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Unit 14 > SC disease pathology > Flashcards

SC disease pathology Flashcards

1
Q

Name the six categories of SC diseases

A 
Degenerative
Traumatic
Metabolic/toxic
Infectious/inflammatory
Tumor
Vascular
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2
Q

What is Amyotrophic lateral sclerosis? What category of disease does it fit in?

A

ALS

DEGENERATIVE

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3
Q

What category does syringomyelia fit in?

A

Traumatic

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4
Q

What category does disc herniation fit in?

A

traumatic

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5
Q

What category does Friedreich’s ataxia fit in?

A

Degenerative

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6
Q

Subacute combined system degeneration fits in what category?

A

Metabolic/toxic

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7
Q

What category does Cervical spondylosis fit in?

A

Degenerative

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8
Q

What category does Myelopathy an radiculopathy fit in?

A

Degenerative

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9
Q

What category does Caisson disease fit in?

A

Metabolic/toxic

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10
Q

What category does radiation myelopathy fit in?

A

Degenerative

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11
Q

What category does extrameduallary and intramedullary fit into

A

SC tumors

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12
Q

What category does spinal hemorrhage fit into?

A

Vascular

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13
Q

What category does

Tabes dorsalis fit into

A

infectious/inflammatory

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14
Q

Meningitis and encephalitis fits into what category

A

infectious/inflammatory

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15
Q

GB syndome fits into what category

A

infectious/inflammatory

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16
Q

Transverse myelitis fits into what category

A

infectious/infalmmatory

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17
Q

Poliomyelitis fits into what category

A

infectious/inflammatory

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18
Q

Myopathy definition

A

issue with muscle

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19
Q

Myelopathy

A

issue with SC

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20
Q

Myelinopathy

A

issue with myelin

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21
Q

Fibrillation vs. fasiculation

A

Fibrillation: small contraction in single muscle fiber; diagnostic you cannot see it

Fasiculation: brief observable muscle twitch, you can see these they’re generally due to nerve irritability, seen in ALS

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22
Q

ALS is progressive degeneration of what

Disease of what?

A

motor neurons!

specifially the chronic, progressive wasting and atrophy of anterior horn cells

Disease of the nerve cell bodies

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23
Q

In ALS UMN or LMN signs?

SC, brainstem, motor cortex?

A

SC and brainstem (site of CN): LMN

Cortex: UMN

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24
Q

What accounts for the spasticity you see in ALS?

A

UMN of cortex

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25
Q

LMN signs

A

hypotonicity, hyporeflexia, atrophy of muscle cells. also happens to the CN due to brainstem involvement so paralysis of face, swallowing issues, vision etc.

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26
Q

UMN signs

A

hypertonicity/spasticity, hyperreflexia

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27
Q

picture of a person at risk for ALS

A

male (1.5 to 1 ratio to females)

mid 50’s

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28
Q

Rizuzle/rilutek

extends life for how long?

A

stops glutamate cytotoxicity at the motor neurons

extends life for ~6months

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29
Q

Half of ALS population live how many years after diagnosis?

A

3 yrs

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30
Q

During primary lateral sclerosis what tract is targeted?

A

CST

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31
Q

During progressive bulbar pasly what tract is targeted?

A

corticobulbar tract

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32
Q

loss of AHC in SC and lower Brainstem results in what?

A

progressive muscular atrophy

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33
Q

Demyelination and gliosis of the CST and CBT lead to what?

A

primary lateral sclerosis and progressive bulbar palsy

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34
Q

What is the most common form of ALS

A

some combination of primary lateral sclerosis and progressive bulbar palsy with progressive muscular atrophy

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35
Q

What two things deteriorate in ALS

A

cell nerve body, muscle itself

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36
Q

What does an ALS spinal cord look like?

A

it looks huge but thats because there are fewer nerves running along the side

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37
Q

Where is very noticeable atrophy in individuals with ALS early on?

A

hands

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38
Q

ALS is a disease of the ______ where are the three places it happens?

A

Nerve cell bodies

1) Betz cells: nerve cell bodies in the cortex which are the beginning of the CST; UMN as they degenerate
2) CN nuclei, they are the AHC of the brainstem; LMN as they degenerate
3) spinal nerve nuclei affecting motor neurons; LMN/flaccid paralysis as they degenerate

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39
Q

What is the deal with the corticobulbar pathway and its influence, how does it differ than what we normally see in the CN nuclei if it is also affected?

A

it runs with the CST but then affects the nerve cell bodies of the CNS above the level of the CNS leading to UMN signs instead of what we’re used to seeing which is LMN symptoms in the face in ALS

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40
Q

Are fasiculations UMN or LMN?

A

LMN

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41
Q

What two areas are fasiculations common in the body.

Why here?

