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Slide 1-

Rehabilitation Management of Parkinsons Disease Susan Stickevers, MD Residency Program Director & Assistant Clinical Professor, SUNY Stony Brook Dept of PM&R
Slide 2-

Parkinsons Disease Is a chronic, progressive neurodegenerative disorder with a multifactorial etiology. It is superseded only by Alzheimer’s Disease as the most common neurodegenerative disorder
Slide 3-

Demographics of Parkinsons Disease Prevalence of 0.3 % in the US population 1 – 2% of all persons > 65 yrs old 4 – 5% of all persons > 85 yrs old In US : > 1 million have diagnosis of Parkinsons – this is greater than the combined number of MS, ALS, and muscular dystrophy patients added together Usual age at onset – early 60s 10% of all those affected are < 45 yrs old – referred to as young onset Parkinsons 40, 000 new cases of PD will diagnosed this year Lifetime risk of Parkinsons for men : 2.0% Lifetime risk for women : 1.3% Incidence of the disease is lower in African Americans than in Caucasians in the USA
Slide 4-

An Interesting Fact The Chinese have the lowest rates of Parkinsons Disease It has been suggested by Fahn & Jankovic that this is may be due to consumption of large amounts of green tea by the Chinese which contains antioxidants
Slide 5-

Etiology Parkinsonian symptoms can arise from either the neuropathological condition PD (idiopathic PD) or other forms of Parkinsonism For neuropathological PD, 90% of cases are sporadic 10% are of genetic origin – 6 different gene mutations have been identified – the Parkin genes Genetic forms of PD are seen more frequently in young onset PD A combination of environmental factors or toxins, genetic susceptibility, and the aging process may account for many of the sporadic cases
Slide 6-

Secondary Parkinsons Can be caused by : Medications – antipsychotics & antiemetics, lithium, reserpine, aldomet Sequelae of CNS infection – Prion Diseases, Jakob Creuzfeldt, SSPE, HIV, post encephalitic Toxin Exposure – Manganese, Rotenone, Paraquat Vascular Metabolic Disorders – Binswanger’s Disease Drug Induced – MPTP – byproduct of Ecstasy production Certain neurodegenerative conditions may exhibit also exhibit Parkinsonian features, these are called the Parkinsons Plus Syndromes – included in this category are progressive supranuclear palsy, MSA, Lewy Body Dementia and CBD Trauma – Pugilistic encephalopathy
Slide 7-

Risk Factors for Parkinsons Disease The most important risk factor for Parkinsons is advancing age. Other environmental or lifestyle risk factors associated with Parkinsons include : Rural living Exposure to herbicides & pesticides – exposure to the synthetic pesticide paraquat is associated with Parkinsons (organic pesticides are not necessarily safe - rotenone or Derris Dust exposure can induce Parkinsonism) Drinking well water Working with solvents – in particular – hexane Manganese toxicity – sometimes seen in welders, or patients exposed to incorrectly prepared TPN solutions
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Idiopathic Parkinsonism Most common form of Parkinsonism : Idiopathic form first described by James Parkinson, A British surgeon & paleontologist in 1817 in his “Essay on the Shaking Palsy”
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Pathophysiology of Idiopathic Parkinsons Pathological hallmark of PD : degeneration of dopaminergic neurons in the substantia nigra compacta, resulting in depletion of striatal dopamine This neurotransmitter regulates excitatory & inhibitory outflow from the basal ganglia Some of the dopaminergic neurons survive, and these are found to contain Lewy Bodies
Slide 10-

Pathophysiology of Parkinsons Lewy Bodies are eosinophilic intracytoplasmic inclusions, composed of numerous proteins Protein accumulation plays a prominent role in the pathogenesis of both sporadic & familial forms of PD Lewy bodies may actually be cytoprotective
Slide 11-

Lewy Bodies The neurodegenerative process in PD is not limited to the substantia nigra compacta Neuronal loss also happens in other brain regions, which accounts for the motor & non motor features of the disease
Slide 12-

Parkinsons Disease – The Six Cardinal Features Tremor at rest Rigidity Bradykinesia Loss of postural reflexes Flexed Posture Freezing (Motor Block) Diagnostic Criteria : Definite Parkinsons : at least two of these features must be present, one of them being # 1 or # 2 Probable : Feature # 1 or feature # 2 is present Possible : at least two of features # 3 – 6 must be present
Slide 13-

