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Neuro D&D > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is the pattern of a normal muscle biopsy?

A
  • Mosaic Pattern

- -Fiber types are scattered and not grouped in a particular pattern

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2
Q

What do neurogenic diseases involve?

A

*Involves nerve cell bodies, axons and/or dendrites involved

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3
Q

What is a needle EMG?

A
  • Denervated muscle is spontaneously active at rest (fibrillation potentials)
  • Short duration (<3 ms) and low amplitude (<300 µv), fibrillation potentials occur in semi-rhythmical runs (<30/second).
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4
Q

How does regeneration occur?

A

*through collateral sprouting

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5
Q

What does neuron atrophy cause?

A

*Causes muscle atrophy of the same muscle fiber type

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6
Q

What occurs with reinnervated muscle fibers?

A
  • since motor neuron type determines muscle fiber type, re-innervated muscle fibers assume histochemical properties of neuron (change fiber type).
  • results in muscle fiber type grouping due to re-innervation (as opposed to the mosaic pattern of normal muscle).
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7
Q

What do myogenic/myopathies involve?

A

*Involve muscle degeneration

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8
Q

What occurs with a myogenic disease needle EMG?

A

*Low muscle activity at rest

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9
Q

What would occur in a muscle biopsy of a myogenic disease?

A
  • Muscle fiber atrophy in a random fashion
  • all muscle fiber types are affected
  • retains the mosaic pattern but fewer overall number and size of all types of muscle fibers
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10
Q

What are examples of Neurogenic diseases?

A
  • Compression of nerve roots or peripheral nerves (PTP 565 – Fundamentals class)
  • Bell’s Palsy*
  • Diabetic polyneuropathy*
  • Alcoholic polyneuropathy
  • Polio and post-polio syndrome
  • Amyotrophic lateral sclerosis (ALS)*
  • Guillian-Barre syndrome (GB)*
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11
Q

What is an example of a myogenic disease?

A

*Muscular dystrophy

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12
Q

What are the fibers in a normal muscle biopsy?

A

*Muscles may have proportionately more fast-glycolytic (FG) muscles fibers as compared to slow, oxidative (SO) secondary to its function

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13
Q

What is Bell’s Palsy

A
  • Lesion of CN VII
  • -demyelination in mild cases
  • -demyelination and axonal damage in more severe cases
  • Innervation to upper face is bilateral
  • Innervation to lower face is unilateral (from opposite hemisphere)
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14
Q

How does Bell’s Palsy typically present?

A

*Presents as flaccid paralysis on the ipsilateral side of the face, affecting the upper and lower quadrants of the face

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15
Q

What is the Etiology of Bell’s Palsy?

A
  • Unknown in most cases
  • May be secondary to viral infection causing swelling in auditory canal (remember that CN VII goes through the auditory canal)
  • In a small number of cases, secondary to acoustic neuroma impinging on nerve
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16
Q

What are the motor signs of Bell’s Palsy?

A
  • Flaccidity
  • –Mouth droops
  • -Nasolabial fold is flattened
  • -Eyelid does not close
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17
Q

What are the sensory signs of Bell’s Palsy?

A

*Decreased taste on ipsilateral tongue

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18
Q

What are the ANS signs of Bell’s Palsy?

A

*Decreased tearing (dry eye)

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19
Q

What is the incidence of Bell’s Palsy?

A
  • 20/100,000 US each year

* Affects 20,000-100,000 people in US per year

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20
Q

What is the onset of Bell’s Palsy?

A
  • Typical onset is overnight

* Onset more common between 20-40 YO

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21
Q

What populations will have a greater risk of getting Bell’s Palsy?

A

*Diabetics and pregnant women and people with MS

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22
Q

What is the Medical treatment for Bell’s Palsy?

A
  • High-dose corticosteroids for 5 days followed by a tapered dose for another 5 days
  • Antiviral medications, e.g. acyclovir
  • –Improves outcomes when paired with corticosteroids
  • Eye patch, artificial tears (methylcellulose eye drops every 4 hours)
  • Gentle massage and gentle heat occasionally used
  • PT for muscle retraining only if problems persist
  • –E-stim for facial muscles
  • 70% of people completely recover within 2-3 weeks (in simple cases) or 3-6 months (in severe cases)
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23
Q

What is diabetic polyneuropathy?

A

*Affects PNS axons primarily (some de-myelination

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24
Q

What is the etiology of Diabetic polyneuropathy?

A

*Disrupted microcirculation

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25
Q

What is the onset of Diabetic polyneuropathy?

A
  • After long duration diabetes
  • –In diabetics who have had diabetes for 25+ years, 50% have this condition
  • Occurs in insulin-dependent and non-insulin dependent diabetes
  • Some regeneration with control of diabetes
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26
Q

What is the large nerve fiber involvement in diabetic polyneuropathy?

A

*Large nerve fiber sensory involvement of MANY NERVES IN LOWER LEGS & FEET
(Ia, Ib & II – from muscle spindles & GTOs)
—most common
—painless paresthesias in bilateral feet and lower legs
decreased vibration and proprioception sense

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27
Q

What is the small nerve fiber involvement in diabetic polyneuropathy?

