Disorders of consciousness

Disorders of Consciousness
Classification and external resources
Specialty
ICD-10	R40
ICD-9-CM	780.0
Patient UK	Disorders of consciousness
MeSH	C10.597.606.358

Disorders of consciousness are organic mental disorders in which there is impairment of the ability to maintain awareness of self and environment and to respond to environmental stimuli. Dysfunction of the cerebral hemispheres or brain stem reticular formation may result in this condition. Consciousness is the state of awareness of self and environment, and responsiveness to external stimulation and inner need. Unconsciousness is a state of unawareness of self and environment or a suspension of those mental activities by which people are made aware of themselves and their environment, coupled always with a diminished responsiveness to environmental stimuli and remain behaviorally unresponsive to all external stimuli. Sleep is a recurrent, reversible physiologic, form of reduced consciousness in which the responsiveness of brain systems responsible for cognitive function is globally reduced, so that the brain does not respond readily to environmental stimuli. A key difference between sleep and coma is that sleep is intrinsically reversible on sufficient stimulation to a normal waking state. In contrast, if patients with pathologic alterations of consciousness can be awakened at all, they rapidly fall back into a sleep-like state when stimulation ceases.

Disorder of consciousness leading to acute confusional state and coma are one of the commonest neurological emergency in clinical practice over last century. There are long list of causes leading to alteration of consciousness. Classical approach to reach the final diagnosis depends on systematic approach.

Physiological Basis of Consciousness and Alteration of Consciousness

Main article: Neural correlates of consciousness

Consciousness has two component

a. Arousal or wakefulness and loss of arousal is the most important cause of alteration of level of consciousness in clinical practice.

b. Content reflecting the quality and coherence of thought and behavior reflecting the sum of cognitive and affective function.

• —Perception -Awareness of self and environment ( Sensory integration)
• —Reaction – Meaningful responsiveness of behavior (Motor response)

Arousal is predominantly a function of the ascending reticular activating system (ARAS), located in in pons and midbrain and the axons ascend in the central tegmental tract. ARAS receives collaterals from somatic and special sensory systems and projects to the reticular nucleus of thalamus and to hypothalamus (which projects to limbic cortex and basal forebrain), in addition, the midline raphe nuclei and locus ceruleus project diffusely to cerebral cortex.

Awareness of content is a direct function of the cerebral hemispheres and the projections to them from thalamus,hypothalamus and brainstem.

Different States of Disorders of Consciousness

Consciousness is the quality or state of being aware especially of something within oneself, or the state or fact of being conscious of an external object, state, or fact, c. awareness; especially :  concern for some social or political cause

Unconscious patient as a result of brain injury rarely lasts more than 2–4 weeks. Based on this observation it is logical to classify disorders of consciousness into two broad categories. A. Acutely Altered States of Consciousness and B. Chronically Altered States of Consciousness.

States of Disorders of Consciousness

Acute Disorders of Consciousness	ICD-10	ICD-10-CM	ICD-11-Beta
Clouding of consciousness: Is a term applied to minimally reduced wakefulness or awareness, which may include hyperexcitability and irritability alternating with drowsiness. Drowsiness is often prominent during the day, but agitation may predominate at night.	-	-	21MB93
Confusion: Lacks precision, but in general it denotes an inability to think with customary speed, clarity, and coherence. Almost all states of confusion are marked by some degree of inattentiveness and disorientation. In this condition the patient does not take into account all elements of his immediate environment. This state also implies a degree of imperceptiveness and distractibility, referred to traditionally as "clouding of the sensorium."
Somnolence: Somnolance or drowsiness denotes an inability to sustain a wakeful state without the application of external stimuli. A disorder characterized by characterized by excessive sleepiness and drowsiness and a sleep disorder characterized by excessive sleepiness and drowsiness.	R40.0	R40.0	21MB90
Delirium: Delirious patients are disoriented, first to time, next to place, and then to persons in their environment. Rarely are patients unaware of who they are, although sometimes married women will revert to their maiden name. Patients are often fearful or irritable and may overreact or misinterpret normal activities of physicians and nurses. Delusions or hallucinations may place the patient completely out of contact with the environment and the examiner. Full-blown delirious states tend to come on rapidly and rarely last more than 4 to 7 days.	-	-	7D90
Obtundation: From the Latin ‘‘to beat against or blunt,’’ literally means mental blunting or torpidity. In amedical setting, such patients have a mild to moderate reduction in alertness, accompanied by a lesser interest in the environment. Such patients have slower psychologic responses to stimulation. They may have an increased number of hours of sleep and may be drowsy between sleep bouts. Stupor: From the Latin ‘‘to be stunned,’’ is a condition of deep sleep or similar behavioral unresponsiveness from which the subject can be aroused only with vigorous and continuous stimulation. Even when maximally aroused, the level of cognitive function may be impaired. Such patients can be differentiated from those with psychiatric impairment, such as catatonia or severe depression, because they can be aroused by vigorous stimulation to respond to simple stimuli.	R40.1	R40.1	21MB91
Coma: Coma is a prolonged period of unconsciousness. Unconsciousness is the lack of appreciation of (or reaction to) a stimulus. Coma differs from sleep in that one cannot be aroused from a coma.	R40.2	R40.2	21MB92

