Coma

Coma is a state of unconsciousness in which a person cannot be awakened; fails to respond normally to painful stimuli, light, or sound; lacks a normal wake-sleep cycle; and does not initiate voluntary actions.[1] A person in a state of coma is described as being comatose. A comatose state may derive from natural causes, or may be medically induced.

A comatose person exhibits a complete absence of wakefulness and is unable to consciously feel, speak, hear, or move.[2] Clinically, a coma can be defined as the inability to consistently follow a one-step command.  It can also be defined as a score of ≤ 8 on the Glasgow Coma Scale (GCS) lasting ≥ 6 hours. For a patient to maintain consciousness, two important neurological components must function. The first is the cerebral cortex—the gray matter that forms the outer layer of the brain. The other is a structure located in the brainstem, called reticular activating system (RAS).[3][4]

Injury to either or both of these components is sufficient to cause a patient to experience a coma. The cerebral cortex is a group of tight, dense, "gray matter" composed of the nuclei of the neurons whose axons then form the "white matter," and is responsible for perception, relay of the sensory input via the thalamic pathway, and many other neurological functions, including complex thinking.

RAS, on the other hand, is a more primitive structure in the brainstem which includes the reticular formation (RF). The RAS area of the brain has two tracts, the ascending and descending tract. Made up of a system of acetylcholine-producing neurons, the ascending track, or ascending reticular activating system (ARAS), works to arouse and wake up the brain, from the RF, through the thalamus, and then finally to the cerebral cortex.[5] A failure in ARAS functioning may thus lead to a coma.

Coma
SpecialtyNeurology, psychiatry

Etymology

The word is from the Greek κῶμα koma, meaning "deep sleep".[6]

Signs and symptoms

Aaron in Coma1
Image of a man in a coma.[7]
Comaventilator
Image of the man still unresponsive to stimuli.[8]

Generally, a person who is unable to voluntarily open the eyes, does not have a sleep-wake cycle, is unresponsive in spite of strong tactile (painful) or verbal stimuli, and who generally scores between 3 and 8[9] on the Glasgow Coma Scale is considered in a coma.[1] Coma may have developed in humans as a response to injury to allow the body to pause bodily actions and heal the most immediate injuries before waking. It therefore could be a compensatory state in which the body's expenditure of energy is not superfluous. The severity and mode of onset of coma depends on the underlying cause. For instance, severe hypoglycemia (low blood sugar) or hypercapnia (increased carbon dioxide levels in the blood) initially cause mild agitation and confusion, but progress to obtundation, stupor, and finally, complete unconsciousness. In contrast, coma resulting from a severe traumatic brain injury or subarachnoid hemorrhage can be instantaneous. The mode of onset may therefore be indicative of the underlying cause.

Causes of coma

Coma may result from a variety of conditions, including intoxication (such as drug abuse, overdose or misuse of over the counter medications, prescribed medication, or controlled substances), metabolic abnormalities, central nervous system diseases, acute neurologic injuries such as strokes or herniations, hypoxia, hypothermia, hypoglycemia, eclampsia or traumatic injuries such as head trauma caused by falls, drowning accidents, or vehicle collisions. It may also be deliberately induced by pharmaceutical agents during major neurosurgery, to preserve higher brain functions following brain trauma, or to save the patient from extreme pain during healing of injuries or diseases.[10]

Forty percent of comatose states result from drug poisoning.[11] Drugs damage or weaken the synaptic functioning in the ARAS and keep the system from properly functioning to arouse the brain.[5] Secondary effects of drugs, which include abnormal heart rate and blood pressure, as well as abnormal breathing and sweating, may also indirectly harm the functioning of the ARAS and lead to a coma. Seizures and hallucinations have shown to also play a major role in ARAS malfunction. Given that drug poisoning is the cause for a large portion of patients in a coma, hospitals first test all comatose patients by observing pupil size and eye movement, through the vestibular-ocular reflex.[5]

The second most common cause of coma, which makes up about 25% of comatose patients, is lack of oxygen, generally resulting from cardiac arrest.[11] The Central Nervous System (CNS) requires a great deal of oxygen for its neurons. Oxygen deprivation in the brain, also known as hypoxia, causes neuronal extracellular sodium and calcium to decrease and intracellular calcium to increase, which harms neuron communication.[12] Lack of oxygen in the brain also causes ATP exhaustion and cellular breakdown from cytoskeleton damage and nitric oxide production.

Twenty percent of comatose states result from the side effects of a stroke.[11] During a stroke, blood flow to part of the brain is restricted or blocked. An ischemic stroke, brain hemorrhage, or tumor may cause such cessation of blood flow. Lack of blood to cells in the brain prevents oxygen from getting to the neurons, and consequently causes cells to become disrupted and eventually die. As brain cells die, brain tissue continues to deteriorate, which may affect functioning of the ARAS.

The remaining 15% of comatose cases result from trauma, excessive blood loss, malnutrition, hypothermia, hyperthermia, abnormal glucose levels, and many other biological disorders.

Diagnosis

Diagnosis of coma is simple, but diagnosing the cause of the underlying disease process is often challenging. The first priority in treatment of a comatose patient is stabilization following the basic ABCs (standing for airway, breathing, and circulation). Once a person in a coma is stable, investigations are performed to assess the underlying cause. Investigative methods are divided into physical examination findings and imaging (such as CAT scan, MRI, etc.) and special studies (EEG, etc.)

