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Neurological Diseases > MN Disease and MS > Flashcards

MN Disease and MS Flashcards

1
Q

MND

A
  • Kills within 2 yrs
  • Cause unknown and no cure
  • Sensation is preserved
  • Few groups of MNs spared: sphincter control and extraocular muscles
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2
Q

MND: treatment

A
  • Only current licensed treatment is riluzole
  • NMDA antagonist (glutamate)
  • Extends life by only 3 months
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3
Q

MND: Symptoms

A
  • Characterised by upper and/or lower motoneuronal loss
  • (-) muscle weakness, cramps, flaccid paralysis
  • (+) hyperreflexia, spastic paralysis
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4
Q

MND: Diagnosis

A
  • Possible/probably MND is diagnosed
  • Confirmation only viable post-mortem
  • Rule of other diseases
  • Motoneuronal degeneration determined by: clinical tests and electrophysiological studies
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5
Q

Types of MND

A
  • 95% is sporadic (unknown cause)

- 5% is genetic/familial

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6
Q

Sporadic (Typical) MND

A
  • Middle-late onset
  • Slight preference for males to fremales
  • UMN +/- LMN loss
  • Muscle weakness, cramps, wasting, paralysis
  • Death ~2yrs due to respiratory-related issues
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7
Q

Genetic Example: MND

A

Spinal Muscular Atrophy

  • Progressive loss of LMNs
  • Types: infantile and juvenile
  • Characterised by LMN symptoms (weakness, wasting, loss of reflexes and fasciculations)
  • Recessive mutation in survival motor neuron gene (SM1)
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8
Q

Hypothesis on the causes on MND

A
  1. genetic
  2. excititoxicity
  3. oxidative stress
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9
Q

MND: Excitotoxicity

A
  • Loss of glial glutamate transporters
  • Excessive glutamate
    -> act on NMDA receptors
    BUT:
  • only some reports of decreased glutamate transporters and increased glutamate in CSF of MND patients
  • Most work done invitro
  • NMDA antagonist (riluzole) only extends life by 90 days
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10
Q

MND: Oxidative stress

A
  • SOD-1 scavenges free-radicals
    -> mutation in SOD-1, increased free-radicals
    BUT:
  • SOD-1 mutations kill other cells too -> not specific to motoneuronal death as seen in MND
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11
Q

Other Hypotheses

A
  • Smoking
  • Immune disorder
  • Mitochondrial abnormalities
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12
Q

MND research at Adelaide Uni

A
  • Young MNs don’t equal old MNs
  • > difference in target-dependency
  • Inflammaging and glial environment
  • > old MNs in an inflamed environment unlike young MNs
  • > could glia of OLD injured cells be diff?
  • Care should be taken when extrapolating from young and genetic models of research to clinical settings of old and non-genetic patients
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13
Q

MS

A
  • Autoimmune demylinating disorder
  • Elapsing episodes of immunologically mediated demyelination and the lesions are separated in time and space
  • Diagnosis usually 20-40yrs
  • 1M:2F
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14
Q

Types MS

A
  • Relapsing remitting pattern (85%0

- Progressive pattern (15%)

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15
Q

Relapsing Remitting MS

A

RRMS
- Acute episodes of neurological symptoms lasting for days, weeks or months, before completely for partially resolving
- The intervals between attacks can be varied but one average occur every 1-2 yrs
SRRMS
- occur in ppl with RRMS
- symptoms worsen over time, with or without the occurrence of relapses and remissions
- 60% of people who start with RRMS, develop secondary RRMS after 15 yrs

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16
Q

Progressive MS

A

Primary Progressive MS
- Affects around 10% of people with MS from the onset
- They experience no relapses or remissions, with slowly worsening symptoms
Progressive Relapsing MS
- rare form in about 5% of the people from the outset
- characterised by a steadily worsening disease state from the beginning, with acute relapses but no remissions, with or without recovery

17
Q

MS Course

A
  • MS starts as a mainly inflammatory disease with bouts of new disease attacks and remissions
  • Overtime it then develops into a chronic progressive disease
  • The no of relapses in the first and second year tend to correlate with progression of the disease over many years
18
Q

Pathogenesis MS

A
  • T cell mediated inflammatory disease
  • T cells enter the CNS when they are activated in the peripheral circulation
  • When they encounter their antigen in the CNS they get reactivated
  • These reactivated T cells then activate macrophages and microglia
  • These cells either alone or in conjunction with antibodies damage the myelin sheaths and the oligodendrocytes
19
Q

5 Major Health Problems of MS

A
  1. Motor control: muscular spasms and problems with weakness, coordination, balance and functioning of the arms and legs, tendency to drag one foot
  2. Fatigue: including heat sensitivity
  3. Other neurological problems: including vertigo, pins and needles, neuralgia and visual disturbances
  4. Continence problems: including bladder incontinence and constipation
  5. Neuropsychological symptoms: including memory loss, depression and cognitive (thought-related difficulties)
20
Q

Clinical Symptoms MS

A

Early common clinical symptoms:

  • limb weakness
  • blurring of vision
  • incoordination
  • abnormal sensation
  • optic neuritis
21
Q

Diagnosis MS

A

MRI: diagnosis and monitoring - detecting brain lesions (plaques)
CSF: elevated IgG levels, increased IgG synthesis rate and oligoclonal bands
- However, oligoclonal bands and elevated CSF IgG are MS- specific

22
Q

MS Macroscopic

A
  • Plaques in brain and SC
  • Most cases have at least 12 plaques
  • Active lesions: salmon pink and granular
  • Old lesions: demarcated, grey pink and firm, may contain cavitations
  • General correlation between location of lesions and clinical symptoms
  • Can occur anywhere in white matter, at a junction between the cerebral grey and white matter and within the cortical grey matter and deep grey nuclei
23
Q

MS Microscopic

A
  • Active lesions = hypercellular

- Inactive lesions = hypocellular

Neurological Diseases (24 decks)

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