1
Q
Normal Muscle Biopsy
A
- mosaic pattern
- muscles may have proportionately more fast-glycolytic (FG) muscles fibers as compared to slow, oxidative (SO) secondary to its function
2
Q
Neurogenic Diseases
A
- involves nerve cell bodies, axons and/or dendrites
- needle EMG
3
Q
Needle EMG for Neurogenic Diseases
A
- denervated muscle is spontaneously active at rest (fibrillation potentials)
- short duration (<3 ms) and low amplitude (<300 uv), fibrillation potentials occur in semi-rhythmical runs (<30/sec)
4
Q
Muscle biopsy of neurogenic disease
A
- neuron atrophy causes muscle atrophy of the same muscle fiber type
- regernation occurs through collateral sprouting
- 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)
5
Q
Myogenic diseases
A
- myogenic or myopathies involve muscle degeneration
- little/less muscle activity at rest with a needle EMG
6
Q
Muscle biopsy of Myogenic diseases
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
7
Q
Examples of neurogenic diseases
A
- compression of nerve roots or periopheral nerves
- bell’s palsy
- diabetic plyneuropathy
- alcoholic poluneuropathy
- polio and post-polio syndrome
- amyotrophic lateral sclerosis (ALS)
- Guillian-Barre syndrome (GB)
8
Q
Demylinating diseases
A
- multiple sclerosis
9
Q
Myogenic diseases
A
- Muscular Dystrophy
10
Q
Bell’s Palsy
A
- lesion of CN VII
- demylination in mild cases
- demyelination and axonal damage in more severe cases
- innervation to upper face is bilateral
- “a” is Bell’s Palsy
- “b” is stroke
- person is asked to smile and close eyes
- Bell’s Palsy typically presents as flaccid paralysis on the ipsilateral side of face, affecting the upper and lower quadrants of the face
11
Q
Bell’s Palsy Etiology
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
12
Q
Motor S&S of Bell’s Palsy
A
- mouth droops
- nasolabial fold is flattened
- eyelid does not close
13
Q
Sensory S&S of Bell’s Palsy
A
- decreased taste on ipsilateral tongue
14
Q
ANS S&S of Bell’s Palsy
A
- decreased tearing (dry eye)
15
Q
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)
- eye patch, artificial tears (eye drops every 4 hrs)
- 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)
16
Q
Diabetic Polyneuropathy sensory loss
A
- sensory loss is not usually in dermatome or periphery pattern
- usually in sock or glove-like patterns
17
Q
Diabetic Polyneuropathy
A
- affects PNS axons primarily (some demyelination)
18
Q
Diabetic Polyneuropathy Etiology
A
- disrupted microcirculation
19
Q
Diabetic Polyneuropathy Onset
A
- after long duration diabetes
- in diabetics who have diabetes for 25+ years, 50% have this condition
- occurs in insulin-dependent and non-insulin dependent diabetes
- some regeneration with control of diabetes
- common in those who are not routinely caring for their diabetes
20
Q
Diabetic Polyneuropathy characteristics
A
- large nerve fiber sensory involvement of MANY NERVES IN LOWER LEGS AND FEET
- Ia, Ib, II from mm spindle and GTOS
- most common
- painless paresthesias in BILATERAL feet and lower legs
- decreased vibration and proprioception sense
- small nerve fiber sensory involvement (A delta and C afferent fibers)
- deep aching pain in legs and burning feeling in feet
- decreased touch, pain, and temp sensations
- nocturnal pain and paresthesias
21
Q
Screening/Examination Tests for Diabetic Polyneuropathy
A
- NCVs
- Monofilament screening with 5.07/10 gm. filament
- vibration
22
Q
Complications with Diabetic Polyneuropathy
A
- diabetic ulcers
- 50% of non-traumatic amputations in US are performed on individuals with diabetes
