Coma

1- Introduction:

– Consciousness is a function of the cerebral cortex and basal ganglia; vigilance is a function of the brainstem through the ascending reticular activating (FARA)

– The existence of specific afferent spinothalamic cortical origin and to the FARA explains the influence of pain and consciousness on vigilance.

– Stiffness decortication -> subcortical lesions hemispherical or capsular

Coma – The common risk comas are all related to the failure of the autonomic functions of the CNS and not to neurological distress mechanism.

– In a stupor, the patient alternates between periods of wakefulness imperfect with pathological sleepiness phases.The performance of the functions of consciousness are limited to the performance of elementary verbal instructions or the correct orientation movements to nociceptive stimuli.

– Coma is a disorder of vigilance which prohibits stably clinical evaluation of all functions of consciousness. This definition does not preclude a cortical activity in a coma (no function clinically detectable consciousness).

– Confusion is altered strategic conscious functions (memory, time orientation, planning …). It can be accompanied by reduced alertness, exacerbated (transient global amnesia) or adapted to the environment (Korsakoff’s syndrome).

– It is dangerous to look at the intersection aerodigestive, seek to insert a gastric tube or testing the gag reflex as the airways are not protected.

– The circulatory failure of purely neurological frequently complicates certain drug intoxications (barbiturates, tricyclic, carbamates)

– Operation of Pierre Marie and Foix -> quiz motor hemifacial in a comatose posterior compression of the ascending branches of the mandible.

2- Tonus, corticospinal signs, abnormal movements:

– The coma is usually accompanied by hypotonia. The finding of hypertension is a major etiological factor.

– A extrapyramidal hypertension is described in some poisoning (carbon monoxide, phenothiazines, strychnine see neurophysiology) and neuroleptic malignant syndrome and serotonin.

– Senior members pronated flexion and leg extension -> extensive lesions of the pyramidal tract sustentorielles (decortication motion).

– Extension of the limbs, trunk (opisthotonos) and lockjaw -> extensive lesions involving the pyramidal tract in the brainstem (decerebration movement).

– These tonic postures reflect the typically large mechanical or vascular lesions, but they also occur in case of hypoglycemia; hyperosmolar states; hepatic encephalopathy.

– A very sharp ROT with extension of the trigger zone evoke a focal brain processes; but during hypoglycemia.

– The cause subarachnoid hemorrhage important bilateral pyramidal syndrome even without visible parenchymal involvement.

– The myoclonus is frequent during postanoxic or uremic coma. The recognition of same localized clonies (eyelid) and even transient is a very strong argument in favor of a status epilepticus.

– When stupor hepatic encephalopathies or hypercapnia, patients frequently present asterixis, which will disappear as the coma will be.

3- eye signs:

– The abolition of the corneal reflex translated ipsilateral lesion of the pons or nerve V or VII.

– A anisocoria can occur when toxic comas (phenothiazines, antihistamines)

– The symmetrical puncture wards (in “pinhead”) occur during opiate poisoning and injuries when the roof of the protuberance.

– A unilateral or bilateral miosis occurs when hypothalamic lesions posterior (central commitment …)

– Bilateral Myosis puncture -> pontine lesion (damage to the sympathetic system and parasympathetic tract irritation)

– Reflex ipsilateral motor (light reflex) / Reflex contralateral motor (consensual response)

– Unilateral Mydriase nonreactive: III ipsilateral lesion (often associated with exotropia and ptosis)  beginner temporal commitment

– Moderate bilateral mydriasis (pupil aréactives moderate size) -> midbrain lesions III: Edinger-Westphal nucleus

– Nonreactive mydriasis occurs in certain intoxications (anticholinergics, imipramine, organophosphorus …) and during severe neurological distress (hypothermia, barbiturate poisoning, postanoxic encephalopathy, brain death).

– Balanced and responsive pupils demonstrate the integrity of the brainstem and moving towards hemispheric lesions or metabolic causes

– Skew deviation (vertical disjunction eyes) -> loss of parallelism between the two eyes in the vertical direction (oblique deviation). Is seen in lesions of the thalamus, brainstem or cerebellum.

– Eye Bobbing (succession of rapid eye movements down and re-ascension slower)  pontine lesion

– Opsoclonies (rapid eye movement combined and anarchic)  brain stem injury and / or cerebellum

– A conjugate deviation of the head and eyes to the opposite side of hemiplegia sign a hemispheric lesion.

– A deviation of the eyes down was observed in thalamic lesions and subthalamic

– Poisoning: Myosis tight (opioids); mydriasis (anticholinergics, tricyclic antidepressants, barbiturates)

4- Breathing:

– Lower midbrain roof Lesions or upper protuberance cause hyperventilation, like acidosis, hypoxia or fever.

– Cheyne-Stokes respiration is characterized by respiratory movements of variable amplitude in a cyclic manner; it may be present in the lesions of the diencephalon or upper part of the midbrain or with metabolism coma or heart failure.

– The apneustique Kussmaul breathing is characterized by pauses at least the end of inspiration, indicates involvement of the lower projection

– Hyperventilation reflex to hypoxia or metabolic acidosis

– Hypoventilation due to poisoning by respiratory depressants (opiates, benzodiazepines, barbiturates).

– Dyspnea Cheyne-Stokes respiration periodic in time, CO2 hypersensitivity; by diencephalic injury or superior pedicle

– Ataxic respiration: irregular chaotic breathing, apnea, gasping with bulbar injury.

5- Differential diagnosis:

A- Locked-in syndrome:

– Usually ischemic lesion of the pons (thrombosis of the basilar artery)

– Conscious and alert patient, a quadriplegic with facial diplegia

– Only are possible eyelid movements and vertical eye (level stem supralésionnel)

B- Akinetic mutism:

– Akinesia driving even to painful stimuli

– Due to a bifrontal injury or acute hydrocephalus

C- Other:

– Gélineau Syndrome: sleep attacks Associates (narcolepsy) and abrupt fall of the tone (trance) in consciousness disorder

– Hysteria, simulation

6- Treatment:

– In the absence of contributory history, all serum glucose infusion should be accompanied by parenteral vitamin B1 (thiamine pyrophosphate).

– A possible HTA must be respected if it is well tolerated and if it shows no malignancy criteria

– Antidotes: flumazenil for benzodiazepine and naloxone for opiates.

– Note: The biochemistry necessarily includes a determination of electrolytes, blood glucose, blood urea and creatinine.

– Hypercalcemia, hyperparathyroidism and hypermagnesemia can manifest as coma, loss of deep tendon reflexes and a beginner paralysis by extraocular muscles.

– Intrinsic ocular motility and normal extrinsic makes it unlikely an expansive process or lesion in the posterior fossa as causing coma.

– The central commitment reflects a shift of the diencephalon. It begins by movements of decortication and a bilateral miosis, while the patient is already in a coma. Then movement decerebration bilateral and nonreactive mydriasis;photomoteurs abolition of reflexes and vertical eye movements