Final Flashcards
1
Q
Herpes Simplex and Varicella remain dormant
A
In sensory ganglia
2
Q
Post Herpetic Neuralgia
A
Severe pain along nerve pathway
Condition seen especially in people >60 y/o
Rarely is also motor paralysis
3
Q
PT role in management of person with varicella zoster
A
Keep track of strength
Possibly manage pain
4
Q
Stages of HIV infection
A
Early stage (Asymptomatic): CD4 count >500. No need for retroviral txt Middle stage (symptomatic): CD4 count 200-500. Retroviral probably needed Late stage (advanced disease): CD4 count
5
Q
Goal of txt of HIV
A
Minimize viral load
More load = more rapid disease progression
Viral load is prognostic indicator
6
Q
Opportunistic infections for HIV pt
A
ADC = HIV Encephalopathy or Dementia Complex
Cryptococcal Meningitis
Viral Encephalitis
Progressive multi focal leukoencephalopathy
Toxoplasmosis
Herpes
Cytalomegavirus
7
Q
AIDS Dementia Complex
A
The most common neurological complication of AIDS; major cause of dementia in the young
“HIV encephalopathy”
1/4 ppl with HIV
8
Q
Symptoms of ADC
A
Apathy Social withdrawal Difficulty concentrating Difficulty with complex mental tasks May be mistaken for depression
All changes in affect
9
Q
Patient with HIV walks into your clinic. The patient exhibits these behaviors upon your examination that make you think ADC
A
Slowing of verbal and motor tasks
Unsteady gait
Decreased ability to perform repetitive movements (not dysdiakinesia)
Needs txt because pt will eventually be mute, bedridden, paraplegic, and incontinent.
10
Q
What is the link between Cerebral Toxoplasmosis and HIV patients?
A
CATS!
Patients should be using gloves and masks when cleaning litterbox
11
Q
Inflammatory Demyelinating Polyneuropathy (IDP)
A
Asymptomatic patients present with weakness but without sensory loss
12
Q
Primary CNS tumors
A
Develop/start in the brain, SC or supporting tissues
Do not typically metastasize from the brain to other parts of the body due to the lack of a Lymphatic system in the brain
13
Q
Metastatic Tumors
A
Travel to the CNS from other sites (lungs, breast, GI tract, GU tract, Melanomas)
Can spread from one part of the CNS to another via the CSF
14
Q
Effects of a Space Occupying Lesion
A
Mechanical displacement of brain and SC. Will damage and destroy brain tissue
Blockage of CSF circulation. In young -> hydrocephalus. In adult -> increased ICP
15
Q
What is a focal neurological deficit?
A
A problem in nerve, spinal cord, or brain function that affects a specific location. Ie: left arm, right arm
Also refers to any problem with a specific nervous system function
16
Q
Clinical signs of Elevated ICP
A
Headache
Seizures
17
Q
Headache associated with increased ICP
A
Worse with straining activities (coughing, lifting, etc)
Awakens person from sleep
Worse in AM; may get better during the day d/t erect position causing drainage
Often accompanied by nausea, vomiting and papilledema
18
Q
Seizures are more likely to accompany
A
Slow growing tumors
19
Q
Differentiation
A
The extent to which parenchyma like cells resemble their normal forbearers morphologically and functionally
The more differentiated the cell, the more similar it is to its original cell type, both morphologically and functionally. Is better than poorly differentiated
20
Q
Anaplasia
A
Hallmark of malignancy
When malignant cells are composed of undifferentiated cells; Do not have specialized functional activity
21
Q
The less differentiated the cell
A
The less similar it is to its original cell type, both morphologically and functionally
The tumor cell cannot perform the originally intended/needed functions
22
Q
“Cells are well differentiated” is this good or bad? What does it mean?
A
It’s good bc cells are able to do their specialized function
23
Q
“Cells have high degree of Anaplasia” is this good or bad? What does it mean?
A
It’s bad. Means they’re malignant, undifferentiated. Have no specialized function
24
Q
“Cells in sample are undifferentiated” is this good or bad? What does this mean?
