Coma Deep sleeplike state Can not be aroused. Stupor Lesser degrees of unarousability. Require vigorous stimuli Drowsiness Simulates light sleep Easy arousal Persistence of alertness for a brief periods. Vegetative state Out come of severe brain injury Preserved sleep-wake cycles (normal arousal) No meaningful interaction with the environment (No content)
Akinetic mutism • Partially or fully awake • Able to form impressions & think but remains immobile & mute,particularly when unstimulated. Locked–in sate • An awake patient with no means of producing speech or volitional movement in order to indicate that he is awake • Vertical eye movement & lid elevation remains unimpaired, allowing patient to signal. e. g - Infarction or hemorrhage of ventral pons, GBS pharmacologic neuromuscular blockade
The anatomic substrate for consciousness involves the cerebral hemispheres and the RAS • Cerebral hemispheres- For all complex waking behaviors • RAS - maintains the cerebral cortex in a state of wakeful consciousness (arousal) Pathophysiology of coma • Structural - Operate by compressing the brainstem • Metabolic - May affect either region
Subtentorial lesions Posterior fossa lesions cause coma in three ways; • Intrinsic brain stem process may destroy RAS • Extrinsic mass by compression or upward herniation through the tentorium cerebelli • Down ward herniation via foramen magnum.
lateral shift • Displacement of deep brain structures by a mass, with or with out herniation, is adequate to compress the region of the RAS & result in coma. • Drowsiness & stupor typically occur with moderate horizontal shift at the level of diencephalon well before transtentorial or other hernations are evident. • Acutely appearing masses are more likely to affect level of consciousness.
Metabolic causes • Many systemic metabolic abnormalities cause coma either; • By interrupting the delivery of energy substrates eg- hypoxia, ischemia, hypoglycemia • By altering neuronal excitabillity e.g – drug & alcohol intoxication,anesthesia & epilepsy. • Conditions such as hypoglycemia, hyponatremia, hyperosmolarity, hypercapnia, hypercalcemia, and hepatic & renal failure are associated with a variety of alterations in neurons & astrocytes. • The reversible effect of these conditions on the brain are not understood, but may result from impaired energy supply, change in ion fluxes across neuronal memberanes, & neuro transmitter abnormalities
metabolic cont… • Coma & seizures are a common accompaniment of any large shifts in sodium & water balance. e .g DKA, NHHS, hyponatremia from any cause ( e. g water intoxication, SIADHS ) • The severity of neurologic changes depends to a large degree on the rapidity with which the serum changes occur. • The pathophysiology of other metabolic encephalopathies such as hypothtroidism, vitamin B12 deficiency, & hypothermia are incompletely understood but must also reflect derangements of CNS biochemistry & memberane function.
Approach to the patient • Acute respiratory & cardiovascular problems should be attended to prior to neurologic assessment. • Vital signs, funduscopy & examination for nuchal rigidity • Neurologic assessment • Complete medical evaluation
History • In many cases, the cause is immediately evident like trauma, cardiac arrest , or known drug ingestion • In the remainder,certain points are especially useful; • Circumstances & rapidity with which neurologic symptoms developed • The antecedent symptoms (confusion, weakness, headache, fever, seizure, vomiting) • The use of medications , illicit drugs , or alcohol • Chronic liver, kidney, lung, heart , or other medical disease
General physical examination • Hyperthermia -Infection, brain lesion disturbing temperature regulating center, heat stroke, anticholinergic drug intoxication • Hypothermia -alcoholic, barbiturate, phenothiazine intoxication, hypothyroidism • Hypertension-Hypertensive encephalopathy Rapid rise in ICP • Hypotension- Alcohol ,barbiturate intoxication MI , internal hemorrhage, Addisonian crisis. • Funduscopy • Hypertensive encephalopathy (exudates, hemorrhage, AV nicking, papilledema). • Increased ICP • Petechiae TTP , meningococcemia, or a bleeding diathesis from which an intracerebral hemorrhage arises.
Respiration • Less localizing value • Cheyne-stokes Bilateral hemispheral damage or metabolic suppression Commonly accompanied by light coma • Kussmaul Usually metabolic acidosis Also in pontomesencephalic lesion . • Agonal gasp Bilateral lower brain stem damage terminal respiratory pattern of severe brain damage.
Pupils Horner’s syndrome • Lesion in sympathetic efferents originating in hypothalamus & descending in the brain stem to the cervical cord produces miosis with ptosis. • Seen in thalamic & hypothalamic lesions from cerebral, thalamic hemorrhage or from herniation. • Bilateral miosis in pontine stroke • Light reaction is preserved in all cases of oculosympathetic paralysis.
Pupil cont… Unreactive pupils • Normally reactive & round pupils of mid size essentially exclude mid brain damage. • Bilaterally dilated, unreactive suggest intraxial involvement of third nerve at mid brain, could be result of stroke, tumor • Unilaterality implies a peripheral third nerve palsy : • uncal herniation at the tentorium • nerve compression by PCA • traction at the superior orbital fissure.
