Neurology II Flashcards
Brainstem death
Brainstem death is regarded as the legal equivalent of death as customarily defined by cessation of heart beat and spontaneous respiration. In order to make the diagnosis of brain death, certain preconditions must be satisfied:
• The patient’s condition must be known to be due to irreversible brain damage of known aetiology.
• The patient must be in apnoeic coma, i.e. deeply unconscious and dependent on artificial ventilation.
Brainstem death exclusion criteria
There should be no doubt that other, potentially reversible, causes of the state of unconsciousness have been excluded, these include:
• Residual drug effects – effects of narcotics, hypnotics, tranquillisers and muscle relaxants
• Hypothermia – this must be excluded; the core
temperature must be 35degrees celsius
• Circulatory, metabolic and endocrine disturbances, e.g. hypernatraemia, diabetic coma.
Brainstem reflexes
• Pupillary
• Absent corneal reflexes
• No motor response to central stimulation
• Absent gag reflex
• Absent cough reflex
• Absent vestibulo-ocular reflex
• Absence of spontaneous breathing
Brainstem reflexes: Pupillary
• Pupillary: There should be no pupillary response to light. The pupils do not respond either directly or consensually to sharp changes of the intensity of incident light. Cranial nerves involved in this reflex are II and III.
Brainstem reflexes: Corneal reflexes
• Absent corneal reflexes. There should be no response to direct stimulation of the cornea. This would normally result in blinking of the eye. The cranial nerves tested are V and VII.
Brainstem reflexes: Central stimulation
• No motor response to central stimulation. There should be no motor response within the cranial nerve distribution in response to adequate stimulation of any somatic area. The usual test is to apply supraorbital pressure.
Brainstem reflexes: Absent gag reflex
• Absent gag reflex. The back of the throat is touched with a catheter. There should be no gagging. This tests cranial nerves IX and X.
Brainstem reflexes: Cough reflex
• Absent cough reflex. There should be no response to bronchial stimulation by a catheter passed via the endotracheal tube. This tests cranial nerves IX and X.
Brainstem reflexes: vestibulo-ocular reflex
• Absent vestibulo-ocular reflex. There should be clear access to the tympanic membrane which is confirmed by visual inspection with an auriscope. The head is flexed at 30o. There should be no eye movements following slow injection of 50 mL of ice cold water over one min into each external auditory meatus in turn. This tests cranial nerves VIII, III and VI.
Spontaneous breathing
1) Finally, spontaneous respiration must be demonstrated to be absent despite a stimulus that should provoke it. Performed by disconnecting the patient from the ventilator in the presence of a PaCO2 above the threshold for respiratory stimulation. This is performed by preoxygenating the patient with 100% oxygen for at least ten min.
2) The PaCO2 is allowed to rise to 5.0 kPa before test- ing. The patient is then disconnected from the ventilator. Oxygen is insufflated at 6 L/min via an endotracheal tube to maintain adequate oxygenation during the test, and the PaCO2 is allowed to rise above 6.65 kPa.
3) There should be no spontaneous respirations noted. These tests should be carried out on two occasions, the time interval between the tests being a matter of clinical judgement. The tests should be carried out by two medical practitioners registered for more than five years, at least one of whom should be a consultant. They should be competent in the field and not members of the transplant team.
The legal time of death is on completion of the first set of brainstem tests, although death is not confirmed until the second set of tests is satisfied.
Head injury
Head injuries may be classified according to their aetiology, i.e. missile or non-missile (blunt) injuries. Missile injuries have been referred to as penetrating injuries in the past, but in some cases the missile does not penetrate but causes a depressed fracture without penetrating brain substance.
Head injury: missile injury
These may be divided into three types:
• Depressed injury, where the missile causes a depressed fracture but does not enter the brain;
• Penetrating injuries, where the missile enters the skull cavity but does not leave
• Perforating injuries, where the missile enters and leaves the skull cavity. This type of injury is usually caused by high velocity bullet wounds, and the brain damage is extensive.
Head injury: Non-missile injury
These most commonly occur in road traffic accidents, falls and assaults. Damage may be minor or may result in severe injuries which are rapidly fatal. Brain damage occurs often as a result of acceleration/deceleration creating rotational and shearing forces which act on the mobile brain anchored within the rigid skull. Head injuries which may be fatal can occur without skull fractures.
Two main patterns of brain damage occur which are referred to as primary and secondary.
Primary brain damage
Contusions
These occur when the brain is crushed when coming into contact with the skull. They usually occur at the site of impact but may be severe on the side opposite the impact, i.e. contre-coup lesions.
Large contusions may be associated with intracerebral haemorrhage.
Diffuse axonal injury This occurs as a result of acceleration/deceleration and rotational move- ments. It may occur in the absence of a skull fracture. The majority of changes are usually only detectable on histology. Patients who have sustained diffuse axonal injury and survive are usually severely disabled.
Treatment cannot reverse primary brain injury. It is aimed at prevention, recognition and treatment of secondary brain damage.
Secondary brain damage
This occurs as a result of complications developing after the time of injury. Secondary brain damage may result from:
• intracranial haemorrhage
• cerebral hypoxia
• cerebral oedema
• intracranial herniation
• infection
Sequelae of head injuries
Most patients make a satisfactory recovery unless the head injury is severe, when up to 10% may be severely disabled. Consequences of severe head injuries include:
• Death (often diagnosed as brainstem death)
• Persistent vegetative state;
• Post-traumatic epilepsy;
• Traumatic hemiplegia;
• Post-traumatic dementia
• Cranial nerve palsies.
