Chapter 42 Disorders of consciousness
NEUROANATOMY AND PHYSIOLOGY OF WAKEFULNESS
A normal level of consciousness depends on the interaction between the cerebral hemispheres and the rostral reticular activating system (RAS) located in the upper brainstem. Although the RAS is a diffuse projection, the areas of RAS of particular importance to the maintenance of consciousness are those located between the rostral pons and the diencephalon. In contrast, consciousness is not focally represented in any of the cerebral hemispheres and is in many ways related to the mass of functioning cortex. Thus anatomical bilateral hemispheric lesions or brainstem lesions may result in an altered conscious state.1 Large unilateral hemispheric lesions may produce impairment of consciousness by compression of the upper brainstem. In addition metabolic processes may result in coma from interruption of energy substrate delivery or alteration of neuronal excitability. Disorders of consciousness are characterised by an alteration in either the level or content of consciousness (Table 42.1). The last few conditions described in Table 42.1 are a frequent source of confusion and require further discussion (Table 42.2). These neurological states are seen more frequently in modern-day clinical practice partly because of the advances in therapy of severe brain injury and intensive care which have led to the survival of many patients who would otherwise have died.
Consciousness | An awake individual demonstrates full awareness of self and environment |
Confusion | Inability to think with customary speed and clarity, associated with inattentiveness, reduced awareness and disorientation |
Delirium | Confusion with agitation and hallucination |
Stupor | Unresponsiveness with arousal only by deep and repeated stimuli |
Coma | Unarousable unresponsiveness |
Locked-in syndrome | Total paralysis below third cranial nerve nuclei; normal or impaired mental function |
Persistent vegetative state | Prolonged coma > 1 month, some preservation of brainstem and motor reflexes |
Akinetic mutism | Prolonged coma with apparent alertness and flaccid motor tone |
Minimally conscious state | Preserved wakefulness, awareness and brainstem reflexes, but poorly responsive |
CLINICAL EXAMINATION OF THE COMATOSE PATIENT
LEVEL OF CONSCIOUSNESS
This is assessed by the Glasgow Coma Scale (GCS),2 which takes into account a patient’s response to command and physical stimuli. The GCS (Table 42.4) which was originally developed to grade the severity of head injury and prognosticate outcome, has now been extended for all causes of impaired consciousness and coma. Although it is a simple clinical score, easily performed by both medical and nursing staff by the bedside, there are a number of caveats:
Eye opening | Points |
---|---|
Spontaneous | 4 |
To speech | 3 |
To pain | 2 |
Nil | 1 |
Best verbal response | |
Oriented | 5 |
Confused | 4 |
Inappropriate | 3 |
Incomprehensible | 2 |
Nil | 1 |
Intubated | T |
Best motor response | |
Obeys commands | 6 |
Localises to pain | 5 |
Withdraws to pain | 4 |
Abnormal flexion | 3 |
Extensor response | 2 |
Nil | 1 |
PUPILLARY RESPONSES IN COMA3
The presence of normal pupils (2–5 mm and equal in size and demonstrating both direct and consensual light reflexes) confirms the integrity of the pupillary pathway (retina, optic nerve, optic chiasma and tracts, midbrain and third cranial nerve nuclei and nerves). The size of the pupil is a balance between the opposing influences of both sympathetic (causing dilatation) and parasympathetic (causing constriction) systems. Pupillary abnormalities have localising and diagnostic value in clinical neurology (Table 42.5). When the pupils are miosed, the light reaction is difficult to appreciate and may require a magnifying glass.
