1

coma

2

Coma • Deep sleeplike state • Can not be aroused.Stupor • Lesser degrees of unarousability.• Require vigorous stimuliDrowsiness• 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)

3

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

4

• 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

5

structural

supratentorial infratentorialLateral

shift

Central uncal

6

Central

Diencephalic level

•Drowsy

•Miotic pupil but reactive

•Intact reflex eye movement

•Babinski signs, grasp reflexes & decorticate posturing contra-laterally to the mass.

Midbrain & upper pons

•Lapses into coma

•Pupils dilate to mid position & unreactive to light•Reflex eye movement difficult to elicit & may take the form of an Inter-nuclear ophthalmoplegia

•Decerebrate posturing

Lower pons & medulla

•Ataxic breathing, irregular pulse & blood pressure •Pupil-remain mid position & unreactive

•Absent reflex eye movement

•Flaccid tone, No response to deep pain.

7

uncal

Early

•Approach normal wakefulness

•Ipsitateral pupil dilatation, reacts sluggishly

•Normal eye movement

•Evolution to coma is rapid & focal motor signs develop ipsilateral to the mass with bilateral decerebrate posturing

Mid brain

• Pupils mid dilated & unreactive to light

• Subsequent rostro caudal deterioration merges with that of central syndrome.

8

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.

9

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.

10

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

11

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.

12

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

13

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

14

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.

15

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.

16

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.

17

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.

18

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

19

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.

20

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.

21

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.

22

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.

23

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.

24

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.

25

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

26

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.

27

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.’’

28

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.

29

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.