Nutri Sci 631 Exam 3

Types of acute neurologic trauma

Stroke

Aneurysm

TBI

Spinal cord injuries

Progressive neurodegenerative diseases

Parkinsons

AD

MS

ALS
Myasthenia Gravia

Guillain-Barre Syndrome

Stroke etiology

Interruption of blood flow to NS caused by blockage or rupture

Stroke classifications

Ischemic

Hemorrhagic

Ischemic stroke

Obstruction or blockage of blood vessel in the brain

80% of strokes

Transient ischemic attacks

Episodes of ischemia that lead to stroke-like symptoms that resolve in 24 hours

Mini-strokes

Hemorrhagic strokes

Rupture of blood vessel in the brain

Less common

MNT for stroke

Acute phase: nutrition support is needed, where nutrients provided parenterally or enterally

Rehab: combating dysphagia

7 health metrics for optimal CV health

Smoking

BMI

PA

Healthy diet pattern

Cholesterol

BP

Blood sugar

Stroke pathophysiology

Lack of blood supply → hypoxia → cell death

Clinical manifestations of stroke

Varies by brain area affected

Change in mental status

FAST

What does FAST stand for in strokes

Facial drooping

Arm weakness

Slurred speech

Emergency services

Stroke diagnosis

Acute stroke evaluation with NIHSS

Brain imaging asap to determine characteristics of the stroke

What does NIHSS evaluate

Consciousness

Visual loss

Sensory loss

Language

Motor skills

tPA

Tissue plasminogen activator

Produced normal after vascular injury to dissolve clots

Recombinant tPA

Thrombolytic drug created by DNA technology

Improves patient outcomes if given a few hours after a stroke

Aspirin role for stroke

Antiplatelet drug

Reduces risk of recurrent ischemic stroke

What does long-term stroke therapy focus on

Neuroprotection (protect neurons from ongoing damage)

Rehab (prevent complications, minimize impairments, maximize function)

Causes of neurodegenerative diseases

Impaired communications within the nervous system

Damage to neurons or altered NTs

Excitatory NTs

ACh

Glutamate

Serotonin

Inhibitory NTs

Dopamine

GABA

Glycine

Serotonin

Impairments from neurologic diseases

Weakened muscle strength and poor body coordination

Ataxia

Hemiparesis

Tremor

Rigidity

Bradykinesia

Vision impairment

Cognitive impairment

Ataxia

Lack of muscle control or coordination of voluntary movements

Hemiparesis

Weakness/paralysis on one side of body

Often leads to postural instability

Tremor

Involuntary, rhythmic shaking

Rigidity symptom

Stiffness due to increased muscle tone

Bradykinesia

Slowed/delayed body movements

Hemianopsia

Blindness in half of visual field

Types of cognitive impairment from neurologic diseases

Memory loss

Confusion

Trouble learning new things, concentrating, making decisions

Apraxia

Apraxia

Inability to perform familiar movements on command

Muscle function is normal and command is understood and person is willing to perform movement

Like putting socks on after shoes

Nutritional consequences of neurological impairment

Problems with access to food (meal prep/cooking, feeding)

Difficulties eating (chewing, swallowing)

Management for food access problems

Provide convenient, pre-packaged single-serving food items

Simplify cooking

Arrange home delivery for meals

Calorie and nutrient dense supplements

Supervise and assist when eating

Adaptive utensils/cups

Normal swallowing requires

Integration of cranial nerves

Synchronized muscle movements

Dominance over respiratory system

Invoking autonomic system

Phases of swallowing

Oral prep

Oral transit

Pharyngeal

Esophageal

Oral phase of swallowing

Voluntary

Prep phase then transit phase

Oral prep phase of swallowing

Mastication

Food mixed with saliva

Tongue movement

Jaw motion

Formation of bolus

Oral transit phase of swallowing

Bolus propelled to rear of oral cavity

Reaches pharynx to initiate swallowing

Pharyngeal phase of swallowing

Involuntary

Early: Bolus → pharynx → stimulates nerve impulses to swallowing center in brain

Middle: Nasal passage sealed, epiglottis tilts up, glottis sealed, respiration stops momentarily