Diagnostic Testing There are no clinical tests widely available to definitively make the diagnosis, however, if confirmation of the clinical diagnosis is desired, order serial 6 – fluoro L dopa PET scans which will demonstrate a gradual decline in uptake in the putamen & caudate in the Parkinsons patient Alternative Imaging Study - Serial Beta CIT SPECT imaging revealing gradual loss of function in the striatum On the right, see the PET scan of a patient who underwent implantation of fetal tissue into the right putamen - note the recovery of function in the right putamen and the progressive loss of function in the left putamen
Slide 14-

Typical MRI Appearance in Parkinsons Disease Standard MRI studies in Parkinsons are normal If warranted, consider High Field Strength 1.5 Tesla T2 weighted Brain MRI Typical Appearance in Parkinsons : wider area of lucency will be noted in the subthalamic nucleus that is probably indicative of increased accumulation of iron – iron deposition occurs when there is a loss of connectivity to the cortex
Slide 15-

Early Non - Specific Signs of Parkinsons Generalized stiffness Pain or Paresthesias of the limbs – in particular, shoulder pain Constipation Low Uric Acid Levels Sleeplessness Reduction in volume of the voice Loss of sense of smell Seborrheic Dermatitis – see photo on the right These symptoms precede onset of the motor symptoms of Parkinsons A Retrospective Study of Early Symptoms of Parkinsons Disease, Przuntek, 1992)
Slide 16-

Early Signs of Parkinsonism Problems with fine motor skills Decreased sense of smell Loss of appetite Tremor occurring with anxiety Decreased arm swing on one side – a principal finding in Parkinsons is asymmetry in neurological findings Decreased emotional expression Personality changes, especially introversion & inflexibility
Slide 17-

Parkinsonism is Frequently Misdiagnosed Clinical presentation may vary from patient to patient It is not uncommon for PD symptoms to go unrecognized or unreported for years
Slide 18-

Two Major Forms of Parkinsonism Tremor Dominant – has a better prognosis PIGD – Postural Instability & Gait Dysfunction Variant – has a poorer prognosis
Slide 19-

The Cardinal Features : Bradykinesia Bradykinesia manifests itself as : Slow reaction times Impaired fine motor coordination that interferes with ADL Drooling due to failure to swallow saliva Monotonic & hypophonic dysarthria : due to incoordination of the muscles of vocalization Loss of facial expression (hypomimia) – leads to mask facies & decreased blink rate Reduced armswing when walking Micrographia – small cramped handwriting Bradyphrenia – slowness of thought The extreme form of bradykinesia is akinesia : the inability to initiate movement Bradykinesia is the most disabling feature of Parkinsonism. With a sudden surge in emotional energy, the bradykinetic patient may be able to catch a ball or make a fast movement This phenomenon is called kinesia paradoxica
Slide 20-

Pathophysiology of Bradykinesia Thought to result from failure of basal ganglia output to reinforce the cortical mechanisms that prepare & execute the commands to move Reduced dopaminergic function disrupts normal motor cortex activity Secondary factors which contribute to bradykinesia include muscle weakness, tremor, and rigidity Bradykinesia results from excessive activity in the subthalamic nucleus and the internal segment of the globus pallidus
Slide 21-

The Cardinal Symptoms : Tremor Resting tremor may be considered to be the most typical sign of Parkinsons A common initial symptom of the disease is an asymmetrical resting tremor – seen in 70 – 90% of patients at presentation Asymmetrical resting tremor usually involves the thumb or wrist If resting tremor is not present, consider that the patient’s Parkinsonian symptoms are caused by a disorder other than PD The typical resting tremor has a frequency between 4 – 6 Hz Tremor is most prominent in the distal part of an extremity – in the hand, called a pill rolling tremor Pill rolling tremor involves the forefinger & thumb at a frequency of 3 -6 cycles per second is the classical presentation of tremor When tremor is present in the head, it occurs in the region of the lips, chin and jaw – only occasionally in the neck **Tremor is more likely to be the presenting symptom in young patients, whereas older patients have more prominent bradykinesia**
Slide 22-

Treatment of Tremor Anticholinergics are effective in treatment of resting tremor Usually used in younger patients ( < 60 yrs) with intact cognition & predominant tremor Benztropine Trihexyphenidyl Side Effects : constipation, blurry vision, urinary retention, confusion, hallucinations
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Prognostic Significance of Tremor Presentation with tremor as the initial symptom often confers a positive prognosis – slower progression There is a subset of patients with Parkinsons who have “benign tremulous parkinsonism” – these patients have : A family history of tremor Minimal progression of the disease process Poor response to levodopa
Slide 24-

