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NM differential Dx Flashcards

1
Q

What is MS?

A

chronic, progressive, demyelinating disease of the CNS

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2
Q

What population does MS commonly affect?

A

Female adults (20-50 y/o)

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3
Q

Description

  • demyelinating lesions impair neural transmission which causes the nerves to fatigue rapidly
  • lesions are common in pyramidal tract, dorsal columns, optic tract, periventricular areas of cerebrum, and cerebellar peduncles
  • variable course with fluctuating episodes progressing to permanent dysfunction
  • transient worsening of symptoms
A

MS

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4
Q

The following s/s are indicate what diagnosis?
- mild to moderate cognitive impairment
- euphoria
- emotional dysregulation
- dysarthria
- dysphagia
- decreased ROM
- Sensory symptoms (parasthesia, hyperpathia, dysesthesias, trigeminal neuralgia, Lhermitte’s sign)
- diplopia and blurred vision (possible optic neuritis, blind spots (scotoma), and/or nystagmus)
- spasticity and hyperreflexia
- paresis
- ataxia
- intention tremors
- dysmetria
- dysdiadokinesia
- vestibular s/s
- fatigue

A

MS

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5
Q

What is the #1 complaint of MS?

A

fatigue

w/ activity and as the day progresses

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6
Q

What are the clinical subtypes of MS?

A
  1. relapsing-remitting (RRMS)
  2. primary-progressive (PPMS)
  3. secondary-progressive (SPMS)
  4. progressive-relapsing (PRMS)
  5. clinically isolated syndrome (CIS)
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7
Q

Definition

Subtype of MS that is characterized by discrete attacks of neuro deficits with either full or partial recovery in subsequent weeks or months; periods between relapses are characterized by lack of disease progression

A

relapsing-remitting MS

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8
Q

What subtype of MS is common in 85% of cases?

A

Relapsing-remitting

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9
Q

definition

subtype of MS characterized by disease progression and a deterioration in function from onset; patient can experience moderate fluctuations in neurological disability but discrete attacks do not occur

A

primary-progressive

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10
Q

definition

Subtype of MS characterized by an initial relapsing-remitting course, followed by a change to a progressive course with a steady decline in function, with or without continued acute attacks

A

secondary-progressive

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11
Q

definition

Subtype of MS characterized by a steady deterioration in disease from onset but with occasional acute attacks; time between attacks are characterized by continued disease progression

A

progressive-relapsing

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12
Q

definition

Subtype of MS that is the first episode of inflammatory demyelination that could become MS if additional activity occurs

A

clinically isolated syndrome (CIS)

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13
Q

What type of MS can CIS progress to if a patient continues to have additional activity indicating possible MS?

A

relapsing-remitting

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14
Q

What is recommended for diagnosis of MS?

A

brain MRI with gladiolum

spinal cord MRI if brain MRI is non-diagnostic

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15
Q

Degeneration of what CNS structures lead to PD?

A
  1. dopaminergic substantia nigra neurons
  2. nigrostriatal pathways

  • deficiency of basal ganglia corpus striatum
  • loss of inhibitory dopamine results in excessive excitatory output from the cholinergic system of the basal ganglia (ACh)
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16
Q

Diagnosis

  • rigidity
  • bradykinesia
  • resting tremor
  • impaired postural reflexes
  • altered gait: shuffling, freezing, festination (involuntary increase in walking speed)
  • fatigue
  • anxiety and depression
  • slow progression with emergence of secondary impairments and permanent dysfunction
  • altered cognition
  • dysphagia
  • orthostatic hypotension
  • akathisia (restlessness)
  • visual changes
  • integumentary changes (edema, circulation, integrity)
  • weakness
A

PD

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17
Q

What is the Hoehn and Yahr classification used for?

A

staging PD

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18
Q

What is stage 1 of Hoegn and Yahr classification?

A

Minimal or absent disability - unilateral symptoms

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19
Q

What is stage 2 of Hoegn and Yahr classification?

A
  • Minimal bilateral or midline involvement
  • no balance involvement
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20
Q

What is stage 3 of Hoegn and Yahr classification?

