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Case

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Case A 32 year old woman comes with complaint of numbness and tingling sensation in her right hand. Her symptoms began several days ago and have progressively ... – PowerPoint PPT presentation

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Title: Case


1
Case
  • A 32 year old woman comes with complaint of
    numbness and tingling sensation in her right
    hand. Her symptoms began several days ago and
    have progressively worsened over the last several
    hours. When asked, she states that 3 years ago
    she had an episode of seeing double that lasted
    for 2 days and resolved on its own. Physical
    examination is significant for hyperreactive
    reflexes bilaterally in her lower extremities.
    Increased spasticity is also noted in her lower
    extremities. What is the Most Likely diagnosis?

2
MULTIPLE SCLEROSIS
3
MULTIPLE SCLEROSIS
  • Multiple sclerosis is an inflammatory disease of
    CNS white matter characterized by relapsing or
    progressive course
  • Multiple sclerosis is a common disease of unknown
    cause in which there are multiple areas of
    Demyelination within brain and the spinal cord.
  • Peak incidence 20-40 years
  • Male Female 12

4
Etiology
  • Multifactorial causation
  • Genetic, environmental (Infectious, dietary,
    climatic), immunologic
  • MS lesions most commonly involve white matter
    areas close to the ventricles of the cerebellum,
    brain stem, basal ganglia, spinal cord and the
    optic nerve.
  • Immune mechanism against CNS myelin sheath is
    suggested due to presence of increased levels of
    activated T-Lymphocytes in the CSF, and increased
    immunoglobulin synthesis within the CNS

5
Pathology
  • Activation of lymphocytes in response to myelin
    proteins (auto antigen).
  • Destruction of the myelin.
  • Initiation of inflammation and infiltration of
    the macrophage and lymphocytes
  • Later on healing by gliosis, loss of neuronal
    function
  • Initially inflammation leads to transient loss of
    function but later permanent deficit occur due to
    disruption of axonal integrity
  • Demyelination may impair nerve conduction that
    lowers the efficiency of CNS function
  • It also causes ectopic impulse generation that
    causes Paresthesia .

6
Nerve
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8
Clinical features
  • Presentation-
  • Weakness, numbness, tingling or unsteadiness of a
    limb.
  • Urinary urgency or retention
  • Blurry vision
  • Double vision
  • Relapsing and remitting MS80 of patients have a
    relapsing and remitting course of neurological
    deficit
  • Characterized by recurrent attacks of neurologic
    dysfunction . The attacks generally evolve over
    days to weeks and may be followed by complete,
    partial or no recovery. Recovery occurs usually
    spontaneously within weeks to several months
  • 2. 20 follow a slowly progressive
  • Secondary progressive MS? The disease has
    relapsing-remitting course at first but evolves
    to be progressive and this phase may begin
    shortly after disease onset or delayed for
    several months or years.
  • Primary progressive MS? Characterized by gradual
    progression of disability from the onset of
    disease
  • 3. And minority have fatal disease causing early
    death
  • Peak age of onset is in the fourth decade
  • Frequent relapse and incomplete recovery indicate
    poor prognosis.
  • Physical signs observed in multiple sclerosis
    depend on the anatomical site of Demyelination

9
Scenario
  • Young patient (Usually lt55years)
  • H/O multiple neurological complaints that cannot
    be explained by presence of one CNS lesion

10
Initial presenting features of Multiple sclerosis
  • Blurring of vision due to optic neuritis
  • Diplopia
  • Weakness in one or more limbs
  • Paresthesia
  • Ataxia
  • Urinary symptoms

11
End stage multiple sclerosis
  • Patient is severely disabled with spastic
    paraparesis, ataxia, optic atrophy, nystagmus,
    pseudobulbar palsy, incontinence of urine,
    dementia
  • Death occurs usually due to bronchopneumonia and
    renal failure.