Rigidity & Flexed Posture Rigidity is manifested by increased resistance throughout the range of motion Rigidity can manifest itself proximally – in the neck, shoulders, and hips Gait in Parkinsons is characterized as : Short & shuffling steps Stooped posture Narrow base of support Flexed knees
Slide 25-

The Cardinal Signs : Flexed Posture - Camptocormia Patient on the left had camptocormia due to unrecognized, untreated Parkinsonism The picture on the right depicts his response to a single test dose of Sinemet. Camptocormia is a postural deformity seen in the Parkinsons patient This manifestation of Parkinsonism is often dismissed by physicians as hysteria
Slide 26-

The Cardinal Signs – Freezing Freezing is also known as motor block Most often affects the legs when walking, but it can also affect the arms and eyelids Freezing consists of a sudden, transient inability to move It typically causes hesitation when initiating walking & sudden inability to move feet when turning or walking thru narrow passages – such as doors or elevators – or when patients are about to reach a target destination Freezing is thought to related to noradrenergic deficiency related to degeneration of the locus coeruleus
Slide 27-

The Use of Gestes Antagonistes to Overcome Freezing Patients learn (or may be taught) a variety of tricks (French : gestes antagonistes) to overcome freezing attacks, such as : Marching to command (left, right,left, right) Stepping over objects, such as a crack in the pavement, the end of a walking stick Walking to music or a metronome Shifting body weight Rocking movements trunk Train your patient to perform gestes antagonistes !!!
Slide 28-

Association of Freezing with the Parkinsons Plus Syndromes When freezing occurs early in the disease process, (< 3 yrs.) or early postural instability (< 3yrs) is present, or is a predominant symptom : Consider that your patient may have a Parkinsons Plus Syndrome – not Parkinsons - such as PSP MSA Vascular Parkinsons
Slide 29-

Non Motor Features of Parkinsons The clinical course of Parkinsons is not limited to motor symptoms Non motor symptoms & disorders significantly affect the health related quality of life (HRQOL) Surveys of PD patients reveal that approximately 90% have at least 1 non motor symptom 10% of PD patient have 5 non motor symptoms The non motor symptoms contribute to shortened life expectancy
Slide 30-

Common Non - Motor Features of Parkinsons Neuropsychiatric Impulse Control Disorders Sleep Disorders Autonomic Dysfunction – orthostatic hypotension, hyperhidrosis, hypohidrosis, sexual impotence can be seen in Parkinsons – but if these features are noted early in disease process, your patient may have MSA Sensory Symptoms – paresthesias, oral & genital pain are common – as is olfactory dysfunction Other – Fatigue, Seborrhea, Diplopia, Blurred Vision, Weight Loss
Slide 31-

Neuropsychiatric Disorders in Parkinsons Disease Depression Anxiety, including panic attacks Cognitive Dysfunction Dementia Psychosis Confusion or delirium Apathy
Slide 32-

Depression in Parkinsons Most common neuropsychiatric disorder in PD patients, affecting up to 50% Depression is often comorbid with anxiety disorder Can be observed at any stage of the illness – including prior to onset of motor symptoms Depression is associated with increased disability, poor HRQOL, and a more rapid progression of motor impairment It is unclear whether or not the depression is reactive or related to neuropathology Most patients with Parkinsons who are depressed are not treated or treated inadequately for depression – resulting in increased disability Weintraub et al, J. of Geriatric Psychiatry & Neurology, 2003 Routine screening for depression & anxiety with a validated instrument is recommended Validated Instruments : Beck Depression Inventory, Geriatric Depression Screen, Hamilton Depression Inventory, Beck Anxiety Inventory, Speilberger State Trait Anxiety Inventory
Slide 33-

Risk Factors for Depression in the Parkinsonian Patient Increasing severity of cognitive impairment Female gender Early onset disease Personal history of depression prior to onset of disease
Slide 34-

Treatment of Depression – Evidence Based Medicine Meta – Analysis : Fewer than 30 studies exist in the literature which evaluate the effectiveness of antidepressants in PD The AAN recommends the use of amitriptyline for the treatment of depression in PD based on their review of available studies TCAs may not be well tolerated by all Parkinsons patients due to the side effect profile – particularly the orthostasis & worsening cognition
Slide 35-

Most Frequently Used Antidepressants in Parkinsons SSRIs are the most commonly used antidepressants Well tolerated by the major of patients This class of drugs do not appear to worsen motor symptoms in PD In open label clinical trials, most PD patients did not experience side effects with maximal dosages **Citalopram, escitalopram, and sertraline are recommended** - less prone to drug – drug interactions than paroxetine or fluoxetine
Slide 36-

