21. Neurological conditions
Karen Green
LEARNING OBJECTIVES
By the end of this chapter the reader will be able to:
• Appreciate the impact of Parkinson’s disease (PD) or a head injury (HI) on nutritional status and nutritional requirements;
• Understand the role of the dietitian in the management of people living with PD or HI;
• Assess the nutritional status of people living with PD or HI; and
• Advise on the suitability of different types of nutrition support and provide appropriate dietary counseling.
Brief scene setting/historical context
The UK Department of Health launched the National Service Framework for Long-Term Conditions in March 2005 and it has a particular focus on the needs of people with neurological conditions and brain or spinal injuries. 1 The role of the dietitian in the management of these patients is highlighted in this key policy. It is now recognised that the dietititian is as an important team member of any neurological multidisciplinary team (MDT) responsible for the care of the neurological patient.
The incidence and prevalence of head injury (HI), and Parkinson’s disease (PD) in the UK is considerable.
The incidence of new HI cases in the UK is 175 per 100,000 of the population per year; all require hospital admission and lead to long-term problems. 1 In the case of PD, there are approximately 120,000 people living with this condition in the UK. 1
Head injury
Physiology
There are two general categories of HI: closed and penetrating. A closed head injury is one in which the skull is not broken open, which can be caused by a direct blow to the head. In a penetrating injury, the skull is broken open, and damage occurs to the brain as well. This can occur when an object, e.g. a bullet, passes through the skull into the brain. Both closed and penetrating HI can cause damage that ranges from mild to very serious. In the most severe cases, HI can result in death. 4
Pathophysiology
HI can take many forms. These include skull fractures (broken bones in the skull), blood clots between the brain and the skull and damage to the brain itself. Brain damage can occur even if the skull itself is undamaged. The brain may move around inside the skull with enough force to cause bruising and bleeding.
Bleeding such as an intracranial haemorrhage inside the skull may accompany a HI and may cause additional damage to the brain. A blood clot (haematoma) may also form between the brain and the skull. The clot can press against the brain and interrupt the flow of blood and oxygen through the brain. A reduced flow of oxygen prevents the brain from functioning normally.
Several types of intracranial haemorrhage can occur, including the following:
• Extradural haematoma (EDH) occurs inside the head. It results in a collection of blood in between the skull and dura matter (the outer protective lining that covers the brain). EDH is usually caused by fractured bones of the skull.
• Subdural haematoma (SDH) is a collection of clotting blood that forms in the subdural space (the area between two of the meninges that form the dura matter). The associated mortality rate is high, approximately 60–80%.
• Intracerebral haemorrhages (ICH) occur when a diseased blood vessel within the brain bursts, allowing blood to leak inside the brain. The most common cause of ICH is hypertension.
• Intraventricular haemorrhage (IVH) tends to occur due to a rupture of aneurysm accounting for ~25% of IVH in adults; or brain tumour; or arterio-ventricular malformation (AVM).
• Subarachnoid haemorrhage (SAH) can occur spontaneously or be due to trauma, resulting in ruptured aneurysms. About 10–15% die before medical care can be administered, and ~50% die within two weeks. It may lead to a communicating hydrocephalus if blood products obstruct the arachnoid villi or in the event of a non-communicating hydrocephalus secondary to a blood clot obstructing the third or fourth ventricle. 5
Severity of HI can be determined using the Glasgow Coma Scale (GCS) within 48 hours of injury. 6 This scale is based on a patient’s ability to open his or her eyes, give answers to questions and respond to physical stimuli, such as a doctor’s touch. A person can score anywhere from 3 to 15 points on this scale. A score of less than 8 points on the scale suggests the presence of serious brain damage. 7
The lowest possible GCS (the sum) is 3 (deep coma or death), whilst the highest is 15 (fully awake). Generally comas are classified as:
• Severe, with GCS < 8;
• Moderate, GCS 9–12; and
• Minor, GCS > 13.
