Imaging of the head, neck and spine

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c) Trauma

Computed tomography is the imaging method of choice for demonstrating intracranial complications secondary to trauma.

Indications for computed tomography following head injury:

  1. Skull fracture

  2. Disorientation or depressed consciousness

  3. Confusion lasting longer than 6-8hrs

  4. Signs of fracture of base of skull – cerebrospinal fluid/blood from nose or ear.

  5. Focal neurological signs

  6. Seizures

  7. Suspected penetrating injury

  8. Uncertain diagnosis

In children, if there is a history of loss of consciousness, neurological signs or symptoms or an inadequate history, imaging is indicated.

Intracerebral haematoma. In the acute stage this appears as a white area due to increased attenuation. There are often multiple small haemorrhages. Later the lesion becomes darker and at 2 weeks will appear darker than the surrounding brain.

Extradural (Epidural ) haematoma: this shows as a peripheral biconvex shaped lesion of high attenuation in the acute phase. The inner margin is convex .

ubdural haematoma
– this shows as a peripheral high attenuation lesion (white) in the acute phase. It is concavo-convex in appearances with a concave inner margin. It spreads over the surface of the hemisphere. Chronic subdurals are dark in appearance and resemble cerebro-spinal fluid. Subdural haemorrhages of 2-3 weeks duration are isodense and difficult to distinguish. Both extradurals and subdurals cause mass effect with midline shift and both may be associated with underlying brain contusion or oedema
Contusion – this causes areas of mixed attenuation due to oedema and haemorrhage. There is often mass effect with compression of the ventricle or midline shift. There may be a contra-coup injury i.e. abnormality on the opposite side of the brain than the trauma.

Skull fracture may be identified by “windowing” which is examining the images at different attenuation levels.

Pneumocephalus (air in the cranial cavity) may be present. Air shows as black on computed tomography and collects anteriorly in the supine position.

Fluid level may be seen in a sinus if there is a fracture communicating with the cranial cavity.

Foreign body may be seen if it is a penetrating injury e.g.gunshot

Scalp swelling will direct you to the site of injury

Skull trauma is often associated with injury to the cervical spine. Magnetic resonance imaging does not show acute haemorrhage and is not used for acute trauma.

Diffuse Brain Damage:
May lead to prolonged unconsciousness after head injury. There are several forms:

  • multiple petechial haemorrhages – usually only seen at post-mortem examination. It is rapidly fatal

  • diffuse axonal injury – secondary to a shearing injury. There is usually little change on computed tomography. It leads to brain death

  • brain swelling – recoverable. On computed tomography the ventricles are compressed and appear slit like. The basal cisterns are occluded and the sulci compressed and obliterated.

- hypoxic brain damage – may lead to areas of infarction i.e. low density areas on computed tomography.

  1. Cerebral infarction

Infarction of the brain is caused by interruption of the blood supply or oxygen to part of the brain. It commonly presents as a stroke and may be caused by:

  • Thrombosis

  • Embolus

  • Hypoxia

A transient ischaemic attack (TIA) presents as a focal neurological deficit persisting only for a short time, usually 24 hours or less. With a stroke the deficit persists. A lacunar infarct is a very small area of infarction, a result of occlusion of a small intracerebral artery.

On computed tomography a brain infarct shows as an area of decreased attenuation (i.e. darker than the surrounding brain) within the territory of a major artery, usually the middle or posterior cerebral artery. Another common site is in the basal ganglia and internal capsule. Infarcts usually only become visible after 24 hours on computed tomography and if the scan is done too early it will appear normal. The changes may be very subtle with just a little alteration in attenuation gradually becoming more obvious with time. There is loss of the grey-white matter differentiation initially, followed by the appearance of a darker area corresponding to the territory of the occluded vessel. An infarct is often accompanied by oedema, which may be marked if the infarct is massive, with midline shift, mimicking a tumour on CT. With time the infarct changes in density. At around 3 weeks it is isodense with the surrounding brain and difficult to recognise. A scan done at this time may be normal. Later it becomes darker and may remain visible for many years as an area of low attenuation becoming darker with time. Old infarcts may have a cystic appearance. With time there is also shrinkage of the affected part resulting in dilatation of the adjacent ventricle and widening of the adjacent sulci.