Diagnostic steps

When an unconscious patient enters a hospital, the hospital utilizes a series of diagnostic steps to identify the cause of unconsciousness. According to Young,[5] the following steps should be taken when dealing with a patient possibly in a coma:

  1. Perform a general examination and medical history check
  2. Make sure the patient is in an actual comatose state and or is not in locked-in state (patient is either able to voluntarily move their eyes or blink) or psychogenic unresponsiveness (caloric stimulation of the vestibular apparatus results in slow deviation of eyes towards the stimulation followed by rapid correction to mid-line. This response cannot be voluntarily suppressed, so if the patient does not have this response, psychogenic coma can be ruled out.)
  3. Find the site of the brain that may be causing coma (i.e., brain stem, back of brain…) and assess the severity of the coma with the Glasgow coma scale
  4. Take blood work to see if drugs were involved or if it was a result of hypoventilation/hyperventilation
  5. Check for levels of “serum glucose, calcium, sodium, potassium, magnesium, phosphate, urea, and creatinine”
  6. Perform brain scans to observe any abnormal brain functioning using either CT or MRI scans
  7. Continue to monitor brain waves and identify seizures of patient using EEGs

Initial assessment and evaluation

In the initial assessment of coma, it is common to gauge the level of consciousness by spontaneously exhibited actions, response to vocal stimuli ("Can you hear me?"), and painful stimuli; this is known as the AVPU (alert, vocal stimuli, painful stimuli, unresponsive) scale. More elaborate scales, such as the Glasgow Coma Scale, quantify an individual's reactions such as eye opening, movement and verbal response on a scale; Glasgow Coma Scale (GCS) is an indication of the extent of brain injury varying from 3 (indicating severe brain injury and death) to a maximum of 15 (indicating mild or no brain injury).

In those with deep unconsciousness, there is a risk of asphyxiation as the control over the muscles in the face and throat is diminished. As a result, those presenting to a hospital with coma are typically assessed for this risk ("airway management"). If the risk of asphyxiation is deemed high, doctors may use various devices (such as an oropharyngeal airway, nasopharyngeal airway or endotracheal tube) to safeguard the airway.

Physical examination findings

Decorticate
Decorticate posturing, indicating a lesion at the red nucleus or above. This positioning is stereotypical for upper brain stem, or cortical damage. The other variant is decerebrate posturing, not seen in this picture.

Physical examination is critical after stabilization. It should include vital signs, a general portion dedicated to making observations about the patient's respiration (breathing pattern), body movements (if any), and of the patient's body habitus (physique); it should also include assessment of the brainstem and cortical function through special reflex tests such as the oculocephalic reflex test (doll's eyes test), oculovestibular reflex test (cold caloric test), nasal tickle, corneal reflex, and the gag reflex.

Vital signs in medicine are temperature (rectal is most accurate), blood pressure, heart rate (pulse), respiratory rate, and oxygen saturation. It should be easy to evaluate these vitals quickly to gain insight into a patient's metabolism, fluid status, heart function, vascular integrity, and tissue oxygenation.

Respiratory pattern (breathing rhythm) is significant and should be noted in a comatose patient. Certain stereotypical patterns of breathing have been identified including Cheyne–Stokes, a form of breathing in which the patient's breathing pattern is described as alternating episodes of hyperventilation and apnea. This is a dangerous pattern and is often seen in pending herniations, extensive cortical lesions, or brainstem damage.[3] Another pattern of breathing is apneustic breathing, which is characterized by sudden pauses of Inhalation and is due to a lesion of the pons.[1][3] Ataxic breathing is irregular and is due to a lesion (damage) of the medulla.

Assessment of posture and body habitus is the next step. It involves general observation about the patient's positioning. There are often two stereotypical postures seen in comatose patients. Decorticate posturing is a stereotypical posturing in which the patient has arms flexed at the elbow, and arms adducted toward the body, with both legs extended. Decerebrate posturing is a stereotypical posturing in which the legs are similarly extended (stretched), but the arms are also stretched (extended at the elbow). The posturing is critical since it indicates where the damage is in the central nervous system. A decorticate posturing indicates a lesion (a point of damage) at or above the red nucleus, whereas a decerebrate posturing indicates a lesion at or below the red nucleus. In other words, a decorticate lesion is closer to the cortex, as opposed to a decerebrate cortex that is closer to the brainstem.

Oculocephalic reflex also known as the doll's eye is performed to assess the integrity of the brainstem. Patient's eyelids are gently elevated and the cornea is visualized. The patient's head is then moved to the patient's left, to observe if the eyes stay or deviate toward the patient's right; same maneuver is attempted on the opposite side. If the patient's eyes move in a direction opposite to the direction of the rotation of the head, then the patient is said to have an intact brainstem. However, failure of both eyes to move to one side, can indicate damage or destruction of the affected side. In special cases, where only one eye deviates and the other does not, this often indicates a lesion (or damage) of the medial longitudinal fasciculus (MLF), which is a brainstem nerve tract. Caloric reflex test also evaluates both cortical and brainstem function; cold water is injected into one ear and the patient is observed for eye movement; if the patient's eyes slowly deviate toward the ear where the water was injected, then the brainstem is intact, however failure to deviate toward the injected ear indicates damage of the brainstem on that side. Cortex is responsible for a rapid nystagmus away from this deviated position and is often seen in patients who are conscious or merely lethargic.

An important part of the physical exam is also assessment of the cranial nerves. Due to the unconscious status of the patient, only a limited number of the nerves can be assessed. These include the cranial nerves number 2 (CN II), number 3 (CN III), number 5 (CN V), number 7 (CN VII), and cranial nerves 9 and 10 (CN IX, CN X). Gag reflex helps assess cranial nerves 9 and 10. Pupil reaction to light is important because it shows an intact retina, and cranial nerve number 2 (CN II); if pupils are reactive to light, then that also indicates that the cranial nerve number 3 (CN III) (or at least its parasympathetic fibers) are intact. Corneal reflex assess the integrity of cranial nerve number 7 (CN VII), and cranial nerve number 5 (CN V). Cranial nerve number 5 (CN V), and its ophthalmic branch (V1) are responsible for the afferent arm of the reflex, and the cranial nerve number 7 (CN VII) also known a facial nerve, is responsible for the efferent arm, causing contraction of the muscle orbicularis oculi resulting in closing of the eyes.