Transient alteration of awareness	-	R40.4	-
Locked-in syndrome: Describes a state in which the patient is de-efferented, resulting in paralysis of all four limbs and the lower cranial nerves.	G83.5	G83.5	AJ02
Subacute or Chronic
Dementia: defines an enduring and often progressive decline in mental processes (content of consciousness) owing to an organic process not usually accompanied by a reduction in arousal.	-	-	-
Hypersomnia: Refers to a state characterized by excessive but normal-appearing sleep from which the subject readily, even if briefly, awakens when stimulated. A sleep disorder characterized by excessive sleepiness during the daytime, that may impair cognitive functioning.	G47.1	G47.1	8A20
Abulia: From the Greek for ‘‘lack of will’’ is an apathetic state in which the patient responds slowly if at all to verbal stimuli and generally does not initiate conversation or activity.	-	-	21MA24.3
Akinetic mutism: Describes a condition of silent, alert-appearing immobility that characterizes certain subacute or chronic states of altered consciousness in which sleep-wake cycles have returned, but externally obtainable evidence for mental activity remains almost entirely absent and spontaneous motor activity is lacking.	R41.8	R41.89
Minimally conscious state: Identifies a condition of severely impaired consciousness in which minimal but definite behavioral evidence of self (this can only be assessed verbally, of course) or environmental awareness is demonstrated. Like the vegetative state, MCS often exists as a transitional state arising during recovery from coma or worsening of progressive neurologic disease. In some patients, however, it may be an essentially permanent condition.	-	-	10AH72
Minimally conscious state plus	-	-	10AH72.1
Minimally conscious state minus	-	-	10AH72.2
The vegetative state (VS): Refers to the neurocognitive status of individuals with severe brain damage, in whom physiologic functions (sleep-wake cycles, autonomic control, and breathing) persist, but awareness (including all cognitive function and emotion) is abolished.[6]Very few surviving patients with severe forebrain damage remain in eyes-closed coma for more than 10 to 30 days. In most patients, vegetative behavior usually replaces coma by that time. The recovery of crude cycling of arousal states heralded by the appearance of ‘‘eyes-open’’ periods in an unresponsive patient.
Persistent vegetative state: Is now commonly reserved for patients remaining in a vegetative state for at least 30 days.	-	R40.3	10AH70
Persistent vegetative state: Prognostic term applied to patients in a persistent vegetative state for whom no recovery is expected.	-	-	10AH71
Brain death: is defined as the irreversible loss of all functions of the entire brain, such that the body is unable to maintain respiratory and cardiovascular homeostasis. R.D. Adams defined the state as one of complete unresponsiveness to all modes of stimulation, arrest of respiration, and absence of all EEG activity for 24 h.	-	G93.82	10MN50

Causes of Disorders of Consciousness

This disturbance can be caused by lesions in the ascending reticular activating system or both hemispheres or by lesions outside this structures but capable of affect their normal function causes alteration of consciousness.

