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Neuro -Test II
Neuro Test 2 - AD, PD, ALS & GBS
| Question | Answer |
|---|---|
| Alzheimer’s (AD) causes | No single identifiable cause. Amyloid plaques & neurofibrillary tangles. (ex Vit. B12 deficiency, hypothyroidism, age) |
| Is Alzheimer's a UMNL or LMNL | UMNL |
| What causes NT exhaustion in AD? | Stress and depression; lack of curiosity |
| Risk Factors for Alzheimer’s | Markers on different genes and chromosomes (Trisomy 21), cardiovascular disease, type 2 Diabetes, Heart disease, increased BP, increased cholesterol and increased free radicals, obesity, & family history |
| Indications that point to having Alzheimer’s (AD) | Dr’s look at Hx, physical exam and neuropsychological tests |
| Manifestation of AD | Resembles natural aging; mild memory loss for recent events. Visiospatial events; navigating the environment, cooking & fixing or manipulating mechanical objects in the home. |
| Alzheimer’s libido suppressed or heightened? | AD affects each person differently and can change throughout the disease; however, it either doesn’t change much or heightens libido |
| What is the only way to know if someone has Alzheimer’s? | Only way to truly know if someone has AD is to do an autopsy |
| Distribution (epidemiology)for AD | Equal for men and women |
| T/F: AD interferes with intellectual f(x)? | True |
| What increases and decreases with Alzheimer’s? | With AD you see a decline in ADLs, memory, decision-making but increase in anxiety and agitation |
| When does AD occur? | Late Adulthood. |
| Which part of the brain is affected in AD? | Limbic System: memory loss, behavioral changes, emotional and personality changes |
| Major differences between AD and PD | AD: limbic system: memory/mental/spiritual/emotional decline and PD: Basal Ganglia: movement decline (primary target is mov’t) |
| Which lobe of the brain is for initiation of mov’t? | Frontal Lobe |
| What does the cerebellum do? | Balance, coordination and equilibrium |
| What is the Tx for AD? | There is no cure. Get pt’s to live w/in their limits of disability. Group therapy with simple exercises. *NO LIGHT THERAPY* |
| Q. …controversy about cause of AD? | A) Al3+ poisoning, level of Al3+ is the issue; if more than trace, then causes problems; Al3+ is found in deodorant and non-coated utensils |
| What year was AD first reported? | 1907 |
| Is AD reversible? | No |
| In AD what part of the brain is affected? | Memory |
| In an autopsy exam of someone with AD, there is an abundance of what abnormal substance? | Amyloid Plaques and neurofibrillary tangles |
| In AD what do you notice about the brain? | Enlargement of canals (ventricles); brain shrinks so canals become enlarged |
| What is not essential for Tx-ing for AD? | Light Therapy |
| What is not a risk factor for those affected with AD? | Gender |
| AD and PD - highlights of PT: | Group therapy, visual cues, don’t exhaust, cool environment, regular routine ex’s, better in the a.m., and sun going down can affect them |
| Oxidative Dementia (PD) | Need water, veggies, beans; water very impt; need antioxidants to get rid of oxidants * MOST IMPORTANT ANTIOXIDANT - WATER* |
| Sundowning (AD) | Pt’s become more aggressive, signs/symptoms increase; can just take off; caretakers have to be alert towards sundown to prevent pt from wandering off |
| Characteristic signs of PD: | Festinating gait, pill rolling tremors, masked facial expression, slowness (bradykinesia), freezing, mm rigidity, unstable posture |
| What part of the brain is involved with PD? | Basal Ganglia |
| Is Parkinson's a UMNL or LMNL? | UMNL |
| What is NOT having the ability to perform rapid, alternating mov’ts? | Diadochokinesia |
| Who discovered PD? | James Parkinson |
| When was Parkinson's discovered | 1817 |
| With PD what decreases? | There is a decrease in the production of Dopamine |
| Why is depression not good? | NE/epinephrine are decreased due to stress; produce adrenaline from dopamine, so low level dopamine = low level adrenaline = less ability to handle stress |
| What does Dopamine do for the human? | Mov’t (if not emotionally involved then mov’t) |
| What affects production of Dopamine apart from exhaustion/depression? | Free radicals (oxidants): need antioxidants to combat |
| What is the most important antioxidant? | Water |
| Relate PD to ADL/Relate AD to ADL | better to deal with ADLs than someone with AD????? |
| Parkinson's Risk factors | Environmental toxins, gene mutations, high levels of Fe2+, O2 released by cells and damaging them |