Late: UES opens, food passes into esophagus without entering trachea, breathing resumes

Esophageal phase of swallowing

Involuntary

Bolus moves from oral cavity to stomach

Peristaltic waves move bolus from proximal to distal end of esophagus

LES opens, food enters stomach, swallowing complete

Dysphagia

Difficulty swallowing

Cause by many conditions

Dysphagia in oral phase manifestations

Drooling, spitting, coughing, sore mouth

Food pocketing

Poor bolus formation, slow oral transit time

Dysphagia in pharyngeal phase

Gagging

Choking

Lump in throat sensation

Aspiration

How can people compensate for impaired swallowing

Chin tuck

Tilt head to one side when swallowing

What may change in terms of eating habits for people with dysphagia

Eat slower

Leave food on plate

Changed food preference

Aspiration

Entrance of materials below level of vocal cords into airways

Aspiration symptoms/signs

Coughing during/after swallowing

Wet gurgled voice

Fever

Chest sounds

Pneumonia or infection

How is dysphagia diagnosed by MBS

Modified barium swallow performed by SLP

Eat/drink food/liquids mixed with barium

Assess bolus formation, transit time, clearance, breathing/swallowing coordination, UES function, aspiration

How is dysphagia diagnoses by FEES

Fiberoptic endoscopic evaluation of swallowing can be used at bedside

Easy to use and well tolerated

Primarily assesses pharyngeal phases

Correlates well with MBS in pharynx and pharyngeal-laryngeal area

Oral phase abnormalities from swallow studies

Decreased lip tone, lip closure, poor tongue control

Decreased rotary jaw movement or range of jaw motion

Mucositis, xerostomia

Mucositis

Mouth sores

Xerostomia

Dry mouth

Pharyngeal phase abnormalities in swallow studies

Delayed/absent swallow reflex

Decreased bolus movement through pharynx

Decreased laryngeal closure

Esophageal phase abnormalities in swallow studies

Decreased esophageal peristalsis

Esophageal obstruction

Dysphagia severity scale

0-6 (normal, minimal, milk, mild-moderate, moderate, moderately severe, severe)

Speech/physical therapies for dysphagia

Oral exercises (chin tuck, tongue strengthening)

Dietary therapy for dysphagia

Dysphagia diet (modified solid food texture and liquid consistency, increased caloric and nutrient density in diet, adjust meal frequency, supplementation)

Eating environment modifications for dysphagia

Decrease distractions during mealtimes

Ensure proper sitting position

Avoid laying down <2hr after eating

Supervise and assist while eating

Nutritional implications of dysphagia

Reduced dietary intake

Weight loss

Nutrient deficiencies

Nutrition assessment and diagnosis for dysphagia

Inadequate oral intake

Malnutrition (anthropometric or biochemical)

NFPE for swallow ability

What are the most challenging foods/liquids for people with dysphagia

Dry solids

Thin liquids

How can food texture be modified for people with dysphagia

Small pieces and soft food reduce risk of choking, preserve energy

Pureed easiest to swallow but least appealing

How can liquid thickness be modified for people with dysphagia

Thin liquid most easily aspirated since most oropharyngeal muscle control and fast coordination

Thickening agents alter liquid thickness

2 dysphagia diet frameworks

NDD

ISSI

IDDSI framework

0- thin liquids

1- slightly thick liquids

2- mildly thick liquids

3- moderately thick liquids and liquidized food

4- extremely thick liquids and pureed food

5- minced and moist food

6- soft and bite sized food

7- ez chew or regular

NDD levels for food (and comparison to IDDSI)

Dysphagia pureed (pureed)

Dysphagia mechanically altered (minced and moist)

Dysphagia advanced (soft and bite sized)

NDD liquid levels (and comparison to IDDSI)

Thin (thin)

Naturally thick liquids (slightly thick)

Nectar thick (mildly thick)

Honey thick (moderately thick)

spoon thick (extremely thick)

Parkinsons disease definition

Brain disorder that leads to tremors, rigidity, bradykinesia, and postural instability characterized by difficulty with walking, balance and coordination

