Neurons

Neurons (Fig 33.1) are the primary components of the nervous system. Functioning alone, or as units, neurons detect internal and external changes and initiate body responses needed to maintain homeostasis. Each neuron is composed of a cell body, with projections forming dendrites, and one long axon. The dendrites are short-branched fibres, which receive impulses and conduct them towards the cell body of a neuron. The axon, which may vary in length from miniscule to over a metre, conducts impulses away from the cell body of a neuron. Generally, a neuron has only one axon but many dendrites. Axons leave the grey matter and become the fibres of the white matter. Each axon has a covering called a neurilemma, and most have a fatty sheath, the myelin sheath. The myelin sheath protects and insulates the axon and increases the transmission rate of nervous impulses. Neurons are bound together by a special type of connective tissue called neuroglia.

Figure 33.1 A typical neuron

Neuroglia

The neuroglia includes many types of cells that support and protect the neurons. They play a role in regulating neuronal activity, and in providing neurons with nutrients. Neuroglia differ from neurons in that they are not capable of transmitting nerve impulses and never lose their ability to divide. The neuroglia in the central nervous system (CNS) are comprised mainly of two types of cells: astrocytes, cells with small cell bodies and processes like dendrites, which protect the neurons from harmful substances that may be in the blood by forming a living barrier between the capillary blood supply and the neurons; and oligodendrocytes in the CNS, which have few processes and produce the myelin sheath around the processes of the neurons. The Schwann cells in the CNS protect, nourish and form myelin.

Functions of neurons

Neurons have two major functional properties: irritability and conductivity. Irritability is the ability to respond to a stimulus and convert it into a nerve impulse. Conductivity is the ability to transmit the impulse to other neurons, muscles or glands. An impulse is a complex electrical and chemical signal transmitted along a nerve pathway in response to a stimulus. The speed of transmission varies with the size of the nerve fibre, and may be as much as 120 metres per second.

A synapse is the space between the terminal axon of one neuron and the dendrites of another. By means of a chemical substance (neurotransmitter) released by the axons, impulses are transmitted through this space from one neuron to another. Examples of neurotransmitters are acetylcholine and noradrenaline. Many different types of stimuli can excite neurons so that they become active and generate an impulse. Most neurons are excited by the neurotransmitters released by other neurons, but other stimuli can excite neurons. For example, sound excites some of the neuronal receptors of the ear, and pressure excites some cutaneous receptors of the skin. Receptors, or sensory nerve terminals, act as transducers, converting the energy of a stimulus into impulses that pass to the brain.

The nervous system can be divided into two primary divisions: the central nervous system, consisting of the brain and spinal cord; and the peripheral nervous system, consisting of nerves that connect the central nervous system with the body tissues.

The brain

The brain is a large organ weighing about 1.4 kg in the adult, held in position within the skull by membranes called the meninges. In most parts of the brain the outer portion, or cortex, consists of grey matter, while white matter forms the inner portion. The grey matter is convoluted to provide a greater surface area. The brain is divided into the:

The cerebrum

The cerebrum (Fig 33.2) is the largest part of the brain, filling the vault of the cranium from front to back. It is divided by fissures into the left and right hemispheres, and each hemisphere is further divided by fissures into four lobes:

Figure 33.2 The brain—cerebral hemispheres (left) and major structures (right)

The left hemisphere is usually associated with language, mathematical skills and reasoning. The right hemisphere is generally associated with skills such as artistic awareness and imagination. Within each hemisphere is a cavity called the lateral ventricle, which is concerned with the formation of cerebrospinal fluid.

The cerebrum is divided into several areas, some of which are sensory and some of which are motor areas. The sensory areas of each hemisphere receive and interpret sensations from the opposite side of the body, including touch, temperature, pain, pressure and an awareness of the position of the body in its environment. The motor areas of each hemisphere control all voluntary movement on the opposite side of the body. The centres of special sense are located in the various lobes, including the centres for hearing, speech, smell, taste and sight (Fig 33.3).

Figure 33.3 The sensory and motor areas of the cerebrum

The functions of the cerebrum are therefore to receive and interpret impulses from the sensory organs, to initiate and control the movements of skeletal muscles and to perform the higher levels of mental activity such as thinking, reasoning, intelligence, learning and memory.

The diencephalon

The thalami are two oval masses of grey matter that form the lateral walls of the third ventricle. Each thalamus is subdivided into a number of nuclei. Most sensory pathways (except smell) synapse here. The thalamus plays a role in the control of somatic motor activity and also influences mood and strong emotions.

The hypothalamus lies beneath the thalami, and the pituitary gland is closely connected to it. The hypothalamus controls all the activities of the autonomic nervous system, which is described later in this chapter. The hypothalamus is important in controlling the endocrine system, as it regulates pituitary gland function.

The brainstem

The midbrain. The midbrain is a short narrow segment connecting the cerebrum with the pons varolii. It is composed primarily of ascending and descending fibre tracts. Its functions are to provide a pathway for impulses passing between the cerebrum and spinal cord, and to receive stimuli that initiate eye and postural movements.

The pons varolii. The pons varolii is about 2.5 cm long, lying anterior to the cerebellum and above the medulla oblongata. It contains two respiratory centres, the pneumotaxic centre and the apneustic centre. Its functions are to act as a relay station from the cerebrum to the cerebellum, and to modify the activity of the medullary respiratory centres through the pneumotaxic and apneustic centres.

The medulla oblongata. The medulla oblongata is about 2.5–3.0 cm long, lying between the pons and the spinal cord. It provides the link between the brain and the spinal cord and contains the cardiac, respiratory, vasomotor and reflex centres. Its functions are:

The cerebellum

The cerebellum lies behind the pons and medulla and below the occipital lobes of the cerebrum. Like the cerebrum, the cerebellum is divided into two hemispheres that have shallow convolutions in their surface of grey matter. Its functions are coordination of muscular activity and regulation of muscle tone, and maintenance of balance and posture.

Blood supply to the brain

The carotid and the vertebral arteries supply blood to the brain. These arteries branch and join up again, forming a circle of arteries at the base of the brain called the circle of Willis. From here smaller cerebral arteries branch off to supply each region of the brain. Blood returns from the brain via the jugular veins to the superior vena cava.

The blood–brain barrier is a barrier that prevents or delays the entry of certain substances into brain tissue. The relatively low permeability of the capillaries supplying the brain means that some substances are either completely or partially prevented from gaining access to brain tissue. The blood–brain barrier thus acts as a protective mechanism, preventing substances such as bilirubin, which could disrupt brain function, from crossing the barrier.

The spinal cord

The spinal cord is a cylindrical structure that lies within a canal inside the vertebral column. It extends from an opening on the underside of the skull (the foramen magnum) to the level of the first or second lumbar vertebra. Below this level the vertebral canal is occupied by nerves from the lumbar and sacral segments of the cord; these constitute the cauda equina (‘horse’s tail’). The spinal cord, which is about 46 cm in length, consists of nervous tissue, with the white matter on the outside and the grey matter arranged roughly in an ‘H’ formation in the centre (Figs 33.4 and 33.5). The two anterior projections of grey matter are called the anterior horns, and the posterior projections are called the posterior horns. Sensory nerve fibres enter the posterior horns, and motor nerve fibres leave the anterior horns.

Figure 33.4 Vertical section of the meninges and spinal cord

Figure 33.5 Cross-section of the spinal cord

Leaving the spinal cord at intervals throughout its length are 31 pairs of spinal nerves. The functions of the spinal cord are:

A reflex action, or arc, is an automatic motor response to a sensory stimulus without conscious involvement (Fig 33.6). Most reflex actions are protective in nature and take place more quickly than voluntary actions. The structures involved in a reflex action are:

Figure 33.6 A reflex arc

An example of a reflex action is when the hand comes into contact with a very hot object. The skin on the hand receives the stimulus of heat, and an impulse travels from the sensory nerve endings in the skin to the posterior horn of the spinal cord. From there, the impulse is transmitted to the anterior horn, then passed along the motor nerves to the muscles of the shoulder, arm and hand. As a result, the hand is pulled rapidly away from the source of heat before the brain has even processed the information.

The meninges

The meninges are the three membranes that cover the brain and the spinal cord. The individual membranes are:

The subarachnoid space is the space between the arachnoid mater and pia mater, filled with cerebrospinal fluid in circulation. The functions of the meninges are to form a protective covering against physical injury around the brain and spinal cord, and to help secure the brain to the cranial vault.

