Consciousness, RAS and approach to coma

Consciousness, RAS and approach to comaDr. Nishtha JainSenior residentDepartment of neurologyGMC, kota.

Consciousness may be defined as a state of awareness of self and surroundings.

Reticular activating systemfound in the reticular formation in the core of the upper brainstem.

Inputs from every sensory system.

Physiologically involved in sleep/wake regulation and arousal/consciousness.

Coma is a state of complete unresponsiveness to arousal in which the patient lies with the eyes closed.

Rapid Initial Examinationand Emergency Therapyto ensure that the comatose patient is medically and neurologically stable.

to rule out the need for immediate medical or surgical intervention.

Emergency Treatment A baseline serum glucose level should be obtained before glucose administration.

Empirical use of supplemental oxygen, intravenous (IV) thiamine (at least 100 mg), and IV 50% dextrose in water (25 g).

Naloxone hydrochloride IV- 0.4 to 2 mg if opiate overdose is the suspected cause.

General Examination

Head and Neck ExaminationLaceration or edema of the scalp : head trauma.

raccoon eyes refers to orbital ecchymosis : anterior basal skull fracture.

The Battle sign : hematoma overlying the mastoid, originating from basilar skull fracture extending into the mastoid portion of the temporal bone.

Meningismus neck stiffness : infectious or carcinomatous meningitis, subarachnoid hemorrhage, or central or tonsillar herniation.

Scars on the neck : endarterectomy, implying vascular disease, or from thyroidectomy or parathyroidectomy, suggesting concomitant hypothyroidism, hypoparathyroidism, or both.

Goiter : hypothyroidism or hyperthyroidism.

Systemic Examination

Cardiac examination- arrythmias, cardiac murmurs

Abdominal examination- abnormal bowel sounds, organomegaly, masses, and ascites.

Neurological Examinationstate of consciousness, respiratory pattern,pupillary size and response to light, spontaneous and reflex eye movements, and skeletal muscle motor response.

Respiratory pattern

Pupil Size and ReactivityThalamic lesions cause small, reactive pupils, often referred to as diencephalic pupils.

Similar pupillary findings are noted in many toxic-metabolic conditions resulting in coma.

Hypothalamic lesions or lesions elsewhere along the sympathetic pathway : Horner syndrome.

Midbrain lesions produce three types of pupillary abnormality, depending on the lesion:

Dorsal tectal lesions interrupt the pupillary light reflex, resulting in midposition pupils, which are fixed to light but react to near vision.

Spontaneous fluctuations in size occur, and the ciliospinal reflex is preserved.

Nuclear midbrain lesions usually affect both sympathetic and parasympathetic pathways, resulting in fixed, irregular midposition pupils, which may be unequal.

Lesions of the third nerve fascicle in the brainstem, or after the nerve has exited the brainstem, cause wide pupillary dilation unresponsive to light.

Pontine lesions interrupt sympathetic pathways and cause small, so-called pinpoint pupils which remain reactive.

Lesions above the thalamus and below the pons should leave pupillary function intact, except for Horner syndrome in medullary or cervical spinal cord lesions.

Ocular MotilityEvaluation of ocular motility consists of (1) observation of the resting position of the eyes, including eye deviation; (2) rotation of spontaneous eye movements; and (3) testing of reflex ocular movements.

Abnormalities in Resting PositionUnilateral third nerve palsy from either an intramedullary midbrain lesion or extramedullary compression causes the affected eye to be displaced downward and laterally.

A sixth nerve palsy produces inward deviation.

Isolated sixth nerve palsy, however, is a poor localizer.

Conjugate lateral eye deviation : ipsilateral lesion in the frontal eye fields, a lesion anywhere in the pathway from the ipsilateral eye fields to the contralateral parapontine reticular formation.

Dysconjugate lateral eye movement : sixth nerve palsy in the abducting eye, a third nerve palsy in the adducting eye, or an internuclear ophthalmoplegia.

An internuclear ophthalmoplegia may be differentiated from a third nerve palsy by the preservation of vertical eye movements.