A
  • Small nerve fiber sensory involvement (A delta & C afferent fibers)
  • –deep aching pain in legs and burning feeling in feet
  • –decreased touch, pain, and temperature sensations
  • –nocturnal pain and paresthesias
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28
Q

What are the S&S of peripheral neuropathy?

A
  • Numbness or reduced ability to feel pain or changes in temperature, especially in the feet and toes
  • A tingling or burning feeling
  • Sharp, jabbing pain that may be worse at night
  • Pain when walking
  • Extreme sensitivity to the lightest touch — for some people, even the weight of a sheet can be agonizing
  • Muscle weakness and difficulty walking
  • Serious foot problems, such as ulcers, infections, deformities, and bone and joint pain
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29
Q

What are the screening/examination tests of diabetic polyneuropathy?

A
  • NVCs
  • Monofilament screening with 5.07/10 gm. filament
  • Vibration
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30
Q

What are the complications with diabetic polyneuropathy?

A
  • Diabetic ulcers

* 50% of non-traumatic amputations in US are performed on individuals with diabetes

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31
Q

Where are the lesion sites of ALS?

A

*anterior horn cells (alpha & gamma motor neurons (LMN signs)), lateral corticospinal tract, motor nuclei of brainstem, and motor area of frontal lobe

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32
Q

What occurs in ALS?

A
  • primary pathologic defect is in the motor neuron cell body (specific to anterior horn cell in the spinal cord)
  • motor cells in the brainstem motor nuclei (cranial nerves)
  • pyramidal cells in the primary motor cortex thus loss of the upper motor neurons in corticospinal tracts (Betz cells)
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33
Q

What are the possible causes of ALS?

A
  • Definitive cause is unknown currently
  • Mitochondria
  • Currently, the most prevalent theory is that a SOD1 gene mutation causes the superoxide dismutase (SOD) enzyme to function improperly. This SOD enzyme is a strong anti-oxidant that the mitochondria need to perform their respiratory function. The respiratory and ATP function is compromised and the nerve cell begins to atrophy.
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34
Q

What are OTHER possible causes of ALS?

A
  • Glutamate (and certain related neuropeptides) are elevated in the cerebrospinal fluid and blood in ALS patients up to concentrations that could be neurotoxic. Over-excitation of glutamate-sensitive cells in the nervous system may result in their premature degeneration and death.
  • Premature aging
  • Exogenous toxins (e.g. heavy metals)
  • Viral diseases (due to similarities between ALS and poliomyelitis (both are anterior horn diseases) > suggest viral origins)
  • Immunologic disturbances (frequent occurrence of unusual antibodies in the blood or nervous system of patients with ALS and animal studies)
  • Heredity:  5% to 10% of all cases of ALS are familial
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35
Q

What are the stats of ALS?

A
  • 0.1% of adult deaths in U.S.
  • ALS is a disease of late middle life and is rarely seen prior to age 40.
  • 90% of all cases begin between the ages of 40 and 70 years
  • some predominance in men (estimated at 1.5-2.0 males to 1 females)
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36
Q

What are the S&S of ALS?

A
  • First sign is usually asymmetric, distal weakness (e.g. difficulty in manipulating objects with the fingers or dragging one leg during walking)
  • By the time the patient’s complain of weakness, they often have lost 80% of their alpha motor neurons in the areas of weakness
  • Early signs: severe muscle cramps and/or fasciculations at rest
  • EMG
  • –spontaneous fibrillations
  • –fasciculations with giant unit spikes upon voluntary activity
  • Progress to muscle atrophy and severe muscle weakness
  • –decrease in number of muscle fibers
  • –type II fibers tend to atrophy earlier and more rapidly than type I fibers
  • Cranial nerve cell atrophy leads to dysarthria, dysphagia, difficulty in chewing, tongue weakness and fasciculations may be prominent (the hypoglossal, facial, and trigeminal nuclei are most severely involved)
  • Control of bladder, bowel, and autonomic function is largely unimpaired, however, some studies report sub-clinical involvement
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37
Q

What are the sensory S&S of ALS?

A
  • THERE ARE NONE!!!
  • sensory systems or the special senses are rarely involved (this is primarily a motor neuron cell body disease), however, pain and paresthesia are often reported
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38
Q

What are the LMN signs of ALS?

A
  • Progressive muscle atrophy
  • Weakness (asymmetric weakness is often a presenting sign)
  • Fasciculations (especially evident in tongue, deltoid)
  • Muscle cramps (painful)
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39
Q

What are the UMN signs of ALS?

A
  • Spasticity
  • Hyperreflexia
  • Positive Babinski
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40
Q

What are the Statistics of ALS?

A
  • Death in 2-5 years commonly from respiratory compromise
  • Life expectancy of a patient with ALS can vary from less than 1 year to more than a decade with ventilator support
  • Average survival rate is 4.1 years
  • 20% survive more than 5 years
  • Those who have ALS before age 50 generally live longer
  • Those that have early CN involvement usually live less years post-Dx
  • Stephen Hawkins is the exception
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41
Q

What are the interventions for ALS?