23
Q
Diabetic PERIPHERAL Neuropathy S&S
A
- numbness or reduced ability to feel pain or changes in temp, esp in feet/toes
- serious foot problems, such as ulcers, infections, deformities, and bone and joint pain
- a tingling or burning feeling
- sharp, jabbing pain that may be worse at night
- pain when walking
- extreme sensitivity to the lightest touch
- muscle weakness and difficulty walking
24
Q
ALS
A
- amyotrophic lateral sclerosis
- lou gehrig’s diseases
25
LMN Signs for ALS
- anterior horn cells (alpha and gamma motor neurons (LMN SIGNS))
- lateral corticospinal tract
- motor nuclei of brainstem
- motor area of frontal lobe
- loss of function in hands in feet starts DISTAL and progresses PROXIMAL
26
UMN Signs for ALS
- anterior horn cells
- lateral corticospinal tract
- motor nuclei of brainstem (red nucleus)
- motor area of frontal lobe
27
ALS is caused by what
- atrophy/degeneration of cell bodies in ventral grey horn
| - therefore degenerating the grey matter in the SC
28
ALS S&S
- motor signs and symptoms only
- asymmetric, distal weakness (first sign)
- by time patient complain of weakness, often have lost 80% of their ALPHA MOTOR NEURONS in area of weakness
- EMG: spontan fibrillations, fasciculations with giant unit spikes upon voluntary activity
29
ALS
- primary pathologic defect is in the motor neuron cell body (specific to anterior horn cell in SC)
- 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)
30
Theory as to why ALS occurs
- technically unknown
- could be due to mitochondria
- SOD1 gene mutation causing the superoxide disputes (SOD) enzyme to function improperly
31
Other possible causes for ALS
- glutamate
- premature aging
- exogenous toxins
- viral diseases
- immunologic distrubances
- premature aging
32
How many ALS cases are familal
- 5-10% of cases
33
ALS stats
- 0.1% of deaths in US
- ALS disease of late middle life and rarely seen prior to age 40
- 90% of all cases begin between the ages of 40 and 70 years
- slight predominance in men
34
What is the first sign of ALS usually?
- asymmetric, distal weakness
35
What are the early signs of ALS?
- severe muscle cramps
| - fasciculations at rest
36
ALS signs and symptoms progression
- 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 1 fibers
- cranial nerve cell atrophy leads to dysarthria, dysphagia, difficulty in chewing, tongue weakness, and fasciculations may be prominent
- control of bladder, bowel, and autonomic function is largely unimpaired, however, some studies report sub-clinical involvement
37
LMN signs of ALS
- Progressive muscle atrophy
- Weakness (asymmetric weakness is often a presenting sign)
- Fasciculations (especially evident in tongue, deltoid)
- Muscle cramps (painful
38
UMN signs of ALS
- Spasticity
- Hyperreflexia
- Positive Babinski
39
ALS Stats
- 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
40
ALS Brief Intervention
- 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
41
PALS
- organization with equipment closet
42
Guillain-Barre Syndrome (GBS) History
- named after the french physicians Georges Guillain and Jean Alexandre Barre, 1916
- an acute polyneuropathy affecting the peripheral nervous system
- may be autoimmune attack on both the schwann cells and peripheral and cranial nerves by circulating antibodies
43
GBS
- acute: develops rapidly
- often follows the flu or respiratory infection
- may be idiopathic
- is rare (1-2 cases per 100,000 people annually), but is most common cause of acute non-trauma paralysis
44
GBS
- 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.
