Neurological Problems

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Questions Received:

  1. Can you explain the mechanism and manifestation of intracranial pressure, and how this relates to the Glasgow Coma Scale?

  2. What happens in a closed head injury?

  3. I'm an amateur Spanish novel writer, and I need information about catalepsy (symptoms, diagnoses,...).I don't find any interesting in Internet. Can you help me?

  4. What is a space-occupying lesion (in the brain) with cerebral oedema? Why are Dexamethasone and Dilantin used? And what is the complication of insulin dependent diabetes mellitus on nursing care with someone with an SOL?

Responses:

Can you explain the mechanism and manifestation of intracranial pressure, and how this relates to the Glasgow Coma Scale?

17th August 1999

The bones of the skull form a rigid enclosure of fixed volume for the brain. The cranial cavity contains brain tissue, cerebral blood and cerebrospinal fluid. The proportions of these components remain relatively constant under normal conditions: brain tissue 78%, cerebral blood 12%, and cerebrospinal fluid 10%. It is the balance of these three which contributes to the intracranial pressure, as first noted by Monro in 1783 and later by Kellie in 1824. The brain requires a constant supply of oxygen and nutrients and receives a blood flow of 30 - 50 ml per 100g of brain tissue per minute (approximately 700ml/min for the whole brain). The brain has the ability to regulate its own blood supply (autoregulation) and it does this by three physiological mechanisms: changes in intracranial pressure, dilatation of the cerebral blood vessels, and metabolic factors (Walleck 1987).

The normal cerebrospinal fluid pressure is between 60 and 150 mm H2O. If intracranial pressure is to remain constant, an increase in volume of one intracranial component must be compensated for by a decrease in one or more of the other components. A variety of everyday activities can influence this balance transiently, for example changes in arterial or venous pressure, changes in intra-abdominal and intrathoracic pressure during coughing and straining, posture, blood gases, and temperature, especially hypothermia (Walleck 1987). Temporary changes in intracranial pressure are not a problem, but a sustained increase in intracranial pressure can damage brain tissue.

Raised intracranial pressure constitutes a life-threatening condition and arises if one or more of the three intracranial components are increased. Cerebral oedema is an important underlying cause in many cases of raised intracranial pressure, and this may be triggered by neoplasms (tumours), cerebral haemorrhage (intra- or extra-cerebral), cerebral vascular events such as thrombosis and embolism, head injuries, or poisoning. Raised intracranial pressure may manifest itself in many ways, but key features are alterations in consciousness and changes in vital signs (pulse, blood pressure, and body temperature).

The Glasgow Coma Scale has become a standard tool for assessing people with neurological dysfunction (Teasdale and Jennett, 1974).

The Glasgow Coma Scale

Assessing Levels of Consciousness
EYES OPEN
Spontaneously 4
To sound 3
To pain 2
None 1
VERBAL RESPONSE
Orientated 5
Confused Conversation 4
Inappropriate Words 3
Incomprehensible Words 2
None 1
BEST MOTOR RESPONSE
Obeys Commands 6
Localises Pain 5
Normal Withdrawal 4
Abnormal Flexion 3
Extension 2
None 1

Maximum score 15 Minimum score 3

A score of less than 8 is considered to indicate unconsciousness.

Pupil sizes using a score from 1 - 8 are also assessed with 1 being pin-point and 8 being widely dilated. The pupil reaction to light is also assessed. The pupil responses indicate the progress of the underlying condition. Uncorrected cerebral oedema leads to compression of the third cranial nerve, first on one side and then on the other. This results in the pupils losing their ability to react to light.

The frequency at which neurological observations using the Glasgow Coma Scale are conducted depends upon the patient's clinical condition and the outcome of investigations such as, computerised axial tomography (CT). These criteria enable the medical and nursing teams to decide on the most appropriate interval to use. The Glasgow Coma Scale was designed to allow comparisons to be made between different centres, although some doubts have been raised about its clinical sensitivity and value (Hinds 1998; Lowry 1998).

A device that can measure intracranial pressure accurately over time, the Codman subdural bolt, is now coming into use in Intensive Care Units within District General Hospitals. The bolt has been in use in specialist neurosurgical centres within the U.K. for the last three to four years. It is mainly used when caring for patients who have sustained a severe head injury. The bolt is inserted, by a member of the medical team, in the prefrontal region of the head when a patient has a Glasgow coma scale of 8 or less and surgery is not indicated (Odell 1996). Following insertion the device is connected to a continuous monitoring system via a transducer. Removal of the bolt usually takes place when the patient's intracranial pressure is less tha 20mmHg. for 24 hrs post extubation, with no need for sedation (Goodwin et al, 1993).

The Codman bolt enables staff in Intensive Care Units to monitor intracranial pressure with greater sensitivity, and by liasing closely with neurosurgical specialists the patient who has sustained a head injury is nursed under optimum conditions.

References

What happens in a closed head injury?

26th March 2000

A closed head injury is one in which there is no communication between the intracranial space and the external environment. This is the opposite of an 'open' head injury where a communication does exist, normally as a result of a fractured skull and trauma to the skin and meninges.