A
  • General care revolves around the relief of discomfort and minimization of musculoskeletal, integumentary, and systemic effects
  • Problems with swallowing, speech, postural control, and respiration are common so that equipment/therapy must be targeted to these needs (IPE – team approach)
  • Therapy is directed at preventing contractures, skeletal deformity and/or respiratory complications, maintaining activity level, and recommending and issuing equipment as needed.
  • Muscle spasms – stretching, increased movement, quinine or baclofen
  • Diet – anti-oxidants – vitamins E and C
  • In general, encourage a balance between activity and rest. “Do no harm” philosophy.
  • If more than one third of the motor units are intact, exercise led to hypertrophy. If less than one third of the motor units are intact, vigorous exercise damaged the muscles
  • If the patient shows evidence of significant, persistent weakness following institution of an exercise program or persistent morning fatigue, the therapist must redesign the HEP and monitor the patient’s activity level and response to HEP carefully
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42
Q

What is GB?

A
  • An acute polyneuropathy affecting the peripheral nervous system
  • May be an autoimmune attack on both the Schwann cells and peripheral and cranial nerves by circulating antibodies
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43
Q

What is the etiology of GB?

A
  • acute – develops rapidly
  • often follows the flu or respiratory infection
  • may be idiopathic
  • Guillain–Barré syndrome is rare (1-2 cases per 100,000 people annually), but is the most common cause of acute non-trauma-related paralysis.
  • can occur at any age, but mostly 50-80
  • More common in men than women
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44
Q

What are the characteristics of GB?

A
  • The disorder is characterized by symmetrical weakness that usually affects the lower limbs first, and rapidly progresses in an ascending fashion.
  • Individuals generally notice weakness in their legs, manifesting as “rubbery legs” or legs that tend to buckle, with or without numbness or tingling (“Jeff”)
  • As the weakness progresses upward, usually over periods of hours to days, the arms and facial muscles also become affected.
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45
Q

When the cranial nerves are involved with GB what can it lead to?

A
  • Oropharyngeal dysphagia (drooling, or difficulty swallowing and/or maintaining an open airway)
  • Respiratory complications
  • –Can cause life-threatening complications, in particular if the respiratory muscles are affected or if the autonomic nervous system is involved
  • –Most patients require hospitalization and about 30% require ventilator assistance
  • Facial weakness is also common
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46
Q

What form does Sensory loss occurs with GB?

A

*takes the form of loss of proprioception

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47
Q

What are common symptoms of GB?

A
  • Pain is a common symptom in GBS, presenting as deep aching pain, usually in the weakened muscles
  • In severe cases of GBS, loss of autonomic function is common, manifesting as wide fluctuations in blood pressure, orthostatic hypotension, cardiac arrhythmias
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48
Q

What is the course of the disease of GB?

A
  • Maximal onset in less than 4 weeks (often in a few days)
  • Static phase (plateau of 2-4 weeks)
  • Recovery takes months to years
  • Recurs in 10% of cases
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49
Q

When is there poor prognosis with GB?

A
  • Onset at an older age
  • Extended time before recovery begins
  • Need for artificial respiration
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50
Q

What is the mortality rate of GB?

A

*5%

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51
Q

What is the progression of weakness of GB?

A
  • At 6 months, 85% are ambulatory
  • At 1 year, 20% remain significantly handicapped by weakness
  • At 2 years, 8% have not achieved full recovery
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52
Q

What is the diagnosis of GB?

A
  • Nerve conduction studies

* Studies of the cerebrospinal fluid

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53
Q

What is the intervention of GB?

A
  • Supportive medical care
  • Plasmaphoresis – filtering the blood plasma to remove circulating antibodies responsible for the destruction of the Schwann cells and peripheral and cranial nerves
  • Intravenous immunoglobulins
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54
Q

What is the Etiology of MS?

A
  • more than 2.3 million people worldwide
  • female > males (women 2-3 x more often than men)
  • predominantly Caucasian population
  • high frequency: Northern US, Scandinavian countries and northern Europe
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55
Q

How does age affect MS?

A
  • Most people are diagnosed between the ages of 20 and 50

* Although MS can occur in young children and significantly older adults

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56
Q

What are the genetic factors of MS?

A
  • MS occurs in most ethnic groups, including African-Americans, Asians and Hispanics/Latinos, but is more common in Caucasians of northern European ancestry.
  • More common in areas farthest from the equator.
  • United States - about one chance in 750 of developing MS
  • For first-degree relatives of a person with MS, such as children, siblings or non-identical twins, the risk rises to approximately one in 40
  • The identical twin of someone with MS (who shares all the same genes) has a one in four chance of developing the disease.
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57
Q

What are found in MS?

A
  • Demyelinating lesions and plaques are found throughout the CNS especially in the periventricular areas of cortex, cerebellum, brainstem and spinal cord
  • Does not involve the PNS
58
Q

What does De-myelination lead to in MS?