45
GBS S&S
- Frequently, the cranial nerves may be affected, leading to; 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
- Sensory loss, if present, usually takes the form of loss of proprioception
- 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
46
GBS Prevalence
- can occur at any age
- mostly 5-8th decade
- more common in men than woman
47
GBS Disease Course
- 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
48
GBS Mortality rate
- 5% relatively low mortality rate
49
GBS Has poorer prognosis with what
- onset at older age
- extended time before recovery begins
- need for artificial respiration
50
Time frame with recovery in GBS
- at 6 months, 85% are ambulatory
- at 1 year, 20% remain significantly handicapped by weakness
- at 2 years, 8% have NOT achieved full recovery
51
GBS Diagnosis
- nerve conduction studies
| - studies of the cerebrospinal fluid
52
GBS Intervention
- supportive medical care
- plasmaphoresis: filtering blood plasma to remove circulating antibodies responsible for destruction of Schwann cells and peripheral and cranial nerves
- Intravenous Immunoglobins
53
MS Prevalence
- more than 2.3 million people worldwide
- female > male (2-3X more)
- predominantly caucasians
- high frequency: northern US, scandinavian and European countries
54
Age with MS
- Most people are diagnosed between the ages of 20 and 50
| - Although MS can occur in young children and significantly older adults
55
Genetic Factors with MS
- 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.
56
MS Disease
- 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
- 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
- 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
57
MS Diagnosis
- can be difficult to diagnose.
- no single test for MS, the diagnosis can be missed, delayed or even incorrect.
- 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
58
S&S of MS
- Multiple symptoms (dependent upon where the plaques, inflammation and demyelination 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
59
MS Exacerbated Symptoms due to what?
- Adverse reaction to heat (internal and external) - may exacerbate symptoms
- Hot packs
- Immersion in water
- Hot weather
- Illness with fever
60
Relapsing-Remitting MS Course
- RRMS
- most common course of disease
- characterized by clearly defined attacks of worsening neurologic function
- attacks are also called relapses, flare-ups, exacerbations
- they are followed by a partial or complete recovery periods (remissions), where symptoms improve partially or completely with no apparent progression of disease
- 85% of people with MS are in this course
61
Secondary-Progressive MS Course
- SPMS
- it follows after relapsing-remitting course
- those who are initially diagnosed with RRMS will eventually transition to SPMS, meaning disease will begin to progress more steadily (with or without relapses)
62
Progressive-relapsing MS Course
- PRMS
- least common of four disease courses
- characterized by steadily progressing disease from beginning and occasional exacerbations along way
- may or may not experience some recovery following these attacks
- disease continue to progress without remissions
63
Primary-Progressive MS Course
- PPMS
- steadily worsening neurologic function from beginning
- rate of progression may vary over time
- occasional plateaus
- temporary, minor improvements, no distinct relapses or remissions
- about 10% are diagnosed with this type
64
Myogenic Disease
- muscular dystrophies
65
Overview of Muscular Dystrophy
- genetically determined
- progressive degenerative course
- muscle fiber changes (degeneration, regeneration, fibrosis)
- abnormal function of DYSTROPHIN causing contraction of muscle
66
S&S of Muscular Dystrophy
- muscular degeneration
- hypotonia
- muscle atrophy
- pseudohypertrophy (calf)
- usually involves core and proximal muscles first
- increased lumbar lordosis
- child walks on toes b/c PF contractors
- positive Trendelenburg
- scoliosis
67
Duchenne's Muscular Dystrophy Prevelance
- 1 in 5,000 male births
- males only (inherited X-linked recessive disorder)
- begins 3-5 y.o.
- weakness first in legs!!
- rapid progression : often in WC by age 12, death in 3rd decade
68
Duchenne's Muscular Dystrophy
- gene produces dystrophin (protein forming part of muscle plasma membrane) is lacking; dystrophin gene Xp21
- early in diagnostic process doctors often order a creatine kinase (CK) blood test
69
MD with CK
- early in 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
70
Muscular Dystrophy
- symmetrical weakness and atrophy in para-axial (trunk) and proximal muscles
- Pseudohypertrophy due to connective tissue and fatty deposits in the muscles (most commonly in bilateral calf)
- Hypotonia
- PT: no strenuous exercise!
