PARKINSON’S DISEASE&
COMPLICATIONS OF THIS DISORDER
PARKINSON’S DISEASE
.Originally described by James Parkinson in 1817 and characterized as Shaking Palsy.
. Chronic slowly prog, neurodegenerative disease of the Basal Ganglia (BG).
. Basic path-lack of dopamine-producing cells in the BG.
BACKGROUND MOSTLY known as movement disorder 1-2% > 65 y/o 15% between ages of 65 and 74Cardinal signs;
tremor, bradykinesia, rigidity & postural instability.
Dx: 2/3 Onset: unilateral progressing to B/L
TREMOR Resting . Pill-rolling motion Suppressed by
activity, sleep, concentration
Intensified by stress, fatigue
Mostly begin unilateral.
BRADYKINESIA
Required for dx Most disabling Sx Slowness of movement/motion Affects facial muscle & masked face Inability to change direction while walking/dif
walking around obstacle Causes gait/postural abnormality Clumsy or weak limb maybe early sign
RIGIDITY refers to an increase in resistance to passive movement about
a joint; either osclillating (cogwheel) or smooth (lead pipe). Rigidity usually is tested by flexing and extending the patient's relaxed wrist.
Cogwheeling Racheting through the ROM due to subtle tremor
superimposed on the rigidity Lead pipe
Smooth resistance to passive movement that is independent of velocity (in contradistinction to spasticity, which is velocity dependent)
Lead pipe tone can be made more obvious with voluntary movement or mental task in the c/l limb.
POSTURAL INSTABILITY 4th cardinal sign, but it emerges late in the disease, usually after 8 years or more
Imbalance and loss of righting reflexes. Assumption by patient of a stooped-forward
posture Presence, usually, of a festinating gait pattern
(stumbling forward).Decreased arm swing during ambulation
CONSEQUENCES OF DISEASE Stiffness and slowed movements Tremor or shaking at rest Difficulty getting out of a chair or rolling over in
bed Frequent falls or tripping Difficulty walking Memory loss Shifting forward of posture into a stoop Speech changes (eg, whispering, rapid speech) Smaller handwriting Slowness in performing activities of daily living
(ADL)
CLINICAL MANIFESTATION
PHYSICAL EXAM Painful dystonia, usually occurring in the early morning Rapid, monotonous, low-volume speech Hypokinetic dysarthria Dysphagia Masklike facies Depression
Can affect up to 50% of patients Suicide risk
Akathisia (inability to sit still) . Olfactory dysfunction (hyposmia), which may be present
prior to motor symptoms and often is not recognized by the patient
PHYSICAL EXAM Autonomic Dysfunction Slowed enteric motility and constipation Urinary retention and incontinence Orthostatic hypotension
Patients may experience freezing when starting to walk (start-hesitation), during turning, or while crossing a threshold, such as going through a doorway
CLASSIFICATION OF PARKINSON’S
Idiopathic PD – 85% of all PS cases Drug induced Parkinsonism – 7-9% Parkinson-Plus Syndrome Vascular Parkinson syndrome -3% Toxin-induced –rare Recurrent Head trauma-rare
IDIOPATHIC PD D/O of the Basal Ganglia (BG) Loss of dopamine producing cells in the
substantia nigra (SN) and locus ceruleus (LC) Degeneration of nigrostriatal pathway Sx manifest if decreased dopamine content by
> 50%) Loss of inhibitory input to the cholinergic
system> > excess excitatory output Imbalance of cholinergic input in the striatum
EPIDEMIOLOGY/M&M
Male to female ratio = 3:2 Prevalence = 160/100,000 Incidence = 20/100,000 per year /general
population Morbidity=progressive Mortality=mean survival after onset @ 15 yrs
PD survival >MSA,PSP MC cause of death: pulmonary infection/aspiration,
UTI, PE, of falls/fractures
ACCELERATED AGINGNormal aging is associated with clinical features that may resemble PD.
Aging is associated with a decline of pigmented neurons in the substantia nigra and with decreased levels of striatal dopamine and dopa decarboxylase.