Axis I - Anatomical Localization of Disorder of Consciousness

• Supratentorial lesions
  • Rhinencephalic and subcortical destructive lesions
    • Thalamic infarcts
  • Supratentorial mass lesions
    • Hemorrhage
      • Intracerebral
      • Hypertensive
      • Vascular anomaly
      • Other
        • Epidural
        • Subdural
        • Pituitary apoplexy
    • Infarction
      • Arterial occlusions
      • Thrombotic
      • Embolic
      • Venous occlusions
    • Tumors
      • Primary
      • Metastatic
    • Abscess
      • Intracerebral
      • Subdural
    • Closed head injury
• Subtentorial lesions
  • Compressive lesions
    • Cerebellar hemorrhage
    • Posterior fossa subdural or extradural hemorrhage
    • Cerebellar infarct
    • Cerebellar tumor
    • Cerebellar abscess
    • Basilar aneurysm
  • Destructive or ischemic lesions
    • Pontine hemorrhage
    • Brainstem infarct
    • Basilar migraine
    • Brainstem demyelination
• Diffuse and/or metabolic brain dysfunction
  • Diffuse intrinsic disorders of brain
    • ‘‘Encephalitis’’ or encephalomyelitis
    • Subarachnoid hemorrhage
    • Concussion, nonconvulsive seizures, and postictal states
    • Primary neuronal disorders
  • Extrinsic and metabolic disorders
    • Anoxia or ischemia
    • Hypoglycemia
    • Nutritional
    • Hepatic encephalopathy
    • Uremia and dialysis
    • Pulmonary disease
    • Endocrine disorders (including diabetes)
    • Remote effects of cancer
    • Drug poisons
    • Ionic and acid-base disorders
    • Temperature regulation
    • Mixed or nonspecific metabolic coma
• Psychiatric ‘‘coma’’
  *Conversion reactions *Depression *Catatonic stupor

Summary of anatomical Localization

Supratentorial Lesions	Infratentorial Lesions	Diffuse Encephalopathies	Psychogenic
Epidural or Subdural Hematoma Large Isquemic Infarction Tumor Intraparenchymal hemorrhage Trauma Abscess	Basilar artery thrombosis Pontine or Cerebellar Hematoma Ischemic Cerebellar Infarction Tumor Abscess	Infections— Ischemic hypoxic Metabolic —Organ failure —Endocrine —Toxic	Catatonic States Acute Psychotic Deliria Hysteria-malingering

Axis II Clinical syndrome of Disorders of Consciousness

1. Diseases that cause no focal or lateralizing neurologic signs, usually with normal brainstem functions; CT scan and cellular content of the CSF are normal
   1. Intoxications: alcohol, sedative drugs, opiates, etc.
   2. Metabolic disturbances: anoxia, hyponatremia, hypernatremia, hypercalcemia, diabetic acidosis, nonketotic hyperosmolar hyperglycemia, hypoglycemia, uremia, hepatic coma, hypercarbia, addisonian crisis, hypo- and hyperthyroid states, profound nutritional deficiency
   3. Severe systemic infections: pneumonia, septicemia, typhoid fever, malaria, Waterhouse-Friderichsen syndrome
   4. Shock from any cause
   5. Postseizure states, status epilepticus, subclinical epilepsy
   6. Hypertensive encephalopathy, eclampsia
   7. Severe hyperthermia, hypothermia
   8. Concussion
   9. Acute hydrocephalus
2. Diseases that cause meningeal irritation with or without fever, and with an excess of WBCs or RBCs in the CSF, usually without focal or lateralizing cerebral or brainstem signs; CT or MRI shows no mass lesion
   1. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous malformation, trauma
   2. Acute bacterial meningitis
   3. Viral encephalitis
   4. Miscellaneous: Fat embolism, cholesterol embolism, carcinomatous and lymphomatous meningitis, etc.
3. Diseases that cause focal brainstem or lateralizing cerebral signs, with or without changes in the CSF; CT and MRI are abnormal
   1. Hemispheral hemorrhage (basal ganglionic, thalamic) or infarction (large middle cerebral artery territory) with secondary brainstem compression
   2. Brainstem infarction due to basilar artery thrombosis or embolism
   3. Brain abscess, subdural empyema
   4. Epidural and subdural hemorrhage, brain contusion
   5. Brain tumor with surrounding edema
   6. Cerebellar and pontine hemorrhage and infarction
   7. Widespread traumatic brain injury
   8. Metabolic coma (see above) with preexisting focal damage
   9. Miscellaneous: cortical vein thrombosis, herpes simplex encephalitis, multiple cerebral emboli due to bacterial endocarditis, acute hemorrhagic leukoencephalitis, acute disseminated (postinfectious) encephalomyelitis, thrombotic thrombocytopenic purpura, cerebral vasculitis, gliomatosis cerebri, pituitary apoplexy, intravascular lymphoma, etc.

