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Pathophysiology 212 > Disorders of neuromuscular function > Flashcards

Disorders of neuromuscular function Flashcards

1
Q

Muscle Tone Terminology

A
  1. Hypotonia
    - Diminished resistance to passive movement
    - Soft muscles on palpation
    - Diminished deep tendon reflexes
  2. Hypertonia
    - Hyperexcitable stretch reflex causing rigidity & spasticity
  3. Clonus
    - Involuntary rhythmic muscular contractions and relaxations
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2
Q

Motor Dysfunction Terminology

A 
Plegia = stroke or paralysis
Paralysis = loss of movement
Paresis = weakness
Mono- = one limb
Hemi- = both limbs on one side
Di- or para- = both upper limbs or both lower limbs

Quadri- or tetra- = all four limbs

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3
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
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4
Q

Lower Motor Neuron Damage (where it connects to the muscle)

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

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5
Q

Skeletal Muscle Disorders: muscle atrophy & muscular dystrophy

A
  1. Muscle Atrophy
    - Disuse
    - Denervation
  2. Muscular Dystrophy
    - Contractile proteins not properly attached to cytoskeleton of muscle cell (muscle issue, not nerve)
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6
Q

Muscular Dystrophy

A
  1. Genetic (inherited X-linked recessive trait)
    - Primarily males
    - 9 major types
  2. Progressive degeneration (protein breakdown) and necrosis of skeletal muscle fibers & tissues
    - Sarcoma do not attach properly
    - Fat and connective tissue replace it
    Note: muscles, not nerves are affected
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7
Q

Muscular Dystrophy: Duchene MD & Becker

A
  1. Duchene MD (most common form)
    - Recessive X-linked
    - Affects 1:3500 male births
    - Females usually asymptomatic if carrier (or milder symptoms)
  2. Becker MD
    - slower, less severe
    - Later in childhood than DMD
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8
Q

MD Presentation

A
  • Boys asymptomatic at birth
  • Hips/shoulder 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
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9
Q

MD Diagnosis

A
  • Family history
  • Observation of voluntary movement
  • Elevated creatine kinase (CK-MM)
  • Muscle biopsy
  • Echo, ECG
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10
Q

MD Treatment

A
  • Maintain ambulation
  • Prevent deformities
  • Prevent respiratory infections
  • Death in young adulthood common
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11
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
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12
Q

Myasthenia Gravis Risk Factors

A
  1. Women > Men
  2. Early adulthood (women)
    - 50 years of age for men
  3. Placental transfer from Mom
    - 10-15% only, and often spontaneous resolution within months
  4. Thymus tumor or hyperplasia in 75% of cases (unclear connection)
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13
Q

Myasthenia Gravis: autoimmune

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 antibody response
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14
Q

MG Manifestations

A

> Initial: progressive throughout day
- Muscle weakness (periorbital muscles: ptosis, diplopia)
- Fatigue
Progression
- Respiratory muscle weakness, difficulty speaking/chewing/swallowing, weak limbs

> Myasthenia Crisis
- d/t stress, infection, emotional upset, pregnancy, alcohol, cold, surgery, etc.

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15
Q

MG Diagnosis

A
  • History, physical exam
  • Acetylcholine receptor blood test
  • Electrophysiologic studies to assess stage
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16
Q

MG Treatment

A
  • Corticosteroid (immunosuppressant)
  • Thymectomy (if thymoma)
  • Plasmapheresis (remove antibodies from the blood)
  • IgG IV
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17
Q

Carpal Tunnel Syndrome Causes

A
  • Mononeuropathy
  • Compression of median nerve passing through carpal bones and ligaments
    > Causes:
  • Inflammation of tendons, synovial swelling, tumor, RA, DM
  • Repetitive flexion-extension movements
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18
Q

Carpal Tunnel Manifestations

A
  • Pain, patesthesis
  • Numbness of thumb, 1st, 2nd, 3rd, and part of 4th digit
    Wrist and hand pain, worse at night (unable to clench effectively)
  • Atrophy of abductor pollicus muscle
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19
Q