Intracranial haemorrhage
This is usually an expansile haematoma within brain tissue. Most arise in hypertensive patients who have weak spots (microaneurysms) on their arteriosclerotic cerebral vessels.
Other causes include
1) Bleeding into a tumour
2) Vascular malformations
3) Bleeding associated with coagulopathies
Extracerebral haemorrhage
These are divided into different types according to where they occur in relationship to the meninges. Extradural and subdural haemorrhages usually occur following trauma. Subarachnoid haemorrhage usually occurs following rupture of a ‘berry’ aneurysm and may also occur following trauma.
Extradural haemorrhage
This is bleeding into the extradural space between the skull and dura. It is caused by a head injury, usually with a skull fracture which causes tearing of an artery or a venous sinus.
Classically the injury is to the middle meningeal artery following fracture of the temporal bone. The haematoma lies outside the dura and causes compression of the underlying brain as it expands.
Clinically there is usually a lucid interval followed by a rapid increase in intracranial pressure.
Transtentorial herniation may occur and manifest itself by reduction in conscious level and by brainstem compression. The condition is fatal unless diagnosed early and treated surgically by evacuation of the clot.
Subdural haemorrhage
This is bleeding into the subdural space between the dura and arachnoid mater. Bleeding is usually from small ‘bridging’ veins which cross the subdural space. Trauma is the usual cause. Two types are described as follows.
Acute subdural haematoma This is commonly seen following head injury, often associated with a lacer- ated brain resulting from high speed injuries. The haematoma spreads over a large area. The patient usually has marked brain injury from the outset and is comatose, but the condition deteriorates further.
Chronic subdural haematoma This is usually seen in the elderly. Brain shrinkage makes the ‘bridging’ veins between cerebral cortex and venous sinuses more vulnerable. It may result from a trivial and forgotten head injury. It may occur weeks or months after the injury. Presentation is with personality change, memory loss, confusion, and fluctuating level of consciousness.
Subarachnoid haemorrhage
This is bleeding into the subarachnoid space between the arachnoid and pia mater. Causes include:
• trauma in association with head injury;
• rupture of a ‘berry’ aneurysm;
• rupture of a vascular malformation;
• hypertensive haemorrhage;
• coagulation disorders;
• rupture of an intracerebral haematoma into the
subarachnoid space;
• tumours; and
• vasculitis.
Subarachnoid haemorrhage presents with sudden onset of severe headache. Blood spreads over the cerebral surface of the subarachnoid space. In approximately 15% of cases it is instantly fatal, a further 45% of cases dying later due to rebleeding.
Blood accumulates in the basal cisterns and may block the egress of CSF, caus- ing hydrocephalus. This can occur early or later in survivors where fibrous obliteration of the subarachnoid space occurs due to organisation of the clot.
Space occupying lesions
These may result from a variety of causes. They cause an expansion in volume of the cranial contents and will eventually cause raised intracranial pressure.
Intracranial space-occupying lesions may be either diffuse or focal. Diffuse brain swelling results from either vasodilatation or oedema.
Focal brain swellings include tumours, abscess and haematomas. The consequences of intracranial space-occupying lesions include:
• Raised intracranial pressure
• Intracranial shift
• intracranial herniation
• hydrocephalus
Raised intracranial pressure
The skull is a rigid container in which brain, CSF and blood are the only contents. At normal intracranial pressures (10–15 mmHg or 12–18 cmH2O), these three components are in volumetric equilibrium, i.e. ICP =CSF + Brain + Blood. This formula is the basis for the Monro-Kellie hypothesis which states that the ICP will increase if the volume of one component is increased. The increase in ICP can only be compensated for by a decrease in one or both of the other components. The compensatory properties among the intracranial con- tents follow a pressure/volume exponential curve.
Increased volume of any of the three components can be balanced up to a certain level without any increase in the intracranial pressure. However, eventually a critical volume is reached when any further vol- ume increase results in raised intracranial pressure.
The effects of raised intracranial pressure are:
• hydrocephalus;
• cerebral ischaemia;
• brain shift and herniation
• systemic effects.
Raised intracranial pressure: hydrocephalus
This is a common complication of space-occupying lesions where an increase in ICP may result in the interruption of CSF flow. This is most commonly seen in lesions of the posterior cranial fossa which compress the cerebral aqueduct and fourth ventricle.
Raised intracranial pressure: Cerebral ischaemia
The effects of raised intracranial pressure are exerted on the vascular component and result in progressive reduction in cerebral perfusion pressure. (Cerebral perfusion pressure = blood pressure – intracranial pressure.)
Brainshift and herniation
These usually occur following a critical increase in intra- cranial pressure. Lumbar puncture is contraindicated in any patient with raised intracranial pressure, as there is a risk of precipitating a potentially fatal brainstem herniation. Herniations occur at some specific sites:
Transtentorial herniation
Tonsillar herniation
Subfalcial herniation
Diencephalic herniation
Transtentorial herniation
Transtentorial herniation
A laterally placed supra- tentorial mass may push the uncus and hippocampus over the tentorium cerebelli. The oculomotor nerves, cerebral peduncles, cerebral aqueduct, posterior cerebral artery, and brainstem may be compressed by the displaced temporal lobe. Transtentorial herniation is
frequently fatal because of the secondary haemorrhage into the brainstem.
Tonsillar herniation
Tonsillar herniation Herniation of the cerebellar tonsils into the foramen magnum causes compres- sion of the medulla. Medullary compression results in decerebrate posture, respiratory failure, and subsequent death.
