Class 7 chapter 36 Flashcards
(68 cards)
1
Q
Hypotonia
A
Diminished resistance to passive movement
Soft muscle on palpation
Diminished deep tendon reflexes
2
Q
Hypertonia
A
Hyperexcitable stretch reflex causing rigidity and spasticity
3
Q
Clonus
A
Involuntary rhythmic muscular contractions and relaxations
4
Q
Plegia
A
Stroke or paralysis
5
Q
Paralysis
A
Loss of movement
6
Q
Paresis
A
Weakness
7
Q
Mono
A
One limb
8
Q
Hemi
A
Both limbs on one side
9
Q
Di or para
A
Both upper limbs or both lower limbs
10
Q
Quadri or tetra
A
All 4 limbs
11
Q
Upper Motor Neuron Damage
A
Weakness and loss of voluntary motion Spinal reflexes remain intact but cannot be modulated by the brain Increased muscle tone Hypertonia/Hyperreflexia Spasticity
12
Q
Lower Motor Neuron Damage
A
Neurons directly innervating muscles are affected
- Irritated neurons
- Involuntary muscle contractions called fasciculation (small/local) - Death of neurons
- Spinal reflexes are lost
- Flaccid paralysis
- Denervation atrophy of muscles
13
Q
Skeletal Muscle Disorders
A
- Muscle Atrophy
- Disuse
- Denervation - Muscular Dystrophy
- Contractile proteins not properly attached to cytoskeleton of muscle cell
14
Q
Muscular Dystrophy
A
Genetic (inherited X-linked recessive trait) - Primarily males - 9 major types Progressive degeneration (protein breakdown and necrosis of skeletal muscle fibers and tissues) - Sarcoma do not attach properly - Fat and connective tissue replace it Duchene MD Becker MD
15
Q
Duchene muscular dystrophy
A
Most common form
Recessive x-linked
Affects 1:3500 male births
Females usually asymptomatic if carrier (or milder symptoms)
16
Q
Becker muscular dystrophy
A
Slower, less severe
Later in childhood than DMD
17
Q
Muscular Dystrophy presentation
A
Boys asymptomatic at birth Hips/shoulders muscles often affected first Calf muscles hypertrophy (fat/tissue) By 2-3 years, abnormal posture, falls, contractures, joint immobility, scoliosis Wheelchair by teen years Incontinence Resp: weak cough = resp infections CVS: cardiomyopathy
18
Q
Muscular Dystrophy diagnosis
A
Family history Observation of voluntary movement Elevated creatine kinase (CK-MM) Muscle biopsy Echo, ECG
19
Q
Muscular Dystrophy treatment
A
Maintain ambulation
Prevent deformities
Prevent respiratory infections
Death in young adulthood common
20
Q
Disorders of Neuromuscular Junction
A
Decreased acetylcholine release
Decreased acetylcholine effects on muscle cell (receptors are lost)
- Myasthenia Gravis
Decreased acetylcholinesterase activity resulting too much acetylcholine at neuromuscular junction, also interfering with nerve impulse
21
Q
Myasthenia Gravis Risk Factors
A
Women > Men
Early adulthood (women)
50 years of age for men
Placental transfer from Mom
10-15% only and often spontaneous resolution within months
Thymus tumor or hyperplasia in 75% of cases (unclear connection)
22
Q
Myasthenia Gravis
A
Decreased motor response d/t loss of functional acetylcholine receptors
Autoimmune
- Gradual destruction of acetylcholine receptors in neuromuscular junction
- Injury to postsynaptic muscle membrane
- Receptor sites degraded and blocked d/t antibodies
23
Q
Myasthenia Gravis manifestations
A
- Initial
- Progressive throughout day
- Muscle weakness (periorbital muscles: ptosis - droopy eyelid, diplopia - double vision)
- Fatigue - Progression
- Respiratory muscle weakness, difficulty speaking/chewing/swallowing, weak limbs
24
Q
Myasthenia Crisis
A
D/t stress, infection, emotional upset, pregnancy, alcohol, cold, surgery etc
25
Myasthenia Gravis diagnosis
History, physical exam
Acetylcholine receptor blood test
Rise in acetylcholine receptor antibodies
Electrophysiologic studies to assess stage
26
Myasthenia Gravis treatment
Corticosteroid (immunosuppressant)
Thymectomy (if thymoma)
Plasmapheresis
IgG IV (suppresses thymus production by providing alternative antibody)
27
Carpal Tunnel Syndrome
Mononeuropathy
| Compression of median nerve passing through carpal bones and ligaments
28
Carpal Tunnel Syndrome causes
Inflammation of tendons, synovial swelling, tumor, RA, DM
| Repetitive flexion-extension movements
29
Carpal Tunnel Syndrome manifestations
Pain, paresthesis, numbness of thumb, 1st, 2nd, 3rd and part of 4th digit
Wrist and hand pain, worse at night
- Unable to effectively clench
Atrophy of abductor pollicus muscle
30