Axis III - Etiology of Disorder of Consciousness

1. 1. Vascular
      1. Ischemic stroke
         1. bihemispheric,
         2. diencephalic,
         3. upper brainstem
         4. Cerebral venous thrombosis
      2. Hemorrhage
         1. subarachnoid,
         2. intraparenchymal,
         3. subdural,
         4. epidural
         5. Pituitary apoplexy
         6. Hypertensive encephalopathy
      3. Infections
         1. Cerebral abscess
         2. Subdural empyema
         3. Viral encephalitis
         4. Malaria
         5. Typhoid fever
         6. Sepsis
         7. Syphilis
         8. Postinfectious encephalomyelitis
      4. Inflammatory
         1. Acute demyelinating encephalomyelitis
         2. Multiple sclerosis (fulminant)
         3. Multifocal leukoencephalopathy
      5. Neoplastic
         1. Any neoplasm—bihemispheric,
         2. unilateral hemisphere with midline shift and herniation,
         3. diencephalic, upper brainstem, associated with hydrocephalus
         4. Paraneoplastic Limbic encephalitis
      6. Metabolic
         1. Addisonian crisis
         2. Diabetic ketoacidosis
         3. Dialysis encephalopathy
         4. Hepatic encephalopathy
         5. Hyper- or hypocalcemia Hypermagnesemia
         6. Hyper- or hypoglycemia
         7. Hypercapnia
         8. Hyper- or hyponatremia
         9. Hypothyroid
         10. Hyper- or hypothermia
         11. Lactic acidosis and mitochondrial disease
         12. Diffuse hypoxia
         13. Porphyria
         14. Uremia
         15. Wernicke’s encephalopathy
      7. Toxins
         1. Carbon monoxide
         2. Cyanide
         3. Ethylene glycol
         4. Lead
         5. Methanol
      8. Medications, Drugs
         1. Alcohol
         2. Anticholinergics
         3. Barbiturates
         4. Lithium
         5. Opiates
         6. Psychotropics
         7. Benzodiazepines
      9. Others
         1. Status epilepticus
         2. Hydrocephalus
         3. Trauma
         4. Reye’s syndrome
      10. Mimics
          1. Locked-in syndrome
          2. Catatonia
          3. Conversion reaction
          4. Neuromuscular weakness—
          5. Guillain-Barré syndrome,
          6. myasthenia gravis

Approach to Patient of Disorders of Consciousness

Emergency Management

Disorder of consciousness leading to acute confessional state and coma are one of the commonest ( 3-5%) neurological emergency in any clinical practice over last century. Large proportion of comatose patient recover, U\untreated coma may lead to further brain damage, to reach the final diagnosis depends on systematic approach.

Primary Objective:

To stabilize, evaluate, and treat the comatose patient in the emergent setting by:

1. Secure airway
2. Establish Adequacy of Ventilation
3. Establish Adequacy of Circulation
4. Insert Intravenous cannula
5. Draw blood for laboratory studies
6. Treat Immediately Reversible causes of coma
   1. Hypoglycemia - 25g of glucose I.V
   2. Opiate overdose - Naloxe 2 mg I.V
   3. Wernicke's Encephalopathy - Thiamine 100 mg I.V
7. Treat seizures
8. Evaluation as to whether there is significant increased ICP or mass lesions. Treatment of ICP to temporize until surgical intervention is possible.
9. Send for CT scan brain once general patient is stabilized to find the structural cause of alteration of consciousness.

Secondary Objectives

To understand and recognize the cause of coma.

Psychogenic Coma

• Holds eye tight, resist opening
• Fixed stare, quick blink
• Normal pupil
• Normal oculocephalic
• Normal oculovestibular
• Normal posture, breathing, bp,pulse

Supratentorial mass lesions

• Initiating signs usually of focal cerebral dysfunction
• Signs of dysfunction progress rostral to caudal
• Neurologic signs at any given time point to one anatomic area - diencephalon, midbrain, brainstem
• Motor signs are often asymmetrical

Subtentorial mass lesions

• History of preceding brainstem dysfunction or sudden onset of coma
• Localizing brainstem signs precede or accompany onset of coma and always include oculovestibular abnormality
• Cranial nerve palsies usually present
• “Bizarre” respiratory patterns common, usually present at onset of coma

• Confusional state -> coma , fluctuation
• No focal neurological sign
• No neck stiffness
• Normal brainstem reflexes
• Coarse tremor 8-10hz
• Multifocal myoclonus
• Asterixis
• Generalized/periodic myoclonus