- usually lose ability to ambulate by 10-12
- significant amount are intellectually or mentally impaired
71
Gower's Sign
- usually present in all forms of MD
| - walking arms up their legs to come to standing
72
MD Scoliosis
- creatine kinase (CK) blood test
- genetic testing
- EMG, Ultrasonography, muscle biopsy
73
Medications and Diet of MD
- corticosteroids (Prednisone) have been found effective in slowing the course of DMD
- Calcium supplements and vit 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
74
Intervention for MD
- surgery, bracing, assitive devices
- physical therapy:
- provide regular ROM exercises and flexibility
- avoid strenuous exercise since it can exacerbate muscle cell death
75
Anatomic NS Changes with Age
- overall brain weight decreases with age
- weight of brain decreases as we age
- by 8th decade, NCV can decrease by 10-15% especially in myelinated nerves
76
Changes with Aging
- decreased # of sensory receptors
- decreased synthesis of neurotransmitters
- may have decreased control of emotions and attention
- reduction of serotonin, reduced memory, sleep pattern effects, thermoregulation
77
TAO is associated with what
- with tangles of the neurons which destroy them
78
Senile Plaques
- extracellular deposits of amyloid (starch-like protein-carbohydrate complex) in the gray matter of brain
- occur most often in the cortex and hippocampus
- associated with Alzheimer's disease and Dementia
79
Proportion of people with plaques
- age 60 years (10%)
| - age 80 years (60%)
80
Senile Plaques and Acetylcholine
- 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
81
Neurofibrillary Tangles
- pathological accumulate 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
- increase much more in Dementia and Alz puts
82
PNS Changes in Vestibular System as age
- 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
83
PNS Changes in Somatosensory System as age
- 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
84
PNS Changes in Motor System as age
- loss of alpha MN with age
- remaining alpha MN 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
85
PNS changes in Autonomic NS as age
- reduce sympathetic control of vasculature in skin
| - results in reduced wound repair efficiency
86
Benign Senescent Forgetfulness
- age-related cognitive issue
- a mild decline in ST memory
- does not progress to other mental impairments
- NOT DIMENTIA
- difficult to partition from memory impairments secondary to polypharmacology
87
Dementia
- 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
- usually involves cognitive impairments affecting memory and orientation plus one or more of: abstract thinking, judgement and problem solving, language (reduction in frequency), personality (behavior, temperament, emotions, mental issues)
88
Types of Dementia
1) Alzheimer's dementia
2) Vascular dementia
3) Dementia with Lewy bodies (DLB)
89
The most common dementia among older adults
- Alzheimer's
| - 50-70% of cases
90
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
91
Dementia with Lewy bodies (DLB)
- third most common cause of dementia (after alzheimer's and vascular)
- 10-25% cases
- levy bodies also found in other brain disorders, including Alzheimer's disease dementia and Parkinson's disease dementia
- overlap in symptoms and other evidence suggest that DLB and Parkinsons may be linked to same underlying abnormalities in how brain processes protein alpha-synuclein
92
Causes of Irreversible Dementia
- Alzheimer's disease
- vascular dimentia
- dementia with lewy bodies
- parkinson's disease
- huntington's disease
- HIV
93
Treatable, Reversible conditions that can cause dementia-like symptoms
- depression
- medication side effects
- drug interactions
- hypothyroidism
- chronic alcoholism
- Vit B12 deficiency
- benign brain tumor
- brain infection
94
CDC Alzheimers definition
- Alzheimer's 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
95
NIH Alzheimers Definition
- 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
96
Alzheimer's Epidemiology
- 5 million Americans
- 7th leading cause of death
- 5% older adults age 65-74 have AD
- nearly 1/2 of those age 85+ may have the disease
- time from onset to death is typically 7-11 years
97
Lesion site for AD
- cerebral cortex
- accumulation of fibrous material called amyloid
- amyloid forms "senile plaques"
98
Amyloid Plaques with AD
- abnormal clumps of protein fragments
- build up between nerve cells
- found throughout the cortex
99
Neurofibrillary tangles with AD
- twisted strands of protein inside dead and dying nerve cells
- most common in the temporal lobe structures, such as hippocampus and amygdala
100
What part of the brain shrinks with AD
- the cortex shrinks
- damages areas involving in thinking, planning and remembering
- executive functions
- severe shrinkage in hippocampus (key role in formation of new memories)
- VENTRICLES BECOME LARGER
101
Executive Functions
- 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
- organization, attention, decision making, self-monitoring, self-control, etc
102
Progression through the brain with AD
- plaques and tangles tend to spread through the cortex in a predictable pattern as Alzheimer's disease progresses
- the rate of progression varies greatly
- people with Alzheimer's live avg 7-8 years after Dx
- course of disease depends in part on age at diagnosis and whether a person has other health conditions
103
Early AD
- may not be detected yet
- slight changes in thinking and planing and learning and memory
- plaques and tangles begin to form
104
Mild to Moderate AD
- generally lasts 2-10 years
- often diagnosable
- 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
105
Severe/Advanced AD
- may last 1-5 years
- most of 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
106
How many AD stages are there?