Carpal Tunnel Syndrome diagnosis
```
1. Tinel sign
Light percussion over median nerve at wrist
Tingling sensation into palm = positive
2. Phalen maneuver
Complete flexion x 1 minute
Paresthesia = positive
```
31
Carpal Tunnel Syndrome treatment
Anti-inflammatories, immobilization
32
Peripheral Nerve Disorders
Guillain-Barre Syndrome
33
Guillain-Barre Syndrome
```
Demyelinating polyneuropathy
Acute onset
Life threatening
Immune-mediated
Linked to Campylobacter jejuni, cytomegalobvirua, Epstein-Barr virus: as influenza like illness often before onset
```
34
Guillain-Barre manifestations
```
Progressive/variable
Ascending muscle weakness/paralysis
Starts at toes and moves upward
Respiratory muscle involvement
Paresthesia, numbness
Loss of tendon reflexes
ANS involvement = postural hypotension, arrhythmias, flushing, sweating, urinary retention
Pain common in shoulder, back, posterior thighs
```
35
Guillain-Barre treatment
Support of ventilation
Prevent complications
Plasmapheresis
IV immunoglobulin
80-90% have full recovery in 6-12 months
36
Disorders of the Cerebellum & Basal Ganglia
```
Tourette’s Syndrome
Parkinson Disease
Movement disorders (Tremors, tics, Hyperkinesia)
Hyperkinesia
- Choreiform - jerks
- Athetoid – twisting movement
- Ballismus – violent flinging movement
- Dystonia - rigidity
```
37
Tourette’s Syndrome
```
Dysfunction in cortical and subcortical regions (thalamus, basal ganglia, frontal cortex)
Inherited
Onset in childhood
Multiple physical tics and phonic tics
- Coprolalia (small %)
Limited treatment options
```
38
Parkinson Disease
Progressive disorder of basal ganglia and substantia nigral resulting in depletion of dopamine
2nd most common neurogenerative disorders after Alzheimer's
Usually occurs after 50 years of age
39
Parkinson Disease risk factors
```
Post encephalitic syndrome
Antipsychotic drug s/e
- Block dopamine receptors and output
Toxins
Carbon monoxide poisoning
Genetics
Brain tumors, CVA, head trauma, degenerative neurological diseases
```
40
Parkinson Disease manifestations
```
Unilateral at first, then bilateral
1. Rhythmic tremor of distal limbs
- Ceases with purposeful movement/sleep
2. Rigidity
- Passive joint movement causes jerks
Bradykinesis
- Slow to move; difficulty stopping voluntary movements
- Shuffling when walking, freeze, lean forward to keep moving
```
41
Parkinson Disease late manifestations
Difficulty planning, starting or carrying out tasks
Dementia/cognitive dysfunction (20-30%)
Motor function abnormalities
- Falls
- Voluntary facial movements become limited and slow = stiff, masklike expression
- Tongue, palate, throat muscles becoming rigid
- Slow speech, poor articulation
Sleep disorders
Neuropsychiatric disorders
- Unable to express emotions
ANS: Lacrimation, sweating, dysphagia, orthostatic hypotension, thermal regulation, constipation, impotence, incontinence
42
Parkinson Treatment
Individualized
43
Parkinson non pharmacological treatment
- Group support, education, exercise, nutrition guidance
44
Parkinson pharmacological treatment
- Increase dopamine levels (Levodopa)
- Stimulate dopamine receptors
- Slow breakdown of dopamine
45
Amyotrophic Lateral Sclerosis
Lou Gehrig Disease
- Etiology unclear
- 5-10% familial
- Mapped genetically
- Middle to late adulthood, male
- 80% die within 2-5 years of diagnosis
Amyotrophy = denervation/shrinkage of muscle fibers leading to atrophy
Lateral sclerosis = gliosis (scarring) of lateral columns of white matter
- 3000 affected currently in Canada
Genetic mutation
Glutamate (neurotransmitter) accumulation
Opens calcium channels > normal
Damages both upper and lower neurons controlling voluntary movement
Distal affected first in lower spinal cord, then disease moves toward parent nerve
46
ALS affects motor neurons in
Anterior horn of SC: decreased motor neuron firing = irritation, weakness, denervation atrophy, hyperflexia
Motor nuclei of brain stem
Cerebral cortex (weakness, lack of motor control, stiffness, spasticity)
47
ALS doesn't effect
Entire sensory system
Intellect
Ocular motility
48
ALS early manifestations
```
Muscle cramps
One extremity progressively weakness and atrophy
Generalized weakness
Hyporeflexia
Fasciculations
Impaired fine motor control
```
49
ALS late manifestations
```
Progressive
Limbs, head weakness
Weakness of palate, pharynx, tongue
