Medical Nutrition Therapy For Neurologic Disorders

MEDICAL NUTRITION THERAPY
FOR NEUROLOGIC DISORDERS

Introduction
• Some neurologic disorders result from a simple deficiency or
excess of a nutrient, such as the neuropathy associated with
thiamin deficiency, whereas others have more complex
causes such as diabetic neuropathy, stroke, or trauma.
• Some conditions arise with the interaction of genetics and
metabolic or environmental factors, as is the case with
multiple sclerosis (MS), Parkinson’s disease (PD), and
alcoholism.
• Numerous symptoms and malnutrition may accompany
neurologic diseases.
• Although not all neurologic diseases have a nutritional
cause, nutritional considerations are integral to effective
medical and clinical management
THE CENTRAL NERVOUS
SYSTEM
• The central nervous system (CNS) is differentiated
functionally into three segments, so lesions in the nervous
system leave a unique “calling card” for localized
dysfunction.
• Localizing the defect (lesion) to muscle, nerve, spinal
cord, or brain is part of the medical diagnosis. Nerve
tracts coming to and from the brain cross to opposite
sides in the CNS.
• Therefore a lesion in the brain that affects the right arm
is found on the left side of the brain.
• Signs of weakness are the most quantifiable clinical signs of
nervous system disease.
• The neurons in the motor strip (upper motor neurons) receive
input from all parts of the brain and project their axons all
the way to their destinations in the spinal cord.
• Axons connect to the spinal cord motor neurons (lower motor
neurons).
• These neurons extend from the spinal cord to muscles
without interruption.
• The location of a lesion in the nervous system often can be
deduced clinically by observing stereotypical abnormalities
and function of either upper or lower motor neurons.
Nutritional Considerations for Neurologic Conditions
Medical Condition Relevant Nutrition Therapy
Adrenoleukodystrophy Dietary avoidance of VLCFAs has not been proven.
Lorenzo’s oil may lower VLCFA levels
Alzheimer’s disease Recommend antioxidants and antiinflammatory diet.
Minimize distractions at mealtime.
Initiate smell or touch of food.
Guide hand to initiate eating.
Provide nutrient-dense foods, omega-3 fatty acids
Amyotrophic lateral Intervene to prevent malnutrition and dehydration.
sclerosis Possibly ketogenic diet.
Monitor dysphagia.
Antioxidant use (vitamins C, E, selenium, methionine)
is well tolerated, but not proven.
Epilepsy Provide ketogenic diet
Nutritional Considerations for Neurologic
Conditions
Guillain-Barré Attain positive energy balance with highenergy, high-
protein tube feedings.
Possibly gluten-free diet.
Assess dysphagia
Migraine headache Follow general recommendations for food
avoidance.
Maintain adequate dietary and fluid intake.
Keep extensive records of symptoms and foods.
Myasthenia gravis Provide nutritionally dense foods at beginning of
meal.
Small, frequent meals are recommended.
Limit physical activity before meals.
Place temporary feeding tube.
Conditions
Multiple sclerosis Recommend antioxidants and antiinflammatory diet.
Possibly recommend linoleic acid supplement.
Evaluate health and especially vitamin D status of
patient.
Nutrition support may be needed in advanced
stages.
Distribute fluids throughout waking hours; limit before
bed.
Neurotrauma Enteral or parenteral nutrition support when needed.
Parkinson’s disease Focus on drug-nutrient interactions.
Minimize dietary protein at breakfast and lunch.
Recommend antioxidants and antiinflammatory diet.
Pernicious anemia Administer vitamin B12injections.
Provide diet liberal in HBV protein.
Provide diet supplemented with Fe, vitamin C, and B
complex vitamins.
Conditions
Spinal trauma Spinal trauma Provide enteral or parenteral nutrition
support.
Provide high-fiber diet, adequate hydration to
minimize constipation.
Provide dietary intake to maintain nutrition health and
adequate weight.
Stroke Dietary alterations for primary prevention.
Maintain good nutrition status.
Assess possible dysphagia.
Nutrition support may be needed.
Wernicke-Korsakoff Provide thiamin supplementation.
syndrome Provide adequate hydration.
Provide diet liberal in high-thiamin foods.
Eliminate alcohol.
Dietary protein may have to be restricted.
Neurologic Syndromes Attributed to Nutritional
Deficiency or Excess
NUTRITIONAL DEFICIENCY
Site of Major Syndrome Name
Encephalon Hypocalcemia and tetany seizures from lack
of vitamin D.
Impaired intellectual and cognitive function
(protein-calorie deprivation).
Cretinism (iodine deficiency).
Wernicke-Korsakoff syndrome (thiamin
deficiency
Optic nerve Nutritional deficiency optic neuropathy
(“tobacco-alcohol amblyopia”)
Brainstem Central pontine myelinolysis (sodium)
Cerebellum Alcoholic cerebellar degeneration.
Vitamin E deficiency caused by bowel disease.
NUTRITIONAL DEFICIENCY
Site of Major Syndrome Name
Spinal cord Combined system disease (B12deficiency).
Tropical spastic paraparesis.
Peripheral nerves Beriberi (thiamin deficiency), pellagra
(nicotinic acid deficiency)
Hypophosphatemia
Tetany (vitamin D deficiency)
Muscle Myopathy of osteomalacia
NUTRITIONAL EXCESS
Syndrome Condition Agent
Increased intracranial Self-medication Vitamin A
pressure
Encephalopathy Phenylketonuria. Phenylalanine
Water intoxication. Water
Hepatic encephalopathy. Protein (and NH₃)
Ketotic or nonketotic coma Glucose, insulin
in diabetes.
Stroke Hyperlipidemia Lipid
Peripheral neuropathy Hypochondriasis Pyridoxine
Myopathy Insomnia, anxiety Tryptophan
Anorexia nervosa, Emetine, ipecac
bulimia
Myoglobinuria Constipation Licorice
Parts of the brain
Spinal cord lying within the vertebral canal
Pathophysiology and Signs of Mass Lesions
• The frontal lobes in the brain are the source of the most
complex activities and commonly offer the most complex
presentations.
• Psychiatric manifestations such as depression, mania, or
personality change may herald a tumor or other frontal lobe
mass, either right or left.
• With a lesion or tumor near the skull base, one may lose the
sense of smell or have visual changes because olfactory and
optic nerves track along the bottom of these frontal lobes.
• Chemosensory losses of smell have been described as
anosmia (absence of smell), hyperosmia (increased
sensitivity of smell), or dysosmia(distortion of normal smell).
• Frontal lobes are larger and the posterior portions of the
frontal lobes contain the motor strips, which control
muscle movement.
• Lesions that develop in the central frontal lobe may
present as motor apraxia. A person with apraxia cannot
perform a complex activity such as independent eating
despite a willingness to do so.
• Temporal lobes control memory and speech; lesions there may
affect these abilities, as seen with the dementia of Alzheimer’s
and with stroke.
• Although any lesion of cerebral gray matter may produce
seizures, the temporal lobes are particularly prone to
seizures. A right parietal lobe mass or insult may result in chronic
inability to focus attention, thus completely ignoring the body’s left
side.
• Because speech centers are located near the junction of the left
temporal, parietal, and frontal lobes, pathologic conditions in this
region may cause speech problems.
• The occipital lobes are reserved for vision, and dysfunction here
may bring about cortical blindness of varying degrees.
• In this condition the person is unaware that he or she cannot see.
• Lesions of the cerebellum and brainstem may obstruct the ventricular
system where it is the narrowest.