Pupil assessment is often a critical portion of a comatose examination, as it can give information as to the cause of the coma; the following table is a technical, medical guideline for common pupil findings and their possible interpretations:[3]

Pupil sizes (left eye vs. right eye) Possible interpretation
Darkblue Normal eye with two pupils equal in size and reactive to light. This means that the patient is probably not in a coma and is probably lethargic, under influence of a drug, or sleeping.
Myosis due to opiate use "Pinpoint" pupils indicate heroin or opiate overdose, and can be responsible for a patient's coma. The pinpoint pupils are still reactive to light, bilaterally (in both eyes, not just one). Another possibility is the damage of the pons.[3]
Anizokoria One pupil is dilated and unreactive, while the other is normal (in this case, the right eye is dilated, while the left eye is normal in size). This could mean a damage to the oculomotor nerve (cranial nerve number 3, CN III) on the right side, or possibility of vascular involvement.
Cyclopentolate 1 percent Pupils Both pupils are dilated and unreactive to light. This could be due to overdose of certain medications, hypothermia or severe anoxia (lack of oxygen).

Imaging and special tests findings

Imaging basically encompasses computed tomography (CAT or CT) scan of the brain, or MRI for example, and is performed to identify specific causes of the coma, such as hemorrhage in the brain or herniation of the brain structures. Special tests such as an EEG can also show a lot about the activity level of the cortex such as semantic processing,[13] presence of seizures, and are important available tools not only for the assessment of the cortical activity but also for predicting the likelihood of the patient's awakening.[14] The autonomous responses such as the skin conductance response may also provide further insight on the patient's emotional processing.[15]

History

When diagnosing any neurological condition, history and examination are fundamental. History is obtained by family, friends or EMS. The Glasgow Coma Scale is a helpful system used to examine and determine the depth of coma, track patients progress and predict outcome as best as possible. In general a correct diagnosis can be achieved by combining findings from physical exam, imaging, and history components and directs the appropriate therapy.

Severity and classification

A coma can be classified as (1) supratentorial (above Tentorium cerebelli), (2) infratentorial (below Tentorium cerebelli), (3) metabolic or (4) diffused.[3] This classification is merely dependent on the position of the original damage that caused the coma, and does not correlate with severity or the prognosis. The severity of coma impairment however is categorized into several levels. Patients may or may not progress through these levels. In the first level, the brain responsiveness lessens, normal reflexes are lost, the patient no longer responds to pain and cannot hear.

The Rancho Los Amigos Scale is a complex scale that has eight separate levels, and is often used in the first few weeks or months of coma while the patient is under closer observation, and when shifts between levels are more frequent.

Treatment

Medical treatment

The treatment hospitals use on comatose patients depends on both the severity and cause of the comatose state. Although the best treatment for comatose patients remains unknown, hospitals usually place comatose patients in an Intensive Care Unit (ICU) immediately.[5] Attention must first be directed to maintaining the patient's respiration and circulation, using intubation and ventilation, administration of intravenous fluids or blood and other supportive care as needed. Once a patient is stable and no longer in immediate danger, the medical staff may concentrate on maintaining the health of patient’s physical state. The concentration is directed to preventing infections such as pneumonias, bedsores (decubitus ulcers), and providing balanced nutrition.[16] Infections may appear from the patient not being able to move around, and being confined to the bed. The nursing staff moves the patient every 2–3 hours from side to side and depending on the state of consciousness sometimes to a chair. The goal is to move the patient as much as possible to try to avoid bedsores, atelectasis and pneumonia. Pneumonia can occur from the person’s inability to swallow leading to aspiration, lack of gag reflex or from feeding tube, (aspiration pneumonia). Physical therapy may also be used to prevent contractures and orthopedic deformities that would limit recovery for those patients who awaken from coma.

A person in a coma may become restless, or seize and need special care to prevent them from hurting themselves. Medicine may be given to calm such individuals. Patients who are restless may also try to pull on tubes or dressings so soft cloth wrist restraints may be put on. Side rails on the bed should be kept up to prevent the patient from falling.[16]

Methods to wake comatose patients include reversing the cause of the coma (e.g., glucose shock if low sugar), giving medication to stop brain swelling, or inducing hypothermia. Inducing hypothermia on comatose patients provides one of the main treatments for patients after suffering from cardiac arrest. In this treatment, medical personnel expose patients to “external or intravascular cooling” at 32-34 °C for 24 hours; this treatment cools patients down about 2-3 °C less than normal body temperature.[17] In 2002, Baldursdottir and her coworkers[17] found that in the hospital, more comatose patients survived after induced hypothermia than patients that remained at normal body temperature. For this reason, the hospital chose to continue the induced hypothermia technique for all of its comatose patients that suffered from cardiac arrest.[17]

Emotional challenges

Coma has a wide variety of emotional reactions from the family members of the affected patients, as well as the primary care givers taking care of the patients. Common reactions, such as desperation, anger, frustration, and denial are possible. The focus of the patient care should be on creating an amicable relationship with the family members or dependents of a comatose patient as well as creating a rapport with the medical staff.[18]

Prognosis

Comas can last from several days to several weeks. In more severe cases a coma may last for over five weeks, while some have lasted as long as several years. After this time, some patients gradually come out of the coma, some progress to a vegetative state, and others die. Some patients who have entered a vegetative state go on to regain a degree of awareness. Others remain in a vegetative state for years or even decades (the longest recorded period being 42 years).[19][20]

The outcome for coma and vegetative state depends on the cause, location, severity and extent of neurological damage. A deeper coma alone does not necessarily mean a slimmer chance of recovery, because some people in deep coma recover well while others in a so-called milder coma sometimes fail to improve.

