Disorders of consciousness

Published on 27/02/2015 by admin

Filed under Anesthesiology

Last modified 27/02/2015

Print this page

This article have been viewed 2655 times

Chapter 42 Disorders of consciousness

Balasubramanian Venkatesh

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

Table 42.2 Coma-like syndromes and related states

DIFFERENTIAL DIAGNOSIS OF COMA

Although the aetiology of coma is invariably multifactorial, the differential diagnosis of coma can be broadly grouped into three classes:

1 diseases that produce focal or lateralising signs

2 coma without focal or lateralising signs, but with signs of meningeal irritation

3 coma without focal or lateralising signs or signs of meningeal irritation

These are considered in greater detail in Table 42.3.

Table 42.3 Differential diagnosis of coma

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.

GENERAL EXAMINATION

General examination of the patient may point to the aetiology of coma. Skin changes may be seen in carbon monoxide poisoning (cherry-red discoloration of skin), alcoholic liver disease (telangiectasia, clubbing), hypothyroidism (puffy facies) and hypopituitarism (sallow complexion). The presence of cutaneous petechiae or ecchymoses may point to meningococcaemia, rickettsial infection or endocarditis as possible causes of coma. Needle puncture marks may suggest substance abuse. Bullous skin lesions are a feature of barbiturate overdose. An excessively dry skin may indicate diabetic ketoacidosis or anticholinergic overdose.

Periorbital haematomas (raccoon eyes) indicate an anterior basal skull fracture, particularly if there is associated cerebrospinal fluid rhinorrhoea. The other signs of a basal skull fracture include Battle’s sign and cerebrospinal fluid otorrhoea. Nuchal rigidity may be seen in meningoencephalitis and subarachnoid haemorrhage, although this sign may not be present in the elderly and in patients in deep coma.

The presence of hepatomegaly or stigmata of chronic liver disease may suggest hepatic encephalopathy. Bilateral enlarged kidneys may indicate polycystic kidney disease and should prompt one to consider subarachnoid haemorrhage as a possible aetiology of coma. The breath may smell of alcohol or other poisons (organophosphates). The smell of ketones on the breath is an unreliable sign and hepatic and uraemic foetor are rare.

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:

1 The GCS should always be determined prior to administration of sedative drugs or endotracheal intubation.

2 It should also be defined with regard to a patient’s vital signs, namely blood pressure, heart rate and temperature.

3 The GCS must be interpreted in the light of previous or concomitant drug therapy.

4 The presence of alcohol in the breath or in the serum should always be documented.

5 Because of the considerable interobserver variation in scoring, it is important to define the responses in descriptive terms rather than emphasising the numerical score associated with each response.

6 Measurement of awareness by the GCS is limited. Subtle changes in brainstem reflexes are not adequately assessed by the GCS.

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 COMA ³

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

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 COMA ⁵

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.

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 SYSTEM ⁸

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.

Table 42.6 Disorders of respiratory rate and pattern in coma

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)