• This obstruction may precipitate life-threatening hydrocephalus, a
condition of increased intracranial pressure (ICP) that may quickly result in
death.
• Other signs of hydrocephalus include trouble with balance, walking and
coordination, marked sleepiness, and complaints of a headache that is
worse on awakening.
• Lesions in the brainstem may infiltrate any of the cranial nerves that
innervate structures of the face and head, including the eyes, ears, jaw,
tongue, pharynx, and facial muscles.
• These lesions have consequences for nutrition because the patient is often
unable to eat without risking aspiration of food or liquids into the lung.
• Tumors or other lesions in may infiltrate respiratory and cardiac centers,
and dysregulation of these centers has grim consequences.
• Lesions in the spinal cord are much less common than
brain tumors and ordinarily cause lower motor neuron
signs at the level of the lesion and upper motor signs in
segments below the level of the lesion.
• Spinal cord injury (SCI) is the most common pathologic
condition in this region. Other examples of spinal cord
abnormalities are MS, amyotrophic lateral sclerosis (ALS),
tumor, syrinx (fluid-filled neurologic cavity), chronic
meningitis, vascular insufficiency, and mass lesions of the
epidural space.
• Lesions of the pituitary gland and hypothalamus are
often heralded by systemic manifestations that may include
electrolyte and metabolic abnormalities secondary to
adrenocortical, thyroid, and antidiuretic hormone
dysregulation.
• Because of the proximity to the visual pathways, changes
may occur in visual field or acuity.
• The syndrome of inappropriate antidiuretic hormone
secretion (SIADH) is often a complication; volume status
and hyponatremia are part of the medical diagnosis.
• Because the hypothalamus is the regulatory center for
hunger and satiety, lesions here may present as anorexia
or overeating.
• Finally, disorders of peripheral nerves and the
neuromuscular junction affect one’s ability to maintain
proper nutrition.
• Disorders such as Guillain-Barré syndrome (GBS) or
myasthenia gravis (MG) may counteract the efforts to
maintain nutritional balance.
• To eat and drink effectively, many parts of the nervous
system are required. A problem at any location of the
nervous system can affect ability to meet nutritional
requirements.
Basic Functions of Cranial Nerves
Number Nerve Function
Olfactory (I) Smell
Optic (II) Vision
Oculomotor (III) 1. Eye movement
2. Pupil constriction
Trochlear (IV) Eye movement
Trigeminal (V) 1. Mastication
2. Facial heat, cold, touch
3. Noxious odors
4. Input for corneal reflex
Abducens (VI) Eye movement
Facial (VII) 1. All muscles of facial expression
2. Corneal reflex
3. Facial pain
4. Taste on anterior two thirds of tongue
Basic Functions of Cranial Nerves
Number Nerve Function
Vestibulocochlear (VIII) Hearing and head acceleration and
input for oculocephalic reflex
Glossopharyngeal (IX) 1. Swallowing
2. Gag reflex
3. Palatal, glossal, and oral sensation
Vagus (X) 1. Heart rate, gastrointestinal activity,
sexual function
2. Cough reflex
3. Taste on posterior third of tongue
Spinal accessory (XI) 1. Trapezius
2. Sternocleidomastoid muscle
Hypoglossal (XII) Tongue movement
ISSUES COMPLICATING NUTRITION
THERAPY
• The nutritional management of patients with neurologic disease is
complex.
• Severe neurologic impairments often compromise the mechanisms
and cognitive abilities needed for adequate nourishment.
• A common result is dysphagia(difficulty swallowing), and the ability to
obtain, prepare, and present food to the mouth can be compromised.
• Modified food textures are often required for the individual with
swallowing problems.
• Early recognition of signs and symptoms, implementation of an
appropriate care plan to meet the nutritional requirements of the
individual, and counseling for the patient and family members on
dietary choices are essential.
• Regular evaluation of the patient’s nutrition status and disease
management are priorities, with the ultimate goal of improving
outcomes and the patient’s nutritional quality of life.
THERAPY
• Nutrition assessment requires detailed histories.
• The diet history and mealtime observations are used to
assess patterns of normal chewing, swallowing, and rate
of ingestion.
• Weight loss history establishes a baseline weight; a
weight loss of 10% or more is indicative of nutritional risk.
• Assessment for nutrients involved in neurotransmitter
synthesis is particularly important in these patients.
THERAPY
• Nutrition diagnoses common in the neurologic patient
population include the following:
a. Chewing difficulty
b. Increased energy expenditure
c. Inadequate energy intake
d. Inadequate fluid intake
e. Physical inactivity
f. Poor nutritional quality
g. Difficulty with independent eating
h. Swallowing difficulty
i. Underweight
j. Elimination problems
k. Inadequate access to food or fluid
THERAPY
1. Meal Preparation
 Confusion, dementia, impaired vision, or poor ambulation may
contribute to difficulty with meal preparation, thus hindering oral
food and beverage intake.
 Assistance with shopping and meal planning are frequently
necessary.
THERAPY
2. Eating Difficulties and Inadequate Access to Food
or Fluid
 With chronic neurologic diseases, a decline in function may
hinder the ability for self-care and nourishment.
 Access to food and satisfying basic needs may depend on the
involvement of family, friends, or professionals.
 With acute neurologic situations such as seizures, trauma,
stroke, or GBS, the entire process of eating can be interrupted
abruptly.
 The patient may require enteral nutrition for a time until overall
function improves and adequate oral intake is resumed
THERAPY
3. Eating Issues: Presentation of Food to the Mouth
 The patient with neurologic disease may be unable to eat
independently because of limb weakness, poor body positioning,
hemianopsia, apraxia, confusion, or neglect.
 Tremors in PD, spastic movements, or involuntary movements that
occur with cerebral palsy, Huntington disease, or tardive
dyskinesia may further restrict dietary intake.
 The affected region of the CNS determines the resulting disability.
 If limb weakness or paralysis occurs on the dominant side of the
body, poor coordination resulting from a new reliance on the
nondominant side may make eating difficult and unpleasant.
 The patient may have to adjust to eating with one hand and also to
using the nondominant hand.
 Hemiparesisis weakness on one side of the body that causes the
body to slump toward the affected side; it may increase a patient’s
risk of aspiration.
THERAPY
3. Eating Issues: Presentation of Food to the Mouth
 Hemianopsiais blindness for one half of the field of vision.
 The patient must learn to recognize that he or she no longer has a
normal field of vision and must compensate by turning the
head.
 Neglect is inattention to a weakened or paralyzed side of the body;
this occurs when the nondominant (right) parietal side of the
brain is affected.
 The patient ignores the affected body part, and his or her
perception of the body’s midline is shifted.
 Hemianopsia and neglect can occur together and severely impair
the patient’s function.
 A patient may eat only half of the contents of a meal because he or
she recognizes only half of it.
A. Normal vision
B. Vision with hemianopsia
Common Impairments with Neurologic Diseases
Site in the Brain Impairment Results
Cortical lesions of the Sensory deficits Fine regulation of muscle activities
parietal lobe (perception of impossible if the
sensory stimuli) patient is unable to perceive joint
position and motion
and tension of contracting
muscles.
