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Neuroanatomy term 2 > Neurological Rehab- amyotrophic lateral sclerosis, muscular dystrophy, guillian-barre syndrome > Flashcards

Neurological Rehab- amyotrophic lateral sclerosis, muscular dystrophy, guillian-barre syndrome Flashcards

1
Q

Upper motor lesion on the basal ganglia

A

-common, tremor at rest, increased tone, bradykinesia, flexed posture

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2
Q

Upper motor lesion on the cerebellum

A

Incoordination of muscle activity, no weakness, unilateral cerebellar lesion

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3
Q

Upper Motor lesion affecting sensation

A

due to loss of touch sensation and feedback, ataxia or clumsiness of movement, uses eyes to compensate, no weakness

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4
Q

Motor neuron disease overview

A
  • generalized wasting, fasciculation and weakness of muscles
  • bulbar muscle involvement common
  • associated with upper neuron symptoms and signs
  • no sensory symptoms and signs
  • steadily progressive and fatal
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5
Q

Motor neuron disease

A

selective loss of lower motor neurons (pons, medula, spinal cord) and upper motor neurons in the motor cortex

  • cerebellar, sensory and autonomic functions intact
  • varied clinical picture: bulbar (medulla oblongata), upper limb, trunk and lower limbs
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6
Q

Motor neuron disease

A
  • Absence of sensory signs

- most death is resulted from the involvement of bulbar and respiratory muscles that lead to chest infection

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7
Q

4 clinical syndromes associated with motor neuron disease

A
  1. Bulbar palsy- Lower motor neurons-weakness, wasting, and fasciculation of the lower facial muscles, and muscles moving the palate, pharynx, larynx and tongue
  2. Pseudobulbar palsy- upper motor neuron weakness, slowness, and spasticity of the lower facial muscles, jaw, palate, phaynx, larynx and tonuge muscles- exaggerated jaq-jerk, emotional lability
  3. Progressive muscular atrophy: weakness, wasting and fasciculation of any of the limb or trunk muscles- often associated with frequent muscle cramps, no sensory loss, small muscles of the hand are frequently involved
  4. ALS- UN- weakness, spasticity, clonus, and increased deep tendon reflexes- any limb, but more common in the legs- sphincter control not affected- no sensory loss
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8
Q

Upper Motor neuron involvement characteristics

A
  • no wasting, increased tone of clasp-knife type- plastic like resistance- weakness most evident in anti-gravity position- increased reflexes and clonus
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9
Q

Lower motor neuron involvement characteristics

A
  • wasting, fasciculation- small, involuntary muscle contraction and relaxation which may be visible under the skin or in deep areas (twitching)- result of spontaneous depolarization of a lower motor neuron leading to the spontaneous contraction of all of the skeletal muscle fibers within a single motor unit
  • decreased tone
  • weakness
  • decreased or absent reflexes
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10
Q

ALS= muscle wasting

A

affects 5 per 100,000
there are 2 forms: familial and sporadic
-onset for familial is 45-52- first or second degree relative with ALS significantly increases the risk
-onset for sporadic is 55-62- presumed to be acquired- viral
- men are more affected
- most common motor neuron disease in adults

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11
Q

ALS etiology

A

fatal, progressive, degenerative
- scars form on the neurons in the corticopsinal pathways, the motor nuclei of the brainstem, and the anterior horn cells of the spinal cord

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12
Q

Path

A

progressive-

  • beginning from loss of strength in the small muscles of the hands and feet
  • loss of muscle movement
  • difficulty speaking and swallowing
  • loss of emotional control, reduced body temperature regulation
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13
Q

Possible causes

A
  • motor neuron distruction: dyfunction of the mitochondrial pathways results in buildup of proteins that lead to motor neuron death
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14
Q

Three subtypes of ALS- 1. Progressive Bulbar Palsy

A
  • includes the corticobular tracts and brainstem nuclei
    the corticobulbar tract is responsible for the control of facial and jaw musculature, swallowing and tongue movements
  • characterized by upper motor neuron involvement and loss of muscles innervated by cranial nerves: glosspharyngeal, vagus, and hypoglossal
  • Symptoms include dysarthria, dysphagia, facial and tongue muscle weakness and wasting
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15
Q