- Speech disorders, dysphagia
Neck, shoulders, respiratory muscles
Aspiration
Death d/t cerebral and respiratory complications
```
50
ALS Treatment
Riluzole (antiglutamate) decreases glutamate accumulation and slows progression
Support of ADLs
Nutrition
Psychological assistance
51
Demyelination Disorders of the Central Nervous System
Multiple sclerosis
52
Multiple sclerosis
Inflammation and destruction of CNS myelin
Usually 20-40 year of age, women
Immune-mediated
Genetically susceptible
- 15 x more likely if immediate relative has it
53
Multiple sclerosis pathophysiology
Dyemyelination of nerve fibers of white matter in brain, spinal cord and optic nerve
- Either increased or decreases conduction
Plaques: hard, sharp-edged, sclerotic, patchy
- Lack oligodendrocytes
1st stage: sequential development of small inflammatory lesions
2nd stage: lesions extend and consolidate, demyelination and gliosis occurs
54
Multiple sclerosis manifestations
Unpredictable/dependent on location/extent
If healthy, symptoms occur, last for days or weeks, then resolve (next occurrence differs)
Paresthesia (mild to severe)
- Numbness, tingling, burning, pressure
Sexual & bladder dysfunction
Fatigue, speech disturbances, mood swings
Optic nerve and muscle abnormalities
- Neuritis, diplopia, gaze paralysis, nystagmus, vertigo
```
Lhermitte sign
Flex neck = shock-like response down back/legs
Muscle spasticity
Corticobulbar tracts (speech/swallowing)
Corticospinal tracts (muscle strength)
Cerebellar tracts (gait, coordination)
Spinocerebrellar tracts (balance)
Posterior cell columns of spinal cord (position, vibratory sensation)
```
Fatigue with depression
55
Multiple sclerosis diagnosis
```
A) Relapsing-remitting
Acute worsening episodes, stabilizing between episodes
B) Secondary progressive
Gradual worsening with episodes of improvement, previously had relapses-remittent
C) Primary progressive
Continuous deterioration
D) Progressive relapsing
Gradual but with superimposed relapses
```
Evidence of CNS lesions occurring in different parts at least 3 months apart
MRI – lesions (CT can be normal)
CSF: elevated IgG, elevated lymphocytes possible
56
Multiple sclerosis treatment
```
Manage symptoms
Healthy lifestyle
Physiotherapy
Corticosteriods
Adrenocorticotropic hormone (ACTH)
Plasmapheresis
Interferon (enhances immune system)
Glatiramer acetate (decoys t-cells)
Mitroxantrone (suppresses leukocytes)
```
57
Vertebral and Spinal Cord Injury
Primary young people
MVA, fall, violence, GSW
Most involve vertebral columns or supporting ligaments and the spinal cord
Life expectancy has increased with recent treatment advances
58
Acute Spinal Cord Injury
Direct trauma to cord (penetrating wound) or indirect (vertebral fracture, dislocation, subluxation of spine)
59
Spinal cord shock
Complete loss of motor, sensory, reflex and autonomic function below level of injury
Muscles, bowels, bladder, vasomotor tone
May recover in hours/days
60
Conus Medullaris Syndrome
Damage/compression to conus medullaris
61
Conus Medullaris Syndrome manifestations
```
Low back pain
Sciatica (usually bilateral)
Flaccid bowel/bladder
Sexual dysfunction
Possible motor/sensory loss
To legs/feet
```
62
Spinal cord secondary injuries
Neurons and white matter damage d/t
63
Spinal cord secondary injuries
Neurons and white matter damage d/t
- Blood vessel damage
- Decreased vasomotor tone
- Local release of vasospastic substances
- Release of enzymes from damaged cells
64
Spinal cord injury management
Reduce neurological deficit and limit additional loss
Immobilization, traction, alignment
Decompression
Surgery: internal skeletal stabilization to enable early ambulation
65
Classifications of SCI
```
1. Tetraplegia/quadraplegia
Cervical damage = loss of sensory motor or both
2. Paraplegia
Thoracic, lumbar, sacral damage
Arm function spared, trunk/legs/pelvis involvement varies
3. Muscle Grading
0 = total paralysis
5 = full movement
4. Impairment Scale
A = complete muscle strength loss
E = normal
```
66
Complication of SCI: Autonomic Dysreflexia
Post SCI above T6
| Unpredictable, exaggerated ANS response
67
Autonomic Dysreflexia triggers
Pain, full/spasm bladder, dressing change, uterine contraction, ejaculation, wrinkled sheets
68
Autonomic Dysreflexia manifestations
Sudden onset
| Vasospasm, hypertension, bradycardia, diaphoresis, headache
