Disorders of Function
We will separate this chapter in 3 parts:
CONSCIOUSNESS AND UNCONSCIOUSNESS
ANATOMY AND PHYSIOLOGY
There is a broad distinction between the content of consciousness, that is, what we are at any moment conscious of, sensations, emotions, ideas, or memories, for example, and the process of consciousness itself. This is bome out by everyday clinical experience. A person may be at one moment conscious of one thing and at another moment conscious of another, but on each occasion he is equally conscious. Moreover, the content of consciousness may be impaired by disease, as when a patient loses part of a visual field or sensation over part of the body. Nevertheless, such a person remains fully conscious. On the other hand, a person may be completely unconscious, and between full conscidusness and unconsciousness there are states in which he is partially conscious, that is, he has some degree of awareness of his surroundings, but it is incomplete. Hence the content of consciousness may be reduced without any alteration in consciousness as a process, or consciousness as a process may be impaired in which case none of the functions normally associated with it can be adequately carried out. Recent research has shown that the maintenance of consciousness depends to an important extent upon the central reticular formation.
The Central Reticular Formation
This structure occupies a central position in the brain stem and is situated in the tegmentum of the medulla, pons and midbrain, above which it merges into the thalamic reticular system (Figure 1). It has been shown experimentally that damage to the central reticular formation which spares the lemniscal ascending sensory pathways causes persistent unconsciousness in animals, which then show the electroencephalographic changes normally associated with sleep. The central reticular formation is therefore regarded as the anatomical basis of an alerting system which acts in a complex manner upon both the cerebral cortex and the afferent pathways in order to maintain the brain in a condition in which consciousness can occur. The experimental lesions just described can be paralleled in human pathology, and there is now evidence that lesions of the central reticular formation in man, even as low as the medulla, may cause loss of consciousness. Lesions of the cerebral cortex and subcortical white matter, including extensive ablations, do not cause loss of consciousness. Discharging cortical lesions, however, may do so, especially when they are situated in the temporal or frontal lobes. How loss of consciousness is produced in epileptic attacks is not fully understood, but it would appear that when a discharging lesion causes loss of consciousness it probably does so by intrefering with the activity of the central reticular formation, and it has been suggested that the disturbance occurs in the upper part of the diencephalon in the neighbourhood of the thalami.
COMA
The word coma (Greek kwµa, meaning a
deep sleep) is the term used for prolonged states of unconsciousness. From what has
already been said it will be clear that coma may be produced by lesions involving the
central reticular formation. This may be the area of the brain primarily damaged, or it
may indirectly as the result of, for example, a space-occupying or vascular lesion
elsewhere. It may be assumed that when coma occurs in a patient suffering from a focal
lesion of the brain, it is to an important extent the resultof disturbance of function of
the central reticular formation. In many cases,
however, coma is the result of some disorder which acts diffusely upon the nervous system,
for example a toxic state, however produced. While there an some substances, for example
anaesthetics, which seem to act to some extent selectively upon the central reticular
formation, when a toxic substance is carried to the nervous system in the blood stream and
causes coma, though the coma may be the result of its effect upon the central reticular
formation, it is usually impossible to separate this from its effects upon the rest of the
brain, including the cerebral cortex.
We shall first consider the causes of coma, then the examination and investigation of the
comatose patient, and finally his management.
The Cause of Coma
Cerebral Vascular Lesions
Space-occupying Lesions
Head Injury
Meningitis and Encephalitis
Narcotic Drugs
Metabolic Disorders
Hepatic Coma
Coma of Endocrine Origin
Coma due to CO2 Intoxication (Carbon Dioxide Intoxication)
Coma due to CO Intoxication (Carbon Monoxide Intoxication)
Epilepsy
Hysteria
These were some fine ideas about the Consciousness and Unconsciousness, with a particular space reserved to Coma.
EPILEPSY
THE NATURE OF EPILEPSY
What is epilepsy ? Only a speculative answer to this question was possible before Berger in 1929 discovered a method of recording the electrical rhythms of the brain known as electroencephalography . This showed that different varieties of epileptic attack are associated with abnormal electrical rhythms recorded from the surface of the head, and differing in their characteristics and localization, and led to the description of epilepsy as a cerebral dysrhythmia. This was a great step forward, but it still leaves some questions unanswered, for we do not yet understand the physiological relationship between the dysrhythmia and the epileptic attack or the nature of the physicochemical disturbance which causes the dysrhythmia. There seems no doubt, however, that whatever its immediate or remote cause, an epileptic attack is the manifestation of a paroxysmal discharge of abnormal electrical rhythms in some part of the brain. If one adds that such discharges are likely to be repetitive, one has defined the cardinal features of epilepsy. It will be noted that loss of consciousness is not an essential feature of the epileptic attack. Loss or impairment of consciousness frequently occurs in association with an attack, but a paroxysmal electrical discharge may involve certain limited areas of the brain without interfering with consciousness.
CLINICAL VARIETIES OF EPILEPTIC ATTACK
We can't explain more about epilepsy because of the complexity of this chapter such as we will don't explain in some other chapters because of the complexity and higher degrees that are needed, to understand.
HEADACHE AND MIGRAINE
HEADACHE
There are many causes of pain in the head, but comparatively few ways in which it can be produced. The principal pain-sensitive structures within the skull are the large blood vessels, and there is abundant evidence that many of the common causes of headache produce it through their effect upon the intracranial vessels. The extracranial branches of the external carolid artery are also pain-sensitive and contribute to some forms of headache. The other important pain-sensitive structures in the head are the sensory nerves and nerve roots, and they are responsible for the pain associated with the various forms of neuritis, neuralgia, and radiculitis. Pain in the head may be referred either from some structure within the head itself, chiefly the eye, nasal sinuses, temporomandibular joint, or teeth, or occasionally from one of the thoracic or even abdominal viscera. Finally, and probably overall most commonly pain in the head may be psychogenic. The mode of production of headache will now be considered in relation to its commoner causes.
MIGRAINE
Definition
The cardinal feature of migraine, derived from the term hemicrania, is a paroxysmal headache, commonly but not invariably unilateral, recurring at irregular intervals, and often associated with visual disturbances and other disorders of cerebral function, and vomiting. Migraine is one of the commonest neurological disorders. Some 5 per cent of the population are estimated to have suffered from it at some time in their lives and there can be few who have not on some occasion experienced a headache which has some of the features of migraine.