2- Primary Lateral Sclerosis

A 
only affects upper motor neurons
- may involve both the corticospinal and corticobular
- symptoms:
progressive spastic paralegia
can live with PLS for many years
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16
Q

3- Progressive Muscular Atrophy

A

affects mostly lower motor neurons
- characterized by weakness and atrophy
- fasciculation of the limbs, trunks, and bulbar muscles
- muscle cramps in thigh muscles
usually associated with a better prognosis than other subtypes

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17
Q

Signs and Symptoms

A

Most common is weakness of small muscles of hands and feet- assymmetrical foot drop
May present with night cramps in the calf muscles
Symptoms progressive, from distal to proximal- symptoms can be divided into lower motor neuron, coritcospinal tract, and corticobulbar tract
Corticospinal tract- fine voluntary motor control of the limbs- voluntary control of body posture adjustments

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18
Q

Picture of ALS

A

starts with focal muscle weakness beginning in the arm, leg or bulbar muscles
- marked muscle atrophy, weight loss, spasticity, muscle cramping and fasciculation
rarely affects eye function, cognition, bowel or bladder function or sensation at the beginning

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19
Q

Prognosis

A

usually progressive and rapid
duration of survival is 1-5 years
most die within 3 years
death is usually from respiratory failure
prognosis is better if either upper or lower motor neurons effected but not both

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20
Q

Diagnosis

A 
based on clinical symptoms
- EMG
 MRI CT scan to rule out other causes
blood test- usually normal
CSF- usually normal but may show raised protein levels
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21
Q

Medical management

A

Little effect

Medications- antispasmodic, non-steriodal anti-inflammatory, anti-glutamatergic, antibiotics

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22
Q

Medical Management

A

Gastrostomy and non-invasive positive pressure ventilation- increase length of life
- low dose radiation or botulinum toxin injections into salivary glands
palliative care

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23
Q

OT assessment

A

MMT, ROM, Balance, coordination, find and gross skills

  • swallowing and eating
  • psychosocial- family support, carer support, environment, spiritual
  • depression- beck depression inventory- cognition MMSE cognistat
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24
Q

OT Assessment

A

Productivity- consider patients age and premorbid occupation

Leisure

Role Checklists- 15 minutes, self-report questionnaire focusing on person’s occupational roles

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25
Q

OT Assessment

A

Functional Autonomy Measuring System (SMAF)- 5 subscales: ADLS, Mobility, Communication, Mental Function and IADLS

Occupational performance history interview:
45-60 min, semi-structured narrative interview,
looking at occupational roles, daily routines, activity and occupational choices, critical life events

26
Q

Clinical phases

A

6 stages and 3 phases
Phases:

  1. independent (stages 1-3)
  2. partially independent (stages 4-5)
  3. dependent (stage 6)
27
Q

Stage 1

A

Overall: mild weakness, clumsiness, minor limitations and some pain may be present, endurance is less

OT Intervention

  • energy conservation techniques to increase activity level
  • Begin some ROM and stretching
  • Work simplification
28
Q

Stage 2

A

Overall: Moderate, selective weakness

OT Intervention

  • adaptive equipment to facilitate ADLS
  • Hand orthotic use & orthotic support as ankle-foot orthosis
  • Continue stretching to avoid contractures
  • safety considerations
29
Q

Stage 3

A

Overall: severe, selective weakness in ankles, wrists and hands
becomes easily fatigued with ambulation, client is still ambulatory

OT intervention

  • prescribe manual or power wc
  • aids and equipment to compensate for function
  • being discussing need for home modifications
30
Q

Stage 4

A

Overall:hanging arm syndrome with shoulder pain and edema, depends on wc for ambulation, LE weakness

OT intervention

  • arm slings
  • evaluate need for environmental control systems such as voice activated computer
  • heat, massage, to control spasms
  • discuss client and family wishes for future interventions
31
Q

Stage 5

A

Overall- severe LE weakness, moderate to severe UE weakness

OT intervention
family training to learn proper transfer, positioning, and turning techniques assistance in ADLs
select essential control devices, ex. for electric bed, telephone and stereo
adapt wc for respiratory device
psychosocial intervention

32
Q

Stage 6

A

Totally dependent and confined to bed/chair

OT intervention:
Evaluate dysphagia & provide with augmentative speech devices
Continue with PROM and massage

