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syposium control and movement > MS > Flashcards

MS Flashcards

1
Q

What are symptoms of Optic neuritis??

A

Pain in the right eye with blurred vision

Can lose complete vision in one of the eyes

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2
Q

What is optic neuritis?

A

Inflammation of the optic nerve

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3
Q

On examination what would identify on a patient with optic neuritis?

A

Reduced colour vision (Ishihara chart)

Reduced pupillary light responses (RAPD)

Hole in visual field (scotoma)

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4
Q

What is the prognosis of optic neuritis?

A

Good prognosis: 95% return to visual acuity of 6/12 or greater within 12 months

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5
Q

What is the treatment of optic neuritis?

A

High dose steroids speed up rate of recovery but have no effect on final acuity

Prednisolone is used

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6
Q

What percentage of people with optic neuritis will develop Ms?

A

50% go on to develop MS within 10 years

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7
Q

What is the role of MRI scan in optic neuritis?

A

Role of MRI tell you what type of optic neuritis it is and give some sort of insight whether or not it will lead to MS

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8
Q

What is transverse myelitis?

A

Inflammation inside the spinal chord

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9
Q

What is the prognosis of transverse myelitis?

A

Often mild with good prognosis

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10
Q

What is the symptoms of transverse myelitis?

A

Can get complains of tingly numbness starting in both feet and gradually ascending to level around chest

Lhermittes phenomenon–> is an electrical sensation that runs down the back and into the limbs which occurs when bending the head forward

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11
Q

What can be a complication of transverse myelitis?

A

May affect the bladder

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12
Q

What type of sensation is lost in transverse myelitis?

A

Pure sensory

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13
Q

What is the percentage chance of developing Ms if you have transverse myelitis?

A

50% go on to develop Multiple Sclerosis

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14
Q

How do you diagnose Ms?

A

Having 2 different diseases such as optic neuritis and transverse myelitis at different times.

They cannot happen at the same time and the same disease cannot occur twice for it to be diagnosed as Ms.

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15
Q

What is the treatment for Transverse myelitis?

A

Treated with intravenous methylprednisolone 1g daily for 3 days

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16
Q

What is Ms?

A

MS is a disease of the central nervous system (CNS)

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17
Q

What is the mechanism in causing MS?

A

An inflammatory reaction in the CNS causes loss of myelin and slowing of nerve conduction

Areas of demyelination

Loss of axons

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18
Q

How common is MS in the UK?

A

It is the most common cause of neurological disability in young adults in the uk

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19
Q

Is MS more common in males or ladies?

A

2F/1M

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20
Q

What is the age of onset of MS and ethnicitiy suscepitbility?

A

Age of onest is 30-40yrs

Northern Europeans, US caucasians and Canadians are at high risk while African blacks and orientals are at low risk.

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21
Q

What is the epidemiology and latitude effect on MS?

A

Prevelance strongle dependent on latitude

Environmental factors such as habitat, diet and infections also have a part to play

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22
Q

What is action of lymphocytes in MS?

A

The CD4 T lymphocytes release a large amount of cytokines that cuase activation of immune system which leads to a problem in myelnation

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23
Q

What occurs in terms of myelination during MS?

A

There is demyelination as the immune system damages the oligodendryocytes that are invovled in the process of myelination.

There is also damage to the meylination and therefore diffuclt for the process of signaling

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24
Q

What is the main treatment for MS?

A

Interferon beta 1-b

Interferon beta-1a)

Glatiramer acetate

Alemtuzumab

Natalizumab (Tysabri

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25
Q

What is the aim of treatments for MS?

A

Not a cure but try to prevent a relapse as every time you have a relapse the disability increases

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26
Q

What is the effectivness of inferferon beta drug work on preventing MS?

A

Reduces the number of relapses by a third

Effective early in the disease course

No evidence on long-term effect on disability

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27
Q

What is the site of infection, frequency and side effects of Betaferon 1b?

A

SC

Alternative days

Flu- like symtpoms

Injection sight reactions

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28
Q

What is the site of infection, frequency and side effects of Avonex 1a?

A

IM

Once week

FLS

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29
Q

What is the site of infection, frequency and side effects of Rebif 1a?

A

SC

3 times/week

ISR

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30
Q

What is the site of infection, frequency and side effects of Glatiramer acetate?

A

SC

daily

Acute reaction

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31
Q

What is (Natalizumab) Tysabri ?