A
  • impaired balance
  • some activity restrictions
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21
Q

What is stage 4 of Hoegn and Yahr classification?

A
  • all PD symptoms are present and severe
  • standing and walking with assistance
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22
Q

What is stage 5 of Hoegn and Yahr classification?

A

confinement to bed or WC

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23
Q

What should you examine for when you have a patient taking Levodopa for PD management?

A

fluctuating symptoms (on-off phenomenon)

Common with disease progression and long-term use of levodopa

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24
Q

What are adverse effects of levodopa (sinemet)?

A
  • n/v
  • orthostatic hypotension
  • arrythmia
  • dyskinesia/involuntary movements
  • psychoses/hallucinations
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25
Q

What causes presyncope?

A

CVD reducing cerebral perfusion

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26
Q

Blurred vision is gaze instability secondary to ______.

A

VOR dysfunction

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27
Q

(true/false) Vestibular symptoms are seen in 87% of patients with chronic TBI

A

FALSE (acute TBI)

PVH occurs in 19%

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28
Q

diagnosis

Acute infection of vestibular system (bacterial or viral) with prolonged attack of symptoms, persisting for several days to weeks

A

vestibular neuronitis, labyrinthitis

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29
Q

Diagnosis

episodic vertigo syndrome associated with low to medium frequency sensorineural hearing loss and fluctuating aural symptoms in the affected ear accompanied by vertigo

Etiology unknown but believed to be accumulation of endolymph

A

meniere’s disease

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30
Q

How long do symptoms of vertigo last in those with menieres disease?

A

20 minutes - 12 hours

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31
Q

Diagnosis

brief attacks of vertigo and nystagmus that occurs with a change in head position

Can be related to disloged otoconia into the semicircular canal

A

BPPV

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32
Q

What can cause unilateral peripheral vestibular hypofunction (PVH)?

A
  • menieres disease
  • BPPV
  • trauma
  • vestibular neuritis/labyrinthitis
  • tumor
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33
Q

What kind of injury is the most common cause of SCI in the lumbar spine?

A

FLX

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34
Q

What kind of injury is most common to cause SCI in the cervical spine?

A

FLX-ROT

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35
Q

What spinal areas have the greatest frequency for experiencing SCI?

A
  1. C5
  2. C7
  3. T12
  4. L1
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36
Q

What is designated as the lesion level for an SCI?

A

Most distal uninvolved nerve root with normal function

MMT must be 3+/5

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37
Q

What levels cause quadriplegia?

A

C1-C8

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38
Q

What levels cause paraplegia?

bilateral LEs and trunk

A

T1-T12

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39
Q

What are the levels of the ASIA scale?

A

A= complete

B= incomplete; sensory function is preserved below neural level

C= incomplete; motor function is preserved below neural level and are < 3/5

D= incomplete; motor function is preserved below the functional level and most have a MMT of 3/5 or higher

E= Normal

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40
Q

Diagnosis

  • Loss of centrally located cervical tracts (arm functioning)
  • loss of B/B functioning with spasticity
  • preservation of peripherally located lumbar and sacral tracts (LE functioning)
A

Central cord syndrome

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41
Q

What MOI typically causes central cord syndrome?

A

hyperextension injury of the cervical spine

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42
Q

Diagnosis

  • ipsilateral loss of tactile discrimination, pressure, vibration, and proprioception (dorsal columns)
  • ipsilateral loss of motor function and paralysis below level of lesion (corticospinal tracts)
  • contralateral loss of pain and temperature below level of lesion (spinothalamic tract)
  • bilateral loss of pain and temperature at the level of lesion (spinothalamic tract)
A

Brown Sequard syndrome

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43
Q

What MOI commonly causes brown-sequard syndrome?

A

puncture wounds

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44
Q

Diagnosis

  • loss of lateral corticospinal tracts
  • loss of spinothalamic tracts
  • bilateral loss of motor function (spastic paralysis below level of lesion - lateral corticospinal tracts)
  • bilateral loss of pain and temperature (spinothalamic tracts)
A

Anterior cord syndrome

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45
Q

What is preserved with anterior cord syndrome?

