Parkinson's Disease NPTEFF Book Chapter 6 PDF

138 NPTE Final Frontier – Mastering the NPTE Parkinson disease (PD) Chronic progressive neurodegenerative disorder Depletion of dopami...

138 NPTE Final Frontier – Mastering the NPTE Parkinson disease (PD) Chronic progressive neurodegenerative disorder Depletion of dopamine from substantia nigra in the basal ganglia (BG) Loss of inhibitory dopamine results in excessive excitatory output from cholinergic system (acetylcholine) of BG ➤ Acetylcholine: main transmitter for parasympathetic nervous system (PNS) As disease progresses and neurons degenerate, Lewy bodies accumulate Etiology Infection (postencephalitic parkinsonism), atherosclerosis, idiopathic, toxin- or drug-induced Parkinsonism: S/S like PD but without the official diagnosis S/S Appear after 40% damage Mnemonic: “TRAP” ➤ T = resting Tremor: pill rolling presentation ‡ Worsens with emotional stress ‡ Often occurs first in one hand ➤ R = Rigidity: affects agonist and antagonist (not velocity-dependent) ‡ In early stages, often asymmetrical and involves proximal muscles (shoulders and neck) ⚬ Progresses to involve muscles of face and extremities ‡ Cogwheel rigidity: jerky ratchetlike resistance to passive range of motion (PROM) ⚬ Occurs when tremor exists with rigidity ‡ Lead-pipe rigidity: sustained resistance to PROM with no fluctuations ⚬ Next, inspect voluntary repetitive movements to determine active limita- tions due to rigidity ➤ A = Akinesia (cannot initiate movement) and bradykinesia (slow movements) ‡ Akinesia in later stages of PD ‡ Freezing episodes (fixed postures) ‡ Difficulty with sit-to-stand transfers ➤ P = Postural instability ‡ Thoracic kyphosis; head forward posture ‡ Decreased trunk rotation and arm swing ⚬ Emphasize trunk rotation (facilitation, PNF, rhythmic initiation) ⚬ Cross midline ‡ Leaning forward or backward when upright Festinating gait: progressive increase in speed with short stride → quick shuffling ➤ Unable to stop on command ➤ General lack of extension; stooped posture ➤ Gait can be anteropulsive → forward festinating gait ‡ Can treat by adding toe wedge or flat heel to displace center of gravity (COG) posteriorly ‡ Often prescribing a rolling walker is contraindicated due to forward festinat- ing gait Freezing of gait: sudden abrupt inability to initiate any movement ➤ Cognitive load (eg, counting) and music help ➤ Climbing stairs can be easier than walking for some with PD due to visual cues ➤ Doorways or turns can lead to freezing episodes Hypophonia: decreased volume of speech ➤ Mutism and masklike face (hypomimia) (infrequent blinking, lack of expressions) in advanced stages Dysphasia, dysarthria Orthostatic hypotension: common ➤ Cardiac arrhythmias uncommon in PD Book_5566_Ch06.indd 138 18-04-2024 22:17:07  Neuromuscular Physical Therapy 139 Decreased ROM: from disuse and inactivity ➤ Contractures common in flexors, adductors, rotators, and plantar flexors ➤ Kyphotic posture (stooped) with head forward ‡ Due to weak antigravity muscles ➤ Often OP with risk of fracture (Fx) Akathisia: Extreme restlessness Autonomic changes ➤ Sialorrhea: excessive saliva production; drooling ➤ Abnormal thermoregulation: excessive sweating ➤ Seborrhea: excessive secretion of sebum; greasy skin ➤ Urinary incontinence and erectile dysfunction Reduced endurance ➤ Fatigue is one of the most common symptoms ‡ Often due to progressive sympathetic denervation of the heart ‡ Altered heart rate (HR) and blood pressure (BP) Decreased thoracic expansion ➤ Restrictive lung disease ➤ Low inspiratory reserve capacity (IRC), forced vital capacity (FVC), and forced expiratory volume in 1 second (FEV1) and higher residual volume (RV) ➤ Cardiovascular disease (CVD) and pneumonia are most common causes of death ➤ Erratic breathing ‡ Due to dyskinetic movement patterns of respiratory muscles Poor dexterity: smaller writing (micrographia) Dysthymic disorder: chronic depression Early S/S: anosmia, sleep disorders, constipation ➤ Insomnia at night