A

tongue, hands

motor units are so small it doesn’t take much chemical change (from nerve cells degenerating causing chemical changes around the nerve cell creating irritability)

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42
Q

Are Riluzole/Rilutek and Myotrophin used to treat ALS effective?

A

no!

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43
Q

causes of ALS?

A

Unknown but suggestions include

toxicity, deficiency of nerve growth factor, excess of extracellular glutamate, autoimmune process, viral

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44
Q

Diagnostic criteria for ALS

A

UMN the LMN signs in 3 spinal regions OR 2 spinal region + Bulbar signs

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45
Q

Can you do a procedure to diagnose ALS?

A

nope just symptomology

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46
Q

do individuals with ALS have sensory loss?

A

no

No cognitive loss either, autonomic involvement are not a thing either (CV, sphincter)

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47
Q

Oculomotor nerve vs. optic nerve involvement in ALS

A

Oculomotor NOT affected

Optic can be affected

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48
Q

What is the common first signs of ALS generally?

A

clumsy, slurring of words, difficulty swallowing

Something that shows some type of weakness

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49
Q

____% of motor neuron loss by the time weakness is noted?

A

80% there is so much redundency in the system

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50
Q

When do fasciculation’s and cramps tend to be a symptom in patients with ALS?

A

further down the line

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51
Q

Typically distal or proximal loss first with ALS?

A

distal!

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52
Q

is speech involved in ALS

A

yes eventually all motor function is lost including speech

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53
Q

when is ventilation required for individuals with ALS?

A

40-50% VC

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54
Q

When should supplements or feeding tube start. What % of BW loss?

A

10% BW loss

PEG tubes are placed relatively early in the disease process generally

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55
Q

What are the three things Friedrich’s ataxia is a degeneration of?

A

Spinocerebellar tracts (unconscious proprioception), CST and posterior columns (DCML)

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56
Q

What is the most common hereditary ataxia?

How is it passed down?

Age of onset?

A

Friedreich’s Ataxia

Autosomal recessive disorder

Onset 8-15 years

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57
Q

Age of onset for Freidreich’s ataxia

Progression? Lose ability to walk by? WC By?

A

8-15 years

Variable progression
Lose ability to walk ~15 years after onset
WC by 45

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58
Q

What does spinocerebellar carry?

A

proprioception unconsciously

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59
Q

Pes Cavus and Kyphotocolionis are sequelae of what disease?

A

Friedrich’s ataxia

60
Q

Describe pes cavus

What do we need to do for it?

What are the implications?

A

hyperextension of MTP and flexion of the IP joints

Generally they’ll be braced

Generally they cannot ambulate

61
Q

Signs and symptoms of Freidricks ataxia

A

Progressive ataxia
Increasing weakness
Loss of tendon reflexes (DCML gone)
Impaired proprioception (no spinocerebellar)
DM
Scoliosis, ataxia in UE, cardiomyopathy, abnormal occular movements
Affective disorders

62
Q

What disease generally has affective disorders associated with it?

A

Fredrick’s ataxia

63
Q

Degenerative disc disease with bone spurs is called what

A

cervical spondylosis

64
Q

what is the most common cause of myelopathy?

A

Cervical spondylosis

65
Q

Gradual onset of neck pain, radicular arm pain, LMN signs and UMN signs in legs stems from what?

A

cervical spondylosis

66
Q

What two tx are common for cervical spondylosis

A

prophylactic as well as possible decompression laminectomy (trying to expand the space)

67
Q

if the disc impinges on the SC what will you see in the LE

A

UMN signs all down the legs

68
Q

what procedure is done on the spine to primarily remove pressure on the SC?

A

posterior laminectomy

69
Q

Is radiation myelopathy progressive or transient?

A

Both!

Transient: 3-6 months after radiation, normally sensory&raquo_space; motor problem and sensation generally resolves (Lhermite’s sign; pain with flexion of neck)

Progressive: 9-15 month post radiation. Has more of a weakness component than transient. Progression stops but does not reverse

70
Q

Cysts in the SC around the central canal (typically in the cervical area) is called what?

A

Syringomyelia (traumatic)

71
Q

What two things are syringomyelia caused by?

TEST QUESTION

A

Congenital: hydrocephalus commonly via Chiari Malmformation

Trauma

72
Q

Explain traumatic syringomyelia

A

central canal runs through SC this is carrying CSF. When the central canal enlarges it impinges on the SC and tissue is compressed affecting sensory and motor components

73
Q

What is a syrinx formation?

A

enlarged central canal (where CSF flows)

74
Q

Do syrinx formations happen in traumatic or congenital syringomyelia?

A

both!

75
Q

Chiari Malformation is associated with what disease

A

syringomyelia

76
Q

Explain chiari malformation

A

posterior skull is deformed, CB sinks posterior and presses on the skull. This stops CSF from flowing down SC as it should –> hydrocephalus and enlargement of ventricles –> syrinx in the SC –> pressure eventually kills neural tissue in brain and SC

77
Q

Posterior decompression/decompression laminectomy is done for what?