A
  • light touch
  • proprioception
  • sense of positioning
  • vibration

Dorsal columns

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46
Q

What is preserved with central cord syndrome?

A
  • proprioception
  • discriminatory sensation
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47
Q

What is the MOI of anterior cord syndrome?

A

FLX injury of cervical spine

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48
Q

Diagnosis

  • loss of posterior columns
  • bilateral loss of proprioception, vibration, pressure ,and epicritic sensations (stereognosis, 2-point discrimination)
  • preservation of motor function, pain, and light touch
  • rare
A

posterior cord syndrome

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49
Q

What is preserved with posterior cord syndrome?

A
  • light touch
  • pain
  • motor function
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50
Q

diagnosis

injury below L1 that results in LMN lesion of lumbar and sacral roots

A

cauda equina injury

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51
Q

What does cauda equina injury cause?

A
  • sensory loss
  • paralysis
  • autonomous or nonreflex bladder
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52
Q

(true/false) There is some capacity for regeneration of motor and sensory functioning with cauda equina injury

A

true

incomplete recovery that stops after 1 year

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53
Q

Definition

Sparing of tracts of sacral segments with preservation of perianal sensation, rectal sphincter tone, or active toe FLX

A

sacral sparing

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54
Q

(true/false) voluntary saccadic or smooth pursuit eye exercises should NOT be offered in isolation (without head movement)

A

true

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55
Q

Describe spinal shock.

A

period of reflex depression and flaccidity

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56
Q

how long can spinal shock occur?

A

hours - 24 weeks

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57
Q

What are the s/s of autonomic dysreflexia?

A
  • HTN
  • bradycardia
  • severe HA
  • anxiety
  • constricted pupils
  • blurred vision
  • flushing and piloerection
  • increased spasticity
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58
Q

What should you do if a person may be experiencing autonomic dysreflexia?

A
  • sit them in upright position
  • loosen tight clothing
  • examine for blockage of urinary drainage
  • monitor BP and HR
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59
Q

What WC is most appropriate for those with high cervical lesions (C1-C4)?

A
  • electric WC
  • tilt in space seating
  • puff and sip control/microswitch
  • portible respirator
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60
Q

What WC is most appropriate for those with C5 injury?

preservation of shoulder function and elbow FLX

A

manual with propulsion aids

Independent for short distances
- may require electric WC for longer distances

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61
Q

What WC is most appropriate for patients with C6 or C7 lesion?

preservation of radial wrist extensors and/or triceps

A

manual WC with friction-surface rims

independent

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62
Q

What would locomotor training result in for those with midthoracic lesions (T6-T9)?

A
  • supervision with short distances
  • use of AD
  • bilateral KAFO

may prefer standing devices for physiological standing (standing WC)

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63
Q

What would locomotor training result in for those with high lumbar lesions (T12-L3)?

A
  • independence with ambulation on all surfaces and stairs
  • independent household ambulation
  • WC use for community distances
    -bilateral KAFOs
  • swing-through pattern or four-point pattern with crutches
  • possible use of FES system with reciprocating gait orthoses
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64
Q

What will locomotor training result in for those with low lumbar lesions (L4-L5)?

A
  • independent ambulators with bilateral AFOs
  • crutches or cane
  • may use WC for high-endurance activity
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65
Q

What are the absolute contraindications for exercise testing and training in individuals with a SCI?

A
  • autonomic dysreflexia
  • severe or infected skin on WB surfaces
  • symptomatic hypotension
  • UTI
  • unstable Fx
  • uncontrolled temperature envirnoments
  • insufficient ROM for task performance
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66
Q

What is another name for ALS?

A

Lou gehrig’s disease

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67
Q

diagnosis

degenerative disease affecting UMNs and LMNs through degeneration of anterior horm cells, descending corticobulbar, and corticospinal tracts.

A

ALS

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68
Q

What is the etiology of ALS?