Abnormality | Cause | Neuroanatomical basis |
---|---|---|
Miosis (< 2 mm in size) | ||
Unilateral | Horner’s syndrome | Sympathetic paralysis |
Local pathology | Trauma to sympathetics | |
Bilateral | Pontine lesions | |
Thalamic haemorrhage | Sympathetic paralysis | |
Metabolic encephalopathy | ||
Drug ingestion | ||
Organophosphate | Cholinesterase inhibition | |
Barbiturate | ||
Narcotics | Central effect | |
Mydriasis (> 5 mm in size) | ||
Unilateral fixed pupil | Midbrain lesion | Third-nerve damage |
Uncal herniation | Stretch of third nerve against the petroclinoid ligament | |
Bilateral fixed pupils | Massive midbrain haemorrhage | Bilateral third-nerve damage |
Hypoxic cerebral injury Drugs | Mesencephalic damage | |
Atropine | Paralysis of parasympathetics | |
Tricyclics | Prevent local reuptake of catecholamines by nerve endings | |
Sympathomimetics | Stimulation of sympathetics |
OPHTHALMOSCOPY IN COMA
The pupils should never be dilated pharmacologically without prior documentation of the pupillary size and the light reflex. The presence of papilloedema suggests the presence of intracranial hypertension, but is frequently absent when the lesion is acute. Subhyaloid and vitreous haemorrhages are seen in patients with subarachnoid haemorrhage.4
EYE MOVEMENTS IN COMA5
The position and movements of the eyes are observed at rest. The presence of spontaneous roving eye movements excludes brainstem pathology as a cause of coma. In a paralytic frontal-lobe pathology, the eyes will deviate towards the side of the lesion, whilst in pontine pathologies, the eyes will deviate away from the side of the lesion. Ocular bobbing, an intermittent downward jerking eye movement, is seen in pontine lesions due to loss of horizontal gaze and unopposed midbrain controlled vertical gaze activity.6 Skew deviation (vertical separation of the ocular axes) occurs with pontine and cerebellar disorders.7
LIMB MOVEMENTS AND POSTURAL CHANGES IN COMA
Restlessness, crossing of legs and spontaneous coughing, yawning, swallowing and localising movements suggest only a mild depression of the conscious state. Choreoathetotic or ballistic movements suggest a basal ganglion lesion. Myoclonic movements indicate a metabolic disorder, usually of postanoxic origin. Asterixis is seen with metabolic encephalopathies. Hiccup is a non-specific sign and does not have any localising value.
Decerebrate rigidity is characterised by stiff extension of the limbs, internal rotation of the arms and plantar flexion of the ankles. With severe rigidity, opisthotonos and jaw clenching may be observed. These movements may be unilateral or bilateral, and spontaneous or in response to a noxious stimulus. Whereas animal studies suggest that the lesion is usually in the midbrain or caudal diencephalon (leading to exaggeration of antigravity reflexes), in humans such posturing may be seen in a variety of disease states: midbrain lesion, certain metabolic disorders such as hypoglycaemia, anoxia, hepatic coma and in drug intoxication.Decorticate posturing is characterised by flexion of elbows and wrists and extension of the lower limbs. The lesion is usually above the midbrain in the cerebral white matter.
RESPIRATORY SYSTEM8
Abnormal respiratory rate and patterns have been described in coma, but their precise localising value is uncertain. As a general rule, at lighter levels of impaired consciousness tachypnoea predominates, whereas respiratory depression increases with the depth of coma. Some of the commonly observed respiratory abnormalities are summarised in Table 42.6. Respiratory failure in comatose patients may result from hypoventilation, aspiration pneumonia and neurogenic pulmonary oedema, a sympathetic nervous system-mediated syndrome seen in acute brain injury.
Abnormality | Significance |
---|---|
Bradypnoea | Drug-induced coma, hypothyroid coma |
Tachypnoea | Central neurogenic hyperventilation (midbrain lesion), |
metabolic encephalopathy | |
Cheyne–Stokes respiration | Deep cerebral lesions, metabolic encephalopathy (hyperpnoea alternating regularly with apnoea) |
Apneustic breathing (an inspiratory pause) | Pontine lesions |
Ataxic breathing | Medullary lesions |
(Ataxic breathing normally progresses to agonal gasps and terminal apnoea) |
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