NEUROLOGY

CARLOS EDUARDO REIS, MD

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Coma

Coma is a state in which the patient is unresponsive to environmental stimuli, unable to communicate in any manner and from which he or she cannot be aroused. The examination requires a special approach because the patient cannot give a history and cooperation is absent.

Normal Physiology of Consciousness

Consciousness is maintained by the normal functioning of the brain stem reticular activating system and it's bilateral projections to the thalamus and cerebral hemispheres.

Etiology

Coma results from a disturbance in the function of either the brain stem reticular activating system above the mid pons or both cerebral hemispheres.
This disturbance can be caused by lesions in the reticular activating system or both hemispheres or by lesions outside this structures but capable of affect their normal function. The many causes of coma are shown in table 1.

**Table 1. Causes of Coma**
Category	Possible Etiologic Factors
Supratentorial Lesions	Epidural or Subdural Hematoma Large Isquemic Infarction Tumor Intraparenchymal hemorrhage Trauma Abscess
Infratentorial Lesions	Basilar artery thrombosis Pontine or Cerebellar Hematoma Ischemic Cerebellar Infarction Tumor Abscess
Diffuse Encephalopathies	Hypoglycemia Drug Intoxication Hepatic Encephalopathy Hyperosmolar States Hyponatremia Global Cerebral Ischemia Hyperthermia Meningitis and Encephalitis Subarachnoid Hemorrhage Myxedema Renal Failure Hypercarbia Thiamine Deficiency Hydrocephalus
Psychogenic	Catatonic States Acute Psychotic Deliria Hysteria-malingering

Emergency Management

The approach to diagnosis of the comatose patient consists of two steps. First you need to stabilize the patient and treat presumptively life-threatening disorders. After that, efforts are directed to establish an etiologic diagnosis

Secure airway
Establish Adequacy of Ventilation
Establish Adequacy of Circulation
Insert Intravenous cannula
Draw blood for laboratory studies

Treat Immediately Reversible causes of coma
a) Hypoglycemia - 25g of glucose I.V
b) Opiate overdose - Naloxe 2 mg I.V
c) Wernicke's Encephalopathy - Thiamine 100 mg I.V
Treat seizures
Draw blood for arterial blood gas determinations

History

After the emergency measures have been taken with successful, you will need to obtain a description of the onset of coma and a history of any chronic illness, eg, diabetes, hypertension or drug abuse.
It is very important because some aspects like the time over which coma develops is crucial to guide your clinical investigation. For example: a sudden onset of coma suggest a vascular origin and in contrast a more protracted course is seen with tumor, Abscess or chronic subdural hematoma

General Physical Examination

Posture - Look for muscle jerks or tremors. Inspect the respiratory movements for tachypnea, bradypneia, Cheyne-Stokes breathing and Kussmaul breathing.

Color - Look for pallor, icterus, the cherry-red color of carbon monoxide hemoglobin and the cyanosis of methemoglobinemia.

Facial muscles - Look for asymmetry of the face which may indicate hemiplegia

Oral Cavity - Look for lacerations in the tongue which may indicate biting during a convulsive seizure. Smell the breath for alcohol or ammonia.

Ears - Look for pus

Neck - Test for nuchal rigidity, Brudzinski sign, Kernig sign, for evidence of meningeal irritation.

Vital signs

Blood Pressure - Elevation of blood pressure can indicate
1. Long-standing hypertension, which predisposes to intracerebral hemorrhage or stroke).
2. Hypertensive Encephalopathy
3. May be a consequence of the process causing the coma ( intracerebral or subarachnoid hemorrhage
Temperature
1. Hypothermia - can occur in ethanol or sedative drug intoxication, Wernicke's encephalopathy, hepatic encephalopathy, and Myxedema.
2. Hyperthermia - can occur in status epilepticus, pontine hemorrhage, heat stroke, malignant hyperthermia and anticholinergic intoxication.

Optic Fundi - Look for Papilledema or retinal hemorrhage which may indicate chronic or acute hypertension or an elevation in intracranial pressure.
subhyaloid hemorrhages in an adult suggest subarachnoid hemorrhage.