A

unknown

5-10% genetic

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69
Q

Diagnosis s/s

  • progressive disease leading to death within 2-5 years
  • muscular weakness progressing from limbs to whole body; atrophy, cramping, muscle fasciculations, twitching (LMN s/s)
  • hyperreflexia (UMN s/s)
  • spasticity (UMN s/s)
  • dysarthria
  • dysphagia
  • dysphonia secondary to pseudobulbar palsy
  • autonomic dysfunction (1/3 of cases)
  • respiratory weakness
  • depression
A

ALS

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70
Q

What is stage I of ALS?

A
  • Early disease with mild focal weakness
  • asymmetrical
  • s/s are hand cramping and fasciculations
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71
Q

What is stage II of ALS?

A
  • moderate weakness
  • start of atrophy
  • modified independence with AD
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72
Q

What is stage III of ALS?

A
  • severe weakness
  • increased fatigue
  • mild to moderate functional limitations
  • ambulatory
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73
Q

What is stage IV of ALS?

A
  • severe weakness and LE wasting
  • mild UE weakness
  • mod A with AD
  • WC user
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74
Q

What is stage V of ALS?

A
  • progressive weakness with deterioration of mobility and endurance
  • increased fatigue
  • moderate to severe weakness of limbs and trunk
  • hyperreflexia
  • spasticity
  • loss of head control
  • max A
  • use of WC
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75
Q

What is stage VI of ALS?

A
  • bedridden
  • dependent
  • progressive respiratory distress
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76
Q

What is bulbar palsy?

A

weakness or paralysis of the muscles innervated by the motor nuclei of the lower brainstem
- affects the muscles of the face, tongue, larynx, and pharynx

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77
Q

What is the etiology of bulbar palsy?

A
  • tumors
  • vascular disease
  • degenerative diseases

… of the lower CN motor nuclei

78
Q

diagnosis

bilateral dysfunction of the corticobulbar innervation of brainstem nuclei – UMN lesion analogous to corticospinal lesions disrupting the function of anterior horn cells

A

pseudobulbar palsy

similar s/s of bulbar palsy

79
Q

What is another name for trigeminal neuralgia?

A

Tic Douloreux

80
Q

What is trigeminal neuralgia?

A

lesion of trigeminal nerve

can result from compression and occurs in older adults

81
Q

Trigeminal neuralgia has a (gradual/abrupt) onset.

A

abrupt

82
Q

What is Bell’s palsy?

A

Lesion of facial nerve (CN VII) resulting in unilateral facial paralysis

83
Q

diagnosis s/s

  • muscles of face on one side are weakened or paralyzed (facial droop, altered taste in anterior 2/3 of tongue)
  • loss of control over salivation or lacrimation
  • acute onset
  • maximal severity within a few hours or days
  • followed behind pain in the air for 1-2 days
A

bell’s palsy

84
Q

(true/false) sensation is not affected with bell’s palsy

A

true

85
Q

What medications are used to treat bell’s palsy?

A

corticosteroids and analgesics

86
Q

definition

nerve injury that causes a transient and focal chemical/structural loss of function (conduction block/demyelination)
- often related to compression causing ischemia
- can be rapidly reversed or persist for weeks to month

A

neurapraxia

87
Q

definition

focal damage to the axon/myelin and varying degrees of peripheral nerve connective tissue (endoneurium, perineurium, and epineurium)
- seen with increased duration or larger amplitude compression or tension
- traction injuries results in disruption of the peripheral nerve connective tissue

A

axonotmesis

88
Q

What does axonomesis result in?

A

Wallerian degeneration within the disrupted axons

axonal regrowth is related to the degree of the connective tissue damage, PMH, and overall health of the patient

89
Q

How much axonal regrowth occurs within a day?

A

1-3 mm (1inch/month)

90
Q

definition

Severance of axon/myelin and all the connective tissue structures including the epineurium
- complete loss of nerve function and wallerian degeneration with no connective tissue path
- requires surgical intervention

A

neurotmesis

91
Q

Describe collateral sprouting.

