Wilkinson. Essential Neurology 2005

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Epilepsy

Chapter 12 deals with epilepsy in detail. Epilepsy may be generalized or focal. In generalized epilepsy the abnormal electrical activity starts in deep midline brain structures and spreads to all parts of the cerebral cortex simultaneously. This gives rise to tonic–clonic and absence seizures in which consciousness is invariably lost.

In focal epilepsy, the abnormal electrical activity is localized to one area of the cerebral cortex. In focal seizures, there is grossly deranged function in that part of the brain where the epileptic activity is occurring, whilst the rest of the brain remains relatively normal. So long as the seizure remains localized, consciousness is maintained. It is only when focal epileptic activity occurs in the temporal lobe, when regions subserving memory are disrupted during the attack, that patients seek help for blackouts which they cannot properly remember. Memory, rather than consciousness, is lost in such attacks.

‘Psychogenic non-epileptic’attacks

Some patients attract attention to themselves, at a conscious or subconscious level, by having blackouts. The attacks may consist of apparent loss of consciousness and falling, sometimes with convulsive movement of the limbs and face. The patient may report no memory or awareness during the attack, or he may acknowledge awareness at a very distant level without any ability to respond to his environment or control his body during the attack.

Such psychologically mediated non-epileptic attacks:

•are more common in teenage and young adult life;

•are associated with self-reported previous physical or sexual abuse;

•may be suggested by the coordinated purposeful kinds of movements which are witnessed in the attacks (shouting, grasping, pelvic thrusting, turning the head from side to side);

•may occur in association with epilepsy. It is easy to understand why a young person with epilepsy might respond to adversity by having non-epileptic attacks rather than developing some other psychosomatic disorder;

•are disabling, very difficult to manage, and potentially dangerous if treated inappropriately with anticonvulsant drugs such as intravenous benzodiazepines.

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Treatment of the common causes of blackouts

Apart from a general explanation of the nature of the attacks to the patient and his family, there are two other aspects of management.

Specific treatment suggestions

Vasovagal syncope: lower head at onset.

Postural hypotension: remove offending drug, consider physical and pharmacological methods of maintaining the standing blood pressure (sleep with bed tilted slightly head up, fludrocortisone).

Hyperventilation: reassurance, and exercises to control breathing.

Cardiac arrhythmia: pharmacological or implanted pacemaker control of cardiac rhythm.

Hypoglycaemia: attention to drug regime in diabetics, removal of insulinoma in the rare instances of their occurrence.

Vertebro-basilar TIAs: treat source for emboli, aspirin. Epilepsy: anticonvulsant drugs.

‘Psychogenic non-epileptic’ attacks: try to establish the reason for this behaviour, and careful explanation to the patient.

Care of personal safety

People who are subject to sudden episodes of loss of consciousness:

•should not drive motor vehicles;

•should consider showering rather than taking a bath;

•may not be safe in some working environments which involve working at heights, using power tools, working amongst heavy unguarded machinery, working with electricity wires;

•may have to curtail some recreational activities involving

swimming or heights.

A firm but sympathetic manner is necessary in pointing out these aspects of the patient’s management.

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Treatment

Sensible, but often unpopular restrictions

•Sudden irresistible need to sleep, for short periods

•Legs give way, when highly amused or angry

Ashort period, lasting hours, of very selective memory loss, other cerebral functions remaining intact

Before leaving the causes of blackouts, there are two rare neurological conditions to mention briefly. One condition predisposes the patient to frequent short episodes of sleep, narcolepsy, and the other gives rise to infrequent episodes of selective loss of memory, transient global amnesia.

Narcolepsy

In this condition, which is familial and very strongly associated with the possession of a particular HLA tissue type, the patient has a tendency to sleep for short periods, e.g. 10–15 minutes. The sleep is just like ordinary sleep to the observer, but is unnatural in its duration and in the strength with which it overtakes the patient. Such episodes of sleep may occur in circumstances where ordinary people feel sleepy, but narcoleptic patients also go to sleep at very inappropriate times, e.g. whilst talking, eating or driving.

The condition is associated with some other unusual phenomena:

•cataplexy: transient loss of tone and strength in the legs at times of emotional excitement, particularly laughter and annoyance, leading to falls without any impairment of consciousness;

•sleep paralysis: the frightening occurrence of awakening at night unable to move any part of the body for a few moments;

•hypnogogic hallucinations: visual hallucinations of faces occurring just before falling asleep in bed at night.

Narcolepsy, and its associated symptoms, are helped by

dexamphetamine, clomipramine and modafinil.

Transient global amnesia

This syndrome, which tends to occur in patients over the age of 50, involves loss of memory for a few hours. During the period of amnesia, the patient cannot remember recent events, and does not retain any new information at all. All other neurological functions are normal. The patient can talk, write and carry out complicated motor functions (e.g. driving) normally. Throughout the episode, the patient repeatedly asks the same questions of orientation. Afterwards, the person is able to recall all events up to the start of the period of amnesia, remembers nothing of the period itself, and has a somewhat patchy memory of the first few hours following the episode.

