The ‘biological clock’

The circadian rhythm set by our ‘biological clock’ of approximately 16 hours awake/8 hours asleep is controlled, specifically by the suprachiasmatic nucleus of the hypothalamus. The pattern of 16/8 varies from person to person and will also change as we go through life from birth to old age. If an individual was allowed to go to sleep in an environment with no cues as to the time of day, they would develop a regular sleep/wake cycle of approximately 25 hours’ duration. It is the various external factors that we employ (use of an alarm, daylight entering the bedroom, social habits and activities) that result in the ‘training’ of the cycle to 24 hours.

Arousal

The cortex of our brain is constantly bombarded by information coming in through all of our senses (visual, auditory, touch, taste, smell, proprioception) and as this information passes up through the brain via the various pathways, collaterals branch off and send impulses to the reticular formation. The more sensory input there is, the greater the excitation of the reticular formation will be. If there is sufficient stimulation of the reticular formation, it will fire impulses up to the thalamus, switching off the thalamic pulsing to the cortex – and we waken. This process helps to explain why we can sometimes find it difficult to get to sleep, even if we want to, if there is a high level of sensory stimulation. Conversely, it also helps to explain why we can drop off to sleep at inappropriate moments, e.g. a warm lecture theatre with the lights dimmed, the quiet monotonous voice of the lecturer (not us obviously!). In this situation there will be less reticular formation stimulation, leading to a reduced firing to the thalamus and a subsequent return of thalamic pulsing to the cortex.

Non-REM sleep

Four separate stages (I–IV) of non-REM sleep have been identified using EEG recordings. Stage IV is often referred to as deep sleep, or slow wave sleep due to the characteristic EEG trace observed, and it is during this level of sleep that we are most difficult to rouse. It is also during stage IV that sleepwalking, talking, tooth-grinding and nightmares occur in some individuals (particularly the young). The time spent in stage IV does start to reduce as we grow older, so we can say that there may be some advantages to being older!

There is a rapid progression through the first four stages of sleep, followed by a short time spent at level IV and then a return back up through the stages. This occurs in a cyclical fashion throughout the period of sleep, with each cycle lasting about 90–100 minutes, although the depth lessens as the night progresses.

REM sleep

As well as the four stages of non-REM sleep, a distinctly different form occurs at regular intervals throughout the period, namely REM sleep. There are four key features associated with REM sleep:

As we move from non-REM to REM sleep there is a notable change in EEG pattern, i.e. it starts to resemble the EEG pattern observed in an awake individual. However, as the individual is still very much in a deep sleep, this has resulted in REM sleep also being labelled ‘paradoxical sleep’. As noted above, dreaming occurs during the REM phase and the term REM sleep is derived from the fact that the eyeballs are moving as the mind of the individual is following the events unfolding in their dream. It is also during REM sleep that, even though our motor activity is significantly reduced, occasional twitches can occur. As well as the increases in the cardiorespiratory parameters noted above, there is also a greater variability in these values compared to non-REM sleep. During periods of both REM and non-REM sleep there is a general level of muscle relaxation; however, it is during the transition from REM to non-REM that we would change our body position.

Post-stroke fatigue

Fatigue is common after stroke, its prevalence ranging from 16% (Glader et al. 2002) to 70% (Carllson et al. 2003), depending on the definition of fatigue and the population studied.

There is often an increase in the level of fatigue felt by an individual after a stroke, particularly if the level of ischaemia has occurred subcortically, in the brainstem or in the thalamus. In fact, in certain cases, fatigue can be the only major disability and is often accepted as a common part of the disease process. Since, as we stated earlier, the definition of fatigue is so vague, it can be difficult to identify what actually causes it after a stroke. Consequently, it often goes undiagnosed – and thus untreated. In order to mediate this problem, a case definition and interview protocol was developed by Lynch et al. (2007), with one version for inpatients and one for people living in the community. The definition of post-stroke fatigue for inpatients is as follows (p. 543):

