Gait observation in linear motion, in changes of direction; if pt uses >5 steps to complete 180 degree turn, PD shld be consideredBradykinesia refers to slowness of movement but also includes a paucity of spontaneous movements and decreased amplitude of movement. Bradykinesia also is expressed as micrographia (small handwriting), decreased blink rate, and hypophonia (soft speech). hypomimia (decreased facial expression),
Cogwheeling may be appreciated in tremors not associated with an increase in tone (ie, essential tremor). Rigidity
There s sometimes confusion differentiating a parkinsonian tremor from ET.ET shld have tremor alone, no other signs of parkinsonism nor any other neurologic signs such hyperreflexia,weakness,or sensory loss. Both d/o may have kinetic and rest component although traditionally pt w/ ET have more postural & kinetic tremor w/ dampening upon rest,where as PD more often have rest tremor dampens with action. In addition,ET pts may exhibit mild signs of bradykinesia & cogwheeling when examined when examined for rigidity.in the early tremor pt,the historical findings of famhx suggesting AD inheritance, a long hx of tremor w/o progression of motor difficulties & tremor response to alcohol r helpful n the dx of ET.lastly ET does not respond to antiPD drugs but may improve w/ propanolol,primidone,andbenzos
No definite preventative tx available there is however wide range of sxmatic tx including pharmacologic and surgical methods. The non motr mgt include tx of depression,OH,excessive drowsiness,& psychosis. Finally, restorative therapies such as fetal or porcine cell transplantation are n expe use & neurotrophic factors susch as GDNF & small molecules such as neuroimmunophillins are being explored Rehabilitaion part is where I’m going to focus more since neurologist are by practice the ones managing their medications. Besides it will takeperhaps another hour to discuss the pharmacologic, side effects of these meds, we certainly discuss them some other time if you like.
Briefly on medical management; Dopaminergic therapy is d cornerstonr of sxmatic mngt of PD LD replaces dopamine presynaptically while dopamine agonists act directly on receptors post synaptically. LD is administered w/ peripheral decarboxylase inhibitor either benserazide or carbidopa. The newest class r the COMT inhibitors, also increase bioavailability of LD by inhibiting peripheral or central catechol o-methyl transferase. Other agents r anticholinergics, the MAO-B inhibitors selegiline and the antiviral amantadine.Bromocriptine=parlodel, pergolide=Permax,ropinirole=requip,pramipexole=mirapexCOMT inhibitors-Tolcapone(Tasmar),Entacapone (Comtan) L-Dopa + Entacapone (Stalevo)MAO-B inhibitors- Selegiline (Eldepryl)Anticholinergics-Trihexyphenidyl(Artane),Benztropine (Cogentin)Antivirals-AmantadineL-Dopa(Sinemet), Dopamine Agonists- Bromocriptine (Parlodel), Ropinirole(Requip),Pramipexole(Mirapex)
When pts develop confusion,sedation,dizziness,halluci or delusions the simplest intervention is to reduce or eliminate sedating meds or antiPD meds of lesser priority.commonly used sedating meds includes hypnotics, sedatives,muscle relaxant,urinary antispasmodics. Low potency antiPD meds that may contribute significantly to confusion include anticholiner, amantadine and selegiline. When this option is not adequate, dosage reduction of LD, DA or COMT inhibitor m/b necessary. Drug related psychotic symptoms in early illness are often associated w/ atypical parkinsonian syndromes
Management of late stages of PD involves tx of motor response fluctuations, dyskinesias,dystonia,freezing and falls. In add, besides these motor fluctuations there r behavioral & neuropsychological concerns, such as depression, sleep d/o, & psychosis. Autonomic problems include OH, hyperhidrosis, constipation, impotence, u inc or retention.
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 74 Cardinal 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 patients 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.
4th cardinal sign, but itINSTABILITY in the POSTURAL emerges late 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
Stiffness and slowed movements DISEASE CONSEQUENCES OF 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)
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 Autonomic Dysfunction EXAM 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
Normal Aaging is associated with clinical CCELERATED AGING 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 UNCLEAR Environmental factors.Genetic susceptibility use of pesticides, - Twin studies living in a rural inconclusive environment Genetic factors play a consumption of well greater role with early water onset PD Increased incidence of a exposure to herbicides family history PD proximity to industrial observed plants or quarries
Head Trauma TIOLOGY UNCLEAR E increases the risk of developing Parkinson . The former champion boxer Muhammad Ali was diagnosed with Parkinsons in 1984 at the age of 42, and is one of the most high-profile people battling the condition.
OXIDATIVE STRESS Free radical damage, Hydrogen peroxide reactions with ferrous ions, resulting in resulting from dopamines formation of hydroxyl radical. oxidative metabolism, - hydroxyl radicals can cause plays a role in the damage to lipids, DNA, amino acids development or PD associated with: progression of PD. increased dopamine Dopamine oxidation via turnover, decreased protective mechanisms MAO result in formation of (glutathione), hydrogen peroxide. increased iron (a pro- Hydrogen peroxide oxidation molecule), evidence of increased lipid normally cleared by peroxidation. glutathione
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 Parkinson-Plus Survival syndromes approximates US Shorter survival, more population when frequent treated complications Slow progressive Early instability onset of asymmetric Rapid disease bradykinesia progression Onset with either Poor response to classic pill-rolling Levodopa tremor or rigidity Pyramidal and cerebellar signs Early dysarthria, dysphasia
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.
Deep drain URGICAL MANAGEMENT S stimulation Thalamic Dec. tremor in 90% of pt No effect on cardinal signs Pallidal Improves cardinal signs, dyskinesia Subthalamic Improves cardinal signs, dyskinesia, motor fluctuations
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
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
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 patients 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 patients 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.
Maintain or increase TREATMENT PLAN ROM in all joints Efforts to improve postural control and standing balance Prevent disuse /atrophy and muscle weakness Improve motor function and mobility
Improve gait TREATMENT pattern PLAN Upper extremity fine Improve speech, breathing motor skills patterns chest expansion, Functional transfers mobility Swallowing Maintain functional evaluation independence in adl’s Cognitive evaluation Assist in psychological Recreational therapy adjustment to new lifestyle 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
Patient and caregiver education O CCUPATIONAL goals of program THERAPY transfers, task simplification, positioning, etc. Home exercise program Home and workplace modifications
Swallowing evaluationTHERAPY SPEECH 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 patients 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 RECOMMENDATIONSEat 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.
Poor PROGNOSIS/COMPLICATIONS Prognostic Complications indicators Underlying medical illness ( sepsis, pneumonia, fecal Old age of impaction, urinary tract infection) should be onset suspected in a PD patient Early cognitive deficits Lack of tremor