The thumbs, fingers, lips, tongue and vocal cords are more sensitive than the trunk, due to the greater number of receptors found in them. The homunculus (Figure 9.5) illustrates how the various parts of the body are represented in the corresponding motor and sensory areas of the cerebral hemispheres, i.e. representation is proportional not to the relative size of the body parts, but to each part’s complexity of movement or the extent of its sensory innervation.

Figure 9.5 A. The motor homunculus showing how the body is represented in the motor area of the cerebrum. B. The sensory homunculus showing how the body is represented in the sensory area of the cerebrum.

(Reproduced from Montague et al 2005 with permission.)

The cerebellum is located below the posterior part of the cerebrum and is separated from it by a fold of dura mater (p. 305). It consists of two hemispheres separated by a narrow strip called the vermis. The cortex of the cerebellum consists of grey matter, folded to increase its surface area. The interior comprises white matter presented in a branching configuration termed the arbor vitae (tree of life). Links to the rest of the brain and spinal cord allow the cerebellum to receive sensory information and thereby to maintain equilibrium and modify voluntary movement, making it smooth and coordinated.

Pituitary gland

The pituitary gland is situated at the base of the brain in a depression or fossa in the sphenoid bone called the ‘sella turcica’. It is attached to the brain via a stalk which is continuous with the hypothalamus, and communication is by means of nerve fibres and blood vessels (see Ch. 5, Part 1).

Diencephalon

Three bilaterally symmetrical structures comprise the diencephalon:

• the thalamus

• the hypothalamus

• the epithalamus.

The thalamus

consists of two oval-shaped masses, mainly consisting of grey matter, situated within the cerebral hemispheres just below the corpus callosum. Sensory impulses associated with pain, temperature, pressure and touch are conveyed to the thalamus, which acts as a ‘gateway’. Chaos would reign if all sensory information were allowed to reach the sensory cortex.

The hypothalamus

is situated below the thalamus and forms the walls and floor of the third ventricle. It controls the output of the hormones from the pituitary gland. Other functions include the regulation of hunger, thirst and body temperature (see Chs 20, 21, 22).

The epithalamus

forms the roof of the third ventricle. Extending from its posterior border is the pineal gland that contains high concentrations of melatonin and is thought to influence circadian rhythms, e.g. the sleep/wake cycle (see Ch. 25).

Brain stem

This comprises three structures: the medulla, the pons and the midbrain. Inferiorly the medulla is continuous with the spinal cord and connects with the pons above. The pons is continuous with the midbrain, which connects with the lower portion of the diencephalon.

The medulla

All the spinal pathways pass through the medulla. Descending motor pathways (corticospinal and corticobulbar) cross to the opposite side in triangular-shaped structures called the pyramids, a process known as decussation. The medulla:

• contains the reticular formation, a diffuse area of grey and white matter that connects with the rest of the brain stem and cerebral cortex, within which is the reticular activating system (RAS), responsible for consciousness and arousal

• accommodates the reflex centres that control vital functions:

– the cardiac centre – regulates heartbeat and force of contraction

– the medullary rhythmicity area – adjusts the rhythm of breathing

– the vasomotor centre (VMC) – regulates the diameter of blood vessels

• contains other non-vital centres, including those responsible for coordinating swallowing, vomiting, coughing, sneezing and hiccupping

• contains the nuclei of cranial nerves VIII to XII (see Table 9.1, p. 309).