Antidepressant Doses
Slide 37-

Anxiety in Parkinson Patients Avoid benzodiazepines as these increase the risk to fall Consider the use of an antidepressant which is also effective against anxiety Escitalopram is a good choice of an antidepressant which can also act as an anxiolytic Buspirone is well tolerated but has not been formally tested for its effectiveness in PD patients
Slide 38-

Cognitive Dysfunction & Dementia in PD Prevalence of dementia : 20 – 40% of PD patients : Six times higher than in the general population Characterized by : Psychomotor slowing Impaired executive function Inattention Impaired visuospatial abilities Memory impairment – due to poor retrieval of information in PD – as opposed to poor encoding of new information seen in Alzheimers Disease Verbal cueing may aide recall in Parkinsons patients – this is not usually helpful in Alzheimers
Slide 39-

Neurobiology of Development of Dementia in PD Neurotransmitter deficits are responsible : Decreased levels of the following are observed in PD : Acetylcholine Dopamine Serotonin Norepinephrine Cholinergic & dopaminergic deficits have been linked to memory dysfunction & dysexecutive syndrome Noradrenergic deficits have been linked to inattention **Consider neuropsychological testing on all your PD patients at regular intervals**
Slide 40-

Recommended Screening Tools for Dementia in the Parkinsons Patient Cambridge Cognitive Examination Folstein Mini Mental Status Exam Montreal Cognitive Assessment – highly effective in detecting early cognitive changes Hopkins Verbal Learning Test – assesses verbal memory abilities & recognition recall Clock Drawing Test – useful to asses visuospatial & executive abilities
Slide 41-

Comparison of the Clinical Features of Lewy Body Dementia, Parkinsons Dementia, & Alzheimers Disease
Slide 42-

Risk Factors for Development of Dementia in Parkinsons Patients Old age Older age at onset Increased severity of PD Depression Psychosis Early executive impairment Early memory deficits
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Is it Lewy Body Dementia or Parkinsons? The presence of dementia & psychosis early in the disease course is highly uncharacteristic of PD and favors a diagnosis of Lewy Body dementia
Slide 44-

Treatment of Dementia in Parkinsons Rivastigmine (Exelon) was found to be moderately effective in Parkinsons dementia in a large placebo controlled study & has received FDA approval for this indication In small studies, the anticholinesterase donepezil in PD patients with dementia Very rarely do these medications cause a worsening of Parkinsonian symptoms
Slide 45-

Drugs for Cognitive Dysfunction in Parkinsons Disease
Slide 46-

Impulse Control Disorders (ICD) Impulse control disorders are defined as failure to resist an impulse, drive, or temptation to perform an act that is harmful to the person or others Manifestations include compulsive gambling, hypersexuality, shopping, and binge eating. ICD occurs at a frequency of 1.5% of the general population In Parkinson Disease, one large scale study suggests that ICD affects 10 – 15% of patients with PD
Slide 47-

Etiology of ICD in Parkinsons Primary Etiology of ICD in Parkinsons – dopamine agonist therapy No one agent has been identified to be more likely than another to induce ICD Higher doses predict a greater risk for ICD A history of ICD before onset of Parkinsons is a risk factor for exacerbation of this syndrome after initiation of dopamine agonist therapy When prescribing dopaminergic agonist therapy, patients must be warned about the potential for developing an ICD Screen patients on dopaminergic agonists for an ICD with the Minnesota Impulse Disorders Interview
Slide 48-

Treatment of ICDs in Parkinsons When ICDs develop in the Parkinsons patient, consider : Dose reduction Discontinuing dopaminergic agonist Switching to another dopaminergic agonist Consider a trial of an SSRI Consider a trial of an atypical antipsychotic
Slide 49-

Sleep Disturbance in Parkinsons Some patients remain awake 30 – 40% of the night Sleep dysfunction is manifested as : Parasomnias Nocturnal Insomnia Difficulty initiating or maintaining sleep Daytime Hypersomnolence
Slide 50-

Etiologies of Sleep Disturbance in Parkinsons Nocturia “Wearing off” motor disability Sleep Apnea – due to rigidity in phargyneal & respiratory musculature & neuropathological changes Periodic Leg Movements Restless Leg Syndrome – occurs in 20% of Parkinsons patients Depression / Anxiety Neuropathological Changes – degeneration of the brainstem nuclei involved in respiration Medication related – for example, selegiline has amphetamine derative metabolites
Slide 51-