Parkinsonism

Clinical syndrome characterized by PD-like symptoms

Multiple causes

PD cause

Loss of dopamine producing cells and reduced dopamine synthesis

Parkinsonism causes

Multiple

Brain disorders, head injuries, metabolic diseases, drugs, toxins, etc

Risk factors for PD

Age (increases with age, rarely diagnosed before 40)
Genetics contribute to EOPD (only 10-15%)

PD Epidemiology

Prevalence: 1% of people >70

Incidence: ~60k new diagnoses/year

50% more common in men

Pathophysiology of PD

Neuronal death in substantia nigra → decreased DA → imbalance of DA and GABA

Motor symptoms of PD

Resting tremor, rigidity, bradykinesia (classic 3)

Stooped posture

Shuffling gait

Change in facial expressions

Micrographia

Micrographia

Words written very small and crowded together

Size of handwriting decreases as they write

PD Diagnosis

No specific diagnostic test

Diagnosis based on symptoms and response to a trial period of levodopa

PD Medication treatments

L-dopa

DA agonists

Inhibitors of enzymes that metabolize L-dopa and DA (AAAD, COMT, MAO-B inhibitors)

Combination drugs

Levodopa

Precursor of DA

Works better because it can cross BBB

DA Agonists

Mimic DA and act directly on DA receptors

Combination drugs for PD

lower dosage of Levodopa and DA agonists/inhibitors

Sinemet (L-dopa and AAAD inhibitor)

Other PD treatments (other than medication)

Surgery (deep brain stimulation, pallidotomy, thalamotomy)

Neuroprotective treatments (controversial; vit E, CoQ)

Deep brain stimulation

Implantation of a battery device that electrically stimulates brain

Pallidotomy and thalamotomy goal

Control tremor symptoms by destroying particular brain cells

Levodopa metabolism

Transported into blood, crosses BBB

Converted to DA

AAAD and COMT inhibitor mechanism

Reduce breakdown of L-dopa in the peripheral blood

Higher amount of L-dopa that can reach the brain

MAO-B inhibitor mechanism

Reduce degradation of DA into its downstream metabolites

PD nutrition implications

Dysphagia

Managing drug-nutrient interactions (GI side effects, protein, vit B6)

How does protein and B6 affect PD treatment

Reduce amount of L-dopa availability to the brain

B6 may expedite the conversion (since it is a cofactor) in the blood, not allowing the L-dopa to reach the brain

Protein redistribution diet in PD role

AA (F analogue) compete with L-dopa for absorption and transport in GI tract and blood

Lower protein intake → increased L-dopa absorbed in GI → increased L-dopa transported into brain

PRD guidelines

Adequate but not excessive protein in diet

Low protein for breakfast and lunch, high in dinner

L-dopa 15-30 mins before meals

Decrease on-off fluctuations during daytime

PRD case-control study population

600 cases with PD and normal cognitive function

600 control

PRD case control study nutritional data

Fairly comprehensive nutritional assessment

Anthropometry, dietary habits (including protein), PA, TDEE, and REE

PRS case control study GI and PD symptoms

Constipation

Duration and severity of disease

Daily dose of L-dopa

Motor symptoms (dyskinesia, fluctuations)

PRD case control study results

Adherence group have lower L-dopa dosage but off-state score better

Protein intake lower in adherence group

Higher protein means higher L-dopa dosage

Adherence means lower L-dopa dosage

What is the suggestion for total protein intake for PRD diet

0.8 g/kg

Also RDA

What are concerns with PRD and low protein intake

May increase risk of weight loss

Increased risk of micronutrient deficiencies (Zn, Ca, B12)

Seizure

Disruption in electrical communication of the brain

Epilepsy

Chronic neurologic disorder defined as having >2 unprovoked seizures at least 24 hours apart

Primary generalized seizures and types

Affect the entire brain

Tonic-clonic seizures (loss of conscious, involuntary movement)

Absence seizures (lose awareness, look dazed)

Partial seizures and types

Involve only one area of the brain

Simple seizures (maintained consciousness)

Complex seizures (loss of conscious, person confused)