Table 9.1 Outline of the cranial nerves

Cranial Nerve Name And Number	Type	Functions
Olfactory (I)	Sensory	Smell (olfaction)
Optic (II)	Sensory	Vision
Oculomotor (III)	Motor Sensory	Controls four of the extrinsic (external) muscles that move the eyeball, and the muscle that raises the upper eyelid Some fibres control the iris muscle that constricts the pupil, and the ciliary muscle, which changes lens shape Proprioception
Trochlear (IV)	Motor Sensory	Controls the external muscle that moves the eyeball down and outwards Proprioception
Trigeminal (V) (three branches: ophthalmic, maxillary, mandibular)	Motor Sensory	Motor to the muscles of chewing (mastication) Sensory to the face, mouth, teeth and the nose
Abducens (VI)	Motor Sensory	Controls the extrinsic (external) muscle that moves the eyeball outwards Proprioception
Facial (VII)	Motor Sensory	Controls the facial, scalp and some neck muscles – facial expression. Autonomic fibres to the lacrimal (tear), nasal and some salivary glands – lacrimation and salivation Also controls the tiny stapedius muscle in the middle ear Taste
Vestibulocochlear (VIII)	Sensory	Hearing (audition) and balance
Glossopharyngeal (IX)	Motor Sensory	Controls the pharyngeal muscles involved in swallowing. Autonomic fibres to some salivary glands – salivation Taste Carotid sinus – regulation of blood pressure Proprioception
Vagus (X)	Motor Sensory	Supplies external ear, heart, larynx, trachea, bronchi, lungs, pharynx, oesophagus, stomach, small intestine and proximal part of large intestine, the liver, gallbladder and pancreas – swallowing, digestive secretions and movement, etc. Taste and other sensory inputs from structures innervated
Accessory (XI)	Motor Sensory	Controls muscles of the neck and shoulders – head movement, shoulder shrugging. The pharynx, soft palate and larynx – swallowing Proprioception
Hypoglossal (XII)	Motor Sensory	Tongue movements during speech and swallowing Proprioception

(adapted from Bowie & Woodward 2003)

The pons

The pons is a bridge between the medulla and the midbrain. It comprises fibres that connect with the cerebellum and fibres that link between the spinal cord and the brain. It contains the nuclei of cranial nerves V to VIII inclusive (see Table 9.1, p. 309). Other important nuclei also exert an influence on respiration.

The midbrain

The midbrain contains the centres for visual, auditory and postural reflexes. It is located above the pons and contains the nuclei of cranial nerves III and IV (see Table 9.1, p. 309). Cranial nerves I and II originate in the cerebrum.

The limbic system

A diffuse collection of nuclei, the limbic system, comprises an interconnected complex of structures, with links to the hypothalamus, cerebral cortex and the olfactory system. These are thought to be responsible for behaviour associated with emotions, subconscious motor and sensory drives and feelings of pain and pleasure.

The meninges

The brain and spinal cord are surrounded and protected by three meninges. From inside working out they are:

• pia mater

• arachnoid mater

• dura mater.

Pia mater

has its own blood supply and is a delicate layer that closely follows and adheres to the contours of the brain and spinal cord.

Arachnoid mater

is a fibrous layer between the pia and dura maters. It is separated from the pia mater by the subarachnoid space which contains cerebrospinal fluid (CSF). The arachnoid mater projects villi into the venous sinuses, which are responsible for the absorption of CSF.

Dura mater

is a double layer of dense fibrous tissue. It is separated from the arachnoid mater by the subdural space. The outer layer adheres closely to the underside of the cranial bones, whilst the inner, meningeal layer is much thinner. The spinal dura mater has only one layer, which corresponds to the meningeal layer of the cranium. The two layers of the dura mater separate at several locations and these spaces contain the venous sinuses, e.g. the falx cerebri and the tentorium cerebelli. The former forms an incomplete division dipping down between the two cerebral hemispheres (Figure 9.6). The tentorium cerebelli forms a division between the occipital lobes of the cerebrum and the cerebellum.

Figure 9.6 The meninges.

The ventricular system

The ventricular system of the brain comprises four fluid-filled irregular cavities (ventricles) interconnected by narrow pathways (Figure 9.7) and connected with the central canal of the spinal cord and the subarachnoid space. There are two lateral ventricles, one in each cerebral hemisphere, one ventricle (the third) located in the diencephalic region and the fourth located in the medulla.

Figure 9.7 The ventricular system.

