quest for a Cure. New York, NY: Penguin Books; 1989. Kunkel SE, Warner MA. Human T-cell lymphotropic virus type III (HTLV-III) infection: how it can affect you, your patients, and your anesthesia practice. Anesthesiology. 1987;66:195-207. LaCharite CL, Huyett J. Understanding the disease. In: Meisenhelder JB, LaCharite CL, eds. Comfort in Caring: Nursing the Person with HIV Infection. Boston, Mass: Scott, Foresman and Company; 1989:89-101.

Bateson MC, Goldsby R Thnking AIDS: The Social Response to the Biological Threat. Reading, Mass: Addison-Wesley Publishing Company Inc; 1988. Cohen BA. Neurologic complications of HIV infection. Prim Care. 1997;24:575-595. Simpson DM, Berger, JR Neurologic manifestations of HIV infection. Part I: Management of the HIVinfected patient. Med Clin North Am. 1996;80:13631394.

7 Hollander H. Neurologic and pschiatric manifesta tions of HIV disease. J Gen Intern Med. 1991;6(1 Suppl):S24-S31.

8 Gabuzda DH. Neurologic disorders associated with HIV inteaions. JAm Acad Dermatol. 1990;22(6 Pt 2):1232-1236.

9 Price RW Neurological complications of HIV infection. Lancet.1996;348(9025):445-452. 10 Nes,on HB. Common neurologic complications of HIV-1 infection and AIDS. Am Fam Physician. 1995;51:387 398.

11 Rachlis AR Neurologic manifestations of HIV infec tion: using imaging studies and antiviral therapy effectively Post,#rad Med. 1998;103:147-150. 12 Berger JR, Moskowitz L, Fischl M, et al. Neurologic disease as the presenting manifestation of acquired immunodeficiency syndrome. South Med J 1987;80:683-686.

13 Le ? Et, Bredesen DE, Rosenblum ML. Neurological manifestations of the acquired immunodeficiency syndrome (AIDS): experience at the UCSF and review of the literature. J Neurosurg. 1985;62:475-495. 14 McArthur JC. Neurologic manifestations of AIDS. Medicine. 1987;66:407-437.

Snider WD, Simpson DM, Nielsen S, et al. Neurological complications of acquired immune deficiency syndrome: analysis of 50 patients. Ann Neurol. 1983;14:403-418.

Burns DK, Risser RC, White CL III. The neuropathologs of human immunodeficiency virus infection: the Dallas, Texas, experience. Arch Pathol Lab Med. 1991;115:1112-1124.

17 Gray F, Gherardi R, Scaravilli P The neuropathology of the acquired immune deficiency syndrome (AIDS): a review. Brain. 1988;111:245-266. Kure K, Llena JF, Lyman WD, et al. Human immunodefidency virus-1 infection of the nervous system: an autopsy study of 268 adult, pediatric, and fetal brains. Hum Pathol. 1991;22:700-710. Lang W, Miklossy J, Deruaz JP, et al. Neuropathology of the acquired immune deficiency syndrome (AIDS): a report of 135 consecutive autopsy cases from Switzerland. Acta Neuropathol (Berl). 1989;77:379-390.

Kwasa TO. Neurological manifestations of human immunodeficiencv virus infection and acquired immune deficiency syndrome: a review. East Afr Med J.1995;72:664-668.

Petito CK, Cho ES, Lemann W, et al. Neuropathology of acquired immunodeficiency syndrome (AIDS): an autopsy review. J Neuropathol Exp Neurol. 1986;45:635-646.

Dalsgaard Hansen NJ, Madsen C, Stenager E. Progressive multifocal leukoencephalopathy Ital J Neurol Sci. 1996:17:393-399.