History

• Circumstances and temporal profile of the onset of coma
• Details of preceding neurological
• Symptoms headache, weakness seizure
• Any fall
• Use of drug and alcohol
• Previous medical illness liver, kidney
• Previous psychiatric illness
• Yawning
  • —Poor localizing value
  • —Posterior fossa expanding lesion
  • —Medial temporal, third ventricular Hiccup
  • —Medullary lesion in the region of Third ventricle
• Vomiting
  • —Lateral reticular formation of the medulla
  • —Projectile ( usually nausea)
  • —Medulloblastoma ependymoma
  • —Raised Intracranial Pressure -> compression of medulla
  • —Basal meningitis
  • —Intraventricular hemorrhage -> irritating fourth ventricle
  • —Lateral medullary infarct (vestibular)

Physical Examination

Emergent Examination

1. The level of consciousness
2. The pattern of breathing
3. Circulation - blood pressure and pulse
4. The size and reactivity of the pupils
5. The eye movements and oculovestibular responses
6. The skeletal motor responses.

The level of consciousness

Glasgow coma scale (GCS) is the best way to objectively document level of consciousness in emergency and ICU.

The Pattern of Breathing

Forebrain

1. —Post hyperventilation apnea
2. —Cheyne stoke respiration¢Forebrain
3. —Post hyperventilation apnea
4. —Cheyne stoke respiration

Hypothalamus midbrain

1. —Central neurogenic hyperventilation

Basis pontis

1. —Pseudobulbar paralysis of voluntary center

Lower pontine tegmentum

1. —Apneustic breathing
2. —Cluster breathing
3. —Short cycle periodic breathing
4. —Ataxic breathing

Medulla

1. —Ataxic breathing
2. —Slow regular respiration
3. —Gasping

Respiration altered in

• —Acid-base derangements
• —Hypoxia
• —Cardiac influences

Circulation

Kocher-Cushing response - rise in BP->bradycardia due to rise in ICP -> compression of floor of the iv ventricle fall in BP and tachycardia usually terminal event due to medullary failure.

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)

Pupil

1. 1. Bilateral dilated pupils - Are greater than 7 mm in diameter and do not react to light stimulation. Are seen in:
      1. Transtentorial herniation of both medial temporal lobes
      2. Anticholinergic or Sympathomimetic drug intoxication
   2. Bilateral pinpoint pupils - Have 1-1,5 mm in diameter and are seen in:
      1. Morphine poisoning
      2. Pontine hemorrhage
      3. neurosyphilis
      4. Organophosphates poisoning
      5. Miotic eyes drops
   3. 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.
   4. Fixed midsized pupils - Are about 5 mm in diameter, do not react to light and are the result of midbrain lesion.

Pupil Summary

• Metabolic: Small reacting
• Diencephalic: Small reacting
• Tectal (Midbrain) : Large fixed hippus
• 3rd Nerve Uncle herniation: Large fixed
• Midbrain; Midsize not reacting
• Pons: Small pinpoint
• Opiate Pinpoint
• Organophosphorus Small
• Atropine Wide dilated

The eye movements

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:
  1. Impaired unilateral adduction - Indicates lesions of the oculomotor nerve or midbrain lesions involving the oculomotor nucleus.
  2. Downward deviation of one or both eyes - is suggestive of sedative drug intoxication.
  3. 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).
  4. —Moving: Roving, dipping, bobbing are signs of pontine lesion with Ipsilateral 6th, —Ipsilateral gaze palsy, —One and half syndrome, —Bilateral gaze palsy, —Ocular bobbing, —MLF (median longitudinal fasciculus) syndrome

Eye movement Summary

• Symmetric responses seen with metabolic or structural causes
• Asymmetric responses seen with structural causes
• The hemispheres (smart) are responsible for:
  • —Inhibiting Doll’s eyes
  • —Fast component of nystagmus
• The brain stem (dumb) is responsible for:
  • —Allowing Doll’s eyes
  • Slow component of nystagmus

Motor Response

• Assess tone, presence of asterixis
• Response to painful stimuli
  • —none
  • —abnormal flexor
  • —abnormal extensor
  • —normal localization/withdrawal
• Symmetric responses seen with metabolic or structural causes
• Asymmetric responses seen with structural causes