A
  • De-myelination leads to NCV abnormalities (slowing of transmission or conduction blocks) or cross-talk (neurons “talk” to each other since myelin no longer insulates)
  • Produce patches of demyelination = plagues in the white matter
59
Q

What is MS?

A
  • Autoimmune disease in which the oligodendrocytes (myelin) is attacked by the person’s own antibodies
  • Immunological mediated pathogenesis
  • –Slow virus theory - acquire virus during puberty lies dormant (mean approximately 12 years) before MS begins
  • –Autoimmune reaction theory - CNS reaction against itself resulting in demyelination
60
Q

What is the Diagnosis of MS?

A
  • MS can be difficult to diagnose.
  • Since there is no single test for MS, the diagnosis can be missed, delayed or even incorrect.
  • MS is not a “reportable” disease, which means that the government does not require physicians to inform any central database when they make the diagnosis. Without this kind of centralized reporting system, there is no easy way to count people with MS.

*Multiple courses - relapses and remissions, relentless progression, very slow progression

61
Q

What are the symptoms of MS?

A
  • *Dependent on where the plaques, inflammation and demyelintion are located
  • Sensory disturbances
  • Paresis of one or multiple limbs
  • Cerebellar movement disorders (intention tremor, ataxia, dysmetria, loss of balance, poor coordination, ataxic gait)
  • Fatigue – major problem is persistent fatigue, loss of energy, decreased tolerance to exercise
  • Visual disturbances
  • Bowel, bladder, and/or sexual disturbances
62
Q

What is Relapsing-remitting MS?

A

*The most common disease course. It’s characterized by clearly defined attacks of worsening neurologic function. These attacks, also called relapses, flare ups or exacerbations, are followed by partial or complete recovery periods (remission), during which symptoms improve partially or completely and there is no apparent progression of disease. Approximately 85% of people with MS are initally diagnosed with relapsing-remitting MS.

63
Q

What is secondary-progressive MS?

A

*Follows after RRMS. Most people who are initially diagnosed with RRMS will eventually transition to SPMS, which means that the disease will begin to progress more steadily (although not necessarily more quickly) with or without relapses

64
Q

What is primary progressive MS?

A

*characterized by steadily worsening neurologic function from the beginning. Although the rate of progression may vary over time with occassional plateaus and temporary, minor improvements, there are no distinct relapses or remissions. About 10 percent of people with MS are diagnosed with PPMS

65
Q

What is progressive relapsing MS?

A

*Least common of 4 disease courses. Characterized by steadily progressing disease from the beginning and occassional exacerbations along the way. People with this form of MS may or may not experience some recovery following these attacks; the disease continues to progress without remissions.

66
Q

What do PTs need to know in regards to MS?

A

Adverse reaction to heat (internal and external) - may exacerbate symptoms

  • Hot packs
  • Immersion in water
  • Hot weather
  • Illness with fever
67
Q

What is the overview of Muscular Dystrophy?

A
  • Genetically determined
  • Progressive degenerative course
  • Muscle fiber changes
  • -Degeneration
  • -Regeneration (collateral sprouting)
  • -Fibrosis
68
Q

What are the general S&S of Muscular Dystrophy?

A
  • Muscular degeneration
  • Hypotonia
  • Muscle atrophy
  • Pseudohypertrophy
69
Q

What is dystrophin and what disease is it abnormal in?

A

Dystrophin is a protein that links the muscle surface membrane [sarcolemma]
with the contractile muscle protein [actin]). Dystrophin is not normal in MD

70
Q

What is the occurrence of MD?

A

1 in 500,000 male births

*Males only (x-linked recessive disorder)

71
Q

When does MD begin?

A
  • Around 3-5 YO, weakness in legs is first S&S
  • Rapid progression-often in wheelchair by age 12, death in 3rd decade
  • Gene produces dystrophin (a protein forming part of muscle plasma membrane) is lacking; dystrophin gene Xp21
72
Q

What is an early diagnostic process in MD?

A
  • Early in the diagnostic process doctors often order a creatine kinase (CK) blood test
  • CK is an enzyme that leaks out of damaged muscle.
  • When elevated CK levels are found in a blood sample, it usually means muscle is being destroyed by some abnormal process, such as a muscular dystrophy or inflammation.
  • High CK level suggests that the muscles themselves are the likely cause of the weakness, but must differentiate what the muscle disorder might be.
73
Q

Where does the weakness occur in MD?

A

*Symmetrical weakness and atrophy in para-axial (trunk) & proximal muscles

74
Q

What is pseudohypertrophy?

A
  • Pseudohypertrophy due to connective tissue and fatty deposits in the muscles (most commonly in bilateral calf muscles)
  • They look bigger but it’s atrophy, not hypertrophy
75
Q

What should a PT do for MD?

A

*no strenuous exercise—causes muscle breakdown! (pushing into muscular fatigue > damages cells)

76
Q

What is Gower’s Sign?

A
  • Usually present in all forms of MD
  • The pt walks their hands up their body in order to stand up, sometimes they even make a wider base to make it shorter/easier
77
Q

What are some signs of MD?