Cerebrospinal fluid

Cerebrospinal fluid (CSF) is a clear watery fluid with a composition similar to plasma. It contains substances including water, glucose, sodium, chloride, potassium, protein and waste products such as urea. The CSF is formed from the blood and is produced by a combination of filtration and active secretory processes by the choroid plexus in the ventricles of the brain. CSF circulates in the subarachnoid space surrounding the brain and spinal cord. The total volume of the CSF is about 150 mL. The fluid is formed continuously in the ventricles at a rate of about 600–700 mL/day, and is reabsorbed into the blood at about the same rate. The normal CSF pressure when the body is horizontal is 5–10 mmHg. The functions of CSF are to:

The cranial nerves

Twelve pairs of cranial nerves leave the brainstem. The numbers (Roman numerals are the convention), names and functions of the cranial nerves are:

The spinal nerves

The spinal nerves project out of the vertebral canal, one pair emerging below each vertebra, and one pair emerging between the cranium and the first cervical vertebra. The spinal nerves are mixed nerves, containing both sensory and motor fibres. They allow for sensation and movement in peripheral parts of the body not supplied by the cranial nerves, such as skin, muscles, bones and joints of the trunk and limbs. The spinal nerves are arranged in groups according to their region of origin in the cord. There are:

In some regions the nerves divide immediately after leaving the cord. These then branch and unite with each other to form what is called a plexus (meaning braid). The major plexuses are:

The sciatic nerve is the largest nerve in the body, running over the hip posteriorly down the back of the thigh to the knee where it divides into the peroneal nerve and tibial nerve (Marieb 2012).

The sympathetic nervous system

The sympathetic nervous system arises from grey matter in the spinal cord from T1 through to L2. Sympathetic nerves then synapse in a chain of ganglia that lies on either side of the vertebral column, before reaching organs or tissues. A ganglion (plural ganglia) is a knot-like mass of cell bodies. Plexuses are formed by fibres from these ganglia; for example, the solar plexus lying behind the stomach and supplying the abdominal organs, and the cardiac plexus supplying the heart and lungs (Marieb 2012).

The parasympathetic nervous system

The parasympathetic nervous system consists of cranial nerves III, VII, IX and X and nerves that emerge from the sacral region of the spinal cord. The vagus nerve (cranial nerve X) is the largest autonomic nerve.

Functions of the autonomic nervous system

The functions of the autonomic nervous system are to control the movements of internal organs and the secretions of glands. The system provides dual control: the activity of an organ is stimulated by one set of nerves, and inhibited by the other set of nerves. This dual control achieves smooth rhythmic action of involuntary muscles and internal organs, maintaining a balance between activity and rest.

The sympathetic nerves are called adrenergic nerve fibres and release the neurotransmitter noradrenaline. These nerves can be affected by strong emotions such as anger, fear or excitement, and have a stimulating effect on most organs. The effect resembles that produced by adrenaline, a hormone secreted by the adrenal glands. This effect is called the ‘fright, fight or flight’ effect, in which the body responds to a fright either by preparing to fight or by running away. The response of the body includes:

The parasympathetic nerves are called cholinergic fibres and release the neurotransmitter acetylcholine. These nerves tend to slow down body processes, so that the end result of the antagonistic action of each division of the autonomic nervous system is a balance between acceleration and retardation. After the ‘fright’ or stressful situation is over, the parasympathetic nervous system returns things to normal. The digestive organs receive more blood, the glands increase their secretions, the heartbeat is decreased and the blood pressure falls. The effects of sympathetic and parasympathetic stimulation on various body organs are compared in Table 33.1.

Table 33.1 Effects of sympathetic and parasympathetic stimulation

Congenital disorders

The central nervous system of the developing fetus is very vulnerable to damage. Factors that may cause nervous system damage include the passage of microorganisms and drugs across the placental barrier into the fetal circulation. Other factors that may cause nervous system defects and result in physical and intellectual deterioration include chromosomal abnormalities, metabolic disorders, cranial malformations and structural abnormalities. The central nervous system may also be damaged during the birth process; for example, by cerebral anoxia or cerebral haemorrhage.

Inflammatory and infectious conditions

Bacterial or viral infective processes affecting the central nervous system may result in the destruction of nervous tissue through the action of toxins released by the living microorganisms and from the material released from dead microorganisms, which stimulates the inflammatory process. Infection and inflammation of nervous tissue may result in altered behaviour, altered consciousness and sensory or motor deficits.

Trauma

Trauma to the nervous system may result from elements within the system or from external forces. Trauma occurring from elements within the nervous system includes: bleeding from an aneurysm or ruptured intracranial vessel; transient interruption of the cerebral blood flow, causing ischaemia; and occlusion of a cerebral blood vessel by a thrombus or embolus. The most common causative factors in these conditions are hypertension and atherosclerosis.

Trauma from external forces may be caused by a direct or an indirect injury. A direct acceleration brain injury occurs when the head is struck by a moving object, and a direct deceleration injury occurs when the head in motion strikes a stationary object. In an indirect brain injury, the traumatic force is transmitted to the head through an impact to another part of the body, such as the neck or buttocks.

In open head trauma, a penetrating injury damages the integrity of the skull and/or meninges and brain. Infection may occur, as the injury allows the entry of microorganisms. A closed head injury is non-penetrating, with generally no disruption to the integrity of the cerebral meninges. Closed head injuries can result in jarring, bruising or tearing of brain tissue, which can cause haemorrhage, cranial nerve damage and cerebral oedema. An important event in closed head injury is known as coup and contrecoup. The coup injury is cerebral bruising resulting from impact to the skull, and contrecoup refers to the rebound effect of the injury, the movement of the brain opposite to the site of impact.

The nervous system response to trauma, which may cause more damage than the actual injury, results in oedema, bleeding and increased intracranial pressure. These factors destroy nervous tissue by compression or restriction of the circulation.

The spinal cord may be damaged as a result of a crushing or penetrating injury, dislocation of the spinal column, prolapsed intravertebral discs or neoplasia. In addition to tearing of, and pressure on, the spinal cord tissues, damage may be caused by haemorrhage, oedema or disruption of the blood supply to the spinal cord.

Damage to the peripheral nerves may result in loss of sensory and/or motor function (Marieb & Hoehn 2010).

Neoplasia

Tumours of the nervous system, which may be either benign or malignant, cause symptoms related to pressure, destruction of nervous tissue, oedema and disruption of the blood supply. The neurological manifestations of a tumour affecting the nervous system depend on the location of the tumour and on its rate of growth.

Degenerative conditions

The causes of degenerative disorders of the nervous system are varied and involve atrophy of neurons and nerve fibres. The course of a degenerative disorder is generally gradual and progressive over many years. The effects of degenerative disorders include: progressive muscular atrophy; impaired speech, chewing, swallowing and breathing; deterioration of intellectual capacity; impaired motor function; and dementia.

Metabolic and endocrine disorders

Nervous system dysfunction may result from the effects of certain metabolic and endocrine disorders. Some nutritional deficiencies may affect nerve cells, resulting in their damage or death. For example, degeneration of the posterior and lateral columns of the spinal cord may occur from the vitamin B12 deficiency of pernicious anaemia. Disorders of cortical function, leading to confusion or coma, may result from a deficiency of thiamine (vitamin B1).

Specific endocrine disorders such as hypothyroidism result in decreased metabolic rate, and hypothermia can develop. If the body temperature falls below 30°C, unconsciousness will result. Myxoedema coma is characterised by exaggeration of the signs and symptoms of hypothyroidism, with neurological impairment leading to loss of consciousness.

Headaches, or cephalalgia

Headaches, or cephalalgia, are common in a variety of disorders and situations ranging from functional disturbances of blood vessels to tension and stress. In neurological disorders, headaches are one of the most common symptoms. Headaches can result from compression, traction, displacement or inflammation of the cranial periosteum, the dura mater, cerebral arteries or branches of the cranial nerves. Headaches may also occur as a result of tension within extracranial structures such as muscles, air sinuses and blood vessels. Headaches are commonly classified as vascular, tension or traction–inflammatory.

Vascular headaches include migraine, cluster headaches, hypertension headaches and headaches resulting from temporal arteritis. Although the mechanisms of migraine are not completely understood, migraine appears to result from an inherited predisposition and seems to be precipitated by trigger factors such as stress, abrupt falls in oestrogen levels, low blood glucose levels and dietary intake. One theory is that migraine results from spasm of intracranial blood vessels and dilation of extracranial blood vessels. The classic characteristics of migraine headache include throbbing and a tendency for the attacks to be unilateral. Some attacks are preceded by a variety of visual disturbances, such as loss of half of the visual field or flashing lights across the visual fields. Some individuals experience vertigo, nausea and vomiting.

