Download Topic 25 Nutritional Support In Neurological diseases

Nutritional Support
in Neurological Diseases
Topic 25
Module 25.1
Nutritional and Metabolic Consequences of Neurological
Diseases
Irene Breton
Endocrinology and Nutrition
Nutritional Support Unit
Hospital General Universitario Gregorio Marañón
Dr Esquerdo 46, 28007 Madrid, Spain
Learning Objectives
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To identify different factors that may favour malnutrition in patients with
neurological diseases, including the effect of drug therapy;
To know the gastrointestinal consequences of neurological disease, that are
relevant for nutritional support;
To know the main characteristics of dysphagia and its relevance for nutritional
support in patients with neurological diseases;
To understand the effect of neurological disease on energy expenditure;
To recognize the clinical consequences of malnutrition in patients with
neurological diseases.
Contents
1. Introduction
2. Factors leading to malnutrition in chronic neurological diseases
2.1. Decreased intake
2.2. GI dysfunction
2.3. Energy expenditure disturbance
2.4. Effect of drug therapy
3. Nutritional consequences of chronic neurological diseases
4. Summary
5. References
Key Messages
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Diet and nutritional factors have been involved in the pathogenesis of
neurological diseases;
Malnutrition is common in neurological patients and can increase the risk of
mortality, clinical complications and disability;
A decreased intake is one of the main factors leading to malnutrition in
patients with neurological disease;
Oropharyngeal dysphagia is common in these patients. Both efficacy and
security of swallowing can be impaired, leading to malnutrition, dehydration
and aspiration pneumonia;
Neurological disorders may be associated with alterations in resting energy
expenditure, leading to hyper or hypo-metabolism. Nutritional status, body
composition and altered neuromuscular function can be responsible for these
alterations.
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1. Introduction
There is a close relationship between nutrition and neurological diseases. Some
nutritional factors may be involved in the pathogenesis of neurological diseases (1).
Diet can favour atherosclerosis and neurological ischaemic disease. High saturated
fat and salt intake and low fruit and vegetable diet have been related to a higher risk
for stroke (2). Vitamin D deficiency and insufficiency have been associated with
multiple sclerosis (3). The aetiology of amyotrophic lateral sclerosis (ALS) is far from
clear; some dietary factors, including high fruit and vegetable intake, have been
reported to decrease the risk of the disease in case-control studies (4). Meta-analyses
of cohort studies, comprising more than one million subjects, have shown a protective
role of omega-3 fatty acid (5) and carotenoid (6) intake on ALS. Epidemiological
studies found that high intake of fruits, vegetables and fish was inversely associated
with risk of Parkinson’s disease (PD), and dietary patterns characteristic of a
Mediterranean diet are emerging as a potential neuroprotective alternative (7).
Higher adherence to the Mediterranean diet may protect from Alzheimer’s Disease in
patients with mild cognitive impairment (8). Peripheral neuropathy can be due to
vitamin deficiency (thiamine, B6).
Neurological patients are at increased nutritional risk of malnutrition and
micronutrient deficiency when intake is low or metabolic rate is high. Alternatively
obesity may occur due to immobility and reduced total energy expenditure.
Patients with neurological diseases comprise 15 percent of acute care hospital
inpatients, over 30 percent of rehabilitation centre inpatients and 50 percent of
nursing home patients. Malnutrition can increase mortality, decrease the efficacy of
the rehabilitation process and increase the risk of disability in these patients.
In this module we will describe the different factors that may favour malnutrition in
neurological patients and the clinical consequences of this common complication.
Acute neurological diseases
Infectious, vascular, or immunological disorders, and also trauma can cause acute
neurological disease. The nutritional and metabolic consequences of acute CNS
trauma (brain trauma and spinal cord injury) have been studied for many years, as
nutritional impairment is a significant prognostic factor in these patients. Traumatic
brain injury (TBI) is a major cause of disability, death and economic cost to our
society. Brain and spinal cord injury patients are at nutritional risk, and clinical
guidelines recommend nutritional screening to identify those patients who require
more formal nutritional evaluation and support (9, 10). There is evidence suggesting
that malnutrition increases mortality rates in ABT patients.