Simpson D, Tagliati M. Neurologic manifestations of HIV infection. Ann Intern Med. 1994;121:770. Whiteman ML, Post MJ, Berger JR, et al. Progressive multifocal leukoencephalopathy in 47 HIV-seropositire patients: neuroimaging with clinical and pathologic correlation. Radiology. 1993;187:233-240. 25 Centers for Disease Control and Prevention: 1993 Revised Classification System for HIV Infection and Expanded Surveillance Case Definition for AIDS among Adolescents and Adults. MMWR. 1992;41:2. Mark AS, Atlas SW Progressive multifocal leukoencephalopathy in patients with AIDS: appearance on MR images. Radiology. 1989;173:517-520. Trotot PM, Vazeux R, Yamashita HK, et al. MRI pattern of progressive multifocal leukoencephalopathy in AIDS: pathological correlations. J Neuroradiol. 1990;17:233-254.

Poon TP, Tchertkoff V, Win H. Fine needle aspiration biopsy of progressive multifocal leukoencephalopathy in a patient with AIDS: a case report. Acta Cytol. 1997;41:1815-1818. Padgett BL, Walker DL, ZuRhein GM, et al. Cultivation of papova-like sims from human brain with progressive multifocal leukoencephalopathy LAncet. 1971;1:1257-1260.

30 Walker DL, Padgett B. Progressive multifocal leukoencephalopathy. In: Frankel-Conrat H, Wagner RR, eds. Comprehensive Virology. New York, NY: Plenum; 1983.

Berger JR, Pall L, Lanska D, Whiteman M. Progressive multifocal leukoencephalopathy in patients with HIV infection. J Neurovirol. 1998;4(1):59-68.

Berger JR, Pall L, Whiteman M. Progressive multical leukoencephalopathy in HIV infection. Neurology. 1996;46:A268. Abstract.

Major EO, Ault GS. Progressive multifocal leukoencephalopathy: clinical and laboratory observations on a viral induced demyelinating disease in the immunodeficient patient. Curr Opin Neurol. 1995;8(3):184-190.

Weber T, Major EO. Progressive multifocal leukoencephalopathy: molecular biology,, pathogenesis and clinical impact. Intervirology. 1997;40(2-3):98-111. Berger JR, Kaszovitz B, Post JD, et al. Progressive multifocal leukoencephalopathy associated with human immunodeficiency virus infection: a review- of the literature with a report of sixteen cases. Ann Intern Med. 1987;107:78-87.

Fong IW, Britton CB, Luinstra KE, et al. Diagnostic value of detecting JC virus DNA in cerebrospinal fid of patients with progressive multifocal leukoencephalopathy. J Clin Microbiol 1995;33:484-486. Gibson PE, Knowles W, Hand JF, et al. Detection of JC virus DNA in the cerebrospinal fluid of patients with progressive multifocal leukoencephalopathy J Med Virol. 1993;39:278-281.

McGuire D, Barhite S, Hollander H, et al. JC virus DNA in cerebrospinal fluid of human immunodeficiency virus-infected patients: predictive value for progressive multifocal leukoencephalopathy. Ann Neurol. 1995;37:395-399.

Perrons CJ, Chinn RJ, Fox JD, et al. Progressive multifocal leukoencephalopathy in patients with AIDS: detection of JC virus DNA in CSF and brain. Genitourin Med. 1995;71(1):35 40. 40 Tornatore C, Berger JR, Houff SA, et al. Detectin of JC virus DNA in peripheral lymphocytes from patients ssith and without progressive multifocal leukoencephalopathy. Ann Neurol. 1992;31:454462.

41 Richardson EP Jr. Progressive multifocal leukoencephalopathy In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology, vol 9 Multiple Sclerosis and Other Demyelinating Diseases. North Holland, NY: Elsevier; 1970:486-499. 42 Thurnher hIM, Thurnher SA, Muhlbauer B, et al. Progressive multifocal leukoencephalopathy in AIDS: initial and follow up CT and MRI. Neuroradiology. 1997;39:611-618.