ETIOLOGY
Unknown Theories
Accelerated aging Genetic susceptibility Environmental Factors Oxidative stress
ETIOLOGY UNCLEAR
.Genetic susceptibility - Twin studies inconclusive Genetic factors play a
greater role with early onset PD
Increased incidence of a family history PD observed
Environmental factors use of pesticides, living in a rural
environment consumption of well
water exposure to herbicides proximity to industrial
plants or quarries
ETIOLOGY UNCLEAR Head Trauma increases the risk of developing
Parkinson . The former champion
boxer Muhammad Ali was diagnosed with Parkinson's in 1984 at the age of 42, and is one of the most high-profile people battling the condition.
OXIDATIVE STRESS
Free radical damage, resulting from dopamine's oxidative metabolism, plays a role in the development or progression of PD.
Dopamine oxidation via MAO result in formation of hydrogen peroxide.
Hydrogen peroxide normally cleared by glutathione
Hydrogen peroxide reactions with ferrous ions, resulting in formation of hydroxyl radical.
- hydroxyl radicals can cause damage to lipids, DNA, amino acids
PD associated with: increased dopamine turnover, decreased protective mechanisms (glutathione),increased iron (a pro-oxidation molecule),
evidence of increased lipid peroxidation.
CLUES SUGGESTING ATYPICAL PARKINSONISM
Early onset of, or rapidly progressing dementia
Rapidly progressive course Supranuclear gaze palsy Cerebellar signs-dysmetria, ataxia Early urinary incontinence.
PARKINSON’S SYNDROME Parkinson’s Disease
Survival approximates US population when treated
Slow progressive onset of asymmetric bradykinesia
Onset with either classic pill-rolling tremor or rigidity
Parkinson-Plus syndromesShorter survival,
more frequent complications
Early instabilityRapid disease
progressionPoor response to
LevodopaPyramidal and
cerebellar signsEarly dysarthria,
dysphasia
PARKINSON-PLUS SYNDROME
PSPSupranuclear downgaze palsy, square wave
jerksUpright posture/frequent fallsPseudobulbar emotionalityFurrowed brows/stare
Corticobasal degenerationcognitive impairmentUnilat, coarse tremor,limb apraxia/limb
dystonia-myoclonus/alien limb
PD VS ESSENTIAL TREMOR
ET should be tremor with no other signs of parkinsonism
Both can have kinetic and rest component
Cogwheel rigidity can be found in ET
TREATMENT OPTIONS Preventive = no definite one available Symptomatic
Pharmacological Surgical
Non-motor management Restorative-experimental only
Transplantation Neurotrophic factors
Nonpharmacologic approaches PT/OT/ST
DRUG CLASSES IN PD Dopaminergic agents
Levodopa (LD) Dopaminergic Agonists- Bromocriptine, Ropinirole,
Pramipexole
COMT inhibitors Tolcapone, Entacapone LD + Entacapone (Stalevo)
MAO-B inhibitors- Selegiline (Eldepryl) Anticholinergics
Trihexyphenidyl, Benztropine
Antivirals-Amantadine
SURGICAL MANAGEMENT Candidates for deep brain
stimulation disabling medication-resistant
tremor
levodopa-responsive patients with medication-resistant disabling motor fluctuations and/or levodopa-induced dyskinesia.
no significant cognitive impairment, mood or behavioral disturbances
No other factors that may increase the risk of surgery.
SURGICAL MANAGEMENT Deep drain stimulationThalamic
Dec. tremor in 90% of pt
No effect on cardinal signs
Pallidal Improves cardinal signs,
dyskinesiaSubthalamic
Improves cardinal signs, dyskinesia, motor fluctuations
FUTURE MANAGEMENT
Neural transplantation dopamine-producing
cells, ex. fetal nigral cells.
Gene therapy
MANAGING EARLY COMPLICATIONS :ALTERED MENTAL
STATES
Confusion, sedation, dizziness, hallucinations, delusions
Reduce /eliminate CNS-active drugs of lesser priority Anticholinergics - Sedatives and many other
medications.