A

TYSABRI, the first humanized monoclonal antibody approved for the treatment of MS

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32
Q

How do leukocytes get through the BBB in MS?

A

The interaction of the adhesion molecules, alpha4-integrin on the activated leukocyte with VCAM-1 on the blood-brain barrier are the key components involved in immune cell adhesion and migration

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33
Q

How does Natalizumab TYSABRI work?

A

Natalizumab is the first in a class of SAM inhibitors that prevent the migration of immune cells across the blood-brain barrier by selectively attaching to alpha 4-integrin

It inhibits adhesion molecules on the surface of immune cells.

Research suggests TYSABRI works by preventing immune cells from migrating from the bloodstream into the brain

Where they can cause inflammation and potentially damage nerve fibers and their insulation.

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34
Q

What is the main therapeutic monoclonal antibody treatment?

A

Alemtuzumab

35
Q

What is the possible complications of Tysabri?

A

If a person has John Cunningham virus and takes Tysabri then there is a chance they can develop Progressive Multifocal Leukoencephalopathy (PML),

36
Q

What is PML?

A

Rare and fatal viral disease causing progressive damage or inflammation of the white matter of the brain at multiple locations

37
Q

What are the new oral treatment for Ms?

A

Fingolimod
Teriflunomide
Dimethyl Fumarate

38
Q

What is fingolimod?

A

Sphingosine 1-phosphate (S1P) receptor modulator

39
Q

How does Fingolimod work?

A

Prevent T cell invasion of CNs

By trapping ciruclating lymphocytes in peripheral lymph nodes

40
Q

What is possible side effect of Fingolimod?

A

Lymphopenia which is abnormal low levels of lymphocytes but not a problem

41
Q

When will treatment for Ms by symptomatic?

A

When there is no relapse but progression fo the disease.

42
Q

What are the different types of MS progression?

A

Relapsing remitting MS

Primary progressive MS

Secondary progressive MS

Progressive-relapsing multiple sclerosis

43
Q

What is relapsing remitting MS?

A

In relapsing remitting MS, people have distinct attacks of symptoms which then fade away either partially or completely.

Most common type of MS occurs in 85% of patients

44
Q

What is primary progressive MS?

A

The symptoms progress and get gradually worse over time rather than appearing as sudden attacks.

45
Q

What is secondary progressive Ms?

A

Secondary progressive MS is a sustained build up of disability, independent of any relapses often occurs after relapsing remitting MS.

46
Q

What is Progressive-relapsing multiple sclerosis (PRMS)?

A

Progressive-relapsing multiple sclerosis (PRMS) refers to a pattern of relapses within primary-progressive MS  experience symptoms that worsen over time

47
Q

What percentage of MS patients are confined to a wheelchair within 10 years of diagnosis?

A

15%

48
Q

What does symptomatic treatment involve?

A 
Treating 
Fatigue, mood problems
Pain and sensory problems
Genitosphincteral problems
Tremor and spasticity
49
Q

Whta are the potential targets for neuroprotective therapy in MS?

A

Apoptotic mechanism, excitotoxic and inflammatory mechanisms, energy depletion, demyelination induced, genetically determined and depletion of growth factors.

50
Q

what is the potential use of stem cells in treatment of MS?

A

Stem cell can be used to produce more oligodendrocytes, type 1 and 1 astrocytes and neurons which will help with myelination

51
Q

How do oligodendrocytes cause mylenation?

A

Arms of oligodendrocytes reach out and wrap around axons creating insulation that allows electrical signals to flow
production of the arms of oligodendrocytes and produce more myelin

52
Q

What is the current problems in Ms management?

A

We don`t know if treating the relapsing phase aggressively helps delay or prevent the progressive phase.

Still no effective treatment for progressive multiple sclerosis

There is no way of telling benign patients at the start of their disease

53
Q

What is a spinal cord injury?

A

A spinal cord injury is a disruption to the spinal cord

usually due to trauma

54
Q

What is cauda equina injury?

A

A cauda equina injury is a disruption to the nerve roots that lie with in the spinal column

55
Q

Is it more common for males or females to have a spinal cord injury?

A

males

56
Q

Why is the incidence of spinal cord injury higher or lower in elderly people?

A

It is higher as Over time as you get older you get osteoporosis, osteophytes, less flexibility so fall has greater damage

57
Q

What are the 4 congenital causes of spinal cord injury?