Cerebrospinal fluid

circulates within the closed ventricular system. The normal features of CSF are:

• colour – crystal clear

• cells – <5 × 10⁶/L (all mononuclear)

• protein (total) – 100–400 mg/L

• glucose – 2.5–4.0 mmol/L.

The CSF production–absorption cycle is continuous and a fairly constant volume of 120–150 mL is maintained. When this process is interrupted and the volume is increased beyond normal limits, hydrocephalus occurs.

Most CSF is produced by the choroid plexus, a collection of specialised capillaries located within the lining of the ventricles, the largest amount being produced in the lateral ventricles. From here, the CSF passes through two interventricular foramina (foramen of Monro) to the third ventricle, then via the single cerebral aqueduct (aqueduct of Sylvius) to the fourth ventricle. Some CSF passes down into the central canal of the spinal cord but most passes up through the two lateral and one medial foramina in the roof of the fourth ventricle, to circulate round the brain and spinal cord in the subarachnoid space before being reabsorbed into the blood via the arachnoid villi.

The functions of CSF are to:

• protect and cushion the brain and spinal cord

• provide nourishment

• maintain a uniform intracranial pressure

• remove waste products.

Blood supply and drainage

The brain cannot survive without a constant supply of oxygen and glucose and receives 850 mL of oxygenated blood per minute. The blood supply to the head arises from the left and right common carotid arteries, which subdivide to form the internal and external carotid arteries. These supply blood to the anterior part of the brain, and the vertebral arteries supply the posterior part.

The greater part of the brain is supplied with blood by the arteries branching from the circulus arteriosus (circle of Willis), a ring of blood vessels located at the base of the brain (Figure 9.8).

Figure 9.8 The blood supply to the brain.

Venous drainage is by small veins in the brain stem and cerebellum, and external and internal veins draining the cerebrum. Some of the external and internal veins empty into one large vein called the vein of Galen (great cerebral vein). Unlike other parts of the body, these veins do not correspond with their arterial supply. All these veins empty directly into a system of venous sinuses, including the superior and inferior sagittal, the straight, transverse, sigmoid and cavernous sinuses.

See website Figure 9.3

The blood–brain barrier

This selective barrier normally prevents many harmful substances crossing from the blood to the brain, e.g. microorganisms. The blood–brain barrier (BBB) is formed by the capillary endothelial cells which have ‘tight junctions’ and are supported by astrocytes (a type of neuroglial cells) to ensure that the capillary wall is relatively impermeable. The barrier allows the passage of oxygen, nutrients and metabolic waste, and some drugs, alcohol and other toxic substances.

The spinal cord

The spinal cord is an oval cylinder that lies within the spinal cavity of the vertebral column. In adults, it is approximately 45 cm long and extends from the medulla to the first or second lumbar vertebrae. Beyond this, the spinal nerves from the lumbar and sacral segments of the cord form the cauda equina, or ‘horse’s tail’. The lower part of the cord is attached to the coccyx by the filum terminale and is tapered in shape (Figure 9.9).

Figure 9.9 The spinal cord.

The cord is segmented into five parts or regions, each corresponding to the specific vertebrae:

• cervical (C1–7)

• thoracic (T1–12)

• lumbar (L1–5)

• sacral (S1–5 fused bones)

• coccygeal (C1 fused bones).

A labelling system identifies different levels within the spinal cord and vertebrae; the third cervical vertebra becomes C3, the fourth lumbar vertebra becomes L4 and so on.

Two enlargements of the spinal cord are seen: (i) from C4 to T1 containing the nerve supply for the upper limbs; and (ii) from L2 to S3 which supplies innervation to the lower limbs. Paired spinal nerves, part of the PNS, are attached by two short roots to the cord (see pp. 308, 309).

The structure of the spinal cord is illustrated in cross-section in Figure 9.10.