Lesions of the Hemi inattention Patient neglects that side of the
nondominant hemisphere syndrome (neglect) body
Optic tract lesions (usually Visual field cuts Patient reads one half of a page,
of the middle cerebral eats from only half of the
artery or the artery near plate, etc.
the internal capsule)
Loss of subcortically stored Apraxia Inability to perform a previously
pattern of motor skills learned task (e.g., walking,
rising from a chair), but paralysis,
sensory loss, spasticity,
and incoordination are not present
Common Impairments with Neurologic Diseases
Site in the Brain Impairment Results
No identification with a Language apraxia Inability to produce meaningful
particular brain disorder or speech, even though oral
a specifically located lesion muscle function is intact and
language production has
not been affected
Lesion of Broca area Nonfluent aphasia Thought and language formulation
are intact, but the patient
is unable to connect them into
fluent speech production
Lesion of Wernicke area Fluent aphasia Flow of speech and articulation
seem normal, but language
output makes little or no sense
Extensive brain damage Global aphasia Expression and speech perception
are severely impaired
Brainstem lesions, bilateral Dysarthria Inability to produce intelligible
hemispheric lesions, words with proper
cerebellar disorders articulation
DYSPHAGIA
• Dysphagia often leads to malnutrition because of
inadequate intake.
• Symptoms of dysphagia include drooling, choking, or
coughing during or following meals; inability to suck
from a straw; a gurgly voice quality; holding pockets
of food in the buccal recesses (of which the patient may
be unaware); absent gag reflex; and chronic upper
respiratory infections.
• Patients with intermediate or late-stage PD, MS, ALS,
dementia, or stroke are likely to have dysphagia.
DYSPHAGIA
• A swallowing evaluation by a speech-language pathologist
(SLP) is important in assessing and treating swallowing
disorders.
• The SLP is often consulted for individual patients
following traumatic brain injury (TBI), stroke, or cancers of
the head and neck, and for those at risk of
aspiration(inhaling foreign material into the lungs) or with
other conditions that result in a lack of coordination in
swallowing.
Phases of Swallowing
a. Oral Phase
b. Pharyngeal Phase
c. Esophageal Phase
MNT for Dysphagia
• Weight loss, anorexia, and dehydration are key concerns
with dysphagia.
• The Academy of Nutrition and Dietetics (formerly the
American Dietetic Association) published the National
Dysphagia Diet (NDD) developed through consensus
from a panel of dietitians, speech pathologists and
scientists.
• The NDD is prescribed by a speech pathologist that
evaluates the individual’s ability to safely swallow both food
textures and liquids.
• Standard levels of dysphagia from severe to mild were
designated with assigned diet texture modifications for each
level to promote the safety of swallow.
MNT for Dysphagia
• The levels of dysphagia severity range from:
i. Severe Dysphagia: inability to clear the pharynx,
nonfunctional volitional cough and silent aspiration
ii. Moderate Dysphagia: moderate retention in the
oral cavity requiring cues and or supervision to clear
iii. Mild Dysphagia: retention in the pharynx that is
able to be cleared through spontaneous cough
Dysphagia
Dysphagia
Dysphagia
MNT for Dysphagia
1. Liquids
 Swallowing liquids of thin consistency such as juice or water is the
most difficult swallowing task because of the coordination and
control required.
 Liquids are easily aspirated into the lungs and may pose a life-
threatening event because aspiration pneumonia may ensue, even
from sterile water in the lungs.
 Sterile water is no longer sterile once it is introduced to the
bacterial load of the oral cavity.
 Dry milk powder as a thickener alters the taste and might raise
protein content too high for children, especially with limited free
water.
 Commercial thickeners now have xanthan gum or modified
food starches as ingredients.
Levels of Thickening Liquids
• The Frazier Water Protocol, which allows for
drinking water in those who otherwise require
thickened liquids is being increasingly used in
long term care. This protocol is based on the
following assumptions:
1. Aspiration of water poses little risk to the patient
if oral bacteria associated with the development of
aspiration pneumonia can be minimized.
2. Allowing free water decreases the risk of dehydration.
3. Allowing free water increases patient compliance with
swallowing precautions and improves quality of life.
4. Good oral hygiene is a key ingredient of the water
protocol and offers other benefits to swallowing.
MNT for Dysphagia
2. Textures
 As chronic neurologic disease progresses, cranial nerves
become damaged, leading to neurologic deficits often
manifested by dysphagia or elimination of entire food groups.
 Nutrition intervention should be individualized according to the
type and extent of dysfunction.
 Vitamin and mineral supplementation may be necessary.
 If chewable supplements are not handled safely, liquid forms
may be added to acceptable foods.
MNT for Dysphagia
3. Enteral Tube Nutrition
 Patients with acute and chronic neurologic diseases may benefit
from nutrition support. Well-managed nutrition support helps to
prevent pneumonia and sepsis, which can complicate these
diseases.
 Enteral tube feedings may be necessary if the risk of aspiration
from oral intake is high, or if the patient cannot eat or drink
enough to meet his or her nutritional needs.
 In most instances the gastrointestinal tract function remains intact,
and enteral nutrition is the preferred method of administering
nutrition support.
 Malnutrition itself can produce neuromuscular weakness that
negatively affects quality of life; it is a prognostic factor for poor
survival.
NEUROLOGIC DISEASES OF NUTRITIONAL
ORIGIN
• Dietary deficiencies of thiamin and niacin can directly result in
neurologic symptoms.
• With Wernicke-Korsakoff synrome (WKS), the neurologic effect
occurs secondary to alcoholism.
• Most neurologic symptoms arising from nutritional deficiencies
can be corrected with increased food intake or supplements.
• A new era of treating neurologic disorders with diet therapy is
emerging, stemming from the effective use of ketogenic diets for
epilepsy.
• Gluten sensitivity is yet another genetic condition with
neurologic implications.
• Numerous reports of patients with neurologic dysfunction related
to gluten sensitivity have been reported since 1966 including
ataxia, headache, and seizures.
Neurologic Diseases Arising from Nutritional
Deficiencies
NEUROLOGIC DISORDERS FROM TRAUMA
• Cerebrovascular Accident (Stroke)
 an acute onset of focal or global neurologic deficit lasting more
than 24 hours; it is attributable to diseases of the intracranial
or extracranial neurovasculature.
 severe strokes are often preceded by transient ischemic
attacks (TIAs), brief attacks of cerebral dysfunction of vascular
origin with no persistent neurologic defect.
 advanced age is the most significant risk factor for stroke.
 among modifiable risk factors, hypertension and smoking are the
major contributors.
 other factors include obesity, coronary heart disease, diabetes,
physical inactivity, and genetics.
Pathophysiology
• Embolic stroke occurs when a cholesterol plaque is
dislodged from a proximal vessel, travels to the brain, and
blocks an artery, most commonly the middle cerebral
artery (MCA).
• In patients with dysfunctional cardiac atria, clots may
be dislodged from there and embolize.
• In thrombotic stroke a cholesterol plaque within an artery
ruptures, and platelets subsequently aggregate to clog an
already narrowed artery.
• Most strokes are incited by a thromboembolic event,
which may be aggravated by atherosclerosis,
hypertension, diabetes, and gout.
Pathophysiology
• Intracranial hemorrhage occurs in only 15% of strokes but is often fatal
immediately.
• Intracranial hemorrhage occurs more commonly in individuals with
hypertension.
• In intraparenchymal hemorrhage, a vessel inside the brain ruptures.
• A variation of intraparenchymal hemorrhage is a lacunar (deep pool)
infarct.
• These smaller infarcts occur in the deep structures of the brain such as
the internal capsule, basal ganglia, pons, thalamus, and cerebellum.
• Even a small lacunar infarct can produce significant disability because
the brain tissue in the deep structures is so densely functional.