A

Intact axons pick up deinnervated terminal targets

92
Q

What happens to muscle fibers if collateral sprouting occurs?

A

Muscle fiber type switches

type I - type II

93
Q

(true/false) Both polyneuropathic conditions impact the axon AND myelin.

A

true

peripheral nerve diseases are more chronic in nature

94
Q

(true/false) old age is a key risk factor in forming a polyneuropathy.

A

true

95
Q

What test is used for diagnosis of small fiber cutaneous neuropathies?

A

skin punch biopsy

96
Q

Diagnosis

Acute inflammatory demyelinating polyradiculoneuropathy presenting with rapid non-symmetric loss of myelin in nerve roots and peripheral nerves (LMN disease)
- muscle weakness has abrupt onset and immediate medical attention is warranted

A

guillain-barre syndrome (GBS)

97
Q

diagnosis s/s

  • sensory loss/parasthesia
  • motor paresis or paralysis; symmetrical distribution of weakness
  • dysarthria
  • dysphagia
  • diplopia
  • facial weakness
  • progresses within a few days to weeks
A

GBS

98
Q

There is (less/more) sensory loss than motor loss with GBS

A

less sensory loss

99
Q

(true/false) GBS can cause full tetraplegia with respiratory failure

A

true

100
Q

How long does GBS evolve/progress?

A

few days to weeks

101
Q

How long does it take to recover from GBS?

A

6 months to 2 years

102
Q

Diagnosis

Slow progressive muscle weakness occurring in individuals with a confirmed history of acute polio

A

post-polio syndrome (PPS)

103
Q

When does PPS occur?

A

after a stable period of functioning (15 years after initial polio diagnosis)

104
Q

What are the signs and symptoms of PPS?

A
  • gradual onset of muscle weakness or fatigue with or without atrophy
  • slow progression; new symptoms progressing > 1 yr
  • abnormal fatigue
  • pain
  • decreased endurance
  • cold intolerance
  • sleep disturbance
105
Q

Those with PPS have (cold/heat) intolerance

A

cold intolerance

106
Q

Is sensation affected by PPS?

A

no

107
Q

What is the most common NMJ disorder encountered in clinical practice?

A

Myasthenia gravis

108
Q

What is the common treatment for hypertonia, dystonia, chronic pain, and muscle spasms?

A

botulinum toxin

109
Q

Diagnosis

  • females 20-30 y/o
  • males = females at 60-80 y/o
  • progressive muscular weakness during activity that improves with rest
  • fatigue with sustained activity
A

myasthenia gravis

110
Q

What is the primary impairment reported by patients with myasthenia gravis?

A

fatigue

111
Q

What are the 4 classifications of myasthenia gravis?

A
  1. ocular myasthenia (confined to extraocular muscles)
  2. mild generalized myasthenia
  3. severe generalized myasthenia
  4. myasthenic crisis
112
Q

What is myasthenic crisis?

A

myasthenia gravis with respiratory failure

medical emergency

113
Q

What muscles do general myasthenia gravis involve?

A
  • bulbar muscles (extraocular, facial, muscle of mastication
  • proximal limb-girdle muscles
114
Q

How long does it take for myasthenia gravis to progress?

A

can progress from mild to severe within 18 months

115
Q

When examining for myasthenia gravis, what should you look for indicating involvement of cranial nerves?

A
  • diplopia
  • ptosis
  • progressive dysarthria
  • nasal speech
  • dysphagia
  • difficult facial expression
  • facial droop
116
Q

What is the ice pack test? What is it normally used for?

A

Used for myasthenia gravis

(+) test is decreased ptosis after a 2-minute application of an ice pack to the affected eyelid

117
Q

Are proximal or distal muscles more affected by myasthenia gravis?

A

proximal muscles

118
Q

Nerve conduction studies on myasthenia gravis show a (increased/decreased) response to repetitive nerve stimulation at baseline

A

decreased

119
Q

What medications can be used for treatment of myasthenia gravis?

A
  • acetylcholinesterase
  • corticosteroids
  • immunosuppressants

Alternative treatments: plasmapheresis or thymectomy

120
Q

What is plasmapheresis?