Posture

1. Cerebral hemisphere: —Decorticate posture
2. Diencephalon supratentorial:—Diagonal posture
3. Upper brain stem: —Decerebrate posture
4. Pontine: —Abnormal ext arm, —Weak flexion leg
5. Medullary: —Flaccidity

Detail Examination

General physical examination

• Evidence of external injury
• Colour of skin and mucosa
• Odour of breath
• 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.
• 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.
• Signs of trauma:
  1. Battle's sign ( swelling and discoloration overlying the mastoid bone behind the ear)
  2. Raccoon eyes (Periorbital ecchymosis)
  3. Cerebrospinal fluid rhinorrhea or otorrhea
  4. Skull fractures

Systemic examination

Neurologic Examination

Systematic assessment of brainstem function via reflexes

Cranial Nerve Exam

• —Pupillary light response (CN 2-3)
• —Occulocephalic/calorics (CN 3,4,6,8)
• —Corneal reflex (CN 5,7)
• —Gag refelx (CN 9,10)
• Funduscopy
  • 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.

Heart lung

Abdomen

Investigation

• Complete blood count, MP, B.sugar
• Blood urea, s. creatinine, s.electrolyte
• Blood gases, ALT, AST
• CSF examination
• CT scan/ MRI
• X-ray chest, ECG

ECG changes in coma (SAH, ICH, INFARCT)

• —Tall T, prolonged QT
• —Q wave with st depression
• —SVT, AF, AFL
• —Sinus bradycardia,arrest, nodal rhythm
• —A-V block or dissociation
• PVc's, VFL, VF

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.

Subsequent management

• Eye, mouth, skin
• Fluid electrolyte, feeding
• Respiration, circulation
• Urine, bowel
• Stimulation
• Infection control

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.

Methodological problems

Metabolic studies are useful, but they are not able identify neural activity within a specific region to specific cognitive processes. Functionality can only be identified at the most general level: Metabolism in cortical and subcortial regionas that may contribute to cognitive processes.

At present, there is no established relation between cerebral metabolic rates of glucose or oxygen as meaured by PET and patient outcome. The decrease of cerebral metabolism occurs also when patients are treated with anaesthetics to the point of unresponsiveness. Lowest value (28% of normal range) have been reported during propofol anaesthesia. Also deep sleep represents a phase of decreased metabolism (down to 40% of the normal range) In general, quantitative PET studies and the assessment of cerebral metabolic rates depends on many assumptions. PET for example requires a correction factor, the lumped constant , which is stable in healthy brains. There are reports, that a global decrease of this constant emerges after a traumatic brain injury. But not only the correction factors change due to TBI. Another issue is the possibility of anaerobic glycosis that could occur after TBI. In such a case the glucose levels measured by the PET are not tightly connected to the oxygen consumption of the patient's brain. Third point regarding PET scans is the overall measurement per unit volume of brain tissue. The imaging can be affected by the inclusion of metabolically inactive spaces e.g. cerebrospinal fluidin the case of gross hydrocephalus, which artificially lowers the calculated metabolism. Also the issue of radiation exposure must be considered in patients with already severely damaged brains and preclude longitudinal or follow-up studies.

Ethical issues

Disorders of consciousness present a variety of ethical concerns. Most obvious is the lack of consent in any treatment decisions. Patients in PVS or MCS are not able to decide for the possibility of withdrawal of life-support. It is also a general question whether they should receive life-sustaining therapy and, if so, for how long? The problems regarding a patient's consent also account for neuroimaging studies. Without patient's consent, such studies are perceived as unethical. Additionally only few patients have created advance directives before losing decision-making capacity. Typically approval must be obtained from family or legal representatives depending on governmental and hospital guidelines. But even with the consent of representatives, researchers have been refused grants, ethics committee approval and publication.
Social issues arise from the enormous costs that are caused by people with disorders of consciousness. Especially chronic comatose and vegetative patients, when recovery is highly unlikely and treatment in the ICU is considered futile by clinicians. In addition to the aforementioned problems, the question rises why medical resources were being used not for the broader public good but for patients who seemed to have only little to gain from them. Still research is everything but sure about irreverebility of these conditions. Some studies demonstrated that some patients suffering from disorders of consciousness may be aware despite clinical unresponsivesness. These recent findings could have a major impact on ethical and social issues.

See also

• Neural Correlates of Consciousness
• Coma
• Neuropsychology
• Neuropsychological assessment