A
  • Increased lumbar lordosis
  • Child walks on toes due to PF contractures
  • Positive Trendelenburg sign
  • Scoliosis happens in most cases
78
Q

What can be effected on boys with MD in their early teens?

A

*The heart and respiratory muscles

79
Q

When do kids lose the ability to ambulate with MD?

A
  • By 10-12 YO

- -The longer you keep them out of a WC the better

80
Q

How do you diagnose MD?

A
  • Creatine kinase (CK) blood test
  • Genetic testing
  • EMG, Ultrasonography, Muscle biopsy
81
Q

What are medications and diets for MD?

A
  • Corticosteroids such as Prednisone have been found effective in slowing the course of DMD.
  • Calcium supplements and vitamin D are often prescribed with prednisone to counteract the osteoporosis
  • Low-calorie, low-sodium diet is usually recommended to help offset the weight gain and fluid retention seen with corticosteroids
82
Q

What are the interventions for MD?

A
  • Surgery, bracing, assistive devices
  • Physical therapy
  • -As muscular dystrophy progresses and muscles weaken, joint contractures can develop and tendons can shorten, restricting flexibility and mobility
  • -One goal of physical therapy is to provide regular range-of-motion exercises to keep joints as flexible as possible, delaying the progression of contractures and scoliosis
  • -Avoid strenuous exercise since can exacerbate muscle cell death
  • -Assist in maintaining function and functional mobility as long as possible
83
Q

What are the Anatomic NS Changes with age?

A
  • Overall brain weight decreases with age
  • -1,260 grams – 21-40 years old
  • -1,061 grams – women > than 80 years old
  • By 8th decade, NCV can decrease by 10-15% especially in myelinated nerves
84
Q

What are the changes with Aging?

A
  • Decreased # of sensory receptors
  • Decreased synthesis of neurotransmitters
  • -May have decreased control of:
  • —Emotions
  • —Attention
  • Reduction of Serotonin
  • -Reduced memory
  • -Sleep pattern effects
  • -Thermoregulation
85
Q

What are Senile Plaques?

A
  • Extracellular deposits of amyloid (starch-like protein-carbohydrate complex) in the gray matter of the brain
  • -Occur most often in the cortex and hippocampus
  • -Associated with Alzheimer’s disease and Dementia
  • -Proportion of people with plaques:
  • —Age 60 years (10%)
  • —Age 80 years (60%)
  • Direct relationship between number of senile plaques and acetylcholine
  • Because acetylcholine is associated with memory loss, it is believed that the senile plaques are a major cause of short term memory loss in Alzheimer’s disease.
86
Q

What are Neurofibrillary Tangles?

A
  • Pathological accumulation of paired helical filaments
  • Found primarily in the cytoplasm of nerve cells of the brain
  • Cerebral cortex and hippocampus
  • Found in higher concentration in older adults
  • Occurs in Alzheimer’s disease and Dementia
87
Q

What are the changes to the vestibular system with aging?

A
  • Hair cell receptors decline beginning at age 30
  • Vestibular receptor cells decrease by age 55-60
  • Myelinated fiber loss in vestibular system is 40% by age 80
  • May lead to c/o dizziness
88
Q

What are somatosensory changes with aging?

A
  • Decreased # of unmyelinated and myelinated nerve fibers
  • Blood vessels become atherosclerotic  loss of blood supply to nerve fibers
  • –Major contributor to increased prevalence of peripheral neuropathies in older adults
89
Q

What are the motor system changes with aging?

A
  • Loss of αMN occurs with age.
  • -Remaining αMN will innervate the denervated muscle cells
  • -Results in larger motor units, which can effectively reduce motor coordination for finely tuned movements
  • Space between nodes of Ranvier (myelin) is reduced  leads to reduced NCV
90
Q

What are the Autonomic NS changes with age?

A
  • Reduce sympathetic control of vasculature in the skin

- -Results in reduced wound repair efficiency

91
Q

What is benign senescent forgetfulness?

A
  • A mild decline in short-term memory
  • Does not progress to other mental impairments
  • NOT dementia
  • Difficult to partition from memory impairments secondary to polypharmacology
92
Q

What is dementia?

A

*A decline in intellectual function (memory and other mental abilities) severe enough to interfere with a person’s relationships and ability to carry out daily activities

93
Q

What problems can occur in dementia?

A
  • Dementia usually involves cognitive impairments affecting memory and orientation plus one or more of the following problems:
  • -Abstract thinking
  • -Judgment and problem solving
  • -Language – reduction in frequency
  • -Personality – behavior, temperament, emotions, mental issues
94
Q

What are the two types of dementia?

A
  • Alzheimer’s Dementia
  • —Most common among older adults (50-70% of cases)
  • Vascular dementia (multi-infarct or “mini” strokes)
  • –An insidiously, subtly-progressive worsening of memory and cognition
  • –Due to chronic, reduced blood flow in the brain as a result of age-related vascular changes
  • Dementia with Lewy Bodies
95
Q

What is Dementia with Lewy Bodies?