A

removal of blood with filtering and separation of the cellular elements within the plasma

121
Q

What is the mechanism of botulinum toxin?

A

decreases the release of ACh resulting in flaccidity and/or hypotonia (dependent on dose)

binds presynaptically to high-affinity sites on cholinergic nerve terminals

122
Q

What are the adverse side effects of botulinum toxin?

A
  • weakness of unintended muscles
  • flaccidity
  • dysphagia
  • local hemotoma
  • generalized fatigue
  • dry mouth
  • dizziness
  • pain
  • flu-like symptoms

complications are dependent on the muscles injected

higher risk of complications when head, neck, and trunk muscles are involved

123
Q

(true/false) myopathic disorders are classified as inherited or acquired.

A

true

inherited (muscular dystrophy)
acquired (inflammatory myopathies, infectious myopathies (HIV), toxic/drug related myopathy, systemic disease myopathy)

124
Q

What do acquired myopathies result in?

A

Muscle cell structure and/or metabolism dysfunction

125
Q

diagnosis

  • muscle cramps and pain with exertional fatigue
  • progression of weakness from proximal to distal muscles
  • difficulty with overhead activity and getting in/out of chairs
  • pelvic girdle weakness w/ associated gait deviations
  • normal sensation
A

myopathic disorders

  • joint pain with polymyositis
  • skin changes with dermatomyositis
126
Q

What lab tests can confirm myopathy?

A

Elevated:
- creatine kinase
- aldolase
- lactate dehydrogenase
- liver function enzymes

To identify the etiology:
- metabolic panel
- thyroid hormone
- PTH
- sedimentation rate
- C-reactive protein

127
Q

(true/false) EMG test can be normal in those with mild myopathies

A

true

128
Q

What is meningitis?

A

inflammation of the meninges of the CNS

typically caused by infection

129
Q

diagnosis

  • fever
  • HA
  • stiff neck
  • irritability
  • mental confusion
  • light sensitivity
  • increased HR and RR
  • sleepiness
  • sluggishness
A

meningitis

130
Q

What special test in used in diagnosis of meningitis?

A

kerning’s sign

along with other dural stretches

131
Q

What medications are used for meningitis?

A
  • corticosteroids
  • anticonvulsants
  • antiviral medication
132
Q

What is primary encephalitis caused by?

A

virus that infects the brain

Examples:
- can be mosquito-borne
- can be tick-borne
- rabies virus

133
Q

What causes secondary encephalitis (post-infection encephalitis)?

A

faulty immune system reaction resulting from an infection in another area of the body

  • immune system attacks the brain
134
Q

What are the symptoms of mild encephalitis?

A

No symptoms
OR
flu-like symptoms

135
Q

(true/false) severe cases of encephalitis are not deadly

A

false

s/s include:
- confusion
- agitation
- hallucinations
- Sz
- muscle weakness
- paralysis
- loss of sensation
- LOC

136
Q

What is the treatment for mild encephalitis?

A
  • bedrest
  • fluids
  • anti-inflammatory drugs
  • antiviral medications
137
Q

What is transverse myelitis?

A

Inflammation of a section of the spinal cord
- myelin is damaged with interruption of signals that the spinal cord sends to the body

138
Q

What causes transverse myelitis?

A
  • infection: bacterial, viral, fungal
  • immune system disorder
  • autoimmune inflammatory disorders
  • myelin disorders
139
Q

How long does it take for transverse myelitis to develop?

A

hours to weeks

gradual

140
Q

diagnosis

  • gradual progression
  • affects both sides of body below level of affected spinal lesion (although can affect only one side)
  • pain (sharp, shooting along level of lesion)
  • abnormal sensation
  • weakness or paralysis
  • stiffness/tightness/painful muscle spasms
  • fatigue
  • B/B dysfunction
  • sexual dysfunction
A

transverse myelitis

141
Q

When does recovery occur for transverse myelitis?