and excessive daytime sleepiness Examination It is important to ask if patient has taken dopaminergic medication prior to examina- tion or treatment Bradyphrenia: slowing of thought process Dementia in late stages (Lewy body dementia) Poor dual-tasking Decreased muscle strength due to disuse atrophy Treatment Becomes increasingly more challenging to manage with stage 3 or higher Caregiver education and training is key to keeping individual safely ambulating in the home Taking medications consistently and on a fixed schedule is also key For home exercise program (HEP), patient should be prone lying for flexion contractures For festinating gait, use a toe wedge to displace COG backward ➤ Do not want to increase cadence or stride length ➤ Improve the limits of stability and improve the alignment of the center of pressure (focus on reducing anterior displacement) Levodopa/carbidopa combination (brand name Sinemet): gold standard drug ➤ Examine for end-of-dose deterioration, on–off phenomenon ‡ Sudden change with loss of function, immobility, and severe dyskinesia ➤ Ensure that physical therapy occurs when patient is in an “on phase” of medication (1 hour after administration) ➤ Effective for approximately 4 to 6 years (wears off after this time frame) ➤ Long-term adverse effects of medication use ‡ Dyskinesia: dynamic involuntary movements ⚬ Occurs at peak levodopa dose or transition between “on” and “off” phases ‡ Dystonia: prolonged involuntary contraction (twisting, torsion) ‡ Nausea and vomiting ‡ Orthostatic hypotension (but no bradycardia) ‡ Arrhythmias Book_5566_Ch06.indd 139 18-04-2024 22:17:07  140 NPTE Final Frontier – Mastering the NPTE ‡ Hallucinations Anticholinergic drugs: used to control tremor ➤ Can cause visual disturbances (blurred vision, photophobia, presbyopia) Amantadine: enhances dopamine release Selegiline (l-deprenyl): used in early stages to slow progress of disease Deep brain stimulation: in thalamus or subthalamic nucleus Huntington disease (HD) Autosomal-dominant progressive neurodegenerative disorder; caused by cytosine-ade- nine-guanine (CAG) trinucleotide repeat Degeneration of BG and cerebral cortex Most common age range for diagnosis is 35 to 55 years S/S Movement disorders ➤ Chorea: involuntary, rapid, irregular or jerky movements ‡ Upper extremity (UE) more commonly involved ➤ Dystonia: rigidity, muscle contractures ➤ Difficulty with physical production of speech and swallowing ➤ Slow or abnormal eye movements Cognitive decline Behavioral changes Basal ganglia disorders Hyperkinesia: abnormally increased muscle activity or movement Hemiballismus: sudden, violent, and large-amplitude flailing motions of arm and leg on 1 side of body (unilateral) ➤ Axial and proximal muscles most commonly affected ➤ Due to lesion in the C/L subthalamic nucleus ➤ “Hemi” = half Dystonia: rigidity or muscle contracture (agonist and antagonist) ➤ Causes abnormal posturing (dystonic posture) or twisting movement ➤ Common in trunk and extremities ➤ Spasmodic torticollis can occur Athetosis: “wormlike ” movements (can occur) ➤ Slow, involuntary writhing or twisting ➤ Distal UE commonly involved (hyperextension to hyperflexion of wrist and fingers) Amyotrophic lateral sclerosis (ALS) Degeneration of anterior horn cells and corticobulbar and corticospinal tract Fatal → up to 5-year life expectancy following diagnosis (progressive disease) S/S UMN and LMN presentation without sensory loss ➤ Only motor neurons are affected ‡ Decreased amplitude and duration of motor unit action potentials ‡ Decreased polyphasic action potentials No change in sensory-evoked potentials (no sensory issues) Cervical spine extensor weakness is common Denervated muscles (twitching and cramping are common) ➤ Muscle atrophy and fasciculations (LMN) Spasticity, hyperreflexia (UMN) Dysphagia, dysarthria, pseudobulbar palsy (bulbar onset) ➤ Pseudobulbar affect: random laughing or crying (change in emotion) for no ­apparent reason Book_5566_Ch06.indd 140 18-04-2024 22:17:07