Figure 9.10 Cross-section of the spinal cord. The cord is incompletely divided into right and left halves by the posterior and anterior median fissures. In the centre is the central canal which contains CSF originating from the fourth ventricle. Extending the entire length of the cord, this is located within an H-shaped area of grey matter with posterior and anterior and, at some levels, lateral horns. The remainder of the cord is made up of white matter organised in columns in the posterior, lateral and anterior segments.

The spinal pathways are described as:

• sensory – ascending from the body and transmitting impulses to the sensory cerebral cortex for interpretation

• motor – descending from the brain to skeletal muscles, where they initiate a motor response.

Each pathway has a name, derived from the spinal column in which it travels, the origin of the cell bodies and the termination of the axon.

Sensory pathways

These consist of the:

• posterior column pathway

• spinothalamic pathway

• cerebellar pathway.

Posterior column pathway

Each pathway comprises a chain of three neurones which transmit information such as discriminative touch and vibration sense from the appropriate receptors to the sensory cortex.

See website Figure 9.4

Spinothalamic pathways

are the lateral and anterior spinothalamic tracts. The first order neurone in both pathways connects the receptor with the spinal cord where it synapses with the second order neurone in the posterior grey horn. The pathway crosses over to the opposite side of the cord and ascends in either the lateral or anterior spinothalamic tract to the thalamus. The second order neurone synapses with the third order neurone, which then continues, terminating in the sensory cortex. Between them the spinothalamic tracts are responsible for conveying information about pain (see Ch. 19) and temperature, light touch and pressure.

Cerebellar pathways

are the posterior spinocerebellar and anterior spinocerebellar tracts. Both tracts convey impulses about joint position sense (proprioception) from muscles and joints, terminating in the cerebellum instead of the cerebral cortex. This time there are only two neurones involved, synapsing in the posterior grey horn.

See website Figure 9.5

Motor pathways

Once a motor process is initiated within the cerebral cortex, the impulses descend via two main motor pathways:

• pyramidal tracts that pass through the internal capsule and form the main pathway for impulses to voluntary muscles

• extrapyramidal tracts consisting of all the descending motor pathways that do not pass through the pyramids; extrapyramidal tracts collectively assist in maintaining muscle tone, posture and balance and gross automatic skeletal muscle movements.

See website for further content

Upper and lower motor neurones

These are the functional units of the motor system and convey motor impulses. Damage to one or the other will result in very different functional impairment. Damage to an upper motor neurone results in spasticity, while damage to a lower motor neurone results in flaccid paralysis.

Upper motor neurones

extend from the motor cortex to either the cranial nerve nuclei in the brain stem or the anterior horn of the spinal cord. The upper motor neurone is contained entirely within the CNS.

Lower motor neurones

start within the brain stem or anterior horn of the spinal cord and pass via cranial or spinal nerves respectively to the motor end-plate of muscles.

The peripheral nervous system

The PNS has two functional parts:

• somatic nervous system, which is further subdivided into motor and sensory divisions

• autonomic nervous system (ANS), which conducts impulses from the CNS to smooth muscle, cardiac muscle and glands.

The cranial nerves

The 12 pairs of cranial nerves pass from their origin, principally within the brain stem, out via small openings in the skull to innervate structures around the head and neck, and beyond (Table 9.1). Cranial nerves were formerly described as either motor or sensory, or mixed nerves; however, most motor nerves are now considered to be mixed, but with a dominance of motor or sensory fibres. (See Further reading, e.g. Tortora & Derrickson 2009.)

Spinal nerves

There are 31 pairs of spinal nerves, named and grouped according to the vertebrae with which they are associated. There are:

It should be noted that there is one more pair of cervical spinal nerves than there are vertebrae. This is because the first pair leave the vertebral canal between the occipital bone and the atlas, i.e. above C1, and the eighth pair leave below C7. Thereafter, the spinal nerves are named according to the vertebra immediately above.