A
  • Most experts estimate that dementia with Lewy bodies (DLB) is the third most common cause of dementia after Alzheimer’s disease and vascular dementia, accounting for 10 to 25 percent of cases.
  • Lewy bodies are also found in other brain disorders, including Alzheimer’s disease dementia and Parkinson’s disease dementia.
  • –Many people with Parkinson’s eventually develop problems with thinking and reasoning, and many people with DLB experience movement symptoms, such as hunched posture, rigid muscles, a shuffling walk and trouble initiating movement.
  • This overlap in symptoms and other evidence suggest that DLB and Parkinson’s disease dementia may be linked to the same underlying abnormalities in how the brain processes the protein alpha-synuclein.
96
Q

What are causes of irreversible dementia’s?

A
  • Alzheimer’s Disease
  • Vascular dementia
  • Dementia with Lewy bodies
  • Parkinson’s Disease
  • Huntington’s Disease
  • HIV
97
Q

What are treatable, reversible conditions that can cause dementia?

A
  • Depression
  • Medication side effects
  • Drug interactions
  • Hypothyroidism
  • Chronic alcoholism
  • Vitamin B12 deficiency
  • Benign brain tumor
  • Brain infection
98
Q

What is the CDC definition of Alzheimer’s Disease?

A
  • Alzheimer’s disease is the most common form of dementia among older adults.
  • Alzheimer’s disease involves parts of the brain that control thought, memory, and language and can seriously affect a person’s ability to carry out daily activities.
99
Q

What is the NIH definition of Alzheimer’s disease?

A

*Alzheimer’s disease (AD) is an irreversible, progressive brain disease that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks of daily living.

100
Q

What does the textbook say about Alzheimer’s disease?

A
  • Alzheimer’s disease is not synonymous with dementia, but rather, is one of the many causes of dementia.
  • Definitive diagnosis is not possible until an autopsy or brain biopsy has been performed.
101
Q

What is the epidemiology of Alzheimer’s disease?

A
  • Prevalence: ~ 5 million Americans
  • 7th leading cause of death in US
  • ~5% older adults age 65-74 have AD
  • Nearly ½ of those age 85 and older may have the disease
  • Time from onset to death is typically 7-11 years
102
Q

Where is the lesion site in Alzheimer’s?

A
  • Lesion site: cerebral cortex
  • –Accumulation of fibrous material called amyloid
  • –Amyloid forms “senile plaques”
103
Q

What shrinks in alzheimer’s and what is damaged?

A
  • The cortex “shrinks”, damaging areas involved in thinking, planning and remembering (executive functions)
  • Shrinkage is especially severe in the hippocampus, an area of the cortex that plays a key role in formation of new memories
  • –Damage to hippocampus explains memory loss and inability to learn new things
  • *Ventricles become larger
104
Q

What are the executive functions?

A
  • “Executive Functions” is often used to explain certain higher-level cognitive abilities that enable an individual to successfully engage in independent goal-directed behavior
  • Frontal or pre-frontal cortex: complex behavior
  • Executive Functions include:
  • –Organization: attention, decision-making, planning, sequencing, problem solving
  • –Regulation: initiation of action, self-control, self-regulation
105
Q

What does the course of Alzheimer’s depend on?

A

*The course of the disease depends in part on age at diagnosis and whether a person has other health conditions.

106
Q

What occurs in the early AD?

A

*May not be detected in this stage
*Slight changes in thinking/planning and learning/memory
*In the earliest stages, before symptoms
can be detected with current tests,
plaques and tangles begin to form in
brain areas involved in higher cortical functions

107
Q

What occurs in mild to moderate AD?

A

*
Mild to moderate Alzheimer stages – generally lasts for 2-10 years
*Often definitive diagnosis in this stage
*Develop problems with memory or thinking serious enough to interfere with work or social life
*May also get confused and have trouble handling money, expressing themselves and organizing their thoughts
*Experience changes in personality and behavior and have trouble recognizing friends and family members
*Speech impairments: Speaking and comprehension
*Sensory integration: association cortex
*Somatosensation deficits  perception issues
*Visual-spatial deficits
—e.g. difficulty knowing where your body is in relation to the surrounding environment, difficulty reading, judging distance and determining color or contrast
—Stop reading or being able to watch TV because cannot follow it anymore

108
Q

What occurs in severe AD?

A
  • Severe Alzheimer’s stage – may last from 1-5 years
  • Most of the cortex is seriously damaged
  • Brain shrinks dramatically due to widespread cell death
  • Individuals lose their ability to communicate, to recognize self, family and loved ones and to care for themselves
109
Q

What is death often secondary to in AD?

A

*secondary to dehydration or infection

110
Q

How do you diagnose AD?

A
  • Physical exam
  • MRI
  • -Rule out other reversible causes of dementia
  • -Difficult to see tangles and plaques (rather see atrophy)
  • Rate of cognitive change
  • -Progressive decline without improvement or fluctuation
  • Cognitive screening test
  • -Mini-Mental State Examination (MMSE)
  • -Clock drawing test
  • Neuropsychological testing (extremely detailed, but lengthy)
111
Q

What is the Mini-Mental State Exam (MMSE)?