Common symptoms of HI include loss of consciousness, confusion, drowsiness, cognitive decline, personality change, swallowing difficulties, headache, nausea and vomiting or in some cases speech and language difficulties. HI accounts for about 30% of traumatic deaths and long-term disability. 8
The immediate objective in severe HI is to prevent secondary damage from hypoxia or raised intracranial pressure (ICP); therefore the initial priorities are to maintain (a) oxygenation and (b) adequate cerebral circulation.
Intubation and ventilation may also be necessary to help in the control of cerebral vasodilation and prevent a rise in ICP. 9 Special attention should be given to the following to prevent secondary complications, thus ensuring a smooth progression to rehabilitation:
• Timely and appropriate nutrition and fluid balance to meet the increased metabolic demands;
• Prevention of contractures;
• Maintenance of postural reflexes;
• Bladder and bowel management;
• Skin care to avoid pressure sores; and
• Management of agitation/confusion.
Attention to these details is all too easily forgotten in the process of saving a patient’s life. However, the development of limb contractures or pressure sores at this stage can take months to heal later. Ideally the rehabilitation team should be involved in the patient’s care as early as possible to ensure that these aspects are addressed. 9
Once the patient is stable enough to leave intensive care, they should be transferred to an acute specialist brain injury rehabilitation unit. These patients frequently have continuing medical and surgical requirements, so immediate post-acute rehabilitation often needs to be provided in an acute hospital setting. As the patient’s condition continues to improve, continuation of the rehabilitation programme on a day-patient or outpatient basis may be appropriate. These programmes and needs will vary from patient to patient as they move from the differing stages of rehabilitation. Therefore a network of integrated MDT services must be provided, with excellent communication systems, so that the patient can pass from one level to another in a seamless continuum of care. 9
Nutritional therapy and dietetic application
Severe undernutrition can exacerbate complications caused by a HI, and can continue throughout the course of rehabilitation. 10 Undernutrition has been shown to increase length of stay (LOS) by up to 28 days on rehabilitation units compared with patients who were well nourished also having sustained a HI. Therefore this highlights the importance of providing continuous monitoring and review of the patient’s nutritional status and nutrition provision throughout their admission. 10
Underfeeding should be avoided at all costs. 11 At least 60% of patients who are admitted to rehabilitation units were found to exhibit severe undernutrition. 12 Feeding difficulties in these patients can be attributed to unconsciousness, drowsiness, being in a vegetative state, bulbar paralysis/palsy, dysphagia, agitation and facial trauma. 10
Nutritional requirements
Energy
The severe hypermetabolic (HM) response to traumatic HI has been well documented since the 1980s. 13.14.15. and 16. The brain normally regulates metabolism through the sympathetic nervous system. In HI the normal regulatory mechanisms of the brain are disrupted and a disordered HM state develops. 17
It has been found that an acute severe HI, even in a patient that is sedated and paralysed, is accompanied by energy expenditure values 130–135% above the predicted basal metabolic rate (BMR). 10,18,19 BMR will further escalate due to agitation, spasticity, autonomic storming and vegetative dysfunction and also when both the sedation and paralysing agents are discontinued. 10,20 Agitation is common in these patients and can be associated with fever, posturing, tachycardia, hypertension and diaphoresis. This stress response is known as autonomic storming. It is also thought to be a stage of recovery from severe HI. Other well-documented, associated complications such as infections, fever, septicaemia and pressure sores can affect the patient’s energy requirements. 10
An increased metabolic rate, with rapid protein breakdown in patients with moderate and severe HI during the early, post-injury phase and the related depletion of muscle mass and depressed immunofunction, are reported to increase complication rates and worsen long-term outcome. 21.22. and 23.
One suggested preventative approach has been to provide nutrition in accordance with the accelerated metabolism; 24 unfortunately, evidence-based guidelines in this area are lacking.
It has been found that only 27% of patients are able to spontaneously eat post-HI. 25 They often require artificial nutritional support because of their accelerated metabolism and a prolonged inability to eat. 25 The duration of the HM state is variable, lasting from 1 week to 1 year post-HI. 26 Because of this duration, even patients who have recovered and are in rehabilitation facilities may be HM and at risk of developing malnutrition.