A
Bad. Cells are different from what they were originally
25
Tumor grading
G1: well-differentiated (low grade)
G2: moderately differentiated (intermediate grade)
G3: poorly differentiated (high grade)
G4: undifferentiated (high grade)
26
TMN staging system
T - tumor size
M - metastasis
N - nodes
27
I-IV staging system of CNS tumors
I - no spread beyond structure of origin
II - spread into adjacent tissue
III - spread beyond own region, but not distant
IV - involves another organ or distant site
28
Neurinomas
Slow growing benign tumors that originate from Schwann cells
Typically develop in vestibular portion
Clinical presentation is sensorineural hearing loss, tinnitus, and vertigo
29
CD4 Count
Normal T cell count = 500-1500
30
LMN lesion signs
```
Hyporeflexia or Areflexia
Hypotonia
Fasciculations and Fibrillations
Muscle weakness
Atrophy
```
31
LSN lesion signs
Hyporeflexia/Areflexia
| Dermatomal pattern of paraesthesia/anesthesia, hypoesthesia, hyperesthesia
32
Neuropathy
Disorder of the nerve
33
Myelinopathy
Disorder of the myelin; due to disease state
34
Dying Back Neuropathy
Progression of disease state and signs/symptoms distally to proximally. Starts at the most distal parts of the nerve fiber and progresses proximally approaching the cell body.
35
Guillan-Barre Syndrome (GBS)
Acute Inflammatory Demyelinating Polyneuropathy (AIDP)
Most common in 5th-8th decades of life. Females > Males. White > Black
Is idiopathic
Possible autoimmune response that damages peripheral nerves
36
Risk Factors linked to Guillan-Barre Syndrome
Most cases are preceeded by cases of:
Infections: Bacterial (Campylobacter jejuni)
Viral (Haemophilus influenza), Epstein-Barr, CMV
Surgery
Vaccination (H1N1)
37
Pathogenesis of Guillan-Barre Syndrome (GBS)
Believed to be autoimmune attack on PNS myelin
Affects PNS from spinal nerve roots to distal termination of motor and sensory fibers
Inflammatory response results in macrophages and lymphocytes that strip myelin from PNS nerves
*Affects nerve roots and peripheral nerves
*Damages myelin sheath
38
Remyelination
Mediated by Schwann cells
| Recovery results in shorter internodal distances
39
Clinical Presentation of GBS
Rapidly evolving
Ascending symmetrical motor and sensory deficits with sparing of extraocular muscles
Usual progression of bilateral paralysis/paresis is from distal to proximal
Weakness may be only in extremities or may result in tetraplegia along w/ involvement of respiratory muscles and cranial nerves. Dysphagia often present
Areflexia
Paraesthesias and hypersthesias. Pain often present. "Stocking-glove presentation"
Some ANS involvement: Decreased cardiac output, tachycardia, BP fluctuations, cardiac rhythm changes, possible sudden death
40
Most common cause of mortality in GBS
Respiratory failure, so mechanical ventilation required ~30% of patients
41
Recovery from GBS
Can last months to years, occurs in a proximal to distal manner
42
GBS Phases
```
Actue phase (Onset to about 2-4 weeks)
Static phase (weeks 3-5, about a 4 week period w/ stable conditions but sxs still present)
Gradual Recovery (months to years)
```
43
Medical Management of GBS
Plasmapheresis
| High does IV administration of immunoglobulin
44
Interventions for Management of GBS
```
Pulmonary PT
Position and ROM
Motor Learning
Strengthening
Functional Training
Education
```
45
More is better w/ a GBS patient RIGHT?! No Pain no gain
No it's a possible contraindication to exercise
Avoid muscle fatigue; it can lead to significant loss of strength
Provide freq rest periods
Only GENTLE stretches
Return to bedrest if decrease in function or strength occurs
Overwork of respiratory muscles may lead to profound decrease in respiratory function
46
Acute Poliomyelitis
Viral in origin
Affects the anterior horn cell
Presentation is asymmetrical: Effects proximal > distal; including trunk. LE > UE
47
SxS of Acute Poliomyelitis
1st 2 weeks: fever, malaise, myalgia, sore throat, GI upset
Flaccid paralysis
Hyporeflexia or areflexia
Sensation intact. Myalgia can be intense
Bulbar symptoms: Dysarthria, Dysphagia, Extraocular sparing, Death d/t respiratory involvement
48
Recovery from Acute Poliomyelitis
Restoration of neurons not irreversibly damaged. Collateral sprouting from surviving axons
Compensation via hypertrophy of undamaged muscles = "denervation hypertrophy"
Many individuals use muscle substitution to achieve functional goals
Often ligaments are used for stability -> ligamentous hypermobility and eventually malalignment of trunk and limbs
49
Polio is long gone right?