Carpal Tunnel Syndrome Diagnosis & Treatment

A 
Diagnosis
Tinel sign
Light percussion over median nerve at wrist
Tingling sensation into palm = positive 
Phalen maneuver
Complete flexion x 1 minute
Paresthesia = positive 
	Treatment
Anti-inflammatories, immobilization
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20
Q

Peripheral Nerve Disorders: Guillain-Barre Syndrome

A
  • Demyelinating polyneuropathy
  • Acute onset… Life-threatening!
  • Immune-mediated
  • Linked to Campylobacter jejuni, cytomegalobvirua, - - Epstein-Barr virus: as influenza like illness often before onset
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21
Q

GB Manifestations

A
  • Progressive/variable
  • Ascending muscle weakness/paralysis
    (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
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22
Q

GB Treatment

A
  • Support of ventilation
  • Prevent complications
  • Plasmapheresis
  • IV immunoglobulin

80-90% have full recovery in 6-12 months

23
Q

Disorders of the Cerebellum & Basal Ganglia

A
  1. Tourette’s Syndrome
  2. Parkinson Disease
    Movement disorders (no paralyisis involved)
    - Tremors, tics
    - Hyperkinesia
    Choreiform (jerks)
    Athetoid (twisting movement)
    Ballismus (violent flingling movements)
    Dystonia (rigidity)
24
Q

Tourette’s Syndrome

A
  • Dysfunction in cortical and subcortical regions (thalamus, basal ganglia, frontal cortex)
  • Inherited
  • Onset in childhood
  • Multiple physical tics and phonic tics (coprolalia- small % excessive swearing)
  • Limited treatment options
25
Q

Parkinson Disease

A
  • Progressive disorder of basal ganglia and substantia nigral pathway resulting in depletion of dopamine
  • 2nd most common neurogenerative disorders after Alzheimer’s
  • Usually occurs after 50 years of age
26
Q

Parkinson: Risk Factors

A
  1. Post encephalitic syndrome
  2. Antipsychotic drug s/e (block dopamine receptors and output)
  3. Toxins
  4. Carbon monoxide poisoning
  5. Genetics
  6. Brain tumors, CVA, head trauma, degenerative neurological diseases
27
Q

Parkinson Manifestations

A
  1. Unilateral at first, then bilateral
  2. Rhythmic tremor of distal limbs
    - Ceases with purposeful movement/sleep
  3. Rigidity
    - Passive joint movement causes jerks
  4. Bradykinesis
    - Slow to move; difficulty stopping voluntary movements
    - Shuffling when walking, freeze, lean forward to keep moving
28
Q

Parkinson Manifestations: Late

A
  • 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 become rigid
  • Slow speech, poor articulation
29
Q

Parkinson Manifestations: Late Cont.

A

Sleep disorders
Neuropsychiatric disorders
- Unable to express emotions

ANS: lacrimation, sweating, dysphagia, orthostatic hypotension, thermal regulation, constipation, impotence, incontinence

30
Q

Parkinson Treatment

A
  • Individualized
    > Nonpharmacologic:
  • Group support, education, exercise, nutrition guidance
  • Botulinum toxin injections for dystonias for those people not responding to traditional treatments
31
Q

Parkinson Treatment: Pharmacologic

A
  1. Increase dopamine levels
    - Levodopa
  2. Stimulate dopamine receptors
    - Bromocriptine, Pramipexole, Amantadine
  3. Slow breakdown of dopamine
    - Selegiline, Rasagiline
32
Q

Amyotrophic Lateral Sclerosis (Low Gehrig Disease)

A 
> Lou Gehrig Disease
- Etiology unclear
- 5-10% familial; SOD 1 gene
Mapped genetically
Middle to late adulthood, male
80% die within 2-5 years of diagnosis
	Amyotrophy = denervation/shrinkage of muscle fibers = atrophy
	Lateral sclerosis = sliosis (scarring) of lateral columns of white matter
3000 affected currently in Canada
33
Q

ALS (genetic mutation)

A

Genetic mutation
Glutamate (neurotransmitter) accumulation
- Opens calcium channels > normal