The aim of nutritional therapy during this highly variable HM phase is to supply adequate caloric intake to meet the increased metabolic demand. 27 It is important to note that when providing and maintaining optimal nutritional status in the acutely ill HI patient that the dietitian has realistic expectations of what artificial nutrition support can accomplish. It is unlikely that a positive nitrogen (N) balance and significant weight gain can be achieved by meeting or exceeding energy expenditure at the hypermetabolic/catabolic state. 3
At this stage overfeeding does not prevent muscle wasting and may exacerbate hyperglycaemia, which can induce anaerobic metabolism in the brain, increasing lactate levels, which in turn may contribute to secondary neuronal damage. 18,28.29. and 30. In addition to this, overfeeding with high carbohydrate/glucose-based formulas in particular can increase oxygen consumption and therefore yield excess carbon dioxide (CO 2) production. Hypercapnia increases a patient’s requirement for artificial ventilatory support, and can cause dilation of cerebral vessels, thereby increasing ICP and the risk of further brain injury. 30
Protein
Unfortunately very few studies have looked at the protein requirements of critically ill patients. However, early nutrition support in the HI patient has been shown to improve the profound negative N balance caused by excessive protein catabolism. 27,31 Optimal protein use has been found to be heavily dependent on the adequacy of caloric intake. As already discussed, energy requirements increase in severe HI and N excretion also increases. 32
In a normal fasting human, the N catabolism is in the region of 3–5 g N/day. In severely head injured patients, N catabolism has been found to be 14–25 g N/day. 33,34 This can be equated to a 10% decrease in lean muscle mass in 7 days. 35 Underfeeding for 2–3 weeks could result in a weight loss of 30%, which is potentially detrimental and has been observed in clinical practice. 35
Excessive protein intakes, like excessive energy intakes, are unlikely to correct negative N balance in critically hypermetabolic/catabolic patients. 3 This is particularly true during the first 2 weeks following HI. Achieving the lowest possible level of negative N balance should be the goal during this early catabolic period. 27
Some research has demonstrated that N excretion sharply increases throughout the weeks post-HI, peaking in the second week, and remaining increased well above normal throughout hospital admission. 25,36 Young et al. studied the protein losses of head injured patients and concluded that negative N balance persisted even when protein intake exceeded 1.5 g/kg/day. 25,37
Studies providing high intakes of N (>17 g/day) via artificial nutrition support have found that less than 50% of N is retained by the body. Therefore, the level of N intake that generally results in less than 10 g of N loss per day is 15–17 g N/day, or 0.3–0.5 g N/kg. This equates to about 2 g protein/kg/day (20% of the caloric composition of a 50 kcal/kg/day feeding protocol). Twenty percent is the maximal protein content and amino acid content of most enteral nutrition support (ENS) and parenteral nutrition support (PNS) formulations. 38
In a HM patient, N equilibrium is rarely achievable, although it has been shown that increasing the N content of enteral feeding from 14 to 20% does result in improved N retention. 39 The survival rate is better when an increased protein diet is commenced within 1–10 days post-injury versus the same diet administered more gradually or after a long period. 25,40 Ishibashi and colleagues measured protein balance in a critically ill population; each group was randomised to receive intakes of protein ranging from 0.9 to 1.5 g/kg/day. 41 Although the patients in all groups were reported to be in a negative protein balance, protein intake of 1.2 g/kg/day was found to be associated with a 50% improvement in the protein balance. Intakes >1.2 g/kg/day conferred no further benefit.
Some studies have noted that exact values for individual therapy cannot be reliably calculated using clinical predictive formulas and are further distorted in individual patients because of treatment with barbiturates, paralytics and sedatives, and the presence or absence of infection, fever and the severity of injury/depth of coma. 25 For these reasons, routine repeated monitoring of a patient’s energy and protein needs should ideally be carried out using indirect calorimetry and urinary urea or total N measurements. Energy expenditure is quantified under specific conditions (usually resting) by measuring respiratory gases (oxygen consumed and carbon dioxide produced) usually undergoing mechanical ventilation on ICU. The measurement of energy expenditure is the most accurate method for assessing energy needs, especially in acutely ill patients. Although accurate, this method is expensive, is not readily accessible and requires technical expertise.