A

Birth trauma
Spinal muscular atrophy
Spina bifida
Congenital spinal anomaly

58
Q

What are the 5 main causes of acquired spinal cord injury?

A 
Degenerative
Vehicle trauma
Bacterial infection
Inflammatory 
Secondary malignant tumour
59
Q

What happens in a Traumatic transection of the thoracic spinal cord?

A

Crush fracture of vertebra

Disruption of spinal cord

60
Q

At what levels is a tetraplegia spinal cord injury?

A

Cervical lesion –> C1 to T1

61
Q

At what level is it a paraplegia spinal cord injury?

A

Thoracic lesion–> T2 to L5

62
Q

What is the AISA impairment scale?

A

A (Complete)
No motor or sensory function is preserved in S5

B (Incomplete)
Sensory but not motor function is preserved below the neurological level to S5

C (Incomplete)
Motor function preserved, and more than half of key muscles below the neurological level have a muscle grade less than 3

D (Incomplete)
Motor function preserved, and at least half of key muscles below the neurological level have a muscle grade of 3 or more

63
Q

Why is grade 3 so important in the AISA impairment scale?

A

Grade 3 is power against gravity so below that you cannot walk

64
Q

What are the descending motor tracts in the spinal pathway?

A

Lateral corticospinal

Anterior corticospinal

65
Q

What are the ascending sensory tracts in spinal pathways?

A

Dorsal columns
Anterolateral spinothalamic
Spinocerebellar

66
Q

What is the prognosis for mobility for the diffrent levels of the AISA impairment scale?

A 
A	(Complete)		1% chance of walking 
B (Incomplete)		35%
C (Incomplete)		75%
D (Incomplete)		100%
E (Normal)		100%
67
Q

What is the adjusted life expectancy at time of injury of a person up to the age of 65yrs?

A

88% of age adjusted life expectancy

68
Q

What is the assoicated injuries of a acute spinal cord injury?

A

Head injury
Chest injuries
Abdominal injuries
Limb injuries

69
Q

How do you manage acute spinal cord injury?

A 
Bed rest/positioning/skull traction
Prevent further damage to spinal cord
Skin care
Bladder and bowel care
Prevention of thromboembolic and GI complications
70
Q

What causes excessive vagal stimulation?

A

Lesions above T6 and spinal shock

Loss of some or all parasympathetic control

71
Q

What does excessive vagal stimulation lead to?

A

Bradycardia

Asystole

72
Q

How is vagal stimulation prevented?

A

Prevent by avoiding vagal stimulation

Atropine prior to intubation, suctioning

73
Q

What causes vagal stimulation?

A

Stimulation can be due to NG tube or some sort of instrumental device

74
Q

What is autonomic dysreflexia?

A

Lesions above T6 in established patients

75
Q

What precipitates after autonmic dysreflexia?

A

Bladder distension,
constipation

Skin, soft tissue, bony injuries

Blood pressure goes up and up

76
Q

How does autonomic dysreflexia present?

A

Presents with headache, hypertension, facial flushing

77
Q

How is autonomic dysreflexia relieved?

A

Relieve cause, antihypertensives ( fast acting to bring BP down), pain relief

78
Q

What are acute complications of spinal cord injury?

A

Urinary tract infections
Urinary tract stones
Progressing to renal failure

Respiratory infection
Progressing to respiratory failure

Pressure sores
Osteomyelitis, amyloid, neoplastic change

79
Q

What is the management of chronic spinal cord injury?

A

Appropriate skin care
Bladder and bowel care
Prevention of thromboembolic complications

Different presentations
e.g. acute abdomen

80
Q

What are the complications of chronic spinal cord injury?

A

Progressive neurological decline
Syringomyelia
Neuronal “drop-out”
Pain and spasticity

Rheumatological complications
Degenerative joint disease
Hetertopic ossification

81
Q

What is Heterotopic ossification?

A

Heterotopic ossification (HO) is the presence of bone in soft tissue where bone normally does not exist

82
Q

What is the future of spinal cord injury?

A

Spinal cord regeneration
Assistive technology
New rehabilitation techniques

83
Q

Why would a person with spinal cord injury have crouched gait and not be able to accelerate his foot?

A

Would firstly have foot drop that would also lead to having crouched gait because of weakness of the quadriceps muscles.

Would also not be able to accelerate their foot forward as it leaves the ground because his calf muscles aren’t able to contract effectively

syposium control and movement (11 decks)

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