A

relieving the pressure caused by a chiari malformation

its the bone flap taken off the posterior aspect of the skull

78
Q

Where does the ventriculoperitoneal shunt travel?

Tx for what?

A

ventricles –> neck –> abdomen

Syringomyelia

79
Q

Where in the body does syringomyelia generally stem from?

A

C-spine

80
Q

Complication of trauma, meningitis, hemorrhage, tumor or arachnoiditis can all be a cause of what even months or years after the initial injury?

A

acquired/traumatic Syringomyelia

81
Q

most common syringomyelia sx? Why?

A

pain in the area of the injury as well as pain and temperature loss. Touch generally in tact.

Its a central issue, think about central cord, ALS crosses in the middle. DCML would be in tact

82
Q

If you were to see CST issues due to syringomyelia, how and where would you see it?

A

weakness and wasting in hands and scapula

83
Q

Two common medical tx for syringomyelia?

A

1) posterior/decompression laminectomy

2) shunt

84
Q

What areas of the SC are lost in subacute combined degeneration?

A

Posterior columns: DCML

Lateral columns: CST and spinocerebellum

85
Q

Etiology of subacute combined degeneration?

A

inability to absorb vitamin B12 = pernicious anemia

86
Q

Loss of what sensations?

A

light touch, vibration, proprioception, weakness, tingling in hands and feet, stiff limbs, irritable, drowsy, confused

87
Q

tx for subacute combined degeneration?

A

replacement therapy, replace B12

88
Q

Common population you see Subacute combined degeneration in?

A

elderly bc they don’t absorb B12

89
Q

Etiology of Caisson disease

A

accumulated nitrogen that cannot be exhaled forming bubbles in blood and tissues

90
Q

2 pathologies of Caisson disease and is it central or peripheral?

A

AGE: central damage

DCS: peripheral damage

91
Q

Explain AGE as part of Caisson disease

A

occlusion of epidural venous sinus by nitrogen bubbles leading to impaired venous return and patchy hemorrhagic infarcts in SC

92
Q

Explain sx of DCS as part of Caisson disease

severe reaction?

recovery?

A

joint pain, skin rash, edema

Severe reaction: 10-30 min after surfacing paresthesias and paralysis LE>UE

Recovery: over weeks in 60-80% especiallyi f they’re in a compression chamber

93
Q

Air embolisms cause what?

A

infarct in the SC or brain

94
Q

Inflammation of the leptomeninges (two most internal layers; arachnoid and pia) and underlying subarachnoid cerebrospinal fluid is what?

A

meningitis

95
Q

What are the two most internal layers of the leptomeninges?

What disease is this in relation to?

A

arachnoid and pia matter

Meningitis

96
Q

Bacteria colonize in the nasopharynx or enteroviruses are common causes for what disease?

A

meningitis

97
Q

Brain inflammation caused by a virus is what?

A

encephalitis

98
Q

Meningitis and encephalitis lead to ____ which leads to _____

A

inflammation –> pressure which can cause damage quickly

99
Q

Whats the deal with CSF and meningitis?

A

Just like syrincomyelia CSF may not be able to exit causing back pressure down the line.

100
Q

What is Tabes Dorsalis a degeneration of?

Specifically in what are?

A

dorsal columns/dorsal spinal roots = loss of DCML

Specifically in the lumbosacral area

101
Q

What disease is associated with sharp leg pain, ataxia, urinary incontinence, absent knee and ankle reflexes?

A

Tabes dorsalis (inflammatory/disease issue)

Side note: develops 10-20 years after syphillis

102
Q

What does poliomyelitis attack?

A

AHC and sometimes motor nuclei of the brainstem

103
Q

Loss of AHC in poliomyelitis leads to UMN or LMN?

A

LMN asymmetrical weakness with prominent atrophy overtime

104
Q

What disease do you get systemic illness prior to neurologic symptoms?

A

poliomyelitis

105
Q

What happens to muscle fiber and motor unit ration in poliomyelitis

A

more muscle fibers per motor unit

surviving AHC’s sprout to re-innervate orphaned fibers creating a ton of muscle fibers per motor units

Unaffected muscle fibers hypertophy due to overload

106
Q

MMT grading came about due to what disease?

A

polio

107
Q

Normal MMT grade could still have how much %AHC loss?

A

60%

There is such a high degree of redundancy in the system

108
Q

Pes cavus and scoliosis are common in what two diagnosis?

A

Friedrich’s ataxia and Polio

109
Q

Whats the big picutre in post polio for PT

A

these people have worked hard all their life with these overworked motor units! We don’t want them overdoing it! You need a definite stop so they do not overexercise.

110
Q

How long after the original disease does post polio come about?

