Disorders of consciousness

Disorders of Consciousness
Classification and external resources
Specialty Psychiatry
ICD-10 R40
ICD-9-CM 780.0
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.[1][2] Consciousness is the state of awareness of self and environment, and responsiveness to external stimulation and inner need.[3] 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[3] and remain behaviorally unresponsive to all external stimuli.[4] 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.[4] 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.[4]

Disorder of consciousness leading to acute confusional state and coma are one of the commonest neurological emergency in clinical practice over last century.[3][4] There are long list of causes leading to alteration of consciousness. Classical approach to reach the final diagnosis depends on systematic approach.[4]

Physiological Basis of Consciousness and Alteration 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.[3]

b. Content reflecting the quality and coherence of thought and behavior reflecting the sum of cognitive and affective function.[3]

Arousal is predominantly a function of the ascending reticular activating system (ARAS), located 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.[6]

Awareness of content is a direct function of the cerebral hemispheres and the projections to them from thalamus,hypothalamus and brainstem.[6]

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[7]

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.[4]

States of Disorders of Consciousness[4]

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 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.[5] 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.[8] - - 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.[7] - - 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.[9] 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.[3] - 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.[4]

Axis I - Anatomical Localization of Disorder of Consciousness[4]

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
  1. Catatonic States
  2. Acute Psychotic Deliria
  3. Hysteria-malingering

Axis II Clinical syndrome of Disorders of Consciousness[10]

  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[6]

    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

Disorders of consciousness leading to acute confessional states and comas are one of the most common ( 3-5%) neurological emergencies in any clinical practice over last century. A large proportion of comatose patients recover, but untreated coma may lead to further brain damage, anf to reach the final diagnosis depends on systematic approach.[3][4]

Primary Objective:[6]

To stabilize, evaluate, and treat the comatose patient in the emergent setting by:[10]

  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.[4]

Psychogenic Coma[4]
Supratentorial mass lesions[4]
Subtentorial mass lesions[4]
[4]

History[4]

Physical Examination[4]

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[4]

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

Circulation[4]

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[4]
    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

The eye movements[4]

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.

Eye movement Summary[4]

Motor Response[4]

Posture[4]

  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[4]
Systemic examination
Neurologic Examination[4]

Systematic assessment of brainstem function via reflexes

Cranial Nerve Exam

Heart lung

Abdomen

Investigation[4]

ECG changes in coma (SAH, ICH, INFARCT)

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

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)[11][12] 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.[13] But not only the correction factors change due to TBI. Another issue is the possibility of anaerobic glycolysis 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.[14] 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.[15] 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.[16] 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.[17]

See also

References

  1. ↑ "No items found - MeSH - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2016-02-25.
  2. ↑ Bernat JL (8 Apr 2006). "Chronic disorders of consciousness". Lancet. 367 (9517): 1181–1192. doi:10.1016/S0140-6736(06)68508-5. PMID 16616561.
  3. 1 2 3 4 5 6 7 Ropper, Allan H. (2014). Adams and Victor's PRINCIPLES OF NEUROLOGY. McGraw-Hill education. ISBN 978-0-07-180091-4.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 Posner, Jerome B. (2007). PLUM AND POSNER’S DIAGNOSIS OF STUPOR AND COMA. Oxford University Press, Inc. ISBN 978-0-19-532131-9.
  5. 1 2 Vinken, P; Bruyn, G (1969). "Coma and other disorders of consciousness". Handbook of Clinical Neurology. 3. Amsterdam: North-Holland Publishing Company. ISBN 9780444812889.
  6. 1 2 3 4 Mowzoon, Nima (2007). Neurology Board Review, An Illustrated Study Guide. Canada: Mayo Clinic Section of Scientific Publications. pp. 401,.
  7. 1 2 "Definition of CONSCIOUSNESS". www.merriam-webster.com. Retrieved 2016-02-24.
  8. ↑ Giacino, Joseph T.; Ashwal, S.; Childs, N.; Cranford, R.; Jennett, B.; Katz, D. I.; Kelly, J. P.; Rosenberg, J. H.; Whyte, J. (2002-02-12). "The minimally conscious state: definition and diagnostic criteria". Neurology. 58 (3): 349–353. doi:10.1212/wnl.58.3.349. ISSN 0028-3878. PMID 11839831.
  9. ↑ "2016 ICD-10-CM Diagnosis Code R40.0 : Somnolence". www.icd10data.com. Retrieved 2016-02-24.
  10. 1 2 Hauser, Stephen L. (2010). HARRISON’S Neurology in Clinical Medicine. California, San Francisco USA: McGraw-Hill Companies. pp. 2,. ISBN 978-0-07-174123-1.
  11. ↑ Maquet P, Degueldre C, Delfiore G; et al. (1997). "Functional neuroanatomy of human slow wave sleep". J Neurosci. 17: 2807–12.
  12. ↑ Buchsbaum MS, Gillin JC, Wu J; et al. (1989). "Regional cerebral glucose metabolic rate in human sleep assessed by positron emission totgraphy". Life Sci. 45: 1349–56. doi:10.1016/0024-3205(89)90021-0.
  13. ↑ Wu HM, Huang SC, Hattori N; et al. (2004). "Selective metabolic reduction in gray matter acutely following human traumatic brain injury". J Neurotrauma. 21: 149–61. doi:10.1089/089771504322778613.
  14. ↑ Hovda DA, Becker DP, Katayama Y. Secondary injury and acidosis. J Neurotrauma 1992; 9 (suppl 1): S47-60
  15. ↑ Meltzer CC, Zubieta JK, Links JM; et al. (1996). "MR-based correction of brain PET measurements for heterogeneous gray matter radioactivity distribution". J Cereb Blood Flow Metlab. 16: 650–58.
  16. ↑ Fins JJ (2003). "Constructing an ethical stereotaxy for severe brain injury: balancing risks, benefits and access". Nat Rev Neurosci. 4: 323–27. doi:10.1038/nrn1079.
  17. ↑ Jox RJ, Bernat JL, Laureys S, Racine E. Disorders of consciousness: responding to request for novel diagnostic and therapeutic interventions. Lancet Neurol. 2012; 11(8): 732-38
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