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Caroline Summer 25 2.0 > Lecture 7 - Demyelination Ataxia > Flashcards

Lecture 7 - Demyelination Ataxia Flashcards

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1
Q

What is ADEM (Acute disseminated encephalomyelitis)

A

Acute demyelinating illness that commonly follows an infection or vaccine (75%)

rare

MRI shows BILATERAL symmetric inflammation of the same age (meaning it started at the same time) “fluffy” brain

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2
Q

ADEM is most common in what patients

A

Children

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3
Q

how does ADEM look on an MRI?

A

big fluffy areas of inflammation on both sides

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4
Q

What does “sensory level noted at T4” mean?

A

Sensory issues below T4

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5
Q

Remember if you see SC S&S (B weakness, B&B issues) but reduced reflexes, it could be during the period of ___________ (still be a SC issue)

A

spinal shock

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6
Q

What is Acute Transverse Myelitis?

A

Inflammation of spinal cord causing lesions

Can be first episode of multiple sclerosis (MS), especially if brain MRI is also abnromal

caused by several infections and autoimmune causes

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7
Q

How will MS acute Transverse myelitis appear on an MRI?

A

Small patchy lesions limited to two vertebral segments

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8
Q

How will Acute Transverse myelitis present

A

Back pain, sensory level problems at spine (example: everything under T4 doesnt work), sphincter disturbances (bowel and bladder), paraparesis

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9
Q

How will optic neuritis present?

A

Pain w/ eye movement
pale and inflamed optic disc

vision loss, (acute, monocular) loss of color vision

APD: Consensual pupillary constriction no longer works when shining light into that eye, nor does the right eye constrict when you shine light into the right eye itself

however, the L can consensually constrict the R eye still

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10
Q

Optic neuritis is a common initial symptom of ________________

A

MS

w/ abnormal brain MRI, 56% had MS in 10 years

w/ normal brain MRI, 22% had MS in 10 years

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11
Q

What factors increase the risk for MS?

A

Younger age, female, previous neuro symptoms, multiple MRI lesions

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12
Q

What is the normal treatment for optic neuritis?

A

IV steroids

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13
Q

Optic neuritis on its own is usually ___________

A

monophasic

but not if its related to MS

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14
Q

How can Transverse Myelitis and Optic Neuritis be confirmed to be MS

A

Recurrent or other attacks elsewhere

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15
Q

What is MS (Multiple Sclerosis)

A

Immune mediated disease of CNS

leading cause of non-traumatic disability in young adults

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16
Q

What is a huge indicator of MS

A

2 episodes separated in time

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17
Q

what is dawsons fingers

A

sign of MS on MRI, projections from the lateral ventricle into/alongside the corpus callosum that look like fingers

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18
Q

Where is MS more common?

What is the peak onset age of MS?

What gender is more common?

How does it affect life expectancy?

A

North of equator, greater rates w/ greater distance

20-30

female

reduces by 7-14 years

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19
Q

What are MS risk factors?

A

Note: exact cause of MS is not known

Risk factors: EBV exposure (Epstein-Barr virus)

Low sun exposure

Obesity

Smoking

Genetic risk factor (20% heritability risk increase)

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20
Q

Considering the risk factors for MS, what is a supplement you might give someone with MS?

A

vitamin D

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21
Q

How does the demyelination happen in MS?

A

movement of auto-reactive T cells and demyelinating antibodies from the systemic circulation into the CNS through disruption of blood brain barrier

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22
Q

How does MS usually progress?

A

unpredictable Recurrent attacks with partial recovery, each time you acquire more and more disability

(called RRMS) Relapsing-Remittent Multiple Sclerosis

Note: disability can also trend up in straight line (primary progressive MS)

80-90% of cases

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23
Q

Have progression of MS typically follows relapsing-remitting MS?

A

secondary progressive MS: initial-remitting MS that suddenly begins to decline without periods of remission

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24
Q

After 10 years what MS progression is more common?