Treatment of Sleep Dysfunction in PD Sleep study to rule out sleep apnea Avoid nighttime doses of selegiline – or consider another MAOB inhibitor, rasagiline, which is less likely to affect sleep Consider use of small doses of immediate release levodopa / carbidopa before bedtime which can alleviate insomnia caused by motor symptoms Consider use of amitriptyline 5 – 40 mg po QHS or quietiapine to reduce sleep maintenance insomnia Deep brain stimulation of the subthalamic nucleus significantly reduces motor symptoms and can improve sleep duration and quality
Slide 52-

Treatment of Motor Symptoms In PD There is no cure for Parkinsons Disease No therapy has been shown to slow or reverse progression of the disease The most effective agent, levodopa / carbidopa has been associated with an increased risk of motor fluctuations Levodopa induced motor fluctuations & dyskinesias are difficult to treat & are socially stigmatizing The risk of motor fluctuations is greatest in younger patients The current treatment paradigm for Parkinsons involves maximizing therapy with levodopa sparing medications for as long as possible before starting levodopa
Slide 53-

Starting Parkinsons Disease Medication Management for Mildly Affected Patient Delay medication therapy for as long as possible – until disease process interferes with function When clinically significant disability or functional impairment begins, consider starting with dopaminergic agonist therapy : Amantidine 100 mg po BID OR MAOB Inhibitors : Seligiline 5 mg po BID Rasagiline 1 mg po QD : more potent than selegiline
Slide 54-

Amantidine Side Effects : Nausea Confusion Dizziness Livedo Reticularis Insomnia Hallucinations Edema Abrupt discontinuation can precipitate worsening of Parkinsonian symptoms & potential for neuroleptic malignant syndrome & delirium Severe psychosis has been reported in the elderly with high plasma levels Dose reduction is required in renal insufficiency
Slide 55-

MAOB Inhibitors : Seligiline & Rasagiline Side Effects : Nausea Orthostatic Hypotension Possible Interactions with tricyclics, SSRIs, meperidine No significant adverse reaction with tyramine rich foods at usual doses
Slide 56-

Other Dopaminergic Agonists for Possible Monotherapy Side Effects with these agents are more common than with levodopa / carbidopa May be used for early monotherapy The non ergot dopamine agonists, pramipexole (Mirapex) or ropinirole (ReQuip) can delay the need for levodopa Pramipexole 0.25 mg – 1 mg po TID Ropinirole 2 mg po TID
Slide 57-

Levodopa The most effective agent for the treatment of motor symptoms of PD It is the prodrug of dopamine, and it crosses the blood brain barrier It is then decarboxylated to dopamine in the nigrostriatal pathways Levodopa is always given with carbidopa,(marketed as Sinemet) which prevents peripheral metabolism of levodopa & allows a higher percentage of of levodopa to cross the blood brain barrier Administration of carbidopa minimizes the adverse effects of peripheral dopamine – including nausea & hypotension
Slide 58-

Response to Levodopa Initially patients have a good & sustained response to levodopa with small amounts given three times per day This honeymoon period may last 5 – 7 yrs. As the disease and the treatment progresses, motor complications occur in most patients Motor complications include a shortened duration of drug benefit – called “wearing off” and drug induced dyskinesias
Slide 59-

Wearing Off The half life of levodopa is 90 minutes With progressive disease, the benefits of each dose become shorter, with a wearing off of benefit before the next dose Patients may also experience loss of benefit from a usually effective dose – an unpredictable, sudden loss of drug effect & recurrence of severe PD symptoms - This is known as an on – off motor fluctuation
Slide 60-

Managing Motor Fluctuations Reduce each individual dose of levodopa & increase frequency of administration Add a dopamine agonist, such as ropinirole or pramipexole or amantidine Consider the use of a COMT inhibitor – a drug which inhibits a peripheral enzyme which metabolizes levodopa – examples entacapone (Comtan) 200 mg po TID – QID or tolcapone (Tasmar) 100 mg po TID – LFTs must be monitored for patients on Tasmar Levodopa & entacapone are available in a combination tablet called Stalevo for convenience in this situation Switch from standard levodopa / carbidopa to sustained release formulations of the drug *Often Parkinsons patients have delayed gastric emptying & malabsorption of Sinemet from chronic Helicobacter pylori infection – if your patient has motor fluctuations, consider workup & treatment for Helicobacter*
Slide 61-