Cluster headaches are a rapid succession of attacks over several days, followed by remission. Previously thought to be caused by histamine sensitisation, cluster headaches are now considered to have a vascular cause. Headaches associated with severe hypertension may be intense and similar to those caused by intracranial lesions. Temporal arteritis causes severe, throbbing headaches in the region of the temporal artery and is sometimes accompanied by visual loss.

Tension headaches are caused by prolonged contraction (tension) of the neck, head or facial muscles. Tension headaches are frequently associated with psychological factors such as anxiety or depression. The pain tends to be bilateral and, unlike vascular headaches, is not throbbing in character.

Traction–inflammatory headaches: headaches of this type are related to increased intracranial pressure, which causes irritation of, and traction on, blood vessels and the dura mater within the skull. Inflammation of the meninges (meningitis) can also result in severe headache. Headaches of intracranial origin related to increased intracranial pressure vary from mild to excruciating depending on the location and cause, such as a tumour, lesion or cerebral oedema.

Sensory changes

Sensory changes, which can result from disorders of the brain, spinal cord or peripheral nerves, include alterations in the sense of touch, pain, temperature sensitivity and the loss of a sense of position. The loss of these sensations may be partial or complete. Common sensory disturbances include neuritis and neuralgia. Neuritis, characterised by pain and tenderness along the path of a nerve, can progress to complete loss of sensory and motor function. Neuralgia is characterised by severe stabbing pain, and can be caused by a variety of disorders affecting the nervous system. Other sensory changes that may accompany nervous system disorders include a loss of taste or smell, visual changes and hearing loss.

Motor changes

Alterations in motor function include localised or generalised weakness, with difficulty in moving normally. Muscle tone may be abnormally increased or decreased. A pronounced increase in tone is referred to as rigidity. Spasticity of muscles is an increased resistance to passive stretch, with rapid flexion of a joint. Abnormal movements include:

Symptoms of ataxia, a condition characterised by impaired ability to coordinate movement, may be caused by a lesion in the spinal cord or cerebellum. Dizziness or vertigo, when the individual is unable to maintain normal balance in a standing or seated position, may also be related to a disorder of the nervous system. Unusual gait or stance may result from motor or sensory deficits caused by a disorder of the nervous system, such as Parkinson’s disease. Paralysis, a symptom of motor disturbances, can occur in varying degrees with many nervous system disorders. Upper motor neuron lesions, in which the reflex area remains intact, generally cause spastic paralysis. Flaccid paralysis generally occurs in lower motor neuron lesions, which disrupt the reflex area.

Reflex changes

Reflex changes can provide evidence of damage to the nervous system. The absences of normal reflexes, or the presence of abnormal reflexes, generally indicate nervous system dysfunction. Reflexes are classed as either superficial (cutaneous) or deep tendon (muscle stretch). Superficial reflexes are elicited when a stimulus is applied to the skin surface or to mucous membrane. Deep tendon reflexes are elicited when a stimulus is applied to a tendon, bone or joint.

Altered awareness, personality or level of consciousness

A neurological disorder that results in altered brain structure may cause impairment of a person’s cognitive functions. They may experience difficulty in being able to think, remember, reason or understand. The person may also be confused in that orientation to time, place and person is impaired. Signs of reduced alertness or responsiveness may also be shown. Brain damage, for example as a result of a head injury, can cause a confused state characterised by fluctuating disorientation and incoherence.

Cerebral impairment may also cause mood changes and/or inappropriate emotional responses. Diffuse brain damage such as that caused by a large cerebral infarction may result in emotional instability or lability (a tendency to show alternating states of happiness and sadness that seem to be inappropriate). The person may also show signs of emotional flatness or apathy, demonstrated by a reactive absence of emotions. Alternatively, the client may become euphoric.

Damage to the brain can also result in altered states of consciousness, ranging from drowsiness and difficulty in being aroused by normal stimuli, to coma. More information on assessment of level of consciousness is provided later in this chapter.

Seizures

Seizures, which are paroxysmal events associated with sudden abnormal discharges of electrical energy in the neurons of the brain, may be secondary to central nervous system disease. Seizure disorders are described later in this chapter.

Level of consciousness

The level of consciousness is a most important factor in neurological assessment, providing valid information about changes in neurological status. Change can occur slowly over the course of many days, or it can occur rapidly in a few minutes or hours. The rapidity of change is an indicator of the severity of the neurological problem. The client’s level of consciousness is evaluated by providing stimuli and observing the response. Sound and pain are the major stimuli used. Speaking to the client is the most common method of applying an auditory stimulus, while painful stimuli are reserved for the client with obviously decreased levels of consciousness. When spoken to, a fully conscious client should reply with an appropriate verbal response. A person with a decreased level of consciousness may respond in a puzzled way or may not respond at all, showing no response even when someone speaks directly into their ear (Crisp & Taylor 2009).

Painful tactile stimuli

Painful tactile stimuli may be necessary to arouse the semi-comatose client. Painful stimuli can be provided by exerting firm digital pressure on the nail beds, the Achilles tendon or the gastrocnemius muscle. Response to painful stimuli can be classified into:

The Glasgow Coma Scale (GCS) (Fig 33.7) was originally designed to assess the level of consciousness in people with head injuries but is now used in a variety of settings. It has gained increasing acceptance as an accurate and effective means of evaluating levels of consciousness. Using the GCS, a score of 15 reflects a fully alert, well-oriented person, while a score of 8 or less is considered to indicate coma. The lowest possible score of 3 is indicative of brain death. The GCS is standardised world wide.

Figure 33.7 The Glasgow Coma Scale

Evaluation of the pupils

Evaluating the pupils provides vital information about the brain and raised intracranial pressure. The findings in one pupil are compared with the findings in the other, and the differences between the two pupils are documented. The pupils are assessed for size, shape and reaction to light. Normally the pupils are equal in size (average diameter of 3.5 mm), round and they constrict briskly when light is shone into the eye. A pupil gauge may be used to estimate the size of each pupil. Abnormal responses of a pupil to light may be described as sluggish, non-reactive or fixed. Generally, any change in a pupil’s size, shape or reaction is indicative of an intracranial change.

Assessment of motor function

Assessment of motor function usually focuses on the arms and legs, and the identification of significant changes is important for denoting improvement, stabilisation or deterioration in the client’s condition. The techniques used to evaluate motor function depend on the client’s level of consciousness. In the conscious client, the assessment can be made by observing motor responses to directions; for example, by asking the client to squeeze the assessor’s hands. If the client is unconscious or is unable to provide accurate responses, the assessor must rely on observational skills to evaluate motor function.

Assessment of sensory function

Assessment of sensory function is described earlier in this chapter.

Assessment of the vital signs

Assessing the vital signs (see Ch 18) provides data concerning vital functions of the body. The client’s temperature, pulse, ventilations and blood pressure are monitored and documented at a frequency that depends on their condition. Data from neurological assessments are documented according to the healthcare institution’s policy. Many institutions use a special neurological assessment chart, similar to the one illustrated in Figure 33.7.

Evaluation of motor function

Evaluating motor function involves assessing the client’s gait, posture, muscle strength and tone, balance and coordination. The assessor observes for abnormalities and compares the findings on both sides of the body for asymmetry.

Evaluation of sensory function

Evaluating sensory function involves assessing the client’s ability to perceive various sensations with their eyes closed. Assessment includes testing of sensitivity to touch, pain, temperature, testing of joint motion and position and assessment of discriminative function and vibratory sensation.

Evaluation of reflexes

Evaluation of reflexes involves testing the two types of reflex to assess the integrity of the motor and sensory systems.

X-ray

Plain x-ray films of the skull may be performed to detect fractures, to aid in the diagnosis of pituitary tumours or to detect congenital abnormalities. X-ray films of the spine may be performed to detect trauma to the vertebral column or to aid in the diagnosis of conditions that cause motor or sensory impairment.

Computerised tomography scan

Computerised tomography (CT) is commonly used to diagnose intracranial and spinal cord lesions. It is usually non-invasive but a contrast dye is sometimes administered to visualise blood vessels or to define lesions. The client lies on an x-ray table, with the head immobilised and face uncovered. The head is moved into the scanner, and a moveable frame revolves around it while x-ray films are taken. If a contrast agent is used the client may feel warm and experience a transient headache, a salty taste and nausea.