Downward deviation of the eyes : brainstem lesions (most often from tectal compression); metabolic disorders such as hepatic coma.

Thalamic and subthalamic lesions produce downward and inward deviation of the eyes : looking at the tip of the nose.

Skew deviation usually indicates a posterior fossa lesion (brainstem or cerebellar).

Spontaneous Eye MovementsPurposeful-appearing eye movements in a patient who seems unresponsive : locked-in syndrome, catatonia, pseudocoma, or PVS.

When roving eye movements are present : brainstem is relatively intact and coma is due to a metabolic or toxic cause or bilateral lesions above the brainstem.

Nystagmus occurring in comatose patients suggests an irritative or epileptogenic supratentorial focus.

An epileptogenic focus in one frontal eye field causes contralateral conjugate eye deviation.

An electroencephalogram (EEG) is required to ascertain the presence of this condition.

Ocular bobbing : rapid downward jerks of both eyes followed by a slow return to the midposition.

In the typical form, there is associated paralysis of both reflex and spontaneous horizontal eye movements.

Monocular or paretic bobbing occurs when a coexisting ocular motor palsy alters the appearance of typical bobbing.

Atypical bobbing : ocular bobbing when lateral eye movements are preserved.

Typical ocular bobbing : specific but not pathognomonic for acute pontine lesions.

Atypical ocular bobbing occurs with anoxia and is nonlocalizing.

Ocular dipping, also known as inverse ocular bobbing : spontaneous eye movements in which an initial slow downward phase is followed by a relatively rapid return.

associated with diffuse cerebral damage.

Reverse ocular bobbing : slow initial downward phase followed by a rapid return that carries the eyes past the midposition into full upward gaze.

Reverse ocular bobbing : nonlocalizing.

Vertical nystagmus due to an abnormal pursuit or vestibular system is slow deviation of the eyes from the primary position, with a rapid (saccadic) immediate return to the primary position.

It is differentiated from bobbing by the absence of latency between the corrective saccade and the next slow deviation.

Ocular-palatal myoclonus occurs after damage to the lower brainstem involving the Guillain-Mollaret triangle, which extends between the cerebellar dentate nucleus, red nucleus, and inferior olive.

Ocular flutter is back to- back saccades in the horizontal plane, a manifestation of cerebellar disease.

Reflex Ocular Movements

Motor SystemBilateral midbrain or pontine lesions responsible for decerebrate posturing. Less commonly, deep metabolic encephalopathies or bilateral supratentorial lesions involving the motor pathways may produce a similar pattern.

Decorticate posturing : much poorer localizing posture result from lesions in many locations, although usually above the brainstem.

Decorticate posture is not as ominous a sign as decerebrate posture, because the former occurs with many relatively reversible lesions.

Myoclonic jerking : anoxic encephalopathy or other metabolic comas such as hepatic encephalopathy. Rhythmic myoclonus : a sign of brainstem injury. Tetany : hypocalcemia.

Cerebellar fits : intermittent tonsillar herniation and characterized by deterioration of level of arousal, opisthotonos, respiratory rate slowing and irregularity, and pupillary dilatation.

Coma and Brain Herniation Supratentorial herniation1. Uncal (transtentorial)2. Central3. Cingulate (subfalcine/transfalcine)4. Transcalvarial Infratentorial herniation5. Upward (upward cerebellar or upward transtentorial)6. Tonsillar (downward cerebellar)

Coma and Brain Herniation

Classically, the uncal pattern includes early signs of third nerve and midbrain compression.

The pupil initially dilates as a result of third nerve compression returns to the midposition with midbrain compression that involves the sympathetic as well as the parasympathetic tracts compression of ipsilateral PCA compression of contralateral midbrain and multiple haemorrhages in brainstem.

Central pattern : mild impairment of consciousness, with poor concentration, drowsiness, or unexpected agitation; small but reactive pupils; loss of the fast component of cold caloric testing; poor or absent reflex vertical gaze; and bilateral corticospinal tract signs, including increased tone of the body ipsilateral to the hemispheric mass lesion responsible for herniation.