- SEVEN
| - death is often secondary to dehydration or infection
107
AD Medical Diagnosis
- physical exam
- MRI (rule out other reversible cause of dementia. difficult to see tangles and plaques)
- rate of cognitive change (progressive decline without improvement)
- cognitive screening test (mini-mental state exam MMSE, clock-drawing test)
- Neuropsychological testing (detailed by lengthy)
108
MMSE (Mini-mental state exam)
- score <20/30 indicates cognitive impairment
- test items: orientation to time, place, immediate recall (3 words), attention, delayed verbal recall, naming, repetition, 2-stage command, reading, writing, copying
109
AD Interventions
- no cure
- anti-cholinesterase
- antioxidants, vit E to control free radical damage
- anti-inflammatory drugs (NSAIDs)
- experimental hormone replacement and immunotherapy
110
Rehabilitation for individuals with brain tumors
- progress shown in rehab
- advances in medical and surgical interventions have improved survival rates and is associated with longer life expectancy
- goals of rehab: improve body structure and function, activity and participation limitations, improve QOL, opportunity to return home, takes interdisciplinary team
111
Incidence and Etiology of brain tumors
- adults: 63,000 new cases of primary benign or malignant brain and CNS tumors
- children: 4,000 new cases
- appears that tumors are being diagnosed (improved tumor imaging) rather than true increase in occurrence
- bimodal distribution: children: 0-15 y.o, adults: 50-70 y.o
112
CNS Tumors that are Glioblastomas
- 16.7%
| - malignant tumor
113
CNS Tumors that are Meningioma
- 34.4%
| - frequently begnin
114
Where are most CNS tumors located
- meninges!