12
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16
MRI scans (post-contrast) of the same brain slice
at monthly intervals. Bright spots indicate
active lesions.
17
Investigations
  • Clinical picture
  • Identify multiple sites of neurological
    involvement i.e., plaques of Demyelination by
    imaging MRI and Myelography
  • Provide evidence for an inflammatory disorder
    CSF examination(cell count and protein
    electrophoresis)
  • Demonstrate other sites of involvement by Visual
    and other evoked potentials
  • Exclude other conditions CXR, Serum ACE and
    serum B12 antibodies

18
Differential diagnosis
  1. SLE
  2. Stroke
  3. Friedreichs ataxia
  4. CNS sarcoidosis
  5. Bechcets syndrome
  6. Sjogrens syndrome

19
Treatment
  • Acute relapse
  • High-dose intravenous steroids (Methylprednisolone
    1 g daily for 3 days followed by tapering dosage
    of oral Prednisolone for next 4 weeks)
  • Preventing relapses
  • Immunosuppressive agents including Azathioprine
    have a marginal effect in reducing relapses and
    improving long-term outcome
  • Interferon Beta-1A
  • Interferon Beta 1B reduces the number of relapses
  • Glatiramer acetate(Immune modulator)

20
Treatment of complications
  • Spasticity
  • Regular Physiotherapy
  • Baclofen (most effective)
  • Painful Paresthesia
  • Carbamazepine
  • Amitriptyline
  • Ataxia
  • Isoniazid and clonazepam
  • Care of bowel and bladder

21
Treatment
  • MS and fatigue? Amantidine
  • MS with Urinary incontinence? Oxybutanine
  • MS and urinary retention? Bethanicol

22
Prognosis
  • About 15 of those having one attack of
    Demyelination do not suffer any more events
  • Approximately 5 of patients die within 5 years
    of onset
  • After 10 years, about one-third of patients are
    disabled to the point of needing help with walking

23
Cavernous sinus thrombosis
  • Cavernous sinus thrombosis (CST) is the formation
    of a blood clot within the cavernous sinus, a
    cavity at the base of the brain which drains
    deoxygenated blood from the brain back to the
    heart.
  • The cause is usually from
  • a spreading infection in the sinuses, ears, or
    teeth.
  • Staphylococcus aureus and Streptococcus are often
    the associated bacteria.
  • Cavernous sinus thrombosis causes
  • decrease or loss of vision
  • drooping or bulging eyes
  • Headaches
  • paralysis of the cranial nerves which
    courses/runs through the cavernous sinus.
  • This infection is life-threatening and requires
    immediate treatment, which usually includes
    antibiotics and sometimes surgical drainage.

24
Cavernous sinus thrombosis
25
WERNICKE-KORSAKOFF DISEASE
  • Due to a deficiency of thiamine
  • Causes are
  • Malnutrition
  • Alcoholism
  • Malabsorption
  • Protracted vomiting.
  • There is failure of carbohydrate metabolism
    (because thiamin is a co-factor in many enzymes
    of the citric acid cycle) and accumulation of
    glutamate.
  • Clinical triad is that of Ophthalmoplegia,
    ataxia, and global confusion
  • Patients are profoundly disoriented,
  • If the disease is not treated?stupor, coma, and
    death may ensue.

26
  • Approximately half recover incompletely, ataxia
    is very slow to recover or may not recover.
  • Later on Korsakoffs psychosis may occur
    (characterized by loss of recent memory,
    confabulation, impaired temporal sequencing of
    events)
  • Treatment
  • Administer to all chronic alcoholic patients
    especially before giving intravenous glucose for
    suspected hypoglycemia.
  • Intravenous or intramuscular thiamin 50 mg TDS
  • Later on switched over oral therapy 100 mg TDS

27
Qs
  1. Difference between UMNL and LMNL
  2. Causes of spinal cord injury and its C/F
  3. Clinical features and causes of spinal cord
    compression
  4. Management of Spinal cord compression
  5. Short notes on
  6. Cervical Spondylosis
  7. Brown sequard syndrome
  8. Syringomyelia
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