Central nervous system

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TOPIC 4 Central nervous system

Assessment of consciousness

Test: Glasgow Coma Scale (GCS)

Indications

• Assessment of consciousness initially used after traumatic brain injury but now also applied to other situations.

How it is done

• Sum the scores of the three eye, verbal and motor tests (Tables 4.1 and 4.2).

Table 4.1 Glasgow coma scale scores for the three tests, plus variables in children

Best eye response
Score	Description
4	Eyes open spontaneously
3	Eyes open to speech. Do not confuse with arousal of sleeping patient
2	Eyes open to pain. Try fingernail bed pressure. Supraorbital pressure will cause grimace and eye closure
1	No eye opening, ensure painful stimulus is adequate

Best verbal response
Score	Description
5	Orientated in time, person and place
4	Responds to questions but is disorientated and confused
3	Inappropriate, random words
2	Incomprehensible sounds and moans but no words
1	None

Verbal response is adjusted in children
Score	Verbal response	Preverbal/grimace response
5	Appropriate babbles, words or phrases to usual ability	Normal facial oromotor activity
4	Inappropriate words, or spontaneous irritable cry	Less than usual ability, response only to touch
3	Cries inappropriately	Vigorous grimace to pain
2	Grunts to pain, occasional whimpers	Mild grimace to pain
1	No vocal response	No response to pain

Best motor response, test and record in each limb^*
Score	Description
6	Obeys commands
5	Localizes pain. Hand should cross midline or get above clavicle in attempt to remove the stimulus
4	Withdraws from pain. Pulls limb away from fingernail bed pressure. Normal flexion observed
3	Abnormal flexion, decorticate response (spastic wrist flexion)
2	Extension to pain, decerebrate response (extensor posturing)
1	No motor response. Ensure adequate painful stimulus and no spinal injury

* Upper limb responses are more reliable as lower limb responses could be spinal reflexes.

Table 4.2 Severity of acute head injury

GCS score	Coma
≤8	Severe
9–12	Moderate
≤13	Minor

CSF analysis

Test: Lumbar puncture

Contraindications

• Reduced GCS.

• Focal neurological signs.

• Papilloedema.

• Coagulation disorders.

• Local infection at site.

Normal values

See Table 4.3

Table 4.3 Lumbar puncture results

Measure	Normal values
Opening pressure	7–20 cmH₂O
Cell count	0–5/mm³, all lymphocytes
Protein concentration	0.15–0.45 g/L
Glucose concentration	2.8–4.2 mmol/L
CSF: blood glucose ratio	65%

Limitations and complications

• Headache:

– Incidence of post dural puncture headache (PDPH) is reduced with smaller needle size. The average frequency of headache is 20–40% using 20–22 G and 5–12% using 24–27 G needles

– Incidence also reduced by using a noncutting (Whittacre or Sprotte) type needle rather than cutting (Quinke) type, and by replacement of stylet before needle withdrawal. There is no evidence increased fluids or bed rest prevents headache.

• Traumatic tap – defined as CSF containing >1000 RBC per high-powered field.

• Backache – may occur in up to 40% of patients.

• Failure.

• Spinal cord or nerve root damage–replacement of stylet before needle withdrawal may avoid damage to nerve roots and dura.

• Cerebral herniation is rare and can be avoided by using CT to exclude a space-occupying lesion (SOL) prior to lumbar puncture.

• Subdural, epidural haematomas.

• Cranial nerve palsies.

• Discitis.

• Pneumocephalus.

• Infection.

Test: CSF appearance (spectrophotometry)

• Xanthrochromia is the yellowish discoloration of Cerebrospinal fluid (CSF) due to the presence of bilirubin, a haemoglobin breakdown product.

• Visual inspection alone is not a reliable method to detect xanthochromia. Spectrophotometry is necessary.

Indications

• In a suspected subarachnoid haemorrhage (SAH), an LP should be done ideally 12 hours after the suspected haemorrhage to allow for the in vivo formation of CSF bilirubin.

How it is done

• If possible collect four sequential CSF specimens and ensure the last sample is sent for bilirubin analysis.

• Check with the laboratory for the volume required and ensure availability of spectrophotometry.

• Protect sample from light and when possible avoid vacuum transport systems that may haemolyze red blood cells (RBCs), produce oxyhaemoglobin (oxyHb) and hence a false-positive result.

• A simultaneous blood specimen should be taken for serum bilirubin and total protein.

• After centrifugation the supernatant is analyzed with a spectrophotometer.