| Who can get PD | Anyone can get it but higher incidence of young onset in Japan |
| Is there a cure for PD? | No cure |
| What is the cause of personality changes in PD? | The limbic system |
| Dance Therapy for PD | New & innovative; one of the best things ppl can do regardless of illness or not |
| What type of disease is PD? | Chronic, progressive disease of CNS |
| Basal Ganglia disorder? | Deficiency of dopamine and degeneration of the substantia nigra; loss of inhibitory dopamine results in excessive excitatory output from cholinergic system of basal ganglia |
| Causes of PD? | Commonly idiopathic but can also be infectious, atherosclerosis, toxic or drug induced |
| Clinical picture of PD | slowly progressive with emergence of secondary impairments and permanent disability |
| Mentation deficits (PD) | Bradyphrenia (slowing of thought processes), depression and dementia in advanced stages |
| Communication (PD) | Dysarthria, hypophonia, masked face and micrographia |
| Musculoskeletal (PD) | Contractures commonly present in flexors and adductors, persistent posturing in kyphosis with forward head, and osteoporosis leading to high risk of Fx |
| Sensory impairments (PD) | Abnormal cramp-like sensations poorly localized & perceptual deficits; Visual problems,skin integrity, tone/reflexes:rigidity,resting tremors,pill-rolling,mm atrophy,motor control,balance & postural rxns,festinating gait,mm &general endurance |
| Festinating Gait (PD) | shortened stride, decreased speed, increased cadence, decreased arm swing and trunk rotation |
| Impaired motor control (PD) | bradykinesia, akinesia (results in freezing episodes), and slowed rxn time and mov’t time |
| What is ALS? | Malnourishment of the mm resulting in atrophy; sensory still intact |
| Why ALS results in atrophy? | Progressive; amyotrophic: mm fiber atrophy from peripheral nerve involvement; Degeneration and scarring of the motor neurons in the lateral aspect of the spinal cord, brainstem and cerebral cortex |
| True or False, ALS usually starts unilateral but eventually becomes bilateral. | True |
| IS ALS UMNL or LMNL | ALS is both UMNL and LMNL |
| ALS LMNL signs | asymmetrical, distal weakness w/ eventual progressive atrophy, facial weakness that results in difficulty with swallowing |
| ALS UMNL signs | hyperactive tendon reflexes and spasticity |
| T/F: ALS is characterized by irreversible denervation? | True |
| What is the most common neurodegenerative disease among adults | ALS |
| Epidemiology of ALS | 1 per 100,000; typically btw ages of 50-60 yrs; men > women |
| Is there a cure for ALS | No cure; younger you are Dx’d, the slower the progression |
| How quickly does ALS progress? | Death usually results in 2-5 yrs due to respiratory compromise |
| Differences between ALS and GBS | GBS: LMN, temporary, starts fingers & toes ALS: UMN/LMN, permanent and fast, feet to head distal to proximal, starts unilaterally and goes bilaterally with sensory still intact |
| What is GBS | GBS is multiple neuropathies; distal to proximal; usually in the appendages |
| GBS | Polyneuritis with progressive muscular weakness that develops rapidly |
| Epidemiology of GBS | Unknown but associated with autoimmune attack; Usually occurs after recovery from an infectious illness; Evolves over a few days or weeks w/ slow recovery (months to a year) back to or near full f(x)ing |
| Pathology of GBS | Acute demyelination of both cranial and peripheral nerves |
| What does GBS resemble that it can be mis-Dx’d as? | Carpal Tunnel Syndrome |
| Btw ALS and GBS: which one quickly need adaptive devices (orthoses)? | ALS b/c starts at feet |
| Ratio of men to women with GBS | 2:1 (men to women) |
| Why does GBS need aggressive PT? | GBS will need aggressive exercise b/c mm’s waste rapidly; so need this aggressive exercise to prevent that from happening |
| GBS Tx | Plasmaphoresis - filter blood (all cells WBC, RBC, platelets filtered out; removes defective cells/proteins) and put plasma back; 50/50 chance body will make correct cells that aren’t defective |
| Clinical Picture of GBS | Aerobic capacity and endurance may be severely limited, especially w/ pulmonary involvement. Integumentary integrity: pain and paresthesias; typically less sensory involvement than motor |
| Motor Function GBS | Motor paresis or paralysis: relative symmetrical distribution or weakness; Progresses from lower extremities to upper and from distal to proximal; May produce full tetraplegia with respiratory failure; Not uncommon to have residual bilateral foot-drop |
Created by:
srussel
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