Each spinal nerve has an anterior (motor nerve fibres) and a posterior root (sensory) (see Figure 9.10). The posterior root can be distinguished by its root ganglion, a cluster of nerve cell bodies.

Shortly after leaving the intervertebral foramina, both roots join together to form a mixed nerve. From here the spinal nerves continue to form a complex network all over the body, carrying motor signals to effectors such as the skeletal muscles and conveying sensory information such as touch to the CNS for interpretation. (See Further reading, e.g. Tortora & Derrickson 2009.)

The autonomic nervous system

The ANS comprises the nerves carrying motor impulses to the internal organs; thus it is exclusively peripheral and motor. Its activity is influenced by many factors, including sensory information from the internal organs, numerous peptides and hormones, and signals from higher control centres such as the hypothalamus. It is described as having two divisions, the sympathetic and parasympathetic, each imposing different effects (Figures 9.11, 9.12). (See Further reading, e.g. Tortora & Derrickson 2009.)

Figure 9.11 The sympathetic outflow, the main structures supplied and the effects of stimulation. Solid lines, preganglionic fibres; broken lines, postganglionic fibres.

Figure 9.12 The parasympathetic outflow, the main structures supplied and the effects of stimulation. Solid lines, preganglionic fibres; broken lines, postganglionic fibres. Where there are no broken lines, the second neurone is in the wall of the structure.

Neurological investigations

Patients may undergo a range of neurological investigations depending on their condition. Pre-procedure preparation and post-procedure care is identified in Table 9.2. The specific investigations performed for each condition are detailed throughout the chapter.

Table 9.2 Neurological investigations (adapted from Woodward & Waterhouse 2009)

Head injury and raised intracranial pressure

In 2006/2007 almost 156 000 people were admitted to hospital in England as a result of head injury, the majority of whom were young males. These figures have risen significantly since the implementation of the NICE head injury guidelines in 2003, which were updated in 2007 (Goodacre 2008). The majority of head injuries are mild (Glasgow coma scale [GCS] 13–15) but moderate (GCS 9–12) or severe injuries (GCS 3–8) are more likely to result in morbidity and mortality (see Ch. 28).

Falls (24–43%) and assaults (30–50%) are the most common causes of mild head injury in the UK, followed by road accidents (25%), although these account for a far greater proportion of moderate to severe head injuries. Alcohol may be implicated in up to 65% of all adult head injuries (NICE 2007a).

Pathophysiology

The adult skull can be considered as a rigid box divided into two major compartments, containing non-compressible components. A uniform pressure, called intracranial pressure (ICP), is maintained, defined as the pressure exerted within the cerebral ventricular system. When an individual sustains a head injury or there is some abnormal pathology, e.g. a tumour, it can cause ICP to rise.

Three intracranial components contribute to maintaining ICP:

• brain tissue

• CSF

• blood.

The brain tissue contributes 80% of the content. The remaining 20% is taken up in equal proportion by the CSF and the blood. Under normal circumstances, ICP is maintained within normal limits (0–15 mmHg), but when there is an increase in the volume of one of these components within the confined space of the skull a rise in ICP may occur. Transient rises in pressure occur with activities such as coughing or sneezing and this is a normal physiological response.

Changes to the brain and its associated structures following trauma may cause ICP to rise to a dangerous level, resulting in coma and leading to permanent brain damage or even death.

The causes and presenting symptoms of raised ICP

A raised ICP can be due to intracerebral or extracerebral causes (Box 9.2).

A rise in ICP can develop over a number of months in a slow-growing brain tumour, with the patient hardly noticing any symptoms, or it can occur in a matter of minutes following severe head injury, when the patient becomes immediately unconscious. A distinct correlation exists between ICP and conscious level; as ICP rises, conscious level deteriorates.

A relationship exists between the volume of a lesion inside the head and ICP, represented by the pressure–volume curve (Figure 9.13).

Figure 9.13 Volume–pressure curve.