NOO!
50
Diabetic Neuropathy presents
Distal symmetrical presentation, occasional focal pattern
51
Most common findings in Diabetic Neuropathy
```
Painless distal paraesthesia
Loss of vibration and proprioception
Diminished DTRs
Sensory Ataxia gait
"Dysvascular Symptoms", usually arterial disorders
Person may have had MI w/o knowing it
```
52
Vertigo
The characteristic symptom is a false sense of spinning or rotation. Has 2 types of true vertigo: Central and peripheral
53
Central Vertigo
```
Structures involved include the cerebellum, brainstem, medulla, and pons
Vertebro-basilar insufficiency
Cerebellar hemorrhage
Brainstem ischemia
MS
Migraines
Neurolabyrinthitis
TIAs
```
54
Peripheral Vertigo
Results from abnormalities in the vestibular end organs (semicircular canals and the utricle), the vestibular nerve, and the vestibular nuclei
Benign Paroxysmal Positional Vertigo (BPPV)
Labyrinthitis
Vestibular Neuritis
Otitis Media
Meniere's disease
55
Central vs Peripheral Vertigo
Central: Purely vertical, horizontal, or torsional; not inhibited by fixation of eyes onto object. Rarely hearing loss. Severe unable to stand still or walk
Peripheral: combined horizontal and torsional; inhibited by fixation of eyes onto object; fades after a few days; does not change direction w/ gaze to either side; Commonly hearing loss; Mild to moderate imbalance when walking
56
Benign Paroxysmal Positional Vertigo
Most common cause of sudden onset vertigo. Easily treated. Remove otoconia from semicircular canal
Positional testing may include Dix Hallpike (posterior and anterior canals)
Roll test (for horizontal canals)
57
Selective Brain Atrophy in Elderly
More cell loss in the hippocampus and cortex than in the cerebellum and brainstem
58
Changes in NT activity w/ Elderly
Decrease especially in dopamine, epinephrine, and norepinephrine. Decrease in receptor
Serotonin appears to be reduced; involved in central regulatory activities like thermoregulation, sleep, respiration, and memory
59
Muscle strength in Elderly
Muscle strength is fairly well maintained in adults thru 50 y/o
10-20% decrease in strength between ages 60-70
30-50% decrease in strength between ages 70-80
60
Muscle atrophy in Elderly
Postural muscles (Quads, soleus) show greater atrophy than non-postural muscles
61
Age-Related Changes in Muscle Tissue
Decrease in both type I and II. Greater loss proportionately of type II fibers (fast twitch)
62
The 2 most important elements needed to maintain balance are
Center of Gravity
| Base of Support
63
Postural stability is the ability to
Maintain Center of Gravity within Base of Support
64
Postural orientation
Maintenance of correct alignment of body segments
| Normally utilizes input from visual, somatosensory and vestibular systems
65
Limits of stability (LOS)
The farthest distance in any direction a person can lean (away from midline) w/o altering the original BOS by stepping, reaching or falling
66
Quiet Stance
Attain and maintain steady state
67
Reactive/Adaptive Stance
Modifying postural responses to changing demands
| Ex: boat, gust of wind, subway
68
Proactive/Anticipatory Stance
Pre-tuning to meet expected postural demands
| Ex: moving couch on stairs, lifting child, being thrown their groceries
69
Balance Coordination in Elderly Change in Strategies
Dominated by hip and stepping strategies
D/t decreased muscle strength and vibration and proprioception sense
70
Multiple Systems Involved in Balance
```
Motor System
Peripheral Sensory (Somato, vestib, visual)
Higher level systems - Cb and BG for Feedback and feedforward functions
```
71
Ambulation in the Elderly
Decrease gait speed, decrease vertical head movement, increase in lateral head movement
Increase in stride width and toe-out
Decrease in hip, knee, and ankle flexion
Decreased stride length
Longer double support stance time
Decrease plantarflexion force at pushoff
More flat-food landings (decrease force absorbed by quads at beginning of stance phase)
All of these a strategy to increase stability
72
Arndt-Schultz Principle
The elderly need a longer period of stimulation and a higher threshold for stimulation
The elderly have a smaller response to stimulus, less visible response and less consistent response
The elderly have a narrower range of safe, therapeutic stimulation
73
Balance in the elderly is
decreased
74
The ability to register, retain, recall recent experiences in the elderly is
decreased
75
The rate of learning new material in the elderly is
decreased
76
Performing motor tasks requiring speed in the elderly is
decreased
77
Fine motor coordination in the elderly is
decreased
78
Difference between seizures and epillepsy
```
Seizures = finite event caused by sudden, excessive electrical discharge of cerebral neurons
Epilepsy = family of disorders characterized by recurrent seizures
```
79
Ictal refers to
Seizure
80
Prodrome
Early SxS or set of SxS that may indicate the start of a disease - Premonition.