• A second type of intracranial hemorrhage is subarachnoid hemorrhage
(SAH). SAH occurs commonly as a result of head trauma but more
often as a result of a ruptured aneurysm of a vessel in the subarachnoid
space.
Medical Management
• Hemorrhage is suspected when the patient presents with headache,
decreased level of consciousness, and vomiting, all of which occur
within minutes to hours.
• A thromboembolic stroke is more likely to occur when the patient
is fully conscious, but the onset of motor or sensory changes occurs
suddenly.
• As with all neurologic disease, the clinical presentation depends on
the location of the abnormality.
• An infarct of a particular cerebrovascular territory can be suspected by
seeking out various neurologic deficits.
• An MCA occlusion produces paresis, with sensory deficits of limbs on
the opposite side of the body because this artery supplies the motor
and sensory strips.
• If the left MCA is occluded, aphasia, or loss of speech or
• expression may be present.
Medical Management
• In the past, treatment for embolic stroke was supportive; it
focused on prevention of further brain infarction and
rehabilitation.
• Use of thrombolytic, “clot-busting” drugs reverses brain
ischemia by lysing the clots.
• Initiation of therapy needs to occur within 6 hours of the
onset of symptoms.
• Use of aspirin may be of some value in preventing further
cerebrovascular events, but its effectiveness varies from
one patient to another.
Medical Nutrition Therapy
• Lifestyle and behavior changes that include diet are key components to
primary prevention of stroke.
• A diet high in omega-3 fatty acids has been shown in some
studies to provide a protective benefit against stroke, however,
omega-3 fat supplements have not shown the same benefit.
• Omega-3 fat supplements should be avoided by anyone taking a
blood thinner such as warfarin or aspirin.
• Eating difficulties and resulting behavioral problems are determined
by the extent of the stroke and the area of the brain affected.
• Dysphagia, an independent predictor of mortality, commonly
accompanies stroke and contributes to complications and poor
outcome from malnutrition, pulmonary infections, disability, increased
length of hospital stay, and institutional care.
• In some instances nutrition support is required to maintain
nutritional health until oral alimentation can be resumed.
Nutrition-Related Factors and Stroke Risk
Practical Interventions for Eating-Related Behavioral
Problems
Behavioral Problem Intervention
Attention or concentration Verbally direct client through each step of eating
deficit process; place utensils in hand.
Make food and fluids available and visible
Combative, throws food Identify provocative agent, remove.
Dining assistant stands or sits on nondominant
side.
Provide nonbreakable dishes with suction holder.
Give one food at a time.
Reward appropriate mealtime behavior.
Chews constantly Tell client to stop chewing after each bite.
Serve soft foods to reduce the need to chew.
Offer small bites.
Eats nonedible things Remove nonedibles from reach; provide finger
foods.
Use edible centerpiece or table decorations.
Practical Interventions for Eating-Related
Behavioral Problems
Eats too quickly Set utensils down between bites.
Offer food items separately.
Offer bulky foods that require chewing.
Use a smaller spoon or cup.
Eats too slowly Use a smaller spoon or cup.
Eats too slowly Monitor eating pace and provide
verbal cues: “chew,” “take a bite.”
Serve first to allow more time.
Use insulated dishes to maintain proper
temperatures.
Forgetful or Follow simple routines.
disoriented Provide constant environment.
Provide assigned seating.
Minimize distractions and limit choices
Behavioral Problems
Forgets to swallow Tell client to swallow.
Feel for swallow before offering next bite.
Stroke upward on larynx.
Inappropriate emotional Engage in conversation; ignore emotional
expression display.
Provide a quiet environment.
Paces Sit beside client at table.
Change dining location.
Provide aerobic exercise before meals.
Offer finger foods.
Use cups with covers or spouts.
Plays in food Serve one food at a time.
Fill glass or plate half full at refill.
Offer finger foods.
Use cups with covers or spouts.
Behavioral Problems
Shows paranoia Provide structured routine.
Present food in consistent manner.
Serve foods in closed containers.
Do not put medicine in food.
Spits Evaluate chewing and swallowing ability.
Tell client not to spit.
Place client away from others who would be
offended.
Provide mealtime supervision.
Will not go into dining Ask why; change dining location.
room Provide a single dining partner versus a group.
Serve meals in room if needed.
HEAD TRAUMA OR NEUROTRAUMA
• Traumatic brain injury (TBI) refers to any of the following,
alone or in combination: brain injury, skull fractures,
extraparenchymal hemorrhage—epidural, subdural,
subarachnoid—or hemorrhage into the brain tissue itself,
including intraparenchymal or intraventricular hemorrhage.
• The annual incidence is estimated to be 200 per 100,000
people, with a peak frequency between 15 and 24 years of
age.
• Motor vehicle collisions are the major source of injury.
• Morbidity is high and headache is one of the most common
complaints.
• It is difficult to accurately predict neurologic recovery.
• Despite intensive intervention, long-term disability occurs in a
large portion of the survivors of severe head injury.
Pathophysiology
• Brain injury can be categorized as three types:
concussion, contusion, and diffuse axonal injury.
• A concussion is a brief loss of consciousness, less than
6 hours, with no damage found on computed tomography
(CT) or magnetic resonance imaging (MRI) scans.
• Microscopic studies have failed to find any evidence of
structural damage in areas of known concussion, although
evidence of change in cellular metabolism exists.
• A contusion is characterized by damaged capillaries and
swelling, followed by resolution of the damage.
• Large contusions may dramatically increase ICP and may
lead to ischemia or herniation.
Pathophysiology
• Large contusions may dramatically increase ICP and may lead
to ischemia or herniation.
• Contusions can be detected by CT or MRI scans.
• Diffuse axonal injury results from the shearing of axons by a
rotational acceleration of the brain inside the skull.
• Damaged areas are often found in the corpus callosum
(the bridge between the two hemispheres) and the upper,
outer portion of the brainstem.
• Skull fractures of the calvarium and the base are described in
the same manner as other fractures.
• Comminution refers to splintering of bone into many fragments.
• Displacement refers to a condition in which bones are displaced
from their original positions.
Pathophysiology
• Open or closed describes whether a fracture is exposed to
air.
• Open fractures dramatically increase the risk of infection
(osteomyelitis), and open skull fractures in particular carry an
increased risk for meningitis because the dura mater is often
violated.
• Epidural and subdural hematomas are often corrected by
surgical intervention.
• The volume of these lesions often displaces the brain tissue
and may cause diffuse axonal injury and swelling.
• When the lesion becomes large enough, it may cause herniation
of brain contents through various openings of the skull base.
• Consequent compression and ischemia of vital brain structures
often rapidly lead to death.
Medical Management
• The body’s response to stress from TBI results in production
of cytokines (interleukin-1, interleukin-6, interleukin-8,
and tumor necrosis factor) and inflammation .
• These are elevated in the body after head injury and are
associated with the hormonal milieu that negatively
affects metabolism and organ function.
• Some of the metabolic events include fever, neutrophilia,
muscle breakdown, altered amino acid metabolism,
production of hepatic acute-phase reactants, increased
endothelial permeability, and expression of endothelial
adhesion molecules.
• Specific cytokines tend to cause organ demise; tissue
damage
Medical Management
• Clinical findings of brain injury often include a transient decrease in level of
consciousness.
• Headache and dizziness are relatively common and not worrisome
unless they become more intense or are accompanied by vomiting.
• Focal neurologic deficits, progressively decreasing level of consciousness,
and penetrating brain injury demand prompt neurosurgical evaluation.