Signs of trauma:

Battle's sign ( swelling and discoloration overlying the mastoid bone behind the ear)
Raccoon eyes (Periorbital ecchymosis)
Cerebrospinal fluid rhinorrhea or otorrhea
Skull fractures

Neurologic Examination

The neurologic examination is very important to etiological diagnosis and have to be done with special attention.The results have to be recorded because they will help later in evaluating the treatment. Some aspects of the neurologic examination were explained above and will not be discussed here.

Pupils - Pupillary size(normal 3-4 mm in diameter) and reactivity is dependent on sympathetic parasympathetic innervation. Brain stem reflexes, such as the pupillary reaction to light, offer clues to the location of the lesion responsible for the coma.

Bilateral dilated pupils - Are greater than 7 mm in diameter and do not react to light stimulation. Are seen in:
a. Transtentorial herniation of both medial temporal lobes
b. Anticholinergic or Sympathomimetic drug intoxication
Bilateral pinpoint pupils - Have 1-1,5 mm in diameter and are seen in:
a. Morphine poisoning
b. Pontine hemorrhage
c. neurosyphilis
d. Organophosphates poisoning
e. Miotic eyes drops
Asymmetric pupils(anisocoria) - With a difference of 1 mm or less in diameter and a normal constriction response to light is a normal finding in 20% of the population. If the dilated pupil do not react to light or do it slowly, it usually indicates a rapidly expanding lesion on the ipsilateral side as in subdural or middle meningeal hemorrhage or brian tumor, that is compressing the midbrain or oculomotor nerve directly or by mass effect.
Fixed midsized pupils - Are about 5 mm in diameter, do not react to light and are the result of midbrain lesion.

Extraocular Movements - In the comatose patient eye movements are tested by stimulating the vestibular system by the oculocephalic reflex(doll's head maneuver) which consists of passive head rotation or by the oculovestibular reflex(cold-water calorics test) which uses ice-water irrigation against the tympanic membrane.

Normal - The presence of full reflex eye movements( full conjugate horizontal eye movement during the doll's head maneuver and tonic conjugate movement of both eyes to the side of the ice-water irrigation during caloric test) attests to the integrity of the brain stem from the pontine to the midbrain level.
Abnormal
a. Impaired unilateral adduction - Indicates lesions of the oculomotor nerve or midbrain lesions involving the oculomotor nucleus.
b. Downward deviation of one or both eyes - is suggestive of sedative drug intoxication.
c. No response - Complete absence of response on oculovestibular testing implies either a structural lesion of the brain stem at the level of the pons or a metabolic disorder with a particular predilection for brain stem involvement(sedative drug intoxication).

Classify the seriousness of cerebral dysfunction using the Glasgow Coma Scale

Treatment

The emergency management of comatose patient is the first part of the treatment. It is necessary to stabilize the patient and to permit further evaluation. The continuation of treatment depends on the etiology of the coma and can vary from medical therapy to neurosurgical intervention.

Prognosis

The most important aspect of evaluation of the comatose patient is to decide whether unconsciousness is the result of a structural brain lesion or a diffuse encephalopathy caused by metabolic disturbance, meningitis or seizures, because they need different therapies. Structural brain lesions may need neurosurgical intervention while diffuse encephalopathy may require only medical treatment. Another important part of medical evaluating includes forecasting the outcome of illness, since vigorous treatment may be followed by an unwanted outcome.

References

Coma. In Aminoff MJ, Greenberg DA, Simon RP(eds): Clinical Neurology, Third edition. Appleton & Lange, 1996.

Sustained Impairments of Consciousness. In Wynngaarden JB, Smith LH, Bennet JC(eds): Cecil Textbook of Medicine, 20th edition. W B Saunders Company, 1996.

Coma. In Adams RD, Victor M(eds): Principles of Neurology, fifth edition.

Coma. In Rowland LP(ed): Merritt's Textbook of Neurology, ninth edition.

Disorders of Sleep and Consciousness. In Kandel ER, Schwartz JH, Jessell TH(eds): Principles of Neural Science, Fourth edition. Appleton & Lange.

If you have suggestions or comments send an e-mail to Carlos Eduardo Reis

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