33
Q

PRECAUTIONS

A
  • muscle strengthening through progressive resistance is usually not part of the program as it can cause cramping or fatigue
  • watch for signs of decreased respiratory function
  • avoid fatigue
  • consider the cost, appearance, and acceptability to the person and the family of any assistive devices
34
Q

MUSCLE DISEASES

A
  • Primary pathology causing muscle weakness is in the muscle itself
  • inherited biochemical defect is present
  • acquired
35
Q

Muscular Dystrophy MD

A
  • group of muscle diseases that weaken the musculoskeletal system and hamper locomotion
  • Characterized y progressive skeletal muscle weakness, defects in muscle proteins and the death of muscle cells and tissue
  • generally inherited
  • mutation of the dystrophin gene and nutritional defects at the prenatal stage
36
Q

Common types of MD

A
  1. Duchenne’s (inherited)
  2. Myotonic dystrophy
  3. Facio-scapulo-humeral
  4. Limb-girdle
37
Q

Duchenne’s

A

inherited
most common childhood form of MD
- increase in volume of the calf muscle
- prognosis- death by age 30

38
Q

Myotonic dystrophy

A

-onset at 20-40 years
- several organs and tissues of the body
- Myotonic contraction
Impairments:
intellectual function
cataracts
premature loss of hair
cardiac arrhythmia and failure
Gonadal atrophy and failure
hand muscles

Contraction myotonia- difficulty in rapid relaxation of tightly contracted muscle

Percussion myotonia- tendency for muscle tissue to contract when it is struck by a tendon hammer

cardiomyopathy
facial problems- wasting of temporalis muscles, bilateral ptosis and bilateral facial weakness

39
Q

Facio-scapulo-humeral

A
  • affects muscles in the face, shoulder and upper arms
  • due to an unusual dominantly inherited gene contraction near the telomere of chromosome 4
  • mild and asymptomatic

characteristics:

  • facial, scapular and humeral muscles
  • difficulties in whistling
  • using the arms above shoulder level
  • abnormal position of the scapula
40
Q

Limb-girdle

A

onset in childhood or teens, affects upper arm and legs

  • proximal limb muscles
  • range of causes
  • should not be regarded as due to dystrophy
41
Q

Other common types of MD

A

Becker- mild form
Congenital- onset at birth
Oculopharyngeal- onset 40-70 years- affects muscles of the eyelids, face and throat
Distal- onset 20-60
Emery-Dreifuss- childhood and early teenage years with contractures

42
Q

OT Assessment

A

physical: MMT, ROM, Balance, coordination fine and gross motor

Cognition, perception- depending on age

psychosocial

Self-care, productivity, leisure

43
Q

OT Intervention

A

Using COMP-E
- Progressive so make reference to ALS but the rate of deterioration and disability to less aggressive
- Splinting/orthosis
-transition to wc
- development stages and considerations
- depending on age of onset- consider activities related to school, work, retirement
-safety, especially if lower limbs are involved
Remediation to maintain residual function and assistive device to optimize function

44
Q

Peripheral Neuropathy

A

peripheral nerves- axon of the anterior horn cell and the distal axon of the dorsal root gangion cell

2 types of pathology:
Distal axonal degeneration
segments of the nerve fibers become demyelinated

45
Q

Sign and symptoms

A

Upper limbs:
sensory:
glove distribution of tingling, pins and needles
sensory ataxia in fingers and hands

Motor:
Weakness of grip and pinch
distal lower motor neuron signs in hands
loss of distal reflex

Lower Limbs

Sensory:
Stocking distribution of tingling, pins and needles and numbness
unsteady stance and gait especially in the dark with eyes closed

Motor:
Loss of spring at the ankles
distal lower motor neuron signs in foot
Loss of distal reflexes

46
Q

Guillain-Barre Syndrome

A

acute, rapidly progressive for of polyneuritis ( affecting many nerves)

  • One of the forms of peripheral neuropathy but very different because it is rapid, produces a life-threatening degree of weakness, underlying pathology clearly affects both the nerve roots and the peripheral nerve
  • commonly affects between 30-50 year olds
47
Q

Etiology

A

Unknown cause

  • very likely could be a viral infection where the immune system attacks the peripheral nerves
  • commonly occurs 1-2 weeks after an infection
48
Q