A

Secondary Progressive Multiple Sclerosis - declines without periods of remission

Basically it commonly starts as Relapse/remittent MS followed by a steady decline after a while (no more recover)

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25
what significant changes will you see as someone changes from RRMS to SPMS?
cognitive decline, dec brain volume, increase level of disability
26
Primary progressive MS
only 10-20% of cases steady increase in disability without attacks
27
progressive-relapsing MS
<10 % of cases steady decline since onset with super imposed attacks
28
What happens to brain volume due to MS?
Decreases
29
Who has a better prognosis for MS? Who has worse?
**Better**: Women, Caucasians, Monofocal onset, low relapse rate, low disablity at 5 years **Worse**: Men, Non-white populations, Smoking/obesity, high relapse rate (lots of lesions), high disability at 5 years
30
What bodily systems can MS effect
Every system CNS, Visual,Speech, throat, MSK, sensation, bowel, urinary
31
What are the most common motor symptoms (& what tract) with MS? What occurs later usually?
**UMN spastic weakness** 80% (corticobulbar and corticospinal) spastic paraparesis is most common **Later**: ataxia, tremor, incoordination, scanning speech (cerebellar)
32
What are the most common sensory symptoms (what tract) experienced with MS?
75% of patients expeirence sensory issues most common spinothalamic lesions, resulting in **dysesthesias**, **pain** **DCML** involvement is less often
33
What is the sensory sensation that often happens with MS?
Lhermitte's phenomenon electric sensation passing down neck and limbs upon flexion of neck
34
What are common brainstem symptoms of MS?
Nystagmus, diplopia, facial weakness, vertigo, dysphasia and **Trigeminal neuralgia** **internuclear opthalmoplegia** - due to lesion in medial longitudinal fasiculus- inability to adduct ipsilateral eye note: trigeminal nerve effected because oligodendrocytes myelinate the first bit of the nerve in the CNS
35
What are the most common cognitive problems caused by MS?
Cognitive symptoms affect 60% of MS patients usually have "**subcortical dementia**" which affects information processing, visuospatial, memory, and executive function
36
What kind of conditions make fatigue worse for MS patients?
Heat Note: systemic fatigue very common
37
What is the most common diagnostic test for MS?
**MRI of brainstem and spinal cord** CSF fluid tap to look for inflammatory changes "evoked potentials" of visual, auditory, somatosensory
38
What does MS look like on a brain MRI?
**diffuse** inflammation and damage throughout
39
What do MS medications help with? What do they not help with?
Help with inflammation but cannot fix nerves that are already damaged
40
When testing CSF in MS patients, what will you see?
**WBC** elevated **protein** may be high increased **immunoglobulin** production (**OCB**)oligoclonal bands- presence of 2 or more antibody clons (indicates damaged blood brain barrier or immunoglobulin production in the brain)
41
What does the "Mcdonald criteria" for MS consists of
Includes: * **Prior** attacks, * **new** lesion on subsequent MRI, * MRI with active or enhancing lesions and coexisting inactive lesions * CSF **oligoclonal banding** **Evidence of atleast 2 areas damage at different times**
42
The 2017 MS diagnostic criteria consists of what
2 different clincal attacks with 2 different locations at 2 different times 1 attack with MRI showing lesions, enhancing and non-enhancing (meaning one is progressing and one is old) 1 attack with MRI, and repeat MRI with new lesions 1 month later
43
What is the most common treatment of **acute exacerbations** of MS?
Steroids: IV or PO or Plasma exchange
44
What is the difference between old vs new MS meds?
Older medications: -very safe but not as effective , mainly injections Newer medications - more risk of infection but more effective - by mouth (PO) or by monthly shot
45
What is Progressive Multifocal Leukoencephalopathy (PML)
**Severe** demyelinating disease of CNS due to **JC virus** infecting **oligodendrocytes** note: 86% of the population have a asymptomatic infection of JC virus the risk comes due to immunosupression associated with treatment of other autoimmune disorders (people with MS are at risk) usually **fatal within 1 year** if not caught can be treated by stopping immunosuppressants will present like an MS attack at first
46
What are treatment goals associated w/ MS
Prevent longterm disability no consensus on approach to therapy
47
If **both** optic discs are enlarged what is likely wrong? If only **one** is enlarged?
**Both**: Increased intracranial pressure **one**: Optic neuritis
48
_______ is common for patients with MS, especially in the lower extremities
Spasticity