LATE COMPLICATIONS
Motor fluctuations, dyskinesias,dystonia,freezing,falls
Behavioral/neuropsychological Depression,sleep d/o, psychosis
Autonomic OH, hyperhidrosis ,constipation, impotence, urinary
incontinence or retention
FREEZING AND FALLS
Freezing motoric block; at initiation of gait, turning, narrow
spaces use auditory(marching steps to the beat of a
metronome), visual, proprioceptive cues ( mental rehearsal and imaging)
Falls Physical therapy evaluation Cane, scooter, wheelchair may be necessary
COGNITIVE ASSESSMENT
Memory difficulties: 11-29% of PD patients Benign forgetfulness Delirium Alzheimer’s disease Other dementias
Evaluation Brain imaging Lumbar puncture EEG Blood work for thyroid profile, vitamin B12, serology,
chemistry panel
PSYCHOSIS Features
Vivid dreams/nightmares, disorientation, hallucinations, delusional thought
Simplify medical regimen Stop unnecessary non-PD meds Stop: anticholinergic drugs, amantadine, selegiline,
dopamine agonists, COMT inhibitors Change from CR to standard carbidopa/levodopa Try atypical antipsychotic agents Try low-potency traditional antipsychotic agents
ANXIETY/RESTLESSNESS Primary anxiety disorder: treat with benzodiazepines Associated with
“off-periods” or low-levopoda levels: adjust levopoda dosing
Restless Leg Syndrome:
SLEEP DISORDERS Insomnia
careful history difficulty with sleep initiation treat depression REM-behavioral disorder: clonazepam
Excessive daytime sleepiness correct poor sleep at night discontinue anticholinergics, amantadine reduce dopamine agonist, levopoda dosages if possible
ORTHOSTATIC HYPOTENSION
Tilt table training for severe cases Taper anti-hypertensive agents Taper non-PD drugs Increase salt intake Elevate HOB, arising slowly, isometric exercises Compression stockings, abdl binders
URINARY INCONTINENCE/FREQUENCY
Rule out urinary tract infection Bladder evaluation Urinary frequency
IMPAIRED GI MOTILITY
Constipation Vomiting Impaired absorption Treatment Options
small frequent meals increased fiber/bulking agents stool softeners and suppositories
NAUSEA
Levodopa-related: take with meals, add carbidopa, add domperidone
Other anti-PD medications: same. If no improvement: withdraw newest agent, re-initiate
at minimal doses, slowly increase
EXCESSIVE SWEATING
Usually levodopa related, and may be seen at peak or trough dose drug levels
PROBLEMS THAT MAY RESPOND TO NONPHARMACOLOGICAL APPROACHES
Motor, mobility,balance, posture, gait ADL difficulties Speech : hypophonia, sialorrhea,dysphagia Inadequate nutrition Sleep disturbance Autonomic dysfunction:
OH, delayed gastric emptying, constipation,bladder dysfunction
Sexual dysfunction Depression, Anxiety
REHABILITATION IMPAIRMENTS
¨ Gait disturbance Decreased stride
length, cadence, velocity. Festination
Stooped flexed posture Cautious gait(fear of
falling) Impaired balance
REHABILITATION MANAGEMENTRehabilitation &interventions are directed at the main causes of impairments.
Multidisciplinaryapproach:PT,OT,ST,RT,Neuropsych
RATIONALE FOR REHABILITATION
While rehabilitation services are often given to the patient with Parkinson disease, this occurrence is more based on common practice rather than clear research design. There is a paucity of well-designed research studies looking at specific rehabilitation techniques. The existing literature is both sparse and fraught with confounding variables such as changes in medication regimens. A recent review examined 11 studies involving various physical therapy techniques in Parkinson disease. The authors found insufficient evidence to support or refute the efficacy of any form of physical therapy over another form. Furthermore, there was insufficient evidence found to support the efficacy of any therapy compared with no therapy. Perhaps the best designed study was a prospective randomized crossover investigation of 4 weeks of outpatient physical therapy, in which medication changes were not allowed.
CARDIOPULMONARY IMPAIRMENT
The patient's flexed posture can lead to kyphosis, cause a reduction in pulmonary capacity, and produce a restrictive lung disease pattern.
Breathing exercises, postural reeducation, and trunk exercises may be helpful.
Institution of a general conditioning program can increase the patient's endurance.
If pulmonary function progressively worsens, assisted coughing techniques, incentive spirometry, and respiratory therapy intervention may be required.
REHABILITATION AND RATING SCALE
Stages 0-II are mild disease;
Stage III is moderate disease;
Stages IV and V are marked or advanced disease. There are gray areas between the successive stages.