Which method of artificial nutrition support is best used in HI?
Infections are a frequent complication in patients with traumatic HI. Early nutritional intervention can clearly combat the development of severe malnutrition, although its effect on improving outcome is not clear. Studies have demonstrated that early ENS is the preferred route of nutritional support in ventilated patients with a functioning gastrointestinal (GI) tract. 24,42,43 The advantage of ENS is less risk of hyperglycaemia, low risk of infection and reduced cost. 38
In the vast majority of ventilated HI patients, the general trend is to maintain nutrition via the enteral route. In many cases although provision of ENS is adequate, its absorption in the GI tract may be impaired. 44,45 Early intolerance to ENS can be attributed to gastric dysmotility during periods of raised intracranial pressure, 44 prolonged paralytic ileus, abdominal distension, aspiration pneumonitis and diarrhoea. 46,47 Drugs such as anaesthetics and sedatives, opioids and catecholamines can also cause or augment GI dysmotility. 48
The use of prokinetic agents, such as metaclopramide and erythromycin, during delayed gastric dysmotility can be beneficial when administered intravenously. 49 The effects of erythromycin to improve gastric emptying and to improve tolerance to ENS have been confirmed by studies of critically ill and mechanically ventilated patients. 50,51 However, some intensive care units do not use erythromycin as first-line treatment due to the rising incidence of microbial resistance and the association between erythromycin and ventricular dysrhythmias. 52,53 Metoclopramide on the other hand has been used for the past 35 years for treating gastric dysmotility and is commonly used as a first-line treatment. 48 The only adverse effect of its use is the development of extrapyramidal motor reactions and symptoms of drowsiness, agitation, fatigue and dystonic reactions in long-term usage. 54 Metoclopramide, however, is usually discontinued once normal gastric motility returns. If, however, a post-pyloric feeding tube can be safely inserted, then nasojejunal feeding may be another useful alternative method for providing optimal nutrition.
Attempts at achieving nutrient goals in this case presents a great challenge to the dietitian to maintain optimal energy requirements. Despite this many researchers have demonstrated that the development of enteral feeding protocols and continuous education of critical care staff may improve delivery of ENS. 55,56 Patients should be monitored carefully for signs of gastric dysmotility and subsequent feed intolerance during enteral feeding, so that appropriate treatment can be instigated early to prevent complications such as reflux and aspiration; and optimise nutrition provision. 57
Enteral nutrition support (ENS) versus parenteral nutrition support (PNS)
Studies have demonstrated that more energy in the form of calories and protein are provided by the PNS route than ENS when administered to patients with severe HI. 44,58 It has been recommended that PNS should be considered as an adjunct therapy, while other researchers believe that early PNS improves the outcome after severe HI. 10,31,47 Many studies have demonstrated that, with nearly equivalent quantities of feeding, the mode of administration has no effect on neurologic outcome and either PNS or ENS is equally effective when prescribed according to individually measured energy expenditure (EE) and N excretion. 25,32,46 Agreement concerning the feeding technique of patients with severe HI should be established within the ICU team, to ensure the appropriate nutritional therapy is followed. 10
Fluid and sodium
Appropriate fluid management of patients with HI can be challenging for many clinicians as it plays an important role in the maintenance of cerebral perfusion pressure (CPP) and ICP. 30,59 A negative fluid balance (approx <600 mL/day) has been associated with a significant negative effect on outcome, whereas previously it was believed that a negative fluid balance reduced cerebral oedema. 30,60
Syndrome of inappropriate antidiuretic hormone (SIADH) and cerebral salt wasting (CSW)
Hyponatraemia is a common neuromedical problem seen in survivors of central nervous system injury. The aetiology of this hyponatraemia is often diagnosed as ‘syndrome of inappropriate diuretic hormone’ (SIADH) or cerebral salt wasting (CSW). SIADH is a disorder of sodium and water balance characterised by hypotonic hyponatraemia and impaired water excretion in the absence of renal insufficiency, adrenal insufficiency or any recognised stimulus for the antidiuretic hormone (ADH). 62. Fluid restriction is usually the first line of treatment. However, this can exacerbate vasospasm and produce resultant ischaemia. CSW is a syndrome of renal sodium loss that may occur commonly after central nervous system injury, yet remains unrecognised. Treatment of CSW consists of hydration and salt replacement. Typically, urinary sodium levels are found to be elevated with a low serum osmolality and a serum sodium (Na) level of < 134 mmol/L. 30
Without adequate evaluation of volume status, patients with CSW may be mistaken for those with SIADH. 63 This is concerning because inappropriate fluid restriction may result in volume depletion and potential cerebral ischaemia in the HI population. 62 The primary mechanism of CSW is still not understood but likely reflects a role for the disturbance of atrial naturetic peptide. 60Table 21.1 specifies the differential diagnosis of both types of hyponatraemic conditions.