People may emerge from a coma with a combination of physical, intellectual, and psychological difficulties that need special attention. Recovery usually occurs gradually—patients acquire more and more ability to respond. Some patients never progress beyond very basic responses, but many recover full awareness.[21] Regaining consciousness is not instant: in the first days, patients are only awake for a few minutes, and duration of time awake gradually increases. This is unlike the situation in many movies where people who awake from comas are instantly able to continue their normal lives. In reality, the coma patient awakes sometimes in a profound state of confusion, not knowing how they got there and sometimes suffering from dysarthria, the inability to articulate any speech, and with many other disabilities.

Predicted chances of recovery are variable owing to different techniques used to measure the extent of neurological damage. All the predictions are based on statistical rates with some level of chance for recovery present: a person with a low chance of recovery may still awaken. Time is the best general predictor of a chance of recovery: after four months of coma caused by brain damage, the chance of partial recovery is less than 15%, and the chance of full recovery is very low.[22]

The most common cause of death for a person in a vegetative state is secondary infection such as pneumonia, which can occur in patients who lie still for extended periods.

There are reports of patients coming out of coma after long periods of time. After 19 years in a minimally conscious state, Terry Wallis spontaneously began speaking and regained awareness of his surroundings.[23]

A brain-damaged man, trapped in a coma-like state for six years, was brought back to consciousness in 2003 by doctors who planted electrodes deep inside his brain. The method, called deep brain stimulation (DBS) successfully roused communication, complex movement and eating ability in the 38-year-old American man who suffered a traumatic brain injury. His injuries left him in a minimally conscious state (MCS), a condition akin to a coma but characterized by occasional, but brief, evidence of environmental and self-awareness that coma patients lack.[24]

Comas lasting seconds to minutes result in post-traumatic amnesia (PTA) that lasts hours to days; recovery plateau occurs over days to weeks. Comas that last hours to days result in PTA lasting days to weeks; recovery plateau occurs over months. Comas lasting weeks result in PTA that lasts months; recovery plateau occurs over months to years.[25]

Society and culture

Research by Dr. Eelco Wijdicks on the depiction of comas in movies was published in Neurology in May 2006. Dr. Wijdicks studied 30 films (made between 1970 and 2004) that portrayed actors in prolonged comas, and he concluded that only two films accurately depicted the state of a coma victim and the agony of waiting for a patient to awaken: Reversal of Fortune (1990) and The Dreamlife of Angels (1998). The remaining 28 were criticized for portraying miraculous awakenings with no lasting side effects, unrealistic depictions of treatments and equipment required, and comatose patients remaining muscular and tanned.[26]

See also

  • Brain death, lack of activity in both cortex, and lack of brainstem function
  • Coma scale, a system to assess the severity of coma
  • Locked-in syndrome, paralysis of most muscles, except ocular muscles of the eyes, while patient is conscious
  • Persistent vegetative state (vegetative coma), deep coma without detectable awareness. Damage to the cortex, with an intact brainstem.
  • Process Oriented Coma Work, for an approach to working with residual consciousness in comatose patients.
  • Suspended animation, the inducement of a temporary cessation or decay of main body functions.