TREATMENT PLANMaintain or increase ROM in all joints
Efforts to improve postural control and standing balance
Prevent disuse /atrophy and muscle weakness
Improve motor function and mobility
TREATMENT PLAN Improve gait pattern Improve speech,
breathing patterns chest expansion, mobility
Maintain functional independence in adl’s
Assist in psychological adjustment to new lifestyle
Upper extremity fine motor skills
Functional transfers
Swallowing evaluation
Cognitive evaluation
Recreational therapy
Pt/Family training-education
PHYSICAL THERAPY: GOAL
Maintain or increase activity level Decrease rigidity and bradykinesia Facilitate movement and flexibility; optimize gait Maximize gross motor coordination and balance Maximize independence, safety, function
PHYSICAL THERAPY Relaxation techniques Gentle ROM and
stretching techniques Exaggerated or patterned
movements High stepping,wt
shifting,repitetion, visual &verbal cues
Back extension exercises and pelvic tilt
PHYSICAL THERAPY Static and dynamic postural controls emphazing whole
body movements sitting and standing Stationary bike training to help reciprocal movements Exercise: walking(1+mile/day),swimming,golf,dancing Use of assistive devices, mobility aids, orthotics Family training and home program
Proper and energy conservation techniques After 6 mths benefit of therapy if not coninued will be gone
OCCUPATIONAL THERAPY: GOALS
Maximize independence, safety, function Improve endurance, reduce energy expenditure Training in use Adaptive Equipments Improve body image, self-esteem, psychosocial adjustment Facilitate active movement Maximize fine motor coordination Increase trunk flexibility and upright posture
OCCUPATIONAL THERAPY Patient and caregiver education goals of program transfers, task
simplification, positioning, etc.
Home exercise program Home and workplace
modifications
SPEECH THERAPY Swallowing evaluation including modified barium swallow
Articulatory speech training for dysarthria
Early therapy is effective Teaching compensatory
strategies for safer swallow
DYSPHAGIA If swallowing difficulties do not respond to conservative interventions by the speech therapist, more aggressive treatment may be required.
Such aggressive management can include invasive procedures, such as nasogastric or gastrostomy feeding tube placement.
Discussion should be initiated early on in the disease course to ascertain the patient's wishes about a feeding tube, in case dementia develops and the patient lacks the capacity for decision making when a feeding tube becomes medically indicated.
TECHNIQUES TO IMPROVE SPEECH
Increase loudness Face the listener directly Emphasize key words Use short sentences Range-of-motion exercises for muscle of speech Breathing exercises, breath control Phonatory-respiratory effort model /Lee Silverman Voice
Tx=“think loud, think shout approach”
MANAGEMENT OF SWALLOWING DIFFICULTY
Do not rush Eat soft foods, small bites of food Swallow only well-chewed food Empty mouth before next bite Chin down positioning Family should learn Heimlich maneuver Be aware of saliva accumulation and swallow often Verbal prompting Clinicians might also choose to administer antiparkinsonian
medications prior to meals, so that maximal benefit of drugs occurs during mastication.
RECREATIONAL THERAPY
identifying previous recreational interests new interests can be identified and explored social and recreational pursuits
social and recreational pursuits
COMMUNITY RESOURCES
Social worker intervention: Social Security office Medicare, Medicaid
In-home programs Meals on Wheels, home visiting, etc.
NUTRITIONAL RISK FACTORS
Inactivity Food preparation problems Dyskinesia and feeding problems Chewing and swallowing problems Increased metabolic needs Medication-related dietary restrictions Drug side effects: anorexia, nausea, vomiting,
constipation Depression and dementia
DIETARY RECOMMENDATIONS Eat a balance diet, including all food groups
Consume sufficient calories to maintain weight
Consume adequate fiber and fluids to avoid constipation
Take vitamin D and calcium to prevent osteoporosis
Reduce protein to minimum daily allowance.
PROGNOSIS/COMPLICATIONS Poor Prognostic indicatorsOld age of onset
Early cognitive deficits
Lack of tremor
Complications Underlying medical
illness ( sepsis, pneumonia, fecal impaction, urinary tract infection) should be suspected in a PD patient
REFERENCES
Neuro Rehab Book ( PTA Program) http://www.emedicine.com/pmr/topic99.htm http://www.emedicine.com/NEURO/
topic304.htm
ANY QUESTION?