| Parameters | SIADH | CSW |
|---|---|---|
| Weight | Increased | Decreased |
| Dehydration | Absent | Present |
| Urine Na | Increased | Increased |
| Serum Potassium (K) | Decrease or no change | Increase or no change |
| Osmolality | Decreased | Increased or normal |
| Serum Na | Decreased | Decreased |
| Blood urea Nitrogen (N) | Normal | Increased |
| Uric acid | Decreased | Normal |
Maintaining electrolyte balance in patients with HI
Patients with severe HI are at risk of developing hypomagnesaemia, hypophosphataemia and hypokalaemia. 63 HI may precipitate polyuresis through a variety of mechanisms or can be induced through medication, e.g. mannitol. Mannitol is used clinically to reduce acutely raised ICP.
These electrolytes must be monitored daily especially during the acute phase of injury and supplemented accordingly via the enteral or intravenous route. 30
Key points
• The generally accepted goals of nutrient delivery in patients with HI are to:
○ Prevent nutrient deficiencies, which can be achieved by avoiding overfeeding and underfeeding during the hypermetabolic/catabolic state. 66 Overfeeding at this stage may lead to metabolic complications. 25 Underfeeding particularly at the rehabilitation stage causes patients to exhibit severe malnutrition. 12
• The dietitian plays a very important role in the continuous and timely monitoring of the patient’s nutritional status and provision of adequate nutrition support. This is imperative with respect to gut motility disturbances, whereby an individually tailored treatment is used to prevent further exacerbation of existing motility disturbances. 67
Developing issues
• Use of indirect calorimetry to determine patient’s energy and protein needs. Increased utilisation of indirect calorimetry would facilitate individualised patient care and should lead to improved treatment outcomes;
• Glutamine supplementation may also be beneficial to decrease incidence of infection rate, but it has yet to be adequately studied in HI; and
• Use of and requirements for vitamin, mineral and trace element in patients with post-HI.
Parkinson’s disease (PD)
Pathophysiology
PD is a progressive neurodegenerative disorder. It is characterised by tremor, rigidity, akinesia and postural instability, resulting from dopamine depletion in the substantia nigra area of the brain.
Dopamine is a neurotransmitter that allows messages to be sent from the brain to the muscles to activate voluntary movements. 68 This helps us to perform smooth, coordinated movements. The symptoms of PD usually appear when at least 80% of the dopamine is lost. The level of dopamine will continue to decline over many years.
Most cases of PD are of unknown cause. PD is not one disease but the most common form of Parkinsonism. 68 This is the name for a group of disorders, e.g. progressive supranuclear palsy (PSP) or multiple-systems atrophy (MSA), with similar symptoms and all resulting from the loss of dopamine-producing nerve cells.