• Haem pigments produce characteristic absorbance peaks at 400–460 nm.

Interpretation

Normal CSF appearance is crystal clear and colourless

Abnormalities

• Need to be interpreted carefully as causes of xanthochromia include raised serum bilirubin and CSF protein.

• The exact ratios of RBC, oxyHb and bilirubin found in the CSF will depend upon the timing of the lumbar puncture in relationship to the bleed.

• If a CT scan and CSF spectrophotometry are normal within 2 weeks of a sudden severe headache then SAH is excluded.

Further investigations

• Patients with a CT positive for subarachnoid blood should proceed to either a cerebral angiogram or CT angiogram to try and find the cause of the SAH (an aneurysm in >85% of cases). Treatment can then be undertaken (surgical or radiological) with the aim of preventing a re-bleed and allowing the aggressive management of vasospasm.

• The small group of patients with a history suggestive of a SAH but with a negative CT, can be identified with an appropriately timed lumbar puncture followed by spectrophotometer CSF analysis. They can then also be referred for cerebral angiography.

Limitations and complications

• Sensitivity of bilirubin to diagnose a subarachnoid haemorrhage has been shown to be 96% when undertaken more than 12 hours after haemorrhage.

• A traumatic tap will produce a CSF sample with an increased RBC count, but unlike SAH the sample will not contain bilirubin. Spectrophotometry is the only reliable way to distinguish SAH from a traumatic tap.

• Spectrophotometric findings taken on a second or subsequent LP only reflect the probability that blood has been introduced into the subarachnoid space at an earlier puncture.

Test: CSF cell counts

Indications

• Diagnostic lumbar puncture.

• Monitoring of partially treated meningitis/ventriculitis.

How it is done

• Cell count must be performed manually by an experienced operator using a Neubauer chamber within 30 minutes of sampling.

• White blood cell (WBC) differential is usually performed on concentrated CSF by centrifugation.

Interpretation

Normal range

• Adults <5 WBC/mm³ (70% lymphocytes, 30% monocytes, occasional eosinophil or neutrophil).

• Neonates <20 WBC/mm³, including <60% neutrophils.

Abnormalities

See Table 4.4.

Table 4.4 Causes of elevated CSF white blood cell count

	Characteristics
Bacterial meningitis	Often >1000/mm³, usually PMN
Viral meningitis	<100/mm³, usually lymphocytes
Seizures
Intracerebral haemorrhage
Malignancy
Guillain-Barré syndrome	<50 monocytes/mm³
Multiple sclerosis	<50 monocytes/mm³
Other inflammatory conditions

WBC differential

Viral, fungal and tuberculosis (TB) infections characteristically show lymphocytosis, but early infection may show polymorphonuclear neutrophil (PMN) preponderance. Eosinophilic meningitis >10 eosinophils/mm³ is rare. Causes include parasitic infections, other infections, VP shunts, malignancy and allergic drug reactions.

Limitations and complications

• Cell counts diminish after 30 minutes due to settling, binding to surfaces and cell lysis. Neutrophil counts fall by 50% by 2 hours whereas lymphocytes and monocytes do not.

• Allow 1 WBC per 500 RBCs in the event of traumatic tap.

Test: CSF glucose (Table 4.5)

Interpretation

Normal range

• CSF glucose should be approximately two-thirds serum glucose: a simultaneous serum sample should always be taken.

• Levels rarely go above 17 mmol/L regardless of serum levels.

• Beware: glucose levels are usually normal in viral infections and can be normal in up to 50% of bacterial CNS infections.

Table 4.5 Causes of altered CSF glucose

Low CSF glucose	High CSF glucose
CNS infections	Hyperglycaemia
Chemical meningitis
Subarachnoid haemorrhage
Hypoglycaemia

Test: CSF microbiology

How it is done

• Gram stain for suspected bacterial infections.

• Acid-fast staining for suspected TB.

• India ink stain for cryptococcus.

• CSF culture is essential to determine antimicrobial sensitivity and resistance. A minimum of 2 mL is required. However, fungal and TB cultures require 20–40 mL to provide reasonable sensitivity. This requires multiple CSF samples.

• Polymerase chain reaction (PCR) has replaced tissue culture for most viral and some bacterial CNS disease.

• CSF antigen testing. For cryptococcus this has a sensitivity of 80–95%.

• Latex agglutination and coagglutination are methods that allow detection of bacterial antigens in CSF. For Haemophilus influenza sensitivity is quoted to be 60–100%, but is lower for other bacteria. This can be useful in partially treated meningitis where cultures may not yield an organism.