References

  1. ^ a b c Weyhenmyeye, James A.; Eve A. Gallman (2007). Rapid Review Neuroscience 1st Ed. Mosby Elsevier. pp. 177–9. ISBN 0-323-02261-8.
  2. ^ Bordini, A.L.; Luiz, T.F.; Fernandes, M.; Arruda, W. O.; Teive, H. A. (2010). "Coma scales: a historical review". Arquivos de neuro-psiquiatria. 68 (6): 930–937. doi:10.1590/S0004-282X2010000600019. PMID 21243255.
  3. ^ a b c d e f Hannaman, Robert A. (2005). MedStudy Internal Medicine Review Core Curriculum: Neurology 11th Ed. MedStudy. pp. (11–1) to (11–2). ISBN 1-932703-01-2.
  4. ^ "Persistent vegetative state: A medical minefield". New Scientist: 40–3. July 7, 2007. See diagram.
  5. ^ a b c d e Young, G.B. (2009). "Coma". Ann. N. Y. Acad. Sci. 1157 (1): 32–47. Bibcode:2009NYASA1157...32Y. doi:10.1111/j.1749-6632.2009.04471.x.
  6. ^ "Coma Origin". Online Etymology Dictionary. Retrieved 14 August 2015.
  7. ^ "Video of man at beginning of documented 3 month coma".
  8. ^ "Video of man still nonresponsive to stimuli while in coma".
  9. ^ Russ Rowlett. "Glasgow Coma Scale". University of North Carolina at Chapel Hill.
  10. ^ Benjamin Werdro. "Induced Coma".
  11. ^ a b c Liversedge, Timothy; Hirsch, Nicholas (2010). "Coma". Anaesthesia & Intensive Care Medicine. 11 (9): 337–339. doi:10.1016/j.mpaic.2010.05.008.
  12. ^ Busl, K. M.; Greer, D. M. (2010). "Hypoxic-ischemic brain injury: Pathophysiology, neuropathology and mechanisms". NeuroRehabilitation: 5–13.
  13. ^ Daltrozzo J.; Wioland N.; Mutschler V.; Lutun P.; Jaeger A.; Calon B.; Meyer A.; Pottecher T.; Lang S.; Kotchoubey B. (2009c). "Cortical Information Processing in Coma" (PDF). Cognitive & Behavioral Neurology. 22 (1): 53–62. doi:10.1097/wnn.0b013e318192ccc8.
  14. ^ Daltrozzo J.; Wioland N.; Mutschler V.; Kotchoubey B. (2007). "Predicting Coma and other Low Responsive Patients Outcome using Event-Related Brain Potentials: A Meta-analysis" (PDF). Clinical Neurophysiology. 118: 606–614. doi:10.1016/j.clinph.2006.11.019.
  15. ^ Daltrozzo J.; Wioland N.; Mutschler V.; Lutun P.; Calon B.; Meyer A.; Jaeger A.; Pottecher T.; Kotchoubey B. (2010a). "Electrodermal Response in Coma and Other Low Responsive Patients" (PDF). Neuroscience Letters. 475 (1): 44–47. doi:10.1016/j.neulet.2010.03.043. PMID 20346390.
  16. ^ a b "Coma" (PDF). Archived from the original (PDF) on 2010-06-27. Retrieved 2010-12-08.
  17. ^ a b c Baldursdottir, S.; Sigvaldason, K.; Karason, S.; Valsson, F.; Sigurdsson, G. H. (2010). "Induced hypothermia in comatose survivors of asphyxia: a case series of 14 consecutive cases". Acta Anaesthesiol. Scand. 54 (7): 821–826. doi:10.1111/j.1399-6576.2010.02248.x. PMID 20497127.
  18. ^ Coma Care (2010-03-30). "Caring for Care Giver and Family". Retrieved 2010-12-08.
  19. ^ Edwarda O’Bara, who spent 4 decades in a coma, dies at 59
  20. ^ Aruna Shanba, who spent 42 years in coma.
  21. ^ NINDS (October 29, 2010). "Coma Information Page: National Institute of Neurological Disorders and Stroke (NINDS)". Archived from the original on December 4, 2010. Retrieved December 8, 2010.
  22. ^ Formisano R; Carlesimo GA; Sabbadini M; et al. (May 2004). "Clinical predictors and neuropleropsychological outcome in severe traumatic brain injury patients". Acta Neurochir (Wien). 146 (5): 457–62. doi:10.1007/s00701-004-0225-4. PMID 15118882.
  23. ^ "Mother stunned by coma victim's unexpected words". The Sydney Morning Herald. 2003-07-12.
  24. ^ "Electrodes stir man from six-year coma-like state". Cosmos Magazine. 2 August 2007. Archived from the original on 6 March 2014.CS1 maint: BOT: original-url status unknown (link)
  25. ^ "Post-traumatic amnesia". Archived from the original on 2012-05-11. Retrieved 2012-04-06.
  26. ^ Eelco F.M. Wijdicks, MD; Coen A. Wijdicks, BS (2006). "The portrayal of coma in contemporary motion pictures". Neurology. 66 (9): 1300–1303. doi:10.1212/01.wnl.0000210497.62202.e9. PMID 16682658. Retrieved 2009-11-25.

External links

External resources
Black Veil Brides

Black Veil Brides is an American rock band based in Hollywood, California. The group formed in 2006 in Cincinnati, Ohio and is currently composed of Andy Biersack (lead vocals), Ashley Purdy (bass, backing vocals), Jake Pitts (lead guitar), Jinxx (rhythm guitar, violin) and Christian "CC" Coma (drums). Black Veil Brides are known for their use of black makeup, body paint, tight black studded clothing, and long hair, which were all inspired by the stage personas of KISS and Mötley Crüe, as well as other 1980s glam metal acts.

Coma (cometary)

The coma is the nebulous envelope around the nucleus of a comet, formed when the comet passes close to the Sun on its highly elliptical orbit; as the comet warms, parts of it sublime. This gives a comet a "fuzzy" appearance when viewed in telescopes and distinguishes it from stars. The word coma comes from the Greek "kome" (κόμη), which means "hair" and is the origin of the word comet itself.The coma is generally made of ice and comet dust. Water dominates up to 90% of the volatiles that outflow from the nucleus when the comet is within 3-4 AU of the Sun. The H2O parent molecule is destroyed primarily through photodissociation and to a much smaller extent photoionization. The solar wind plays a minor role in the destruction of water compared to photochemistry. Larger dust particles are left along the comet's orbital path while smaller particles are pushed away from the Sun into the comet's tail by light pressure.

On 11 August 2014, astronomers released studies, using the Atacama Large Millimeter/Submillimeter Array (ALMA) for the first time, that detailed the distribution of HCN, HNC, H2CO, and dust inside the comae of comets C/2012 F6 (Lemmon) and C/2012 S1 (ISON). On 2 June 2015, NASA reported that the ALICE spectrograph on the Rosetta space probe studying comet 67P/Churyumov–Gerasimenko determined that electrons (within 1 km (0.62 mi) above the comet nucleus) produced from photoionization of water molecules by solar radiation, and not photons from the Sun as thought earlier, are responsible for the degradation of water and carbon dioxide molecules released from the comet nucleus into its coma.

Coma Berenices

Coma Berenices is an ancient asterism in the northern sky which has been defined as one of the 88 modern constellations. It is located in the fourth galactic quadrant, between Leo and Boötes, and is visible in both hemispheres. Its name means "Berenice's Hair" in Latin and refers to Queen Berenice II of Egypt, who sacrificed her long hair as a votive offering. It was introduced to Western astronomy during the third century BC by Conon of Samos and was further corroborated as a constellation by Gerardus Mercator and Tycho Brahe. Coma Berenices is the only modern constellation named for a historic person.