• Skull fractures underneath lacerations often can be felt as a “drop off” or
discontinuity on the surface of the skull and are readily identifiable by CT
scan.
• Basilar skull fractures are manifested by otorrhea(fluid leaking from the ear)
or rhinorrhea (salty fluid dripping from the nose or down the pharynx).
• Other signs include raccoon eyes and Battle’s sign—blood behind the
mastoid process.
• Basilar skull fractures may precipitate injuries to cranial nerves, which are
essential for chewing, swallowing, taste, and smell.
Medical Management
• Hematomas are neurosurgical emergencies because they
may rapidly progress to herniation of brain contents through the
skull base and to subsequent death.
• These lesions may present similarly, with decreased level of
consciousness, contralateral hemiparesis, and pupillary
dilation.
• These lesions damage brain tissue by gross displacement and
traction.
• Classically the epidural hematoma presents with progressively
decreasing consciousness after an interval of several hours
during which the patient had only a brief loss of
consciousness.
• Subdural hematoma usually features progressively decreasing
consciousness from the time of injury.
• The goal of nutrition therapy is to oppose the
hypercatabolism and hypermetabolism associated with
inflammation.
• Hypercatabolism is manifested by protein degradation,
evidenced by profound urinary urea nitrogen excretion.
• Nitrogen catabolism in a fasting normal human is only 3 to 5
g of nitrogen per day, whereas nitrogen excretion is 14 to 25
g of nitrogen per day in the fasting patient with severe
head injury.
• In the absence of nutritional intake, this degree of nitrogen
loss can result in a 10% decrease in lean mass within 7
days.
• A 30% weight loss increases mortality rate.
• Hypermetabolism contributes to increased energy
expenditure.
• Correlations between the severity of brain injury as
measured by the Glasgow Coma Scale and energy
requirements have been shown.
• The Glasgow Coma Scale is based on a 15-point
scale for estimating and categorizing the outcomes of
brain injury on the basis of overall social capability
or dependence on others.
• Replacement of 100% to 140% resting metabolism
expenditure with 15% to 20% nitrogen calories reduces
nitrogen loss.
• Immune enhancing nutrition formulas are available for
critically ill head-injured patients that are enhanced with
glutamine, arginine and omega-3 fatty acids.
SPINE TRAUMA AND SPINAL CORD INJURY
• Spine trauma encompasses many types of injuries,
ranging from stable fractures of the spinal column to
catastrophic transection of the spinal cord.
• A complete spinal cord injury (SCI) is defined as a lesion
in which there is no preservation of motor or sensory
function more than three segments below the level of the
injury.
• With an incomplete injury there is some degree of residual
motor or sensory function more than three segments
below the lesion.
Pathophysiology
• The spinal cord responds to insult in a manner similar to
the brain.
• Bleeding, contusion, and shorn axons appear first,
followed by a several-year remodeling process consisting
of gliosis and fibrosis.
• The location of the SCI and the disruption of the
descending axons determines the extent of paralysis.
• Tetraplegia (formerly known as quadriplegia) exists
when the injury to the spinal cord affects all four
extremities.
• When the SCI location results in only lower extremity
involvement, it is called paraplegia.
Medical Management
• Spinal cord injuries have numerous clinical
manifestations, depending on the level of the injury.
• Complete transection results in complete loss of function
below the level of the lesion, including the bladder and
sphincters.
• After the patient is stabilized hemodynamically, the
doctor evaluates the degree of neurologic deficit.
• Patients with suspected SCI are usually immobilized
promptly in the field.
• Complete radiographic evaluation of the spinal column
is obligatory in multitrauma and unconscious patients.
Medical Management
• In the awake patient, clinical evidence of spine
compromise is usually sufficient to determine the need for
further workup.
• CT and MRI are used to more accurately delineate bony
damage and spinal cord compromise. A dismal 3% of
patients with complete spinal cord insults recover
some function after 24 hours.
• Failure to regain function after 24 hours predicts a
poor prognosis for reestablishment of function in the
future.
• Incomplete spinal cord syndromes may have somewhat
better outcomes.
• Technologic advances in enteral and parenteral
feeding techniques and formulas have played a role in
maintaining nutrition status of these patients.
• Although the metabolic response to neurotrauma has
been studied extensively, the acute metabolic
response to SCI has not; but it is similar to other
forms of neurotrauma during the acute phase.
• Initially paralytic ileus may occur but often resolves
within 72 hours after injury.
• Because DHA and EPA have antioxidative,
antiinflammatory, antiapoptosis effects, patients may
benefit from fish oil supplementation.
• Individuals with SCI have significantly higher fat mass
and lower lean mass.
• Loss of muscle tone caused by skeletal muscle paralysis
below the level of injury contributes to decreased metabolic
activity, initial weight loss, and predisposition to
osteoporosis.
• Guidelines for accepted weights adjusted for paraplegia and
tetraplegia are as follows: the paraplegic should weigh 10 to
15 lb less than the ideal body mass index (BMI) would
indicate; the tetraplegic should weigh 15 to 20 lb less
than ideal weight dictated by the BMI.
• The higher the injury, the lower the metabolic rate; a
lower energy requirement occurs.
• Tetraplegic patients have lower metabolic rates than paraplegic
patients, proportional to the amount of denervated muscle in their
arms and legs, caused in part by the loss of residual motor
function.
• In the rehabilitation phase, tetraplegics may require approximately
25% to 50% fewer calories than conventional equations predict.
• Thus, these patients have the potential to become overweight.
• It has been proposed that obesity may slow the eventual rehabilitation
process by limiting functional outcome.
• As a consequence of bone loss resulting from the loss of
mineralization caused by immobilization, SCI is associated with
osteopenia and osteoporosis, and the prevalence of longbone
fractures increases.
• Adequate intake of vitamin D and calcium should be planned
without excessive daily intakes.
NEUROLOGIC DISEASES
• Adrenomyeloleukodystrophy
• Amyotrophic Lateral Sclerosis
• Epilepsy
• Guillain-Barré Syndrome and Chronic Inflammatory
Demyelinating Polyneuropathy
• Myasthenia gravis
• Multiple sclerosis
• Parkinson’s disease
The role of curcumin and resveratrol in
neuroprotection
Adrenomyeloleukodystrophy
• Adrenomyeloleukodystrophy (ALD) is a rare congenital enzyme
deficiency that affects the metabolism of very-long-chain fatty acids
(VLCFAs) in young men.
• This leads to accumulation of VLCFAs, particularly hexacosanoic acid
(C26:0) and tetracosanoic acid (C24:0) in the brain and adrenal
glands.
• It is an X-linked recessive disorder characterized by myelopathy,
peripheral neuropathy, and cerebral demyelination.
• The adult variant, adrenomyeloneuropathy, has chronic distal
axonopathy of spinal cord and peripheral nerves marked by cerebral
inflammatory demyelination; head trauma is an environmental
factor that is detrimental in those people genetically at risk.
• The mental and physical deterioration progresses to dementia,
aphasia, apraxia, dysarthria, and blindness.
Medical Management
• Clinical manifestations usually occur before age 7 and
may manifest as adrenal insufficiency or cerebral
decompensation.
• Dysarthria (impairment of the tongue or other muscles
needed for speech) and dysphagia may interfere with oral
alimentation.
• Bronzing of the skin is a late clinical sign.
• With adrenal insufficiency, replacement of steroids is indicated
which may improve neurologic symptoms and prolong life.
• Numerous therapies have been directed at the root of the
disorder but have been disappointing.