Includes headache, mood alterations, lethargy, myoclonic jerking (sudden rapid twitching)
Last from 30 mins to several hours
Prodromes are pre-ictal
81
Aura
Changes in subjective sensations:
Bodily sensations, e.g., strange taste in mouth
Ability to interact w. things happening around you
How familiar outside world is – e.g., deja vu
May occur right before seizure (sz)/at start of seizure. Lasts up to 15 mins.
82
What kind of generalized seizure is characterized by stare, fluttering eyes, and lasts 2-15 seconds?
Absence (Petite Mal)
83
Call 911 if a patient is having a seizure and
Prolong duration >5 minutes
Pregnant pt (this could be a sign of preclampsia)
>1 seizure occurs w/in 24 hours
Pt does not respond normally w/in 1 hour post sz
Seizure accompany by CVA, TBI, DM, severe HA, post ingestion of poison or breathing fumes
Pt c/o severe pain after waking up or develops fever w/in 24 hrs post seizure
84
A PT should educate the family of an individual who has seizures to position her in a (blank) position during/after a seizure.
Sidelying
85
You are a PT working with a person who suddenly has a seizure. What are appropriate actions to take?
Move objects away to prevent injury to person with seizure
Time the seizure
Do not place anything in the patient's mouth
86
Signs of tardive dyskinesia are
Stereotypical facial movements, e.g., facial grimacing, chewing movements, tongue writhing &/or protrusions
Choreiform (dancelike) movements of extremities: “piano-playing” of fingers, larger choreiform movements of limbs
Can have respiratory dyskinesias
When severe, can be dysarthria and dysphagia leading to need for feeding tube
Condition worsens when patient does dexterity tasks, walking and doing cognitive task at same time, is fatigued or anxious
87
PTs role in management of Tardive Dyskinesia
Early recognition
| Communication w/ the health care team
88
Medications associated w/ an increased incidence of Tardive Dyskinesia?
antiepileptic, antiemetic and antipsychotic medications
89
Why is early recognition of Tardive Dyskinesia important?
The effects can be irreversible
90
Lewey Body Dementia
Every person with LBD is different
Progressive dementia - deficits in attention and executive function are typical. Prominent memory impairment may not be evident in the early stages.
Fluctuating cognition with pronounced variations in attention and alertness.
Recurrent complex visual hallucinations, typically well formed and detailed.
Spontaneous features of parkinsonism.
Severe sensitivity to neuroleptics occurs in up to 50% of LBD patients who take them.
Repeated falls and syncope (fainting).
Transient, unexplained loss of consciousness.
Autonomic dysfunction.
Hallucinations of other modalities.
Visuospatial abnormalities.
Other psychiatric disturbance
91
Lewey Body Dementia Diagnosis requires
Dementia plus two or more core features, or
Dementia plus one core feature and one or more suggestive features. AND THIS JUST FOR A PROBABLE DIAGNOSIS
Dementia plus one core feature, or
Dementia plus one or more suggestive features.
FOR POSSIBLE DIAGNOSIS
92
The most common form of demyelinating disease
Multiple Sclerosis
93
Multiple Sclerosis
A demyelinating disease characterized by a course of demyelination-mediated relapses and remissions, superimposed upon gradual neurologic deterioration. The demyelinating lesions are called plaques
94
Origin of the Name MS
```
Multiple = Multiple CNS sites
Sclerosis = Hardening = the plaques that result
```
95
MS Incidence is most prominent in
20-50 y/o
Caucasians
"Temperate Climates": Northern US; There is an environmental trigger in where a person spends their first 15 years of life
Genetic link
96
MS is considered a (blank) disease
Autoimmune
97
Primary Impairments and Conditions of Multiple Sclerosis
```
Fatigue
Sensory Impairments
Weakness
Optic neuritis
Spasticity (UMN)
Heat sensitivity (for some the humidity is worse than actual heat)
Cerebellar signs [typically bilateral] (dizziness, vertigo, ataxia, other cerebellar signs)
Pain
Psychiatric issues
Bladder dysfunction
Bowel dysfunction
Sexual dysfunction
```
98
PT considerations w/ working w/ an MS patient
Careful in prescribing exercise. They are prone to fatigue so want to be mindful of that. Fatigue is one of the biggest complaints from an MS patient.