Nutritional support is considered a critical component of care for patients with CNS
trauma, and is a factor contributing to survival and optimal rehabilitation (11).
Malnutrition is common in patients with acute stroke and is associated with a higher
mortality, poor outcome and more disability (12). Nutritional support, with adapted
oral diet, oral supplements or enteral nutrition, may be necessary.
Chronic neurological diseases
Patients with chronic neurological disease are at nutritional risk. Several factors may
be involved, including decreased intake and increased energy expenditure. Some of
these diseases are briefly described:
Dementia is a syndrome of many causes and is defined as an acquired deterioration
in cognitive abilities that impairs the successful performance of activities of daily
living. Alzheimer’s disease is the most common cause of dementia in western
countries and is the cause in more than half of demented patients, followed by
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neurological ischaemic disease. Weight loss is a very common finding in advanced
dementia and is related to a worse prognosis (13).
Parkinson’s disease is one of the most frequent neurological diseases, affecting 1%
of individuals over age 55. Parkinson’s disease results from dopamine depletion in
the brain, leading to the characteristic symptoms of the disease: tremor, rigidity and
bradykinesia. As the disease progresses, other symptoms become evident, including
dysphagia, monotonous speech, impaired gastrointestinal motility, fatigue,
depression and cognitive impairment (14).
Amyotrophic lateral sclerosis (ALS) is the most common adult-onset motor neurone
disease (15). It has a prevalence of 3-4 cases:100,000 and is a progressive
neurodegenerative disorder, involving motor neurons in the cerebral cortex,
brainstem and spinal cord, presenting with a combination of upper and lower motor
neurone signs (16). It is a purely motor syndrome, without clinically significant visual,
sensory, autonomic, sphincter or early cognitive dysfunction. Bladder and bowel
function is usually preserved. Bulbar onset is associated with a worse prognosis.
Multiple sclerosis is a demyelinating disorder characterized by inflammation and
selective destruction of central nervous system myelin; the course can be relapsingremitting or progressive. Its prevalence can be 250:100,000 in Northern Europe. It
is the second most common cause of neurological disability (after trauma) in young
adults. Weight loss in these patients can be due to decreased intake, dysphagia and
depression. Some patients experience weight gain and obesity due to immobility and
steroid drug therapy.
Peripheral neuropathy, neuromuscular diseases (such as myasthenia gravis),
muscular dystrophy, and other muscle diseases complete the spectrum of
neurological diseases. All of them can have metabolic and nutritional consequences.
2. Factors Leading to Malnutrition in Chronic Neurological
Diseases
2.1 Decreased Intake
The ingestion of food is a complex process. Some patients are not able to handle
cutlery properly, or have difficulty in chewing or swallowing.
Depression is common in chronic neurological disease, affecting up to 40% of patients
and may contribute to malnutrition risk. Patients with impaired cognitive function
are also at increased risk of malnutrition, due to their impaired ability to find, buy
and prepare food. Apraxia, a common symptom of Alzheimer’s disease, can also
decrease food intake. Self-imposed or improperly prescribed dietary restriction can
also induce malnutrition. Patients with dysarthria can have difficulty in
communicating needs. Dyspnoea can get worse in relation to food intake.
Dysphagia
Dysphagia is defined as difficulty or discomfort during swallowing, i.e. the progression
of the alimentary bolus from the mouth to the stomach. Dysphagia is classified as
oesophageal or oropharyngeal, and from a functional point of view, as organic or
functional.
Normal swallowing comprises four stages:
1. The oral preparatory stage is voluntary, ie mastication and bolus formation;
2. The oral stage is also voluntary. Bolus is propelled by the tongue;
3. The pharyngeal phase is involuntary.
An activation of pharyngeal;
mechanoreceptors sends information to the CNS and triggers the pharyngeal
swallowing motor pattern. An elevation of the soft palate closes the
nasopharynx. The airway is then closed by elevation and anterior
displacement of the hyoid bone, and by descent of the epiglottis and vocal
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cord closure. The upper oesophageal sphincter opens and there is a
contraction of the pharyngeal constrictor muscles;
4. The oesophageal phase begins with the opening of the upper oesophageal
sphincter, which is followed by oesophageal peristalsis.