Management of Dyskinesias Reduce each dose of levodopa Add agents to treat dyskinesias, such as amantidine Reduce or discontinue anticholinergic therapy
Slide 62-

Surgery for PD Pallidotomy is no longer performed in the management of Parkinsons – it is not as effective as Deep Brain Stimulation (DBS) DBS is indicated for patients with drug resistant motor fluctuations Bilateral Deep brain stimulation (DBS) of the subthalamic nucleus (STN) reduces both the primary symptoms of PD and its motor complications including tremor, bradykinesia, wearing off, dyskinesias, and dystonia
Slide 63-

Effects of DBS Reduction in daily levodopa dose by 55% 69% reduction in dyskinesias 68% reduction in off periods 34.5% improvement in quality of life
Slide 64-

Patient Selection for DBS & Potential Complications Patient Selection – Medically refractory motor fluctuations or tremor Stable medical problems Normal cognitive function Complications : Hemorrhage Stroke Infection Failure of stimulator Memory Loss
Slide 65-

Exercise Interventions in Parkinsons Disease A meta – analysis found that physical & occupational therapy improved gait speed, stride length, and ADL, but no change in the neurological cardinal signs – De Goede et al, Archives of PM&R, 2001 Train your patient to perform gestes antagonistes, such as marching with the metronome – this is not frequently done by therapists
Slide 66-

Weight Supported Ambulation Training Weight supported ambulation training with Lite Gait or Biodex has been shown to improve gait in Parkinsons patients, as published in the Archives of PM&R
Slide 67-

Speech & Language Pathology Services Dysphagia in Parkinsons is observed due to the weakness of pharnygeal & esophageal musculature, as well as due to lower esophageal sphincter dysfunction Consider regular screening of the PD patient for dysphagia with modified barium videofluoroscopic swallowing studies
Slide 68-

Speech & Language Pathology Services Helpful in the management of dysarthria associated with Parkinsons For PD related hypomimia, training the PD patient to shout has been found to be effective – this is known as the Lee Silverman technique
Slide 69-

Diet Levodopa absorption can be impaired by ingestion of amino acids, especially in patients with motor fluctuations, which can potentially reduce its effectiveness A high fiber diet (or fiber supplementation) as well as adequate fluid intake can minimize the constipation commonly seen in the Parkinsons patient
Slide 70-

Vitamin D Deficiency in Parkinsons
Slide 71-

NEJM April 1, 2010 Case Report – Cycling for Tx. Of Freezing in A Parkinsons Patient A 58-year-old man with a 10-year history of idiopathic Parkinson's disease presented with an incapacitating freezing of gait The patient had severe difficulties initiating gait and was able to take only a few shuffling steps when provided with a visual cue (the examiner's foot placed in front of the patient). Attempts to walk evolved rapidly into forward festination and ultimately a fall to the ground. Axial turning was impossible. However, the patient's ability to ride a bicycle was remarkably preserved Gait freezing recurred instantaneously after he dismounted the bicycle. This striking kinesia paradoxica may be explained by the bicycle's rotating pedals, which may act as an external pacing cue. Alternatively, the motor-control mechanisms involved in gait as compared with other activities engaging the legs, such as cycling, could be affected differentially in Parkinson's disease. Cycling may offer a useful approach for exercise training in patients with Parkinson's who are "grounded" by freezing
Slide 72-

Treatment of Sialorrhea in Parkinsons Sialorrhea often results from the PD patient’s inability to swallow their own secretions If severe, it can interfere with fluid & nutrient intake Botulinum Toxin A & B have been used to curtail sialorrhea Dose of Botulinum Toxin A : 10 units per parotid gland, 15 units per submandibular gland – procedure must be done bilaterally
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Equipment for the Parkinsons Patient Rolling Walkers are best – canes & standard walkers are frequently carried by the patient Shower chairs Grab Bars Raised Toilet Seats with armrests – ie Versaframe Chairs with arms to assist patient to lower themselves to the chair without falling
Slide 74-

Considerations for the Primary Care Physician Parkinsons patients have a lower incidence of cancer than the general population with the exception of … Malignant melanoma – Parkinsons patients are at 2 x greater risk of developing melanoma than the general population – order sunblock !
Slide 75-

On the Horizon Implantation of fetal tissue Implantation of retinal tissue Gene Therapy Neuroprotection Strategies : for patients with early Parkinsonism & their family members Antioxidant Trials - Vitamins E & C Coenzyme Q 10 at doses 2400 mg / day
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Thanks for Your Attention Questions ?