A

Most recovery occurs within first 3 months and can continue up to 2 years

1/3 of patients have permanent disability

relapsing or recurrent transverse myelitis can occur

142
Q

Relapsing or recurrent transverse myelitis can occur when what diagnosis is found to be the cause?

A

MS

143
Q

Diagnosis

Rare and polio-like condition that affects the motor neurons in the gray matter of the spinal cord causing muscles and reflexes to become weak

A

acute flaccid myelitis (AFM)

144
Q

What population commonly develops acute flaccid myelitis (AFM)?

A

children

145
Q

What is the etiology of AFM?

A

unknown

146
Q

Most patients who develop AFM have a prior history of what?

A

respiratory illness or fever

147
Q

diagnosis

  • sudden onset of arm or leg weakness
  • loss of muscle tone
  • hyporeflexia
  • difficulty moving eyes/eyelids
  • facial weakness/drooping
  • dysphagia
  • pain in neck, back, or limbs
  • impaired sensation
  • b/b dysfunction
  • respiratory failure requiring vent support (severe cases)
A

Acute flaccid myelitis

148
Q

What can be an early symptom of acute flaccid myelitis?

A

pain in the neck, back, or limbs

149
Q

(true/false) Those who experience acute flaccid myelitis have full recovery.

A

false

most regain some strength over time but do not recover to full functioning

150
Q

What are the 2 major criteria to suspect myalgic enephalomyelitis/chronic fatigue syndrome?

A
  1. persistent or relapsing fatigue and reduced physical activity for >6 months
  2. 4/8 of symptoms are experienced
151
Q

What are the symptoms of myalgic encephalomyelitis/chronic fatigue syndrome?

A
  • severe/prolonged fatigue
  • post exertional malaise (PEM)
  • muscle pain (myalgia)
  • cognitive impairment
  • difficulty sleeping
  • sore throat
  • HA
  • dizziness
  • deconditioning, anxiety and depression
  • multi-joint pain (anthralgias)
152
Q

What causes AIDS?

A

acquired and severe depression of cell-mediated immunity

  • wide-ranging symptoms
  • 1/3 of patients exhibit PNS or CNS symptoms
153
Q

What are the symptoms of AIDS dementia complex?

A
  • confusion
  • memory loss
  • disorientation
154
Q

What are some s/s of AIDS?

A
  • AIDS dementia complex (ADC)
  • motor deficits
  • peripheral neuropathy
155
Q

Describe the Gate Control Theory.

A

Sensation of spinal cord level is contolled by a balance between large fibers (A- alpha and beta) and small fibers (A delta, C)

Possible initiation of counterirritant theory

156
Q

Describe the counterirritant theory.

A

Temporal summation of large myelinated fibers may block activity of small fibers and pain transmission

157
Q

Describe desending analgesic systems.

A

Endogenous opiates are produced in the CNS and can depress pain transmission at various sites via presynaptic inhibition

158
Q

(true/false) Areas of the cortex and limbic system function to upregulate or downregulate the descending pain modulation systems

A

true

159
Q

Describe nociceptive pain.

A

response to immediate noxious stimuli

inflammatory pain occurs after tissue damage and increases sensitivity

Ex: ankle sprain

160
Q

Describe nociplastic pain.

A

persistent pain that arises from altered nociception, despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system causing the pain.

dysfunction of central pain processing (central sensitization)

  • diffuse pain and persists beyond normal tissue healing
161
Q

Definition

Pain due to a stimulus that does not actually provoke pain

A

allodynia

162
Q

definition

increased pain sensitivity that occurs in directly in the area of damaged or inflammed tissue

A

primary hyperalgesia

Secondary hyperalgesia: pain sensitivity that occurs in surrounding undamaged tissues (ex: phantom limb pain)

163
Q

When does CRPS often develop?

A

After disuse or trauma

164
Q

What is another name for CRPS type I?

A

reflex sympathetic dystrophy

165
Q

What is observed with CRPS I?

A

intense pain throughout the limb but does not involve specific damage to the PNS

166
Q

What is observed with CRPS II?

A

specific damage to the PNS that results in over motor and sensory neuropathic s/s

167
Q

What is another name for CRPS II?