Brain infarcts show well on magnetic resonance imaging appearing bright on T2 images. Magnetic resonance imaging is preferable to computed tomography if available.

Transient ischaemic attacks (TIAs) are the result of small emboli reaching the blood vessels in the brain. These often arise on atheromatous plaques at the origin of the internal carotid artery, or they may be due to a thrombus in the L atrium or ventricle. Computed tomography is negative as the lesions are too small to be demonstrated. Carotid doppler ultrasound may be helpful in these patients by showing arterial narrowing and plaque formation. Magnetic resonance is also more sensitive for detecting very small areas of brain infarction.
a) Abscess. These may occur within the brain itself or outside the brain substance in the subdural space. The infection may be:

  • pyogenic

  • tuberculous

  • fungal

  • parasitic

A pyogenic abscess is the commonest and often occurs secondary to chronic sinus or middle ear infection. It can occur anywhere in the brain or subdural space especially in the frontal or temporal lobes.

Computed tomography shows an area of low attenuation showing ring enhancement after contrast. There is also mass effect. A subdural abscess (subdural empyema) shows as an area of decreased attenuation adjacent to the skull vault or falx. There is marked enhancement of the margins after contrast.

Tuberculomas are usually multiple, show decreased density and ring enhancement but with little oedema and no mass effect.

Parasitic infection is usually Toxoplasmosis . There are two forms of the disease. The congenital form is not associated with abscess formation but causes extensive brain damage and bilateral choroidoretinits. It is commoner in Europe where it is usually transmitted from cats. Computed tomography shows gross ventricular dilatation and extensive calcification in the basal ganglia of the subcortical region. The adult infection is usually associated with AIDS and presents as small brain abscesses. On computed tomography these show as multiple small ring enhancing lesions with surrounding oedema and mass effect.

b) Pyogenic meningitis. This usually shows no change on computed tomography and imaging is not indicated in the uncomplicated case. If the infection is severe thrombosis of a major vessel may occur resulting in ischaemia which shows as an area of decreased attenuation. Occasionally a subdural empyema will develop. In a very severe case, pus may obliterate the basal cisterns, this looks like blood on computed tomography appearing white. Hydrocephalus is a common sequel.
c) Tuberculous meningitis. This causes obliteration of the basal cisterns with marked enhancement following CM. Hydrocephalus is common.

  1. Viral infections usually cause no change on computed tomography except for herpes simplex virus which may cause low density areas in the temporal lobes, which are often bilateral.

5. HYDROCEPHALUS: dilatation of the ventricular system.

This may be focal, secondary to previous infarction or trauma, or generalised.

Generalised hydrocephalus may be obstructive (high pressure) or non obstructive (low pressure) due to brain atrophy.

Non – obstructive hydrocephalus

Brain atrophy has many causes but is often idiopathic and forms part of the normal ageing process. The ventricles of a 50 year old person are considerably larger than those of a child. Loss of cortex leads to secondary dilatation of the ventricles and there is no obstructive element. It may be seen in:

  • Previous trauma - boxers are an example of this.

  • Multiple brain infarcts resulting in shrinkage of the brain

  • Alzheimers disease and other degenerative brain diseases

  • Congenital degenerative brain disorders

  • Alcohol and drug abuse.

On computed tomography there is enlargement of the ventricles, basal cisterns, cerebral and cerebellar sulci which show dark. In Alzheimer’ disease although a diffuse process the temporal lobes are often most severely affected with relative sparing of the cerebellum. It is often not possible to diagnose the cause from the CT appearances alone.

Obstructive hydrocephalus

This may be secondary to obstruction proximal to the outlets of the 4th ventricle (non-communicating) or due to obstruction of CSF flow in the subarachnoid space (communicating). Causes include:

  • Congenital – often associated with spina bifida and meningocele or the Arnold Chiari malformation.

  • Meningitis – pus blocks the ventricular system or exit foramina or interferes with CSF flow over the surface of the brain

  • Intraventricular mass or pressure from an outside tumour mass

  • Subarachnoid haemorrhage – blood blocks the ventricular system

On computed tomography there is ventricular dilatation above the level of obstruction. The sulci remain normal or become compressed as the intracranial pressure increases. This differentiates it from non obstructive hydrocephalus.

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