• The selective use of bone marrow transplant is one current
therapy; gene therapy holds promise for the future.
• Nutritional therapy by dietary avoidance of VLCFAs does
not lead to biochemical change because of endogenous
synthesis.
• A specialty altered fatty acid product, Lorenzo’s oil
(C18:1 oleic acid and C22:1 erucic acid), lowers the
VLCFA level.
• Although the clinical course is not significantly
improved, a slower decline in function may result.
Amyotrophic Lateral Sclerosis
• Amyotrophic lateral sclerosis (ALS), also known as Lou
Gehrig disease, is a neurodegenerative disorder affecting the
motor neurons in the central nervous system.
• ALS involves a progressive denervation, atrophy, and weakness
of muscles; hence the name amyotrophy.
• Men are affected more than women, and the average age of
onset is the mid-50s with 90% having no family history of the
disease.
• The cause of ALS is not clear.
• Thus there is no cure, and survival is typically 3 to 5 years after
disease onset.
• Risk factors related to occupation, trauma, diet, or
socioeconomic status are not consistent, although
environmental toxins have been suspected to play a role.
Pathophysiology
• The pathologic basis of weakness in ALS is the selective death of motor
neurons in the ventral gray matter of the spinal cord, brainstem, and
in the motor cortex.
• Clinical manifestations are characterized by generalized skeletal muscular
weakness, atrophy, and hyperreflexia.
• The typical presentation is lower motor neuron (weakness, wasting,
fasciculation) and upper motor neuron deficits (hyperactive tendon
reflexes, Hoffman signs, Babinski signs, or clonus).
• Muscle weakness begins in the legs and hands and progresses to the
proximal arms and oropharynx. As these motor nerves deteriorate, almost
all of the voluntary skeletal muscles are at risk for atrophy and complete
loss of function.
• The loss of spinal motor neurons causes the denervation of voluntary
skeletal muscles of the neck, trunk, and limbs, resulting in muscle
wasting, flaccid weakness, involuntary twitching (fasciculations), and loss
of mobility.
Pathophysiology
• Progressive loss of function in cortical motor neurons
can lead to spasticity of jaw muscles, resulting in slurred
speech and dysphagia.
• The onset of dysphagia is usually insidious.
• Swallowing difficulties usually follow speech difficulties.
• Although some weight loss is inevitable given the muscle
atrophy, consistent or dramatic loss may be an indicator of
chewing difficulties or dysphagia.
• Eye movement and eye blink are spared, as are the
sphincter muscles of the bowel and bladder; thus
incontinence is rare.
• Sensation remains intact and mental acuity is maintained.
Medical Management
• No currently known therapy cures the disease.
• Treatment with a high dose of methylcobalamin (B12) is
being studied to preserve muscle integrity.
• The ketogenic diet has shown positive results in disease
amelioration in mouse models.
• Although mechanical ventilation can extend the life of
patients, most decline this option.
• Quality of life is poor in advanced ALS and supportive
comfort measures are primarily used.
• There are decreases in body fat, lean body mass, muscle power,
and nitrogen balance and an increase in resting energy
expenditure as death approaches.
• Hypermetabolic status and increased resting energy expenditure
measurements have been noted.
• The relationship between dysphagia and respiratory status is
important.
• As ALS progresses, a progressive loss of function in bulbar and
respiratory muscles contributes to oral and pharyngeal
dysphagia.
• This results in the need for nutrition support, generally via a
gastrostomy tube.
• In late stages, when the respiratory status is impaired, feeding
tube placement is associated with more risk.
Nutritional and Metabolic Changes During the
Progression of Amyotrophic Lateral Sclerosis
Epilepsy
• Epilepsy is a chronic condition characterized by
unprovoked, recurring seizures.
• Seizures are caused by abnormal electrical activity of a
group of neurons.
Pathophysiology
• Most seizures begin in early life, but a resurgence occurs after
• age 60.
• A clinical workup usually reveals no anatomic abnormalities, and
the cause of the seizure may remain unknown (idiopathic).
• Seizures before age 2 are usually caused by fever,
developmental defects, birth injuries, or a metabolic disease .
• The medical history is the key component for suggesting further
avenues of diagnostic investigation and potential treatments,
especially in children.
• An electroencephalogram can help to delineate seizure activity.
• It is most helpful in localizing partial complex seizures.
Medical Management
• The dramatic tonic-clonic (grand mal) seizure is the
most common image of a convulsive seizure, yet
numerous classifications of seizures, each with a different
and often less dramatic clinical presentation, exist.
• A generalized tonic-clonic seizure typically involves the
entire brain cortex from its beginning phases.
• After such a seizure the patient wakes up slowly and will
be groggy and disoriented for minutes to hours.
• This is termed the postictal phase and is characterized by
deep sleep, headache, confusion, and muscle soreness.
Medical Management
• The absence seizure (petit mal)is also generalized in nature.
• A patient with absence seizures may appear to be
daydreaming during an episode, but he or she recovers
consciousness within a few seconds and has no postictal
fatigue or disorientation.
• Partial seizures occur when there is a discrete focus of
epileptogenic brain tissue.
• A simple partial seizure involves no loss of consciousness,
whereas a complex partial seizure is characterized by a
change in consciousness.
• Failure of partial seizure control may prompt consideration
of seizure surgery.
Medical Management
• Medications used in anticonvulsant therapy may alter the nutrition
status of the patient .
• Phenobarbital has been associated with decreased intelligence
quotient when used in children.
• It occasionally is considered for use after failure of other
antiepileptic drugs.
• Phenobarbital, phenytoin, and valproates interfere with intestinal
absorption of calcium by interfering with vitamin D metabolism in
the kidneys.
• Long-term therapy with these drugs may lead to osteomalacia in
adults or rickets in children, and vitamin D supplementation is
recommended.
• Folic acid supplementation interferes with phenytoin metabolism;
thus it contributes to difficulties in achieving therapeutic levels.
Medical Management
• Phenytoin, valproates, and phenobarbital are bound primarily to albumin
in the bloodstream.
• Decreased serum albumin levels limit the amount of drug that can be
bound.
• This results in an increased free drug concentration and possible drug
toxicity even with a standard dose.
• Absorption of phenobarbital is delayed by the consumption of food;
therefore administration of the drug must be staggered around mealtimes
if it is used.
• Continuous enteral feeding slows the absorption of phenytoin, thus
necessitating an increase in the dose to achieve a therapeutic level.
• Stopping the tube feeding 1 hour before and 1 hour after the phenytoin
dose was common practice in the past but is no longer
recommended.
• The phenytoin dose should be adjusted based on the tube feeding.
• The classic ketogenic diet, which has been in
existence since the 1920s, can be used for treatment
of all types of seizures .
• Originally designed using ratios of 4:1 or 3:1 (grams of fat
to nonfat) to achieve strong and consistent ketosis, less
restrictive versions are now available that can also be
effective.
• The modified ketogenic uses lower ratios (e.g., 1:1 and
2:1), modified Atkins, and the Low Glycemic Index
Treatment (LGIT) are also available for those who may
benefit from a less restricted approach.
• Glucose Transporter Type I Deficiency Syndrome (Glut-1
DS) and pyruvate dehydrogenase deficiency (PDHD)
are two genetically inherited disorders that typically
include seizures and are treatable with ketogenic diet
therapy.
• The diet also has been effective for other inherited
disorders in which seizures are also typical: glycogen
storage diseases, nonketotic hyperglycinemia, and
respiratory chain defects.