Test: CSF opening pressure

How it is done

• Connect manometer to lumbar puncture needle hub once CSF is draining. Allow CSF pressure to equilibrate with atmospheric pressure in the manometer tubing.

• Read the pressure in cmH₂O/mmH₂O calibrated onto manometer tubing.

Interpretation

Normal data (Table 4.6)

Pressures can become elevated if the patient holds their breath or strains. It will reduce with hyperventilation. Fluctuations may be seen with respirations.

Table 4.6 Normal range of CSF pressure

Age (years)	Pressure (cmH₂O)
<8	1–10
>8	6–20
Obese adult	<25

Abnormalities

See Table 4.7.

Table 4.7 Causes of altered CSF pressure

High pressure (>25 cmH₂O)	Low pressure (<6 cmH₂O)
Intracranial haemorrhage	CSF leak
Space-occupying lesions	Previous lumbar puncture
Meningitis	Severe dehydration
Cerebral oedema	Inadequate production
Congestive cardiac failure	Shunt
High venous pressure	Obstructive hydrocephalus Excess absorption
Idiopathic/benign intracranial hypertension	Drugs: acetazolamide, diuretics

Test: CSF protein

Indications

• CSF protein concentration is one of the most sensitive indicators of pathology within the CNS.

Interpretation

Normal range

• Adult range 0.15–0.45 g/L is reached between 6 and 12 months of age.

• Newborns have up to 1.5 g/L.

Abnormalities (Table 4.8)

• CSF: serum ratio of albumin is 1:200. Immunoglobulins are normally excluded from CSF; their CSF:serum ratio is >1:500 and essentially consists only of IgG.

• Oligoclonal bands present in the CSF but not serum suggest an immune response within CNS.

• CSF protein levels >2 g/L suggest bacterial infections.

Table 4.8 Causes of altered CSF protein

Elevated CSF protein	Low CSF protein
Infections	Repeated LP
Intracranial haemorrhage	Chronic CSF leak
Multiple sclerosis	Children 6 months to 2 years
Guillain-Barré syndrome	Acute water intoxication
Malignancy
Endocrine abnormalities
Drugs

Limitations and complications

• Allow 0.01 g/L protein for every 1000 RBCs/mm³ in the event of a traumatic tap.

• Measurement is technique dependent; check own laboratory reference range.

Electroencephalogram derivatives

The electroencephalogram (EEG) is produced from the electrical activity in the superficial cerebral cortex. Scalp electrodes are used, the exact location of which has been determined by an international system. Each electrode can detect activity within 2.5 cm. The resulting signal is amplified, filtered and then displayed visually on a plot of amplitude versus time. Computerized Fourier analysis can be undertaken to show amplitude at each frequency, power versus frequency or a compressed spectral array.

Monitors that use the EEG include the bispectral index, cerebral state index, patient state index, narcotrend index and spectral entropy monitors.

Test: Bispectral index (BIS)

Indications

• To attempt to reduce the incidence of awareness during anaesthesia.

• Monitoring hypnosis/depth of anaesthesia.

• Titrate sedation/anaesthesia to reduce side effects.

How it is done

• A single adhesive probe with four sensors is attached over the frontal cortex.

• The probe is connected to the BIS software and a single figure is displayed on screen.

• The BIS is a dimensionless number ranging from 100 (fully awake) to 0 (isoelectric EEG, deep coma). It is calculated from bispectral EEG analysis.

• The BIS calculates subparameters including beta ratio, SynchFastSlow and burst suppression.

– Beta ratio is the log ratio of the power in high and medium frequency bands: this is most influential during light hypnotic states with characteristic high β activity.

– SynchFastSlow is the relative bispectral power in the 40–47 Hz frequency band: this predominates during surgical levels of anaesthesia.

– Burst suppression ratio (SR) is the proportion of isoelectric ‘suppressed’ EEG in the preceding 1 minute. Increasing anaesthetic drug concentrations gives increasing duration of suppressed periods with intermittent high frequency high amplitude ‘burst’ activity. This detects very deep anaesthesia.

• The analysis uses an algorithm that produces a linear relationship between the numerical BIS value and the concentration of sedative.

Interpretation

Abnormalities

• It is advisable to confirm a normal BIS value in patients before induction of anaesthesia, although this is often not undertaken.

• Low voltage EEG occurs occasionally, which can be misinterpreted as burst suppression.

Physiological principles

See Fig. 4.1.

Fig. 4.1 Physiological principles of bispectral index measurement.