49
MS patients also commonly have sexual dysfunction and spastic and flaccid bladder what is the difference between spastic and flaccid bladder
Flaccid bladder - cant get urine out (leads to retention) - treat with scheduled voiding spastic bladder- overactive, frequency urgency - treat with intermittent catheterization
50
many of the medications for MS cause what as a side effect
makes them sleepy
51
MS MEDS DONT HELP
numbness
52
What medication works at the neuromuscular junction (PNS) and is shown to increase walking speed in patients by an average of 25%
Ampyra (D-Alfampridine)
53
how can you qualify for ampyra and what are two common contraindications?
25 ft walk test > 10 sec seizures or significant kidney disease
54
What is neuromyelitis optica (devic's disease)
presents like transverse myelitis combined with **bilateral** optic neuritis **spinal cord transverse myelitis longitudinally extensive lesion across more than 3 vertebrae levels** more severe than MS Female 90% diagnosed through antibody testing **NMO IgG**
55
What is the treatment for acute NMO (neuromyelitis optica) maintenance?
Acute attacks: Steroids, plasma exchange Maintenance: medications
56
What is myelin oligodendrocyte glycoprotein antibody disease? (MOG)
Basically neuromyelitis optica (NMO) but for children and young adults (but all ages can be impacted) Can be **monophasic** or **relapsing** usually has optic neuritis, transverse myelinitis, and ADEM like CNS lesions Has **good recovery** if treated like NMO
57
MOGAD vs AQP4+NMOSD
Basically these are both MOGAD However, the regular **MOGAD** affects the **lower** spinal cord whereas the **AQP4+** affects the **upper** spinal cord Not correct
58
How does ataxia present?
Disturbance in smooth preformance of voluntary motor acts Error in rate, range, force, and duration
59
Quick overview of cerebellum: Vermis is for: Intermediate zone is for: Lateral hemisphere is for: Flocculonodular lobe is for: Answer choices: Proximal coordination distal coordination balance and vestiboccular reflex motor planning for extremities
Vermis is for: Proximal coordination Intermediate zone is for: distal coordination Lateral hemisphere is for: motor planning for extremities Flocculonodular lobe is for: balance and vestiboccular reflex
60
What are the clinical manifestations of cerebellar dysfunction
limb/trunk/gait ataxia ipsilateral to lesions of the cerebellar hemisphere impaired stance (wide) intention tremor Dysmetria Dysdiadochokinesia Impaired checking response **hypo**tonia speech deficits: mutism, scanning, dysarthria Nystagmus/abnormal saccades
61
What does scanning speech sound like?
uneven time and inflection points no problem w/ word findng or speech production
62
Acute causes of ataxia
Intoxication Vascuar lesions (strokes) Trauma Infections
63
Subacute causes of ataxia (days to weeks)
Brain tumors Alcoholic-nutritional thiamine or vitamin E deficiency Related to cancer (paraneoplastic) Demyelinating cause (MS)
64
Causes of chronic ataxia (years)
Friedreich ataxia (common in kids) Spinocerebellar ataxia (SCA) Other cerebellar degeneration Hereditary metabolic diseases
65
Rostral vermis syndrome is usually in what population? What are the features?
Chronic alcoholics features: -wide base stance/gait ataxia gait Fine in supine infrequent nystagmus/hypotonia,dysarthria
66
Caudal vermis syndrome is usually present in what population? What are the features?
Typically in children w/ medulloblastoma Features: axial dysequilibrium and staggering gait little to no limb ataxia sometimes spontaneous nystagmus and rotated postures of head
67
cerbellar hemispheric syndrome is usually present in who? What are the features?
People w/ infarcts, tumors, abscess Features: incoordination of ipsilateral movements, particularly **fine motor control**
68
What are the causes of pancerebellar syndrome? What are the features?
Causes: infection, hypoglycemia, hyperthermia, paraneoplastic, toxic-metabolic, hereditary features: **Bilateral cerebellar signs** affecting limbs trunk and cranial musculature
69
What is the clincial presentation of friedreich ataxia?
Begins in childhood or young adulthood loss of ambulation after 10-15 years areflexia foot deformities scoliosis cardiomyopahty glucose intolerance life expectancy: 40 usually presents w/ "proprioceptive gait w/ foot slap to increase sensation"
70
Why is it important to identify friedreich ataxia early? is friedreich ataxia autosomal dominant or resessive? what chromosome is affected?
New medication can slow progression by 50% recessive chromosome 9
71
How does ADEM usually progress
usually monophasic, but can reoccur

Caroline Summer 25 2.0 (32 decks)

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