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For clinical purposes, the ability of the individual to respond appropriately to environmental stimuli provides a quantifiable definition of consciousness.
The causes of altered conscious state can be divided pathophysiologically into structural and metabolic insults.
A thorough history and examination is the key to guiding investigation choice and identifying the cause of the primary insult. Management is directed towards resuscitation, specific correction of the primary pathology and minimization of secondary injury.
Bedside blood glucose measurement is essential and may be lifesaving.
Consciousness is variously termed lucidity, orientation, awakeness and mentation in the context of emergency department (ED) patients. None of these terms comprehensively defines consciousness. The Glasgow Coma Scale (GCS) ( Box 8.4.1 ), developed for head-injured patients in a time when computed tomography (CT) scanning was unavailable, is routinely used but not specifically suited to measuring conscious state. Ultimately, consciousness is an amalgam of alertness, orientation and clarity of cognition. Of note, isolated absence or derangement of cognition and mentation (e.g. caused by dementia or psychiatric illness or both, considered elsewhere) does not result in the clinical entity of altered conscious state. In the same way, simple lack of orientation does not constitute a clinical alteration in conscious state.
The GCS scores range between 3 and 15, 3 being the worst and 15 the best. This scale is composed of three parameters: best eye response, best verbal response, best motor response, as given below:
Best eye response (score out of 4)
1—No eye opening
2—Eye opening to pain
3—Eye opening to verbal command
4—Eyes open spontaneously
Best verbal response (score out of 5)
1—No verbal response
2—Incomprehensible sounds
3—Inappropriate words
4—Confused
5—Orientated
Best motor response (score out of 6)
1—No motor response
2—Extension to pain
3—Flexion to pain
4—Withdrawal from pain
5—Localizing pain
6—Obeys commands
In the clinical context, an alteration in conscious state requires a drop in alertness and ‘awakeness’. This drop may result in a corresponding loss of orientation and/or a clouding of cognition, thereby altering a patient’s response to environmental stimuli or provocation. The reverse, an increase in alertness, could also be considered an alteration in conscious state but, in practice, is most often due to pharmacological agents or a mood-elevating psychiatric illness, both of which are beyond the scope of the present discussion.
The level of consciousness describes the rousability of the individual, whereas the content of consciousness may be assessed in terms of the appropriateness of the individual’s response. Broadly speaking, the first is a brain stem function and the second is an attribute of the forebrain.
The physical portions of the brain involved in consciousness consist of the ascending arousal system, which begins with monoaminergic cell groups in the brain stem and culminates in extensive diffuse cortical projections throughout the cerebrum. En route there is input and modulation from both thalamic and hypothalamic nuclei as well as basal forebrain cell groups.
Integration of the brain stem and the forebrain is illustrated by individuals who have an isolated pontine injury. They remain aware, but the intact forebrain is unable to interact with the external world, hence the aptly named ‘locked-in syndrome’. At the other end of the spectrum are individuals with unresponsive wakefulness syndrome (persistent vegetative state) who, in spite of extensive forebrain impairment, appear awake but totally lack the content of consciousness. These clinical extremes emphasize the important role of the brain stem in modulating motor and sensory systems through its descending pathways and regulating the wakefulness of the forebrain through its ascending pathways.
Given the pathophysiology, the causes of an altered conscious state are myriad and include any cause of insult or injury either directly or indirectly to the brain ( Box 8.4.2 ). Direct injury resulting in structural insults may be traumatic or non-traumatic (e.g. subdural haemorrhage, stroke). Indirect injury may encompass any change in the metabolic and chemical milieu of the brain, resulting in a depression of neuronal function (e.g. sepsis, hyper- or hypoglycaemia, drug ingestion).
Haematoma
epidural
subdural
Cerebral tumour
Cerebral aneurysm
Haemorrhagic CVA
Cerebellar AVM
Pontine haemorrhage
Brain stem tumour
Hypoxia
Hypoglycaemia
Global ischaemia
Shock
hypovolaemia
cardiogenic
Focal ischaemia
TIA/CVA
vasculitis
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