Despite the fact that post-stroke fatigue is commonplace, very little is known on the actual extent of the problem or, in fact, what impact it has on the recovery of the individual affected. It does beg the question of how much impact an undetermined level of fatigue could be having on the return to ‘pre-stroke’ levels of activity. There is some evidence that post-stroke fatigue may be slightly more commonplace in females (Glader et al. 2002). However, there are also many studies which find that there is no demographic link with the level of occurrence. There is further contradictory evidence when looking at the severity of the fatigue being experienced. Several studies have linked the severity of fatigue to poor general health, pain, anxiety and depression post stroke. However, other studies report no link between fatigue levels and depression post stroke (Naess et al., 2005, van der Werf et al. 2001). There also appears to be no link between the level of fatigue experienced and either the time since the stroke or the level of disability associated with the stroke (van der Werf et al. 2001).

It therefore appears that, although post-stroke fatigue is a very real issue, there is much we do not know about the factors affecting the occurrence and severity of the fatigue experienced by a patient post stroke. In terms of interventions, a Cochrane systematic review only identified three studies, the results of which were inconclusive (McGeough et al. 2009). Exercise can be effective in reducing fatigue; however a Cochrane systematic review on exercise and fitness training after stroke reported insufficient evidence on this issue (Brazzelli et al. 2011). The unknown aspects of post-stroke fatigue could make the role of the therapist involved in post-stroke rehabilitation particularly difficult. It is clear that a considerable amount of further research is required in this important area.

Fatigue in multiple sclerosis

A definition of multiple sclerosis (MS) fatigue is ‘a subjective lack of physical and/or mental energy that is perceived by the individual or caregiver to interfere with usual and desired activities’ (Multiple Sclerosis Council 1998).

Fatigue in patients suffering from MS is very commonplace; in an audit of people with MS living in Oxfordshire, nearly half of the respondents reported fatigue (Wade and Green 2001). One particular problem mentioned is the fact that fatigue can be experienced at rest and, if occurring following activity, is not helped by rest. Levels of fatigue may also vary within the individual. Another interesting aspect that has been uncovered in some studies is that the level of fatigue experienced appears to be worsened by stress as well as heat (e.g. due to a warm environment or exercise). The exact mechanism behind the occurrence of fatigue in MS patients is not really understood, despite the fact that significant levels of information have been gathered from patients. However, it is thought that fatigue in MS may be associated with depression, cognitive impairment and muscle weakness, as well as disability, and, therefore, a comprehensive biopsychosocial approach to the assessment and management of fatigue should be taken.

It is clear that fatigue can have a considerable impact on rehabilitation and life in general; the high and variable levels of fatigue mean that it is often difficult for individuals with MS to plan their activities. They may only be able to engage with rehabilitation to a limited extent, and therapists need to carefully balance the need to avoid over-exertion with the need for sufficient physical activity to maintain optimum function. Outside rehabilitation, together with cognitive impairment, fatigue is one of the most important factors affecting employment prospects of people with this condition.

Fatigue in Parkinson’s disease

As is the case with both stroke and MS patients, fatigue is also widely observed in Parkinson’s disease (PD), with prevalence ranging from 33 to 58% (Friedman et al. 2007), and about half of patients reporting fatigue as a major symptom (Friedman et al. 2007). Having said that, it is not always clearly defined as a symptom by the patient who may not actually use the word ‘fatigue’ spontaneously. The problems with defining fatigue, mentioned in the context of stroke and MS, also apply to PD and there is currently no consensus on the best tool for assessing fatigue in people with PD (Friedman et al. 2007). Therapists, therefore, need to listen carefully for expressions such as ‘tiredness’, ‘exhaustion’ or ‘lack of energy’ (Brown et al. 2005).

Both depression and cognitive impairment are often linked to fatigue, but this is not necessarily the case in PD patients. Chronic fatigue has been observed in some PD patients, lasting as long as 9 years since diagnosis in some cases, while there is evidence to indicate that fatigue increases with time since diagnosis (Friedman et al. 2007).

In conclusion, fatigue is a real issue for PD patients, with a number of the people affected having to deal with a level that is both all-encompassing and persistent.

Post-stroke sleep disorders

There are three separate sleep disorders which can appear in patients who have suffered a stroke: sleep disordered breathing (SDB); sleep–wake disorders (SWD); and insomnia.

