Nutritional Disorders of the Nervous System

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jknell
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195493
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Nutritional Disorders of the Nervous System
Updated:
2013-01-26 14:50:47
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MBB II
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MBB II
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  1. General principles of nutritional disorders of the nervous system
    • -diffuse
    • -subacute
    • -often symmetric
    • -affect selectively vulnerable systems

    • Most common phenotypes:
    • -distal polyneuropathy
    • -ataxia
    • -non-specific cognitive dysfunction

    • Causes:
    • 1. not available in diet
    • 2. inability to absorb or metabolize
    • 3. poor diet due to chronic alcohol/vegan
    • 4. toxic excess of nutrient
  2. Thiamine (B1) deficiency
    • Causes:
    • -Alcoholism
    • -Malabsorption from chronic vomiting, primary GI disorders, short gut syndromes, bariatric surgery
    • -Dietary restriction

    • Two classic syndromes:
    • -Wernicke Korsakoff
    • -BeriBeri (dry and wet)

    • -human body has 7-8 week store of thiamine
  3. Thiamine Deficiency: Wernicke Korsakoff
    • -involves CNS
    • -acute to subacute onset

    • Presentation:
    • 1. Ophthalmoplegia: weakness of EOM --> diplopia (esp LR), nystagmus
    • 2. Ataxia (axial > appendicular)
    • 3. Cognitive Syndrome: delirium, memory problems, basic amnesia syndrome, confabulation

    • Pathology:
    • -mammillary bodies (amnesia)
    • -dorsomedial nucleus of thalamus (amnesia)
    • -midbrain and pontine tegmentum (CNIII, CNVI nuclei --> ophthalmoplegia)
    • -medulla (vestibular nuclei --> nystagmus, ataxia)
    • -dilated capillaries with prominent endothelial cells --> hemorrhagic necrosis

    • Pathophysiology:
    • -unknown
    • -genetic mutation in an enzyme that requires thiamine

    • Treatment:
    • -thiamine administration
    • ***in patients with low thiamine levels glucose administration can trigger Wernicke Korsakoff syndrome

    • Prognosis:
    • -early treatment
    • -ophthalmoplegia resolves (days)
    • -ataxia improves partially (wks to months)
    • -often congitive residua of basic amnesia syndrome
  4. Thiamine Deficiency: BeriBeri
    • -involves PNS
    • -two forms in adults: dry and wet
    • -infantile variant in breastfed infants in areas with heavy white rice consumption

    • Presentation:1. Dry BeriBeri
    • -chronic progressive polyneuropathy
    • -sensorimotor defect, may include pain
    • 2.Wet BeriBeri
    • -similar to dry
    • -with associated heart failure
    • 3. Infantile Variant
    • -wet BeriBeri
    • -eye movement abnormalities of Wernicke Korsakoff

    • Pathology:
    • -lesions most prominently in distal portions of longest and largest myelinated fibers
    • -axonal degeneration

    • Pathophysiology:
    • -see Wernicke Korsakoff

    • Treatment:
    • -thiamine administration
    • -drugs for neuropathic pain

    • Prognosis:
    • -tx prevents worsening
    • -may or may not lead to gradual improvement (months)
  5. Cobalamin (B12) Deficiency
    • -subacute onset (many weeks-months)
    • -human body has 3 year store of cobalamin
    • -may have megaloblastic anemia

    • Presentation:
    • 1. Subacute combined degeneration (dorsal columns and lateral corticospinal tracts) and large fiber polyneuropathy (predominantly sensory)
    • -sensory paresthesias usually hands and feet
    • -worsening distal somatosensory and motor dysfunction
    • -impaired proprioception, vibration and fine touch
    • -UMN findings in distal extremeties
    • -sometimes ataxia
    • 2. Neuropsychiatric effects (absent or mild)
    • -trouble concentrating to overt dementia
    • 3. Optic Neuropathy
    • -decreased visual acuity (often later)

    • Pathology:
    • -demyelinating lesions starting in dorsal columns, lateral corticospinal tracts
    • -low cervical to mid thoracic spinal cord
    • -myelin sheaths swollen
    • -intramyelinic vacuoles

    • Pathophysiology:
    • -often due to pernicious anemia
    • -strict vegan diet, celiac sprue, GI resections, tapeworm etc

    • Diagnosis:
    • -normal range of cobalamin is very wide: can have normal levels and still be deficient
    • -check homocysteine and methylmalonic acid levels

    • Treatment:
    • -IM cobalamin
    • -large does oral supplements in pernicious anemia
    • ***folate will correct the anemia but not neuro dysfxn of cobalamin deficiency

    • Prognosis:
    • -anemia resolves rapidly
    • -neuro changes correct slowly over months and often incompletely
  6. Pyridoxine (B6) Deficiency
    • Presentation:
    • -polyneuropathy
    • -seizures (rarely)

    • Pathophysiology:
    • -often in patients taking isoniazid for TB

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