A
  • Score: < 20/30 indicates cognitive impairment
  • Test items
  • -Orientation to Time
  • -Orientation to Place
  • -Immediate Recall (3 words)
  • -Attention (100-7s, spell WORLD backwards)
  • -Delayed Verbal Recall (3 words)
  • -Naming
  • -Repetition (“No if, ands, or buts”)
  • -3-Stage Command (“Take the paper in your hand, fold it in half, and put it on the floor.”)
  • -Reading
  • -Writing
  • -Copying
112
Q

What is normal for a clock drawing test?

A

*If all numbers are present in the correct sequence and position, and the hands readably display the requested time

113
Q

What are the interventions for AD?

A
  • No cure
  • Anti-cholinesterase (may improve memory)
  • -Cognex
  • -Aricept
  • Antioxidants, vitamin E to control free radical damage
  • Anti-inflammatory drugs (NSAIDs)
  • Experimental: Hormone replacement
  • -Estrogen replacement therapy appears to decrease risk of AD by half
  • Experimental: Immunotherapy
  • -Infusion of antibody specific for amyloid-β peptide
  • -Drugs may slow down the progression, but do not stop or reverse progression
114
Q

What are PT functional considerations with AD?

A
  • Fall prevention
  • General exercises - decreases restlessness and wandering
  • Periodic intervention as decline
  • –Educate caregiver
  • –Assistive devices
  • –PTs may need to teach gait sequence; however, often hard to learn secondary to STM and new learning problem
  • PTs treat because sometimes patients lose motor skills ~ increased rigidity and muscle weakness
115
Q

What is the rehabilitation for individuals with brain tumors?

A
  • Despite the prognosis for limited survival associated with primary brain tumors, individuals have shown progress in the rehabilitation setting1-3
  • Advances in medical and surgical interventions have improved survival rates and is associated with longer life expectancy
116
Q

What are the goals of rehab for brain tumors?

A
  • Improve body structure & function, activity & participation limitations
  • Improve quality of life
  • Opportunity to return to home
  • Takes an interdisciplinary team
117
Q

What is the incidence and etiology of brain tumors in adults?

A

*63,000 new cases of primary benign or malignant brain and CNS tumors (2010, U.S.A.)

118
Q

What is the incidence and etiology of brain tumors in children?

A

*4,000 new cases (2010, U.S.A.)

119
Q

What is the bimodal distribution of brain tumors?

A
  • Children: ages 0 – 15 years

* Adults: ages 50-70 years

120
Q

What does the location of the brain tumor determine?

A

*The impairments and functional limitations that the client will display

121
Q

What is the etiology of brain tumors?

A
  • “Runs in families” is questionable
  • –Heredity
  • –Common toxic environment or infectious exposure
  • Association, but not causal effect, with certain chemicals, materials, environments
  • –Petrochemicals (derived from petroleum)
  • –Organic solvents (carbon-based solvents: such as paints, varnishes, lacquers, adhesives, glues, & degreasing/cleaning agents)
  • –Rubber products
  • –Farming or Manufacturing environments
  • –Radiation
122
Q

What is a primary brain tumor?

A
  • Originates in CNS
  • Primary CNS tumors typically do not metastasize (DR/DF)
  • Lack of lymphatic system in CNS to transport cancerous cells (DR/DF)
123
Q

What are secondary or metastatic tumors?

A
  • Spread to the CNS from systemic sites outside of the brain

* Blood-brain barrier “somewhat” protects the brain from metastasis

124
Q

What are primary tumor examples?

A
  • Gliomas - Four primary categories
  • –Astrocytomas
  • –Oligodendrogliomas
  • –Ependymomas
  • –Medulloblastomas
  • Meningiomas
  • Pituitary adenomas
  • Schwannomas
  • Primary CNS lymphomas
125
Q

What are gliomas?

A
  • Arise from glial cells
  • 42% of all brain tumors
  • Frequently located in the cerebral hemispheres
  • Also occurs in the brain stem, optic nerve, and spinal cord
  • Malignant tumors are more common after age 75
  • Benign forms are more common in children
126
Q

What are astrocytomas?

A
  • Derived from astrocytes (star-shaped glial cells)
  • 35% of all brain tumors are astrocytomas
  • —Most common primary brain tumor in adults and children
  • Morphology
  • —Circumscribed (“contained”) – therefore, less likelihood of metastasis
  • —Diffuse – infiltrate surrounding brain structures
  • Low-grade astrocytomas are the slowest growing (next slide)
  • Intermediate-grade astrocytomas, or anaplastic astrocytomas, grow at a moderate rate
  • Frequently found in the frontal lobes of adults and the cerebellum in children
  • Intervention: Surgery, radiation therapy, chemotherapy
127
Q

What are low grade astrocytomas?

A
  • Slowest growing of all CNS neoplasms
  • Occurs in 3rd and 4th decades of life
  • Typically located in the cerebrum
  • –Frontal lobes especially
  • Characterized by unilateral headaches
  • Tend to see personality changes secondary to frontal lobe damage
  • Frequently easy to surgically remove –> result in better survival rates
128
Q

What is a glioblastoma multiforme?