(Reproduced with permission from Dahaba AA (2005) Anaesth Analg 101:765-773.)

Management principles

• There is currently no gold standard measure of anaesthetic depth.

• Practioners administer anaesthetic agents to keep the BIS value between 40 and 60, generally considered to indicate adequate depth of anaesthesia.

• BIS is drug dependent and no specific BIS value can guarantee unconsciousness, but there is evidence that its use is associated with a reduction in awareness under anaesthesia.

Limitations and complications

Drugs

• Nitrous oxide (N₂O) generally does not alter BIS values, but case reports have shown variable effects.

• Ketamine causes an increase in the β activity accompanied by a reduction in the δ power. This different EEG pattern is reflected by a BIS increase after ketamine administration.

• Opioids at analgesic concentrations do not produce BIS/EEG alterations on the cerebral cortex.

• Suxamethonium causes artefact decrease of BIS values.

• Aminophylline and doxapram will increase BIS values and speed recovery.

• Different anaesthetic drugs have different EEG changes. BIS values may not be the same when using different combinations of anaesthetic agents.

Interference

The following produce interference and have been reported to increase BIS values: electrocautery, pacemakers, forced air warming blankets, endoscopic shaver oscillators, electromagnetic positioning systems and ECG. Newer monitors may be less susceptible to electrical interference.

Clinical conditions

• Hypothermia produces slowing of the EEG below 35°C. Electrical silence occurs between 7 and 20°C.

• Hypoglycaemia can produce a pattern similar to general anaesthesia with BIS values as low as 45. BIS values will increase as blood glucose is restored and consciousness is returned.

• Cerebral ischaemia will cause EEG slowing. Cortical silence can occur within 20 seconds given complete absence of cerebral blood flow.

• A BIS value of 0 has been shown to accurately indicate brain death in the presence of other confirmatory tests of brainstem death.

• Further clinical causes of abnormal EEG patterns include post ictus, Alzheimer’s dementia, cerebral palsy and severe brain injury. Their exact effect upon BIS values has not yet been quantified.

• Performance of BIS has not been studied extensively in the presence of concomitant medications including antidepressants, anticonvulsants and analgesics.

Other limitations

• There are differences in the EEG of children compared to adults. As a result BIS values in children show a much wider spread, and it is unclear if this index can be used to determine depth of anaesthesia in children.

• The algorithm used varies with different models of monitor. This may improve resistance to artefacts but give different BIS values depending on the model used.

• BIS values do not predict the likelihood of movement.

• Case reports have been published of explicit recall despite adequate BIS readings.

Evoked potentials

Evoked potentials (EP) measure action potentials that occur in response to a specific stimulus. The recorded potentials test a specific neural tract, sensory or motor, peripheral or central. Evoked potentials are smaller than EEG and require computer averaging to resolve them from background signals (EEG and ECG). The EP waveform (Fig. 4.2) is a plot of voltage versus time. It is described in terms of amplitude, latency and morphology.

Fig. 4.2 Schematic diagram of an evoked potential.

Guidelines and standards are available from The International Federation of Clinical Neurophysiology at http://www.ifcn.info/ and The American Clinical Neurophysiology Society at http://www.acns.org/.

Intraoperative monitoring should be considered whenever the function of the brain, brainstem, spinal cord or selected peripheral nerve is at risk. This includes surgery for scoliosis, spinal trauma, spinal cord pathologies, tethered cords, brainstem tumours, cranial nerve involvement and thoracoabdominal aortic aneurysms.

Test: Somatosensory evoked potentials (SSEPs)

Indications

• To assess central sensory function and the integrity of the sensory tract.

• To possibly reduce neurological deficit post scoliosis surgery.

• Diagnostic spinal cord injury studies.

• During carotid endarterectomy (CEA) for cortical protection and thus an indication for shunt placement.

• During SAH vasospasm, surgical clipping and embolization of spinal cord AVMs.

How it is done

• A peripheral nerve is stimulated using surface electrodes to deliver an electrical stimulus. Nerves usually used are the tibial, common peroneal, median and ulnar nerves. Unilateral stimulation is usually used with stimuli alternated between legs.

• The stimulus intensity is adjusted to produce a consistent muscle twitch or maximal cortical SEP amplitude.

• The EP is recorded at various points along the neural pathway using surface or needle electrodes.

• Spinal potentials are recorded over cervical and lumbar spinous processes. They may be recorded invasively using epidural or surgically placed wire electrodes.

• Subcortical potentials are recorded over C2 vertebrae.

• Cortical SSEPs are recorded from standard scalp EEG electrodes.

