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Medical Nutrition Therapy in Neurological Disorders Part 2

Medical Nutrition Therapy in Neurological Disorders Part 2. Epilepsy. Intermittent derangement of the nervous system caused by sudden discharge of cerebral neurons 2.3 million Americans have epilepsy; 15% under age 15

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Medical Nutrition Therapy in Neurological Disorders Part 2

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  1. Medical Nutrition Therapy in Neurological Disorders Part 2

  2. Epilepsy • Intermittent derangement of the nervous system caused by sudden discharge of cerebral neurons • 2.3 million Americans have epilepsy; 15% under age 15 • May be caused by head injury, congenital defects, metabolic disorders, other illnesses • Many are idiopathic (cause unknown)

  3. Onset of Seizures by Age Source: University of Cincinnati Department of Neurology http://www.med.uc.edu/neurology/

  4. Causes of Seizures Source: University of Cincinnati Department of Neurology http://www.med.uc.edu/neurology/

  5. Generalized Seizures

  6. Epilepsy: Tonic-Clonic Seizure • Formerly called grand mal. • Generalized seizure that lasts 1-2 minutes • Involves complete loss of muscle tone and consciousness • More common in children

  7. Epilepsy: Absence Seizure • Formerly called petit mal • Also generalized • May appear to be daydreaming, but recovers after a few seconds with no postictal fatigue or disorientation • More common in children

  8. Absence Seizure Pathology

  9. Partial Seizures

  10. Epilepsy: Partial Seizure • Discrete focus of epileptogenic brain tissue • Simple partial seizure involves no loss of consciousness • Complex partial seizure involves change in consciousness • Most common, especially in adults Source: University of Cincinnati Department of Neurology http://www.med.uc.edu/neurology/

  11. Types of Seizures and Prevalence Source: University of Cincinnati Department of Neurology http://www.med.uc.edu/neurology/

  12. Epilepsy: Medical Treatment Generalized seizures • managed with valproate, phenytoin, gabapentin • Drug-drug and drug-nutrient interactions • Liver damage

  13. Epilepsy: Medical Treatment Partial seizures • Managed with carbamazepine or phenytoin • Seizure surgery if fail to control with medications • Localized focus resected produces cure in 75% of patients • Phenobarbital avoided as associated with  IQ in children; may be used in failure of other drugs

  14. Epilepsy: Drug-Nutrient Interactions • Phenobarbital, phenytoin, primidone interfere with absorption of calcium by increasing vitamin D metabolism • Long term therapy may lead to osteomalacia in adults or rickets in children • Vitamin D supplementation is essential

  15. Epilepsy: Drug-Nutrient Interactions • Folic acid supplementation interferes with phenytoin metabolism; may not reach therapeutic levels • Phenytoin and phenobarbital are bound to albumin in the bloodstream; malnutrition results in  free drug and possible toxicity • Alcohol interferes with phenytoin, possibly resulting in seizures

  16. Epilepsy: Drug-Nutrient Interactions • Continuous enteral feeding slows absorption of oral phenytoin; may increase therapeutic dose • If enteral feeding is discontinued,  risk of toxicity • Window enteral feedings around phenytoin administration (stop feeding 2 hours before and after) • Give phenytoin IV or use time-release formula to decrease time the feeding is off

  17. Epilepsy MNT: Ketogenic Diet • Treatment of last resort in children with intractable seizures • Will completely control epilepsy in one-third of children; significantly decrease activity in one-third • Ketones may exert anticonvulsant effect on body

  18. Ketogenic Diet Implementation • Stop antiepileptic drugs • Child fasts in hospital for 24-72 hours until 4+ ketonuria • Evaluate response • Fat: 75% of calories • Protein: sufficient to meet growth needs (1 g/kg) • CHO: added to make up rest of calorie needs (negligible)

  19. Ketogenic Diet Menu Using MCT Oil

  20. Multiple Sclerosis • Chronic disease affecting the CNS • Destruction of the myelin sheath, which transmits nerve impulses • Multiple areas of myelin are replaced with scar tissue • May be genetic and environmental factors, including geographical latitude (northern hemisphere) and diet (high animal fats)

  21. Multiple Sclerosis: Medical Tx • Steroid therapy for exacerbations; ACTH and prednisolone; methotrexate (can cause weight gain, fluid retention) alpha-interferon • Physical therapy

  22. Progression of Multiple Sclerosis

  23. MS Controversial Therapies • Shank diet: low in saturated fat • MacDougal diet: no gluten, low sugar, and no refined sugar • Allergen-free, gluten-free, pectin-free, fructose-restricted, raw food Evers diet • Low fat diet high in linoleic acid may have some beneficial effects

  24. MNT in MS • Diet consistency modifications as needed if dysphagia develops • Suggest prepackaged, single-serving or convenience foods if meal preparation becomes difficult due to impaired vision, poor ambulation • High fiber diet for constipation • Counseling regarding fluid intake, cranberry juice to prevent UTIs • Enteral nutrition support in end stage