The constellation's major stars are Alpha Comae Berenices, Beta Comae Berenices and Gamma Comae Berenices. They form a 45-degree triangle, from which Berenice's imaginary tresses, formed by the Coma Star Cluster, hang. The constellation's brightest star is Beta Comae Berenices, a 4.2-magnitude main sequence star similar to the Sun. Coma Berenices contains the North Galactic Pole and one of the richest known galaxy clusters, the Coma Cluster, part of the Coma Supercluster. Galaxy Malin 1, in the constellation, is the first-known giant low-surface-brightness galaxy. Supernova SN 2005ap discovered in Coma Berenices is the second-brightest known, and SN 1940B was the first observed example of a type II supernova. The star FK Comae Berenices is the prototype of an eponymous class of variable stars. The constellation is the radiant of one meteor shower, Coma Berenicids, which has one of the fastest meteor speeds, up to 65 kilometres per second (40 mi/s).

Coma Berenices (album)

Coma Berenices is an album by the Japanese noise musician Merzbow.

Comet

A comet is an icy, small Solar System body that, when passing close to the Sun, warms and begins to release gases, a process called outgassing. This produces a visible atmosphere or coma, and sometimes also a tail. These phenomena are due to the effects of solar radiation and the solar wind acting upon the nucleus of the comet. Comet nuclei range from a few hundred metres to tens of kilometres across and are composed of loose collections of ice, dust, and small rocky particles. The coma may be up to 15 times the Earth's diameter, while the tail may stretch one astronomical unit. If sufficiently bright, a comet may be seen from the Earth without the aid of a telescope and may subtend an arc of 30° (60 Moons) across the sky. Comets have been observed and recorded since ancient times by many cultures.

Comets usually have highly eccentric elliptical orbits, and they have a wide range of orbital periods, ranging from several years to potentially several millions of years. Short-period comets originate in the Kuiper belt or its associated scattered disc, which lie beyond the orbit of Neptune. Long-period comets are thought to originate in the Oort cloud, a spherical cloud of icy bodies extending from outside the Kuiper belt to halfway to the nearest star. Long-period comets are set in motion towards the Sun from the Oort cloud by gravitational perturbations caused by passing stars and the galactic tide. Hyperbolic comets may pass once through the inner Solar System before being flung to interstellar space. The appearance of a comet is called an apparition.

Comets are distinguished from asteroids by the presence of an extended, gravitationally unbound atmosphere surrounding their central nucleus. This atmosphere has parts termed the coma (the central part immediately surrounding the nucleus) and the tail (a typically linear section consisting of dust or gas blown out from the coma by the Sun's light pressure or outstreaming solar wind plasma). However, extinct comets that have passed close to the Sun many times have lost nearly all of their volatile ices and dust and may come to resemble small asteroids. Asteroids are thought to have a different origin from comets, having formed inside the orbit of Jupiter rather than in the outer Solar System. The discovery of main-belt comets and active centaur minor planets has blurred the distinction between asteroids and comets. In the early 21st century, the discovery of some minor bodies with long-period comet orbits, but characteristics of inner solar system asteroids, were called Manx comets. They are still classified as comets, such as C/2014 S3 (PANSTARRS). 27 Manx comets were found from 2013 to 2017.As of July 2018 there are 6,339 known comets, a number that is steadily increasing as they are discovered. However, this represents only a tiny fraction of the total potential comet population, as the reservoir of comet-like bodies in the outer Solar System (in the Oort cloud) is estimated to be one trillion. Roughly one comet per year is visible to the naked eye, though many of those are faint and unspectacular. Particularly bright examples are called "great comets". Comets have been visited by unmanned probes such as the European Space Agency's Rosetta, which became the first ever to land a robotic spacecraft on a comet, and NASA's Deep Impact, which blasted a crater on Comet Tempel 1 to study its interior.

Diabetic coma

Diabetic coma is a reversible form of coma found in people with diabetes mellitus. It is a medical emergency.Three different types of diabetic coma are identified:

Severe low blood sugar in a diabetic person

Diabetic ketoacidosis (usually type 1) advanced enough to result in unconsciousness from a combination of a severely increased blood sugar level, dehydration and shock, and exhaustion

Hyperosmolar nonketotic coma (usually type 2) in which an extremely high blood sugar level and dehydration alone are sufficient to cause unconsciousness.In most medical contexts, the term diabetic coma refers to the diagnostical dilemma posed when a physician is confronted with an unconscious patient about whom nothing is known except that they have diabetes. An example might be a physician working in an emergency department who receives an unconscious patient wearing a medical identification tag saying DIABETIC. Paramedics may be called to rescue an unconscious person by friends who identify them as diabetic. Brief descriptions of the three major conditions are followed by a discussion of the diagnostic process used to distinguish among them, as well as a few other conditions which must be considered.

An estimated 2 to 15 percent of people with diabetes will suffer from at least one episode of diabetic coma in their lifetimes as a result of severe hypoglycemia.

Extinct comet

An extinct comet is a comet that has expelled most of its volatile ice and has little left to form a tail and coma. In a dormant comet, rather than being depleted, any remaining volatile components have been sealed beneath an inactive surface layer.

Due to the near lack of a coma and tail, an extinct or dormant comet may resemble an asteroid rather than a comet and blur the distinction between these two classes of small Solar System bodies. When volatile materials such as nitrogen, water, carbon dioxide, ammonia, hydrogen and methane in the comet nucleus have evaporated away, all that remains is an inert rock or rubble pile. A comet may go through a transition phase as it comes close to extinction.

Glasgow Coma Scale

The Glasgow Coma Scale (GCS) is a neurological scale which aims to give a reliable and objective way of recording the conscious state of a person for initial as well as subsequent assessment. A person is assessed against the criteria of the scale, and the resulting points give a person's score between 3 (indicating deep unconsciousness) and either 14 (original scale) or 15 (more widely used modified or revised scale).