Myelogram

A myelogram involves fluoroscopy and radiography to evaluate the spinal cord and vertebral column after injection of a contrast medium into the subarachnoid space. A needle is inserted, most often in the lumbar area, into the subarachnoid space and about 10 mL of CSF is removed. Contrast medium is then injected through the needle and the client is positioned to allow the medium to flow through the subarachnoid space. A series of x-ray films are taken, after which the contrast medium may be either withdrawn or allowed to remain in the CSF. Water-soluble agents are allowed to remain, as they will eventually be excreted by the kidneys.

Angiography

Cerebral angiography involves injecting a radio-opaque contrast medium into an artery for radiological visualisation of the intracranial and extracranial blood vessels. Common injection sites are the carotid or femoral arteries, with x-ray films taken at various intervals after injection of the medium. Cerebral angiography may be performed using either local or general anaesthetic. Digital subtraction angiography is a computer-assisted radiographic procedure for visualising extracranial and intracranial vessels and involves injection of a contrast medium through a catheter into the superior vena cava. Cerebral vessels are visualised on a screen, and pictures taken.

Pneumoencephalography

Pneumoencephalography is performed infrequently since the advent of the CT scan. Pneumoencephalography allows radiographic examination of the cerebral ventricles after injection of air or oxygen into the subarachnoid space.

Magnetic resonance imaging (MRI)

An MRI is a non-invasive procedure in which the individual is placed in a strong magnetic field and is subjected to precise computer-programmed bursts of radio pulse waves. The sharpness and detail of the images produced assist diagnosis by providing identification of abnormalities and can detect neurological disorders with structural changes, for example, stroke, tumour, infection. MRI is contraindicated in clients with pacemakers, metallic aneurysm clips and some metallic prostheses.

Positron emission tomography (PET) scanning

PET scanning is a non-invasive nuclear imaging technique used to detect biochemical and physiological abnormalities. The client is injected with a nuclide that reacts with electrons and produces gamma-ray photons. A scanner detects the gamma rays and codes this data into a computer. Radioisotopes evaluate cellular metabolism, and may show a typical pattern for Alzheimer’s disease, and can be used to differentiate tumour reoccurrence from radiation necrosis. The computer then reconstructs cross-sectional images of the tissues being examined. PET is not widely available.

Radionuclide scan

This test uses a camera or scanner to provide images of the brain after administration of a radioisotope. The rays emitted by the radioisotope are converted into images that are displayed on a screen.

Queckenstedt’s test

Queckenstedt’s test is sometimes performed as part of the lumbar puncture if an obstruction of the spinal subarachnoid space is suspected. While the lumbar puncture needle is in place, an assistant manually compresses both jugular veins for 10 seconds. The CSF pressure is read and recorded at 5-second intervals and again after release of jugular pressure. Normally, occlusion of the veins of the neck causes an immediate rise in spinal fluid pressure; if the vertebral canal is blocked, no rise occurs. The test is contraindicated if the client has increased intracranial pressure or cerebral bleeding, because brainstem herniation or further bleeding can occur.

Cisternal puncture

A cisternal puncture may be performed to obtain a sample of CSF when a lumbar puncture is contraindicated. A needle, with stylus, is inserted into the cisterna magnum and a sample of CSF withdrawn. Cisternal puncture is a potentially dangerous procedure because the needle is positioned close to the brainstem.

Echoencephalography (ECHO)

An echoencephalogram (ECHO) is a test that uses pulsating ultrasonic waves to indicate deviation of the cerebral midline structures. Since the advent of computerised tomography, echoencephalography is used infrequently.

Electromyography

This procedure involves recording the electrical activity of a muscle and peripheral nerve and may be performed to aid in diagnosis of neuromuscular disorders. Needle electrodes are inserted into the muscle to be examined, and recordings are made of the electrical activity of the muscle at rest and during contraction.

Nerve conduction studies

These studies involve application of an electrical stimulus to peripheral nerves, and measurement of their response by means of an oscilloscope.

Caloric testing for vestibular function

Caloric testing is a diagnostic procedure designed to evaluate the vestibular portion of the eighth cranial (acoustic) nerve. The underlying principle of the procedure is that thermal stimulation of the vestibular end organs with warm and cold water will elicit the oculovestibular reflex. This reflex, if intact, results in induced nystagmus and eye movement in response to cold or warm water irrigation of the external auditory canal. Each external meatus is irrigated for up to 3 minutes with both cold and warm water, with a pause of at least 5 minutes between irrigations. Irrigation with cold water should result in slow nystagmic eye movements on the same side, followed by rapid nystagmus to the opposite side. Irrigation with warm water should produce rapid nystagmus on the same side.

Anencephaly

Anencephaly is the failure of normal development of the brain (cerebral hemispheres and cerebellum) and scalp. The precise cause is unknown, and babies with the disorder do not live.

Spinal cord defects

These include spina bifida, meningocele and myelo-meningocele. These conditions are the result of incomplete closure of the neural tube during the first 3 months of embryonic development. Causes are thought to include maternal exposure to viruses, radiation and other environmental factors.

In severe forms, spina bifida involves incomplete closure of one or more of the vertebrae, causing protrusion of the spinal contents in an external sac. In spina bifida with meningocele, the sac contains meninges and CSF. In spina bifida with myelomeningocele the sac contains meninges, CSF and a portion of the spinal cord or nerve roots. Manifestations of congenital spinal cord defects vary and include a depression, dimple or tuft of hair on the skin over the spinal defect. The more severe defects cause neurological dysfunction such as paralysis of the legs, bowel and bladder incontinence and hydrocephalus.

Hydrocephalus

Hydrocephalus is an excessive accumulation of CSF within the ventricles of the brain. It may result from an obstruction in CSF flow or from faulty absorption of CSF. The condition can also occur as a result of cerebral injury or disease. In infants, the obvious manifestation of hydrocephalus is abnormal enlargement of the head. Other characteristics include distended scalp veins, thin and fragile scalp skin, downward displacement of the eyes, a shrill high-pitched cry, irritability and abnormal muscle tone of the legs.

Muscular dystrophy

Muscular dystrophy is a group of congenital disorders characterised by progressive wasting and weakness of muscles. Duchenne’s muscular dystrophy, which begins to manifest between the ages of 3 and 5 years, is the most common and severe form. Initially it affects the leg and pelvic muscles but there is progressive involvement of all voluntary muscles. Later in the disease, progressive weakening of cardiac and respiratory muscles results in heart or respiratory failure. Early manifestations of Duchenne’s muscular dystrophy include a waddling gait, lordosis (increased curvature of the lumbar spine) and marked difficulty rising from a supine to a standing position. As the disease progresses, facial, oropharyngeal and respiratory muscles become involved.

Huntington’s chorea

Huntington’s chorea is a disorder in which degeneration of the cerebral cortex and basal ganglia causes chronic progressive choreiform movements and mental deterioration. Onset is generally in early middle age, and the individual gradually develops progressively severe choreiform movements and dementia. The movements usually begin slowly, with facial grimacing and jerking arm actions. Over time, the movements become frequent, erratic and violent, affecting the trunk and lower limbs. Dementia may be mild at first but eventually severely disrupts the personality.

Neurofibromatosis

Neurofibromatosis is characterised by a variety of congenital abnormalities and the condition is usually classified according to which parts of the nervous system are affected. In the peripheral form, multiple cutaneous and subcutaneous nodules of varying size occur. Subcutaneous nodules may attach to the peripheral portion of the nerve, causing pain or pressure and, rarely, sensory loss in the distribution of the affected nerve. Neuromas, which are an overgrowth of subcutaneous tissue, may reach enormous sizes and commonly affect the face, scalp, neck and chest. Neurological symptoms may appear if the tumours cause pressure on the brain or spinal cord.

Cerebral palsy

Cerebral palsy comprises a group of neuromotor disorders resulting from prenatal, perinatal or postnatal cerebral hypoxia or damage. The incidence of cerebral palsy is highest in premature infants or in infants who have experienced a difficult birth resulting in cerebral damage. Causative factors include: chromosomal abnormalities; prenatal factors such as maternal infections, exposure to harmful chemicals or malnutrition; perinatal factors such as premature birth or instrumental delivery causing cerebral anoxia; and postnatal factors such as trauma, infection or malnutrition causing cerebral damage.

The manifestations of cerebral palsy range from mild muscle incoordination to severe spasticity. The spastic form of the disorder is characterised by rapid alternating muscle contraction and relaxation, muscle weakness and underdevelopment and muscle contraction in response to manipulation. The athetoid form of cerebral palsy is characterised by grimacing, writhing and jerking involuntary movements, which become more severe during stress. Ataxic cerebral palsy is characterised by disturbed balance, incoordination, muscle weakness and tremor. In addition to the range of motor deficits, the individual may experience sensory deficits such as speech, visual or hearing impairment. Intellectual disability accompanies cerebral palsy in about 40% of cases.