A

causalgia

168
Q

What type of CRPS is most common?

A

Type I

90% of cases

169
Q

diagnosis

  • intense and diffuse pain
  • continuous burning and throbbing pain
  • hyperalgesia and allodynia
  • decreased movement of affected area
  • cold sensitivity
  • edema in painful area
  • change in skin temperature, color, and texture
  • hyperhidrosis
  • change in hair and nail growth
  • atrophy

risk of osteoporosis

A

CRPS

170
Q

What is fibromyalgia syndrome (FMS)?

A

Chronic condition with widespread pain and fatigue (> 3 months)

171
Q

What population is commonly diagnosed with fibromyalgia?

A

females (80-90%)

–> tends to run in families

172
Q

When do symptoms of fibromyalgia begin?

A

after physical trauma, surgery, infection, or significant psychological stress

Those with the following are more likely to develop fibromyalgia:
- RA
- lupus
- ankylosis spondylitis

173
Q

What are the s/s of fibromyalgia syndrome (FMS)?

A
  • widespread pain (>3 months)
  • persistent fatigue
  • trigger points
  • sleep disturbance
  • cognitive changes
  • sensory changes (atypical pattern)
  • anxiety and depression

Stress can make symptoms worse

174
Q

What medications can be used for management of fibromyalgia?

A
  • analgesics
  • antiseizure drugs
  • antidepressants
175
Q

What are the two criteria for diagnosis of fibromyalgia?

A
  1. widespread pain for > 3 months
  2. positive tender point exam
176
Q

What is the D1F pattern for UE proprioceptive neuromuscular facilitation (PNF)?

A

FLX, ADD, ER

“close hand, turn inward, and pull arm across body”

177
Q

What is the D1E pattern for UE proprioceptive neuromuscular facilitation (PNF)?

A

EXT, ABD, IR
Pronation
hand EXT

“open hand, turn, and push arm out”

178
Q

What is the D2F pattern for UE proprioceptive neuromuscular facilitation (PNF)?

A

FLX, ABD, ER

“open hand, turn, and lift arm up and out”

179
Q

What is the D2E pattern for UE proprioceptive neuromuscular facilitation (PNF)?

A

EXT, ADD, IR
Pronation
Wrist/finger FLX

“close hand, turn, pull arm down and across body”

180
Q

What is the D1F pattern for LE proprioceptive neuromuscular facilitation (PNF)?

A

FLX, ADD, ER

181
Q

What is the D1E pattern for LE proprioceptive neuromuscular facilitation (PNF)?

A

EXT, ABD, IR

182
Q

What is the D2F pattern for LE proprioceptive neuromuscular facilitation (PNF)?

A

FLX, ABD, IR

183
Q

What is the D2E pattern for LE proprioceptive neuromuscular facilitation (PNF)?

A

EXT, ADD, ER

184
Q

What techniques can be used for sensory stimulation in those wtih reduced sensory response?

A
  1. spatial summation (multiple techniques)
  2. temporal summation (repeated application of the same technique)
185
Q

When does substitution occur?

A

When functions are assumed, replaced, or substituted by different areas of the brain using different effectors or body segments

Indication: to offset or adapt to residual impairments and disabilities

186
Q

Pain type

  • Dull ache/pain
  • LBP increases with bending/lifting around 30 minutes
  • relieved within few minutes of walking
A

nociceptive pain

187
Q

Pain type

  • dull pain/ache
  • shooting/sharp/tingling pain
  • increased pain with bending
A

neuropathic pain

188
Q

pain type

dull ache/pain is constant

A

nociplastic pain

189
Q

Out of the following diagnoses, which have CN involvement?

  1. ALS
  2. polyneuropathy
  3. GBS
  4. myasthenia gravis
A

ALS, GBS, myasthenia gravis

190
Q

Severe cases of myasthenia gravis will show what gait deviation?

A

trendelenburg

191
Q

What gait deviations can be observed in those with ALS?

A
  • asymmetric foot slap/drop
  • equinus gait

NPTE (20 decks)

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