GCS was initially used to assess a person's level of consciousness after a head injury, and the scale is now used by first responders, EMS, nurses, and doctors as being applicable to all acute medical and trauma patients. In hospitals it is also used in monitoring chronic patients in intensive care.

The scale was published in 1974 by Graham Teasdale and Bryan J. Jennett, professors of neurosurgery at the University of Glasgow's Institute of Neurological Sciences at the city's Southern General Hospital.

GCS is used as part of several ICU scoring systems, including APACHE II, SAPS II, and SOFA, to assess the status of the central nervous system, as it was designed for. The initial indication for use of the GCS was serial assessments of people with traumatic brain injury and coma for at least 6 hours in the neurosurgical ICU setting, though it is commonly used throughout hospital departments. A similar scale, the Rancho Los Amigos Scale is used to assess the recovery of traumatic brain injury.

GCS was updated following a review of the helpfulness and usefulness of the scale from Clinicians. It was decided that several things required updating, like the Eye Response element, meaning that instead of responding to "Painful Stimuli" being regarded as a 2, a person that opens their eyes in response to pressure is now considered a 2 in the Eye Response element.

Hepatic encephalopathy

Hepatic encephalopathy (HE) is an altered level of consciousness as a result of liver failure. Onset may be gradual or sudden. Other symptoms may include movement problems, changes in mood, or changes in personality. In the advanced stages it can result in a coma.Hepatic encephalopathy can occur in those with acute or chronic liver disease. Episodes can be triggered by infections, GI bleeding, constipation, electrolyte problems, or certain medications. The underlying mechanism is believed to involve the buildup of ammonia in the blood, a substance that is normally removed by the liver. The diagnosis is typically made after ruling out other potential causes. It may be supported by blood ammonia levels, an electroencephalogram, or a CT scan of the brain.Hepatic encephalopathy is possibly reversible with treatment. This typically involves supportive care and addressing the triggers of the event. Lactulose is frequently used to decrease ammonia levels. Certain antibiotics and probiotics are other potential options. A liver transplant may improve outcomes in those with severe disease.More than 40% of people with cirrhosis develop hepatic encephalopathy. More than half of those with cirrhosis and significant HE live less than a year. In those who are able to get a liver transplant, the risk of death is less than 30% over the subsequent five years. The condition has been described since at least 1860.

Hyperosmolar hyperglycemic state

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. Symptoms include signs of dehydration, weakness, legs cramps, vision problems, and an altered level of consciousness. Onset is typically over days to weeks. Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis.The main risk factor is a history of diabetes mellitus type 2. Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1. Triggers include infections, stroke, trauma, certain medications, and heart attacks. Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), osmolarity greater than 320 mOsm/kg, and a pH above 7.3.Initial treatment generally consists of intravenous fluids to manage dehydration, intravenous insulin in those with significant ketones, low molecular weight heparin to decrease the risk of blood clotting, and antibiotics among those in whom there is concerns of infection. The goal is a slow decline in blood sugar levels. Potassium replacement is often required as the metabolic problems are corrected. Efforts to prevent diabetic foot ulcers are also important. It typically takes a few days for the person to return to baseline.While the exact frequency of the condition is unknown, it is relatively common. Older people are most commonly affected. The risk of death among those affected is about 15%. It was first described in the 1880s.

Hypoglycemia

Hypoglycemia, also known as low blood sugar, is when blood sugar decreases to below normal levels. This may result in a variety of symptoms including clumsiness, trouble talking, confusion, loss of consciousness, seizures or death. A feeling of hunger, sweating, shakiness and weakness may also be present. Symptoms typically come on quickly.The most common cause of hypoglycemia is medications used to treat diabetes mellitus such as insulin and sulfonylureas. Risk is greater in diabetics who have eaten less than usual, exercised more than usual or have drunk alcohol. Other causes of hypoglycemia include kidney failure, certain tumors, such as insulinoma, liver disease, hypothyroidism, starvation, inborn error of metabolism, severe infections, reactive hypoglycemia and a number of drugs including alcohol. Low blood sugar may occur in otherwise healthy babies who have not eaten for a few hours.The glucose level that defines hypoglycemia is variable. In people with diabetes, levels below 3.9 mmol/L (70 mg/dL) is diagnostic. In adults without diabetes, symptoms related to low blood sugar, low blood sugar at the time of symptoms and improvement when blood sugar is restored to normal confirm the diagnosis. Otherwise, a level below 2.8 mmol/L (50 mg/dL) after not eating or following exercise may be used. In newborns, a level below 2.2 mmol/L (40 mg/dL), or less than 3.3 mmol/L (60 mg/dL) if symptoms are present, indicates hypoglycemia. Other tests that may be useful in determining the cause include insulin and C peptide levels in the blood.Among people with diabetes, prevention is by matching the foods eaten with the amount of exercise and the medications used. When people feel their blood sugar is low, testing with a glucose monitor is recommended. Some people have few initial symptoms of low blood sugar, and frequent routine testing in this group is recommended. Treatment of hypoglycemia is by eating foods high in simple sugars or taking dextrose. If a person is not able to take food by mouth, an injection of glucagon may help. The treatment of hypoglycemia unrelated to diabetes includes treating the underlying problem as well and a healthy diet. The term "hypoglycemia" is sometimes incorrectly used to refer to idiopathic postprandial syndrome, a controversial condition with similar symptoms that occur following eating but with normal blood sugar levels.

Induced coma

An induced coma, also known as a medically induced coma, a barbiturate-induced coma, or a barb coma, is a temporary coma (a deep state of unconsciousness) brought on by a controlled dose of a barbiturate drug, usually pentobarbital or thiopental. Barbiturate comas are used to protect the brain during major neurosurgery, as a last line of treatment in certain cases of status epilepticus that have not responded to other treatments, and in refractory intracranial hypertension following traumatic brain injury.