Interpretation

Data presented as

• Generally amplitude reduction of >50% or latency increase of 10% is usually considered significant.

Physiological principles

• Neuronal activity passes along the nerves, up the ipsilateral dorsal columns, to synapse in the cervicomedullary junction. It crosses the midline, ascends through the contralateral medial lemniscus in the brainstem to synapse again in the thalamus. The final projections reach the parietal sensory cortex.

• Additional components may ascend the spinal cord through the posterior spinocerebellar pathways.

Normal range/graph

See Fig. 4.3.

Fig. 4.3 Somatosensory AP normal range/graph.

Abnormalities

• Surgical factors – direct trauma, retraction, compression, stretching, positioning, blood flow impairment and vascular clamps.

• Anaesthetic agents – anaesthetic agents (inhalational and intravenous) and N₂O produce a dose related increased SSEP latency and decreased amplitude.

• Physiological effects – temperature, ischaemia, hypotension, raised ICP, age, and neurological disorders can all result in EP deterioration.

• Equipment and technical problems – good electrical isolation of equipment is essential.

Management principles

• Aim for a stable steady state anaesthetic, using low concentrations of inhalational agents supplemented with opioid infusions (remifentanil) to produce ideal conditions for monitoring.

• Boluses are avoided as interpretation of the following EP is difficult.

• Neuromuscular block may be necessary to prevent compartment syndrome occurring at the site of the SSEP stimulus.

Limitations and complications

• SSEPs may remain intact despite injury to the anterior spinal cord or nerve root injury. To detect this you require EMG or MEP monitoring.

• To reduce false negatives you measure both latency and amplitude, and maximize the number of recording electrodes.

• SSEPs are averaged over 10–40 seconds, which causes delayed warning to the surgical team.

Test: Motor evoked potentials (MEPs)

MEPs assess the motor pathway from the motor cortex to the NMJ. In combination with SSEP monitoring, addition of MEP improves sensitivity and specificity for detecting neuronal injury.

Indications

• When anterior spinal artery blood supply is jeopardized.

• Spinal vascular malformations and spinal cord tumours.

Advantages

• Direct monitoring of motor tract and improved sensitivity for postoperative motor deficits.

• Allows for individual limb assessment.

• No averaging is required thus prompt corrections can be made.

How it is done

• Baseline recordings are made after induction of anaesthesia.

• Stimulation of the motor cortex using electrical or magnetic techniques. (Magnetic stimulation is more difficult in the anaesthetized patient.)

• Transcranial high frequency repetitive stimulus protocols make it possible to elicit MEPs in anaesthetized patients.

• The evoked response is recorded as either a compound muscle action potential (CMAP) in the peripheral muscle or a spinal cord nerve action potential.

Management principles

• TIVA anaesthetic using propofol and opioids is required as MEPs are abolished by inhalational anaesthetics.

• Cardiovascular stability is crucial as CMAPs are highly sensitive to variation in blood pressure and local blood perfusion.

Limitations and complications

• Tongue/lip bites can occur and require protection with insertion of a bite block.

• Other movement related injuries, burns, arrhythmias and lacerations have been documented. Seizures are rare.

• Epidural electrodes may not monitor motor tracts reliably.

Further investigations

• A wake up test is performed if a change in the recorded evoked potentials occurs and an injury is suspected. This is to check for a clinical deficit.

• EEG may be more useful for detection of cerebral ischaemia.

Test: Auditory evoked potentials (AEPs)

Indications

• Assessment of hearing and VIII cranial nerve function.

• Intraoperative monitoring during cerebellopontine angle surgery, microvascular decompression surgery and posterior fossa tumour removal.

• Monitoring depth of anaesthesia.

How it is done

• Stimulus supplied through headphones – ear receives a clicking sound at intensity 65–70 dB, at repetition 10 Hz.

• Sensor electrodes are placed over the vertex and mastoid process. An extra ground electrode is placed over the forehead.

• The contralateral ear receives noise at 30–40 dB.

• Signal averaging of the EEG yields a sequence of waveforms that corresponds to the neural response along the pathway from the auditory nerve VIII, through the brainstem and to the cortex.

Interpretation

See Fig. 4.4.

Fig. 4.4 Auditory evoked potential normal range/graph.

(Reproduced with permission from Thornton C, Sharpe RM (1998) Evoked responses in anaesthesia 4. Br J Anaesth 81:771–81, and Kumar A, Bhattacharya A, Makhija N (2000) Evoked potential monitoring in anaesthesia and analgesia. Anaesthesia 55:225–41.)