Cerebral aneurysm

A cerebral aneurysm is an abnormality of the wall of a cerebral artery that results in a localised dilation. If the aneurysm ruptures, blood enters the subarachnoid space or cerebral tissue. Causative factors include congenital defects in the arterial walls, sclerotic changes in blood vessels, hypertension and cerebral trauma. Manifestations of a cerebral aneurysm do not generally appear until the aneurysm ruptures. The most common symptom of rupture is the sudden onset of a severe headache, which may be accompanied by nausea and vomiting, motor deficits, visual disturbances and loss of consciousness. A cerebral aneurysm may be detected before it ruptures if the individual shows signs of oculomotor nerve compression, eyelid ptosis and a pupil that is sluggish or non-reactive.

Transient ischaemic attacks

Transient ischaemic attacks (TIAs) are recurrent episodes of neurological deficit. The attacks, which may last from seconds to hours, are generally considered to be warning signs of an impending thrombotic cerebrovascular accident (stroke). The characteristics of a TIA, which may be caused by micro-emboli or arteriole spasm, are various symptoms of neurological dysfunction followed by a return of normal function. Symptoms include double vision, slurred or thick speech, unilateral loss of vision, staggering or uncoordinated gait, unilateral weakness or numbness, dizziness and falling because of leg weakness.

Trigeminal neuralgia

Trigeminal neuralgia is a painful disorder of one or more branches of the trigeminal nerve that produces paroxysmal attacks of excruciating facial pain. While the cause is often unknown, the disorder may be associated with other neurological conditions such as aneurysms, cerebral tumours or multiple sclerosis. The individual experiences excruciating burning pain, which generally occurs suddenly in response to a stimulus, such as a draft of cold air, drinking hot or cold fluids, brushing the teeth or speaking or laughing. The frequency of attacks varies from many times a day to several times a month or year.

Intellectual disability

Intellectual disability is a syndrome of incomplete intellectual development associated with impaired learning and social adjustment. The causes include:

Manifestations include poor motor development, impaired concepts of space and time, learning difficulties, inappropriate behaviour and difficulty with social interactions.

Peripheral neuritis

Peripheral neuritis (polyneuritis) is the degeneration of peripheral nerves, resulting in muscle weakness and atrophy, sensory loss and decreased or absent tendon reflexes. Causes include chronic intoxication (alcohol, arsenic, lead), metabolic and inflammatory disorders (diabetes mellitus, rheumatoid arthritis), nutrient deficiencies (thiamine) and infectious diseases (meningitis or Guillain–Barré syndrome). Manifestations usually develop slowly, beginning with leg pains and numbness or tingling in the feet and hands. As the disease progresses the individual experiences flaccid paralysis, muscle wasting, pain of varying intensity and loss of reflexes in the legs and arms. Footdrop, ataxic gait and inability to walk will eventually occur.

Guillain–Barré syndrome

Guillain-Barré Syndrome (GBS) is an acute inflammatory polyneuropathy disease (Schub et al 2011). It is characterised by rapid and progressive neuromuscular paralysis (Schub et al 2011). There is no known cause of GBS; however, up to two-thirds of clients who are diagnosed with this condition have a 1- to 3-week previous history of upper respiratory or gastrointestinal infection (Lugg 2010). What happens in GBS is antiganglioside antibodies attack Schwann cells of the myelin sheath, causing demyelination, usually of the peripheral nerves which in turn halts nerve conduction (Schub et al 2011). Clients with GBS will initially complain of decreased function, weakness and deceased sensation in their arms and legs, with or without pain (Lugg 2010). This rapidly develops into muscle weakness, commencing distally then travelling to proximal with decreased reflexes and sensations (Lugg 2010). For some clients the disease progression will stop here; they will experience difficulty walking but will be able to be discharged to home (Lugg 2010). Others will progress to total paralysis. Thirty per cent of clients with GBS will require mechanical ventilation due to respiratory dysfunction (Lugg 2010). The disease progression is usually 4–8 weeks and is confirmed with a lumbar puncture, electromyography and nerve conduction studies. Treatment of GBS is supportive, Schwann cells will re-myelinate and most clients can expect a full recovery (Schub et al 2011). When caring for the client with GBS the nurse should assess airway and breathing, refer to speech pathology and maintain the client as nil by mouth until otherwise ordered, ensure adequate analgesia, perform pressure area care and take steps to reassure the client.

Bell’s palsy

Bell’s palsy is a disorder of the seventh cranial nerve that produces unilateral facial weakness or paralysis. An inflammatory reaction occurs in or around cranial nerve VII, resulting in nerve compression and the onset of flaccid facial paralysis. Factors responsible for the inflammatory reaction include infection, prolonged exposure to cold temperature and local trauma. The seventh cranial nerve can also be affected by other conditions such as a cerebral tumour, meningitis or a middle-ear infection. Manifestations are unilateral facial weakness, which is sometimes associated with pain around the angle of the jaw or behind the ear. On the affected side the mouth droops and the individual is unable to wrinkle the forehead, close the eyelid or smile. There may be excessive watering from the affected eye and drooling of saliva from the affected side of the mouth.

Parkinson’s disease

Parkinson’s disease is a degenerative process of nerve cells in the basal ganglia and substantia nigra. The substantia nigra is an area in the basal ganglia considered necessary for motor control. Although the precise cause of the disorder is unknown, research has demonstrated that a dopamine deficiency prevents affected brain cells from functioning normally. Dopamine is a neurotransmitter that plays a role in the transmission of nerve impulses between synapses. Factors implicated in the development of Parkinson’s disease include cerebral atherosclerosis and long-term therapy with drugs such as haloperidol and phenothiazine.

Manifestations of Parkinson’s disease are related to disturbances of movement: tremor, muscle rigidity and dyskinesia. The most common initial symptom is tremor; for example, ‘pill-rolling’ movements of the fingers, and to-and-fro head tremors. Tremors are aggravated by fatigue and stress, and decrease when the individual performs a purposeful activity or is asleep. The person experiences difficulty in initiating voluntary movement and loss of posture control, so that walking is with the body bent forwards. The gait consists of short shuffling steps that are slowly initiated. Facial expression becomes mask-like, and the voice is commonly high-pitched and monotone. The person’s intelligence is not affected.

Amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis, which is the most common form of motor neuron disease, is a progressive degenerative condition that is generally fatal within 3–10 years after onset. The disease affects the upper and lower motor neurons of the central nervous system, resulting in progressive muscular atrophy, progressive bulbar palsy and upper motor neuron deficits. While the cause is unknown, the disease is thought to result from viral, metabolic, toxic, infectious and immunological factors. Manifestations include skeletal muscle weakness and atrophy and impaired speech, chewing, swallowing and breathing. The cause of death is commonly respiratory muscle weakness and bulbar palsy causing respiratory failure.

Alzheimer’s disease

Alzheimer’s disease is a progressive degenerative disorder that causes cerebral atrophy and dementia. Although the precise cause is unknown, several theories propose that the disorder may result from a genetic factor, immunological dysfunction, a toxin or a virus. Recent research has focused on the role of neurotransmitters and on the effect of a deficiency of acetylcholine in the brain as a cause of the condition. Manifestations of the disease generally occur in three stages:

Delirium is a common mental disorder affecting older adults. The characteristics of delirium are listed in Clinical Interest Box 33.3. The acute condition is often misdiagnosed as a form of dementia and the underlying cause therefore being missed. A history of the client’s behaviour before delirium developed is essential in early recognition of the condition.

Multiple sclerosis

Multiple sclerosis is a disorder characterised by progressive demyelination of nerve fibres in the spinal cord and brain. Patches of demyelination throughout the central nervous system result in varied neurological dysfunction. The cause is unknown, but the disease is thought to result from viral or immunological factors. Manifestations vary depending on the areas of the central nervous system that are affected. Some clients experience mild exacerbations, with long remission periods, while others have frequent relapses, with increasing residual deficits. The most common initial symptoms are fatigue, motor weakness and visual disturbances. Other characteristic changes include numbness and tingling sensations, intention tremor, gait ataxia, paralysis, urinary disturbances and emotional lability. Clinical Interest Box 33.4 provides a teaching plan for the client as well as their significant others.

Myasthenia gravis

Myasthenia gravis is a chronic neuromuscular disorder that affects voluntary muscles and is characterised by fluctuating muscle weakness that is exacerbated by exercise. The disease is considered to be autoimmune in origin, resulting in an acetylcholine-receptor deficiency. The thymus gland is also thought to be involved in the disease because the gland is abnormal and remains active after puberty in clients with myasthenia gravis.