Pupil cont… • Metabolic Vs structural lesion • Normally reactive pupils in a comatose patient strongly support a metabolic process • Structural causes with reactive pupil • Early phase of central transtentorial herniation • Pontine hemorrhage • Metabolic conditions with unreactive pupil • Doriden ( gluthetimide ) • Anoxia • Anticholinergic agents – not respond to 1% pilo carpine. • Hypothermia
Eye movement Eyelids • Remain closed in coma. • Exception – some case of pontine stroke with persistent , tonic eyelid retractiion. • Spontaneous blinking indicates intact pontine reticular formatiion • Blinking to light indicates intact functioning visual afferent pathway but not occipital cortex. • Corneal reflex • both metabolic & structural disease of brain- stem or cortex depress it. • Depth of coma may correlate with the degree of depression.
Eye movement cont… Roving eyes • Slow, random, usually horizontal movements that occur spontaneously in coma. • Can not be duplicated by hysterical patients. • Indicate intact oculomotor pathways, one parameter of brain stem function. • Appear in many metabolic & bilateral hemispheric structural processes causing coma, & their presence excludes brain stem structural lesions.
Eye movement cont… Horizontal gaze deviation • congugate horizontal ocular deviation to one side indicates • damage to the pons on the opposite side or • a lesion in the frontal lobe on the same side. • “the eyes looks toward a hemispheral lesion & away from a brainstem lesion.” • epileptic phenomina produce deviation of eyes to the opposite side of the body. • “ wrong way eyes”- the eyes may turn paradoxically away from the side of a deep hemispheral lesion.
Eye movement cont… oculocephalic testing • Depend on the integrity of the oculomotor nuclei & their interconnecting tracts that extend from the mid brain to the pons & the medulla. • Are normally suppressed in the awake patient by visual fixation. • Their presence indicate reduced cortical influence on the brain stem. oculovestibular testing • Assess virtually the same brain stem reflex as oculocephalic test. • Tonic deviation of both eyes to the side of cool water irrigation & nystagmus in the opposite direction. • Absent cold water calories usually suggest structural posterior fossa lesion or drug intoxication. • pupillary reactivity preserved in drug induced coma.
Eye movement cont… ocular bobbing • A brisk down ward & slow upward movement of the eyes. • Associated with loss of horizontal eye movements. • Diagnostic of bilateral pontine damage usually from thrombosis of basilary artery ocular dipping • A slower , arrhythmic down ward movement followed by a faster upward movement • In patients with normal reflex horizontal gaze. • Indicates diffuse cortical anoxic damage.
Motor signs postures • Primitive non purposeful reflex, which may occur spontaneously In response to sensory stimuli (pain) • Lesions producing flexion tend to be more rostral & those producing extension more caudal. • Acute destructive lesions tend to induce the extensor posture, whereas evolution over time results more in a chronic flexor position. • Distinction of weak flexor posturing from purposeful with drawal can be made by noting the response to a painful stimulus applied to the medial upper arm. • Adduction is a reflex response • Abduction suggests a high level (with drawal) response.
posture cont… • In assymmetric /mismatched posturing, the more abnormal posture points to the opposite side of the brain as the more compromised. • Lack of restless movements on one side or an out turned leg suggests a hemiplegia. • Abnormal postural responses do have some relation to out come , extensor tends to fare worse, probably as a function of the acuity and depth of the lesion
Motor signs cont… • Multifocal myoclonus almost always indicates a metabolic disorder (uremia, anoxia, drug intoxication) • Frontal release phenomena • Constitute forced grasping, perioral primitive reflexes ( e.g suck, snout, root ) paratonic rigidity • Unduly marked in a patient who appears awake but immobile- akinetic mutism a disturbance principally of motivation. • Assymetry of a grasp phenomena suggests a hemiparesis on the side of weaker response.
Psychogenic unresponsiveness • May mimic real coma • In coma, the release of eyelids opened by the examiner produces gradual, incomplete closure, this can not be voluntarily duplicated • In psychogenic cases, the lids may voluntarily resist opening , & close too rapidly or in a fluttering manner • Presence of roving eye movements strongly mitigates against a psychogenic state. • Truly comatose patients can not stop their arm from being dropped on their face. • Demonestration of unambiguous full, uninhibited oculocephalic response or complete paralysis of this response during passive head movement strongly supports a diagnosis of nonpsyohogenic coma. • Presence of caloric-evoked nystagmus defines ‘’ coma ‘’ as psychogenic. • In clinical practice , the pain of the procedure most often terminates the ‘’unconsciousness.’’
Brain death • The criteria endorsed by the American Academy of neurology include : • documentation of both cessation of brain function • and the irreversibility of such cessation. • Cessation • Hemispheric function unreceptivity & unresponsivity. • Brain stem function Absence of pupillary light, corneal, oculocephalic , oculovestibular, oropharyngeal, & respiratory reflexes.
Brain death cont… • Irreversiblity • The absence of reversible causes of coma must be documented, like hypothermia (<32.3 ºc ), sedative drugs, neuromuscular blockade , & shock. • Duration of observation • The cessation of brain function must persist for ‘’an approprate period of observation’’ • 6 hours when confirmatory EEG documentation is available. • 12 hours in the absence of confirmatory test • For ischemic brain damage , 24 hours is suggested, in the absence of EEG confirmation.