During the initial rise in ICP, compensatory mechanisms come into play. The cerebral ventricular system can reduce the volume of CSF by displacing it into a distensible spinal dural sac. A reduction in cerebral blood volume also occurs as a result of autoregulation, the ability of blood vessels to constrict according to local conditions. This is represented by the flattened part of the curve. However, this is only a temporary measure and, as the volume of the expanding lesion increases, compensation is overcome and the steep part of the curve is entered. Then for every small increase in volume, the corresponding rise in ICP is dramatic. This process has four identifiable stages (Box 9.3).

Other factors which have an influence on this complex process include cerebral blood flow and cerebral oedema. (See Further reading, e.g. Woodward & Mestecky 2011.)

Herniation

The skull has two compartments:

• the supratentorial compartment above the tentorium

• the infratentorial compartment below the tentorium.

Herniation is the process by which tissue in a high-pressure compartment is compressed and forced through an available opening into an adjoining low-pressure compartment. Such a situation can exist in the patient with raised ICP.

The opening that permits trans-tentorial herniation is the tentorial notch, and that which permits tonsillar herniation is the foramen magnum.

Subfalcine herniation

involves the herniation of brain tissue across the midline from one side of the head to the other, under the falx cerebri.

Trans-tentorial herniation

involves the downward displacement of the cerebral hemispheres, diencephalon and midbrain (central herniation). The nerves and posterior cerebral arteries are stretched and compression of the oculomotor nerve (IIIrd cranial nerve) occurs, resulting in a non-reactive pupil that may also be dilated. These and other structures are displaced into the posterior fossa.

Lateral trans-tentorial herniation occurs in the presence of an expanding lesion located close to the temporal lobe. The medial part of the temporal lobe (the uncus) is forced downwards and can subsequently develop into a central herniation (Figure 9.14).

Figure 9.14 Types of herniation.

Tonsillar herniation

is the downward displacement of the lower part of the cerebellum (the cerebellar tonsils) through the foramen magnum, where compression of the medulla results.

Medical/surgical management

Common presenting symptoms

The head-injured patient with raised ICP may be fully alert and orientated, but consciousness is usually impaired. Neurological deficits can be found, e.g. limb weakness or occurrence of a seizure. Answers to the questions listed below should be obtained as they have an influence on the management and outcome:

• How long has the patient been unconscious? The period of unconsciousness relates to the severity of brain damage, i.e. the longer the patient is unconscious, the more severe the damage.

• Does post-traumatic amnesia (PTA) exist and for how long? The patient’s memory for events following injury is an indicator of the severity of brain damage, i.e. the longer the period of PTA, the worse the brain damage.

• What were the cause and circumstances of the injury? This may indicate if other extracranial injuries exist.

• Does the patient have any headache or vomiting?

Early signs and symptoms of raised ICP include reduction in level of consciousness and focal neurological deficits (e.g. limb weakness or speech deficits), followed by pupil changes and finally systemic changes (Cushing’s triad – bradycardia, hypertension and reduced/irregular respiratory rate). Hyperthermia may also occur due to compression of the hypothalamus and loss of the ability to autoregulate temperature.

Investigations

In the head-injured patient, skull X-ray may reveal a fracture and computed tomography (CT) or magnetic resonance imaging (MRI) may demonstrate cerebral contusions or lacerations and/or an intracranial haematoma (Hickey 2002) (Box 9.4).

Box 9.4 Information

Brain injuries

Contusions

Contusions are bruising of the cerebral tissue, most commonly affecting the frontal, occipital and undersurface of the temporal lobes.

There are two types:

• coup – indicates haemorrhage and oedema immediately under the injury site

• contrecoup – damage occurs directly opposite the injury site. This is caused by the rapid acceleration or deceleration movement of the brain within the skull following severe trauma, resulting in cerebral oedema and raised ICP.

Lacerations

Brain tissue is lacerated as a result of, for example, a skull fracture, resulting in disruption to cellular activity which will produce focal neurological deficits such as hemiparesis (weakness on one side of the body).