One of the most common forms of SDB is obstructive sleep apnoea (see later). Approximately 65% of stroke survivors will show symptoms associated with SDB, in which the patient usually experiences abnormalities in their respiratory pattern resulting in significant interruptions in their sleep patterns. The knock-on effects of this disrupted sleeping pattern are a marked level of fatigue during the day coupled with a difficulty in focusing their attention on any particular task. One aspect of SDB that has been identified was the fact that those suffering from it exhibited a worrying increase in both blood pressure and clotting factors (Golbin et al., 2008, Robinson et al. 2004). In addition to this, other studies suggest that abnormalities in breathing during sleep may increase the risk of vascular disease. However, it has to be pointed out that there is a lot of debate around this controversial area. A number of clinical studies have been carried out which suggest that habitual snoring actually increases the risk of developing high blood pressure and stroke (Lees et al. 2008, Neau et al. 2002). Interestingly, however, such findings have not been backed up in further work when other risk factors such as age, body mass index (BMI) and smoking were controlled for.

Around 30% of those individuals surviving a stroke will display symptoms of SWD, which affects the normal circadian rhythms (mentioned earlier), so that the usual pattern is no longer governed by day/night changes. The consequences of the sleep disturbances observed in SWD can be a high level of fatigue, some level of depression and a degree of attention/memory problems. The sleep fragmentation that can derive from SDB can result in a form of SWD.

Sleep disorders in Parkinson’s disease

Various studies have shown that somewhere between 60 and 88% of PD patients will show some level of night-time sleep disturbance, coupled with a marked increase in the level of daytime sleepiness (Kales et al. 1971, Larsen 2003, Lees et al. 1988, Tandberg et al. 1998). A number of these patients report a range of marked night-time problems, including broken sleep and regular waking, which do not appear to be helped with use of sleep medications (hypnotics such as Zolpidem®) (Dauvilliers, 2007, Gjerstad et al. 2007, Oerlemans and de Weerd 2002, Tandberg et al. 1998). Any form of sleep fragmentation appears to be more commonplace during the lighter stages I and II, with the patients noting that if they waken they find it exceptionally difficult to fall back asleep.

Sleep apnoea is most commonly found in individuals with a high BMI, a factor not frequently found in PD patients. Despite this, the occurrence of sleep apnoea is much higher than predicted in PD patients. It has been observed in a group of patients with a BMI within the normal range (approximately 19–25 kg/m²) that almost 50% have a significant level of sleep apnoea. Around one-quarter to one-half of PD patients exhibit symptoms of REM sleep behaviour disorder (RBD) where there is an increased level of muscle activity during REM sleep. One key piece of research by Iranzo et al. (2006) showed that RBD may even precede the onset of the clinical symptoms of PD. Further research is required to see if RBD could be an early marker for PD. Another common complaint in about 15% of PD patients is excessive daytime sleepiness (EDS) which results in sleep ‘attacks’ and a danger of, for example, car accidents.

It can be seen that sleep disturbance and fatigue is a common feature of a number of neurological conditions, but it still remains an area that is not greatly understood.

Oral phases

The first phase prepares the food so that it is in a suitable format for swallowing and involves the various structures in your oral cavity. Have a look inside your mouth using a mirror. You can see many of the structures which include the lips, teeth and tongue, and looking towards the back of your mouth you can see the soft palate (velum), uvula (dangling soft tissue) and faucial arches (see Fig. 14.2). The tongue is an amazing structure which is composed almost entirely of many muscle fibres. It is composed of six regions – the tip, blade, front, centre, back and the base. The first five regions are largely under voluntary cortical control and are involved in the oral phases of the swallow. The sixth region, the base of the tongue, is employed during the pharyngeal phase of the swallow (see below) and is largely under involuntary neural control coordinated in the brainstem. It is also important to note the oral crevices (spaces) between your upper and lower lips and gums and between your cheeks and gums where food can lodge if not cleared by our tongue.

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Executive dysfunction Synopsis and implications of neuroscience for neurological rehabilitation Problems of emotion and motivation Basic neuroanatomy and neurophysiology Perceptuo-motor control Disorders of attention and memory

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