Manifestations include progressive weakness of certain voluntary muscles, with some improvement in muscle function after rest. The eye muscles are most commonly affected, with drooping of the eyelids (ptosis) and double vision (diplopia). Other affected muscles include those involved with facial expression, speech, chewing and swallowing. The client may experience problems with saliva, nasal regurgitation and choking. The shoulder and neck muscles may be affected so that the head tends to fall forwards. Weakened respiratory muscles make breathing difficult and predispose the person to respiratory tract infections.

Meningitis

Meningitis is inflammation of the meninges and can be caused by viruses, bacteria or fungi. The inflammation may involve one or all three layers of the meninges. Meningitis often begins when the causative organism enters the subarachnoid space, then the infection spreads because of the open communication over the brain’s convexity. The accumulation of exudate from the inflammatory process over the convexities or in the ventricles can obstruct the flow of CSF. Aseptic meningitis is thought to occur from meningeal irritation resulting from encephalitis, leukaemia, lymphoma or the presence of blood in the subarachnoid space. The major manifestations of meningitis are severe headaches, pyrexia, irritability, neck rigidity, photophobia and pain in the back and limbs. Other manifestations are alterations in mental status, altered levels of consciousness and restlessness. Vomiting may occur, and cranial nerve involvement causes visual disturbances, pupil abnormalities, strabismus and vertigo. There may be generalised seizures due to cerebral oedema.

Encephalitis

Encephalitis is inflammation of the brain tissue caused by viruses, bacteria, fungi or protozoans. Endemic encephalitis begins in a non-human host or reservoir from which the virus is transmitted to humans, for example, through mosquito bites. After the pathogen gains access to the central nervous system via the bloodstream or along nerves, the white matter and meninges develop non-suppurative inflammation, and diffuse cerebral oedema results. Initial manifestations are headaches, pyrexia, vomiting, malaise and muscular aches and pains. These are often followed by alterations in the level of consciousness, confusion, motor and sensory deficits, hyperirritability and meningeal signs.

Brain abscess

A brain abscess is a collection of pus, usually occurring in the temporal lobes or the cerebellum. A brain abscess is accompanied by cerebral oedema and congestion. Most brain abscesses develop secondary to a primary source of infection such as mastoiditis or otitis media; or they may develop from a septic focus in the respiratory tract or, less often, from a pelvic or cardiac source. A small percentage result from a penetrating head wound such as a gunshot injury.

Manifestations include headache, pyrexia, vomiting, alterations in the level of consciousness, and local or generalised seizures. Other features differ according to the site of the abscess and include motor, sensory and speech disturbances.

Myelitis

Myelitis is the term that applies to a group of infective and non-infective processes that affect the spinal cord. Myelitis can be due to viruses, occur secondary to meningeal inflammation or be of unknown aetiology. The most common viral diseases causing myelitis are poliomyelitis and herpes zoster. Manifestations include a sudden onset of motor paresis, accompanied by other neurological deficits such as loss of sensory and sphincter functions.

Herpes zoster

Herpes zoster is a viral disorder that causes inflammation of the posterior root ganglia. The condition develops from reactivation of the varicella virus, the virus responsible for chickenpox. There is also evidence of a relationship between herpes zoster and certain systemic infections, neoplasms and immunosuppressive therapy. Manifestations include mild to severe neuralgic pain in the affected nerve root distribution. The pain, which may be burning, tingling, dull or sharp, may occur with or be followed by skin reddening and eruption of vesicles. The vesicles become pustules and develop a crust within 1–2 weeks. If infection or ulceration accompanies the vesicles, permanent scarring may result.

Occasionally, herpes zoster involves the cranial nerves, especially the trigeminal or oculomotor nerve. Trigeminal involvement causes eye pain and, possibly, corneal damage and impaired vision. Oculomotor involvement may result in conjunctivitis or ptosis. Rarely, herpes zoster leads to generalised central nervous system infection. Post-herpetic neuralgia can persist for months or years, and the skin may remain hypersensitive to touch.

Poliomyelitis

Poliomyelitis is an acute infectious disease caused by one of the three poliomyelitis viruses, which generally enter the body through the mouth or nose, multiply in the bloodstream and travel to the central nervous system. The viruses are then spread along neural pathways and destroy cells in the anterior horns of the spinal cord. The brainstem may also be damaged. The incidence of acute anterior poliomyelitis has decreased dramatically in the western world since the introduction of vaccination in 1955.

The virus may cause only a minor illness, or there may be signs and symptoms of viral meningitis and paralysis. The extent of paralysis depends on the location of the affected neurons. The initial manifestations of paralytic poliomyelitis include pyrexia, headaches, vomiting, irritability and pains in the neck, back, arms and legs. About 5–7 days after onset, the individual experiences weakness of various muscles, paraesthesia, hypersensitivity to touch and resistance to neck flexion. If the disease affects the brainstem, the muscles involved in swallowing, chewing and ventilation are affected.

Concussion

Concussion results from a blow to the head and is characterised by a loss of consciousness for less than 5 minutes and memory loss of events preceding and following the injury. Other features include headaches, confusion, dizziness, visual disturbances, vomiting and irritability.

Contusion

Contusion is bruising of the brain that disrupts normal nerve function in the bruised area and which may be associated with haemorrhage or oedema. Manifestations include drowsiness, confusion, behavioural changes, loss of consciousness, hemiparesis, unequal pupil response and decorticate or decerebrate posturing. With decorticate posturing the individual demonstrates hyperflexion of the upper extremities and hyperextension of the lower extremities (Fig 33.10A). With decerebrate posturing, both the upper and lower extremities are hyper-extended (Fig 33.10B).

Figure 33.10 Decorticate and decerebrate posturing A: Decorticate rigidity B: Decerebrate rigidity

Laceration

Laceration is tearing of the brain tissue, followed by intracerebral bleeding. Manifestations include prolonged unconsciousness, immediate neurological deficits and deterioration of the individual’s condition.

Haematomas

Haematomas are collections of coagulated blood and, in the brain, may be epidural, subdural or intracerebral. An epidural haematoma results from haemorrhage in the epidural space between the skull and the dura mater. A subdural haematoma results from an accumulation of blood in the subdural space, between the arachnoid and dura mater. An intracerebral haematoma is a collection of blood within the brain tissue.

Manifestations of cerebral haematomas vary according to the location and whether the haematoma develops rapidly or slowly. Typically an epidural haematoma causes immediate loss of consciousness, followed by a lucid interval that eventually gives way to a rapidly progressive decrease in the level of consciousness. Accompanying features include hemiparesis, severe headaches, unilateral pupil dilation and signs of increased intracranial pressure (decreasing pulse and ventilation rate, increasing systolic blood pressure). Manifestations of a subdural haematoma may not occur until days after the injury. Common features include headaches, drowsiness, confusion, slow responses and seizures. Pupillary changes and motor deficits commonly occur. Manifestations of intracerebral haematoma include neck rigidity, photophobia, nausea and vomiting, dizziness, decreased ventilation rate and seizures.

Cerebral herniation

Increased pressure in the cranial cavity can cause damage to the brain through hypoxia, ischaemia and infarction. Unrelieved or untreated raised pressure results in cerebral herniation. When pressure builds up in one area of the brain, brain tissue will begin to move into an area of lower pressure.

Tentorial herniation occurs when part of the temporal lobe herniates through the tentorial hiatus. Typical signs of this form of herniation are pupil dilation and hemiplegia.

Tonsillar herniation or ‘coning’ occurs when part of the cerebellum and/or brainstem herniates through the foramen magnum. Typical signs of this type of herniation are neck rigidity, dysfunction of the cardiac and respiratory drive and abnormal posturing. Irreversible brain damage and death can occur rapidly.

Spinal cord damage

Spinal cord damage may occur from traumatic injuries as a result of motor vehicle or sports accidents, gunshot or stab wounds or falls from high places. Fractures and dislocations can occur anywhere along the spinal column and, if the spinal cord is injured, may result in temporary or permanent damage.

Peripheral nerve damage

Peripheral nerve damage can result from pressure, compression, constriction or traction on a nerve, or as a consequence of skeletal fractures, lacerations or penetrating wounds. Nerve damage can also result from an injection of a toxic or metabolic substance into the nerve. The peripheral nerves most commonly injured are the radial, axillary and ulnar nerves and the brachial plexus. Manifestations include loss of motor function, loss of sensation and muscle atrophy. Depending on which nerve is damaged, there may be foot drop, wrist drop, limited range of motion or paralysis.