Physiological principles

The waveform allows anatomical location of a dysfunction along the auditory pathway

• Brainstem response (BAEP) <10 ms.

• Early/mid cortical response (MLAEP) 10–80 ms.

• Long latency AEP >80 ms.

Further investigations

• Combined use of other evoked potentials or other cranial nerves (facial nerve function) may be required for optimal functional outcome.

Limitations and complications

• The significance of brainstem AEP changes depends upon the surgery.

• Assessment of AEP latencies and amplitudes is done by visual inspection and is subject to observer bias.

• It requires computer averaging, which can take up to 2 minutes. This time lapse limits usefulness during surgical procedures.

• MLAEP is affected by muscle movement, diathermy and electrical interference.

• There is poor agreement among experts regarding signal quality.

Imaging

Test: Computerized tomography (CT) brain

Head injury

NICE guidelines for head injury (http://www.nice.org.uk) were published in 2003 and updated in 2007. The presence of any of the following risk factors requires CT brain imaging following head injury:

• GCS <13 at any point

• GCS 13–14 at 2 hours post injury

• Suspected open or depressed skull fracture

• Any sign of basal skull fracture

• Post-traumatic seizure

• Focal neurological deficit

• >1 episode vomiting

• Amnesia >30 minutes of events before impact

• Additional high-risk patients include those with coagulopathy, age >65 and dangerous mechanism of injury.

For children under two, it is recommended by NICE (2007) that the best evidence currently available is the ‘CHALICE’ rule (see http://www.nice.org.uk for more details).

How it is done

• CT brain imaging may use a sequential single-slice technique, multislice helical (spiral) protocol or multidetector multislice algorithm.

• Slice thickness <10 mm supratentorial, <5 mm for posterior fossa and children.

• Base of skull slice thickness should be 2–3 mm depending on technique.

• Soft tissue and bony images are required.

• Contrast may be required, e.g. meningioma.

Interpretation

Please see Fig. 4.5 for a normal CT scan.

Fig. 4.5 A normal CT scan.

Abnormalities

• Cerebral oedema: loss of grey-white differentiation, sulcal and ventricular effacement with increased brain volume.

• Subarachnoid haemorrhage (Fig. 4.6): blood in the CSF is seen as hyperdensity in the suprasellar cistern. CT will show subarachnoid blood in 98% of cases within 48 hours.

• Infarction.

• Subdural haematoma (Fig. 4.7): initially the hyperdense space-occupying lesion gradually organizes to become hypodense, which may be difficult to differentiate from surrounding brain tissue. Check for sulcal effacement and mass effect. Compared to an extradural (which looks biconvex; lens shaped) a subdural often has a crescent-shaped appearance.

• Extradural haematoma (Fig. 4.8): due to arterial injury and skull fracture. Requires urgent neurosurgical decompression.

• Skull fractures: bone windows are required to view the cranium.

• Contusions: small areas of hyperdensity in brain substance.

• Hydrocephalus: pathological enlargement of ventricular system (Fig. 4.9).

Fig. 4.6 CT showing subarachnoid haemorrhage with left intraventricular blood.

Figure 4.7 CT showing extensive right subdural haematoma with ventricular compression and midline leftward shift.

Fig. 4.8 CT showing left extradural haematoma: a biconvex (lens shaped) collection with high attenuation.

Fig. 4.9 CT showing pathological enlargement of the ventricular system and intraventricular drain.

Test: MRI brain

Advantages

• Smaller tumours are easier to see.

• MRI may detect and localize cerebral infarction within a few hours when the CT is negative.

Contraindications

Always check with radiology staff as some devices may be MRI compatible. The interference produced with metal implants may produce poor-quality pictures.

Limitations and complications

• Enclosed cylindrical magnet may precipitate claustrophobia.

• Prolonged times required for scanning.

• MRI may miss calcification.

• Specialized equipment for administration of anaesthesia and monitoring.

Cervical spine in trauma

Injuries to the cervical spine occur in approximately 2–6% of blunt trauma patients, and in 10% of patients with severe head injuries with a GCS <8.

Indications

Multiple guidelines exist to suggest which patients require investigations.

• Patients who are alert and orientated, have never lost consciousness, are not under the influence of alcohol or drugs, have no distracting injuries, have no cervical tenderness and no neurological findings, and are between 2 and 65 years of age do not need imaging. All others, including all patients with a GCS <15, require some form of imaging and careful clinical assessment.