Any head injury has the potential to provoke significant disturbances and a closed head injury does not mean the risks are in anyway lessened. Here are some examples of the pathophysiological changes that occur in response to deformation, acceleration, deceleration and rotation of the brain (summarised from Hickey, 1984):

Reference

I'm an amateur Spanish novel writer, and I need information about catalepsy (symptoms, diagnoses,...).I don't find any interesting in Internet. Can you help me?

16th June 2000

Catalepsy - sustained immobility, postural trance (from the Greek: katalepsis - act of seizing) catalepsy - sustained immobility, postural trance (from the Greek: katalepsis - act of seizing)

Catalepsy is a sudden loss of mobility that occurs in humans and other animals. The limbs or other parts of the body remain immobile for an unusual length of time, and during this time the affected parts can be manipulated into different positions and will stay where they are put. In a healthy person or other animal, it can be a response to a sudden frightening stimulus, such as being caught unexpectedly in the light of a car’s headlights at night. Simply placing an animal in an unusual position can sometimes be enough to produce catalepsy (Reese, Newton, and Angel, 1982; Sanberg et al, 1988). Catalepsy can be induced in deep hypnotic states. It is also associated with disorders of brain function such as cerebellar disease, some types of schizophrenia, and in hysteria. A transient catalepsy of the left upper extremity was observed in a patient who experienced a haemorrhage within his right cerebral hemisphere (Fukutake, Hirayama, and Komatsu, 1993).

Certain types of drugs can cause catalepsy, particularly those which interact with neurotransmitter systems in the brain such as dopamine, acetylcholine, noradrenaline, GABA, histamine, opiates, and certain neuropeptides (Klemm, 1989). Most notably, neuroleptics produce catalepsy by influencing the dopamine system of the basal ganglia (Jann, Froemming, and Borison, 1990). The active ingredient of marijuana (Cannabis sativa) and related substances can produce catalepsy and other effects in animals through an effect mainly on the basal ganglia (Rodriguez de Fonseca et al, 1998; Chaperon and Thiebot, 1999). You may be interested to know that in Haiti Voodoo priests use plant-derived chemicals to induce catalepsy in other people (Craan, 1988).

References

What is a space-occupying lesion (in the brain) with cerebral oedema? Why are Dexamethasone and Dilantin used? And what is the complication of insulin dependent diabetes mellitus on nursing care with someone with an SOL?

18th August 2000

Blackwell's Dictionary of Nursing (1994) provides the following definition concerning space-occupying lesions:

"Lesions such as abscesses, haematomas, or tumours which form in an area where there is little room for expansion and which therefore compress the normal structures in the area: frequently they occur in the skull."

Oedema occurs as a result of vascular responses to tissue damage. A developing cerebral tumour brings about changes in the surrounding blood vessels - the capillaries dilate and the permeability of the vessels may increase. If so, fluid then leaks through the walls of these vessels into the surrounding tissues producing oedema. This is an inflammatory response identical to those produced when tissue is subjected to other forms of injury such as heat, cold, or the presence of pathogens.

Dexamethasone is a synthetic glucocorticosteroid used in the treatment of cerebral oedema because it has anti-inflammatory effects and thus helps to reduce the raised pressure within the cranial cavity.

Dilantin, better known as phenytoin, is an anticonvulsant used in the management of epilepsy. This drug may be administered to someone who develops epilepsy as a result of an underlying lesion such as cerebral tumour.

Dexamethasone is a synthetic glucocorticoid which has the potential to raise the person's blood glucose level. It does this by activating liver enzymes that convert amino acids to glucose - gluconeogenesis (Grahame-Smith et al, 1994). Thus it can cause blood glucose levels to rise and may disrupt the treatment regime normally employed to achieve good blood sugar control. Therefore the dose levels of insulin and any oral hypoglycaemic agents used may need to be increased.

There are additional considerations to bear in mind when caring for someone who is taking glucocorticosteroid preparations for cerebral oedema and who also has diabetes mellitus. Steroids can have an effect on a person's mood, sleep pattern and appetite, in which case the person may develop a false sense of well being and play down the seriousness of their illness and the need to comply with medication and other forms of treatment. If sleep is disrupted this may impose further physiological and psychological stress. As a result more energy may be consumed and this may lead to the onset of hypoglycaemia, or hyperglycaemia if carbohydrate is taken to satisfy hunger. An increase in appetite is a further recognised side effect of steroid therapy.

In view of this and the water retaining properties of steroids (although less with Dexamethasone, which has little mineralcorticoid action - British National Formulary, 1999), regular checks on the person's blood glucose and weight should be made. Furthermore it is important to ensure that the person taking steroids and their relatives are fully conversant with both the therapeutic and non-therapeutic effects of these drugs.

Because taking steroids carries serious implications, people taking these drugs are asked to carry a card showing that they are receiving steroid treatment. Nurses responsible for providing care need to make themselves fully conversant with the implications associated with steroid therapy, some of which have been set out here.

References

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