Aphasia

Aphasia is subdivided into three major classifications.

The loss or impairment of the ability to communicate is devastating and frustrating to the client and to their significant others, often resulting in fear and depression. Although the speech therapist will be the key person in the treatment of a client with a communication problem, the nurse must be aware of prescribed therapy so that it can be continued when the speech therapist is not with the client. The nurse should assume a calm, reassuring and supportive manner that conveys a sense of acceptance of the client’s behaviour. Table 33.3 provides guidelines that can be used when working with a client with aphasia.

Table 33.3 Assisting the aphasic client

Communication with the unconscious client is very important because, although the client appears to be completely unaware of their environment, it is impossible to determine their awareness of any stimulus. Many clients have recovered from unconsciousness and given accurate details of events or conversations that took place in their presence while they were unconscious. Therefore the nurse should assume that some stimuli will penetrate the complexities of unconsciousness. Stimuli can be provided by talking to the client, by touch and by playing a radio or CDs. The client should be told what the nurse will be doing—orient the client to time, place and person and describe the surroundings. Coma arousal is a technique whereby the unconscious individual is continuously exposed to a variety of stimuli, such as sounds, touch and smells in an attempt to increase the level of consciousness.

Outcome of unconsciousness

The ultimate outcome of unconsciousness varies from full recovery of brain function, through a wide range of disabilities, to irreversible coma and death. The development of sophisticated monitoring techniques and life-support systems has increased the survival rate for comatose clients with severe brain damage. A small percentage of clients emerge from deep coma to a state of wakefulness without awareness, never regaining any recognisable mental function.

Persistent vegetative state

Persistent vegetative state is a term used to describe a chronic condition occurring after severe cerebral damage. It is characterised by intact autonomic functions, generally intact reflexes, presence of a sleep–wakefulness cycle, spontaneous eye opening to verbal stimuli, no localising motor responses to verbal stimuli and no intact cognitive functions or awareness of self or of the environment.

Brain death

Brain death is a state of irreversible brain damage characterised by absence of cognitive functions and awareness of self and the environment, inability to maintain vital functions and the absence of isoelectric activity on EEG. In brain death (or brainstem death) the higher cortical functions cease, consciousness and awareness are lost, as is voluntary control of movement and all brainstem function. Some functions are not completely dependent on the integrity of the brainstem; for example, heart rate continues, though this is usually for a limited time as the client requires ventilatory support. If brainstem function can be shown to have ceased, then there is no prospect of recovery. The basic criteria for diagnosing brain death usually include:

Before considering a brain death diagnosis there is a need to exclude that brain dysfunction is the result of structural or metabolic disease, rather than the result of depressant drugs, alcohol, poisoning or hypothermia.

Brain death is a controversial legal, ethical and medical dilemma, but it is considered ethical and legal to terminate life support in clients diagnosed as brain dead.

Maintaining a patent airway

With the absence of cough and swallowing reflexes, secretions accumulate in the posterior pharynx and upper trachea. An oral artificial airway may be sufficient to maintain patency, or tracheostomy or endotracheal intubation and mechanical ventilation may be necessary. To prevent airway obstruction:

Monitoring neurological function

The client’s neurological signs are monitored at intervals determined by their condition. The results are documented and compared with previous assessments. Information on assessment of neurological function is provided earlier in this chapter.

Positioning

The client is generally nursed in a lateral position with a small pillow placed under the head and neck to maintain the head in a neutral position. The upper arm is positioned on a pillow to maintain the shoulder in alignment, and the upper leg is supported on a pillow to maintain alignment of the hip. The client’s position is changed so that they lie on alternate sides every 2–4 hours. If hemiplegia is present the client may be positioned on the affected side for brief periods, but care must be taken to prevent injury to soft tissue and nerves, oedema or disruption of the blood supply. Because vasomotor tone is decreased in the affected areas, such adverse effects can develop rapidly from improper positioning. If the correct position is maintained, secretions are able to drain from the client’s mouth, the tongue is less likely to obstruct the airway and postural deformities can be prevented.

Meeting hygiene needs

Care of the skin involves keeping it clean and dry and protected from damage. Areas of the skin, particularly over the bony prominences, should be assessed regularly for the signs of impaired blood circulation and irritation that contribute to the formation of decubitus ulcers. Dry skin may be lubricated with a suitable cream or lotion to prevent cracking and breakdown, and a water-repellent substance may be used to protect the skin against excreta or perspiration. The male should receive a facial shave as part of his daily hygiene care; the client’s nails are kept short and clean; and the hair is brushed, combed and washed as necessary.

Care of the mouth involves cleansing all areas at 2–4-hourly intervals to prevent a build-up of plaque, development of caries and development of a focus of infection. To prevent aspiration of fluid while oral hygiene is being performed, the client’s head is turned to one side and suction equipment made available throughout the procedure. The lips are lubricated with a suitable water-based substance.

Care of the nose involves cleansing the nostrils to keep them free of dried mucus. Cottonwool-tipped applicators and saline solution may be used to remove mucus and dried crusts, and a thin coating of cream may be applied to the rim of the nostrils.

Care of the eyes involves swabbing the eyes with moistened cotton wool to remove secretions, the instillation of artificial tears (or antibiotic eye drops if prescribed) and protecting the eyes from corneal abrasions. If the eyelids do not close fully, the use of eye shields or pads may be necessary to protect the corneas. (See Ch 32 for more information on care of the eye.)

Meeting nutritional and fluid needs

The nutritional and fluid needs of the client must be regularly assessed and met to maintain body function, support tissue repair and combat infection. The dietitian prescribes a nutritional program based on consideration of the individual’s energy needs, requirements for tissue repair, loss of fluid and basic life functions. Methods of administering nutritional and fluid support to the unconscious client include total parenteral nutrition, and enteral feedings administered via a nasogastric, nasojejunal or gastrostomy tube. Parenteral nutrition is only used if there is a long-term gut absorption problem, as the aim is to normalise gut function as soon as possible. Fluid input may be restricted to a specific amount of fluid in a 24-hour period. The purpose of fluid restriction is to control increased intracranial pressure by keeping the client slightly under-hydrated. As fluid input is correlated with output, an accurate input and output record must be maintained.

Meeting elimination needs

Because an unconscious client is incontinent, an external urinary drainage appliance or an indwelling catheter (IDC) may be used to manage urinary drainage. Both methods are used to keep the skin dry, as urinary incontinence can quickly lead to skin breakdown. Urinary drainage devices also enable accurate calculation of urinary output. Long-term IDC is avoided whenever possible due to risk of infection. Frequent checks and meticulous skin care is preferable. (Information on care of the client with a urinary drainage device is provided in Ch 29.)

Constipation and faecal impaction are common complications in an unconscious client because immobility and lack of a normal diet inhibit peristalsis. A program is established whereby aperients and rectal suppositories are administered to promote regular bowel evacuation. The frequency of bowel actions and the amount and nature of the faeces are documented (see Ch 30).

Promoting safety

Providing and maintaining a safe environment is of prime importance because an unconscious client is unable to perceive or react to safety hazards. Clinical Interest Box 33.5 suggests alternative routes for measuring temperature when a client is in a state of altered consciousness.

Preventing complications

Because the unconscious client is not mobile, they are at risk of developing any of the complications associated with immobility (muscle contractures, decubitus ulcers or venous, pulmonary or urinary stasis). Information on preventing these complications is provided in Chapter 26.

Providing sensory stimulation

The extent to which an unconscious client may be aware of what is happening to and around them cannot usually be determined; the nurse should therefore assume that the brain is receiving some sensory input. When the duration of coma extends into weeks or months, it may seem meaningless to keep explaining each activity to a client who gives no sign of comprehension. However, on regaining consciousness some clients have been able to describe accurately events that happened to and around them while they were unconscious. Although they were unable to communicate their feelings they were able to discriminate between the gentle caring manner of some people and the inattentive ways of others. Some clients have reported that they longed for someone to talk to them rather than about them.

The nurse should therefore act as though the client is conscious and demonstrate respect for them as a person. All activities should be explained to them, privacy during procedures should be ensured and they should be treated with dignity. Family members and friends should be encouraged to talk to and touch the unconscious client. They should be encouraged to perform certain activities for the client, such as combing the hair or applying skin lotion. Other sensory stimuli can be provided by playing a radio or CDs, or by placing perfumed flowers in the room.

Recovery from unconsciousness is a gradual process that tends to vary with each individual. Rehabilitation after a prolonged period of unconsciousness includes protecting the client from orthostatic hypotension. When able to tolerate a vertical position, an ambulation program is developed, unless neurological deficits make it infeasible. (Information on rehabilitation nursing is provided in Ch 38.)