Damages both upper & lower neurons controlling voluntary movement
Distal affected first in lower spinal cord, then disease moves toward parent nerve

34
Q

ALS affect on motor neurons

A

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)

35
Q

ALS Does not affect…

A

Does not affect, in most cases:
Entire sensory system
Intellect
Ocular motility

36
Q

ALS Manifestations: Early

A
  • Muscle cramps
  • One extremity progressively weakness and atrophies
  • Generalized weakness
  • Hyporeflexia
  • Fasciculations
  • Impaired fine motor control
37
Q

ALS Manifestations: Late

A
  1. Progressive
  2. Limbs, head weakness
  3. Weakness of palate, pharynx, tongue
    - Speech disorders, dysphagia
  4. Neck, shoulders, respiratory muscles
  5. Death d/t cerebral and respiratory complications
38
Q

ALS Treatment

A
  • Riluzole (antiglutamate) decreases glutamate accumulation and slows progression
  • Support of ADLs
  • Nutrition
  • Psychological assistance
39
Q

Demyelination Disorders of the Central Nervous System: Multiple sclerosis

A

Multiple sclerosis
- Inflammation & destruction of CNS myelin
- Usually 20-40 year of age, women
- Immune-mediated
- Genetically susceptible
15x more likely if immediate relative has

40
Q

MS: patho

A

> Demyelination of nerve fibers of white matter in brain, spinal cord and optic nerve
- Either increased or decreased condction
Plaques: hard, sharp-edged, sclerotic, patchy
- Lack oligodendrocytes
1st stage: sequential development of small inflammatory lesions
2nd stage: lesions extend & consolidate, demyelination and gliosis occurs

41
Q

MS: Manifestations

A

> 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)

42
Q

MS: Manifestations (cont)

A
  • 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

43
Q

MS Stages

A 
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
44
Q

MS Diagnosis: Lesions

A

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

45
Q

MS Treatment

A
  • Manage symptoms
  • Healthy lifestyle
  • Physiotherapy
  • Corticosteriods
  • Adrenocorticotropic hormone (ACTH)
  • Plasmapheresis
  • Interferon (enhances immune system)
  • Glatiramer acetate (decoys t-cells)
  • Mitroxantrone (suppresses leukocytes)
46
Q

Vertebral and Spinal Cord Injury

A
  • Primary young people
  • MVA, fall, violence, gun shot wounds
  • Most involve vertebral columns or supporting ligaments and the spinal cord
  • Life expectancy has increased with recent treatment advances
47
Q

Acute Spinal Cord Injury

A

> Direct trauma to cord (penetrating wound) or indirect (vertebral fracture, dislocation, subluxation of spine)
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 or days

48
Q

Conus Medullaris Syndrome & Manifestations

A 
Damage/compression to conus medullaris
> Manifestations
-Low back pain
-Sciatica (usually bilateral)
-Flaccid bowel/bladder
-Sexual dysfunction
-Possible motor/sensory loss to legs/feet
49
Q

SCI: Primary injuries

A
  • Gray matter hemorrhages
  • White matter edematous
  • Necrosis of neural tissue
50
Q

SCI: Secondary injuries

A
  • Neurons and white matter damage d/t
  • Blood vessel damage
  • Decreased vasomotor tone
  • Local release of vasospastic substances
  • Release of enzymes from damaged cells
51
Q

SCI Management

A
  • Reduce neurological deficit & limit additional loss
  • Immobilization, traction, alignment
  • Decompression
  • Surgery: internal skeletal stabilization to enable early ambulation
52
Q

Classifications of SCI

A
  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
    Muscle Grading
    0 = total paralysis 5 = full movement
    Impairment Scale
    A = complete m/s loss E = normal
53
Q

Complication of SCI: Autonomic Dysreflexia

A
  • Post SCI above T6
  • Unpredictable, exaggerated ANS response
    Triggers
  • Pain, full/spasm bladder, dressing change, uterine contraction, ejaculation, wrinkled sheets
    Manifestations – sudden onset
  • Vasospasm, HTN, bradycardia, diaphoresis, h/a.
    Treatment:
  • Remove cause, support

Pathophysiology 212 (18 decks)

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