Test: Plain cervical radiographs (Fig. 4.10)

The three standard cervical trauma views are the investigation of choice according to NICE guidelines (see http://www.nice.org.uk). They consist of lateral, AP and open mouth views. The sensitivity of this series ranges from 70% to 90%. In practice this is reduced as films are inadequate in up to 50% of patients. Expert interpretation is essential.

Fig. 4.10 A Normal cervical spine on plain lateral radiographs. B Injured cervical spine on plain lateral radiographs

How it is done

Lateral view

An adequate view from the base of the occiput to the top of T1 is mandatory. Repeated attempts to show the C7–T1 border should be avoided. Lateral views of C2 may be required to supplement CT in patients aged >65 years.

AP view

Should be correctly positioned and centered to avoid rotation artifacts and should demonstrate each spinous process from C2 to T1.

Open-mouth view

This allows visualization of the odontoid peg and the lateral masses of C1 and C2. In unconscious, head-injured patients, fractures of C1 and C2 have been missed due to obscuration by endotracheal tubes, gastric tubes and hard collars. In these intubated patients, the open-mouth view should be replaced by a CT scan.

Trauma oblique views

The trauma oblique view can indicate alignment at the C7–T1 level, if the lateral view fails to show the C7–T1 junction. It allows good visualization of the posterior elements of the cervical spine and reveals facet joint dislocations. They are not commonly undertaken in this setting in the UK.

Interpretation

Consider soft tissue and vertebral alignment. Abnormal soft tissue may be associated with a fracture and should draw attention to a hyperextension injury. Four lines can be drawn to assess alignment; disruption of any one of these smooth lines is suggestive of injury:

• Anterior margin of the vertebral bodies

• Posterior margin of the vertebral bodies

• Spinolaminar line

• Spinous processes.

Limitations

• Standard radiographs are notorious for inadequate visualization of C1/C2 and C7/T1 junctions.

• The swimmer’s view requires one arm to be raised and the other pulled down, which tends to twist the spine, and dislocations have been reported. The radiation dose is also high to obtain this view.

Test: Cervical CT scan

Primary CT scanning of the entire cervical spine with sagittal and coronal reconstruction is more sensitive than plain films, particularly with the advent of the newer generation multislice/multidetector CT (MDCT) machines. Thus it has become the primary imaging of choice according to some protocols.

• NICE guidelines advocate that in patients with severe head injuries (GCS <8) CT is the imaging of choice.

• Trauma patients requiring a cranial CT should undergo either routine axial CT of C1/C2 or an MDCT examination of their entire C spine whilst still in the CT suite.

• Once one injury is detected, CT scanning of the whole cervical spine including the cervical-thoracic junction is required as 10–31% of cervical fractures have associated noncontiguous fractures.

Alternatively CT can be used as a supplement to plain films for:

• Evaluation of suspicious and poorly visualized areas

• C1 and C2 evaluation in intubated patients.

How it is done

Conventional (single slice, nonhelical) CT scanners acquire discrete axial slices. False negatives are usually due to axially orientated fractures, dislocations and undisplaced ligamentous injuries not visible with this resolution.

In a helical (spiral) scan the patient moves smoothly through the rotating scanning beam acquiring a helical volume of data, which the computer can then reconstruct in any plane.

The new MDCT machines effectively scan multiple slices simultaneously, making scanning much faster. Current recommendations for cervical spine CT are to perform 1.5–3-mm slices with reformatted sagittal and coronal reconstruction. Sagittal and coronal reconstructions must be closely examined for features suggestive of ligamentous instability, such as widening, subluxation and rotation of the vertebrae relative to one another.

The diagnostic performance of helical CT scanners is good, with reported sensitivity as high as 99% and specificity 93%. Improvements in CT technology are likely to improve sensitivity further.

Limitations

• Helical CT may not exclude unstable ligamentous injuries. Injury to the cervical spinal cord in the absence of a fracture occurs in 0.03% to 0.7% of trauma.

• It must be correctly performed and interpreted. When a fracture is not present, subtle bony malalignment and soft tissue findings may be the only clues to the presence of a potentially serious, unstable injury.

• In children under 10 years, CT of the cervical spine should only be used in cases where patients have a severe head injury (GCS ≤8), or where there is a strong suspicion of injury despite normal or inadequate plain films.

Test: Cervical MRI

Cervical MRI can detect soft tissue, ligament, disc and cord injury that may not be evident even on helical or multislice CT. To date no prospective studies comparing modern multislice CT and MRI have been conducted for the evaluation of occult cervical injuries in unconscious patients.