Contusions and cerebral oedema may also occur.

Diffuse brain injury

Here, there is no specific focal pathology. Shearing of the white matter occurs, causing disruption and tearing of the axons.

ICP monitoring

One of the most important diagnostic measures is the monitoring of ICP. This is an invasive technique involving direct measurement of ICP. A typical system comprises a fibreoptic transducer-tipped catheter, which can be placed in the lateral ventricle, subdural or extradural space. The level of ICP is then transmitted to a digital data display as a waveform. A pulsatile waveform will be demonstrated along with a pressure level indicating if the patient’s ICP is within normal limits (≤15 mmHg) (Figure 9.15).

Figure 9.15 The fibreoptic transducer-tipped catheter system for monitoring intracranial pressure (Camino system).

(Adapted from Hickey 2002.)

Treatment

In the past, the treatment of head injury focused primarily on the interventions required to reduce ICP. However, greater emphasis is now placed on maintaining cerebral perfusion pressure (CPP) which is the pressure needed to perfuse the brain with blood, at more than 70 mmHg (Box 9.5). Those patients with a high ICP, low blood pressure and low CPP make a poorer recovery. The means by which this is achieved are varied according to circumstances.

Hyperosmolar agents

An intravenous infusion of 100 mL of 20% mannitol over 15 min will reduce ICP by establishing an osmotic gradient between the plasma and brain tissue, thus removing water from the oedematous brain tissue to the blood. This will ‘buy’ time to allow the patient to be prepared for transfer to a specialist unit or for surgery. Repeated boluses may be administered over 24 hours, but may lead to a rebound increase in ICP.

Controlled ventilation

In the past it was recommended that the reduction of PaCO₂ would reduce ICP. However, it also causes vasoconstriction, thus reducing cerebral blood volume. The resultant reduction in cerebral blood flow may itself cause ischaemic brain damage (Lindsay & Bone 2004) so patients are ventilated to keep PaCO₂ within normal limits. Maintaining the blood pressure and CPP appear to be as important, if not more important, than lowering ICP.

Fluid management

Dextrose infusions should not be given to patients with head injuries. Due to disruption to the BBB, administration of dextrose could exacerbate cerebral oedema. 0.9% sodium chloride is the fluid of choice initially.

Sedatives

If ICP fails to respond to standard measures then sedation, under carefully controlled conditions, may help by reducing cerebral metabolism and thus offering a degree of protection for the brain (Lindsay & Bone 2004).

Surgical intervention

Surgery may be performed to remove a focal lesion such as an expanding haematoma and this may be combined with decompression. Withdrawal of small amounts of CSF via a ventricular catheter results in a reduction of ICP, but this provides only temporary relief. To be effective, drainage would require to be continuous, but this is often impractical.

Nursing management and health promotion: head injury

Head injury is preventable. This is an area in which nurses should exercise their health promotion skills, e.g. by emphasising the dangers associated with head injury and its detrimental effects when communicating with patients who have experience of minor head injury with good recovery, and with their families. This may include consideration of driver behaviour or unsafe work practices. The use of seatbelts for the driver and all car passengers has led to a reduction in head injuries, as has the use of protective headgear for motorcyclists and horse riders (Headway 2004). Because a common contributing factor in head injury is alcohol intake, where appropriate, the patient can be encouraged to consider personal lifestyle and the consumption of alcohol.

Head-injured patients with raised ICP can present in different ways on admission to hospital. The person may initially appear not to have sustained an injury but can progress to become drowsy or confused, or develop speech problems or limb deficits. Seizures may occur.

Immediate priorities

The immediate nursing aim is to prevent further damaging rises in ICP, and the first priority is to identify any alteration in respiratory function due to an inability to maintain an airway (Box 9.6). The nurse should be aware of the presence of other injuries, e.g. if the patient has been in a road traffic accident (see Chs 18, 27 for detail of assessment and interventions).