Induced coma was a feature of the Milwaukee protocol, a now-discredited method that was promoted as a means of treating rabies infection in people.Induced coma usually results in significant systemic adverse effects. The patient is likely to completely lose respiratory drive and require mechanical ventilation. Gut motility is reduced. Hypotension can complicate efforts to maintain cerebral perfusion pressure and often requires the use of vasopressor drugs. Hypokalemia often results. And the completely immobile patient is at increased risk of bed sores as well as infection from indwelling lines.

La Coma i la Pedra

La Coma i la Pedra is a municipality in the comarca of the Solsonès in Catalonia, Spain. It is situated in the Lord valley in the north of the comarca. The Cardener river has its source in the territory of the municipality. The local economy is traditionally based on livestock raising, although there is also a ski resort in the pyrenean massif of Port del Comte and a power station at Gafa. Local roads link the municipality with Sant Llorenç de Morunys and Josa i Tuixén.

Messier 99

Messier 99 or M99, also known as NGC 4254, is a grand design spiral galaxy in the northern constellation Coma Berenices approximately 15 megaparsecs (49 megalight-years) in distance from the Milky Way. It was discovered by Pierre Méchain on March 17, 1781. The discovery was then reported to Charles Messier, who included the object in the Messier Catalogue of comet-like objects. Messier 99 was one of the first galaxies in which a spiral pattern was seen. This pattern was first identified by Lord Rosse in the spring of 1846.This galaxy has a morphological classification of SA(s)c, indicating a pure spiral shape with loosely wound arms. It has a peculiar shape with one normal looking arm and an extended arm that is less tightly wound. The galaxy is inclined by 42° to the line-of-sight with a major axis position angle of 68°. Four supernovae have been observed in this galaxy: SN 1967H (type II), 1972Q, 1986I (type II), and 2014L (type Ic).A bridge of neutral hydrogen gas links NGC 4254 with VIRGOHI21, an HI region and a possible dark galaxy. The gravity from the latter may have distorted M99 and drawn out the gas bridge, as the two galaxy-sized objects may have had a close encounter before they went their separate ways. However, VIRGOHI21 may instead be tidal debris from an interaction with the lenticular galaxy NGC 4262 some 280 million years ago. It is expected that the drawn out arm will relax to match the normal arm once the encounter is over.

While not classified as a starburst galaxy, M99 has a star formation activity three times larger than other galaxies of similar Hubble type that may have been triggered by the encounter. M99 is likely entering the Virgo Cluster for the first time and is located at the periphery of the cluster at a projected separation of 3.7°, or around one megaparsec, from the cluster center at Messier 87. The galaxy is undergoing ram-pressure stripping as it moves through the intracluster medium.

Myxedema coma

Myxedema coma is a state of decompensated hypothyroidism. A person may have lab values identical to a "normal" hypothyroid state, but a stressful event (such as an infection, myocardial infarction or stroke) precipitates the myxedema coma state, usually in the elderly. Primary symptoms of myxedema coma are altered mental status and low body temperature. Low blood sugar, low blood pressure, hyponatremia, hypercapnia, hypoxia, slowed heart rate, and hypoventilation may also occur. Myxedema, although included in the name, is not necessarily seen in myxedema coma.According to newer theories myxedema coma could result from allostatic overload in a situation where the effects of hypothyroidism are amplified by non-thyroidal illness syndrome.

NGC 4559

NGC 4559 (also known as Caldwell 36) is an intermediate spiral galaxy with a weak inner ring structure in the constellation Coma Berenices. Distance estimates for NCG 4559 range from about 29 million light-years to 51 million light-years, averaging about 29 million light-years.NGC 4559 is a member of the Coma I Group.

Persistent vegetative state

A persistent vegetative state (PVS) is a disorder of consciousness in which patients with severe brain damage are in a state of partial arousal rather than true awareness. After four weeks in a vegetative state (VS), the patient is classified as in a persistent vegetative state. This diagnosis is classified as a permanent vegetative state some months (3 in the US and 6 in the UK) after a non-traumatic brain injury or one year after a traumatic injury. Nowadays, more doctors and neuroscientists prefer to call the state of consciousness a syndrome, primarily because of ethical questions about whether a patient can be called "vegetative" or not.

Son of Coma Guy

"Son of Coma Guy" is the seventh episode of the third season of House and the fifty-third episode overall.

Virgo Cluster

The Virgo Cluster is a cluster of galaxies whose center is 53.8 ± 0.3 Mly (16.5 ± 0.1 Mpc)

away in the constellation Virgo. Comprising approximately 1300 (and possibly up to 2000) member galaxies, the cluster forms the heart of the larger Virgo Supercluster, of which the Local Group (containing the Milky Way galaxy) is an outlying member. The Local Group actually experiences the mass of the Virgo Supercluster as the Virgocentric flow. It is estimated that the Virgo Cluster's mass is 1.2×1015 M☉ out to 8 degrees of the cluster's center or a radius of about 2.2 Mpc.Many of the brighter galaxies in this cluster, including the giant elliptical galaxy Messier 87, were discovered in the late 1770s and early 1780s and subsequently included in Charles Messier's catalogue of non-cometary fuzzy objects. Described by Messier as nebulae without stars, their true nature was not recognized until the 1920s.The cluster subtends a maximum arc of approximately 8 degrees centered in the constellation Virgo. Although some of the cluster's most prominent members can be seen with smaller instruments, a 6 inch telescope will reveal about 160 of the cluster's galaxies on a clear night. Its brightest member is the elliptical galaxy Messier 49; however its most famous member is the elliptical galaxy Messier 87, which is located in the center of the cluster.

This page is based on a Wikipedia article written by authors (here).
Text is available under the CC BY-SA 3.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.