Stages

A
  1. Acute onset- 1st symptom appears and ends and no further symptoms are noted (1-3 weeks)- patient will notice limb weakness and sensory symptoms, worsen day to day for 2 weeks and continue to 4 weeks
  2. Plateau Period- No further changes occur, lasts from several days to 2 weeks
  3. Some will demonstrate a recover phase when remyelination and axonal regeneration occur and may take up to 2 or 3 years
  • common to progress to very serious paralysis in the limbs, trunk and chest mucles and muscles that supply the cranial nerves
  • May involve autonomic nerves, cause erratic rises and falls in HR and BP and profound constipation
49
Q

Medical management

A

-hospitalized until plateau period

50
Q

Prognosis

A

Some with incomplete recovery and further deterioration but most will completely recover over a few weeks or months

10-20% will die due to respiratory paralysis

Schwann cells are able to regenerate

51
Q

Problem Areas

A

Primarily motor and sensory

  • psychological- very anxious, depressed and frustrated- supports are very important
  • OP depends on the progression of the illness
52
Q

Motor

A

Common
- muscle weakness, begins in lower extremities and speed up the body, trunk, and cranial nerves- facial nerve(unable to smile, whistle, drink through a straw), glossopharengeal nerve and vagus nerve (difficulty swallowing, coughing and gagging), hypoglossal nerve (deviation or paralysis of the tongue)
- Loss of ROM
-fatigue until respiratory sufficiency is restored
May appear:
- develop contractures due to lack of active movement
- hypotonia
- Lose superficial and deep reflexes
-Loss of respiratory control

53
Q

Sensory

A

Common:

Temporary loss of touch sensation below the point of the body affected by the disorder

54
Q

OT Treatment- Motor, ,

A

Motor: Maintain passive ROM and encourage active ROM, increase muscle strength and endurance within a tolerable duration,

  • **for Nonresistive activites, muscles should be 3+ or greater
  • splinting to prevent deformity
  • increase hand manipulation, grasp release activities
55
Q

OT Treatment- SensoryCognitive, Psychosocial, Relevant occupational performance areas

A

Sensory- provide opportunities for sensory stimulation when sensory system returns

Cognitive- stress management, task scheduling to cope with muscle fatigue, energy conservation and concepts of joint protection

Psychosocial- relaxations techniques, positive encouragement

ADL- shoulder slings or mobile arm supports, hand splints to promote functionality and functional positions

Work- work simplification, temporary modification of home and work environment

Leisure- Strenuous leisure activities will not be possible until full recover occurs

56
Q

Precautions

A

watch for redness over bony areas
discontinue activities when the patient shows signs of fatigue
never stress the muscle past the point of pain

57
Q

Myasthenia gravis

A
  • autoimmune disease
  • presence of auto-antibody attached to receptor sites on the post-synaptic membrane
  • women more than men
  • fatigue, muscle weakness, worse at the end of the day, repetitive use of the muscles
58
Q

Common symptoms

A

external occular- double vision,
Bulbar- difficulty chewing, swallowing and talking
neck- difficulty in lifting head up from lying position
Proximal limb- Difficulty in lifting arms above shoulder level, standing from low chairs, out of the bath
Trunk- breathing problems and difficulty sitting from the lying position
Distal limb- weak hand-grip, ankles and feet

59
Q

Management

A

medication, surgery-thyectomy, plasma exchange, watch for fatigue signs and take precaution in exercise treatment- muscle strength changes abruptly

60
Q

ADD-ONs- MS

A

MS- lesion is in the CNS, ie the cerebellum, brainstem, cerebellum or spinal cord, but not the peripheral system

  • optic nerve is an outgrow from the CNS– frequently involve the optic nerve
  • Lesion in the other cranial nerves, spinal nerves and peripheral nerves in the limbs do not occur
  • Main insult if the myelin sheaths

Typical Picture:

  • reduce visual acuity, blurred vision caused by optic neuritis
  • a cerebellar deficit
  • an upper motor neuron deficit, mild in the arms, moderate in the trunk and most evident in the legs
  • impaired sexual, bladder and bowel function
  • variable amount of sensory loss
  • cause is unknown, genetic, environmental
61
Q

Precautions

A
  • type of exercise, intensity, duration of workload,
  • avoid exercising outside during the hottest times of the day due to thermosensitivity
  • swimming and water aerobics, gentle yoga, taichi,
    dont overdo
    aspiration

Neuroanatomy term 2 (8 decks)

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