Transient global amnesia may occur a few times in a patient’s life. Its pathological mechanism remains poorly understood, but may be related to that of migraine aura.

UNCONSCIOUSNESS

Regulation of pupils

Regulation of Temperature

BP

Pulse

Respiration

Fig. 11.4 Diagram to show important functions of the brainstem.

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body temperature, blood pressure, pulse and respiration may all indicate trouble in the pons/medulla, where the centres controlling these vital functions exist.

When confronted with a patient in coma, a well-trained doctor will assess:

•vital functions of respiration, temperature control, pulse and blood pressure;

•pupil size and reactivity;

•the patient’s eyes, speech and motor responses according to the Glasgow Coma Scale.

This approach to the assessment of conscious level holds good regardless of the particular cause of coma.

Causes of coma

There is a simple mnemonic to help one to remember the causes of coma (Fig. 11.5). In considering the causes of coma it is helpful to think again in terms of disease processes which impair cerebral hemisphere function generally on the one hand, and in terms of lesions in the brainstem blocking afferent stimulation of the cerebrum on the other. The common causes of coma are illustrated in this way in Fig. 11.6 overleaf.

Fig. 11.5 Asimple mnemonic for the recall of the causes of coma.

UNCONSCIOUSNESS

•Airway

•Level of coma

•Cause of coma

•Cautionoverlumbarpuncture

•Treat cause

•Routine care of unconscious patient

Fig. 11.7 Diagram to show the routine care of the unconscious patient.

(a)

Chart of observations

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Investigation and management of a patient in coma

1.Check that the patient’s airway is clear, that breathing is satisfactory, and that the patient’s colour is good.

2.Assess the level of coma, looking at vital functions, pupils and items of the Glasgow Coma Scale as mentioned above.

3.Try to establish the cause of the coma by taking a history from relatives or witnesses, physical examination and appropriate tests. It is obviously important to have the common causes of coma (A, E, I, O, U) clearly in one’s mind whilst questioning, examining and ordering investigations.

4.Remember the danger of lumbar puncture in patients in whom coning is imminent or present (see p. 44). Reduction of the CSF pressure below the foramen magnum may encourage further downward herniation at the tentorial or foramen magnum level, so no lumbar puncture if papilloedema is present, or until a head scan has excluded a mass lesion or any brain swelling.

5.Treat the specific cause of the coma as soon as this is established, e.g. anticonvulsants for epilepsy, antibiotics for meningitis, intravenous glucose for hypoglycaemia, specific antagonists for specific CNS depressant drug poisonings.

6.Establish the routine care of an unconscious patient regardless of the cause (Fig. 11.7).

(a)Observations: assessment every 15–30 minutes of vital functions, pupils and Glasgow Coma Scale, to monitor improvement or deterioration in the patient’s condition.

(b)Airway, ventilation, blood gases.

(c)Blood pressure, to maintain adequate perfusion of the body, particularly of the brain and kidneys.

(d)Fluid and electrolyte balance.

(e)Nutrition and hydration.

(f)Avoidance of sedative or strong analgesic drugs.

(g)General nursing care of eyes, mouth, bladder, bowels, skin and pressure areas, passive limb mobilization to prevent venous stagnation and contractures, chest physiotherapy.

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Prognosis for coma

Patients whose coma has been caused by drug overdose may remain deeply unconscious for prolonged periods and yet have a satisfactory outcome. They may need respiratory support during their coma if brainstem function is depressed, but proceed to make a full recovery.

Prolonged coma from other causes has a much less satisfactory outcome. As an example of this, if one takes a group of unconscious patients, whose coma is not due to drug overdose, who:

•show no eye opening (spontaneous or to voice),

•express no comprehensible words,

•fail to localize painful stimuli,

•remain like this for more than 6 hours,

more than 50% of them will die, and recovery to independent existence will occur in a minority of the rest. This background knowledge must remain in the doctor’s mind when counselling relatives of patients in coma, and when planning the care of patients in prolonged coma.

Some patients who fail to recover from coma enter a state of unawareness of self and environment, in which they can breathe spontaneously and show cycles of eye closure and opening which may simulate sleep and waking. This is known as the vegetative state, which can become permanent. It is difficult, and takes a long time, to determine the precise state of awareness in such unfortunate patients.

Brainstem death

Deeply unconscious patients whose respiration has to be maintained on a ventilator, whose coma is not caused by drug overdose, clearly have a worsening prognosis as each day goes by. Amongst this group of patients, there will be some who have a zero prognosis, whose brainstems have been damaged to such an extent that they will never breathe spontaneously again.

Guidelines exist to help doctors identify patients who have undergone brainstem death whilst in coma which has been supported by intensive care and mechanical ventilation (Fig. 11.8). Testing for brainstem death must be done by two independent, senior and appropriately trained specialists if treatment is to be withdrawn.

CHAPTER 11