The main symptoms of dysphagia are coughing, choking or drooling with swallowing,
a characteristically wet-sounding voice, changes in breathing when eating or
drinking, frequent respiratory infections and known or suspected aspiration
pneumonia.
The prevalence of oropharyngeal functional dysphagia in neurological patients is very
high: it includes more than 30% of patients with stroke; it affects 40% of patients
with myasthenia gravis and up to 84% of patients with Alzheimer’s disease (17).
Dysphagia in Parkinson’s disease is a consequence of rigidity and bradykinesia, and
can affect 50-82 % of patients, being more prevalent in late-stage disease (18).
Dysphagia is a common finding in ALS patients, especially those with bulbar
involvement. It is one of the presenting symptoms in 10-30% of ALS patients and
affects all patients as the disease progresses; it generally follows a few months after
initial speech impairment. Bulbar muscle involvement is associated with labial and
lingual dysfunction, palatine incompetence, pharyngeal weakness, difficulty in
triggering the swallowing reflex and impairment of laryngeal elevation during
swallowing. The tongue is usually involved before the lips or jaw (19).
In patients with multiple sclerosis, the symptoms of dysphagia can be temporary, for
example, during a period of relapse. It may affect 44% of patients.
The clinical evaluation of neurological patients with dysphagia should include:
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A comprehensive clinical and neurological evaluation.
The use of structured questionnaires, e.g. EAT-10 (20), that is able to
differentiate safe and unsafe swallowing in ALS (21), Parkinson’s disease and
Alzheimer’s disease (22). It is especially useful in chronic neurological
diseases.
Bed-side clinical evaluation of swallowing (23)
o Water swallow test (3 ounce = 90ml). Can also be performed using
oximetry.
o Volume-viscosity swallow test (V-VST), that has shown 83.7%
sensitivity and 64.7% specificity for bolus penetration into the larynx
and 100% sensitivity and 28.8% specificity for aspiration (24).
Evaluation of the characteristics of voluntary cough can also be useful to
identify neurological patients at risk of aspiration (25, 26).
Videofluoroscopy or radiological examination of swallowing function can also
use different consistencies, textures and volumes. It can detect silent
aspiration. Patient collaboration is needed.
FEES: fibre-optic endoscopic evaluation of swallowing, is a bed-side
procedure, easy to repeat, and can check the anatomy and function of the
pharyngeal and laryngeal structures. Not all of the swallowing phases are
visible to this technique.
2.2. Gastrointestinal Dysfunction
Nausea and vomiting
Nausea and vomiting are important symptoms of intracranial hypertension and are
more common in acute than in chronic neurological disease. When intracranial
hypertension is present, third ventricle floor involvement may further increase
vomiting. Some medications used in neurological disease, such as drug therapy for
Parkinson’s disease, can also induce vomiting.
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Delayed gastric empting
Delayed gastric empting in neurological disease can be due to intracranial
hypertension, autonomic neuropathy, myopathy and the effect of drug therapy
(opioids, anticholinergics). This condition can decrease appetite, induce early
satiation, nausea and vomiting, reflux and heartburn, and abdominal bloating. It can
also contribute to decreased or irregular drug absorption. Gastroparesis is specially
common in Parkinson’s disease (27) and in multiple sclerosis patients (28).
Uncontrolled diabetes mellitus can also induce delayed gastric empting.
Constipation
Constipation is a common condition in patients with chronic neurological diseases and
can be a serious, sometimes live-threatening disorder. It can be due to slow gastric
and intestinal motility, weakness of abdominal and pelvic muscles, autonomic
dysfunction, side effects of medications and immobility. Some dietary factors can
also be important, including a decreased intake of fluid and fibre.