99
Uthoff's Phenomena
Related to MS patients
| Worsening of fatigue and weakness w/ elevation of body temperature
100
Psychiatric issues in patients w/ MS
Most common cognitive changes are memory loss and impaired safety awareness
Euphoria is often seen in late stages
Possible Depression
101
Secondary Conditions from MS
Overuse/Tendonitis secondary to spasticity
Progressive weakness d/t inactivity
Osteoporosis - from disuse and steroids
UTIs, respiratory infections, skin breakdown
102
1 problem for MS patients that is commonly seen d/t steroid use (she underlined this multiple times)
OSTEOPOROSIS from steroids. The steroids are supposed to suppress immune function and limit the inflammatory response but the side effect is the osteoporosis.
103
Besides for maintaining strength and preventing secondary problems of infection or skin breakdown a big part of PT should include what when working w/ MS patients
Energy Conservation Techniques (they're fatigued)
104
If you see degeneration of substantia nigra and decrease in dopamine you think
Parkinson's
105
If you see decrease in synaptic connections, amyloid plaques, decrease in ACTH, neuronal death, decrease in number of axons you think
Alzheimers
106
If you see atrophy of basal ganglia, corpus striatum, and autosomal dominant gene you think
Huntington's disease
107
Diagnosis of Parkinson's
Asymmetrical onset
Resting Tremor
Positive initial response to L-Dopa
108
Diagnosis of Alzheimer's
Definitive only made by Biopsy or
| Autopsy finding of Amyloid Plaque formations.
109
Diagnosis of Huntington's
Genetic Marker; All individuals w/ gene will get HD
110
Between Parkinson's Alzheimer's and Huntington's which impacts younger typically?
Huntington 30-50 y/o. The others are usually 65+
111
Risk factors for Parkinson's
Age is the greatest risk factor
Possible family history
Damage to BG
Idiopathic
112
Risk factors for Alzheimer's
Idiopathic
15% have fam hx
Chromosome 21 mutation, esp.
Down Syndrome have high risk.
113
Risk factors for Huntington's
Inheriting gene; 50% chance of inheriting HD if one parent has gene
114
Onset of disease in Parkinson's Alzheimers and Huntingtons
Parkinsons is asymetrical
| The others are insiduous and huntington's is progressive
115
Loss of ability to do math computations (e.g., handling money), sleeping & eating disorders, word-finding difficulty, loss of orientation, lost in familiar environments, subtle personality changes, (irritability, impulsiveness, indifference, paranoia, hoarding). You might be thinking?
Early Alzheimer's
116
Choreic mvmts (reported as “restlessness”), Personality/Behavioral/ Cognitive Changes. You're thinking?
Huntington's
117
Parkinson's TRAP
```
T= Tremor (Resting tremor)
R = Rigidity (Lead pipe, Cogwheel)
A= Akinesia, Bradykinesia (both are considered motor planning deficits)
P = Postural Instability: FALLS RISK!!
```
118
Cell loss in DRG with secondary degeneration in the posterior columns & spinocerebellar tracts
Friedrich Ataxia (Spinocerebellar Degeneration)
119
Demyelination autoimmune in CNS. Scarring is caused by inflammatory process at multiple CNS sites = plaques. As disease progresses, myelin is replaced by Gliosis = fibrous scarring
Multiple Sclerosis
120
Degenrerative scarring or sclerosis in lateral aspects of the SC, Brainstem & Cortex,
Peripheral nerve involvement leads to atrophy (amyotrophy)
= Combination of UMN and LMN
ALS or Amoyotrophic Lateral Sclerosis
121
Diagnosis of Friedrich Ataxia
Absent DTR’s with Positive Babinski
Normal tone w/ flexor spasm
Motor Restlessness
122
MMT of a patients w/ ALS
They won't realize how weak they are, not until 80% of their motor neurons are gone
123
Huntington's disease is a disorder characterized by
Movement abnormalities
Dementia
Personality changes (disturbances)
124
Huntington's disease is a disorder characterized by
Movement abnormalities
Dementia
Personality changes (disturbances)