Indications

• Patients with neurological symptoms and signs suggesting cord or nerve root injury.

Limitations

• The requirement for detailed patient history to exclude ferrous body implants.

• Increased cervical clearance times and availability of MRI scanning.

• Risks associated with the transport of an unconscious patient, requirement of MRI-compatible monitoring equipment and prolonged scanning times.

• The incidence of soft tissue abnormalities on MRI is in the order of 20%, the significance of which is uncertain and does not correlate with other evidence of cervical instability.

Flexion/extension screening

Given the inherent risks in passively flexing and extending the neck of an unconscious patient, this technique should only be undertaken as part of a controlled trial designed to investigate efficacy and safety.

Further management principles

• In critically injured patients, spinal immobilization in hard collars and strapping can lead to decubitus ulceration, compression of the jugular veins, make airway management more difficult, restrict physiotherapy and compromise nursing care and the management of traumatic brain injury.

• Continuous spinal immobilization is therefore not recommended for >48 hours in the unconscious patient.

• To complete spinal clearance in the unconscious trauma patient ideally a CT of the whole cervical spine is obtained and reported by an expert.

• If unstable then await instructions from a spinal team.

• If normal then the hard collar can be removed. There is no need for further log rolling, but a soft Miami J collar is used for waking. When awake the neck is further tested for tenderness or pain.

• Any unexplained limb deficits require an MRI as soon as clinically possible.

Intracranial pressure (ICP) monitoring

Indications

An ICP monitor is used in traumatic brain injury when the following apply:

• Severe head injury defined as GCS <8, with an abnormal admission CT scan.

• Severe head injury with GCS <8, with a normal CT scan if two or more of the following features are present: age >40 years, unilateral or bilateral motor posturing and systolic blood pressure <90 mmHg.

• Traumatic mass lesions in selected patients with mild or moderate head injury.

Further indications for ICP monitoring are listed in Table 4.9.

Table 4.9 Reasons for ICP monitoring

Condition	Comments
Subarachnoid haemorrhage	With associated hydrocephalus to allow CSF drainage
Brain tumours	Selected patients at high risk of post op cerebral oedema, e.g. posterior fossa craniotomy
Reye’s syndrome	Active treatment decreases mortality
Hydrocephalus	Diagnostic tool in complex cases
Benign intracranial hypertension	Monitoring via lumbar drain as diagnostic test and treatment response
Hypoxic brain swelling	Post drowning, CO poisoning
Others	Meningitis, venous sinus thrombosis, hepatic encephalopathy, stroke and craniostenosis

How it is done

Monitoring requires an invasive transducer. Ventricular drainage catheters are the gold standard. A simple catheter is inserted under sterile conditions into a lateral ventricle via a burr hole. When connected to an external pressure transducer this is the most accurate, low cost and reliable method. ICP can be controlled by CSF drainage, and the transducer may be zeroed externally.

The other commonly used method is an intraparenchymal monitor that is zeroed to atmospheric pressure before insertion.

Subdural and subarachnoid bolts are less invasive and have reduced risk of complications, but are less reliable.

Interpretation

Waveform analysis over 30 minutes should be the minimum as instant CSF measurements may be misleading. Normal range varies with age, posture and clinical conditions. Values in children are not well established (Table 4.10).

Table 4.10 Waveform analysis normal ranges

Age group	Normal range (mmHg)
Adults	<10–15
Children	3–7
Term infants	1.5–6

Physiological principles

The Munro Kelly hypothesis states that within the rigid skull the contents are not compressible. Initially intracranial compliance allows compensation for small increases in volume (Fig. 4.11). Once this is exhausted then small increases in volume will cause steep exponential increases in ICP.

Fig. 4.11 Data presented as pressure values and/or pressure waveform against time.

Abnormalities

• Lundberg A (plateau) waves (Fig. 4.12). Steep increases in ICP from near normal values to 50–100 mmHg, persisting for 5–20 minutes and then fall sharply. Always pathological and indicate greatly reduced compliance. Often accompanied by neurological deterioration.

• Lundberg B waves (Fig. 4.13). Rhythmic oscillations occurring every 1–2 minutes. Sharp rhythmic oscillations, occurring every 1–2 minutes, occur in ventilated patients and with Cheyne–Stokes respiration. Indicative of failing intracranial compensation.

• Lundberg C waves. Oscillations with a frequency of 4–8/minute. They are of smaller amplitude and are probably of limited pathological significance.

• Others, for example, due to sudden increases in systemic blood pressure (Fig. 4.14).