A

30-40 years.

111
Q

What disease usually occurs at levels T4-T6 or T10-12?

A

transverse myelitis

112
Q

What disease? non specific sensory loss, symmetrical severe muscle weakness, loss of reflexes and bowel and bladder control (think of th elevels it affects)

A

Transverse myelitis

113
Q

Prognosis for transverse myelitis (inflammatory process following another infection)

A

self limiting w/good recovery

114
Q

Is GB acute or long lasting?

A

acute!!

115
Q

what kind of paralysis do you have with GB syndrome?

what two parts of the nerve are affected?

A

flaccid motor paralysis

entire length of the nerve: Nerve root and peripheral nerve

116
Q

What is the assumed etiology of GB sndrome?

A

autoimmune overreaction to a virus,50% of people have recent viral infections

117
Q

weakness in legs spreading to the arms (ascending paralysis) in a symmetrical pattern

Asymmetric sciatic pain

is indicative of what disease?

A

GBS

118
Q

Male vs. female, which is more common in GBS?

A

same

119
Q

Polyradiculoneeuropathy associated with what disorder?

A

GB syndrome, causes flaccid motor paralysis

120
Q

Do people with GB syndrome recover?

A

yes they do but they often have residual symptoms

121
Q

The older you are, is the prognosis better or worse for GB?

A

worse!

122
Q

Where does weakness normally start for GBS?

A

legs spreading to arms symmetrically

123
Q

Sensory paresthesia or numbness in what pattern in GBS?

A

stocking glove distribution

124
Q

Maximum weakness in GBS within how many weeks?

A

one week

125
Q

Muscle weakness may include muscles of _____ in GBS leading to ____ in ____-% of people

A

muscles of respiration leading to ventilation in 20-30% of patients

126
Q

50% of pts with GBS have what two things?

A

autonomic signs (affecting cardiac rhythm) CN involvement

127
Q

What sx is common throughout GBS entire recovery process

A

pain: deep and aching in large muscle groups

128
Q

When does the recovery process of GBS begin?

A

within 2-3 weeks OF THE ACUTE PROCESS meaning 2-3 weeks after their sx have stopped progressing

129
Q

True or false: PT can help speed up the GBS recovery process?

A

False! you can’t speed it up but you can stop shortening of tissues decrease pain etc.

130
Q

Plasmapheresis and Intravenous immunoglobulin (IVIG) used in what disease

A

GBS

Plasmapheriesis: Shown earlier recovery of walking if given within the first week (it takes mulitiple days)

IVIG: more of a steroid

131
Q

Do PT’s have a role in acute phase of GBS?

A

no! ROM perhaps

132
Q

Would someone with GBS show hyper or hypo reflexive deep tendon reflexes

A

hypo: diminished or absent

133
Q

several days to two weeks but no worsening of symptoms is what phase of GBS?

A

plateau phase

Generally you see asymmetric sciatic pain here

134
Q

Time frame of recovery for GBS depends on what generally/

A

the extent of the inital paralysis

it may take 1-2 years to reach best state and some may have perimant residual weakness as well as fatigue being a continual problem

135
Q

Poorer prognosis in GBS for what three things?

A
  • rapidly progressing sx
  • need for ventilatory support
  • over the age of 70
136
Q

Very general outcomes for GBS

A

people get better, half walk unassisted within three months, majority don’t have neurologic sequelae but are fatigued, many test with some weakness and fatigue but pts feel they are getting stronger due to compensations etc.

137
Q

CIPD is what

A

chronic inflammatory demyelinating polyneuropathy

A type of GBS

138
Q

What is the pattern of CIPD

_____ rather than _____

symmetrical or asymmetrical?

Lasting disability/

A

its a type of GBS following a pattern or RELAPSE rather than PROGRESSIVE

Asymmetrical

Yes some have lasting disability

139
Q

medical tx for CIPD

A

corticosteroids, and plasmapheresis over months instead of days like normal GBS

140
Q

Where is an intrameduallry tumor

A

on the SC itself

141
Q

Where is an extramedullary intradural tumor

A

inside the dura but not adhered to the SC itself

142
Q

Where is an extramedullary, extradural tumor?

A

totally outside of the dura, not attached to the SC at all, THIS IS THE MOST SERIOUS

143
Q

Where is extradural tumor generally coming from?

A

metastatic

144
Q

Sxs from bony instability can be from which of the three kinds of tumors?

A

extradural

Can have a decompression or radiation to reduce size

145
Q

Intramedullary tumor generally medically tx how?

A

surgery, they are less aggressive and benign

146
Q

Most likely artery to have an infarct?

A

anterior spinal artery

147
Q

What does the anterior artery serve?

A

anterior 2/3 of the spinal cord

ALS, CST impacted. DCML in tact. UMN below the level of the lesion.

Unit 14 (6 decks)

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