| - location of tumor determines impairments
115
Brain tumor Etiology
- runs in families, is questionable. heredity, common toxic environment or infectious exposure
- association, but not causal effect with certain chemicals, materials, environments
116
Primary brain tumors
- originate in the CNS
- primary CNS tumors typically do not metastasize
- lack of lymphatic system in CNS to transport cancerous cells
117
Secondary or metastatic tumors
- spread to the CNS from systemic sites outside of the brain
| - blood-brain barrier "somewhat" protects the brain from metastasis
118
Primary Tumor Types
- Gliomas (astrocytomas, oligodendrogliomas, ependymomas, medulloblastomas)
- meningiomas
- pituitary adenomas
- schwannomas
- primary CNS lymphomas
119
Gliomas
- arise from glial cells
- 42% of brain tumors
- frequently located in cerebral semis
- also occurs in brain stem, optic nerve, and SC
- malignant tumors are more common after age 75
- benign forms are more common in kids
120
Astrocytomas
- derived from astrocytes (star-shaped glial cells)
- 35% of all brain tumors
- most common primary brain tumor in adults and kids
- if contained, more successfully removed (less likely of metastasis)
- low-grade astrocytomas are slowest growing
- intermediate-grade astrocytomas, or anaplastic astrocytomas, grown at a moderate rate
- frequently found n frontal lobes of adults and cerebellum in kids
- intervention: surgery, radiation therapy, chemotherapy
121
Diffuse
- infiltrate surrounding structures
122
Low-grade Astrocytomas
- slowest growing of all CNS neoplasms
- occurs in 3rd and 4th decades of life
- typically in cerebrum (frontal lobes)
- characterized by unilateral headaches
- tend to see personality changes secondary to frontal lobe damage
- frequently easy to surgically remove --> result in better survival rates
123
Astrocytomas: Glioblastomas
- glioblastoma multiforme: highly malignant grade IV astrocytoma
- glioblastomas are fastest growing
- most common malignant brain tumor in adults
- first symptom is typically unilateral headache followed by a generalized headache
- rapid progression of symptoms
- have seizures
- intervention: surgical resection, radiation therapy, sterotactic radiosurgery , chemotherapy
124
Oligodendroglioma
- slow-growing, but progressive tumors that develop over several years
- tumors in the myelin-producing oligodendrocytes
- 50% in frontal lobe
- 50% in temporal or parietal lobe
- occurs in adults (40-60 years)
- characterized by chronic headaches, history of partial or generalized seizures (may be the only manifestation)
125
Ependymoma
- affects the ependymal lining of the ventricular system
- can also affect the central canal of SC
- common site is 4th ventricle: more prevalent in children
- get signs/symptoms of increased ICP
126
Medulloblastoma
- arise from primitive embryonic cells (pluripotent stem cells that prevented from maturing to their normal growth-arrested state)
- rapidly growing, malignant tumor of the cerebellum (lateral cerebellar semis in young adults and vermis in kids)
- hydrocephalus is common (4th ventricle compression: increased ICP)
127
Meningiomas
- 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
128
Pituitary Adenomas
- benign epithelial tumors of pituitary gland
- frequently encroach on optic chasm (tunnel vision!!)
- characterized by hyper-or hypo-secretion of hormones
- rate before puberty
- female to male ratio 3:1
129
Schwannomas
- 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 radio surgery
- complications can include facial paralysis, deafness and balance problems
- can involve any cranial or spinal nerve
130
Primary CNS Lymphomas
- 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 CNS lacks lymphatic tissue)
- 60% in cerebral hemi
- frequently presenting symptoms of personality changes, confusion, dizziness, confront enlarged lymph nodes, fever, night sweats, unintended weight loss, fatigue
- also in cerebellum and brain stem
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Metastatic Brain Tumors
- originate from malignancies outside of CNS
- spread to brain, typically through the arterial circulatory system
- 1/3 of secondary brain tumors arise from lung cancer
- followed by breast, skin, GI and kidneys
- intervention: corticosteroids, brain irradiation, surgery, and/or chemotherapy
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Signs and Symptoms of Metastatic Brain Tumors
- typically headaches, seizures, cognitive and personality changes, and/or focal signs
- headaches generally start as dull, intermittent, on same side as tumor, interrupt sleep or is worse upon wakening, elicited by postural changes or coughing, recent onset and severe, nausea, vomitting, can be due to local swelling
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Seizures with Metastatic Tumors
- present in 1/3 cases
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Cognitive and personality changes with Metastatic Tumors
- 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
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Papilledema with Metastatic Tumors
- swelling of optic nerve
| - less frequent due to improved diagnostic imaging
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Focal signs and symptoms with Metastatic Tumors
- frontal lobe
- occipital lobe
- temporal lobe
- cerebellum
- brain stem (reticular formation > consciousness and attention. vital function associated with cardiovascular systems > death)
- pituitary glands (typically large here. compress pituitary gland and causes disorders)
Neuro D&D
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