A
  • highly malignant grade IV astrocytoma
  • Glioblastomas are the fastest growing
  • Most common malignant brain tumor in adults
  • First symptom is typically a unilateral headache followed by a generalized headache
  • Rapid progression of symptoms
  • May have seizures
  • With optimal treatment… (FYI)
  • –70% survive for one year
  • –40% survive for two years
  • –10-20% survive five years
  • Intervention: Surgical resection, radiation therapy, stereotactic radiosurgery and chemotherapy
129
Q

What is an oligodendroglioma?

A
  • Slow-growing, but progressive tumors that develop over several years
  • Tumors in the myelin-producing oligodendrocytes
  • ~ 50 % in the frontal lobe
  • ~ 50% in the temporal or parietal lobes
  • Occurs in adults (40-60 YO)
  • Characterized by:
  • –Chronic headaches
  • –History of partial or generalized seizures (may be the only manifestation)
  • Prognosis:
  • –83-100% survive for 5 years
  • –45-55% survive for 10 years
130
Q

What is an ependymoma?

A
  • Affects the ependymal lining of the ventricular system
  • Can also affect the central canal of the spinal cord
  • Common site is 4th ventricle: More prevalent in children
  • Get signs/symptoms of increased ICP (e.g. headaches)
  • Prognosis:
  • –80% survive at least 5 years
  • –40-60% survive at least 10 years
131
Q

What is a medulloblastoma?

A
  • Arise from primitive embryonic cells (specifically pluripotent stem cells that have been prevented from maturing to their normal growth-arrested state)
  • Rapidly growing, malignant tumor of the cerebellum (lateral cerebellar hemispheres in young adults and vermis in children (20% of childhood brain tumors)
  • Hydrocephalus is common (4th ventricle compression: Increased ICP
  • May metastasize to the spinal cord and higher brain areas
  • Prognosis:
  • –45-70% survive at least 5 years
132
Q

What are meningiomas?

A
  • Slow growing CNS tumors
  • Originate from cells in the dura mater or arachnoid membrane
  • 33% of all brain tumors
  • Also spinal tumors
  • Majority are benign
  • Most are well-encapsulated tumors
  • Resectable tumors are primarily treated with surgery
133
Q

What are pituitary adenomas?

A
  • Benign epithelial tumors of the pituitary gland
  • Frequently encroach on the optic chiasm
  • Characterized by hyper- or hypo-secretion of hormones
  • Rare before puberty
  • Female to Male ratio is 3:1
134
Q

What are Schwannomas?

A
  • Encapsulated tumors composed of neoplastic Schwann cells
  • Usually involves 8th cranial nerve
  • –Schwannomas of 8th CN = Acoustic Neuroma
  • –Frequently treated by surgical resection or stereotactic radiosurgery
  • –Complications can include facial paralysis, deafness, and balance problems
  • Can involve any cranial or spinal nerve
135
Q

What are primary CNS lymphomas?

A
  • Involved the lymphocytes
  • Only 1% of all intracranial tumors
  • Increased frequency in individuals with AIDS
  • Similar in histology to systemic non-Hodgkin lymphoma cell (but uncertainty arises since the CNS lacks lymphatic tissue)
  • 60% in cerebral hemispheres
  • –Frequently presenting symptoms include behavioral and personality changes, confusion, & dizziness
  • –Concurrent enlarged lymph nodes, fever, night sweats, unintended weight loss, fatigue
  • Also in the cerebellum and brain stem
136
Q

What is a metastatic Brain Tumor?

A
  • Originate from malignancies outside of the CNS
  • Spread to the brain, typically through the arterial circulatory system
  • –1/3 of secondary brain tumors arise from lung cancer
  • –Followed by breast, skin, GI and kidneys (in that order)
  • –Intervention: corticosteroids, brain irradiation, surgery, and/or chemotherapy
137
Q

What are S&S of secondary tumors?

A

Typically headaches, seizures, cognitive and personality changes, and/or focal signs

138
Q

How does a headache present when it’s a secondary brain tumor?

A
  • Generally start as dull, intermittent, and non-specific
  • Usually on the same side as the tumor
  • Headaches that interrupt sleep or is worse upon waking and improves throughout the day
  • Elicited by postural changes, coughing, or exercise
  • Recent onset and severe
  • Nausea, vomiting, papilledema, or focal neurological signs
  • May be due to local swelling, distortion of blood vessels, invasion of meninges, and/or increased ICP
139
Q

What are the cognitive/personality changes with secondary brain tumors?

A
  • Altered mental status
  • May start as subtle changes in concentration, memory, affect, personality, initiative, and/or abstract reasoning
  • May progress to severe cognitive problems and confusion
  • Increased ICP causes drowsiness and decreased levels of consciousness to potential coma
140
Q

How prevalent are seizures in secondary brain tumors?

A

*present in 1/3 of cases

141
Q

What is papilledema?

A
  • Swelling of the optic nerve

* Less frequent due to improved diagnostic imaging

Neuro D&D (4 decks)

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