2.3 Energy Expenditure Disturbance
Neurological disorders may be associated with alterations in resting energy
expenditure, leading to hyper- or hypo-metabolism due to changes in body
composition, altered muscle function, paralysis, rigidity, spasticity, fasciculation,
tremor and other motility disorders (Table 1). Decreased energy intake and
malnutrition themselves cause secondary hypometabolism over and above any effect
of the disease itself. Predictive equations may not be accurate in assessing restring
energy expenditure in these patients and indirect calorimetry, if available, is advised.
Table 1
Energy expenditure (EE) alterations in neurological disorders
Neurological condition
Tremor,
fasciculation's,
dyskinesia, myoclonia
spasticity,
Paralysis, paresis
Increase EE
Decrease EE
Nutritional status
Malnutrition, loss of lean body mass
Decrease EE
Refeeding
Increase EE
Physical activity
Decrease in leisure physical activity
Decrease EE
Rehabilitation
Increase EE
Ventilatory function
Respiratory failure
Increase EE
Infections
Increase EE
Drug therapy: sedatives, baclofen
Decrease EE
Huntington’s disease is associated with increase in resting energy expenditure (29),
even in early stages of the disease (30). Energy expenditure in Parkinson’s disease
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may vary according to disease stage and the severity of symptoms. Increased total
energy expenditure can contribute to weight loss in late-stage disease (31). Some
patients with dyskinesias may expend as much energy at rest as people undertaking
moderate physical activity. Subthalamic stimulation decreases EE and can favour
weight gain and obesity.
Some clinical studies have observed increased resting energy expenditure in patients
with ALS, and this can contribute to malnutrition (32).
Resting energy expenditure in ALS patients may depend on many different factors,
including nutritional status (malnutrition decreases REE), the main clinical
neurological manifestations (predominant upper or lower motor neurone signs) and
the need for ventilation. Kasarskis attributed hypermetabolism to increased
respiratory effort (33). Desport (34) evaluated 62 patients and found that measured
energy expenditure was 10% higher than that of control subjects. Multivariate
analysis, however, did not reveal a relationship between hypermetabolism and
ventilatory function. Sherman studied ventilated and non-ventilated patients with
ALS. Patients who were receiving mechanical ventilation had higher energy
expenditure than that predicted by Harris-Benedict equations, whereas those
patients who were not receiving mechanical ventilation had a lower-than-predicted
energy expenditure. Both over- and underestimation of REE have been observed in
these patients using standard equations (35). REE in relation to fat-free mass tends
to increase during the course of the disease (36).
2.4 Effect of Drug Therapy
Drug therapy can decrease food intake due to dysgeusia, nausea and vomiting, dry
mouth, decrease in gastric empting, etc (Table 2). Interactions with micronutrients
have also been described.
Table 2
Nutrition-related side effects of drugs commonly used in neurological
patients
Drug
Side effect
Interferon
Weight loss, anorexia, fever,
depression, dysgeusia
Atypical antipsychotics
Weight gain, central obesity, metabolic
syndrome
Dopaminergic agents
Nausea, vomiting, anorexia, psychosis
Levodopa
Nausea, vomiting, constipation
Steroids
Decrease in muscle mass
Anticholinergics
Dry mouth, dehydration, delayed gastric
emptying, constipation
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Table 3
Micronutrient-related side effects of drugs commonly used in
neurological patients
Drug
Micronutrient
Steroids
Negative calcium balance. Osteoporosis
Phenytoin
Vit D, K, folate, and B6 deficiency
Levodopa
Increased homocysteine, vitamin B6,
B12 deficiency
Phenobarbital
Folate and vit D deficiency
Omeprazole, ranitidine
Vitamin B12, calcium, iron deficiency
Antacids
Phosphate deficiency
Diuretics
Thiamine deficiency
3. Nutritional Consequences of Chronic Neurological Diseases
The consequences of malnutrition are well known and are described in other LLL
modules. In neurological patients, it will exacerbate atrophy, and dysfunction of limb
and respiratory muscles. This further impairs mobility, weakens the respiratory
muscles and increases the risk of pneumonia. The increase in demand for gas
exchange associated with diet-induced thermogenesis during feeding may induce
dyspnoea in patients with respiratory muscle weakness and therefore necessitate a
reduced feeding rate. In addition, malnutrition leads to immunodeficiency and
increases the risk of infection, a common cause of death in these patients.