43 Holtzman DM, Kaku DA, So YT. New-onset seizures associated with human immunodeficiency virus infection: causation and clinical features in 100 cases. Ann J Med.1989;87(2):173-177. 44 Mooignier A, Mikol J, Pialoux G, et al. AIDS-associated progressive multifocal leukoencephalopathy revealed by new-onset seizures. Am J Med. 1995;99:64 68.

45 Lemp GE, Payne SF, Neal T, Rutherford GW. Survival trends for patients with AIDS. JAMA. 1990;263:402 406.

46 O'Dell MW, Levinson SF, Riggs RV. Focused review: physiatric management of HIV-related disability. Arch Phes Med Rehabil. 1996;77(3 Suppl):S66-S73. 47 Blick G, Whiteside M, Griegor P, et al. Successfid resolution of progressive multifocal leukoencephalopathy after combination therapy with cidofovir and cotosine arabinoside. Clin Infect Dis. 1998;26(1):191-192.

Nicoli F, Chave B, Peragut JC, et al. Efficacy of cytarabine in progressive multifocal leukoencephalopathy in AIDS. Lancet. 1992;339:306. 49 Portegies P, Alga AR, Hollak CE, et al. Responses to cytarabine in progressive multifocal leukoencephalopathy in AIDS. Lancet. 1991;337:680-681. 50 Conway B, Halliday WC, Brunham RC. Human immunodeficiency virus associated progressive multifocal leukoencephalopathy: apparent response to 3 azido 3'deoxythymidine. Reviews of Infectious Diseases.1990;12:479 482.

51 Fiala M, Cone LA, Cohen N, et al. Responses of neurologic complications of AIDS to 3'-azido-3'dithymidine and 9-(1,3-dihydroxl-2propoxynethl) guanine: 1. Clinical features. Reviews of Infectious Diseases.1988;10:250 256.

Garrote FJ, Molina JA, Lacambra C, et al. The inetfica

Singer EJ, Stoner GL, Singer P, et al. AIDS presenting as progressive multifocal leukoencephalopathy with clinical response to zidosudine. Acta Neurol Scand. 1994;90:443 447.

von Einsiedel RW, Fife TD, Aksamit AJ, et at. Progressive multifocal leukoencephalopathy in AIDS: a clinicopathological study and reviesv of the literature. J Neurol.1993;240:391 406.

Frank E, Kupfer DJ, Siegel LR Alliance not compli

ance: a philosophy of outpatient care. J Clin Psychiatry. 1995;56(suppl):11-17.

56 Sadovsky R, Gillette P. The initial assessment of the HIV-infected patient. Prim Care. 1997;24(3):497515.

57 Guide to Physical Therapist Practice. Phys Ther. 1997;77:1163-1650.

58 O'Connell PG, Levinson SE Experience with rehabilitation in the acquired immunodeficiency sl>ndrome. Am J Ph^7s Med Rehabil.1991:70:195-200. 59 Galantino ML, ed. Clinical Assessment and Treatment of HIV- Rehabilitation ofa Chronic Illness. Thorofare, NJ: Slack Inc; 1992. 60 Bobath B. Adult Hemiplegia: Evaluation and Treatment. London, England: Wuliam Heinemann Medical Books Ltd; 1970.

61 Kendall FP, McCreary EK, Provance PG. Muscle Testing and Function. 4th ed. Baltimore, Md: Williams & Wilkins Co;1993.

62 Guide for the Uniform Data Set for Medical Rehabilitation (Adult FIM), Version 4.0. Buffalo, NY: State University of New York at Buffalo/UB Foundation Activities Inc; 1993. 63 Lenderking WR, Testa Ma, Katzenstein D, Hammer S. Measuring qualin of life in early HIV disease: the modular approach. Qual Life Res 1997;6:515-530. 64 Chaisson RE, Gallant JE, Keruly JC, Moore RD. Impact of opportunistic disease on survival in patients with HIV infection. AIDS.1998;12(1):29-33. 65 Karahalios D, Breit R, Del Canto MC, et al. Progressive multifocal leukoencephalopathy in patients with HIV infection: lack of impact of early diagnosis by stereotactic brain biopsy Journal of AIDS. 1992;5:1030-1038.