  25. Nutrition Guidelines for Parkinson’s Disease • Eat a variety of healthy foods consistent with the US Dietary Guidelines • Maintain a healthy body weight • Balance food with exercise • Eat foods high in fiber

  26. Food-Drug Interactions in Parkinson’s Disease • Levodopa works best taken on an empty stomach ½ hour before or one hour after meals • Protein competes with levodopa for absorption. Rarely, a high protein diet interferes with levodopa • If so, reduce overall protein intake or divide into many small meals; eat protein late in the day (usually not recommended) Source: Cleveland Clinic Health System, http://www

  27. Food-Drug Interactions in Parkinson’s Disease • Levodopa can cause nausea • Doctor may change to combination of levodopa and carbidopa (Sinemet) or carbidopa by itself • Drink liquids between meals rather than with them • Eat smaller more frequent meals • Avoid fried, greasy or sweet foods • Eat foods at room temperature to minimize odors • Rest after eating with head elevated Source: Cleveland Clinic Health System, http://www.cchs.net/

  28. Protein Redistribution in L-Dopa Therapy

  29. Acute Spinal Cord Injury Source: www.spinal-cord-injury-resources.com/ spinal-i...

  30. Spinal Cord Lying within the Vertebral Canal

  31. Sequelae of Spinal Cord Injury and Rehabilitation Challenges

  32. Acute Spinal Cord Injury (SCI) • Energy requirement for SCI = H/B x 1.1 x 1.3 (Barco et al, NCP 17;309-313, 2002) • Pt with multi-traumas in addition to SCI may have higher needs • Protein needs: 2 g/kg (Rodriguez DJ et al, JPEN 15:319-322, 1991 • Provide enteral/parenteral support as needed

  33. MNT in Chronic Spinal Cord Injury • Risk of weight gain, pressure ulcers due to immobilization • High fiber, adequate hydration to minimize constipation • Dietary intake to maintain nutritional health and adequate weight

  34. Brain Injury • 400,000 new cases of brain injury occur each year in the United States • Most result from motor vehicle crashes. • Incidence is highest in young people and elderly; twice as often in males than females • Almost all patients with a severe head injury have some degree of disability.

  35. Glasgow Coma Scale (GCS) Strong prognostic value for neurologic recovery in head-injured patients (scale evaluating and quantitating the degree of coma by determining best responses to standardized stimuli) • Eye opening (4 Spontaneous–1 None) • Verbal response (5 Oriented–1 None) • Motor response (6 Follows command–1 None) Severity of head injury: mild = GCS 13-15, moderate = GCS 9-12, severe = GCS 3-8

  36. Older age Low Glasgow ComaScale score Pupil dilatation Low blood pressure All these variables have an additive effect on morbidity and mortality Inadequate oxygenation early after injury Prolonged and/or difficult to control intracranial pressure Strong Predictors of Poor Outcome after Head Injury

  37. Neurological Deficits That Affect Nutritional Status • Hemiparesis: weakness that affects one side of the body • May increase risk of aspiration • Hemianopsia: blindness in one half of field of vision. • Must compensate by turning his head

  38. Normal Vision

  39. Hemianopsia

  40. Neurological Deficits That Affect Nutritional Status • Apraxia • Patient has difficulty with perceptual motor planning • Dysphagia • Difficulty swallowing

  41. Symptoms of Dysphagia • Drooling • Choking or coughing during or following meals • Inability to suck from a straw • Gurgly voice quality • Holding pockets of food in the buccal recesses (patient may not be aware)

  42. Symptoms of Dysphagia • Absent gag reflex • Chronic upper respiratory infections • Weight loss and anorexia

  43. Stages of Swallowing • Oral Phase: (voluntary) food is chewed, mixed with saliva, tongue moves it to the back of the mouth • Problems include inability to seal the lips around a cup • Inability to suck through a straw • Food can become pocketed

  44. Stages of Swallowing • Pharyngeal phase: (involuntary) Soft palate closes off the nasopharynx; hyoid and larynx elevate, vocal cords adduct to protect the airway; pharynx contracts and cricopharyngeal sphincter relaxes allowing food to pass into the esophagus • Symptoms of poor coordination include gagging, choking, and nasopharyngeal regurgitation

  45. Stages of Swallowing (cont) • Esophageal phase: (involuntary) bolus continues through esophagus into the stomach • Most difficulties due to mechanical obstruction • Involuntary peristalsis affected by brain stem infarct

  46. Swallowing Occurs in Three Phases

  47. Swallowing Occurs in Three Phases—cont’d

  48. Swallow Animation http://greenfield.fortunecity.com/rattler/46/upali4.htm

  49. Food Textures in Dysphagia Thin liquids: the most difficult to control in the mouth • Easily aspirated into the lungs • Often thickened to nectar thick, honey thick, or pudding thick • Essential for proper hydration

  50. National Dysphagia Diet Survey • Diet covered in Oral and Dental Health lecture • ADA and ASHA surveyed RDs and SLPs regarding use of NDD • 30% had implemented NDD • Of those not using it, some were using modifications of it Reported at FNCE 2007; Shirley L. McCallum

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