Disorders of consciousness

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.


Table 42.1 Disorders of consciousness






























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


The neurological examination of the comatose patient is of crucial importance to assess the depth of coma and to locate the site of lesion. Although the detailed neurological examination which can be carried out in a conscious patient is not possible in a comatose individual, useful information can be obtained by performing a thorough general examination and a neurological examination, particularly evaluating the level of consciousness, brainstem signs and motor responses in coma.




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:








Table 42.4 Glasgow Coma Scale


























































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.


Table 42.5 Pupillary abnormalities in coma











































































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



EYE MOVEMENTS IN COMA5


Horizontal eye movements to the contralateral side are initiated in the ipsilateral frontal lobe and closely coordinated with the corresponding centre in the contralateral pons. To facilitate conjugate eye movements, yoking of the third-, fourth- and sixth-nerve nuclei is achieved by the medial longitudinal fasciculus.


To look to the left, the movement originates in the right frontal lobe and is coordinated by the left pontine region and vice versa. In contrast to horizontal gaze, vertical eye movements are under bilateral control of the cortex and upper midbrain.


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


The presence of full and conjugate eye movements in response to oculocephalic and oculovestibular stimuli demonstrates the functional integrity of a large segment of the brainstem. Corneal reflexes are preserved until late in coma. Upward rolling of the eyes after corneal stimulation (Bell’s phenomenon) implies intact midbrain and pontine function.





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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Disorders of consciousness

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