66 Berger JF, Mucke L. Prolonged survival and partial recovery in AIDS-associated progressive multifocal

leukoencephalopathy. Neurology. 1988;38:10601065. 67. Berger JR Long-term survival in biopsy proven AIDS-associated PML. J NeHroPtrol.

67 Berger JR Long-term survival in biopsy proven AIDS-associated PML. J Neurovirol. 1996;2:31. Ahstran.

Fong IW, Toma E. The natural history of progressive multifocal leukoencephalopathy in patients with AIDS. Clin Infect is. 1995 May;20(5):1305-1310. O'Dell MW HIV-related neurological disability and prospects for rehabilitation. Disabil Rehabil. 1996 Jun;lB(6):285-292.

Bertakis KB. Resident Physician Practice StYles and Patient Outcomes: Final Report. Rockville, Md: Agency for Health Care Policy and Research; 1995. Sadovsky R Psychosocial issues in symptomatic HIV infection. Am Fam PEsician. 1991;46:2065-2072. Levinson SE, O'Connell PG. Rehabilitation dimensions of AIDS: a rc ieA. Arch Phys Med Rehabil. 1991;72:690-696.

O'Dell MW, Crawford A, Bohi ES, Bonner FJ. Disability in persons hospitalized with AIDS. Am J Phys Med Rehabil. 1991;70:91-95.

Silwa JA, Smith JC. Rehabilitation of neurologic disability related to human immunodeficiency virus. Arch Phys Med Rehabil. 1991;72:759-762. O'Dell MW, Sasson NI,. Hemiparesis in HIV infection: rehabilitation approach. Arch Phys Med Rehabil. 1990;71:291-296.

Galantino ML, Mukand J, Freed MM. Physical therapy management of patients with HIV infection. In: Mukand J, ed. Rehabilitation for Patients with HIV Disease. New York, NY: McGraw-Hill; 1991:257282.

77 Knott M, Voss DE. Proprioceptive Neuromascular Facilitation: Patter's and Techniques. 2nd ed. New York, NY: Harper Rz Row; 1968.

Stockmeyer S. An interpretation of the approach of Rood to the treatment of neuromuscular dysfunction. Am JPhys Med. Feb 1967;46:900-956. Perry CE. Principles and techniques of the Brunnstrom approach to the treatment of hemiple gia. Arm JPhvr Med. 1967;46:789-812. Aitkens SG, McCrory MA, Kilmer DD, Bemauer EM. Moderate resistance exercise program: its effect in slowly progressive neuromuscular disease. Arch Phys Med Rehabil.1993;:711-715. Spence DW, Galanono ML, Mossberg KA, Zimmerman SO. Progressive resistance exercise: effect on muscle function and anthropometry of a select AIDS population. Arch Phys Med Rehabil. 1990;71:644-648.

Levy RM, Bredesen DE. Central nervous system dysfunction in acquired immunodeficiency syndrome. In: Rosenblum ML, Levy RM, Bredesen DE, eds. AIDS and the Nervous System. New York, NY: Raven Press; 1988:29-63.

Calabrese LH, LaPerriere A. Human immunodeficiency virus infection, exercise and athletics. Sports Med. 1993:15:6 13.

84 LaPerriere A, Fletcher MA, Antoni MH, Kilmas N, Ironson G, Schneiderman N. Aerobic exercise train ing in an AIDS risk group. Int J Sports Med. 1991;12:S53-S57.

85 LaPerriere A, Kilmas N, Fletcher lMA, et al. Change in CD4+ cell enumeration following aerobic exer cise training in HIV-1 disease: possible mechanisms and practical applications. Int J Sports Med. 1997;18(Suppl 1):S56 S61.

Copyright American Physical Therapy Association Feb 1999
Provided by ProQuest Information and Learning Company. All rights Reserved

Return to Progressive multifocal leukoencephalopathy
Home Contact Resources Exchange Links ebay