• Ketones provided by ketogenic diet therapy offer an
alternative fuel source which improves symptoms,
preserves neurons, and can prevent further decline.
• The ketogenic diet has minimal side effects, and risks of
the diet are low blood sugar, upset stomach at first
caused by the high amounts of fat, and constipation.
• The long-term risk of kidney stones is rare; elevated
serum cholesterol is usually temporary and disappears
with discontinuation of the diet; and growth, which is
sometimes slowed while on the diet, resumes at the
child’s normal rate.
• Although the diet is restrictive and requires continued
effort, it completely controls epilepsy in 10-15% of the
children whose seizures are otherwise uncontrollable.
• The diet is designed to create and maintain a state of ketosis.
• The beneficial effect in epilepsy may be caused by a change in neuronal
metabolism; ketones may inhibit neurotransmitters, thus producing an
anticonvulsant and neuroprotective effect in the brain.
• Initiation of the classic ketogenic diet in children typically begins under close
medical supervision, while administration of the more liberal versions
described earlier may begin at home with prior instructions.
• The classic ketogenic diet is determined in a ratio of 3:1 or 4:1, meaning
that there are 3 or 4 g of fat for every 1 g of protein and carbohydrate
combined in the diet.
• With a 4:1 ratio, the diet is calculated so that at least 90% of the
kilocalories are from fat.
• Goal level of ketones are patient specific; some individuals need to be
in the range of 35 to 60 mg/L (4 to 7 mmol/L) for seizure control while others
may achieve control with little or no ketosis, which is typical with the
liberal diets (modified ketogenic of 1:1 and 2:1 ratios, and LGIT).
Guillain-Barré Syndrome and Chronic
Inflammatory Demyelinating Polyneuropathy
• Guillain-Barré Syndrome (GBS) and chronic
inflammatory demyelinating polyneuropathy (CIDP) are
acquired immune-mediated inflammatory disorders of the
peripheral nervous system.
• The common causative organisms are Campylobacter
jejuni and Mycoplasma spp.
•
Pathophysiology
• Relatively symmetric weakness with paresthesia usually begins in
the legs and progresses to the arms.
• The loss of function in affected nerves occurs because of
demyelination.
• Myelin is the specialized fatty insulation that envelops the
conducting part of the nerve, the axon.
• In GBS the immune system recognizes myelin and mounts an
attack against it.
• Presumably myelin shares a common characteristic with the
pathogen from the antecedent infection; thus the immune
system cannot differentiate what is foreign (the pathogen)
from what is native (myelin).
• When the nerve is demyelinated, its ability to conduct signals is
severely impaired, resulting in neuropathy.
Medical Management
• GBS reveals itself in a matter of days.
• The most common sequence of symptoms is areflexia (absence of reflexes),
followed by proximal limb weakness, cranial nerve weakness, and respiratory
insufficiency.
• These symptoms normally peak by 2 weeks but may progress up to 1 month.
• Medical diagnosis is ordinarily made on clinical grounds, but nerve conduction
studies are also beneficial.
• Before the clinical course is apparent, myelopathic disorders must be
considered.
• Because of the precipitous progression of vital capacity and swallowing function
may rapidly deteriorate such that intensive care is sometimes necessary.
• Intubation and respiratory support should be instituted early in respiratory
decline to avoid the need for resuscitation.
• Plasmapheresis, the exchange of the patient’s plasma for albumin, is often
helpful to reduce the load of circulating antibodies. Intravenous immunoglobulin
or steroids have been shown to be of benefit.
• Guillain-Barré syndrome evolves quickly; during the
acute stage, the metabolic response of GBS is similar to
the stress response that occurs in neurotrauma.
• Energy needs assessed by indirect calorimetry may be
as high as 40 to 45 kcal/kg and protein needs twice
the usual amount.
• Supportive nutritional care should be offered to attenuate
muscle wasting.
• For a small percentage of patients, oropharyngeal
muscles may be affected, leading to dysphagia and
dysarthria.
Myasthenia Gravis
• Myasthenia Gravis (MG)is the most well-known disorder of the
neuromuscular junction.
• The neuromuscular junction is the site on the striated muscle
membrane where a spinal motor neuron connects. Here the
signal from the nerve is carried to the muscle via a submicron-size
gap, a synapse.
• The molecule that carries the signal from the nerve ending to
the muscle membrane is acetylcholine (Ach), and acetylcholine
receptors (AchRs) populate the muscle membrane.
• These receptors translate the chemical signal of Ach into an
electrical signal that is required for contraction of muscle fibers.
• MG is one of the most well-characterized autoimmune diseases,
a class of disorders in which the body’s immune system raises a
response to AchRs.
Pathophysiology
• In MG the body unwittingly makes antibodies to AchR.
• These antibodies are the same that fight off colds and give
immunity.
• The AchR antibodies bind to AchR and make them unresponsive
to Ach.
• There is no disorder of nerve conduction and no intrinsic disorder
of muscle.
• The characteristic weakness in MG occurs because the signal of
the nervous system to the muscle is garbled at the
neuromuscular junction.
• Patients with MG commonly have an overactive thymus gland.
This gland resides in the anterior thorax and plays a role in
the maturation of B-lymphocytes, the cells that are charged
with synthesizing antibodies.
Pathophysiology
• Relapsing and remitting weakness and fatigue, varying
from minutes to days, characterize MG.
• The most common presentation is diplopia (double vision)
caused by extraocular muscle weakness, followed by
dysarthria, facial muscle weakness, and dysphagia.
• Dysphagia or swallowing disorders (resulting from fatigue
after mastication) may cause malnutrition.
• Less commonly, proximal limb weakness in the hips and
shoulders may be present.
• Severe diaphragmatic weakness can result in respiratory
difficulty.
• No involvement of sensory nerves occurs
Medical Management
• Anticholinesterases are medicines that inhibit
acetylcholinesterase, thus serving to increase the amount
of Ach in the neuromuscular junction.
• Corticosteroids are immunosuppressive.
• Removal of the thymus results in symptomatic
improvement in most patients.
• Chewing and swallowing often are compromised in MG.
• Because this compromise occurs with fatigue, it is important
to provide nutritionally dense foods at the beginning of
meals before the patient tires.
• Small, frequent meals that are easy to chew and swallow are
helpful.
• Difficulties holding a bolus on the tongue also have been
observed, suggesting that foods that do not fall apart
easily may be better tolerated.
• For patients treated with anticholinesterase drugs, it is
crucial to time medication with feeding to facilitate optimal
swallowing.
• Physical activity should be limited before mealtime to ensure
maximum strength to eat a meal.
• It is also important not to encourage food consumption
once the patient begins to fatigue because this may
contribute to aspiration.
• If and when respiratory crisis occurs, it is usually temporary.
Nutrition support via a tube may be implemented in the
interim to assist in maintaining vital functions of the patient
until the crisis subsides.
• Once extubated, a swallow evaluation using cinefluoroscopy
is appropriate to assess the degree of deglutitory
dysfunction(swallowing irregularity) or risk of aspiration
associated with an oral diet.
Multiple Sclerosis
• Multiple sclerosis (MS) is a chronic inflammatory disorder of
the central nervous system (CNS) and is one of the most
common causes of nontraumatic disability among young
and middle-aged adults.
• MS affects the CNS and is characterized by destruction of
the myelin sheath, the function of which is transmission of
electrical nerve impulses.
• Multiple areas of optic nerves, spinal cord, and brain
undergo “sclerosis,” whereby myelin is replaced with sclera
or scar tissue.