Box 9.6 Information

Respiratory care priorities in a patient with raised intracranial pressure

• Assess the rate, depth and pattern of respirations to indicate the patency of the airway. Report if the rate is less than 12 and more than 20, and any irregularities in rate or rhythm, as these may indicate a rise in ICP.

• Monitor O₂ saturations and assess the skin/mucosae for cyanosis, which would indicate inadequate respiration as a late sign.

• Apply oropharyngeal and tracheal suctioning only as required to remove secretions. Suction for no more than 15 s and consider preoxygenation prior to suctioning with 100% oxygen to prevent a build-up of carbon dioxide in the blood, resulting in further elevation of ICP.

• Institute measures to achieve optimal respiratory status including insertion of a Guedel airway, positioning the patient on their side with a 30 degree head-up tilt, and administer oxygen as prescribed.

• Assist with monitoring arterial blood gases and mechanical ventilation as required.

Assessment of neurological status

This is performed in order to:

• identify any immediate action that needs to be taken

• record a baseline to detect any changes in neurological condition.

Any deterioration in neurological status may be an early indication that ICP is rising further, thus increasing the likelihood of herniation (Mestecky 2007). Neurological assessment is important, as this may be the only indication that the patient’s condition is deteriorating and a standardised method of monitoring neurological status enhances this process. The gold standard method is the Glasgow Coma Scale (NICE 2007a) (Ch. 28).

The frequency of observations is determined by the patient’s condition, ranging from intervals of 15 min to 2 h. Conducting serial assessments is more important than a one-off set of observations. Medical staff should be promptly informed of any pertinent changes in the patient’s neurological status.

The nurse, as the health care professional who normally spends most time with the patient, should learn to observe changes in the patient’s behaviour which may herald an impending change in neurological status, e.g. the patient who does not answer questions so readily or who is becoming agitated and restless (Box 9.7).

The expert neurosurgical nurse will be alert to the early warning signs that must be reported so that treatment can be carried out as soon as possible (p. 314).

Surgery

Pre-operative care

Urgent surgery (e.g. craniotomy) may be indicated on admission or in response to subsequent deterioration. The nurse may need to prepare the patient in a very short time and also provide adequate explanation and reassurance (see Ch. 26).

Postoperative care

The overall priorities for patients following neurosurgery are:

• continuous assessment of neurological status (see Ch. 28)

• instituting measures to avoid secondary brain damage

• administration of appropriate therapies.

Table 9.3 outlines the main complications of neurosurgery.

Table 9.3 Complications of neurosurgery

Complications	Cause	Interventions
Altered conscious level	Increased ICP due to cerebral haemorrhage/oedema	Frequent assessment of neurological status
Onset of seizures	Cerebral irritation	Observation of seizures. Appropriate interventions if they occur (see section on epilepsy)
Limb weakness	Increased ICP due to cerebral haemorrhage/oedema	Frequent assessment of limb movements
Speech problems	Increased ICP due to cerebral haemorrhage/oedema	Frequent assessment of verbal responses
Respiratory problems	Increased ICP due to cerebral haemorrhage/oedema	Frequent assessment of respiratory status
Loss of swallowing reflex	Increased ICP due to cerebral haemorrhage/oedema	Assessment of swallowing and keep nil by mouth
Loss of corneal reflex	Increased ICP due to cerebral haemorrhage/oedema	Eye care. Keep eyes closed to protect cornea
Periorbital oedema	Direct result of surgery	Observe for swollen/bruised periorbital tissues

As the patient progresses, their needs will require to be reassessed and the nursing interventions adjusted accordingly. The aim of care is to ensure optimal function and the early detection of complications.

Subsequent considerations

All of the nursing interventions identified in Chapter 26 will apply. Only those interventions specific to the patient who is unconscious due to raised ICP are included here. The main aim of care remains that of preventing further rises in ICP.

The patient care outlined in the following sections uses the Roper et al (1980) framework of the activities of living model.