Differentiating Toxic-Metabolic Comafrom Structural ComaTime course of the illness : structural lesions have more abrupt onset, whereas metabolic or toxic causes are slowly progressive.

Focal features or notable asymmetry on neurological examination : structural lesion. Toxic, metabolic, and psychiatric diseases : symmetrical.

Metabolic problems : milder alterations in arousal, typically with waxing and waning of the behavioral state , acute structural lesions : same level of arousal or progressively deteriorate.

Deep, frequent respiration most commonly due to metabolic abnormalities.

Papilledema are almost pathognomonic of structural lesions.

Papilledema does not occur in metabolic diseases except hypoparathyroidism, lead intoxication, and malignant hypertension.

The pupils usually are symmetrical in coma from toxic-metabolic causes.

Asymmetry in oculomotor function typically is a feature of structural lesions.

Roving eye movements with full excursion are most often indicative of metabolic or toxic abnormalities.

Muscle tone usually is symmetrical and normal or decreased in metabolic coma.

Structural lesions cause asymmetrical muscle tone.

Differentiating Psychiatric Comaand Pseudocoma from Metabolicor Structural Coma

The malingering or hysterical patient often gives active resistance to passive eye opening.

It is nearly impossible for the psychiatric or malingering patient to mimic the slow, gradual eyelid closure.

Blinking also increases in psychiatric and malingering patients but decreases in patients in true stupor.

Passive eye opening in a sleeping person or a truly comatose patient (if pupillary reflexes are spared) results in pupillary dilation.

Opening the eyes of an awake person produces constriction.

This principle may help differentiate coma from pseudocoma.

Roving eye movements cannot be mimicked and thus also are a good sign of true coma.

Finally, if during cold caloric testing, the eyes do not tonically deviate to the side of the caloric instillation, and the fast phases are preserved, stupor or true coma is essentially ruled out.

Moreover, cold caloric testing with the resultant vertigo usually awakens psychiatric and malingering patients.

Electroencephalography Metabolic disorders : a decrease in the frequency of background rhythms and the appearance of diffuse theta activity.

Hepatic encephalopathy : bilaterally synchronous and symmetrical, medium- to high-amplitude, broad triphasic waves, often with a frontal predominance.

Herpes simplex encephalitis : unilateral or bilateral periodic sharp waves with a temporal preponderance.

The EEG also can help confirm a clinical impression of catatonia, pseudocoma, the locked-in syndrome, PVS, and brain death.

PrognosisOnly about 15% of patients in nontraumatic coma make a satisfactory recovery. Functional recovery is related to the cause of coma. Cerebrovascular disease including subarachnoid hemorrhage : worst prognosis; coma from hypoxia-ischemia : intermediate prognosis; coma due to hepatic encephalopathy and other metabolic causes: best ultimate outcome.

Age does not appear to be predictive of recovery.

The longer a coma lasts, the less likely the patient is to regain independent functioning.

Factors that adversely impact brain injury following cardiac arrest include cerebral edema, pyrexia, hyperglycemia, and seizures.

Absence of pupillary light or corneal reflexes, and motor response to noxious stimuli no greater than extension : poor prognosis.

Other poor prognostic signs : myoclonic status epilepticus, bilateral absence of the N20 response from the somatosensory cortex.

Referrences Bradleys Neurology in Clinical Practice, sixth edition.The Acutely Comatose Patient: Clinical Approach and Diagnosis. S. A Moore, E F. Wijdicks. Semin Neurol 2013;33:110120.Emergency Neurological Life Support: Approach to the Patient with Coma. J. S Huff, R D. Stevens, S D. Weingart, W S. Smith. Neurocrit Care 2012.Management of the Patient with Diminished Responsiveness. S Hocker, A. A. Rabinstein. Neurol Clin 30 (2012) 19.Evaluation and prognosis of coma. J. J Provencio. Continuum Lifelong Learning Neurol 2009;15(3).