Malnutrition also impairs muscle function (type II fibres) and the recovery of
swallowing ability. Malnutrition and micronutrient deficiency (zinc or iron) increase
the susceptibility to pressure sores (37). Nutritional status and body weight are
important predictors of survival in ALS (38, 39, 40).
Dysphagia is associated with a decrease in both the efficacy and safety of swallowing
(Fig. 1). Because of this, the patient can develop malnutrition, dehydration,
oropharyngeal aspiration and aspiration pneumonia. Aspiration may be silent in
patients with chronic neurological disease.
Fig. 1 Clinical Consequences of dysphagia (18)
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Dehydration is common in patients with neurological diseases and dysphagia, causing
confusion and impaired renal function. Salivary production decreases and respiratory
secretions became thicker. This may further impair swallowing and increase
dyspnoea. Dehydration can also exacerbate orthostatic hypotension in patients with
autonomic dysfunction. Elderly patients are especially prone to dehydration, due to
their decrease in total body water and the relative insensitivity of the osmo-receptors.
Frequent assessment of fluid status is mandatory in patients with neurological
diseases, in order to prevent these complications. It should include a clinical
evaluation, diuresis and body weight recording, and evaluation of fluid intake. Some
laboratory parameters can help, such as haemoglobin, plasma/urine osmolality or
urea-BUN/ creatinine, but there is no gold standard. Dehydration cannot be
diagnosed using simple laboratory variables. Dehydration is usually under-diagnosed
in chronic neurological patients (41). An adequate fluid intake can decrease stroke
recurrence (42).
Aspiration pneumonia is a complex process in which pathogenic bacteria colonize the
oropharynx, and are aspirated into the airway; the patient is unable to clear the
material by coughing and subsequently, respiratory infection can develop (Fig. 2).
In patients with dysphagia, there is a 93% increase in hospitalization because of
aspiration pneumonia (43). Aspiration pneumonia has the highest rate of mortality
of all causes of pneumonia.
Fig. 2 Risk factors for aspiration pneumonia
Dysphagia can decrease quality of life in neurological patients (44).
Osteoporosis is common in patients with chronic neurological disease, due to
immobilization, lack of weight-bearing exercise, decreased food intake and
malnutrition (45). Bone mass density correlates with severity of disease in patients
with Parkinson’s disease (46). Osteoporosis is also common in multiple sclerosis (47),
even in men (48). The risk of osteoporosis in MS patients is related to disability and
disease duration; the effect of high dose pulse corticosteroid therapy is controversial.
Bone mineral density and calcium and vitamin D status need to be assessed in order
to prevent or limit osteoporosis in these patients.
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4. Summary
Neurological patients are at nutritional risk. Several factors may be responsible for
malnutrition in these patients, including decreased intake (dysphagia,
gastrointestinal disturbances, depression, etc), the effects of drug therapy, and
disease-related changes in energy expenditure. A structured nutritional evaluation is
mandatory. Nutritional support is considered a major component of care in patients
with acute and chronic neurological disorders. Changes in energy expenditure have
been described in these patients. Standard equations may be inaccurate and indirect
calorimetry, if available, should be used to assess energy requirements.
Malnutrition in neurological patients is related to a worse prognosis, being an
independent factor for mortality in amyotrophic lateral sclerosis and other
neurological diseases. It exacerbates muscle atrophy and function and impairs the
recovery of swallowing ability. Malnutrition also impairs immune function and
increases the risk of pneumonia and the susceptibility of pressure sores. Dysphagia
increases the risk of malnutrition, dehydration and aspiration. Osteoporosis and high
fracture risk are common in patients with chronic neurological disease.
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