• No single test can ascertain whether a patient has MS;
however, diagnostic criteria (McDonald criteria) were
developed for use by practicing clinicians.
Pathophysiology
• The precise cause of MS remains undetermined.
• A familial predisposition to MS has been noted in a
minority of cases.
• Geographic latitude and diet are therefore implicated.
• Epidemiologic studies have linked the incidence of MS to
geographic location and sunshine exposure.
• Studies have shown that people born in an area with a
high risk of MS who then move —or migrate—to an area
with a lower risk before the age of 15 assume the risk of
their new area.
Pathophysiology
• There is growing evidence that vitamin D may play a role.
• The degree of sunlight exposure catalyzes the
production of vitamin D in the skin.
• Vitamin D produced by the skin is eventually metabolized
to vitamin D₃ which is a selective immune system
regulator and may inhibit MS progression.
• The evidence is also growing that smoking plays an
important role in MS.
• Studies have shown that smoking increases a person’s
risk of developing MS and is associated with more severe
disease and more rapid disease progression.
Medical Management
• Fluctuating symptoms and spontaneous remissions make
treatments difficult to evaluate.
• Currently no proven treatment for changing the course of MS,
preventing future attacks, or preventing deterioration exists.
• Initially recovery from relapses is nearly complete, but over
time, neurologic deficits remain.
• Therefore measures to maximize recovery from initial attacks
or exacerbations, prevent fatigue and infection, and use all of
the available rehabilitative measures to postpone the
bedridden stage of disease are imperative.
• Physical and occupational therapies are standard for
weakness, spasticity, tremor, uncoordination, and other
symptoms.
Medical Management
• Drugs for spasticity can be initiated at a low dose and cautiously
increased until the patient responds.
• Physical therapy for gait training and range-of-motion exercises
helps.
• Steroid therapy is used in treating exacerbations;
adrenocorticotropic hormone (ACTH) and prednisolone are the
drugs of choice.
• However, treatment is not consistently effective and tends to be more
useful in cases of less than 5 years’ duration. Side effects of short-term
steroid treatment include increased appetite, weight gain, fluid
retention, nervousness, and insomnia.
• Reduced cerebrospinal fluid and serum levels of vitamin B12 and folate
have been noted in MS patients who receive high-dose steroids.
• Methotrexate also may be used with ACTH, causing anorexia and
nausea.
• Several dietary regimens for managing MS have been studied, all
of which have yielded equivocal results.
• Various diets such as allergen-free, gluten-free, pectin-free,
fructose-restricted, raw food diet, megadoses of micronutrients,
zinc phosphates with calcium, and other combinations have not
been proven effective.
• Restriction of saturated fat has been evaluated by several
researchers but with inconclusive results.
• Vitamin D status should be assessed by measuring 25-hydroxy
vitamin D, and supplementation may be warranted.
• Neurogenic bowel can cause either constipation or diarrhea, and
incidence of fecal impaction is increased in MS.
• A diet that is high in fiber with additional prunes and adequate fluid
can moderate both problems.
Parkinson’s Disease
• Parkinson’s disease (PD) is a progressive, disabling,
neurodegenerative disease, first described by James
Parkinson in 1817.
• PD is characterized by slow and decreased movement,
muscular rigidity, resting tremor, postural instability, and
decreased dopamine transmission to the basal ganglia.
• Although the natural history of this disease can be
remarkably benign in some cases, approximately 66% of
patients are disabled within 5 years, and 80% are
disabled after 10 years.
• It most commonly occurs between the ages of 40 and
70.
Pathophysiology
• PD is caused by the progressive impairment or deterioration
of neurons (nerve cells) in an area of the brain known as
the substantia nigra.
• When functioning normally, these neurons produce the
vital brain chemical known as dopamine.
• The cause of PD is unknown, but several factors appear to
play a role.
• The presence of Lewy bodies, which are clumps of specific
substances within brain cells, are microscopic markers of
PD.
• Lewy bodies are proteins found in abundance in the
brainstem area that deplete the neurotransmitter dopamine.
Pathophysiology
• The role of endogenous toxins from cellular oxidative
reactions has emerged because aging has been
associated with a loss of neurons containing dopamine
and an increase in monoamine oxidase.
• When metabolized (enzymatic oxidation and
autoxidation), dopamine produces endogenous toxins
(hydrogen peroxide and free radicals), causing
peroxidation of membrane lipids and cell death.
• In the presence of an inherited or acquired predisposition,
severe oxidative injury can lead to substantial loss of
dopaminergic neurons similar to that observed in PD.
Pathophysiology
• Several other environmental factors also have been implicated as
causal factors of PD.
• The connection between smoking and a lowered risk for PD has been
evaluated, but results are inconsistent.
• In older patients, drug-induced PD may occur as a side effect of
neuroleptics or metoclopramide.
• Dairy products have been linked to PD.
• A meta-analysis of dairy intake and PD risk found a 17% increase in
PD for every 200 g/day increment in milk intake.
• PD has also been linked to the exposure to different metals and
industrial compounds (manganese, lead, copper, iron, zinc,
aluminium, or amalgam).
• Nutrient-related findings are biologically plausible and support the
hypothesis that oxidative stress may contribute to the pathogenesis of
PD.
Medical Management
• The “classic triad” signs—tremor at rest, rigidity, and
bradykinesia—remain the criterion for medical
diagnosis.
• However, it was well over a century before l-dopa (a
precursor to dopamine) was introduced for controlling
symptoms.
• Exelon, a cholinesterase inhibitor, was approved by
the FDA in 2006 for use in mild to moderate PD
dementia.
• Pharmacotherapy agents, surgical interventions, and
physical therapy are the best adjunctive therapies.
• The primary focus of nutrition intervention is to optimize dietary
intake particularly to maintain muscle mass for strength and
mobility.
• Nutrition intervention should also focus on drug-nutrient
interactions, especially between dietary protein and L-dopa.
• Side effects of medications for PD include anorexia, nausea,
reduced sense of smell, constipation, and dry mouth.
• To diminish the gastrointestinal side effects of L-dopa, it should be
taken with meals.
• Foods that contain natural L-dopa such as broad beans (fava
beans) should be avoided.
• For some patients dyskinesia may be reduced by limiting dietary
protein at breakfast and lunch and including it in the evening meal.
• Fiber and fluid adequacy lessen constipation, a common
concern for persons with PD. Pyridoxine (vitamin B6) has a
possible interaction with L-dopa.
• Decarboxylase, the enzyme required to convert L-dopa to
dopamine, depends on pyridoxine.
• If excessive amounts of the vitamin are present, L-dopa may
be metabolized in the periphery and not in the CNS, where its
therapeutic activity occurs.
• Therefore vitamin preparations containing pyridoxine should not
be taken with doses of L-dopa.
• Interactions between pyridoxine and aspartame should be
considered as well.
• In addition, manganese should be carefully monitored to avoid
excesses above DRI levels.
• Antiinflammatory and neuroprotective effects come from
phenolic compounds, such as resveratrol from grapes
and red wine, curcumin from turmeric, apocynin from
Picrorhiza kurroa, and epigallocatechin from green tea.
• Sufficient intake of vitamin D₃ and omega-3 fatty acids
should be recommended.

Medical Nutrition Therapy For Neurologic Disorders

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Medical Nutrition Therapy For Neurologic Disorders

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MEDICAL NUTRITION THERAPY

FOR NEUROLOGIC DISORDERS

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