Onset of PD is usually between the ages of 55 and 65, known as ‘late-onset’ PD, but between 5 and 10% of patients are under the age of 40, known as ‘young-onset’ or ‘early-onset’ PD. 69 It can significantly impair the quality of life, especially physical and social functioning. 70 The impact of having young-onset PD is often most profound in terms of the psychological, emotional and social effects on a person’s life. 71 It is worth noting that patients may live with this illness for up to 30 years. 72
There is no cure at present for PD, although the treatments available are directed at minimising the symptoms and disabilities of the patient. 72.73. and 74. The type of medication used varies between individuals according to the nature and severity of symptoms. Since many of the available drugs have significant side effects, the aim of drug therapy is to find a balance between effective symptom control and avoidance of side effects.
Some of the drugs used in the management of PD are levodopa, dopamine agonists, anticholinergics, amantadine and catechol-O-methyl transferase (COMT) inhibitors. Levodopa is used to replace or mimic dopamine in the brain and is used alongside COMT inhibitors to limit the conversion of levodopa to dopamine in the peripheral tissues, therefore enabling a greater proportion of levodopa to cross the blood–brain barrier. Dopamine agonists (mimics dopamine) are usually the first drugs prescribed for those diagnosed with young-onset PD, such as apomorphine hydrochloride and cabergoline. 75 It is also used in conjunction with levodopa.
The effectiveness of drug therapy in PD tends to decrease with time and the duration of benefit after each dose becomes progressively shorter; this is known as ‘end-dose failure’. Side effects of levodopa such as dyskinesia may also begin to appear.
Patients on long-term therapy may also suffer from ‘on/off syndrome’, causing sudden changes in or loss of functional ability. These ‘off’ periods are unpredictable and may last for only a few minutes or many hours. The main feature of the “off” period is increased muscle tone, and increased involuntary movements during the on period. Drug adjustment is often titrated in an attempt to overcome this problem.
Nutritional therapy and dietetic application
The nutritional issues faced by people living with PD are complex and diverse, in particular weight loss. Weight loss is often accompanied by malnutrition and is a very common observation among healthcare professionals. Weight loss in this particular group of patients had not received much attention until recently. 76.77. and 78.
Weight loss is reported frequently by patients living with PD. 79 They exhibit lower body weight and weight loss can occur during the early stages of the disease. 80.81.82. and 83. This can be associated with increased risk of fall and fractures due to low bone mineral density, and is multifactorial. 77,84,85 The symptoms of PD are outlined in Table 21.2.
| Symptom | Action | Result |
|---|---|---|
| Tremor in hands | Increase in spillages | Embarrassment and reluctance to eat in front of others—resulting in social isolation |
| Rigidity and stiffness in muscles | Inability to prepare food and manually feed themselves | Difficulties with chewing and swallowing food may develop, requiring assistance, which can demoralise the patient |
| Bradykinesia | Slow movements can prolong the time taken to eat a meal | Food may be abandoned either because it has become cold and unappetising or because of fatigue arising from the sheer effort involved in eating |
| Motor fluctuations | Unpredictable ‘off’ periods around mealtimes and for extended periods during the day | Can affect ability to eat and drink enough, thus having a direct impact on nutritional intake and weight |
| Dyskinesia | Uncontrolled ‘jerky’ movements | This uses up more energy than the patient consumes, thought to be due to increased energy consumption by skeletal muscle80 |
| Mood changes | Anxiety, depression, irritability, restlessness and cognitive decline | This may impair appetite. Side effects of some anti-Parkinsonian drugs may also exacerbate these problems |
| Drug side effects | Some neuropsychiatric side effects such as confusion, insomnia, hallucinations or psychosis OR gastrointestinal side effects may include nausea, vomiting, dry mouth or constipation | Many of the side effects of anti-Parkinsonian drugs have nutritional implications such as reduced appetite, forgetting to eat, or early satiety |
| Dysphagia | Inability to control/tolerate certain textures and consistencies increasing the risk of aspiration | Certain textures such as puree can be nutritionally dilute and therefore not adequately energy dense to prevent weight loss |
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