Management of the client with impaired motor function

Disturbance of motor function is common among clients who experience disorders of the brain, spinal cord or peripheral nerves, such as cerebral haemorrhage, spinal cord injury or peripheral neuritis. While this chapter addresses the care of a client who has experienced a stroke or a spinal cord injury, the principles of care can be applied to clients who experience impaired motor function from other causes. Some terms relating to impaired motor function are:

Risk factors

Educational programs have been developed to inform the general public about stroke and prevention. Many factors have been identified as predisposing a person to a stroke and, by increasing public awareness, those at risk can seek medical advice to have any preexisting conditions managed, thus reducing the risk of stroke. Risk factors include:

Manifestations of a stroke

In all cases of stroke, areas of the brain are deprived of an adequate oxygen supply. If the blood supply is impaired for an extended period, the involved cerebral tissue may become necrotic, resulting in permanent neurological deficits. In instances of ischaemia, temporary neurological impairment may result. The particular type and degree of neurological deficits depend on the area of the brain involved (see Table 33.4). Table 33.5 lists a comparison of manifestations associated with right- and left-sided hemiplegia.

Table 33.5 Manifestations of stroke

Care during the acute phase

The acute phase begins when the client is admitted, and continues until their condition is stable. Nursing care is directed towards maintaining a patent airway and monitoring vital and neurological signs.

Maintaining a patent airway. This involves positioning the client on their side, administering oxygen as prescribed and suctioning secretions from the airway. Care must be taken when performing oronasopharyngeal suction, as suction applied for longer than 15 seconds at a time may increase intracranial pressure.

Recording fluid input and output. This information should be kept to monitor kidney function and to evaluate fluid and electrolyte balance.

Vital and neurological signs. These signs should be assessed frequently, for example every 15–30 minutes, to detect changes in the client’s condition. Information on neurological assessment is provided earlier in this chapter. If the client is unconscious, the principles of care described previously should be incorporated.

Care after the acute phase

Detailed information about the nursing measures necessary to meet the client’s basic needs for hygiene, safety, elimination, nutrition and fluids, psychological support, mobility and rehabilitation are provided elsewhere in this text. Clinical Interest Box 33.6 provides some suggestions which can facilitate self-care after stroke.

The main aims of care for a client who has experienced a stroke are to:

Rehabilitation

Rehabilitation of the client begins on admission to hospital and continues for as long as necessary including after discharge home. In some healthcare institutions the client may be transferred to a rehabilitation unit after the acute phase of their illness. The focus of rehabilitation is directed at helping the client to relearn lost skills and to become as independent as possible. The client and their significant others are made aware of the plan and goals of the rehabilitative phase, and their active participation is encouraged. Recovery from a stroke is a slow process; therefore the nurse must provide support and positive feedback so that the client does not become discouraged. Rehabilitation of the client includes:

More information on rehabilitation nursing is provided in Chapter 38.

Planning for discharge

Discharge planning is directed at facilitating the transition from the healthcare institution to the home environment. Discharge planning involves assessing the client and the family, identifying specific needs, planning to implement ways of meeting those needs and evaluating the discharge process and the results. After the client is discharged home, they and the family must have contact with support services, such as the district nurse, whom they can rely on for continued help and support.

Classification of spinal cord injuries

Spinal cord injuries can be classified by the type of injury and by syndromes:

Manifestations of spinal cord injury

Generally, the degree of damage to the spinal cord at any level is described as incomplete or complete transection. Incomplete transection of the cord produces loss or impairment of sensation and motor function that reflects the specific nerve tracts that have been damaged. Complete transection of the cord results in permanent loss of voluntary movement, sensation, reflex and autonomic function below the level of injury.

Spinal shock

Spinal shock is an immediate response to an acute spinal cord injury and is the temporary suppression of reflexes controlled by the segments below the level of injury. After a period that may vary from hours to months, the spinal neurons gradually regain their excitability. Subsequent return of some function results from decompression of the cord as oedema resolves.

Functional loss from spinal cord injury

The different functions and dysfunctions associated with spinal cord injuries at specific levels are listed in Table 33.6. The effects of spinal cord injury on sexual response vary depending on the level and degree of injury. Sexual function is controlled by spinal levels S2, S3 and S4. Knowledge of the physiology of alterations in sexual response after spinal cord injury is incomplete, and significant individual differences exist. People with complete loss of sensation in the genitalia may still experience orgasm in response to sensations produced by stimulation of other areas of the body in which sensation is intact. Sexual pleasure can also be increased by psychological stimuli, such as memory, sight, sound and odour. Physical stimulation of the genitalia may produce reflex erection of the penis and vaginal lubrication, even though there is no sensory awareness of stimulation.

Table 33.6 Spinal cord injury—functional loss

Initial management

On arrival of the client in the accident and emergency department, the medical officer assesses the client, and x-rays are taken to determine the extent of the injuries. The medical officer develops a plan of care that may include immediate surgery or a non-surgical approach with traction and immobilisation and insertion of a nasogastric tube, indwelling urinary catheter and intravenous infusion. Generally, glucocorticoid steroids are prescribed to reduce cord swelling.

Early management

After initial assessment and stabilisation of the client, they are admitted to the intensive care or spinal unit. A client with less severe injuries may be admitted to a general ward. Medical management will depend on the type of spinal cord injury and any associated injuries. Treatment may be surgical, non-surgical or a combination of both approaches. Surgical management may take the form of decompression laminectomy, fusion of vertebrae, open or closed reduction of fractures or dislocations or the insertion of rods. Non-surgical management involves immobilisation of the spine (Fig 33.11) using skeletal tongs with traction, halo traction, a cervical collar or a device designed to maintain thoracic or lumbar alignment, such as a fibreglass body jacket.

Figure 33.11 Immobilisation of the spine A: Cervical traction with tongs. The inset shows the position of the tongs on the bone structure of the skull B: Halo traction and vest

Respiratory care

A client with a spinal cord injury can develop varying degrees of respiratory difficulty, depending on the level of spinal injury. The client will require a plan of care directed at preventing pulmonary complications. Intubation and mechanical ventilation will be required if there is impairment of respiratory muscle function. The program of care includes:

Immobilisation and alignment of the spine

After alignment of the spine has been achieved, immobilisation serves to maintain alignment and promotes healing at the site of injury. For most thoracic, lumbar or sacral injuries the client remains confined to bed, with the back positioned and supported to achieve hyperextension of the spine at the site of injury. A bed with a firm mattress and steel base and correctly positioned pillows are necessary to maintain the prescribed posture.

Skeletal traction

When the injury involves dislocation or fracture-dislocation of the cervical or high thoracic spine, skeletal traction is commonly used to accomplish alignment and immobilisation (see Fig 33.11). Skeletal traction may be achieved by means of cervical tongs, such as Crutchfield tongs, or by the halo device. The halo device may also be incorporated with the use of a body vest or jacket to stabilise the spine, thereby allowing the individual to be ambulatory. When skeletal traction is used, the client may be nursed on a firm mattress and fracture board, or on a special bed such as a Stryker frame.

After skeletal traction has been established, pain is decreased and the client’s comfort is enhanced. Turning can be carried out using a special technique (as described in Ch 21) to allow for skin care and a change of position. Alternatively, a client may be lifted in a Jordan frame for hygiene purposes. Management of the client in cervical skeletal traction includes:

Preventing complications

Because prolonged immobility can lead to various complications, specific preventive measures must be implemented. (Information on preventing the complications associated with immobility is provided in Ch 26.)

Meeting basic needs

Clients with impaired motor and sensory function require assistance to meet their needs for hygiene, safety, elimination, nutrition and fluids, temperature regulation and pain relief. (Information on assisting clients to meet these basic needs is provided in other chapters.)

Providing psychological support

A severe spinal cord injury has a devastating effect on the client and their significant others, and they will experience a range of emotional responses, from the time of injury and through the rehabilitation process. The client will have to adapt to the loss of motor function and sensory deprivation, both of which severely threaten self-concept and body image. It is important that the nurse is aware of the impact that the injury has on the client’s emotional and psychological equilibrium. The nurse must be sensitive to the emotional and psychological response of the client to the injury, and be supportive as they deal with the impact of the injury. The nurse can help to support the client by:

Promoting rehabilitation

In most instances of spinal cord injury the client will require long-term rehabilitation. Rehabilitation after spinal cord injury is a lifelong process of learning to live with a disability. The client and family together with the healthcare team members contribute to the development of the rehabilitative plans. (Information on rehabilitation is provided in Ch 38.)